Volume 12, Issue 24

Arterial elementary calcium signaling in aging

Mario Kassmann, Gang Fan, Maik Gollasch,

https://doi.org/10.18632/aging.104220 pp 24476—24478

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Kassmann M, Fan G, Gollasch M, . Arterial elementary calcium signaling in aging. . 12:24476-24478. https://doi.org/10.18632/aging.104220

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Sugar-induced dysregulation of purine metabolism impacts lifespan

Claudia Lennicke, Eliano dos Santos, Helena M. Cochemé,

https://doi.org/10.18632/aging.104223 pp 24479—24480

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The Ercc1^-/Δ mouse model of accelerated senescence and aging for identification and testing of novel senotherapeutic interventions

Alec Wong, Tra Kieu, Paul D. Robbins,

https://doi.org/10.18632/aging.202321 pp 24481—24483

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Wong A, Kieu T, Robbins PD, . The Ercc1^-/Δ mouse model of accelerated senescence and aging for identification and testing of novel senotherapeutic interventions. . 12:24481-24483. https://doi.org/10.18632/aging.202321

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Provider: 
 TY - JOUR
 AU - Wong, Alec 
 AU - Kieu, Tra 
 AU - Robbins, Paul D. 
 TI - The Ercc1-/Δ mouse model of accelerated senescence and aging for identification and testing of novel senotherapeutic interventions
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.202321
 DO - 10.18632/aging.202321
 SP - 24481
 EP - 24483
 PY - 
 AB - Progeroid murine models represent an emerging tool to investigate mechanisms of aging in an expedient and efficient manner. One prominent mechanism of aging is the accumulation of DNA damage and subsequent increase in cellular senescence, leading to age related pathologies. Ercc1-/&#x394; hypomorphic mice, which have a reduced level of the ERCC1-XPF DNA repair endonuclease complex, accumulate spontaneously occurring endogenous DNA damage similar to naturally aged mice, but at a faster rate. The resulting genomic damage gives rise to a senescent cell burden that is comparable to that of a naturally aged mouse. In fact, the expression of senescence and senescence-associated secretory phenotype (SASP) markers in 4-5-month-old Ercc1-/&#x394; mice, along with other measurements of senescence, were equivalent and never exceeded the extent of that found in naturally aged mice. Furthermore, many features of both natural murine aging and human aging are present in Ercc1-/&#x394; mice. An emerging use of these mice is the ability to study age-related signaling pathways, including identifying different types of senescent cells and their key senescent cell anti-apoptotic pathways (SCAPs). Most importantly, this model represents a rapid, cost-effective mouse model for the evaluation in vivo of senolytic drugs and other gerotherapeutics.
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ARDD 2020: from aging mechanisms to interventions

Garik V. Mkrtchyan, Kotb Abdelmohsen, Pénélope Andreux, Ieva Bagdonaite, Nir Barzilai, Søren Brunak, Filipe Cabreiro, Rafael de Cabo, Judith Campisi, Ana Maria Cuervo, Marco Demaria, Collin Y. Ewald, Evandro Fei Fang, Richard Faragher, Luigi Ferrucci, Adam Freund, Carlos G. Silva-García, Anastasia Georgievskaya, Vadim N. Gladyshev, David J. Glass, Vera Gorbunova, Aubrey de Grey, Wei-Wu He, Jan Hoeijmakers, Eva Hoffmann, Steve Horvath, Riekelt H. Houtkooper, Majken K. Jensen, Martin Borch Jensen, Alice Kane, Moustapha Kassem, Peter de Keizer, Brian Kennedy, Gerard Karsenty, Dudley W. Lamming, Kai-Fu Lee, Nanna MacAulay, Polina Mamoshina, Jim Mellon, Marte Molenaars, Alexey Moskalev, Andreas Mund, Laura Niedernhofer, Brenna Osborne, Heidi H. Pak, Andrey Parkhitko, Nuno Raimundo, Thomas A. Rando, Lene Juel Rasmussen, Carolina Reis, Christian G. Riedel, Anais Franco-Romero, Björn Schumacher, David A. Sinclair, Yousin Suh, Pam R. Taub, Debra Toiber, Jonas T. Treebak, Dario Riccardo Valenzano, Eric Verdin, Jan Vijg, Sergey Young, Lei Zhang, Daniela Bakula, Alex Zhavoronkov, Morten Scheibye-Knudsen,

https://doi.org/10.18632/aging.202454 pp 24484—24503

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Mkrtchyan GV, Abdelmohsen K, Andreux P, Bagdonaite I, Barzilai N, Brunak S, Cabreiro F, de Cabo R, Campisi J, Cuervo AM, Demaria M, Ewald CY, Fang EF, et al, . ARDD 2020: from aging mechanisms to interventions. . 12:24484-24503. https://doi.org/10.18632/aging.202454

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Provider: 
                TY  - JOUR
                AU  - Mkrtchyan, Garik V. 
                AU  - Abdelmohsen, Kotb 
                AU  - Andreux, Pénélope 
                AU  - Bagdonaite, Ieva 
                AU  - Barzilai, Nir 
                AU  - Brunak, Søren 
                AU  - Cabreiro, Filipe 
                AU  - de Cabo, Rafael 
                AU  - Campisi, Judith 
                AU  - Cuervo, Ana Maria 
                AU  - Demaria, Marco 
                AU  - Ewald, Collin Y. 
                AU  - Fang, Evandro Fei 
                AU  - Faragher, Richard 
                AU  - Ferrucci, Luigi 
                AU  - Freund, Adam 
                AU  - Silva-García, Carlos G. 
                AU  - Georgievskaya, Anastasia 
                AU  - Gladyshev, Vadim N. 
                AU  - Glass, David J. 
                AU  - Gorbunova, Vera 
                AU  - de Grey, Aubrey 
                AU  - He, Wei-Wu 
                AU  - Hoeijmakers, Jan 
                AU  - Hoffmann, Eva 
                AU  - Horvath, Steve 
                AU  - Houtkooper, Riekelt H. 
                AU  - Jensen, Majken K. 
                AU  - Jensen, Martin Borch 
                AU  - Kane, Alice 
                AU  - Kassem, Moustapha 
                AU  - de Keizer, Peter 
                AU  - Kennedy, Brian 
                AU  - Karsenty, Gerard 
                AU  - Lamming, Dudley W. 
                AU  - Lee, Kai-Fu 
                AU  - MacAulay, Nanna 
                AU  - Mamoshina, Polina 
                AU  - Mellon, Jim 
                AU  - Molenaars, Marte 
                AU  - Moskalev, Alexey 
                AU  - Mund, Andreas 
                AU  - Niedernhofer, Laura 
                AU  - Osborne, Brenna 
                AU  - Pak, Heidi H. 
                AU  - Parkhitko, Andrey 
                AU  - Raimundo, Nuno 
                AU  - Rando, Thomas A. 
                AU  - Rasmussen, Lene Juel 
                AU  - Reis, Carolina 
                AU  - Riedel, Christian G. 
                AU  - Franco-Romero, Anais 
                AU  - Schumacher, Björn 
                AU  - Sinclair, David A. 
                AU  - Suh, Yousin 
                AU  - Taub, Pam R. 
                AU  - Toiber, Debra 
                AU  - Treebak, Jonas T. 
                AU  - Valenzano, Dario Riccardo 
                AU  - Verdin, Eric 
                AU  - Vijg, Jan 
                AU  - Young, Sergey 
                AU  - Zhang, Lei 
                AU  - Bakula, Daniela 
                AU  - Zhavoronkov, Alex 
                AU  - Scheibye-Knudsen, Morten 
                TI  - ARDD 2020: from aging mechanisms to interventions
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202454
                DO  - 10.18632/aging.202454
                SP  - 24484
                EP  - 24503
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Mkrtchyan, Garik V. 
                AU  - Abdelmohsen, Kotb 
                AU  - Andreux, Pénélope 
                AU  - Bagdonaite, Ieva 
                AU  - Barzilai, Nir 
                AU  - Brunak, Søren 
                AU  - Cabreiro, Filipe 
                AU  - de Cabo, Rafael 
                AU  - Campisi, Judith 
                AU  - Cuervo, Ana Maria 
                AU  - Demaria, Marco 
                AU  - Ewald, Collin Y. 
                AU  - Fang, Evandro Fei 
                AU  - Faragher, Richard 
                AU  - Ferrucci, Luigi 
                AU  - Freund, Adam 
                AU  - Silva-García, Carlos G. 
                AU  - Georgievskaya, Anastasia 
                AU  - Gladyshev, Vadim N. 
                AU  - Glass, David J. 
                AU  - Gorbunova, Vera 
                AU  - de Grey, Aubrey 
                AU  - He, Wei-Wu 
                AU  - Hoeijmakers, Jan 
                AU  - Hoffmann, Eva 
                AU  - Horvath, Steve 
                AU  - Houtkooper, Riekelt H. 
                AU  - Jensen, Majken K. 
                AU  - Jensen, Martin Borch 
                AU  - Kane, Alice 
                AU  - Kassem, Moustapha 
                AU  - de Keizer, Peter 
                AU  - Kennedy, Brian 
                AU  - Karsenty, Gerard 
                AU  - Lamming, Dudley W. 
                AU  - Lee, Kai-Fu 
                AU  - MacAulay, Nanna 
                AU  - Mamoshina, Polina 
                AU  - Mellon, Jim 
                AU  - Molenaars, Marte 
                AU  - Moskalev, Alexey 
                AU  - Mund, Andreas 
                AU  - Niedernhofer, Laura 
                AU  - Osborne, Brenna 
                AU  - Pak, Heidi H. 
                AU  - Parkhitko, Andrey 
                AU  - Raimundo, Nuno 
                AU  - Rando, Thomas A. 
                AU  - Rasmussen, Lene Juel 
                AU  - Reis, Carolina 
                AU  - Riedel, Christian G. 
                AU  - Franco-Romero, Anais 
                AU  - Schumacher, Björn 
                AU  - Sinclair, David A. 
                AU  - Suh, Yousin 
                AU  - Taub, Pam R. 
                AU  - Toiber, Debra 
                AU  - Treebak, Jonas T. 
                AU  - Valenzano, Dario Riccardo 
                AU  - Verdin, Eric 
                AU  - Vijg, Jan 
                AU  - Young, Sergey 
                AU  - Zhang, Lei 
                AU  - Bakula, Daniela 
                AU  - Zhavoronkov, Alex 
                AU  - Scheibye-Knudsen, Morten 
                TI  - ARDD 2020: from aging mechanisms to interventions
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202454
                DO  - 10.18632/aging.202454
                SP  - 24484
                EP  - 24503
                PY  - 
                AB  - Aging is emerging as a druggable target with growing interest from academia, industry and investors. New technologies such as artificial intelligence and advanced screening techniques, as well as a strong influence from the industry sector may lead to novel discoveries to treat age-related diseases. The present review summarizes presentations from the 7th Annual Aging Research and Drug Discovery (ARDD) meeting, held online on the 1st to 4th of September 2020. The meeting covered topics related to new methodologies to study aging, knowledge about basic mechanisms of longevity, latest interventional strategies to target the aging process as well as discussions about the impact of aging research on society and economy. More than 2000 participants and 65 speakers joined the meeting and we already look forward to an even larger meeting next year. Please mark your calendars for the 8th ARDD meeting that is scheduled for the 31st of August to 3rd of September, 2021, at Columbia University, USA.
                ER  -

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Neuroprotective effects and mechanisms of action of nicotinamide mononucleotide (NMN) in a photoreceptor degenerative model of retinal detachment

Xiaohong Chen, João A. Amorim, Giannis A. Moustafa, Jong-Jer Lee, Zhen Yu, Kenji Ishihara, Yasuhiro Iesato, Paulo Barbisan, Takashi Ueta, Konstantina A. Togka, Lin Lu, David A. Sinclair, Demetrios G. Vavvas,

https://doi.org/10.18632/aging.202453 pp 24504—24521

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Chen X, Amorim JA, Moustafa GA, Lee J, Yu Z, Ishihara K, Iesato Y, Barbisan P, Ueta T, Togka KA, Lu L, Sinclair DA, Vavvas DG, . Neuroprotective effects and mechanisms of action of nicotinamide mononucleotide (NMN) in a photoreceptor degenerative model of retinal detachment. . 12:24504-24521. https://doi.org/10.18632/aging.202453

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Provider: 
                TY  - JOUR
                AU  - Chen, Xiaohong 
                AU  - Amorim, João A. 
                AU  - Moustafa, Giannis A. 
                AU  - Lee, Jong-Jer 
                AU  - Yu, Zhen 
                AU  - Ishihara, Kenji 
                AU  - Iesato, Yasuhiro 
                AU  - Barbisan, Paulo 
                AU  - Ueta, Takashi 
                AU  - Togka, Konstantina A. 
                AU  - Lu, Lin 
                AU  - Sinclair, David A. 
                AU  - Vavvas, Demetrios G. 
                TI  - Neuroprotective effects and mechanisms of action of nicotinamide mononucleotide (NMN) in a photoreceptor degenerative model of retinal detachment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202453
                DO  - 10.18632/aging.202453
                SP  - 24504
                EP  - 24521
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Chen, Xiaohong 
                AU  - Amorim, João A. 
                AU  - Moustafa, Giannis A. 
                AU  - Lee, Jong-Jer 
                AU  - Yu, Zhen 
                AU  - Ishihara, Kenji 
                AU  - Iesato, Yasuhiro 
                AU  - Barbisan, Paulo 
                AU  - Ueta, Takashi 
                AU  - Togka, Konstantina A. 
                AU  - Lu, Lin 
                AU  - Sinclair, David A. 
                AU  - Vavvas, Demetrios G. 
                TI  - Neuroprotective effects and mechanisms of action of nicotinamide mononucleotide (NMN) in a photoreceptor degenerative model of retinal detachment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202453
                DO  - 10.18632/aging.202453
                SP  - 24504
                EP  - 24521
                PY  - 
                AB  - Currently, no pharmacotherapy has been proven effective in treating photoreceptor degeneration in patients. Discovering readily available and safe neuroprotectants is therefore highly sought after. Here, we investigated nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide (NAD+), in a retinal detachment (RD) induced photoreceptor degeneration. NMN administration after RD resulted in a significant reduction of TUNEL+ photoreceptors, CD11b+ macrophages, and GFAP labeled glial activation; a normalization of protein carbonyl content (PCC), and a preservation of the outer nuclear layer (ONL) thickness. NMN administration significantly increased NAD+ levels, SIRT1 protein expression, and heme oxygenase-1 (HO-1) expression. Delayed NMN administration still exerted protective effects after RD. Mechanistic in vitro studies using 661W cells revealed a SIRT1/HO-1 signaling as a downstream effector of NMN-mediated protection under oxidative stress and LPS stimulation. In conclusion, NMN administration exerts neuroprotective effects on photoreceptors after RD and oxidative injury, suggesting a therapeutic avenue to treating photoreceptor degeneration.
                ER  -

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COVID-19
Mortality in an Italian nursing home during COVID-19 pandemic: correlation with gender, age, ADL, vitamin D supplementation, and limitations of the diagnostic tests

Biagio Cangiano, Letizia Maria Fatti, Leila Danesi, Giacomo Gazzano, Marina Croci, Giovanni Vitale, Luisa Gilardini, Stefania Bonadonna, Iacopo Chiodini, Chiara Francesca Caparello, Antonio Conti, Luca Persani, Marco Stramba-Badiale, Marco Bonomi,

https://doi.org/10.18632/aging.202307 pp 24522—24534

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Cangiano B, Fatti LM, Danesi L, Gazzano G, Croci M, Vitale G, Gilardini L, Bonadonna S, Chiodini I, Caparello CF, Conti A, Persani L, Stramba-Badiale M, et al, . Mortality in an Italian nursing home during COVID-19 pandemic: correlation with gender, age, ADL, vitamin D supplementation, and limitations of the diagnostic tests. . 12:24522-24534. https://doi.org/10.18632/aging.202307

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                TY  - JOUR
                AU  - Cangiano, Biagio 
                AU  - Fatti, Letizia Maria 
                AU  - Danesi, Leila 
                AU  - Gazzano, Giacomo 
                AU  - Croci, Marina 
                AU  - Vitale, Giovanni 
                AU  - Gilardini, Luisa 
                AU  - Bonadonna, Stefania 
                AU  - Chiodini, Iacopo 
                AU  - Caparello, Chiara Francesca 
                AU  - Conti, Antonio 
                AU  - Persani, Luca 
                AU  - Stramba-Badiale, Marco 
                AU  - Bonomi, Marco 
                TI  - Mortality in an Italian nursing home during COVID-19 pandemic: correlation with gender, age, ADL, vitamin D supplementation, and limitations of the diagnostic tests
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202307
                DO  - 10.18632/aging.202307
                SP  - 24522
                EP  - 24534
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cangiano, Biagio 
                AU  - Fatti, Letizia Maria 
                AU  - Danesi, Leila 
                AU  - Gazzano, Giacomo 
                AU  - Croci, Marina 
                AU  - Vitale, Giovanni 
                AU  - Gilardini, Luisa 
                AU  - Bonadonna, Stefania 
                AU  - Chiodini, Iacopo 
                AU  - Caparello, Chiara Francesca 
                AU  - Conti, Antonio 
                AU  - Persani, Luca 
                AU  - Stramba-Badiale, Marco 
                AU  - Bonomi, Marco 
                TI  - Mortality in an Italian nursing home during COVID-19 pandemic: correlation with gender, age, ADL, vitamin D supplementation, and limitations of the diagnostic tests
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202307
                DO  - 10.18632/aging.202307
                SP  - 24522
                EP  - 24534
                PY  - 
                AB  - Introduction: The COVID-19 pandemic caused an increased mortality in nursing homes due to its quick spread and the age-related high lethality.
                Results: We observed a two-month mortality of 40%, compared to 6.4% in the previous year. This increase was seen in both COVID-19 positive (43%) and negative (24%) residents, but 8 patients among those testing negative on the swab, tested positive on serological tests. Increased mortality was associated with male gender, older age, no previous vitamin D supplementation and worse &#x201C;activities of daily living (ADL)&#x201D; scores, such as Barthel index, Tinetti scale and S.OS.I.A. classification.
                Conclusion: Our data confirms a higher geriatric mortality due to COVID-19. Negative residents also had higher mortality, which we suspect is secondary to preanalytical error and a low sensitivity of the swab test in poorly compliant subjects. Male gender, older age and low scores on ADL scales (probably due to immobility) are risk factors for COVID-19 related mortality. Finally, mortality was inversely associated with vitamin D supplementation.
                Design: In this observational study, we described the two-month mortality among the 157 residents (age 60-100) of a nursing home after Sars-CoV-2 spreading, reporting the factors associated with the outcome. We also compared the diagnostic tests for Sars-CoV-2.
                ER  -

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COVID-19
Coagulopathy in patients with COVID-19: a systematic review and meta-analysis

Xiaolin Zhang, Xue Yang, Hongmei Jiao, Xinmin Liu,

https://doi.org/10.18632/aging.104138 pp 24535—24551

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Zhang X, Yang X, Jiao H, Liu X, . Coagulopathy in patients with COVID-19: a systematic review and meta-analysis. . 12:24535-24551. https://doi.org/10.18632/aging.104138

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                TY  - JOUR
                AU  - Zhang, Xiaolin 
                AU  - Yang, Xue 
                AU  - Jiao, Hongmei 
                AU  - Liu, Xinmin 
                TI  - Coagulopathy in patients with COVID-19: a systematic review and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104138
                DO  - 10.18632/aging.104138
                SP  - 24535
                EP  - 24551
                PY  - 
                AB  - COVID-19 patients frequently exhibit coagulation abnormalities and thrombotic events. In this meta-analysis, we investigated the association between coagulopathy and the severity of COVID-19 illness. Using PubMed, Embase, Cochrane, WanFang Database, CNKI, and medRxiv, a systematic literature search was conducted for studies published between December 1, 2019 and May 1, 2020. We then analyzed coagulation parameters in COVID-19 patients exhibiting less severe and more severe symptoms. All statistical analyses were performed using Stata14.0 software. A total of 3,952 confirmed COVID-19 patients from 25 studies were included in the meta-analysis. Patients with severe symptoms exhibited higher levels of D-dimer, prothrombin time (PT), and fibrinogen (FIB) than patients with less severe symptoms (SMD 0.83, 95% CI: 0.70-0.97, I2 56.9%; SMD 0.39, 95% CI: 0.14-0.64, I2 79.4%; and SMD 0.35, 95% CI: 0.17-0.53, I2 42.4%, respectively). However, platelet and activated partial thromboplastin times did not differ (SMD -0.26, 95% CI: -0.56-0.05, I2 82.2%; and SMD -0.14, 95% CI: -0.45-0.18, I2 75.7%, respectively). These findings demonstrate that hypercoagulable coagulopathy is associated with the severity of COVID-19 symptoms and that D-dimer, PT, and FIB values are the main parameters that should be considered when evaluating coagulopathy in COVID-19 patients.
                ER  -

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COVID-19
Clinical outcomes of patients hospitalized for COVID-19 versus SARS: a meta-analysis

Po-Cheng Chang, Chien-Chang Yang, Kuo-Chin Kao, Ming-Shien Wen,

https://doi.org/10.18632/aging.104139 pp 24552—24569

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Chang P, Yang C, Kao K, Wen M, . Clinical outcomes of patients hospitalized for COVID-19 versus SARS: a meta-analysis. . 12:24552-24569. https://doi.org/10.18632/aging.104139

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                TY  - JOUR
                AU  - Chang, Po-Cheng 
                AU  - Yang, Chien-Chang 
                AU  - Kao, Kuo-Chin 
                AU  - Wen, Ming-Shien 
                TI  - Clinical outcomes of patients hospitalized for COVID-19 versus SARS: a meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104139
                DO  - 10.18632/aging.104139
                SP  - 24552
                EP  - 24569
                PY  - 
                AB  - Estimating the case-fatality rate and clinical outcomes for patients with coronavirus disease 2019 (COVID-19) is crucial because health care systems must adequately prepare for outbreaks and design appropriate policies. A systematic search of PubMed, Embase, and Medline+Journal (via OVID) were conducted for relevant journal publications from database inception to May 4, 2020. Articles that reported the fatality rates and clinical outcomes of patients hospitalized for COVID-19 or severe acute respiratory syndrome (SARS) infection were included. Nine clinical reports (four SARS reports and five COVID-19 reports) with a total of 851 patients (367 and 484 patients with SARS and COVID-19, respectively) were analyzed. A greater proportion of hospitalized patients with COVID-19 had bilateral pneumonia (90.0% [76.3%&#x2013;96.2%] vs. 35.9% [21.4%&#x2013;53.6%], p &lt; 0.001) and required ventilators (23.8% [18.8%&#x2013;29.6%] vs. 15.3% [11.9%&#x2013;19.4%], p = 0.010) compared with hospitalized patients with SARS. The case-fatality rate was 9.5% (6.5%&#x2013;13.7%) and 6.1% (3.5%&#x2013;10.3%) among patients with COVID-19 and SARS, respectively (p = 0.186). The case-fatality rate among hospitalized patients with COVID-19 was comparable to that during the 2003 SARS outbreak. A higher incidence of bilateral pneumonia and increased ventilator usage were noted among patients with COVID-19 compared with patients with SARS.
                ER  -

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COVID-19
Association between ageing population, median age, life expectancy and mortality in coronavirus disease (COVID-19)

Xue-Qiang Wang, Ge Song, Zheng Yang, Ren-Jie Chen, Yi-Li Zheng, Hao-Yu Hu, Xuan Su, Pei-Jie Chen,

https://doi.org/10.18632/aging.104193 pp 24570—24578

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Wang X, Song G, Yang Z, Chen R, Zheng Y, Hu H, Su X, Chen P, . Association between ageing population, median age, life expectancy and mortality in coronavirus disease (COVID-19). . 12:24570-24578. https://doi.org/10.18632/aging.104193

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                TY  - JOUR
                AU  - Wang, Xue-Qiang 
                AU  - Song, Ge 
                AU  - Yang, Zheng 
                AU  - Chen, Ren-Jie 
                AU  - Zheng, Yi-Li 
                AU  - Hu, Hao-Yu 
                AU  - Su, Xuan 
                AU  - Chen, Pei-Jie 
                TI  - Association between ageing population, median age, life expectancy and mortality in coronavirus disease (COVID-19)
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104193
                DO  - 10.18632/aging.104193
                SP  - 24570
                EP  - 24578
                PY  - 
                AB  - As of May 5, 2020, the number of confirmed coronavirus disease (COVID-19) cases has been more than 3.5 million with 243,540 deaths. We aimed to determine the associations between ageing population, median age, life expectancy at birth and COVID-19 mortality. The numbers of COVID-19 cases and deaths in the European region were obtained from the World Health Organization database. The data on percentage of the population aged 65 and over, median age and life expectancy at birth were extracted from the World Factbook of Central Intelligence Agency. A total of 56 countries/areas in the Europe reported COVID-19 cases and deaths (1,121,853 cases and 100,938 deaths) on April 20, 2020. The results showed significant positive associations between COVID-19 mortality and ageing population (r =0.274; P =0.021), median age (r =0.255; P=0.029), male median age (r =0.284; P =0.017), female median age (r =0.224; P=0.049), life expectancy at birth (r =0.336; P=0.006), male life expectancy at birth (r =0.342; P=0.005), female life expectancy at birth (r =0.312; P=0.01) in the 56 European countries/areas. This study illustrated that COVID-19 mortality was positively associated with ageing population, median age, and life expectancy at birth.
                ER  -

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COVID-19
Characteristics of mortal COVID-19 cases compared to the survivors

Xianghui Zhou, Zhipeng Cheng, Dan Shu, Wenyi Lin, Zhangyin Ming, Wei Chen, Yu Hu,

https://doi.org/10.18632/aging.202216 pp 24579—24595

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Zhou X, Cheng Z, Shu D, Lin W, Ming Z, Chen W, Hu Y, . Characteristics of mortal COVID-19 cases compared to the survivors. . 12:24579-24595. https://doi.org/10.18632/aging.202216

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                TY  - JOUR
                AU  - Zhou, Xianghui 
                AU  - Cheng, Zhipeng 
                AU  - Shu, Dan 
                AU  - Lin, Wenyi 
                AU  - Ming, Zhangyin 
                AU  - Chen, Wei 
                AU  - Hu, Yu 
                TI  - Characteristics of mortal COVID-19 cases compared to the survivors
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202216
                DO  - 10.18632/aging.202216
                SP  - 24579
                EP  - 24595
                PY  - 
                AB  - The outbreak of coronavirus disease 2019 (COVID-19) initially occurred in December 2019 and triggered a public health emergency. The increasing number of deaths due to this disease was of great concern. Therefore, our study aimed to explore risk factors associated with COVID-19 deaths.
                After having searched the PubMed, EMBASE, and CNKI for studies published as of August 10, 2020, we selected articles and extracted data. The meta-analysis was performed using Stata 16.0 software.
                Nineteen studies were used in our meta-analysis. The proportions of comorbidities such as diabetes, hypertension, malignancies, chronic obstructive pulmonary disease, cardio-cerebrovascular disease, and chronic liver disease were statistically significantly higher in mortal COVID-19 cases. Coagulation and inflammatory markers, such as platelet count, D-dimer, prothrombin time, C-reactive protein, procalcitonin, and interleukin 6, predicted the deterioration of the disease. In addition, extracorporeal membrane oxygenation and mechanical ventilation predicted the poor prognosis during its progression.
                The COVID-19 pandemic is still evolving, placing a huge burden on healthcare facilities. Certain coagulation indicators, inflammatory indicators, and comorbidities contribute to the prognosis of patients. Our study results may help clinicians optimize the treatment and ultimately reduce the mortality rate.
                ER  -

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COVID-19
Dynamic monitoring of immune function indexes in COVID-19 patients

Yaohui Song, Huixiu Zhong, Lin Li, Minggang Yin, Yi Yin, Xiaolong Guo, Bo Zhang, Weiping Liu,

https://doi.org/10.18632/aging.202362 pp 24596—24603

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Song Y, Zhong H, Li L, Yin M, Yin Y, Guo X, Zhang B, Liu W, . Dynamic monitoring of immune function indexes in COVID-19 patients. . 12:24596-24603. https://doi.org/10.18632/aging.202362

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                TY  - JOUR
                AU  - Song, Yaohui 
                AU  - Zhong, Huixiu 
                AU  - Li, Lin 
                AU  - Yin, Minggang 
                AU  - Yin, Yi 
                AU  - Guo, Xiaolong 
                AU  - Zhang, Bo 
                AU  - Liu, Weiping 
                TI  - Dynamic monitoring of immune function indexes in COVID-19 patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202362
                DO  - 10.18632/aging.202362
                SP  - 24596
                EP  - 24603
                PY  - 
                AB  - We conducted a retrospective analysis of the clinical characteristics and dynamic variations of immune indexes in nine COVID-19 patients in Zigong, China. We used flow cytometry and enzyme-linked immunosorbent assays to measure the absolute levels of CD4 and CD8 lymphocytes and SARS-CoV-2 antibodies, respectively. We found that CRP, LDH, HBDH, CD4/CD8 and IgE levels were increased in 6/9 patients, while PA and the absolute numbers of CD4 and CD8 lymphocytes decreased in 7/9 patients. From disease onset through 63 days of follow-up, SARS-CoV-2 IgG levels were consistently higher than those of SARS-CoV-2 IgM, reaching peaks on days 28 and 13, respectively. IgM levels decreased to normal 35 days after disease onset, while IgG levels remained elevated through day 63. IgE levels varied similarly to SARS-CoV-2 IgM. Our results suggest that SARS-CoV-2 may elicit allergic immune responses in patients and that the levels of CRP, PA, LDH, and HBDH, as well as the absolute numbers of CD4 and CD8 lymphocytes could be used as early diagnostic markers of SARS-CoV-2 infection. Lastly, the dynamic variation of SARS-CoV-2 antibodies could guide the timing of blood collection for plasma exchange.
                ER  -

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Control of lifespan and survival by Drosophila NF-κB signaling through neuroendocrine cells and neuroblasts

Sinan Khor, Dongsheng Cai,

https://doi.org/10.18632/aging.104196 pp 24604—24622

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Khor S, Cai D, . Control of lifespan and survival by Drosophila NF-κB signaling through neuroendocrine cells and neuroblasts. . 12:24604-24622. https://doi.org/10.18632/aging.104196

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Provider: 
 TY - JOUR
 AU - Khor, Sinan 
 AU - Cai, Dongsheng 
 TI - Control of lifespan and survival by Drosophila NF-κB signaling through neuroendocrine cells and neuroblasts
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104196
 DO - 10.18632/aging.104196
 SP - 24604
 EP - 24622
 PY - 
 AB - We report a comparative analysis of the effects of immune activation in the fly nervous system using genetic activation models to target Drosophila NF-&#x3BA;B within Toll versus Imd pathways. Genetic gain-of-function models for either pathway pan-neuronally as well as in discrete subsets of neural cells including neuroendocrine insulin-producing cells (IPCs) or neuroblasts reduce fly lifespan, however, these phenotypes in IPCs and neuroblasts are stronger with Toll activation than Imd activation. Of note, while aging is influenced more by Toll/NF-&#x3BA;B activation in IPCs during adulthood, neuroblasts influence aging more substantially during development. The study then focused on Toll/NF-&#x3BA;B inhibition, revealing that IPCs or neuroblasts are important for the effects of lifespan and healthspan extension but in a life stage-dependent manner while some of these effects display sexual dimorphism. Importantly, co-inhibition of Toll/NF-&#x3BA;B pathway in IPCs and neuroblasts increased fly lifespan greater than either cell population, suggesting that independent mechanisms might exist. Toll/NF-&#x3BA;B inhibition in IPCs was also sufficient to enhance survival under various fatal stresses, supporting the additional benefits to fly healthspan. In conclusion, IPCs and neuroblasts are important for Drosophila NF-&#x3BA;B for controlling lifespan.
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The reliability, validity, and sensitivity of the Edmonton Frail Scale (EFS) in older adults with foot disorders

Emmanuel Navarro-Flores, Ricardo Becerro de Bengoa Vallejo, Marta Elena Losa-Iglesias, Patricia Palomo-López, César Calvo-Lobo, Daniel López-López, Eva Maria Martínez-Jiménez, Carlos Romero-Morales,

https://doi.org/10.18632/aging.202140 pp 24623—24632

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Navarro-Flores E, de Bengoa Vallejo RB, Losa-Iglesias ME, Palomo-López P, Calvo-Lobo C, López-López D, Martínez-Jiménez EM, Romero-Morales C, . The reliability, validity, and sensitivity of the Edmonton Frail Scale (EFS) in older adults with foot disorders. . 12:24623-24632. https://doi.org/10.18632/aging.202140

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                TY  - JOUR
                AU  - Navarro-Flores, Emmanuel 
                AU  - de Bengoa Vallejo, Ricardo Becerro 
                AU  - Losa-Iglesias, Marta Elena 
                AU  - Palomo-López, Patricia 
                AU  - Calvo-Lobo, César 
                AU  - López-López, Daniel 
                AU  - Martínez-Jiménez, Eva Maria 
                AU  - Romero-Morales, Carlos 
                TI  - The reliability, validity, and sensitivity of the Edmonton Frail Scale (EFS) in older adults with foot disorders
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202140
                DO  - 10.18632/aging.202140
                SP  - 24623
                EP  - 24632
                PY  - 
                AB  - The Edmonton Frail Scale (EFS) is an index employed to measure alterations related to frailty. The main objective in this research was to develop the EFS short-form (EFS-SF) and to evaluate its validity, reliability, and sensitivity to predict frailty disability outcomes in elderly patients with foot disabilities.
                Results: Exploratory factor analysis (EFA) of the EFS-SF revealed the presence of three components, as in the original EFA. There were significant differences (p &lt; 0.05) in the study population for several of the EFS and 5-item FRAIL scale indicators. The highest correlation (Pearson R = 0.871; p &lt; 0.001) was found for the first component of the EFS-SF. Finally, the Cronbach alpha was 0.864 which indicated a high level of internal consistency.
                Conclusion: The EFS-SF is a reliable and valid instrument to measure frailty in patients with and without foot disabilities.
                Method: A cross sectional descriptive study was carried out. The study population was aged over 60 years (n = 66) and comprised 29 men and 37 women. Frailty disorders were registered by using the EFS, 5-item FRAIL scale, and the Geriatricians&#x2019; Clinical Impression of Frailty (GCIF) scale. EFA was employed to locate potential constituents of the EFS, with scores ranging from 0.596 to 0.946 for each of the sub scales: (1) cognitive and general health status; (2) medication and nutrition status; and (3) functional and physiological status, thus revealing that the EFS-SF comprised three components, a reduction compared to the nine in the original EFS.
                ER  -

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The impact of physical frailty on the response to inactivated influenza vaccine in older adults

Krissy K. Moehling, Bo Zhai, William E. Schwarzmann, Uma R. Chandran, Marianna Ortiz, Mary Patricia Nowalk, David Nace, Chyongchiou J. Lin, Michael Susick, Min Z. Levine, John F. Alcorn, Richard K. Zimmerman,

https://doi.org/10.18632/aging.202207 pp 24633—24650

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Moehling KK, Zhai B, Schwarzmann WE, Chandran UR, Ortiz M, Nowalk MP, Nace D, Lin CJ, Susick M, Levine MZ, Alcorn JF, Zimmerman RK, . The impact of physical frailty on the response to inactivated influenza vaccine in older adults. . 12:24633-24650. https://doi.org/10.18632/aging.202207

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                TY  - JOUR
                AU  - Moehling, Krissy K. 
                AU  - Zhai, Bo 
                AU  - Schwarzmann, William E. 
                AU  - Chandran, Uma R. 
                AU  - Ortiz, Marianna 
                AU  - Nowalk, Mary Patricia 
                AU  - Nace, David 
                AU  - Lin, Chyongchiou J. 
                AU  - Susick, Michael 
                AU  - Levine, Min Z. 
                AU  - Alcorn, John F. 
                AU  - Zimmerman, Richard K. 
                TI  - The impact of physical frailty on the response to inactivated influenza vaccine in older adults
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202207
                DO  - 10.18632/aging.202207
                SP  - 24633
                EP  - 24650
                PY  - 
                AB  - Physical frailty&#x2019;s impact on hemagglutination inhibition antibody titers (HAI) and peripheral blood mononuclear cell (PBMC) transcriptional responses after influenza vaccination is unclear. Physical frailty was assessed using the 5-item Fried frailty phenotype in 168 community- and assisted-living adults &#x2265;55 years of age during an observational study. Blood was drawn before, 3, 7, and 28 days post-vaccination with the 2017-2018 inactivated influenza vaccine. HAI response to the A/H1N1 strain was measured at Days 0 and 28 using seropositivity, seroconversion, log2 HAI titers, and fold-rise in log2 HAI titers. RNA sequencing of PBMCs from Days 0, 3 and 7 was measured in 28 participants and compared using pathway analyses. Frailty was not significantly associated with any HAI outcome in multivariable models. Compared with non-frail participants, frail participants expressed decreased cell proliferation, metabolism, antibody production, and interferon signaling genes. Conversely, frail participants showed elevated gene expression in IL-8 signaling, T-cell exhaustion, and oxidative stress pathways compared with non-frail participants. These results suggest that reduced effectiveness of influenza vaccine among older, frail individuals may be attributed to immunosenescence-related changes in PBMCs that are not reflected in antibody levels.
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Downregulated genes by silencing MYC pathway identified with RNA-SEQ analysis as potential prognostic biomarkers in gastric adenocarcinoma

Jersey Heitor da Silva Maués, Helem Ferreira Ribeiro, Raquel de Maria Maués Sacramento, Rafael Maia de Sousa, Raíssa Pereira de Tommaso, Bruno Dourado Kovacs Machado Costa, Paulo Cardoso Soares, Paulo Pimentel Assumpção, Caroline de Fátima Aquino Moreira-Nunes, Rommel Mário Rodriguez Burbano,

https://doi.org/10.18632/aging.202260 pp 24651—24670

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Heitor da Silva Maués J, Ferreira Ribeiro H, de Maria Maués Sacramento R, Maia de Sousa R, Pereira de Tommaso R, Dourado Kovacs Machado Costa B, Cardoso Soares P, Pimentel Assumpção P, de Fátima Aquino Moreira-Nunes C, Mário Rodriguez Burbano R, . Downregulated genes by silencing MYC pathway identified with RNA-SEQ analysis as potential prognostic biomarkers in gastric adenocarcinoma. . 12:24651-24670. https://doi.org/10.18632/aging.202260

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Provider: 
 TY - JOUR
 AU - Heitor da Silva Maués, Jersey 
 AU - Ferreira Ribeiro, Helem 
 AU - de Maria Maués Sacramento, Raquel 
 AU - Maia de Sousa, Rafael 
 AU - Pereira de Tommaso, Raíssa 
 AU - Dourado Kovacs Machado Costa, Bruno 
 AU - Cardoso Soares, Paulo 
 AU - Pimentel Assumpção, Paulo 
 AU - de Fátima Aquino Moreira-Nunes, Caroline 
 AU - Mário Rodriguez Burbano, Rommel 
 TI - Downregulated genes by silencing MYC pathway identified with RNA-SEQ analysis as potential prognostic biomarkers in gastric adenocarcinoma
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.202260
 DO - 10.18632/aging.202260
 SP - 24651
 EP - 24670
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Heitor da Silva Maués, Jersey 
 AU - Ferreira Ribeiro, Helem 
 AU - de Maria Maués Sacramento, Raquel 
 AU - Maia de Sousa, Rafael 
 AU - Pereira de Tommaso, Raíssa 
 AU - Dourado Kovacs Machado Costa, Bruno 
 AU - Cardoso Soares, Paulo 
 AU - Pimentel Assumpção, Paulo 
 AU - de Fátima Aquino Moreira-Nunes, Caroline 
 AU - Mário Rodriguez Burbano, Rommel 
 TI - Downregulated genes by silencing MYC pathway identified with RNA-SEQ analysis as potential prognostic biomarkers in gastric adenocarcinoma
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.202260
 DO - 10.18632/aging.202260
 SP - 24651
 EP - 24670
 PY - 
 AB - MYC overexpression is a common phenomenon in gastric carcinogenesis. In this study, we identified genes differentially expressed with a downregulated profile in gastric cancer (GC) cell lines with silenced MYC. The TTLL12, CDKN3, CDC16, PTPRA, MZT2B, UBE2T genes were validated using qRT-PCR, western blot and immunohistochemistry in tissues of 213 patients with diffuse and intestinal GC. We identified high levels of TTLL12, MZT2B, CDC16, UBE2T, associated with early and advanced stages, lymph nodes, distant metastases and risk factors such as H. pylori. Our results show that in the diffuse GC the overexpression of CDC16 and UBE2T indicate markers of poor prognosis higher than TTLL12. That is, patients with overexpression of these two genes live less than patients with overexpression of TTLL12. In the intestinal GC, patients who overexpressed CDC16 had a significantly lower survival rate than patients who overexpressed MZT2B and UBE2T, indicating in our data a worse prognostic value of CDC16 compared to the other two genes. PTPRA and CDKN3 proved to be important for assessing tumor progression in the early and advanced stages. In summary, in this study, we identified diagnostic and prognostic biomarkers of GC under the control of MYC, related to the cell cycle and the neoplastic process.
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Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer

Javier A. Menendez, Susan K. Peirce, Adriana Papadimitropoulou, Elisabet Cuyàs, Travis Vander Steen, Sara Verdura, Luciano Vellon, Wen Y. Chen, Ruth Lupu,

https://doi.org/10.18632/aging.202289 pp 24671—24692

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Menendez JA, Peirce SK, Papadimitropoulou A, Cuyàs E, Steen TV, Verdura S, Vellon L, Chen WY, Lupu R, . Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer. . 12:24671-24692. https://doi.org/10.18632/aging.202289

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                TY  - JOUR
                AU  - Menendez, Javier A. 
                AU  - Peirce, Susan K. 
                AU  - Papadimitropoulou, Adriana 
                AU  - Cuyàs, Elisabet 
                AU  - Steen, Travis Vander 
                AU  - Verdura, Sara 
                AU  - Vellon, Luciano 
                AU  - Chen, Wen Y. 
                AU  - Lupu, Ruth 
                TI  - Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202289
                DO  - 10.18632/aging.202289
                SP  - 24671
                EP  - 24692
                PY  - 
                AB  - Progesterone receptor (PR) isoforms can drive unique phenotypes in luminal breast cancer (BC). Here, we hypothesized that PR-B and PR-A isoforms differentially modify the cross-talk between prolactin and fatty acid synthase (FASN) in BC. We profiled the responsiveness of the FASN gene promoter to prolactin in T47Dco BC cells constitutively expressing PR-A and PR-B, in the PR-null variant T47D-Y cell line, and in PR-null T47D-Y cells engineered to stably re-express PR-A (T47D-YA) or PR-B (T47D-YB). The capacity of prolactin to up-regulate FASN gene promoter activity in T47Dco cells was lost in T47D-Y and TD47-YA cells. Constitutively up-regulated FASN gene expression in T47-YB cells and its further stimulation by prolactin were both suppressed by the prolactin receptor antagonist hPRL-G129R. The ability of the FASN inhibitor C75 to decrease prolactin secretion was more conspicuous in T47-YB cells. In T47D-Y cells, which secreted notably less prolactin and downregulated prolactin receptor expression relative to T47Dco cells, FASN blockade resulted in an augmented secretion of prolactin and up-regulation of prolactin receptor expression. Our data reveal unforeseen PR-B isoform-specific regulatory actions in the cross-talk between prolactin and FASN signaling in BC. These findings might provide new PR-B/FASN-centered predictive and therapeutic modalities in luminal intrinsic BC subtypes.
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Beyond the social gradient: the role of lifelong socioeconomic status in older adults’ health trajectories

Lisa Harber-Aschan, Amaia Calderón-Larrañaga, Alexander Darin-Mattson, Xiaonan Hu, Laura Fratiglioni, Serhiy Dekhtyar,

https://doi.org/10.18632/aging.202342 pp 24693—24708

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Harber-Aschan L, Calderón-Larrañaga A, Darin-Mattson A, Hu X, Fratiglioni L, Dekhtyar S, . Beyond the social gradient: the role of lifelong socioeconomic status in older adults’ health trajectories. . 12:24693-24708. https://doi.org/10.18632/aging.202342

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                TY  - JOUR
                AU  - Harber-Aschan, Lisa 
                AU  - Calderón-Larrañaga, Amaia 
                AU  - Darin-Mattson, Alexander 
                AU  - Hu, Xiaonan 
                AU  - Fratiglioni, Laura 
                AU  - Dekhtyar, Serhiy 
                TI  - Beyond the social gradient: the role of lifelong socioeconomic status in older adults’ health trajectories
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202342
                DO  - 10.18632/aging.202342
                SP  - 24693
                EP  - 24708
                PY  - 
                AB  - Inequalities in older adults&#x2019; health rarely consider life-course aspects of socioeconomic status (SES). We examined the association between lifelong SES and old-age health trajectories, and explored the role of lifestyle factors and depressive symptoms in this association. We followed 2760 adults aged 60+ from the Swedish National Study on Care and Aging, Kungsholmen. SES groups were derived using latent class analysis incorporating seven socioeconomic measures spanning childhood, midlife, and late life. We measured health using the Health Assessment Tool, which combines gait speed, cognition, multimorbidity, and disability. Linear mixed models were used to estimate health trajectories. Four SES groups were identified: High (34.9%), Middle (40.2%), Low (21.2%), and Mixed (3.8%). The Mixed group reported greater financial difficulties in childhood and older age, but varying SES attainment in midlife. Baseline health scores indicated that Mixed SES experienced substantial cognitive and physical deficits 12 years earlier than the High SES group. Compared to the High SES group, the Mixed SES group had the fastest health deterioration (&#x3B2;&#xD7;time=&#x2212;0.07, 95% CI:&#x2212;0.11,&#x2212;0.02); other groups followed a gradient (High&gt;Middle&gt;Low). Lifestyle factors and depressive symptoms attenuated the gradient but did not explain Mixed group&#x2019;s health disadvantage. Life-long SES measures are crucial for understanding older adults&#x2019; health inequalities.
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Post-transplant colitis after kidney transplantation: clinical, endoscopic and histological features

Rossella Gioco, Lidia Puzzo, Marco Patanè, Daniela Corona, Giuseppe Trama, Pierfrancesco Veroux, Massimiliano Veroux,

https://doi.org/10.18632/aging.202345 pp 24709—24720

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Gioco R, Puzzo L, Patanè M, Corona D, Trama G, Veroux P, Veroux M, . Post-transplant colitis after kidney transplantation: clinical, endoscopic and histological features. . 12:24709-24720. https://doi.org/10.18632/aging.202345

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                TY  - JOUR
                AU  - Gioco, Rossella 
                AU  - Puzzo, Lidia 
                AU  - Patanè, Marco 
                AU  - Corona, Daniela 
                AU  - Trama, Giuseppe 
                AU  - Veroux, Pierfrancesco 
                AU  - Veroux, Massimiliano 
                TI  - Post-transplant colitis after kidney transplantation: clinical, endoscopic and histological features
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202345
                DO  - 10.18632/aging.202345
                SP  - 24709
                EP  - 24720
                PY  - 
                AB  - Chronic immunosuppression may increase the risk of post-transplant infection and medication-related injury and may also be responsible for the increased risk of gastrointestinal complications in kidney transplant recipients. Differentiating the various forms of post-transplant colitis is challenging, since most have similar clinical and histological features. This study evaluated the incidence of post-transplant gastrointestinal complications during screening colonoscopy. Kidney transplant recipients undergoing a colonoscopy for any reasons in the period 2014-2018 were included. Among the 134 patients completing the colonoscopy, 74 patients (56%) had an abnormal finding: an adenoma was found in 25 patients (18.6%), while 19 patients (14.1%) had colitis. Mycophenolic acid/related colitis was the most common colitis (6%), while 7 patients (5.2%) developed a de novo inflammatory bowel disease. Patients with post-transplant colitis were younger and with shorter time from transplant compared to patients without colitis. In conclusions, immunosuppression may predispose kidney transplant recipients to an increased risk of post-transplant colitis. Diagnostic colonoscopy should be encouraged in all transplant patients with refractory diarrhea and gastrointestinal symptoms to allow a prompt diagnosis and a timely treatment, finally improving the quality of life and long-term outcomes of affected patients.
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Age and gender related differences in load-strain response in C57Bl/6 mice

Hammad Mumtaz, Nuria Lara-Castillo, JoAnna M. Scott, Mark Begonia, Mark Dallas, Mark L. Johnson, Thiagarajan Ganesh,

https://doi.org/10.18632/aging.202350 pp 24721—24733

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Mumtaz H, Lara-Castillo N, Scott JM, Begonia M, Dallas M, Johnson ML, Ganesh T, . Age and gender related differences in load-strain response in C57Bl/6 mice. . 12:24721-24733. https://doi.org/10.18632/aging.202350

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                TY  - JOUR
                AU  - Mumtaz, Hammad 
                AU  - Lara-Castillo, Nuria 
                AU  - Scott, JoAnna M. 
                AU  - Begonia, Mark 
                AU  - Dallas, Mark 
                AU  - Johnson, Mark L. 
                AU  - Ganesh, Thiagarajan 
                TI  - Age and gender related differences in load-strain response in C57Bl/6 mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202350
                DO  - 10.18632/aging.202350
                SP  - 24721
                EP  - 24733
                PY  - 
                AB  - We examined the changes in mechanical strain response of male and female mouse tibia and ulna, using axial compression tests, to assess age-related changes in tibiae and ulnae by a non-contact strain measurement technique called the digital image correlation (DIC) and the standard strain gage. A unique aspect of the study was to compare bones from the same animal to study variations in behavior with aging. This study was conducted using male and female C57Bl/6 mice at 6, 12 and 22 months of age (N=6-7 per age and sex) using three load levels. The DIC technique was able to detect a greater number of statistically significant differences in comparison to the strain gaging method. Male ulna showed significantly higher DIC strains compared to strains captured from strain gage at all three levels of load at 6 months and in the lowest load at 12 months. DIC measurements revealed that the ulna becomes stiffer with aging for both males and females, which resulted in 0.4 to 0.8 times reduced strains in the 22-month group compared to the 6 month group. Male tibia showed three-fold increased strains in the 22 months group at 11.5 N load compared to 6 months group (p&lt;.05).
                ER  -

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Biological characteristics of aging in human acute myeloid leukemia cells: the possible importance of aldehyde dehydrogenase, the cytoskeleton and altered transcriptional regulation

Maria Hernandez-Valladares, Elise Aasebø, Frode Berven, Frode Selheim, Øystein Bruserud,

https://doi.org/10.18632/aging.202361 pp 24734—24777

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Hernandez-Valladares M, Aasebø E, Berven F, Selheim F, Bruserud Ø, . Biological characteristics of aging in human acute myeloid leukemia cells: the possible importance of aldehyde dehydrogenase, the cytoskeleton and altered transcriptional regulation. . 12:24734-24777. https://doi.org/10.18632/aging.202361

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                TY  - JOUR
                AU  - Hernandez-Valladares, Maria 
                AU  - Aasebø, Elise 
                AU  - Berven, Frode 
                AU  - Selheim, Frode 
                AU  - Bruserud, Øystein 
                TI  - Biological characteristics of aging in human acute myeloid leukemia cells: the possible importance of aldehyde dehydrogenase, the cytoskeleton and altered transcriptional regulation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202361
                DO  - 10.18632/aging.202361
                SP  - 24734
                EP  - 24777
                PY  - 
                AB  - Patients with acute myeloid leukemia (AML) have a median age of 65-70 years at diagnosis. Elderly patients have more chemoresistant disease, and this is partly due to decreased frequencies of favorable and increased frequencies of adverse genetic abnormalities. However, aging-dependent differences may also contribute. We therefore compared AML cell proteomic and phosphoproteomic profiles for (i) elderly low-risk and younger low-risk patients with favorable genetic abnormalities; and (ii) high-risk patients with adverse genetic abnormalities and a higher median age against all low-risk patients with lower median age. Elderly low-risk and younger low-risk patients showed mainly phosphoproteomic differences especially involving transcriptional regulators and cytoskeleton. When comparing high-risk and low-risk patients both proteomic and phosphoproteomic studies showed differences involving cytoskeleton and immunoregulation but also transcriptional regulation and cell division. The age-associated prognostic impact of cyclin-dependent kinases was dependent on the cellular context. The protein level of the adverse prognostic biomarker mitochondrial aldehyde dehydrogenase (ALDH2) showed a similar significant upregulation both in elderly low-risk and elderly high-risk patients. Our results suggest that molecular mechanisms associated with cellular aging influence chemoresistance of AML cells, and especially the cytoskeleton function may then influence cellular hallmarks of aging, e.g. mitosis, polarity, intracellular transport and adhesion.
                ER  -

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L-PGDS deficiency accelerated the development of naturally occurring age-related osteoarthritis

Yassine Ouhaddi, Mehdi Najar, Frédéric Paré, Bertrand Lussier, Yoshihiro Urade, Mohamed Benderdour, Jean-Pierre Pelletier, Johanne Martel-Pelletier, Hassan Fahmi,

https://doi.org/10.18632/aging.202367 pp 24778—24797

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Ouhaddi Y, Najar M, Paré F, Lussier B, Urade Y, Benderdour M, Pelletier J, Martel-Pelletier J, Fahmi H, . L-PGDS deficiency accelerated the development of naturally occurring age-related osteoarthritis. . 12:24778-24797. https://doi.org/10.18632/aging.202367

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                TY  - JOUR
                AU  - Ouhaddi, Yassine 
                AU  - Najar, Mehdi 
                AU  - Paré, Frédéric 
                AU  - Lussier, Bertrand 
                AU  - Urade, Yoshihiro 
                AU  - Benderdour, Mohamed 
                AU  - Pelletier, Jean-Pierre 
                AU  - Martel-Pelletier, Johanne 
                AU  - Fahmi, Hassan 
                TI  - L-PGDS deficiency accelerated the development of naturally occurring age-related osteoarthritis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202367
                DO  - 10.18632/aging.202367
                SP  - 24778
                EP  - 24797
                PY  - 
                AB  - Osteoarthritis (OA) is the most common musculoskeletal disorder among the elderly. It is characterized by progressive cartilage degradation, synovial inflammation, subchondral bone remodeling and pain. Lipocalin prostaglandin D synthase (L-PGDS) is responsible for the biosynthesis of PGD2, which has been implicated in the regulation of inflammation and cartilage biology. This study aimed to evaluate the effect of L-PGDS deficiency on the development of naturally occurring age-related OA in mice.
                OA-like structural changes were assessed by histology, immunohistochemistry, and micro&#x2013;computed tomography. Pain related behaviours were assessed using the von Frey and the open-field assays.
                L-PGDS deletion promoted cartilage degradation during aging, which was associated with enhanced expression of extracellular matrix degrading enzymes, matrix metalloprotease 13 (MMP-13) and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5), and their breakdown products, C1,2C, VDIPEN and NITEG. Moreover, L-PGDS deletion enhanced subchondral bone changes, but had no effect on its angiogenesis. Additionally, L-PGDS deletion increased mechanical sensitivity and reduced spontaneous locomotor activity. Finally, we showed that the expression of L-PGDS was elevated in aged mice. Together, these findings indicate an important role for L-PGDS in naturally occurring age-related OA. They also suggest that L-PGDS may constitute a new efficient therapeutic target in OA.
                ER  -

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Effects of choral singing versus health education on cognitive decline and aging: a randomized controlled trial

Lei Feng, Rafael Romero-Garcia, John Suckling, Jasmine Tan, Anis Larbi, Irwin Cheah, Glenn Wong, Maurine Tsakok, Bernard Lanskey, Darius Lim, Jialiang Li, Joanna Yang, Benjamin Goh, Tristan Gwee Chen Teck, Allan Ho, Xiu Wang, Jin-Tai Yu, Can Zhang, Crystal Tan, Michelle Chua, Junhua Li, John J Totman, Caroline Wong, Marie Loh, Roger Foo, Chay Hoon Tan, Lee Gan Goh, Rathi Mahendran, Brian K. Kennedy, Ee-Heok Kua,

https://doi.org/10.18632/aging.202374 pp 24798—24816

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Feng L, Romero-Garcia R, Suckling J, Tan J, Larbi A, Cheah I, Wong G, Tsakok M, Lanskey B, Lim D, Li J, Yang J, Goh B, et al, . Effects of choral singing versus health education on cognitive decline and aging: a randomized controlled trial. . 12:24798-24816. https://doi.org/10.18632/aging.202374

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                TY  - JOUR
                AU  - Feng, Lei 
                AU  - Romero-Garcia, Rafael 
                AU  - Suckling, John 
                AU  - Tan, Jasmine 
                AU  - Larbi, Anis 
                AU  - Cheah, Irwin 
                AU  - Wong, Glenn 
                AU  - Tsakok, Maurine 
                AU  - Lanskey, Bernard 
                AU  - Lim, Darius 
                AU  - Li, Jialiang 
                AU  - Yang, Joanna 
                AU  - Goh, Benjamin 
                AU  - Teck, Tristan Gwee Chen 
                AU  - Ho, Allan 
                AU  - Wang, Xiu 
                AU  - Yu, Jin-Tai 
                AU  - Zhang, Can 
                AU  - Tan, Crystal 
                AU  - Chua, Michelle 
                AU  - Li, Junhua 
                AU  - Totman, John J 
                AU  - Wong, Caroline 
                AU  - Loh, Marie 
                AU  - Foo, Roger 
                AU  - Tan, Chay Hoon 
                AU  - Goh, Lee Gan 
                AU  - Mahendran, Rathi 
                AU  - Kennedy, Brian K. 
                AU  - Kua, Ee-Heok 
                TI  - Effects of choral singing versus health education on cognitive decline and aging: a randomized controlled trial
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202374
                DO  - 10.18632/aging.202374
                SP  - 24798
                EP  - 24816
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Feng, Lei 
                AU  - Romero-Garcia, Rafael 
                AU  - Suckling, John 
                AU  - Tan, Jasmine 
                AU  - Larbi, Anis 
                AU  - Cheah, Irwin 
                AU  - Wong, Glenn 
                AU  - Tsakok, Maurine 
                AU  - Lanskey, Bernard 
                AU  - Lim, Darius 
                AU  - Li, Jialiang 
                AU  - Yang, Joanna 
                AU  - Goh, Benjamin 
                AU  - Teck, Tristan Gwee Chen 
                AU  - Ho, Allan 
                AU  - Wang, Xiu 
                AU  - Yu, Jin-Tai 
                AU  - Zhang, Can 
                AU  - Tan, Crystal 
                AU  - Chua, Michelle 
                AU  - Li, Junhua 
                AU  - Totman, John J 
                AU  - Wong, Caroline 
                AU  - Loh, Marie 
                AU  - Foo, Roger 
                AU  - Tan, Chay Hoon 
                AU  - Goh, Lee Gan 
                AU  - Mahendran, Rathi 
                AU  - Kennedy, Brian K. 
                AU  - Kua, Ee-Heok 
                TI  - Effects of choral singing versus health education on cognitive decline and aging: a randomized controlled trial
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202374
                DO  - 10.18632/aging.202374
                SP  - 24798
                EP  - 24816
                PY  - 
                AB  - We conducted a randomized controlled trial to examine choral singing&#x2019;s effect on cognitive decline in aging. Older Singaporeans who were at high risk of future dementia were recruited: 47 were assigned to choral singing intervention (CSI) and 46 were assigned to health education program (HEP). Participants attended weekly one-hour choral singing or weekly one-hour health education for two years. Change in cognitive function was measured by a composite cognitive test score (CCTS) derived from raw scores of neuropsychological tests; biomarkers included brain magnetic resonance imaging, oxidative damage and immunosenescence. The average age of the participants were 70 years and 73/93 (78.5%) were female. The change of CCTS from baseline to 24 months was 0.05 among participants in the CSI group and -0.1 among participants in the HEP group. The between-group difference (0.15, p=0.042) became smaller (0.12, p=0.09) after adjusting for baseline CCTS. No between-group differences on biomarkers were observed. Our data support the role of choral singing in improving cognitive health in aging. The beneficial effect is at least comparable than that of health education in preventing cognitive decline in a community of elderly people. Biological mechanisms underlying the observed efficacy should be further studied.
                ER  -

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A DNA methylation age predictor for zebrafish

Benjamin Mayne, Darren Korbie, Lisa Kenchington, Ben Ezzy, Oliver Berry, Simon Jarman,

https://doi.org/10.18632/aging.202400 pp 24817—24835

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Mayne B, Korbie D, Kenchington L, Ezzy B, Berry O, Jarman S, . A DNA methylation age predictor for zebrafish. . 12:24817-24835. https://doi.org/10.18632/aging.202400

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                TY  - JOUR
                AU  - Mayne, Benjamin 
                AU  - Korbie, Darren 
                AU  - Kenchington, Lisa 
                AU  - Ezzy, Ben 
                AU  - Berry, Oliver 
                AU  - Jarman, Simon 
                TI  - A DNA methylation age predictor for zebrafish
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202400
                DO  - 10.18632/aging.202400
                SP  - 24817
                EP  - 24835
                PY  - 
                AB  - Changes in DNA methylation at specific CpG sites have been used to build predictive models to estimate animal age, predominantly in mammals. Little testing for this effect has been conducted in other vertebrate groups, such as bony fish, the largest vertebrate class. The development of most age-predictive models has relied on a genome-wide sequencing method to obtain a DNA methylation level, which makes it costly to deploy as an assay to estimate age in many samples. Here, we have generated a reduced representation bisulfite sequencing data set of caudal fin tissue from a model fish species, zebrafish (Danio rerio), aged from 11.9-60.1 weeks. We identified changes in methylation at specific CpG sites that correlated strongly with increasing age. Using an optimised unique set of 26 CpG sites we developed a multiplex PCR assay that predicts age with an average median absolute error rate of 3.2 weeks in zebrafish between 10.9-78.1 weeks of age. We also demonstrate the use of multiplex PCR as an efficient quantitative approach to measure DNA methylation for the use of age estimation. This study highlights the potential further use of DNA methylation as an age estimation method in non-mammalian vertebrate species.
                ER  -

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miR-106b suppresses pathological retinal angiogenesis

Catherine Ménard, Ariel M. Wilson, Agnieszka Dejda, Khalil Miloudi, François Binet, Sergio Crespo-Garcia, Célia Parinot, Frédérique Pilon, Rachel Juneau, Elisabeth MMA Andriessen, Gaëlle Mawambo, John Paul SanGiovanni, Vincent De Guire, Przemyslaw Sapieha,

https://doi.org/10.18632/aging.202404 pp 24836—24852

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Ménard C, Wilson AM, Dejda A, Miloudi K, Binet F, Crespo-Garcia S, Parinot C, Pilon F, Juneau R, Andriessen EM, Mawambo G, SanGiovanni JP, De Guire V, et al, . miR-106b suppresses pathological retinal angiogenesis. . 12:24836-24852. https://doi.org/10.18632/aging.202404

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                TY  - JOUR
                AU  - Ménard, Catherine 
                AU  - Wilson, Ariel M.
                AU  - Dejda, Agnieszka 
                AU  - Miloudi, Khalil 
                AU  - Binet, François 
                AU  - Crespo-Garcia, Sergio 
                AU  - Parinot, Célia 
                AU  - Pilon, Frédérique 
                AU  - Juneau, Rachel 
                AU  - Andriessen, Elisabeth MMA
                AU  - Mawambo, Gaëlle 
                AU  - SanGiovanni, John Paul
                AU  - De Guire, Vincent 
                AU  - Sapieha, Przemyslaw 
                TI  - miR-106b suppresses pathological retinal angiogenesis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202404
                DO  - 10.18632/aging.202404
                SP  - 24836
                EP  - 24852
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ménard, Catherine 
                AU  - Wilson, Ariel M.
                AU  - Dejda, Agnieszka 
                AU  - Miloudi, Khalil 
                AU  - Binet, François 
                AU  - Crespo-Garcia, Sergio 
                AU  - Parinot, Célia 
                AU  - Pilon, Frédérique 
                AU  - Juneau, Rachel 
                AU  - Andriessen, Elisabeth MMA
                AU  - Mawambo, Gaëlle 
                AU  - SanGiovanni, John Paul
                AU  - De Guire, Vincent 
                AU  - Sapieha, Przemyslaw 
                TI  - miR-106b suppresses pathological retinal angiogenesis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202404
                DO  - 10.18632/aging.202404
                SP  - 24836
                EP  - 24852
                PY  - 
                AB  - MicroRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression. We recently demonstrated that levels of miR-106b were significantly decreased in the vitreous and plasma of patients with neovascular age-related macular degeneration (AMD). Here we show that expression of the miR-106b-25 cluster is negatively regulated by the unfolded protein response pathway of protein kinase RNA-like ER kinase (PERK) in a mouse model of neovascular AMD. A reduction in levels of miR-106b triggers vascular growth both in vivo and in vitro by inducing production of pro-angiogenic factors. We demonstrate that therapeutic delivery of miR-106b to the retina with lentiviral vectors protects against aberrant retinal angiogenesis in two distinct mouse models of pathological retinal neovascularization. Results from this study suggest that miRNAs such as miR-106b have the potential to be used as multitarget therapeutics for conditions characterized by pathological retinal angiogenesis.
                ER  -

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Aberrant RhoA activation in macrophages increases senescence-associated secretory phenotypes and ectopic calcification in muscular dystrophic mice

Xiaodong Mu, Chi-Yi Lin, William S. Hambright, Ying Tang, Sudheer Ravuri, Aiping Lu, Polina Matre, Wanqun Chen, Xueqin Gao, Yan Cui, Ling Zhong, Bing Wang, Johnny Huard,

https://doi.org/10.18632/aging.202413 pp 24853—24871

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Mu X, Lin C, Hambright WS, Tang Y, Ravuri S, Lu A, Matre P, Chen W, Gao X, Cui Y, Zhong L, Wang B, Huard J, . Aberrant RhoA activation in macrophages increases senescence-associated secretory phenotypes and ectopic calcification in muscular dystrophic mice. . 12:24853-24871. https://doi.org/10.18632/aging.202413

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                TY  - JOUR
                AU  - Mu, Xiaodong 
                AU  - Lin, Chi-Yi 
                AU  - Hambright, William S. 
                AU  - Tang, Ying 
                AU  - Ravuri, Sudheer 
                AU  - Lu, Aiping 
                AU  - Matre, Polina 
                AU  - Chen, Wanqun 
                AU  - Gao, Xueqin 
                AU  - Cui, Yan 
                AU  - Zhong, Ling 
                AU  - Wang, Bing 
                AU  - Huard, Johnny 
                TI  - Aberrant RhoA activation in macrophages increases senescence-associated secretory phenotypes and ectopic calcification in muscular dystrophic mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202413
                DO  - 10.18632/aging.202413
                SP  - 24853
                EP  - 24871
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Mu, Xiaodong 
                AU  - Lin, Chi-Yi 
                AU  - Hambright, William S. 
                AU  - Tang, Ying 
                AU  - Ravuri, Sudheer 
                AU  - Lu, Aiping 
                AU  - Matre, Polina 
                AU  - Chen, Wanqun 
                AU  - Gao, Xueqin 
                AU  - Cui, Yan 
                AU  - Zhong, Ling 
                AU  - Wang, Bing 
                AU  - Huard, Johnny 
                TI  - Aberrant RhoA activation in macrophages increases senescence-associated secretory phenotypes and ectopic calcification in muscular dystrophic mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202413
                DO  - 10.18632/aging.202413
                SP  - 24853
                EP  - 24871
                PY  - 
                AB  - Duchenne Muscular Dystrophy (DMD) patients often suffer from both muscle wasting and osteoporosis. Our previous studies have revealed reduced regeneration potential in skeletal muscle and bone, concomitant with ectopic calcification of soft tissues in double knockout (dKO, dystrophin-/-; utrophin-/-) mice, a severe murine model for DMD. We found significant involvement of RhoA/ROCK (Rho-Associated Protein Kinase) signaling in mediating ectopic calcification of muscles in dKO mice. However, the cellular identity of these RhoA+ cells, and the role that RhoA plays in the chronic inflammation-associated pathologies has not been elucidated. Here, we report that CD68+ macrophages are highly prevalent at the sites of ectopic calcification of dKO mice, and that these macrophages highly express RhoA. Macrophages from dKO mice feature a shift towards a more pro-inflammatory M1 polarization and an increased expression of various senescence-associated secretory phenotype (SASP) factors that was reduced with the RhoA/ROCK inhibitor Y-27632. Further, systemic inhibition of RhoA activity in dKO mice led to reduced number of RhoA+/CD68+ cells, as well as a reduction in fibrosis and ectopic calcification. Together, these data revealed that RhoA signaling may be a key regulator of imbalanced mineralization in the dystrophic musculoskeletal system and consequently a therapeutic target for the treatment of DMD or other related muscle dystrophies.
                ER  -

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Age-associated deficient recruitment of 53BP1 in G1 cells directs DNA double-strand break repair to BRCA1/CtIP-mediated DNA-end resection

Teresa Anglada, Anna Genescà, Marta Martín,

https://doi.org/10.18632/aging.202419 pp 24872—24893

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Anglada T, Genescà A, Martín M, . Age-associated deficient recruitment of 53BP1 in G1 cells directs DNA double-strand break repair to BRCA1/CtIP-mediated DNA-end resection. . 12:24872-24893. https://doi.org/10.18632/aging.202419

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                TY  - JOUR
                AU  - Anglada, Teresa 
                AU  - Genescà, Anna 
                AU  - Martín, Marta 
                TI  - Age-associated deficient recruitment of 53BP1 in G1 cells directs DNA double-strand break repair to BRCA1/CtIP-mediated DNA-end resection
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202419
                DO  - 10.18632/aging.202419
                SP  - 24872
                EP  - 24893
                PY  - 
                AB  - DNA repair mechanisms play a crucial role in maintaining genome integrity. However, the increased frequency of DNA double-strand breaks (DSBs) and genome rearrangements in aged individuals suggests an age-associated DNA repair deficiency. Previous work from our group revealed a delayed firing of the DNA damage response in human mammary epithelial cells (HMECs) from aged donors. We now report a decreased activity of the main DSB repair pathways, the canonical non-homologous end-joining (c-NHEJ) and the homologous recombination (HR) in these HMECs from older individuals. We describe here a deficient recruitment of 53BP1 to DSB sites in G1 cells, probably influenced by an altered epigenetic regulation. 53BP1 absence at some DSBs is responsible for the age-associated DNA repair defect, as it permits the ectopic formation of BRCA1 foci while still in the G1 phase. CtIP and RPA foci are also formed in G1 cells from aged donors, but RAD51 is not recruited, thus indicating that extensive DNA-end resection occurs in these breaks although HR is not triggered. These results suggest an age-associated switch of DSB repair from canonical to highly mutagenic alternative mechanisms that promote the formation of genome rearrangements, a source of genome instability that might contribute to the aging process.
                ER  -

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Obesity induced by high-fat diet is associated with critical changes in biological and molecular functions of mesenchymal stromal cells present in visceral adipose tissue

Mustafa Burak Acar, Şerife Ayaz-Güner, Giovanni Di Bernardo, Hüseyin Güner, Ayşegül Murat, Gianfranco Peluso, Servet Özcan, Umberto Galderisi,

https://doi.org/10.18632/aging.202423 pp 24894—24913

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Acar MB, Ayaz-Güner Ş, Di Bernardo G, Güner H, Murat A, Peluso G, Özcan S, Galderisi U, . Obesity induced by high-fat diet is associated with critical changes in biological and molecular functions of mesenchymal stromal cells present in visceral adipose tissue. . 12:24894-24913. https://doi.org/10.18632/aging.202423

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                TY  - JOUR
                AU  - Acar, Mustafa Burak 
                AU  - Ayaz-Güner, Şerife 
                AU  - Di Bernardo, Giovanni 
                AU  - Güner, Hüseyin 
                AU  - Murat, Ayşegül 
                AU  - Peluso, Gianfranco 
                AU  - Özcan, Servet 
                AU  - Galderisi, Umberto 
                TI  - Obesity induced by high-fat diet is associated with critical changes in biological and molecular functions of mesenchymal stromal cells present in visceral adipose tissue
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202423
                DO  - 10.18632/aging.202423
                SP  - 24894
                EP  - 24913
                PY  - 
                AB  - The mesenchymal stromal cells (MSCs) residing within the stromal component of visceral adipose tissue appear to be greatly affected by obesity, with impairment of their functions and presence of senescence.
                To gain further insight into these phenomena, we analyzed the changes in total proteome content and secretome of mouse MSCs after a high-fat diet (HFD) treatment compared to a normal diet (ND). In healthy conditions, MSCs are endowed with functions mainly devoted to vesicle trafficking. These cells have an immunoregulatory role, affecting leukocyte activation and migration, acute inflammation phase response, chemokine signaling, and platelet activities. They also present a robust response to stress. We identified four signaling pathways (TGF-&#x3B2;, VEGFR2, HMGB1, and Leptin) that appear to govern the cells&#x2019; functions.
                In the obese mice, MSCs showed a change in their functions. The immunoregulation shifted toward pro-inflammatory tasks with the activation of interleukin-1 pathway and of Granzyme A signaling. Moreover, the methionine degradation pathway and the processing of capped intronless pre-mRNAs may be related to the inflammation process.
                The signaling pathways we identified in ND MSCs were replaced by MET, WNT, and FGFR2 signal transduction, which may play a role in promoting inflammation, cancer, and aging.
                ER  -

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Age-related transcriptome changes in melanoma patients with tumor-positive sentinel lymph nodes

Derek S. Menefee, Austin McMasters, Jianmin Pan, Xiaohong Li, Deyi Xiao, Sabine Waigel, Wolfgang Zacharias, Shesh N. Rai, Kelly M. McMasters, Hongying Hao,

https://doi.org/10.18632/aging.202435 pp 24914—24939

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Menefee DS, McMasters A, Pan J, Li X, Xiao D, Waigel S, Zacharias W, Rai SN, McMasters KM, Hao H, . Age-related transcriptome changes in melanoma patients with tumor-positive sentinel lymph nodes. . 12:24914-24939. https://doi.org/10.18632/aging.202435

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                TY  - JOUR
                AU  - Menefee, Derek S. 
                AU  - McMasters, Austin 
                AU  - Pan, Jianmin 
                AU  - Li, Xiaohong 
                AU  - Xiao, Deyi 
                AU  - Waigel, Sabine 
                AU  - Zacharias, Wolfgang 
                AU  - Rai, Shesh N. 
                AU  - McMasters, Kelly M. 
                AU  - Hao, Hongying 
                TI  - Age-related transcriptome changes in melanoma patients with tumor-positive sentinel lymph nodes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202435
                DO  - 10.18632/aging.202435
                SP  - 24914
                EP  - 24939
                PY  - 
                AB  - Age is an important factor for determining the outcome of melanoma patients. Sentinel lymph node (SLN) status is also a strong predictor of survival for melanoma. Paradoxically, older melanoma patients have a lower incidence of SLN metastasis but a higher mortality rate when compared with their younger counterparts. The mechanisms that underlie this phenomenon remain unknown. This study uses three independent datasets of RNA samples from patients with melanoma metastatic to the SLN to identify age-related transcriptome changes in SLNs and their association with outcome. Microarray was applied to the first dataset of 97 melanoma patients. NanoString was performed in the second dataset to identify the specific immune genes and pathways that are associated with recurrence in younger versus older patients. qRT-PCR analysis was used in the third dataset of 36 samples to validate the differentially expressed genes (DEGs) from microarray and NanoString. These analyses show that FOS, NR4A, and ITGB1 genes were significantly higher in older melanoma patients with positive SLNs. IRAK3- and Wnt10b-related genes are the major pathways associated with recurrent melanoma in younger and older patients with tumor-positive SLNs, respectively. This study aims to elucidate age-related differences in SLNs in the presence of nodal metastasis.
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Time gap between the onset and diagnosis in Werner syndrome: a nationwide survey and the 2020 registry in Japan

Masaya Koshizaka, Yoshiro Maezawa, Yukari Maeda, Mayumi Shoji, Hisaya Kato, Hiyori Kaneko, Takahiro Ishikawa, Daisuke Kinoshita, Kazuki Kobayashi, Junji Kawashima, Akiko Sekiguchi, Sei-ichiro Motegi, Hironori Nakagami, Yoshihiko Yamada, Shinji Tsukamoto, Akira Taniguchi, Ken Sugimoto, Yukiko Shoda, Kunihiko Hashimoto, Toru Yoshimura, Daisuke Suzuki, Masafumi Kuzuya, Minoru Takemoto, Koutaro Yokote,

https://doi.org/10.18632/aging.202441 pp 24940—24956

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Koshizaka M, Maezawa Y, Maeda Y, Shoji M, Kato H, Kaneko H, Ishikawa T, Kinoshita D, Kobayashi K, Kawashima J, Sekiguchi A, Motegi S, Nakagami H, et al, . Time gap between the onset and diagnosis in Werner syndrome: a nationwide survey and the 2020 registry in Japan. . 12:24940-24956. https://doi.org/10.18632/aging.202441

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                TY  - JOUR
                AU  - Koshizaka, Masaya 
                AU  - Maezawa, Yoshiro 
                AU  - Maeda, Yukari 
                AU  - Shoji, Mayumi 
                AU  - Kato, Hisaya 
                AU  - Kaneko, Hiyori 
                AU  - Ishikawa, Takahiro 
                AU  - Kinoshita, Daisuke 
                AU  - Kobayashi, Kazuki 
                AU  - Kawashima, Junji 
                AU  - Sekiguchi, Akiko 
                AU  - Motegi, Sei-ichiro 
                AU  - Nakagami, Hironori 
                AU  - Yamada, Yoshihiko 
                AU  - Tsukamoto, Shinji 
                AU  - Taniguchi, Akira 
                AU  - Sugimoto, Ken 
                AU  - Shoda, Yukiko 
                AU  - Hashimoto, Kunihiko 
                AU  - Yoshimura, Toru 
                AU  - Suzuki, Daisuke 
                AU  - Kuzuya, Masafumi 
                AU  - Takemoto, Minoru 
                AU  - Yokote, Koutaro 
                TI  - Time gap between the onset and diagnosis in Werner syndrome: a nationwide survey and the 2020 registry in Japan
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202441
                DO  - 10.18632/aging.202441
                SP  - 24940
                EP  - 24956
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Koshizaka, Masaya 
                AU  - Maezawa, Yoshiro 
                AU  - Maeda, Yukari 
                AU  - Shoji, Mayumi 
                AU  - Kato, Hisaya 
                AU  - Kaneko, Hiyori 
                AU  - Ishikawa, Takahiro 
                AU  - Kinoshita, Daisuke 
                AU  - Kobayashi, Kazuki 
                AU  - Kawashima, Junji 
                AU  - Sekiguchi, Akiko 
                AU  - Motegi, Sei-ichiro 
                AU  - Nakagami, Hironori 
                AU  - Yamada, Yoshihiko 
                AU  - Tsukamoto, Shinji 
                AU  - Taniguchi, Akira 
                AU  - Sugimoto, Ken 
                AU  - Shoda, Yukiko 
                AU  - Hashimoto, Kunihiko 
                AU  - Yoshimura, Toru 
                AU  - Suzuki, Daisuke 
                AU  - Kuzuya, Masafumi 
                AU  - Takemoto, Minoru 
                AU  - Yokote, Koutaro 
                TI  - Time gap between the onset and diagnosis in Werner syndrome: a nationwide survey and the 2020 registry in Japan
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202441
                DO  - 10.18632/aging.202441
                SP  - 24940
                EP  - 24956
                PY  - 
                AB  - Patients with Werner syndrome present with diverse signs of aging that begin in adolescence. A Japanese nationwide survey was conducted to establish a registry that could clarify the disease profile of patients with Werner syndrome. The questionnaires were sent to 7888 doctors. The survey identified 116 patients diagnosed with Werner syndrome based on the diagnosis criteria. Forty patients were enrolled in the registry. Data on clinical symptoms, treatment information, and laboratory examination from patients who provided informed consent were collected. The data at enrollment were analyzed. The patients&#x2019; average age at enrollment was 50.1&#xB1;7.5 years. The mean onset age was 26.1&#xB1;9.5 years, but the mean age at diagnosis was 42.5&#xB1;8.6 years. Average height and weight of the study patients were lower than those of Japanese individuals. Almost all patients experienced hair change and cataracts. More than 60% of patients presented with glycolipid abnormalities. Overall, 15% of patients had a history of foot amputation. Approximately 30% of the patients&#x2019; parents had a consanguineous marriage. The average grip strength, walking speed, and skeletal muscle mass index met the diagnostic criteria for sarcopenia. The registry revealed that there are opportunities for early diagnosis and intervention; therefore, sensitization about the disease is needed.
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LINC01410 accelerated the invasion and proliferation of osteosarcoma by sponging miR-3128

Quanxiao Xu, Limin He, Lei Ma, Lin Fan, Lihua Yan, Xulin Zhao, Yuanyuan Li,

https://doi.org/10.18632/aging.103464 pp 24957—24966

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Xu Q, He L, Ma L, Fan L, Yan L, Zhao X, Li Y, . LINC01410 accelerated the invasion and proliferation of osteosarcoma by sponging miR-3128. . 12:24957-24966. https://doi.org/10.18632/aging.103464

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                TY  - JOUR
                AU  - Xu, Quanxiao 
                AU  - He, Limin 
                AU  - Ma, Lei 
                AU  - Fan, Lin 
                AU  - Yan, Lihua 
                AU  - Zhao, Xulin 
                AU  - Li, Yuanyuan 
                TI  - LINC01410 accelerated the invasion and proliferation of osteosarcoma by sponging miR-3128
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103464
                DO  - 10.18632/aging.103464
                SP  - 24957
                EP  - 24966
                PY  - 
                AB  - Increasing evidence has shown that lncRNAs are closely correlated with cell apoptosis, autophagy and progression. However, the role of LINC01410 in osteosarcoma has not been verified. We determined that LINC01410 was overexpressed in osteosarcoma specimens and cell lines. The expression of LINC01410 was upregulated in 22 osteosarcoma patients (22/30, 73%) compared to control normal samples. Ectopic expression of LINC01410 promoted the osteosarcoma cell cycle, proliferation and invasion. Overexpression of LINC01410 induced N-cadherin and Vimentin expression and inhibited E-cadherin expression in osteosarcoma cells. LINC01410 acted as a sponge for miR-3128. The results showed that miR-3128 overexpression decreased the luciferase activity of WT-LINC01410 but not mut-LINC01410 in MG-63 cells. Upregulation of LINC01410 expression suppressed miR-3128 expression in MG-63 cells. Moreover, LINC01410 overexpression increased osteosarcoma cell invasion and growth by modulating miR-3128. These data indicated that LINC01410 acted as an oncogene in osteosarcomagenesis and might be a potential new strategy for osteosarcoma treatment.
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HBXIP promotes gastric cancer via METTL3-mediated MYC mRNA m6A modification

Zhi Yang, Xiaodi Jiang, Deming Li, Xiaofeng Jiang,

https://doi.org/10.18632/aging.103767 pp 24967—24982

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Yang Z, Jiang X, Li D, Jiang X, . HBXIP promotes gastric cancer via METTL3-mediated MYC mRNA m6A modification. . 12:24967-24982. https://doi.org/10.18632/aging.103767

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 TY - JOUR
 AU - Yang, Zhi 
 AU - Jiang, Xiaodi 
 AU - Li, Deming 
 AU - Jiang, Xiaofeng 
 TI - HBXIP promotes gastric cancer via METTL3-mediated MYC mRNA m6A modification
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103767
 DO - 10.18632/aging.103767
 SP - 24967
 EP - 24982
 PY - 
 AB - Gastric cancer (GC) is one of the most common malignancies worldwide with limited treatment options and distinct geographical distribution even in countries such as China. Genetic alterations during its carcinogenesis need urgent elucidation. In this study, we propose an intriguing hypothesis that the hepatitis B X-interacting protein (HBXIP) may function as an oncogene in GC. We harvested 45 GC tissues and matched the paracancerous tissues. The c-myc proto-oncogene (MYC) N6-methyladenosine (m6A) mRNA methylation was detected by m6A RNA immunoprecipitation and dot-blot assays. Expressions of HBXIP, methyltransferase like 3 (METTL3) and MYC were all determined to be upregulated in both GC tissues and cells. Silencing HBXIP led to a decreased expression of METTL3, which inhibited GC cell proliferation, migration and invasion while promoting their apoptosis. Furthermore, METTL3 enhanced MYC m6A methylation and increased MYC translation, which could potentiate the proliferation, migration and invasion of GC cells. Finally, the HBXIP knockdown impeded the tumorigenicity of GC cells in vivo. Based on the findings of this study, we conclude that HBXIP plays an oncogenic role in GC via METTL3-mediated MYC mRNA m6A modification. The study offers a comprehensive understanding of HBXIP as a potential therapeutic target to limit GC progression.
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A glycolysis-related gene expression signature in predicting recurrence of breast cancer

Jianing Tang, Yongwen Luo, Gaosong Wu,

https://doi.org/10.18632/aging.103806 pp 24983—24994

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Tang J, Luo Y, Wu G, . A glycolysis-related gene expression signature in predicting recurrence of breast cancer. . 12:24983-24994. https://doi.org/10.18632/aging.103806

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                TY  - JOUR
                AU  - Tang, Jianing 
                AU  - Luo, Yongwen 
                AU  - Wu, Gaosong 
                TI  - A glycolysis-related gene expression signature in predicting recurrence of breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103806
                DO  - 10.18632/aging.103806
                SP  - 24983
                EP  - 24994
                PY  - 
                AB  - Metabolic change is the hallmark of cancer. In the present study, we aimed to develop a glycolysis-related gene signature to predict the prognosis of breast cancer patients. Gene expression profiles and clinical data of breast cancer patients were obtained from the GEO database. A four-gene based signature (ALDH2, PRKACB, STMN1 and ZNF292) was developed to separate patients into high-risk and low-risk groups. Patients in the low-risk group had significantly better prognosis than those in the high-risk group. Time-dependent ROC analysis demonstrated that the glycolysis-related gene signature had excellent prognostic accuracy. We further confirmed the expression of the four prognostic genes in breast cancer and paracancerous tissue samples using qRT-PCR analysis. Expression level of PRKACB was higher in paracancerous tissues, while STMN1 and ZNF292 were overexpressed in tumor samples, no significant difference was observed in ALDH2 expression level. Global proteome data of 105 TCGA breast cancer samples obtained from the Clinical Proteomic Tumor Analysis Consortium (CPTAC) were used to evaluate the prognostic value in protein levels. Consistently, high expression level of PRKACB protein was associated with favorable prognosis, while high ZNF292 and STMN1 protein expression levels indicated poor prognosis. The glycolysis-related gene signature might provide an effective prognostic predictor and a new insight for individualize management of breast cancer patients.
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DZIP3 is a key factor to stratify IDH1 wild-type lower-grade gliomas

Tingyu Liang, Xingang Zhou, Peiliang Li, Gan You, Fang Wang, Peng Wang, Enshan Feng,

https://doi.org/10.18632/aging.103817 pp 24995—25004

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Liang T, Zhou X, Li P, You G, Wang F, Wang P, Feng E, . DZIP3 is a key factor to stratify IDH1 wild-type lower-grade gliomas. . 12:24995-25004. https://doi.org/10.18632/aging.103817

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                TY  - JOUR
                AU  - Liang, Tingyu 
                AU  - Zhou, Xingang 
                AU  - Li, Peiliang 
                AU  - You, Gan 
                AU  - Wang, Fang 
                AU  - Wang, Peng 
                AU  - Feng, Enshan 
                TI  - DZIP3 is a key factor to stratify IDH1 wild-type lower-grade gliomas
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103817
                DO  - 10.18632/aging.103817
                SP  - 24995
                EP  - 25004
                PY  - 
                AB  - Background: Malignant glioma is the most common form of primary malignant brain cancer. Heterogeneity is the hallmark of glioma. DAZ-interacting zinc finger 3 (DZIP3), acts as an RNA-binding RING-type ubiquitin ligase; however, its function in glioma is yet unclear.
                Results: The DZIP3 expression was related to the World Health Organization (WHO) grade and isocitrate dehydrogenase 1(IDH1) status, as well as the clinical outcome. Malignant cases exhibit lower DZIP3 expression. DZIP3 was an independent predictive factor of good prognosis in all grade and lower grade gliomas (p &lt; 0.0001). Gene enrichment analysis and immunohistochemistry indicated that DZIP3 affected the biological behavior of glioma through the angiogenesis pathway. Moreover, based on DZIP3 expression, IDH1 wild-type lower-grade gliomas could be divided into two groups with different survival time.
                Conclusion: In conclusion, the loss of DZIP3 may be involved in the mechanism of angiogenesis in the invasive biological process of glioma. These findings laid an understanding of DZIP3-specific clinical features in glioma.
                Methods: A total of 325 glioma patients from the Chinese Glioma Genome Atlas (CGGA) RNA-seq cohort comprised the training cohort, while 265 patients from the GSE 16011 array cohort formed the validation cohort. The mRNA expression of DZIP3 and clinical characteristics was assessed. DZIP3 protein expression and microvessel density (MVD) were evaluated by immunohistochemistry (IHC).
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Sleep quality and risk of coronary heart disease - a prospective cohort study from the English longitudinal study of ageing

Chenxi Song, Rui Zhang, Jiaqiang Liao, Rui Fu, Chunyue Wang, Qianqian Liu, Weihua Song, Hongjian Wang, Kefei Dou,

https://doi.org/10.18632/aging.103866 pp 25005—25019

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Song C, Zhang R, Liao J, Fu R, Wang C, Liu Q, Song W, Wang H, Dou K, . Sleep quality and risk of coronary heart disease - a prospective cohort study from the English longitudinal study of ageing. . 12:25005-25019. https://doi.org/10.18632/aging.103866

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                TY  - JOUR
                AU  - Song, Chenxi 
                AU  - Zhang, Rui 
                AU  - Liao, Jiaqiang 
                AU  - Fu, Rui 
                AU  - Wang, Chunyue 
                AU  - Liu, Qianqian 
                AU  - Song, Weihua 
                AU  - Wang, Hongjian 
                AU  - Dou, Kefei 
                TI  - Sleep quality and risk of coronary heart disease - a prospective cohort study from the English longitudinal study of ageing
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103866
                DO  - 10.18632/aging.103866
                SP  - 25005
                EP  - 25019
                PY  - 
                AB  - Background: The association between sleep quality and risk of coronary heart disease (CHD) remains unclear in the elderly.
                Results: At eight-year follow up, a total of 411 (4.29%) participants developed CHD. Compared with good quality group, the multivariable hazard ratio [HR] (95% confidence interval [CI]) for CHD was 1.393 (1.005, 1.931) for intermediate quality group and 1.913 (1.206, 3.035) for poor quality group. Consistent results were observed in participants with normal sleep duration.
                Conclusions: Poor sleep quality may be a novel modifiable risk factor for CHD in the elderly independent of conventional cardiovascular risk factors, even when sleep duration was normal.
                Methods: The current study included 9570 CHD-free participants in the English Longitudinal Study of Ageing (ELSA) from wave 4 (2008 to 2009). Incident CHD included new onset angina or myocardial infarction. Sleep quality was measured by a four-item questionnaire. Score ranged from 1 (best) to 4 (poorest). Participants were divided into three groups: good quality (1 &#x2264; score &lt;2), intermediate quality (2 &#x2264; score &lt;3) and poor quality (3 &#x2264; score &#x2264;4). Cox regression model was used to calculate HR for CHD risk according to sleep quality, adjusted for conventional CHD risk factors and sleep duration.
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TRIB3 facilitates glioblastoma progression via restraining autophagy

Zhanbin Tang, Hongping Chen, Di Zhong, Wan Wei, Lili Liu, Qiong Duan, Baichao Han, Guozhong Li,

https://doi.org/10.18632/aging.103969 pp 25020—25034

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Tang Z, Chen H, Zhong D, Wei W, Liu L, Duan Q, Han B, Li G, . TRIB3 facilitates glioblastoma progression via restraining autophagy. . 12:25020-25034. https://doi.org/10.18632/aging.103969

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                TY  - JOUR
                AU  - Tang, Zhanbin 
                AU  - Chen, Hongping 
                AU  - Zhong, Di 
                AU  - Wei, Wan 
                AU  - Liu, Lili 
                AU  - Duan, Qiong 
                AU  - Han, Baichao 
                AU  - Li, Guozhong 
                TI  - TRIB3 facilitates glioblastoma progression via restraining autophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103969
                DO  - 10.18632/aging.103969
                SP  - 25020
                EP  - 25034
                PY  - 
                AB  - The pseudokinase Tribble 3 (TRIB3) is known as a regulator in cellular responses to a variety of stresses, such as glucose insufficiency and endoplasmic reticulum (ER) stress. TRIB3 is upregulated in various cancer tissues and is closely connected to the poor prognosis of patients. However, the underlying regulation and function of TRIB3 in glioblastoma (GBM) is still largely unknown. In this study, the upregulation of TRIB3 was confirmed both in primary specimens from GBM patients and in vitro with GBM cell lines. Overexpression of specific TRIB3 transcripts promoted cell growth and migration in vitro, while knockdown of TRIB3 expression exerted a repressive effect on these cellular processes. The growth-promoting effect of TRIB3 was also demonstrated in a xenograft mouse model. Mechanistic studies further revealed that TRIB3 was able to suppress autophagic flux and that this suppression was responsible for TRIB3 silencing-induced proliferation and migration of GBM cells. These findings indicate that the suppression of autophagic flux by TRIB3 drives the invasion and proliferation of GBM cells, thus suggesting that TRIB3 is a potential novel therapeutic target for the treatment of glioma.
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δ-opioid receptor activation protects against Parkinson’s disease-related mitochondrial dysfunction by enhancing PINK1/Parkin-dependent mitophagy

Yuan Xu, Feng Zhi, Jiahao Mao, Ya Peng, Naiyuan Shao, Gianfranco Balboni, Yilin Yang, Ying Xia,

https://doi.org/10.18632/aging.103970 pp 25035—25059

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Xu Y, Zhi F, Mao J, Peng Y, Shao N, Balboni G, Yang Y, Xia Y, . δ-opioid receptor activation protects against Parkinson’s disease-related mitochondrial dysfunction by enhancing PINK1/Parkin-dependent mitophagy. . 12:25035-25059. https://doi.org/10.18632/aging.103970

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                TY  - JOUR
                AU  - Xu, Yuan 
                AU  - Zhi, Feng 
                AU  - Mao, Jiahao 
                AU  - Peng, Ya 
                AU  - Shao, Naiyuan 
                AU  - Balboni, Gianfranco 
                AU  - Yang, Yilin 
                AU  - Xia, Ying 
                TI  - δ-opioid receptor activation protects against Parkinson’s disease-related mitochondrial dysfunction by enhancing PINK1/Parkin-dependent mitophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103970
                DO  - 10.18632/aging.103970
                SP  - 25035
                EP  - 25059
                PY  - 
                AB  - Our previous studies have shown that the &#x3B4;-opioid receptor (DOR) is an important neuroprotector via the regulation of PTEN-induced kinase 1 (PINK1), a mitochondria-related molecule, under hypoxic and MPP+ insults. Since mitochondrial dysfunctions are observed in both hypoxia and MPP+ insults, this study further investigated whether DOR is cytoprotective against these insults by targeting mitochondria. Through comparing DOR-induced responses to hypoxia versus MPP+-induced parkinsonian insult in PC12 cells, we found that both hypoxia and MPP+ caused a collapse of mitochondrial membrane potential and severe mitochondrial dysfunction. In sharp contrast to its inappreciable effect on mitochondria in hypoxic conditions, DOR activation with UFP-512, a specific agonist, significantly attenuated the MPP+-induced mitochondrial injury. Mechanistically, DOR activation effectively upregulated PINK1 expression and promoted Parkin&#x2019;s mitochondrial translocation and modification, thus enhancing the PINK1-Parkin mediated mitophagy. Either PINK1 knockdown or DOR knockdown largely interfered with the DOR-mediated mitoprotection in MPP+ conditions. Moreover, there was a major difference between hypoxia versus MPP+ in terms of the regulation of mitophagy with hypoxia-induced mitophagy being independent from DOR-PINK1 signaling. Taken together, our novel data suggest that DOR activation is neuroprotective against parkinsonian injury by specifically promoting mitophagy in a PINK1-dependent pathway and thus attenuating mitochondrial damage.
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LINC01235-TWIST2 feedback loop facilitates epithelial–mesenchymal transition in gastric cancer by inhibiting THBS2

Yu-En Tan, Yao Xing, Ban-Lai Ran, Chao Zhang, Si-Wei Pan, Wen An, Qing-Chuan Chen, Hui-Mian Xu,

https://doi.org/10.18632/aging.103979 pp 25060—25075

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Tan Y, Xing Y, Ran B, Zhang C, Pan S, An W, Chen Q, Xu H, . LINC01235-TWIST2 feedback loop facilitates epithelial–mesenchymal transition in gastric cancer by inhibiting THBS2. . 12:25060-25075. https://doi.org/10.18632/aging.103979

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                TY  - JOUR
                AU  - Tan, Yu-En 
                AU  - Xing, Yao 
                AU  - Ran, Ban-Lai 
                AU  - Zhang, Chao 
                AU  - Pan, Si-Wei 
                AU  - An, Wen 
                AU  - Chen, Qing-Chuan 
                AU  - Xu, Hui-Mian 
                TI  - LINC01235-TWIST2 feedback loop facilitates epithelial–mesenchymal transition in gastric cancer by inhibiting THBS2
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103979
                DO  - 10.18632/aging.103979
                SP  - 25060
                EP  - 25075
                PY  - 
                AB  - Although the anomalous expression of long non-coding RNAs (lncRNAs) has been extensively investigated in numerous carcinomas including gastric cancer (GC), their function remains unclear. The aim of our study was to explore the role of LINC01235 in GC. We used real-time quantitative PCR (RT-qPCR) to measure the expression of LINC01235 and twist family bHLH transcription factor 2 (TWIST2) in GC tissues. Scratch and transwell assays were performed to evaluate cellular capacity for migration and invasion. Gene relationships were explored by Weighted Gene Co-Expression Network Analysis (WGCNA). We measured TWIST2, thrombospondin 2 (THBS2) and epithelial-mesenchymal transition (EMT)-related proteins with western blot. We also used Pearson correlation analysis and the Kaplan&#x2013;Meier method to detect associations among genes and overall survival. We found that LINC01235 was upregulated in GC tissues and cells. LINC01235 down-regulation restricted migration and invasion. Interestingly, we found the LINC01235-TWIST2-THBS2 axis induced EMT. Additionally, TWIST2 upregulated LINC01235 transcription in luciferase and chromatin immunoprecipitation (ChIP) assays. Bioinformatics analysis showed that microRNA (miR)-6852-5p might be a key gene involved in the regulation of TWIST2 by LINC01235. The LINC01235-TWIST2 positive feedback loop mainly affected migration and invasion of GC cells, which suggests it may serve as a potential therapeutic target in gastric cancer.
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Secondary data mining of GEO database for long non-coding RNA and Competing endogenous RNA network in keloid-prone individuals

Yu Deng, Yangbin Xu, Shuqia Xu, Yujing Zhang, Bing Han, Zheng Liu, Xiangxia Liu, Zhaowei Zhu,

https://doi.org/10.18632/aging.104054 pp 25076—25089

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Deng Y, Xu Y, Xu S, Zhang Y, Han B, Liu Z, Liu X, Zhu Z, . Secondary data mining of GEO database for long non-coding RNA and Competing endogenous RNA network in keloid-prone individuals. . 12:25076-25089. https://doi.org/10.18632/aging.104054

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                TY  - JOUR
                AU  - Deng, Yu 
                AU  - Xu, Yangbin 
                AU  - Xu, Shuqia 
                AU  - Zhang, Yujing 
                AU  - Han, Bing 
                AU  - Liu, Zheng 
                AU  - Liu, Xiangxia 
                AU  - Zhu, Zhaowei 
                TI  - Secondary data mining of GEO database for long non-coding RNA and Competing endogenous RNA network in keloid-prone individuals
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104054
                DO  - 10.18632/aging.104054
                SP  - 25076
                EP  - 25089
                PY  - 
                AB  - This study aimed to identify long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs) differentially expressed (DE) during keloid formation, predict DElncRNA-DEmiRNA-DEmRNA interactions, and construct a competing endogenous RNA (ceRNA) network through secondary data mining of keloid-related sequencing and microarray data in the open-source Gene Expression Omnibus (GEO) database. The GSE113621 dataset was downloaded from the GEO database, |log2FC|&gt;1 and p&lt;0.05 were set as screening criteria, genes expressed only in keloid-prone individuals were selected as research objects, and DEmRNAs, DElncRNAs, and DEmiRNAs before injury and 6 weeks after injury were screened. A Pearson correlation coefficient (PCC) of &gt; 0.95 was selected as the index to predict the targeting relationships among lncRNAs, miRNAs, and mRNAs; and a network diagram was constructed using Cytoscape. The expression of 2356 lncRNAs was changed in the keloid-prone group&#x2014;1306 were upregulated and 1050 were downregulated. Six lncRNAs, namely, 2 upregulated (DLEU2 and AP000317.2) and 4 downregulated (ADIRF-AS1, AC006333.2, AL137127.1 and LINC01725) lncRNAs, were expressed only in the keloid-prone group and were used to construct a ceRNA network. DLEU2 may regulate fibroblast proliferation, differentiation, and apoptosis through hsa-miR-30a-5p/hsa-miR-30b-5p. In-depth mining of GEO data indicated that lncRNAs and a ceRNA regulatory network participate in the wound healing process in keloid-prone individuals, possibly providing novel intervention targets and treatment options for keloid scars.
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miR-100-3p inhibits the adipogenic differentiation of hMSCs by targeting PIK3R1 via the PI3K/AKT signaling pathway

Tao Wang, Donghuo Zhong, Zhongjun Qin, Shan He, Ying Gong, Weidong Li, Xingnuan Li,

https://doi.org/10.18632/aging.104074 pp 25090—25100

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Wang T, Zhong D, Qin Z, He S, Gong Y, Li W, Li X, . miR-100-3p inhibits the adipogenic differentiation of hMSCs by targeting PIK3R1 via the PI3K/AKT signaling pathway. . 12:25090-25100. https://doi.org/10.18632/aging.104074

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                TY  - JOUR
                AU  - Wang, Tao 
                AU  - Zhong, Donghuo 
                AU  - Qin, Zhongjun 
                AU  - He, Shan 
                AU  - Gong, Ying 
                AU  - Li, Weidong 
                AU  - Li, Xingnuan 
                TI  - miR-100-3p inhibits the adipogenic differentiation of hMSCs by targeting PIK3R1 via the PI3K/AKT signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104074
                DO  - 10.18632/aging.104074
                SP  - 25090
                EP  - 25100
                PY  - 
                AB  - MicroRNAs play an important role in the adipogenic differentiation of human bone marrow mesenchymal stem cells (hMSCs). How miR-100-3p influences such adipogenesis, however, remains uncertain. In this study, hMSC adipogenic differentiation was associated with miR-100-3p downregulation, and overexpressing this miRNA inhibited adipogenesis and the expression of adipogenic marker genes. Through bioinformatics approaches, miR-100-3p can bind the 3&apos;-untranslated region (3&#x2032;-UTR) of the mRNA encoding phosphoinositide 3-kinase regulatory subunit 1 (PIK3R1) such that miR-100-3p overexpression resulted in significant reductions in PIK3R1 expression. Importantly, overexpressing PIK3R1 was sufficient to reverse the anti-adipogenic effects of miR-100-3p overexpression. PIK3R1 is a critical component of the PI3K/AKT signaling pathway, and miR-100-3p overexpression resulted in reduced AKT phosphorylation in the context of adipogenesis. In addition, the adipogenic differentiation of hMSCs in which miR-100-3p was overexpressed was further enhanced upon treatment with the PI3K/AKT agonist 740Y-P relative to miR-100-3p overexpression alone. Taken together, these findings provide evidence that miR-100-3p inhibits the adipogenic differentiation of hMSCs by targeting PIK3R1 via the PI3K/AKT signaling pathway.
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Could microtubule inhibitors be the best choice of therapy in gastric cancer with high immune activity: mutant DYNC1H1 as a biomarker

Jin Bai, BoWen Yang, Ruichuan Shi, Xinye Shao, Yujing Yang, Fang Wang, Jiawen Xiao, Xiujuan Qu, Yunpeng Liu, Ye Zhang, Zhi Li,

https://doi.org/10.18632/aging.104084 pp 25101—25119

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Bai J, Yang B, Shi R, Shao X, Yang Y, Wang F, Xiao J, Qu X, Liu Y, Zhang Y, Li Z, . Could microtubule inhibitors be the best choice of therapy in gastric cancer with high immune activity: mutant DYNC1H1 as a biomarker. . 12:25101-25119. https://doi.org/10.18632/aging.104084

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                TY  - JOUR
                AU  - Bai, Jin 
                AU  - Yang, BoWen 
                AU  - Shi, Ruichuan 
                AU  - Shao, Xinye 
                AU  - Yang, Yujing 
                AU  - Wang, Fang 
                AU  - Xiao, Jiawen 
                AU  - Qu, Xiujuan 
                AU  - Liu, Yunpeng 
                AU  - Zhang, Ye 
                AU  - Li, Zhi 
                TI  - Could microtubule inhibitors be the best choice of therapy in gastric cancer with high immune activity: mutant DYNC1H1 as a biomarker
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104084
                DO  - 10.18632/aging.104084
                SP  - 25101
                EP  - 25119
                PY  - 
                AB  - Immune checkpoint blockade (ICB) has achieved unprecedented breakthroughs in various cancers, including gastric cancer (GC) with high immune activity (MSI-H or TMB-H), yet clinical benefits from ICB were moderate. Here we aimed to identify the most appropriate drugs which can improve outcomes in GC. We firstly compared MSI-H and TMB-H GC samples with normal samples in TCGA-STAD cohort, respectively. After that, Connectivity Map database repurposed nine candidate drugs (CMap score &lt; -90). Then, microtubule inhibitors (MTIs) were screened as the significant candidate drugs with their representative gene sets strongly enriched (p &lt; 0.05) via GSEA. GDSC database validated higher activities of some MTIs in GC cells with MSI-H and TMB-H (p &lt; 0.05). Furthermore, some MTIs activities were positively associated with mutant Dynein Cytoplasmic 1 Heavy Chain 1 (DYNC1H1) (p &lt; 0.05) based on NCI-60 cancer cell line panel. DYNC1H1 was high frequently alteration in GC and was positively associated with TMB-H and MSI-H. Mutant DYNC1H1 may be accompanied with down-regulation of MTIs-related genes in GC or change the binding pocket to sensitize MTIs. Overall, this study suggested that some MTIs may be the best candidate drugs to treat GC with high immune activity, especially patients with DYNC1H1 mutated.
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Apelin protects against ischemia-reperfusion injury in diabetic myocardium via inhibiting apoptosis and oxidative stress through PI3K and p38-MAPK signaling pathways

Songtao An, Xi Wang, Huairui, Shi, Xueqiang Zhang, Hua Meng, Wenbo Li, Dongchang Chen, Junbo Ge,

https://doi.org/10.18632/aging.104106 pp 25120—25137

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An S, Wang X, Shi H, Zhang X, Meng H, Li W, Chen D, Ge J, . Apelin protects against ischemia-reperfusion injury in diabetic myocardium via inhibiting apoptosis and oxidative stress through PI3K and p38-MAPK signaling pathways. . 12:25120-25137. https://doi.org/10.18632/aging.104106

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                TY  - JOUR
                AU  - An, Songtao 
                AU  - Wang, Xi 
                AU  - Shi, Huairui, 
                AU  - Zhang, Xueqiang 
                AU  - Meng, Hua 
                AU  - Li, Wenbo 
                AU  - Chen, Dongchang 
                AU  - Ge, Junbo 
                TI  - Apelin protects against ischemia-reperfusion injury in diabetic myocardium via inhibiting apoptosis and oxidative stress through PI3K and p38-MAPK signaling pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104106
                DO  - 10.18632/aging.104106
                SP  - 25120
                EP  - 25137
                PY  - 
                AB  - Among all diabetes mellitus-associated cardiovascular diseases, morbidity of diabetic myocardium with ischemia reperfusion injury (D-IRI) is increasing year by year. We aimed to discover a therapeutic biomarker and investigate its mechanism in D-IRI. High-fat diet and streptozotocin-induced diabetes rats were operated with IRI or sham. Recombined lentiviral vector encoding Apelin was injected into D-IRI rat via tail vein. Cardiac function, infarct size, cellular death and oxidative stress were major outcome measures. Cardiomyocyte ischemia reperfusion injury was more serious in D-IRI rats than in non-diabetes ischemia reperfusion injury (ND-IRI) rats. The secretion of NTproBNP was increased in D-IRI compared with ND-IRI. Bcl-2 expression was decreased, and Bax and cleaved caspase-3 expression was increased in D-IRI rats compared with ND-IRI rats, which were reversed after treatment with Apelin. Apelin-upregulation improved cardiomyocyte ischemia reperfusion injury and decreased NT-proBNP levels in D-IRI rats. Apelin overexpression enhanced PI3K and eNOS levels while reduced those of p38-MAPK and iNOS in D-IRI rats. Apelin overexpression protected against D-IRI through inhibiting apoptosis and oxidative stress via PI3K and p38MAPK signaling pathways in D-IRI rats. These findings provide critical new insight into understanding of Apelin&apos;s cardio-protective effects, which may become a novel therapeutic target for the diabetic IRI patients.
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Bone marrow mesenchymal stem cell-derived exosomes prevent osteoarthritis by regulating synovial macrophage polarization

Jiyong Zhang, Yuluo Rong, Chunyang Luo, Weiding Cui,

https://doi.org/10.18632/aging.104110 pp 25138—25152

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Zhang J, Rong Y, Luo C, Cui W, . Bone marrow mesenchymal stem cell-derived exosomes prevent osteoarthritis by regulating synovial macrophage polarization. . 12:25138-25152. https://doi.org/10.18632/aging.104110

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                TY  - JOUR
                AU  - Zhang, Jiyong 
                AU  - Rong, Yuluo 
                AU  - Luo, Chunyang 
                AU  - Cui, Weiding 
                TI  - Bone marrow mesenchymal stem cell-derived exosomes prevent osteoarthritis by regulating synovial macrophage polarization
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104110
                DO  - 10.18632/aging.104110
                SP  - 25138
                EP  - 25152
                PY  - 
                AB  - Osteoarthritis is a chronic degenerative disease that can lead to restricted activity or even disability. Bone marrow mesenchymal stem cells can repair cartilage damage and treat osteoarthritis via cell therapies or in-tissue engineering. Research has shown that the paracrine mechanism is the main mode of action of mesenchymal stem cells. Exosomes are the smallest known membrane-bound nanovesicles. Exosomes are also important carriers of paracrine delivery agents and promote communication between cells. We demonstrated that bone marrow mesenchymal stem cell-derived exosomes can delay the progression of osteoarthritis. Exosomes alleviate cartilage damage, reduce osteophyte formation and synovial macrophage infiltration, inhibit M1 macrophage production and promote M2 macrophage generation. In synovial fluid, the expression levels of the proinflammatory cytokines, IL-1&#x3B2;, IL-6, and TNF-&#x3B1; were decreased and the release of the anti-inflammatory cytokine, IL-10 was increased. In vitro, macrophages treated with exosomes maintain chondrocytes&#x2019; chondrogenic characteristics and inhibit hypertrophy. Our results demonstrated that bone marrow mesenchymal stem cell-derived exosomes may relieve osteoarthritis by promoting the phenotypic transformation of synovial macrophages from M1 to M2.
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Integrated analysis of a competing endogenous RNA network reveals an 11-lncRNA prognostic signature in ovarian cancer

Yongjian Zhang, Hu Zhou, Meiyin Zhang, Linan Xing, Chang Yang, Bairong Xia, Ge Lou,

https://doi.org/10.18632/aging.104116 pp 25153—25171

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Zhang Y, Zhou H, Zhang M, Xing L, Yang C, Xia B, Lou G, . Integrated analysis of a competing endogenous RNA network reveals an 11-lncRNA prognostic signature in ovarian cancer. . 12:25153-25171. https://doi.org/10.18632/aging.104116

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                TY  - JOUR
                AU  - Zhang, Yongjian 
                AU  - Zhou, Hu 
                AU  - Zhang, Meiyin 
                AU  - Xing, Linan 
                AU  - Yang, Chang 
                AU  - Xia, Bairong 
                AU  - Lou, Ge 
                TI  - Integrated analysis of a competing endogenous RNA network reveals an 11-lncRNA prognostic signature in ovarian cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104116
                DO  - 10.18632/aging.104116
                SP  - 25153
                EP  - 25171
                PY  - 
                AB  - Long noncoding RNA (lncRNA) can function as a competing endogenous RNA (ceRNA) involved in tumor initiation and progression. However, the prognostic roles of lncRNAs in the integrated analysis of the ceRNA network in ovarian cancer (OVC) are still lacking. This study aimed to identify lncRNAs associated with the prognosis of OVC. Differential expression analysis and WGCNA were used to screen OVC-specific RNAs. A lncRNA-miRNA-mRNA regulatory network consisting of 201 lncRNAs, 85 miRNA and 146 mRNAs was constructed, and functional enrichment and protein-protein network analyses were performed. Then, the OVC-specific RNAs were submitted to Cox regression analysis. Twelve differentially expressed lncRNAs and mRNAs were identified as significantly associated with OS of OVC patients. Meanwhile, 11 lncRNAs (including C4A-AS1, LINC02408, LINC00488) were established as prognostic risk formulas. The low-risk group had better OS and DFS than the high-risk group (P &lt;0.01). Univariate and multivariate Cox regression analyses revealed the 11-lncRNA risk score as an independent prognostic factor. A prognostic nomogram was developed based on independent prognostic factors. Our data provide evidence that the 11-lncRNA signature could serve as an independent prognostic indicator. This study also suggests that these 11 lncRNAs potentially participate in the progression of OVC.
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Vascular endothelial growth factor receptor-2 and its association with tumor immune regulatory gene expression in hepatocellular carcinoma

Ze-Long Liu, Ling-Ling Zhu, Jing-Hua Liu, Zhang-Ya Pu, Zhi-Ping Ruan, Jiang Chen,

https://doi.org/10.18632/aging.104119 pp 25172—25188

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Liu Z, Zhu L, Liu J, Pu Z, Ruan Z, Chen J, . Vascular endothelial growth factor receptor-2 and its association with tumor immune regulatory gene expression in hepatocellular carcinoma. . 12:25172-25188. https://doi.org/10.18632/aging.104119

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                TY  - JOUR
                AU  - Liu, Ze-Long 
                AU  - Zhu, Ling-Ling 
                AU  - Liu, Jing-Hua 
                AU  - Pu, Zhang-Ya 
                AU  - Ruan, Zhi-Ping 
                AU  - Chen, Jiang 
                TI  - Vascular endothelial growth factor receptor-2 and its association with tumor immune regulatory gene expression in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104119
                DO  - 10.18632/aging.104119
                SP  - 25172
                EP  - 25188
                PY  - 
                AB  - Anti-vascular endothelial growth factor (anti-VEGF) drugs have long been the only first-line treatment for advanced or unresectable hepatocellular carcinoma (HCC). Recently, the combination of bevacizumab (an anti-VEGF drug) and atezolizumab (an immune checkpoint blockade, ICB) has been proven to have superior efficacy over sorafenib. However, the complex association between VEGF signaling pathway and tumor immune microenvironment is still largely unknown. Here, we analyzed the RNA sequencing and clinical data of 365 HCC patients obtained from The Cancer Genome Atlas to investigate the potential correlation between VEGF signaling pathway and tumor immune microenvironment, including immune cell infiltration, 66 immune markers, genomic instability, and immune-related pathways. Our study revealed that VEGF signaling pathway score was positively correlated with immune cell infiltration and the expression profile of 66 immune markers. Enrichment analysis indicated that genes differentially expressed between two VEGF score subtypes were enriched in many immune-related Gene Ontology terms. Most importantly, both VEGF signaling pathway and activated CD8+ T cells were positively correlated with prognosis. Our findings suggest the co-activation of VEGF signaling pathway and tumor immune microenvironment in HCC patients, indicating the underlining mechanism of combination therapy including anti-VEGF drugs and ICBs.
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Histone methyltransferase SETD2 inhibits tumor growth via suppressing CXCL1-mediated activation of cell cycle in lung adenocarcinoma

You Zhou, Xiao Zheng, Bin Xu, Haifeng Deng, Lujun Chen, Jingting Jiang,

https://doi.org/10.18632/aging.104120 pp 25189—25206

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Zhou Y, Zheng X, Xu B, Deng H, Chen L, Jiang J, . Histone methyltransferase SETD2 inhibits tumor growth via suppressing CXCL1-mediated activation of cell cycle in lung adenocarcinoma. . 12:25189-25206. https://doi.org/10.18632/aging.104120

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                TY  - JOUR
                AU  - Zhou, You 
                AU  - Zheng, Xiao 
                AU  - Xu, Bin 
                AU  - Deng, Haifeng 
                AU  - Chen, Lujun 
                AU  - Jiang, Jingting 
                TI  - Histone methyltransferase SETD2 inhibits tumor growth via suppressing CXCL1-mediated activation of cell cycle in lung adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104120
                DO  - 10.18632/aging.104120
                SP  - 25189
                EP  - 25206
                PY  - 
                AB  - The histone H3 lysine 36 methyltransferase SET-domain-containing 2 (SETD2) has been reported to be frequently mutated or deleted in many types of human cancer. However, the role of SETD2 in lung adenocarcinoma (LUAD) has not been well documented. In the present study, we found that SETD2 was significantly down-regulated both in LUAD tissues and cell lines. Functionally, the increased expression of SETD2 significantly attenuated the proliferation of cancer cells by affecting the cell cycle, whereas SETD2 deficiency dramatically improved these proliferative abilities of cancer cells. Through conjoint analysis of RNA-seq and ChIP data, we identified a functional target gene of SETD2, CXCL1, and its expression was negatively correlated with that of SETD2. Moreover, SETD2 deletion stimulated cell cycle-related proteins to promote LUAD. Further mechanistic studies demonstrated that histone H3 lysine 36 trimethylation (H3K36me3) catalyzed by SETD2 interacted with the promoter of CXCL1 to regulate its transcription and downstream signaling pathways, contributing to tumorigenesis in vitro and in vivo. Our findings suggested that SETD2 inhibited tumor growth via suppressing CXCL1-mediated activation of cell cycle, indicating that the regulation of H3K36me3 level by targeting SETD2 and/or the administration of downstream CXCL1 might represent a potential therapeutic way for new treatment in LUAD.
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Impairment of Pol β-related DNA base-excision repair leads to ovarian aging in mice

Ke Hua, Liping Wang, Junhua Sun, Nanhai Zhou, Yilan Zhang, Feng Ji, Li Jing, Yang Yang, Wen Xia, Zhigang Hu, Feiyan Pan, Xi Chen, Bing Yao, Zhigang Guo,

https://doi.org/10.18632/aging.104123 pp 25207—25228

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Hua K, Wang L, Sun J, Zhou N, Zhang Y, Ji F, Jing L, Yang Y, Xia W, Hu Z, Pan F, Chen X, Yao B, et al, . Impairment of Pol β-related DNA base-excision repair leads to ovarian aging in mice. . 12:25207-25228. https://doi.org/10.18632/aging.104123

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                TY  - JOUR
                AU  - Hua, Ke 
                AU  - Wang, Liping 
                AU  - Sun, Junhua 
                AU  - Zhou, Nanhai 
                AU  - Zhang, Yilan 
                AU  - Ji, Feng 
                AU  - Jing, Li 
                AU  - Yang, Yang 
                AU  - Xia, Wen 
                AU  - Hu, Zhigang 
                AU  - Pan, Feiyan 
                AU  - Chen, Xi 
                AU  - Yao, Bing 
                AU  - Guo, Zhigang 
                TI  - Impairment of Pol β-related DNA base-excision repair leads to ovarian aging in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104123
                DO  - 10.18632/aging.104123
                SP  - 25207
                EP  - 25228
                PY  - 
                AB  - The mechanism underlying the association between age and depletion of the human ovarian follicle reserves remains uncertain. Many identified that impaired DNA polymerase &#x3B2; (Pol &#x3B2;)-mediated DNA base-excision repair (BER) drives to mouse oocyte aging. With aging, DNA lesions accumulate in primordial follicles. However, the expression of most DNA BER genes, including APE1, OGG1, XRCC1, Ligase I, Ligase &#x3B1;, PCNA and FEN1, remains unchanged during aging in mouse oocytes. Also, the reproductive capacity of Pol &#x3B2;+/- heterozygote mice was impaired, and the primordial follicle counts were lower than that of wild type (wt) mice. The DNA lesions of heterozygous mice increased. Moreover, the Pol &#x3B2; knockdown leads to increased DNA damage in oocytes and decreased survival rate of oocytes. Oocytes over-expressing Pol &#x3B2; showed that the vitality of senescent cells enhances significantly. Furthermore, serum concentrations of anti-M&#xFC;llerian hormone (AMH) indicated that the ovarian reserves of young mice with Pol &#x3B2; germline mutations were lower than those in wt. These data show that Pol &#x3B2;-related DNA BER efficiency is a major factor governing oocyte aging in mice.
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Exposure to ozone impacted Th1/Th2 imbalance of CD⁴⁺ T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling

Yangyang Wei, Baofen Han, Wenjuan Dai, Shufang Guo, Caiping Zhang, Lixuan Zhao, Yan Gao, Yi Jiang, Xiaomei Kong,

https://doi.org/10.18632/aging.104124 pp 25229—25255

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Wei Y, Han B, Dai W, Guo S, Zhang C, Zhao L, Gao Y, Jiang Y, Kong X, . Exposure to ozone impacted Th1/Th2 imbalance of CD⁴⁺ T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling. . 12:25229-25255. https://doi.org/10.18632/aging.104124

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Provider: 
 TY - JOUR
 AU - Wei, Yangyang 
 AU - Han, Baofen 
 AU - Dai, Wenjuan 
 AU - Guo, Shufang 
 AU - Zhang, Caiping 
 AU - Zhao, Lixuan 
 AU - Gao, Yan 
 AU - Jiang, Yi 
 AU - Kong, Xiaomei 
 TI - Exposure to ozone impacted Th1/Th2 imbalance of CD4+ T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104124
 DO - 10.18632/aging.104124
 SP - 25229
 EP - 25255
 PY - 
 AB - This investigation attempted to elucidate whether lncRNA PVT1-led miRNA axes participated in aggravating ozone-triggered asthma progression. One hundred and sixty-eight BALB/c mice were evenly divided into saline+air group, ovalbumin+air group, saline+ozone group and ovalbumin+ozone group. Correlations were evaluated between PVT1 expression and airway smooth muscle function/inflammatory cytokine release among the mice models. Furthermore, pcDNA3.1-PVT1 and si-PVT1 were, respectively, transfected into CD4+T cells and airway smooth muscle cells (ASMCs), and activities of the cells were observed. Ultimately, a cohort of asthma patients was recruited to estimate the diagnostic performance of PVT1. It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of ovalbumin+air group and saline+ozone group (P&lt;0.05). Moreover, pcDNA3.1-PVT1 significantly brought down Th1/Th2 ratio in CD4+ T cells by depressing miR-15a-5p expression and activating PI3K-Akt-mTOR signaling (P&lt;0.05). The PVT1 also facilitated ASMC proliferation by sponging miR-29c-3p and motivating PI3K-Akt-mTOR signaling (P&lt;0.05). Additionally, PVT1 seemed promising in diagnosis of asthma, with favorable sensitivity (i.e. 0.844) and specificity (i.e. 0.978). Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.
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A systematic review and network meta-analysis of single nucleotide polymorphisms associated with pancreatic cancer risk

Zhuo-Miao Ye, Li-Juan Li, Ming-Bo Luo, Hong-Yuan Qing, Jing-Hui Zheng, Chi Zhang, Yun-Xin Lu, You-Ming Tang,

https://doi.org/10.18632/aging.104128 pp 25256—25274

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Ye Z, Li L, Luo M, Qing H, Zheng J, Zhang C, Lu Y, Tang Y, . A systematic review and network meta-analysis of single nucleotide polymorphisms associated with pancreatic cancer risk. . 12:25256-25274. https://doi.org/10.18632/aging.104128

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                TY  - JOUR
                AU  - Ye, Zhuo-Miao 
                AU  - Li, Li-Juan 
                AU  - Luo, Ming-Bo 
                AU  - Qing, Hong-Yuan 
                AU  - Zheng, Jing-Hui 
                AU  - Zhang, Chi 
                AU  - Lu, Yun-Xin 
                AU  - Tang, You-Ming 
                TI  - A systematic review and network meta-analysis of single nucleotide polymorphisms associated with pancreatic cancer risk
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104128
                DO  - 10.18632/aging.104128
                SP  - 25256
                EP  - 25274
                PY  - 
                AB  - In this meta-analysis, we systematically investigated the correlation between single nucleotide polymorphisms (SNPs) and pancreatic cancer (PC) risk. We searched PubMed, Network Science, EMBASE, Cochrane Library, China National Knowledge Infrastructure (CNKI), China Science and Technology Periodical Database (VIP), and Wanfang databases up to January 2020 for studies on PC risk-associated SNPs. We identified 45 case-control studies (36,360 PC patients and 54,752 non-cancer individuals) relating to investigations of 27 genes and 54 SNPs for this meta-analysis. Direct meta-analysis followed by network meta-analysis and Thakkinstian algorithm analysis showed that homozygous genetic models for CTLA-4 rs231775 (OR =0.326; 95% CI: 0.218-0.488) and VDR rs2228570 (OR = 1.976; 95% CI: 1.496-2.611) and additive gene model for TP53 rs9895829 (OR = 1.231; 95% CI: 1.143-1.326) were significantly associated with PC risk. TP53 rs9895829 was the most optimal SNP for diagnosing PC susceptibility with a false positive report probability &lt; 0.2 at a stringent prior probability value of 0.00001. This systematic review and meta-analysis suggest that TP53 rs9895829, VDR rs2228570, and CTLA-4 rs231775 are significantly associated with PC risk. We also demonstrate that TP53 rs9895829 is a potential diagnostic biomarker for estimating PC risk.
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DNA methylation-based lung adenocarcinoma subtypes can predict prognosis, recurrence, and immunotherapeutic implications

Feng Xu, Lulu He, Xueqin Zhan, Jiexin Chen, Huan Xu, Xiaoling Huang, Yangyi Li, Xiaohe Zheng, Ling Lin, Yongsong Chen,

https://doi.org/10.18632/aging.104129 pp 25275—25293

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Xu F, He L, Zhan X, Chen J, Xu H, Huang X, Li Y, Zheng X, Lin L, Chen Y, . DNA methylation-based lung adenocarcinoma subtypes can predict prognosis, recurrence, and immunotherapeutic implications. . 12:25275-25293. https://doi.org/10.18632/aging.104129

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                TY  - JOUR
                AU  - Xu, Feng 
                AU  - He, Lulu 
                AU  - Zhan, Xueqin 
                AU  - Chen, Jiexin 
                AU  - Xu, Huan 
                AU  - Huang, Xiaoling 
                AU  - Li, Yangyi 
                AU  - Zheng, Xiaohe 
                AU  - Lin, Ling 
                AU  - Chen, Yongsong 
                TI  - DNA methylation-based lung adenocarcinoma subtypes can predict prognosis, recurrence, and immunotherapeutic implications
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104129
                DO  - 10.18632/aging.104129
                SP  - 25275
                EP  - 25293
                PY  - 
                AB  - The marked heterogeneity of lung adenocarcinoma (LUAD) makes its diagnosis and treatment difficult. In addition, the aberrant DNA methylation profile contributes to tumor heterogeneity and alters the immune response. We used DNA methylation array data from publicly available databases to establish a predictive model for LUAD prognosis. Thirty-three methylation sites were identified as specific prognostic biomarkers, independent of patients&#x2019; clinical characteristics. These methylation profiles were used to identify potential drug candidates and study the immune microenvironment of LUAD and response to immunotherapy. When compared with the high-risk group, the low-risk group had a lower recurrence rate and favorable prognosis. The tumor microenvironment differed between the two groups as reflected by the higher number of resting dendritic cells and a lower number of monocytes and resting mast cells in the low-risk group. Moreover, low-risk patients reported higher immune and stromal scores, lower tumor purity, and higher expression of HLA genes. Low-risk patients responded well to immunotherapy due to higher expression of immune checkpoint molecules and lower stemness index. Thus, our model predicted a favorable prognosis and increased overall survival for patients in the low-risk methylation group. Further, this model could provide potential drug targets to develop effective immunotherapies for LUAD.
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Multiwalled carbon nanotubes inhibit cell migration and invasion by destroying actin cytoskeleton via mitochondrial dysfunction in ovarian cancer cells

Ping Zhang, Jiangyan Teng, Lijuan Wang,

https://doi.org/10.18632/aging.104130 pp 25294—25303

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Zhang P, Teng J, Wang L, . Multiwalled carbon nanotubes inhibit cell migration and invasion by destroying actin cytoskeleton via mitochondrial dysfunction in ovarian cancer cells. . 12:25294-25303. https://doi.org/10.18632/aging.104130

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                TY  - JOUR
                AU  - Zhang, Ping 
                AU  - Teng, Jiangyan 
                AU  - Wang, Lijuan 
                TI  - Multiwalled carbon nanotubes inhibit cell migration and invasion by destroying actin cytoskeleton via mitochondrial dysfunction in ovarian cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104130
                DO  - 10.18632/aging.104130
                SP  - 25294
                EP  - 25303
                PY  - 
                AB  - Objective: This study aimed to investigate the effects of multiwalled carbon nanotubes (MWCNTs) on cytotoxicity and tumor metastasis in ovarian cancer cells, and further explored its mechanism.
                Results: MWCNTs significantly inhibited cell viability and the clone number, increased the cell number of S phage, promoted cell apoptosis, as well as suppressed cell migration and invasion, and damaged the structure of actin cytoskeleton in a dose-dependent manner in SKOV3. Moreover, MWCNTs treatment obviously damaged the structure of actin cytoskeleton of SKOV3, and inhibited the activities of mitochondrial electron transfer chain complexes I-V.
                Conclusions: MWCNTs might influence the assembly of actin cytoskeleton by disrupting mitochondrial function, thereby inhibiting migration and invasion of SKOV3.
                Methods: The characterization of MWCNTs was analyzed by UV visible light absorption spectroscopy and transmission electron microscopy. SKOV3 cells were exposed to different doses of MWCNTs. Then, in vitro cytotoxicity of MWCNTs was evaluated by MTT assay, colony-forming assay, cell cycle, and cell apoptosis assay. Moreover, the effects of MWCNTs on cell migration and invasion as well as actin cytoskeleton were explored in SKOV3 cells. Furthermore, the mitochondrial membrane potential and the activities of mitochondrial electron transfer chain complexes I-V were measured.
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Identification of novel prognostic biomarkers in renal cell carcinoma

Yuanzhang Zou, Qiu Lu, Qin Yao, Di Dong, Binghai Chen,

https://doi.org/10.18632/aging.104131 pp 25304—25318

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Zou Y, Lu Q, Yao Q, Dong D, Chen B, . Identification of novel prognostic biomarkers in renal cell carcinoma. . 12:25304-25318. https://doi.org/10.18632/aging.104131

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                TY  - JOUR
                AU  - Zou, Yuanzhang 
                AU  - Lu, Qiu 
                AU  - Yao, Qin 
                AU  - Dong, Di 
                AU  - Chen, Binghai 
                TI  - Identification of novel prognostic biomarkers in renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104131
                DO  - 10.18632/aging.104131
                SP  - 25304
                EP  - 25318
                PY  - 
                AB  - Objective: To identify novel prognostic biomarkers in renal cell carcinoma (RCC).
                Results: 12 coding genes and one miRNA were finally identified as prognostic biomarkers. All of them were related to a poor prognosis. Lower expression levels of the coding genes were observed in higher clinical stages. Prognostic signatures including 7 biomarkers were identified. Patients in the high-risk group had worse survival than those in the low-risk group. The areas under the curves in different years indicated that it was a valuable signature in prognosis. It was found that elevated WDR72 inhibited the survival and invasion of 786-O and 769P cells in vitro.
                Conclusions: Thirteen prognostic biomarkers of RCC were identified. Among them, 7 biomarkers comprised a signature to evaluate the RCC prognosis. WDR72 was a cancer suppressor and a potential therapeutic target in RCC.
                Methods: Differentially expressed genes/miRNAs (DEGs/DEMs) and prognosis-related genes/miRNAs were acquired from public database. Prognostic biomarkers were identified by overlapping the significant DEGs/DEMs and prognosis-related genes/miRNAs. The associations between these biomarkers and the clinical stages were analyzed. All of these prognostic biomarkers were further investigated with multi-variable Cox regression. Finally, the inhibitory effect of WDR72 on the growth and invasion of RCC cells was studied.
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Cerebellar-limbic neurocircuit is the novel biosignature of physio-cognitive decline syndrome

Li-Kuo Liu, Kun-Hsien Chou, Chih-Chin Heather Hsu, Li-Ning Peng, Wei-Ju Lee, Wei-Ta Chen, Ching-Po Lin, Chih-Ping Chung, Pei-Ning Wang, Liang-Kung Chen,

https://doi.org/10.18632/aging.104135 pp 25319—25336

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Liu L, Chou K, Hsu CH, Peng L, Lee W, Chen W, Lin C, Chung C, Wang P, Chen L, . Cerebellar-limbic neurocircuit is the novel biosignature of physio-cognitive decline syndrome. . 12:25319-25336. https://doi.org/10.18632/aging.104135

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                TY  - JOUR
                AU  - Liu, Li-Kuo 
                AU  - Chou, Kun-Hsien 
                AU  - Hsu, Chih-Chin Heather 
                AU  - Peng, Li-Ning 
                AU  - Lee, Wei-Ju 
                AU  - Chen, Wei-Ta 
                AU  - Lin, Ching-Po 
                AU  - Chung, Chih-Ping 
                AU  - Wang, Pei-Ning 
                AU  - Chen, Liang-Kung 
                TI  - Cerebellar-limbic neurocircuit is the novel biosignature of physio-cognitive decline syndrome
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104135
                DO  - 10.18632/aging.104135
                SP  - 25319
                EP  - 25336
                PY  - 
                AB  - Both physical and cognitive deficits occur in the aging process. We operationally defined the phenomenon as physio-cognitive decline syndrome (PCDS) and aimed to decipher its corresponding neuroanatomy patterns and neurocircuit. High resolution 3T brain magnetic resonance imaging (MRI) images from a community-dwelling longitudinal aging cohort were analysed. PCDS was defined as weakness (handgrip strength) and/or slowness (gait speed) concomitant with impairment in any cognitive domain (defined by 1.5 standard deviation below age, sex-matched norms), but without dementia or disability. Among 1196 eligible &#x2265; 50-year-old (62&#xB1;9 years, 47.6%men) subjects, 15.9% had PCDS. Compared to the other participants, individuals with PCDS had significantly lower gray-matter volume (GMV) in the bilateral amygdala and thalamus, right hippocampus, right temporo-occipital cortex, and left cerebellum VI and V regions. The regions of reduced GMV in people with PCDS were similar between the middle-aged and older adults; whereas larger clusters with more extensive GMV-depleted regions were observed in &#x2265;65-year-olds with PCDS. Diffusion-weighted tractography showed disrupted hippocampus-amygdala-cerebellum connections in subjects with PCDS. The neuroanatomic characteristics revealed by this study provide evidence for pathophysiological processes associated with concomitant physio-cognitive decline in the elderly. This neurocircuit might constitute a target for future preventive interventions.
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Single cell sequencing reveals cell populations that predict primary resistance to imatinib in chronic myeloid leukemia

Weilong Zhang, Beibei Yang, Linqian Weng, Jiangtao Li, Jiefei Bai, Ting Wang, Jingwen Wang, Jin Ye, Hongmei Jing, Yuchen Jiao, Xixi Chen, Hui Liu, Yi-Xin Zeng,

https://doi.org/10.18632/aging.104136 pp 25337—25355

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Zhang W, Yang B, Weng L, Li J, Bai J, Wang T, Wang J, Ye J, Jing H, Jiao Y, Chen X, Liu H, Zeng Y, . Single cell sequencing reveals cell populations that predict primary resistance to imatinib in chronic myeloid leukemia. . 12:25337-25355. https://doi.org/10.18632/aging.104136

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                TY  - JOUR
                AU  - Zhang, Weilong 
                AU  - Yang, Beibei 
                AU  - Weng, Linqian 
                AU  - Li, Jiangtao 
                AU  - Bai, Jiefei 
                AU  - Wang, Ting 
                AU  - Wang, Jingwen 
                AU  - Ye, Jin 
                AU  - Jing, Hongmei 
                AU  - Jiao, Yuchen 
                AU  - Chen, Xixi 
                AU  - Liu, Hui 
                AU  - Zeng, Yi-Xin 
                TI  - Single cell sequencing reveals cell populations that predict primary resistance to imatinib in chronic myeloid leukemia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104136
                DO  - 10.18632/aging.104136
                SP  - 25337
                EP  - 25355
                PY  - 
                AB  - The treatment of chronic myeloid leukemia (CML), a disease caused by t(9;22)(q34;q11) reciprocal translocation, has advanced largely through the use of targeted tyrosine kinase inhibitors (TKIs). To identify molecular differences that might distinguish TKI responders from non-responders, we performed single cell RNA sequencing on cells (n = 41,723 cells) obtained from the peripheral blood of four CML patients at different stages of treatment to generate single cell expression profiles. Analysis of our single cell expression profiles in conjunction with those previously obtained from the bone marrow of additional CML patients and healthy donors (total = 69,263 cells) demonstrated that imatinib treatment significantly altered leukocyte population compositions in both responders and non-responders, and affected the expression profiles of multiple cell populations, including non-neoplastic cell types. Notably, in imatinib poor-responders, patient-specific pre-treatment unique stem/progenitor cells became enriched in peripheral blood compared to the responders. These results indicate that resistance to TKIs might be intrinsic in some CML patients rather than acquired, and that non-neoplastic immune cell types may also play vital roles in dispersing the responsiveness of patients to TKIs. Furthermore, these results demonstrated the potential utility of peripheral blood as a diagnostic tool in the TKI sensitivity of CML patients.
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Development and validation of a prognostic model for kidney renal clear cell carcinoma based on RNA binding protein expression

Yuzhu Xiang, Shengcai Zhou, Jian Hao, Chunhong Zhong, Qimei Ma, Zhuolun Sun, Chunxiao Wei,

https://doi.org/10.18632/aging.104137 pp 25356—25372

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Xiang Y, Zhou S, Hao J, Zhong C, Ma Q, Sun Z, Wei C, . Development and validation of a prognostic model for kidney renal clear cell carcinoma based on RNA binding protein expression. . 12:25356-25372. https://doi.org/10.18632/aging.104137

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                TY  - JOUR
                AU  - Xiang, Yuzhu 
                AU  - Zhou, Shengcai 
                AU  - Hao, Jian 
                AU  - Zhong, Chunhong 
                AU  - Ma, Qimei 
                AU  - Sun, Zhuolun 
                AU  - Wei, Chunxiao 
                TI  - Development and validation of a prognostic model for kidney renal clear cell carcinoma based on RNA binding protein expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104137
                DO  - 10.18632/aging.104137
                SP  - 25356
                EP  - 25372
                PY  - 
                AB  - Dysregulated expression of RNA-binding proteins (RBPs) is strongly associated with the development and progression of multiple tumors. However, little is known about the role of RBPs in kidney renal clear cell carcinoma (KIRC). In this study, we examined RBP expression profiles using The Cancer Genome Atlas database and identified 133 RBPs that were differentially expressed in KIRC and non-tumor tissues. We then systematically analyzed the potential biological functions of these RBPs and established PPIs. Based on Lasso regression and Cox survival analyses, we constructed a risk model that could independently and accurately predict prognosis based on seven RBPs (NOL12, PABPC1L, RNASE2, RPL22L1, RBM47, OASL, and YBX3). Survival times were shorter in patients with high risk scores for cohorts stratified by different characteristics. Gene set enrichment analysis was also performed to further understand functional differences between high- and low-risk groups. Finally, we developed a clinical nomogram with a concordance index of 0.792 for estimating 3- and 5-year survival probabilities. Our results demonstrate that this risk model could potentially improve individualized diagnostic and therapeutic strategies.
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Effect of paternal age on offspring birth defects: a systematic review and meta-analysis

Yiwei Fang, Yongfeng Wang, Meilin Peng, Jia Xu, Zunpan Fan, Chunyan Liu, Kai Zhao, Huiping Zhang,

https://doi.org/10.18632/aging.104141 pp 25373—25394

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Fang Y, Wang Y, Peng M, Xu J, Fan Z, Liu C, Zhao K, Zhang H, . Effect of paternal age on offspring birth defects: a systematic review and meta-analysis. . 12:25373-25394. https://doi.org/10.18632/aging.104141

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                TY  - JOUR
                AU  - Fang, Yiwei 
                AU  - Wang, Yongfeng 
                AU  - Peng, Meilin 
                AU  - Xu, Jia 
                AU  - Fan, Zunpan 
                AU  - Liu, Chunyan 
                AU  - Zhao, Kai 
                AU  - Zhang, Huiping 
                TI  - Effect of paternal age on offspring birth defects: a systematic review and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104141
                DO  - 10.18632/aging.104141
                SP  - 25373
                EP  - 25394
                PY  - 
                AB  - Objective: This systematic review and meta-analysis was aimed at determining whether paternal age is a risk factor for offspring birth defects.
                Results: A total of 38 and 11 studies were included in the systematic review and meta-analysis, respectively. Compared with reference, fathers aged 25 to 29, young fathers (&lt; 20 years) could increase the risk of urogenital abnormalities (OR: 1.50, 95 % CI: 1.03&#x2013;2.19) and chromosome disorders (OR: 1.38, 95 % CI: 1.12&#x2013;1.52) in their offsprings; old fathers (&#x2265; 40 years) could increase the risk of cardiovascular abnormalities (OR: 1.10, 95 % CI: 1.01&#x2013;1.20), facial deformities (OR: 1.08, 95 % CI: 1.00&#x2013;1.17), urogenital abnormalities (OR: 1.28, 95 % CI: 1.07&#x2013;1.52), and chromosome disorders (OR: 1.30, 95 % CI: 1.12&#x2013;1.52).
                Conclusions: Our study indicated that paternal age is associated with a moderate increase in the incidence of urogenital and cardiovascular abnormalities, facial deformities, and chromosome disorders.
                Methods: PubMed, Web of Science, the Cochrane Library, and Embase were searched for relevant literatures from 1960 to February 2020. The systematic review follows PRISMA guidelines. Relevant meta-analyses were performed.
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Steroid 5 alpha-reductase 3 (SRD5A3) promotes tumor growth and predicts poor survival of human hepatocellular carcinoma (HCC)

Qicong Mai, Dafeng Sheng, Chengcong Chen, Qing Gou, Meng Chen, Xiaoting Huang, Heng Yin, Xiaoming Chen, Zide Chen,

https://doi.org/10.18632/aging.104142 pp 25395—25411

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Mai Q, Sheng D, Chen C, Gou Q, Chen M, Huang X, Yin H, Chen X, Chen Z, . Steroid 5 alpha-reductase 3 (SRD5A3) promotes tumor growth and predicts poor survival of human hepatocellular carcinoma (HCC). . 12:25395-25411. https://doi.org/10.18632/aging.104142

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                TY  - JOUR
                AU  - Mai, Qicong 
                AU  - Sheng, Dafeng 
                AU  - Chen, Chengcong 
                AU  - Gou, Qing 
                AU  - Chen, Meng 
                AU  - Huang, Xiaoting 
                AU  - Yin, Heng 
                AU  - Chen, Xiaoming 
                AU  - Chen, Zide 
                TI  - Steroid 5 alpha-reductase 3 (SRD5A3) promotes tumor growth and predicts poor survival of human hepatocellular carcinoma (HCC)
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104142
                DO  - 10.18632/aging.104142
                SP  - 25395
                EP  - 25411
                PY  - 
                AB  - Steroid 5 alpha-reductase 3 (SRD5A3) is an important molecule in glycosylation metabolism and steroid hormone formation. It is differentially expressed in human fetal liver, endometrial cancer and prostate cancer; however, its prognostic value and biological function in hepatocellular carcinoma (HCC) remain unclear. Here, bioinformatics analysis was employed to explore the expression and prognostic significance of SRD5A3 in various cancers including HCC. Additionally, clinical specimens of HCC were applied to analyze the expression of SRD5A3. SRD5A3-underexpressed HCC cell lines were established to test the effect of SRD5A3 on cell proliferation in in vitro and in vivo. We found that the elevated expression of SRD5A3 was common in many cancers with poor prognosis. Moreover, public datasets and our specimens revealed that SRD5A3 was also upregulated in HCC tissues and associated with clinical stage and patient&#x2019;s gender. Kaplan-Meier survival analysis showed that higher SRD5A3 level predicted poor overall survival, progression-free survival, relapse-free survival and disease specific survival in HCC patients. Further experiments showed that the lack of SRD5A3 inhibited the growth of HCC. Collectively, these findings indicate that SRD5A3 functions as an oncogene and might serve as a potential biomarker for prognosis and a therapeutic target for HCC.
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DNA methylomic homogeneity and heterogeneity in muscles and testes throughout pig adulthood

Min Zheng, Shijun Xiao, Tianfu Guo, Lin Rao, Longyun Li, Zhiyan Zhang, Lusheng Huang,

https://doi.org/10.18632/aging.104143 pp 25412—25431

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Zheng M, Xiao S, Guo T, Rao L, Li L, Zhang Z, Huang L, . DNA methylomic homogeneity and heterogeneity in muscles and testes throughout pig adulthood. . 12:25412-25431. https://doi.org/10.18632/aging.104143

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                TY  - JOUR
                AU  - Zheng, Min 
                AU  - Xiao, Shijun 
                AU  - Guo, Tianfu 
                AU  - Rao, Lin 
                AU  - Li, Longyun 
                AU  - Zhang, Zhiyan 
                AU  - Huang, Lusheng 
                TI  - DNA methylomic homogeneity and heterogeneity in muscles and testes throughout pig adulthood
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104143
                DO  - 10.18632/aging.104143
                SP  - 25412
                EP  - 25431
                PY  - 
                AB  - DNA methylome pattern is significantly different among tissues, ages, breeds, and genders. We assessed 20 methylome and transcriptome data in longissimus dorsi (LD) or testicles from Bamaxiang (BMX) and Large White pigs (LW) by deep sequencing technology. We identified ~55.7M CpGs and 5.30M, 0.20M, 1.20M, and 0.16M differential CpGs (P&lt;0.01) between tissues, ages, breeds, and genders, respectively. Interestingly, 7.54% of differentially methylated regions (DMRs) are co-localized with promoters, which potentially regulate gene expression. RNA-seq analysis revealed that 23.42% CpGs are significantly correlated with gene expression (mean |r|=0.58, P&lt;0.01), most of which are enriched in tissue-specific functions. Specially, we also found that the methylation levels in promoters of 655 genes were strongly associated with their expression levels (mean |r|=0.66, P&lt;0.01). In addition, differentially methylated CpGs (DMCpGs) between breeds in HOXC gene cluster imply important regulatory roles in myocytes hypertrophy and intermuscular fat (IMF) deposition. Dramatically, higher similarity of methylation pattern was observed within pedigree than across pedigrees, which indicates the existence of heritable methylation regions. In summary, a part of CpGs in promoter can change its methylation pattern and play a marked regulatory function in different physiological or natural environments.
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Different doses of ovalbumin exposure on dendritic cells determine their genetic/epigenetic regulation and T cell differentiation

Ying Wang, Zizhong Yu, Yue Zhou, Yun Zhu, Jinhui Wang, Junmei Fu, Yang Yuan, Shan Chen, Yanjun Wang, Wenting Yu, Pei Gao, Wanting Zhu, Qing Cheng, Seong H Cho, Weijia Kong, Jianjun Chen,

https://doi.org/10.18632/aging.104145 pp 25432—25451

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Wang Y, Yu Z, Zhou Y, Zhu Y, Wang J, Fu J, Yuan Y, Chen S, Wang Y, Yu W, Gao P, Zhu W, Cheng Q, et al, . Different doses of ovalbumin exposure on dendritic cells determine their genetic/epigenetic regulation and T cell differentiation. . 12:25432-25451. https://doi.org/10.18632/aging.104145

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                TY  - JOUR
                AU  - Wang, Ying 
                AU  - Yu, Zizhong 
                AU  - Zhou, Yue 
                AU  - Zhu, Yun 
                AU  - Wang, Jinhui 
                AU  - Fu, Junmei 
                AU  - Yuan, Yang 
                AU  - Chen, Shan 
                AU  - Wang, Yanjun 
                AU  - Yu, Wenting 
                AU  - Gao, Pei 
                AU  - Zhu, Wanting 
                AU  - Cheng, Qing 
                AU  - Cho, Seong H 
                AU  - Kong, Weijia 
                AU  - Chen, Jianjun 
                TI  - Different doses of ovalbumin exposure on dendritic cells determine their genetic/epigenetic regulation and T cell differentiation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104145
                DO  - 10.18632/aging.104145
                SP  - 25432
                EP  - 25451
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wang, Ying 
                AU  - Yu, Zizhong 
                AU  - Zhou, Yue 
                AU  - Zhu, Yun 
                AU  - Wang, Jinhui 
                AU  - Fu, Junmei 
                AU  - Yuan, Yang 
                AU  - Chen, Shan 
                AU  - Wang, Yanjun 
                AU  - Yu, Wenting 
                AU  - Gao, Pei 
                AU  - Zhu, Wanting 
                AU  - Cheng, Qing 
                AU  - Cho, Seong H 
                AU  - Kong, Weijia 
                AU  - Chen, Jianjun 
                TI  - Different doses of ovalbumin exposure on dendritic cells determine their genetic/epigenetic regulation and T cell differentiation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104145
                DO  - 10.18632/aging.104145
                SP  - 25432
                EP  - 25451
                PY  - 
                AB  - It has been reported that allergen dosage can impact the differentiation of dendritic cells (DCs)-mediated T cells. However, the mechanisms of such dose-dependent differentiation are poorly understood. In this study, bone marrow-derived immature DCs stimulated with Ovalbumin (OVA) of different concentrations (0, 10, 100, 1000, 10000&#x3BC;g/ml, respectively). DCs were then co-cultured with na&#xEF;ve T cells. RNA-sequencing detection and DNA methylation of DCs were performed. We show that when DCs were stimulated with low-dose (10&#x3BC;g/ml), 77 genes were up-regulated and 87 genes down-regulated. Most activated genes were related to ribosome synthesis and ion channel inhibition. At the medium-dose (100&#x3BC;g/ml), 339 genes were up-regulated and 168 genes down-regulated. Most activated genes involved cytokine synthesis and regulation of immune responses. At high-dose (10000&#x3BC;g/ml), 2497 genes were up-regulated and 1156 genes down-regulated. TNF signaling pathway, NF-kappa B signaling pathway, antigen processing and presentation signaling pathway were mostly up-regulated. The related co-stimulators, co-inhibitory molecules, inhibitory cytokines, negative regulating enzymes were highly expressed. The monocarbate, coenzyme, fatty acid, glucolipid, starch, sucrose and other metabolism-related signaling pathways were down-regulated. The profiles of DNA methylation and RNA synthesis of DCs varied with different doses of OVA, which serves to induce T cells to differentiate in various directions.
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Sevoflurane postconditioning reduces myocardial ischemia reperfusion injury-induced necroptosis by up-regulation of OGT-mediated O-GlcNAcylated RIPK3

Jing Zhang, Peng Yu, Fuzhou Hua, Yanhui Hu, Fan Xiao, Qin Liu, Dan Huang, Fumou Deng, Gen Wei, Wei Deng, Jianyong Ma, Wengen Zhu, Jiru Zhang, Shuchun Yu,

https://doi.org/10.18632/aging.104146 pp 25452—25468

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Zhang J, Yu P, Hua F, Hu Y, Xiao F, Liu Q, Huang D, Deng F, Wei G, Deng W, Ma J, Zhu W, Zhang J, et al, . Sevoflurane postconditioning reduces myocardial ischemia reperfusion injury-induced necroptosis by up-regulation of OGT-mediated O-GlcNAcylated RIPK3. . 12:25452-25468. https://doi.org/10.18632/aging.104146

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                TY  - JOUR
                AU  - Zhang, Jing 
                AU  - Yu, Peng 
                AU  - Hua, Fuzhou 
                AU  - Hu, Yanhui 
                AU  - Xiao, Fan 
                AU  - Liu, Qin 
                AU  - Huang, Dan 
                AU  - Deng, Fumou 
                AU  - Wei, Gen 
                AU  - Deng, Wei 
                AU  - Ma, Jianyong 
                AU  - Zhu, Wengen 
                AU  - Zhang, Jiru 
                AU  - Yu, Shuchun 
                TI  - Sevoflurane postconditioning reduces myocardial ischemia reperfusion injury-induced necroptosis by up-regulation of OGT-mediated O-GlcNAcylated RIPK3
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104146
                DO  - 10.18632/aging.104146
                SP  - 25452
                EP  - 25468
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhang, Jing 
                AU  - Yu, Peng 
                AU  - Hua, Fuzhou 
                AU  - Hu, Yanhui 
                AU  - Xiao, Fan 
                AU  - Liu, Qin 
                AU  - Huang, Dan 
                AU  - Deng, Fumou 
                AU  - Wei, Gen 
                AU  - Deng, Wei 
                AU  - Ma, Jianyong 
                AU  - Zhu, Wengen 
                AU  - Zhang, Jiru 
                AU  - Yu, Shuchun 
                TI  - Sevoflurane postconditioning reduces myocardial ischemia reperfusion injury-induced necroptosis by up-regulation of OGT-mediated O-GlcNAcylated RIPK3
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104146
                DO  - 10.18632/aging.104146
                SP  - 25452
                EP  - 25468
                PY  - 
                AB  - Inhalation anesthetics have been demonstrated to have protective effects against myocardial ischemia reperfusion injury (MIRI). O-linked GlcNAcylation (O-GlcNAc) modifications have been shown to protect against MIRI. This study aimed to investigate whether O-GlcNAcylation and necroptosis signaling were important for sevoflurane postconditioning (SPC) induced cardioprotective effects. Apart from rats in the SHAM and sevoflurane (SEVO) group, rats underwent 30 min ischemia followed by 2 h reperfusion. Cardiac hemodynamics and function were determined. In addition, myocardial infarction size, cardiac function parameters, myocardial lactic dehydrogenase (LDH) content, myocardium histopathological changes, necrotic myocardium, O-GlcNAcylation, and protein expression levels of necroptosis biomarkers were measured, together with co-immunoprecipitation experiments using proteins associated with the necroptosis pathway and O-GlcNAcylation. SPC reduced myocardial infarction size, ameliorated cardiac function, restored hemodynamic performance, improved histopathological changes, and reduced receptor-interacting protein kinase 1 (RIPK1)/receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like (MLKL) mediated necroptosis. In addition, SPC up-regulated O-GlcNAc transferase (OGT) mediated O-GlcNAcylation, increased O-GlcNAcylated RIPK3, and inhibited the association of RIPK3 and MLKL. However, OSMI-1, an OGT inhibitor, abolished SPC mediated cardioprotective effects and inhibited OGT mediated up-regulation of O-GlcNAcylation and down-regulation of RIPK3 and MLKL proteins induced by SPC. Our study demonstrated that SPC restrained MIRI induced necroptosis via regulating OGT mediated O-GlcNAcylation of RIPK3 and lessening the formulation of RIPK3/MLKL complex.
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Tumor necrosis factor superfamily 14 is critical for the development of renal fibrosis

You Li, Ming Tang, Bo Han, Shun Wu, Shu-jing Li, Qian-hui He, Feng Xu, Gui-qing Li, Kun Zhang, Xu Cao, Quan-you Zheng, Jian Chen, Di Yang, Gui-lian Xu, Ke-qin Zhang,

https://doi.org/10.18632/aging.104151 pp 25469—25486

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Li Y, Tang M, Han B, Wu S, Li S, He Q, Xu F, Li G, Zhang K, Cao X, Zheng Q, Chen J, Yang D, et al, . Tumor necrosis factor superfamily 14 is critical for the development of renal fibrosis. . 12:25469-25486. https://doi.org/10.18632/aging.104151

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                TY  - JOUR
                AU  - Li, You 
                AU  - Tang, Ming 
                AU  - Han, Bo 
                AU  - Wu, Shun 
                AU  - Li, Shu-jing 
                AU  - He, Qian-hui 
                AU  - Xu, Feng 
                AU  - Li, Gui-qing 
                AU  - Zhang, Kun 
                AU  - Cao, Xu 
                AU  - Zheng, Quan-you 
                AU  - Chen, Jian 
                AU  - Yang, Di 
                AU  - Xu, Gui-lian 
                AU  - Zhang, Ke-qin 
                TI  - Tumor necrosis factor superfamily 14 is critical for the development of renal fibrosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104151
                DO  - 10.18632/aging.104151
                SP  - 25469
                EP  - 25486
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, You 
                AU  - Tang, Ming 
                AU  - Han, Bo 
                AU  - Wu, Shun 
                AU  - Li, Shu-jing 
                AU  - He, Qian-hui 
                AU  - Xu, Feng 
                AU  - Li, Gui-qing 
                AU  - Zhang, Kun 
                AU  - Cao, Xu 
                AU  - Zheng, Quan-you 
                AU  - Chen, Jian 
                AU  - Yang, Di 
                AU  - Xu, Gui-lian 
                AU  - Zhang, Ke-qin 
                TI  - Tumor necrosis factor superfamily 14 is critical for the development of renal fibrosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104151
                DO  - 10.18632/aging.104151
                SP  - 25469
                EP  - 25486
                PY  - 
                AB  - Objective: Tumor necrosis factor superfamily protein 14 (TNFSF14) was recently identified as a risk factor in some fibrosis diseases. However, the role of TNFSF14 in renal fibrosis pathogenesis remains unknown.
                Results: It was found that TNFSF14 levels were significantly increased both in UUO-induced renal fibrotic mice and in patients with fibrotic nephropathy, compared with those in controls. Accordingly, Tnfsf14 deficiency led to a marked reduction in renal fibrosis lesions and inflammatory cytokines expression in the UUO mice. Furthermore, the levels of Sphk1, a critical molecule that causes fibrotic nephropathy, were remarkably reduced in Tnfsf14 KO mice with UUO surgery. In vitro recombinant TNFSF14 administration markedly up-regulated the expression of Sphk1 of primary mouse renal tubular epithelial cells (mTECs).
                Conclusion: TNFSF14 is a novel pro-fibrotic factor of renal fibrosis, for which TNFSF14 up-regulates Sphk1 expression, which may be the underlying mechanism of TNFSF14-mediated renal fibrosis.
                Methods: We investigated the effect of TNFSF14 on renal fibrosis and the relationship between TNFSF14 and pro-fibrotic factor sphingosine kinase 1 (Sphk1) by using the unilateral urethral obstruction (UUO)-induced mice renal fibrosis as a model and the specimen of patients with fibrosis nephropathy, by Masson trichrome staining, immunohistochemistry, qRT-PCR, and western blot analysis.
                ER  -

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Pentoxifylline enhances antioxidative capability and promotes mitochondrial biogenesis for improving age-related behavioral deficits

Yu Wang, Yunxiao Kang, Chunxiao Qi, Tianyun Zhang, Hui Zhao, Xiaoming Ji, Wensheng Yan, Yuanxiang Huang, Rui Cui, Guoliang Zhang, Geming Shi,

https://doi.org/10.18632/aging.104155 pp 25487—25504

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Wang Y, Kang Y, Qi C, Zhang T, Zhao H, Ji X, Yan W, Huang Y, Cui R, Zhang G, Shi G, . Pentoxifylline enhances antioxidative capability and promotes mitochondrial biogenesis for improving age-related behavioral deficits. . 12:25487-25504. https://doi.org/10.18632/aging.104155

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                TY  - JOUR
                AU  - Wang, Yu 
                AU  - Kang, Yunxiao 
                AU  - Qi, Chunxiao 
                AU  - Zhang, Tianyun 
                AU  - Zhao, Hui 
                AU  - Ji, Xiaoming 
                AU  - Yan, Wensheng 
                AU  - Huang, Yuanxiang 
                AU  - Cui, Rui 
                AU  - Zhang, Guoliang 
                AU  - Shi, Geming 
                TI  - Pentoxifylline enhances antioxidative capability and promotes mitochondrial biogenesis for improving age-related behavioral deficits
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104155
                DO  - 10.18632/aging.104155
                SP  - 25487
                EP  - 25504
                PY  - 
                AB  - Pentoxifylline (PTX) is a non-specific phosphodiesterase inhibitor with pleiotropic effects that is routinely used to treat peripheral vascular disease. In this study, we tested whether PTX could also counteract the detrimental effects of aging in the brain. To accomplish that, we treated aged rats with PTX and measured resulting behavioral alterations as well as changes in dopaminergic neurochemical levels, oxidative balance markers, mitochondrial function, nuclear factor erythroid 2-related factor 2 (Nrf2), peroxisome proliferator activated receptor-gamma coactivator 1-alpha (PGC-1&#x3B1;) and downstream gene expression, and cyclic adenosine monophosphate (cAMP) content in the brain. The results demonstrated that PTX improved motor and cognitive deficits and restored levels of dopamine and its metabolites in the brains of aged rats. PTX also reduced malondialdehyde levels and increased the GSH/GSSG ratio, mitochondrial ATP, nuclear Nrf2, and cAMP levels, and upregulated PGC-1&#x3B1;, nuclear respiratory factor 1, and mitochondrial transcription factor A expression in the substantia nigra and hippocampus of aged rats. Thus, increased nuclear Nrf2 levels and upregulation of PGC-1&#x3B1;, which enhance antioxidative capability and promote mitochondrial biogenesis, may be responsible for PTX-induced amelioration of behavioral deficits in aged rats.
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Sesn2 attenuates the damage of endothelial progenitor cells induced by angiotensin II through regulating the Keap1/Nrf2 signal pathway

Shiao Ding, Nan Ma, Hao Liu, Min Tang, Ju Mei,

https://doi.org/10.18632/aging.104156 pp 25505—25527

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Ding S, Ma N, Liu H, Tang M, Mei J, . Sesn2 attenuates the damage of endothelial progenitor cells induced by angiotensin II through regulating the Keap1/Nrf2 signal pathway. . 12:25505-25527. https://doi.org/10.18632/aging.104156

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                TY  - JOUR
                AU  - Ding, Shiao 
                AU  - Ma, Nan 
                AU  - Liu, Hao 
                AU  - Tang, Min 
                AU  - Mei, Ju 
                TI  - Sesn2 attenuates the damage of endothelial progenitor cells induced by angiotensin II through regulating the Keap1/Nrf2 signal pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104156
                DO  - 10.18632/aging.104156
                SP  - 25505
                EP  - 25527
                PY  - 
                AB  - Endothelial progenitor cell (EPC) dysfunction is an important physiopathological mechanism in the dynamics of the formation of atherosclerosis. It has been reported that angiotensin II (Ang-II) damages the function of EPCs in atherosclerotic plaque through induction of oxidative stress. Sestrin 2 (Sesn2) serves as an antioxidant role in oxidative stress, however, the exact mechanisms underlying the dynamics of how Sesn2 may factor into EPCs after Ang-II treatments needs to be illustrated. We isolated EPCs from human umbilical cord blood samples and treated with Ang-II. Western blotting, qRT-PCR, transwell assays, immunofluorescence and so on were used to investigate the mechanisms underlying the roles of Sesn2 in EPCs treated with Ang-II. Ang-II was found to promote the apoptosis of EPCs as well as inhibited the mRNA and protein expression of Sesn2. Upregulation of Sesn2 attenuated the negative effect of Ang-II. Sesn2 increased the protein expression of Nrf2 by enhancing P62-dependent autophagy. Silencing of Nrf2 enhanced the degree of apoptosis of EPCs as well as resulted in the impairment of EPC functions through inducing the promotion of (reactive oxygen species) ROS production. Our study results indicated that Sesn2 facilitated the viability of EPCs After treatment with Ang-II, as well as provided a potential therapeutic target to alleviate the progression of atherosclerosis.
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miRNA-122-5p stimulates the proliferation and DNA synthesis and inhibits the early apoptosis of human spermatogonial stem cells by targeting CBL and competing with lncRNA CASC7

Fan Zhou, Wei Chen, Yinghong Cui, Bang Liu, Qingqing Yuan, Zheng Li, Zuping He,

https://doi.org/10.18632/aging.104158 pp 25528—25546

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Zhou F, Chen W, Cui Y, Liu B, Yuan Q, Li Z, He Z, . miRNA-122-5p stimulates the proliferation and DNA synthesis and inhibits the early apoptosis of human spermatogonial stem cells by targeting CBL and competing with lncRNA CASC7. . 12:25528-25546. https://doi.org/10.18632/aging.104158

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                TY  - JOUR
                AU  - Zhou, Fan 
                AU  - Chen, Wei 
                AU  - Cui, Yinghong 
                AU  - Liu, Bang 
                AU  - Yuan, Qingqing 
                AU  - Li, Zheng 
                AU  - He, Zuping 
                TI  - miRNA-122-5p stimulates the proliferation and DNA synthesis and inhibits the early apoptosis of human spermatogonial stem cells by targeting CBL and competing with lncRNA CASC7
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104158
                DO  - 10.18632/aging.104158
                SP  - 25528
                EP  - 25546
                PY  - 
                AB  - Epigenetic regulators of human spermatogonia stem cells (SSCs) remain largely unknown. We found that miRNA-122-5p was upregulated in human spermatogonia from obstructive azoospermia (OA) patients compared with non-obstructive azoospermia (NOA). MiRNA-122-5p stimulated the proliferation and DNA synthesis of human SSCs, whereas it inhibited the early apoptosis of human SSCs. CBL was predicted and identified as a direct target of miRNA-122-5p in human SSCs. CBL silencing led to an enhancement of cell proliferation and DNA synthesis and neutralized the effect of miRNA-122-5p inhibitor on the DNA synthesis of human SSCs. The decrease in the early apoptosis of human SSCs was observed after CBL knockdown. By comparing the profiles of lncRNAs between OA and NOA spermatogonia, CASC7 was significantly deficient in OA spermatogonia, and it had a direct association with miRNA-122-5p. LncRNA CASC7 competed with miRNA-122-5p, and it suppressed the inhibition of CBL. Collectively, these results implicate that miRNA-122-5p enhances the proliferation and DNA synthesis and inhibits the early apoptosis of human SSCs by targeting CBL and competing with lncRNA CASC7. Therefore, this study provides novel insights into epigenetic regulation of fate determinations of human SSCs, and it offers new targets for gene therapy of male infertility that is associated with aging.
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LncRNA MAGI2-AS3 inhibits bladder cancer progression by targeting the miR-31-5p/TNS1 axis

Congyi Tang, Yi Cai, Huichuan Jiang, Zhengtong Lv, Changzhao Yang, Haozhe Xu, Zhi Li, Yuan Li,

https://doi.org/10.18632/aging.104162 pp 25547—25563

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Tang C, Cai Y, Jiang H, Lv Z, Yang C, Xu H, Li Z, Li Y, . LncRNA MAGI2-AS3 inhibits bladder cancer progression by targeting the miR-31-5p/TNS1 axis. . 12:25547-25563. https://doi.org/10.18632/aging.104162

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                TY  - JOUR
                AU  - Tang, Congyi 
                AU  - Cai, Yi 
                AU  - Jiang, Huichuan 
                AU  - Lv, Zhengtong 
                AU  - Yang, Changzhao 
                AU  - Xu, Haozhe 
                AU  - Li, Zhi 
                AU  - Li, Yuan 
                TI  - LncRNA MAGI2-AS3 inhibits bladder cancer progression by targeting the miR-31-5p/TNS1 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104162
                DO  - 10.18632/aging.104162
                SP  - 25547
                EP  - 25563
                PY  - 
                AB  - In this study, we performed bioinformatics analysis to identify the competing endogenous RNAs (ceRNAs) that regulate bladder cancer (BCa) progression. RNA-sequencing data analysis identified 2451 differentially expressed mRNAs, 174 differentially expressed lncRNAs, and 186 microRNAs (miRNAs) in BCa tissues (n=414) compared to the normal urothelial tissues (n=19) from the TGCA database. CeRNA network analysis of the differentially expressed lncRNAs and mRNAs showed strong positive correlation between lncRNA MAGI2-AS3 and Tensin 1 (TNS1) mRNA in BCa tissues. Bioinformatics analysis also showed that both MAGI2-AS3 and TNS1 mRNA sequences contain miR-31-5p binding sites. Furthermore, we observed significantly lower MAGI2-AS3 and TNS1 mRNA expression and higher miR-31-5p expression in the BCa tissues and cell lines (T24 and J82) compared with their corresponding controls. Functional and biochemical experiments in BCa cell lines including luciferase reporter assays showed that MAGI2-AS3 upregulated TNS1 by sponging miR-31-5p. Transwell assays showed that the MAGI2-AS3/miR-31-5p/TNS1 axis regulated migration and invasion ability of BCa cell lines. Moreover, immunohistochemical staining of paired BCa and normal urothelial tissues showed that low expression of TNS1 correlated with advanced tumor (T) stages and lymph node metastasis in BCa. In conclusion, our study demonstrates that the MAGI2-AS3/miR-31-5p/TNS1 axis regulates BCa progression.
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TRIM27 acts as an oncogene and regulates cell proliferation and metastasis in non-small cell lung cancer through SIX3-β-catenin signaling

Shiyuan Liu, Ying Tian, Ying Zheng, Yao Cheng, Danjie Zhang, Jiantao Jiang, Shaomin Li,

https://doi.org/10.18632/aging.104163 pp 25564—25580

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Liu S, Tian Y, Zheng Y, Cheng Y, Zhang D, Jiang J, Li S, . TRIM27 acts as an oncogene and regulates cell proliferation and metastasis in non-small cell lung cancer through SIX3-β-catenin signaling. . 12:25564-25580. https://doi.org/10.18632/aging.104163

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                TY  - JOUR
                AU  - Liu, Shiyuan 
                AU  - Tian, Ying 
                AU  - Zheng, Ying 
                AU  - Cheng, Yao 
                AU  - Zhang, Danjie 
                AU  - Jiang, Jiantao 
                AU  - Li, Shaomin 
                TI  - TRIM27 acts as an oncogene and regulates cell proliferation and metastasis in non-small cell lung cancer through SIX3-β-catenin signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104163
                DO  - 10.18632/aging.104163
                SP  - 25564
                EP  - 25580
                PY  - 
                AB  - The Wnt/&#x3B2;-catenin pathway plays vital roles in diverse biological processes, including cell differentiation, proliferation, migration, and insulin sensitivity. A recent study reported that the DNA-binding transcriptional factor SIX3 is essential during embryonic development in vertebrates and capable of downregulating target genes of the Wnt/&#x3B2;-catenin pathway in lung cancer, indicating negative regulation of Wnt/&#x3B2;-catenin activation. However, regulation of the SIX3-Wnt/&#x3B2;-catenin pathway axis remains unknown. We measured the expression of TRIM27 and SIX3 as well as investigated whether there was a correlation between them in lung cancer tissue samples. Herein, we found that the E3 ubiquitin ligase, TRIM27, ubiquitinates, and degrades SIX3. TRIM27 induces non-small cell lung cancer (NSCLC) cell proliferation and metastasis, and the expression of &#x3B2;-catenin, S100P, TGFB3, and MMP-9 were significantly inhibited by SIX3. Furthermore, XAV939 is a selective &#x3B2;-catenin-mediated transcription inhibitor that inhibited TRIM27- and SIX3-mediated NSCLC cell proliferation, migration, and invasion. Clinically, lung tissue samples of cancer patients showed increased TRIM27 expression and decreased SIX3 expression. Taken together, these data demonstrate that TRIM27 acts as an oncogene regulating cell proliferation and metastasis in NSCLC through SIX3-&#x3B2;-catenin signaling.
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A dual inhibitor targeting HMG-CoA reductase and histone deacetylase mitigates neurite degeneration in LRRK2-G2019S parkinsonism

Chin-Hsien Lin, Han-Yi Lin, Jim-Min Fang, Ching-Chow Chen,

https://doi.org/10.18632/aging.104165 pp 25581—25598

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Lin C, Lin H, Fang J, Chen C, . A dual inhibitor targeting HMG-CoA reductase and histone deacetylase mitigates neurite degeneration in LRRK2-G2019S parkinsonism. . 12:25581-25598. https://doi.org/10.18632/aging.104165

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 TY - JOUR
 AU - Lin, Chin-Hsien 
 AU - Lin, Han-Yi 
 AU - Fang, Jim-Min 
 AU - Chen, Ching-Chow 
 TI - A dual inhibitor targeting HMG-CoA reductase and histone deacetylase mitigates neurite degeneration in LRRK2-G2019S parkinsonism
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104165
 DO - 10.18632/aging.104165
 SP - 25581
 EP - 25598
 PY - 
 AB - Parkinson&#x2019;s disease (PD) is among the most common neurodegenerative disorders, and its etiology involves both genetic and environmental factors. The leucine-rich repeat kinase (LRRK2) G2019S mutation is the most common genetic cause of familial and sporadic PD. Current treatment is limited to dopaminergic supplementation, as no disease-modifying therapy is available yet. Recent evidence reveals that HMG-CoA reductase (HMGR) inhibitors (statins) exert neuroprotection through anti-neuroinflammatory effects, and histone deacetylase (HDAC) inhibitors mitigate neurodegeneration by promoting the transcription of neuronal survival factors. We designed and synthesized a dual inhibitor, statin hydroxamate JMF3086, that simultaneously inhibits HMGR and HDAC, and examined its neuroprotective effects on LRRK2-G2019S parkinsonism. JMF3086 restored dopaminergic neuron loss in aged LRRK2-G2019S flies and rescued neurite degeneration in primary hippocampal and dopaminergic neurons isolated from transgenic LRRK2-G2019S mice. The molecular mechanisms included downregulation of ERK1/2 phosphorylation, increased anti-apoptotic Akt phosphorylation, and inhibition of GSK3&#x3B2; activity to maintain cytoskeletal stability in stably transfected LRRK2-G2019S SH-SY5Y human dopaminergic cells. JMF3086 also promoted a-tubulin acetylation and kinesin-1 expression, facilitating antegrade mitochondrial transport in axons. Our findings demonstrate that JMF3086 exerted beneficial effects on restoring LRRK2-G2019S neurite degeneration by maintaining microtubule stability. This dual-target compound may be a promising mechanism-based therapy for PD.
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Silencing hTERT attenuates cancer stem cell-like characteristics and radioresistance in the radioresistant nasopharyngeal carcinoma cell line CNE-2R

Kaihua Chen, Ling Li, Song Qu, Xinbin Pan, Yongchu Sun, Fangzhu Wan, Binbin Yu, Lei Zhou, Xiaodong Zhu,

https://doi.org/10.18632/aging.104167 pp 25599—25613

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Chen K, Li L, Qu S, Pan X, Sun Y, Wan F, Yu B, Zhou L, Zhu X, . Silencing hTERT attenuates cancer stem cell-like characteristics and radioresistance in the radioresistant nasopharyngeal carcinoma cell line CNE-2R. . 12:25599-25613. https://doi.org/10.18632/aging.104167

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                TY  - JOUR
                AU  - Chen, Kaihua 
                AU  - Li, Ling 
                AU  - Qu, Song 
                AU  - Pan, Xinbin 
                AU  - Sun, Yongchu 
                AU  - Wan, Fangzhu 
                AU  - Yu, Binbin 
                AU  - Zhou, Lei 
                AU  - Zhu, Xiaodong 
                TI  - Silencing hTERT attenuates cancer stem cell-like characteristics and radioresistance in the radioresistant nasopharyngeal carcinoma cell line CNE-2R
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104167
                DO  - 10.18632/aging.104167
                SP  - 25599
                EP  - 25613
                PY  - 
                AB  - Objective: This study aimed to explore the effect of silencing hTERT on the CSC-like characteristics and radioresistance of CNE-2R cells.
                Results: Silencing hTERT suppressed CNE-2R cell proliferation and increased the cell apoptosis rate and radiosensitivity in vitro. Moreover, it could also inhibit the growth of xenografts and increase the apoptosis index and radiosensitivity in vivo. Further study discovered that after silencing hTERT, telomerase activity in CNE-2R cells was markedly suppressed, along with remarkably down-regulated stem cell-related protein levels both in vitro and in vivo.
                Conclusion: Silencing hTERT can suppress the CSC-like characteristics of CNE-2R cells to enhance their radiosensitivity, revealing that hTERT may become a potential target for treating radioresistant NPC.
                Methods: An RNAi lentiviral vector specific to the hTERT gene was constructed to infect CNE-2R cells, the hTERT silencing effect was verified through qPCR and Western blot assays, and telomerase activity was detected by PCR-ELISA. Moreover, radiosensitivity in vitro was detected through colony formation assays, CCK-8 assays and flow cytometry. Tumor growth and radioresistance were also evaluated using xenograft models, while the apoptosis index in xenografts was measured through TUNEL assay. Levels of stem cell-related proteins were determined in vitro and in vivo.
                ER  -

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Identification of prognostic chromatin-remodeling genes in clear cell renal cell carcinoma

Yujing Yang, Chengyuan Wang, Ningde Wei, Ting Hong, Zuyu Sun, Jiawen Xiao, Jiaxi Yao, Zhi Li, Tao Liu,

https://doi.org/10.18632/aging.104170 pp 25614—25642

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Yang Y, Wang C, Wei N, Hong T, Sun Z, Xiao J, Yao J, Li Z, Liu T, . Identification of prognostic chromatin-remodeling genes in clear cell renal cell carcinoma. . 12:25614-25642. https://doi.org/10.18632/aging.104170

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                TY  - JOUR
                AU  - Yang, Yujing 
                AU  - Wang, Chengyuan 
                AU  - Wei, Ningde 
                AU  - Hong, Ting 
                AU  - Sun, Zuyu 
                AU  - Xiao, Jiawen 
                AU  - Yao, Jiaxi 
                AU  - Li, Zhi 
                AU  - Liu, Tao 
                TI  - Identification of prognostic chromatin-remodeling genes in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104170
                DO  - 10.18632/aging.104170
                SP  - 25614
                EP  - 25642
                PY  - 
                AB  - The aim of this study was to investigate the effects of chromatin-remodeling genes on the prognosis of patients with clear cell renal cell carcinoma (ccRCC). In TCGA-KIRC patients, two subgroups based on 86 chromatin-remodeling genes were established. The random forest algorithm was used for feature selection to identify BPTF, SIN3A and CNOT1 as characterized chromatin remodelers in ccRCC with good prognostic value. YY1 was indicated to be a transcription factor of genes highly related to BPTF, SIN3A and CNOT1. Functional annotations indicated that BPTF, SIN3A, CNOT1 and YY1 are all involved in the ubiquitin-mediated proteolysis process and that high expression of any of the five associated E3 ubiquitin ligases found in the pathway suggests a good prognosis. Protein network analysis indicated that BPTF has a targeted regulatory effect on YY1. Another independent dataset from International Cancer Genome Consortium (ICGC) showed a strong consistency with results in TCGA. In conclusion, we demonstrate that BPTF, SIN3A and CNOT1 are novel prognostic factors that predict good survival in ccRCC. We predicted that the good prognostic value of chromatin-remodeling genes BPTF and SIN3A is related to the regulation of YY1 and that YY1 regulates E3 ubiquitin ligases for further degradation of oncoproteins in ccRCC.
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Neurofilament degradation is involved in laparotomy-induced cognitive dysfunction in aged rats

Yiyun Cao, Taotao Liu, Zhengqian Li, Jiao Yang, Lijun Ma, Xinning Mi, Ning Yang, Aihua Qi, Xiangyang Guo, Aizhong Wang,

https://doi.org/10.18632/aging.104172 pp 25643—25657

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Cao Y, Liu T, Li Z, Yang J, Ma L, Mi X, Yang N, Qi A, Guo X, Wang A, . Neurofilament degradation is involved in laparotomy-induced cognitive dysfunction in aged rats. . 12:25643-25657. https://doi.org/10.18632/aging.104172

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                TY  - JOUR
                AU  - Cao, Yiyun 
                AU  - Liu, Taotao 
                AU  - Li, Zhengqian 
                AU  - Yang, Jiao 
                AU  - Ma, Lijun 
                AU  - Mi, Xinning 
                AU  - Yang, Ning 
                AU  - Qi, Aihua 
                AU  - Guo, Xiangyang 
                AU  - Wang, Aizhong 
                TI  - Neurofilament degradation is involved in laparotomy-induced cognitive dysfunction in aged rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104172
                DO  - 10.18632/aging.104172
                SP  - 25643
                EP  - 25657
                PY  - 
                AB  - Excessive neuroinflammatory responses play important roles in the development of postoperative cognitive dysfunction (POCD). Neurofilaments (NFs) were essential to the structure of axon and nerve conduction; and the abnormal degradation of NFs were always accompanied with degenerative diseases, which were also characterized by excessive neuroinflammatory responses in brain. However, it is still unclear whether the NFs were involved in the POCD. In this study, the LC-MS/MS method was used to explore the neuroinflammatory response and NFs of POCD in aged rats. Moreover, trichostatin A (TSA), an inflammation-related drug, was selected to test whether it could improve the surgery-induced cognitive dysfunction, inflammatory responses and NFs. Evident cognitive dysfunction, excessive microglia activation, neuroinflammatory responses and upregulated NFs in hippocampus were observed in the POCD group. TSA pretreatment could significantly mitigate these changes. The KEGG analysis revealed that nine pathways were enriched in the TSA + surgery group (versus the surgery group). Among them, two signaling pathways were closely related with the changes of NFs proteins. In conclusion, surgery could impair the cognitive function and aggravate neuroinflammation and NFs. The TSA could significantly improve these changes which might be related to the activation of the &#x201C;focal adhesion&#x201D; and &#x201C;ECM-receptor interaction&#x201D; pathways.
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Up-regulation of circRNA-0003528 promotes mycobacterium tuberculosis associated macrophage polarization via down-regulating miR-224-5p, miR-324-5p and miR-488-5p and up-regulating CTLA4

Zikun Huang, Fangyi Yao, Jun Liu, Jianqing Xu, Yang Guo, Rigu Su, Qing Luo, Junming Li,

https://doi.org/10.18632/aging.104175 pp 25658—25672

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Huang Z, Yao F, Liu J, Xu J, Guo Y, Su R, Luo Q, Li J, . Up-regulation of circRNA-0003528 promotes mycobacterium tuberculosis associated macrophage polarization via down-regulating miR-224-5p, miR-324-5p and miR-488-5p and up-regulating CTLA4. . 12:25658-25672. https://doi.org/10.18632/aging.104175

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                TY  - JOUR
                AU  - Huang, Zikun 
                AU  - Yao, Fangyi 
                AU  - Liu, Jun 
                AU  - Xu, Jianqing 
                AU  - Guo, Yang 
                AU  - Su, Rigu 
                AU  - Luo, Qing 
                AU  - Li, Junming 
                TI  - Up-regulation of circRNA-0003528 promotes mycobacterium tuberculosis associated macrophage polarization via down-regulating miR-224-5p, miR-324-5p and miR-488-5p and up-regulating CTLA4
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104175
                DO  - 10.18632/aging.104175
                SP  - 25658
                EP  - 25672
                PY  - 
                AB  - Background: In this study, we selected several candidate miRNAs to study their possible relationships with tuberculosis.
                Results: The expression of hsa_circ_0003528 was negatively correlated with the expression of miR-224-5p, miR-324-5p, miR-488-5p, miR-587, and miR-668, while the expression of hsa_circ_0003528 was positively correlated with the expression of miR-224-5p, miR-324-5p and miR-488-5p. No evident difference was observed between tuberculosis and healthy control groups in terms of the expression of miR-587 and miR-668.
                Conclusion: The findings of this study demonstrated that miR-224-5p, miR-324-5p and miR-488-5p were all ceRNAs of circRNA-0003528 by sponging each other and CTLA4 was found to be a shared target gene of miR-224-5p, miR-324-5p and miR-488-5p. Furthermore, we found that up-regulation of circRNA-0003528 promoted tuberculosis associated macrophage polarization by promoting expression CTLA4, which was mediated by the down-regulation of miR-224-5p, miR-324-5p and miR-488-5p.
                Methods: RT-qPCR and Western blot were conducted to observe the expression of hsa_circ_0003528, miRNAs and CTLA4 in different patient and cell groups to establish the potential molecular mechanisms underlying the effect of hsa_circ_0003528 on M1 to M2 macrophage polarization.
                ER  -

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Loss of Atg7 causes chaotic nucleosome assembly of mouse bone marrow CD11b⁺Ly6G^- myeloid cells

Yixuan Fang, Yue Gu, Lei Li, Lingjiang Zhu, Jiawei Qian, Chen Zhao, Li Xu, Wen Wei, Yanhua Du, Na Yuan, Suping Zhang, Ye Yuan, Youjia Xu, Cizhong Jiang, Jianrong Wang,

https://doi.org/10.18632/aging.104176 pp 25673—25683

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Fang Y, Gu Y, Li L, Zhu L, Qian J, Zhao C, Xu L, Wei W, Du Y, Yuan N, Zhang S, Yuan Y, Xu Y, et al, . Loss of Atg7 causes chaotic nucleosome assembly of mouse bone marrow CD11b⁺Ly6G^- myeloid cells. . 12:25673-25683. https://doi.org/10.18632/aging.104176

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Provider: 
 TY - JOUR
 AU - Fang, Yixuan 
 AU - Gu, Yue 
 AU - Li, Lei 
 AU - Zhu, Lingjiang 
 AU - Qian, Jiawei 
 AU - Zhao, Chen 
 AU - Xu, Li 
 AU - Wei, Wen 
 AU - Du, Yanhua 
 AU - Yuan, Na 
 AU - Zhang, Suping 
 AU - Yuan, Ye 
 AU - Xu, Youjia 
 AU - Jiang, Cizhong 
 AU - Wang, Jianrong 
 TI - Loss of Atg7 causes chaotic nucleosome assembly of mouse bone marrow CD11b+Ly6G- myeloid cells
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104176
 DO - 10.18632/aging.104176
 SP - 25673
 EP - 25683
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Fang, Yixuan 
 AU - Gu, Yue 
 AU - Li, Lei 
 AU - Zhu, Lingjiang 
 AU - Qian, Jiawei 
 AU - Zhao, Chen 
 AU - Xu, Li 
 AU - Wei, Wen 
 AU - Du, Yanhua 
 AU - Yuan, Na 
 AU - Zhang, Suping 
 AU - Yuan, Ye 
 AU - Xu, Youjia 
 AU - Jiang, Cizhong 
 AU - Wang, Jianrong 
 TI - Loss of Atg7 causes chaotic nucleosome assembly of mouse bone marrow CD11b+Ly6G- myeloid cells
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104176
 DO - 10.18632/aging.104176
 SP - 25673
 EP - 25683
 PY - 
 AB - Atg7, a critical component of autophagy machinery, is essential for counteracting hematopoietic aging. However, the non-autophagic role of Atg7 on hematopoietic cells remains fundamentally unclear. In this study, we found that loss of Atg7, but not Atg5, another autophagy-essential gene, in the hematopoietic system reduces CD11b myeloid cellularity including CD11b+Ly6G+ and CD11b+Ly6G- populations in mouse bone marrow. Surprisingly, Atg7 deletion causes abnormally accumulated histone H3.1 to be overwhelmingly trapped in the cytoplasm in the CD11b+Ly6G-, but not the CD11b+Ly6G+ compartment. RNA profiling revealed extensively chaotic expression of the genes required in nucleosome assembly. Functional assays further indicated upregulated aging markers in the CD11b+Ly6G- population. Therefore, our study suggests that Atg7 is essential for maintaining proper nucleosome assembly and limiting aging in the bone marrow CD11b+Ly6G- population.
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A SNP involved in alternative splicing of ABCB1 is associated with clopidogrel resistance in coronary heart disease in Chinese population

Shasha Zhang, Jing Wang, Anan Zhang, Xiaowei Zhang, Tao You, Dingxiong Xie, Wenke Yang, Yuhong Chen, Xuetian Zhang, Cuixia Di, Xiaodong Xie,

https://doi.org/10.18632/aging.104177 pp 25684—25699

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Zhang S, Wang J, Zhang A, Zhang X, You T, Xie D, Yang W, Chen Y, Zhang X, Di C, Xie X, . A SNP involved in alternative splicing of ABCB1 is associated with clopidogrel resistance in coronary heart disease in Chinese population. . 12:25684-25699. https://doi.org/10.18632/aging.104177

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Provider: 
 TY - JOUR
 AU - Zhang, Shasha 
 AU - Wang, Jing 
 AU - Zhang, Anan 
 AU - Zhang, Xiaowei 
 AU - You, Tao 
 AU - Xie, Dingxiong 
 AU - Yang, Wenke 
 AU - Chen, Yuhong 
 AU - Zhang, Xuetian 
 AU - Di, Cuixia 
 AU - Xie, Xiaodong 
 TI - A SNP involved in alternative splicing of ABCB1 is associated with clopidogrel resistance in coronary heart disease in Chinese population
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104177
 DO - 10.18632/aging.104177
 SP - 25684
 EP - 25699
 PY - 
 AB - Although many scientists are studying the association between genetic polymorphism of ABCB1 and CR in patients, the molecular mechanism has not been further studied in patients with CHD. This study investigated the relationship between SNP of the ABCB1 gene in patients with CHD and CR, and whether the polymorphism of the ABCB1 gene affects the AS of the gene. 741 patients were enrolled in the study, 316 CR cases and 425 NCR cases. The correlation between CR risk and clinical-pathological characteristics were studied. Additionally, the five SNPs were analysed by PCR and Mass Array genotyping methods. Furthermore, silicon analysis was used to predict whether the polymorphism affects the process of AS. Results showed that there was a significant correlation between rs1045642 polymorphism and CR in genotyping and allele analysis. The rs1045642 polymorphism of the ABCB1 gene of CHD patients carrying the A allele are more likely to develop CR. Silicon analysis showed that rs1045642 generated a new ESE sequence which might affect AS of ABCB1 gene. We hypothesize that the mechanism of CR might be caused by a change in the AS caused by the polymorphism of the gene. Thus, this work provides guidance for the clinical use of clopidogrel.
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Inhibition of PAR-1 delays aging via activating AMPK in C. elegans

Di Wu, Waijiao Cai, Xuan Zhang, Jianfeng Lan, Lina Zou, Samuel J. Chen, Zixing Wu, Di Chen,

https://doi.org/10.18632/aging.104180 pp 25700—25717

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Wu D, Cai W, Zhang X, Lan J, Zou L, Chen SJ, Wu Z, Chen D, . Inhibition of PAR-1 delays aging via activating AMPK in C. elegans. . 12:25700-25717. https://doi.org/10.18632/aging.104180

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Provider: 
 TY - JOUR
 AU - Wu, Di 
 AU - Cai, Waijiao 
 AU - Zhang, Xuan 
 AU - Lan, Jianfeng 
 AU - Zou, Lina 
 AU - Chen, Samuel J. 
 AU - Wu, Zixing 
 AU - Chen, Di 
 TI - Inhibition of PAR-1 delays aging via activating AMPK in C. elegans
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104180
 DO - 10.18632/aging.104180
 SP - 25700
 EP - 25717
 PY - 
 AB - The antagonistic pleiotropy theory of aging suggests that genes essential for growth and development are likely to modulate aging later in life. Previous studies in C. elegans demonstrate that inhibition of certain developmentally essential genes during adulthood leads to significant lifespan extension. PAR-1, a highly conserved serine/threonine kinase, functions as a key cellular polarity regulator during the embryonic development. However, the role of PAR-1 during adulthood remains unknown. Here we show that inhibition of par-1 either by a temperature-sensitive mutant or by RNAi knockdown only during adulthood is sufficient to extend lifespan in C. elegans. Inhibition of par-1 also improves healthspan, as indicated by increased stress resistance, enhanced proteotoxicity resistance, as well as reduced muscular function decline over time. Additionally, tissue-enriched RNAi knockdown analysis reveals that PAR-1 mainly functions in the epidermis to regulate lifespan. Further genetic epistatic and molecular studies demonstrate that the effect of par-1 on lifespan requires the AMP-activated protein kinase (AMPK), and RNAi knockdown of par-1 results in age-dependent AMPK activation and reduced lipid accumulation in the metabolic tissue. Taken together, our findings reveal a previously undescribed function of PAR-1 in adulthood, which will help to understand the molecular links between development and aging.
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Central motor conduction time in spinocerebellar ataxia: a meta-analysis

Zhi-Chao Tang, Zhao Chen, Yu-Ting Shi, Lin-Lin Wan, Ming-Jie Liu, Xuan Hou, Chun-Rong Wang, Hui-Rong Peng, Lin-Liu Peng, Rong Qiu, Bei-Sha Tang, Hong Jiang,

https://doi.org/10.18632/aging.104181 pp 25718—25729

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Tang Z, Chen Z, Shi Y, Wan L, Liu M, Hou X, Wang C, Peng H, Peng L, Qiu R, Tang B, Jiang H, . Central motor conduction time in spinocerebellar ataxia: a meta-analysis. . 12:25718-25729. https://doi.org/10.18632/aging.104181

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                TY  - JOUR
                AU  - Tang, Zhi-Chao 
                AU  - Chen, Zhao 
                AU  - Shi, Yu-Ting 
                AU  - Wan, Lin-Lin 
                AU  - Liu, Ming-Jie 
                AU  - Hou, Xuan 
                AU  - Wang, Chun-Rong 
                AU  - Peng, Hui-Rong 
                AU  - Peng, Lin-Liu 
                AU  - Qiu, Rong 
                AU  - Tang, Bei-Sha 
                AU  - Jiang, Hong 
                TI  - Central motor conduction time in spinocerebellar ataxia: a meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104181
                DO  - 10.18632/aging.104181
                SP  - 25718
                EP  - 25729
                PY  - 
                AB  - The dominantly inherited spinocerebellar ataxias (SCAs) are a large class of neurodegenerative diseases. Transcranial magnetic stimulation has been used to evaluate the function of the pyramidal tract, and central motor conduction time (CMCT) is one index used to detect pyramidal tract dysfunction. We conducted a comprehensive search of PubMed, Embase and Web of Science. Eight eligible studies were included in the meta-analysis. For upper limb CMCT, the mean difference (95% confidence interval (CI)) between the combined SCA group and the control group was 2.24 [1.76-2.72], while the mean differences (95% CIs) between the subtypes and the control group were as follows: 4.43 [3.58-5.28] for SCA1, 0.25 [-0.15,0.65] for SCA2, 1.04 [-0.37,2.46] for SCA3 and 0.49 [-0.29,1.28] for SCA6. Additionally, SCA1 significantly differed from SCA2 and SCA3 in terms of CMCT (P=0.0006 and P=0.010, respectively). We also compared lower limb CMCT between the SCA2 and control groups. The mean difference (95% CI) was 6.58 [4.49-8.67], which was clearly statistically significant. The differences in CMCT values among different subtypes suggests diverse pathological mechanisms. In general, CMCT is a promising objective index to judge the severity of disease deserving further investigation.
                ER  -

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Cardamonin induces G2/M phase arrest and apoptosis through inhibition of NF-κB and mTOR pathways in ovarian cancer

Jiang Ruibin, Jin Bo, Wan Danying, Feng Jianguo, Gu Linhui,

https://doi.org/10.18632/aging.104184 pp 25730—25743

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Ruibin J, Bo J, Danying W, Jianguo F, Linhui G, . Cardamonin induces G2/M phase arrest and apoptosis through inhibition of NF-κB and mTOR pathways in ovarian cancer. . 12:25730-25743. https://doi.org/10.18632/aging.104184

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                TY  - JOUR
                AU  - Ruibin, Jiang 
                AU  - Bo, Jin 
                AU  - Danying, Wan 
                AU  - Jianguo, Feng 
                AU  - Linhui, Gu 
                TI  - Cardamonin induces G2/M phase arrest and apoptosis through inhibition of NF-κB and mTOR pathways in ovarian cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104184
                DO  - 10.18632/aging.104184
                SP  - 25730
                EP  - 25743
                PY  - 
                AB  - Cardamonin, a natural chalcone, is reported to induce apoptosis and inhibit cancer cell growth. However, the mechanisms underlying the therapeutic effects of cardamonin remain to be established. Here, we have focused on cardamonin-induced apoptosis in ovarian cancer cells, both in vitro and in vivo. The effects of cardamonin on cell cycle patterns and apoptotic responses of cells were assessed in this study. Western blot was employed to determine the effects of cardamonin on expression of cell cycle- and apoptosis-related proteins. Our results indicate that cardamonin suppresses cancer cell growth by inducing G2/M phase arrest and apoptosis through targeted inhibition of NF-&#x3BA;B and mTOR pathways. The collective findings provide novel insights into the pathways responsible for the anticancer effects of cardamonin and support its potential utility as a clinical therapeutic agent for ovarian cancer.
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Alisol B 23-acetate activates ABCG5/G8 in the jejunum via the LXRα/ACAT2 pathway to relieve atherosclerosis in ovariectomized ApoE^-/- mice

Xi-Chao Yu, Yu Fu, Yun-Hui Bi, Wei-Wei Zhang, Jun Li, Tingting Ji, Ying Chao, Qing-Hai Meng, Qi Chen, Meng-Hua Ma, Yu-Han Zhang, Jinjun Shan, Hui-Min Bian,

https://doi.org/10.18632/aging.104185 pp 25744—25766

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Yu X, Fu Y, Bi Y, Zhang W, Li J, Ji T, Chao Y, Meng Q, Chen Q, Ma M, Zhang Y, Shan J, Bian H, . Alisol B 23-acetate activates ABCG5/G8 in the jejunum via the LXRα/ACAT2 pathway to relieve atherosclerosis in ovariectomized ApoE^-/- mice. . 12:25744-25766. https://doi.org/10.18632/aging.104185

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Provider: 
 TY - JOUR
 AU - Yu, Xi-Chao 
 AU - Fu, Yu 
 AU - Bi, Yun-Hui 
 AU - Zhang, Wei-Wei 
 AU - Li, Jun 
 AU - Ji, Tingting 
 AU - Chao, Ying 
 AU - Meng, Qing-Hai 
 AU - Chen, Qi 
 AU - Ma, Meng-Hua 
 AU - Zhang, Yu-Han 
 AU - Shan, Jinjun 
 AU - Bian, Hui-Min 
 TI - Alisol B 23-acetate activates ABCG5/G8 in the jejunum via the LXRα/ACAT2 pathway to relieve atherosclerosis in ovariectomized ApoE-/- mice
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104185
 DO - 10.18632/aging.104185
 SP - 25744
 EP - 25766
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Yu, Xi-Chao 
 AU - Fu, Yu 
 AU - Bi, Yun-Hui 
 AU - Zhang, Wei-Wei 
 AU - Li, Jun 
 AU - Ji, Tingting 
 AU - Chao, Ying 
 AU - Meng, Qing-Hai 
 AU - Chen, Qi 
 AU - Ma, Meng-Hua 
 AU - Zhang, Yu-Han 
 AU - Shan, Jinjun 
 AU - Bian, Hui-Min 
 TI - Alisol B 23-acetate activates ABCG5/G8 in the jejunum via the LXRα/ACAT2 pathway to relieve atherosclerosis in ovariectomized ApoE-/- mice
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104185
 DO - 10.18632/aging.104185
 SP - 25744
 EP - 25766
 PY - 
 AB - Phytosterols have been shown to improve blood lipid levels and treat atherosclerosis. This research investigated the effects of phytosterol Alisol B 23-acetate (AB23A) on jejunum lipid metabolism and atherosclerosis. The results show that intragastric administration of AB23A can significantly reduce atherosclerotic plaque area and lipid accumulation in the jejunum of ovariectomized ApoE-/- mice fed a high-fat diet and can also improve the lipid mass spectra of the plasma and jejunum. In vitro studies have shown that AB23A can increase cholesterol outflow in Caco-2 cells exposed to high fat concentrations and increase the expression of ATP-binding cassette transfer proteins G5/G8 (ABCG5/G8), the liver X receptor &#x3B1; (LXR&#x3B1;). Furthermore, inhibition of LXR&#x3B1; can significantly eliminate the active effect of AB23A on decreasing intracellular lipid accumulation. We also confirmed that AB23A has a negative effect on Acyl-CoA cholesterol acyltransferase 2 (ACAT2) in Caco-2 cells cultured in the high concentrations of fat, and we found that AB23A further reduces ACAT2 expression in cells treated with the ACAT2 inhibitor pyripyropene or transfected with ACAT2 siRNA. In conclusion, we confirmed that AB23A can reduce the absorption of dietary lipids in the jejunum by affecting the LXR&#x3B1;-ACAT2-ABCG5/G8 pathway and ultimately exert an anti-atherosclerotic effect.
 ER -

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Zinc oxide nanoparticles (ZnO NPs) combined with cisplatin and gemcitabine inhibits tumor activity of NSCLC cells

Chenping Hu, Wenxiu Du,

https://doi.org/10.18632/aging.104187 pp 25767—25777

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Hu C, Du W, . Zinc oxide nanoparticles (ZnO NPs) combined with cisplatin and gemcitabine inhibits tumor activity of NSCLC cells. . 12:25767-25777. https://doi.org/10.18632/aging.104187

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                TY  - JOUR
                AU  - Hu, Chenping 
                AU  - Du, Wenxiu 
                TI  - Zinc oxide nanoparticles (ZnO NPs) combined with cisplatin and gemcitabine inhibits tumor activity of NSCLC cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104187
                DO  - 10.18632/aging.104187
                SP  - 25767
                EP  - 25777
                PY  - 
                AB  - Non-small cell lung cancer (NSCLC) is one of the most common malignancies worldwide. The use of a combination of chemotherapy drugs and zinc oxide nanoparticles (ZnO-NPs), which have proven to induce tumor-selective cell death, reduce the drug resistance and reduce the side effects in vitro. In the present study, we developed ZnO-NPs loaded with both cisplatin (Cp) and gemcitabine (Gem) (ZnO-NPs(Cp/Gem)), then the morphologies and the size distribution of ZnO-NPs(Cp/Gem) particles were observed by transmission electron microscopy (TEM) and dynamic light scattering (DLS). Also, MTT, western blot and Annexin V-PI were used to assess the anti-tumor role of ZnO-NPs(Cp/Gem) in A549 cells. The viability for A549 cells showed a significant decrease in the ZnO NPs(Cp/Gem) group, respectively relative to Cp, Gem, the combination of Cp and Gem (Cp+Gem), and ZnO-NPs loaded with Cp (ZnO-NPs(Cp)) or Gem (ZnO-NPs(Gem)). Furthermore, ZnO-NPs(Cp/Gem) remarkably enhanced the apoptosis-promoting effect of Cp and Gem in A549 cells. The xenograft model showed that Zno-NPS (Cp/Gem) significantly enhanced the inhibition of Cp and Gem on tumor formation. The above results suggested that therapy of NSCLC with ZnO-NPs(Cp/Gem) could enhance the cytotoxic action of chemotherapeutic agents synergistically, indicating a promising potential for ZnO-NPs in antitumor applications.
                ER  -

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Identification of prognostic aging-related genes associated with immunosuppression and inflammation in head and neck squamous cell carcinoma

Jing Yang, Qingshan Jiang, Lijun Liu, Hong Peng, Yaya Wang, Shuyan Li, Yanhua Tang, Jing Yu, Runliang Gan, Zhifeng Liu,

https://doi.org/10.18632/aging.104199 pp 25778—25804

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Yang J, Jiang Q, Liu L, Peng H, Wang Y, Li S, Tang Y, Yu J, Gan R, Liu Z, . Identification of prognostic aging-related genes associated with immunosuppression and inflammation in head and neck squamous cell carcinoma. . 12:25778-25804. https://doi.org/10.18632/aging.104199

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Provider: 
                TY  - JOUR
                AU  - Yang, Jing 
                AU  - Jiang, Qingshan 
                AU  - Liu, Lijun 
                AU  - Peng, Hong 
                AU  - Wang, Yaya 
                AU  - Li, Shuyan 
                AU  - Tang, Yanhua 
                AU  - Yu, Jing 
                AU  - Gan, Runliang 
                AU  - Liu, Zhifeng 
                TI  - Identification of prognostic aging-related genes associated with immunosuppression and inflammation in head and neck squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104199
                DO  - 10.18632/aging.104199
                SP  - 25778
                EP  - 25804
                PY  - 
                AB  - Aging is regarded as a dominant risk factor for cancer. Additionally, inflammation and asthenic immune surveillance with aging may facilitate tumor formation and development. However, few studies have comprehensively analyzed the relationship between aging-related genes (AGs) and the prognosis, inflammation and tumor immunity of head and neck squamous cell carcinoma (HNSCC). Here, we initially screened 41 differentially expressed AGs from The Cancer Genome Atlas (TCGA) database. In the training set, a prognosis risk model with seven AGs (APP, CDKN2A, EGFR, HSPD1, IL2RG, PLAU and VEGFA) was constructed and validated in the TCGA test set and the GEO set (P &lt; 0.05). Using univariate and multivariate Cox regression analyses, we confirmed that risk score was an independent prognostic factor of HNSCC patients. In addition, a high risk score was significantly correlated with immunosuppression, and high expression of PLAU, APP and EGFR was the main factor. Furthermore, we confirmed that a high risk score was significantly associated with levels of proinflammatory factors (IL-1&#x3B1;, IL-1&#x3B2;, IL-6 and IL-8) in HNSCC samples. Thus, this risk model may serve as a prognostic signature and provide clues for individualized immunotherapy for HNSCC patients.
                ER  -

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MRI-visible perivascular spaces are associated with cerebrospinal fluid biomarkers in Parkinson’s disease

Yi Fang, Lu-Yan Gu, Jun Tian, Shao-Bing Dai, Ying Chen, Ran Zheng, Xiao-Li Si, Chong-Yao Jin, Zhe Song, Ya-Ping Yan, Xin-Zhen Yin, Jia-Li Pu, Bao-Rong Zhang,

https://doi.org/10.18632/aging.104200 pp 25805—25818

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Fang Y, Gu L, Tian J, Dai S, Chen Y, Zheng R, Si X, Jin C, Song Z, Yan Y, Yin X, Pu J, Zhang B, . MRI-visible perivascular spaces are associated with cerebrospinal fluid biomarkers in Parkinson’s disease. . 12:25805-25818. https://doi.org/10.18632/aging.104200

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                TY  - JOUR
                AU  - Fang, Yi 
                AU  - Gu, Lu-Yan 
                AU  - Tian, Jun 
                AU  - Dai, Shao-Bing 
                AU  - Chen, Ying 
                AU  - Zheng, Ran 
                AU  - Si, Xiao-Li 
                AU  - Jin, Chong-Yao 
                AU  - Song, Zhe 
                AU  - Yan, Ya-Ping 
                AU  - Yin, Xin-Zhen 
                AU  - Pu, Jia-Li 
                AU  - Zhang, Bao-Rong 
                TI  - MRI-visible perivascular spaces are associated with cerebrospinal fluid biomarkers in Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104200
                DO  - 10.18632/aging.104200
                SP  - 25805
                EP  - 25818
                PY  - 
                AB  - Perivascular spaces in the brain have been known to communicate with cerebrospinal fluid and contribute to waste clearance in animal models. In this study, we sought to determine the association between MRI-visible enlarged perivascular spaces (EPVS) and disease markers in Parkinson&#x2019;s disease (PD). We obtained longitudinal data from 245 patients with PD and 98 healthy controls from the Parkinson&#x2019;s Progression Marker Initiative. Two trained neurologists performed visual ratings on T2-weighted images to characterize EPVS in the centrum semiovale (CSO), the basal ganglia (BG) and the midbrain. We found that a greater proportion of patients with PD had low grade BG-EPVS relative to healthy controls. In patients with PD, lower grade of BG-EPVS and CSO-EPVS predicted lower CSF &#x3B1;-synuclein and t-tau. Lower grade of BG-EPVS were also associated with accelerated Hoehn &amp;Yahr stage progression in patients with baseline stage 1. BG-EPVS might be a valuable predictor of disease progression.
                ER  -

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Association and functional study between ADIPOQ and metabolic syndrome in elderly Chinese Han population

Qiao Wang, Decheng Ren, Yan Bi, Ruixue Yuan, Dong Li, Jianying Wang, Ruirui Wang, Lei Zhang, Guang He, Baocheng Liu,

https://doi.org/10.18632/aging.104203 pp 25819—25827

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Wang Q, Ren D, Bi Y, Yuan R, Li D, Wang J, Wang R, Zhang L, He G, Liu B, . Association and functional study between ADIPOQ and metabolic syndrome in elderly Chinese Han population. . 12:25819-25827. https://doi.org/10.18632/aging.104203

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Provider: 
 TY - JOUR
 AU - Wang, Qiao 
 AU - Ren, Decheng 
 AU - Bi, Yan 
 AU - Yuan, Ruixue 
 AU - Li, Dong 
 AU - Wang, Jianying 
 AU - Wang, Ruirui 
 AU - Zhang, Lei 
 AU - He, Guang 
 AU - Liu, Baocheng 
 TI - Association and functional study between ADIPOQ and metabolic syndrome in elderly Chinese Han population
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104203
 DO - 10.18632/aging.104203
 SP - 25819
 EP - 25827
 PY - 
 AB - Objective: Metabolic syndrome (MetS) is a cluster of health problems that places individuals at higher risk of developing cardiovascular disease, diabetes and stroke. The prevalence of MetS is increasing worldwide. It is also well accepted that genetic and environmental factors play significant roles in the occurrence/development of MetS, but studies exploring genetic factors are still lacking. Here, we aimed to investigate the association of ADIPOQ gene variants with MetS in an elderly Chinese Han population.
 Results: We found that the allelic frequencies of rs6773957 and rs3774261 were significantly different between MetS and the control (p = 0.031; p = 0.049). Furthermore, a reduction in luciferase activity was observed when HEK293T cells were transfected with rs6773957 mutant fragments compared with wild type.
 Conclusion: Our results suggest that rs6773957 and rs3774261 of ADIPOQ were associated with MetS in the elderly Chinese Han population. The functional assays performed indicate that the rs6773957 variant might be pathogenic and may provide evidence for mechanistic studies of MetS in the future.
 Methods: Four single nucleotide polymorphisms (SNPs) were selected and genotyped (rs6773957, rs182052, rs3774261 and rs17366568) in 1337 subjects, including 569 healthy controls and 768 MetS cases. The clinical characteristics of all the subjects were obtained and analyzed. Additionally, a functional study of rs6773957 in regulating the expression of ADIPOQ was performed in this study.
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A glycolysis-related gene signature predicts prognosis of patients with esophageal adenocarcinoma

Huafeng Kang, Nan Wang, Xuan Wang, Yu Zhang, Shuai Lin, Guochao Mao, Di Liu, Chengxue Dang, Zhangjian Zhou,

https://doi.org/10.18632/aging.104206 pp 25828—25844

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Kang H, Wang N, Wang X, Zhang Y, Lin S, Mao G, Liu D, Dang C, Zhou Z, . A glycolysis-related gene signature predicts prognosis of patients with esophageal adenocarcinoma. . 12:25828-25844. https://doi.org/10.18632/aging.104206

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                TY  - JOUR
                AU  - Kang, Huafeng 
                AU  - Wang, Nan 
                AU  - Wang, Xuan 
                AU  - Zhang, Yu 
                AU  - Lin, Shuai 
                AU  - Mao, Guochao 
                AU  - Liu, Di 
                AU  - Dang, Chengxue 
                AU  - Zhou, Zhangjian 
                TI  - A glycolysis-related gene signature predicts prognosis of patients with esophageal adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104206
                DO  - 10.18632/aging.104206
                SP  - 25828
                EP  - 25844
                PY  - 
                AB  - Background: Esophageal adenocarcinoma (EAC) is a growing problem with a rapidly rising incidence and carries a poor prognosis. We aimed to develop a glycolysis-related gene signature to predict the prognostic outcome of patients with EAC.
                Results: Five genes (CLDN9, GFPT1, HMMR, RARS and STMN1) were correlated with prognosis of EAC patients. Patients were classified into high-risk and low-risk groups calculated by Cox regression analysis, based on the five gene signature risk score. The five-gene signature was an independent biomarker for prognosis and patients with low risk scores showed better prognosis. Nomogram incorporating the gene signature and clinical prognostic factors was effective in predicting the overall survival.
                Conclusion: An innovative identified glycolysis-related gene signature and an effective nomogram reliably predicted the prognosis of EAC patients.
                Methods: The Cancer Genome Atlas database was investigated for the gene expression profile of EAC patients. Glycolytic gene sets difference between EAC and normal tissues were identified via Gene set enrichment analysis (GSEA). Univariate and multivariate Cox analysis were utilized to construct a prognostic gene signature. The signature was evaluated by receiver operating characteristic curves and Kaplan&#x2013;Meier curves. A prognosis model integrating clinical parameters with the gene signature was established with nomogram.
                ER  -

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The long noncoding RNA LINC01140/miR-140-5p/FGF9 axis modulates bladder cancer cell aggressiveness and macrophage M2 polarization

Shuiqing Wu, Ran Xu, Xuan Zhu, Haiqing He, Jinhua Zhang, Qi Zeng, Yinhuai Wang, Xiaokun Zhao,

https://doi.org/10.18632/aging.202147 pp 25845—25864

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Wu S, Xu R, Zhu X, He H, Zhang J, Zeng Q, Wang Y, Zhao X, . The long noncoding RNA LINC01140/miR-140-5p/FGF9 axis modulates bladder cancer cell aggressiveness and macrophage M2 polarization. . 12:25845-25864. https://doi.org/10.18632/aging.202147

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                TY  - JOUR
                AU  - Wu, Shuiqing 
                AU  - Xu, Ran 
                AU  - Zhu, Xuan 
                AU  - He, Haiqing 
                AU  - Zhang, Jinhua 
                AU  - Zeng, Qi 
                AU  - Wang, Yinhuai 
                AU  - Zhao, Xiaokun 
                TI  - The long noncoding RNA LINC01140/miR-140-5p/FGF9 axis modulates bladder cancer cell aggressiveness and macrophage M2 polarization
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202147
                DO  - 10.18632/aging.202147
                SP  - 25845
                EP  - 25864
                PY  - 
                AB  - MIBC (muscle invasive bladder cancer) only accounts for only a minority of bladder cancers, however, the disease-specific and overall survival rates of patients with MIBC are low. Macrophage M2 polarization has been reported to be associated with poorer prognosis in bladder cancer. Through cancer bioinformatics and experimental analyses, FGF9 was found to be upregulated in MIBC tissues. FGF9 knockdown in T24 cells strongly suppressed the viability, migratory capacity, and invasive capacity of cells; culture with medium from FGF9 knockdown T24 cells (si-FGF9-CM) significantly inhibited macrophage M2 polarization, while promoting M1 polarization. The long noncoding RNA (lncRNA) LINC01140 was positively correlated with FGF9 and was significantly upregulated in MIBC tissues. LINC01140 knockdown inhibited the viability, migratory capacity and invasive capacity of T24 cells; culture in si-LINC01140-CM also inhibited macrophage M2 polarization, while promoting M1 polarization. LINC01140 targeted miR-140-5p, while miR-140-5p targeted FGF9 to form a lncRNA-miRNA-mRNA axis. The effects of miR-140-5p inhibition on bladder cancer aggressiveness and macrophage M2 polarization were opposite to those of LINC01140 or FGF9 knockdown; additionally, miR-140-5p inhibition partially reversed the effects of LINC01140 knockdown on FGF9 protein levels, bladder cancer phenotype, and macrophage M2 polarization. In conclusion, LINC01140, miR-140-5p, and FGF9 form a lncRNA-miRNA-mRNA axis that modulates the bladder cancer phenotype, affects macrophage M2 polarization through the tumor microenvironment, and in turn affects bladder cancer cell aggressiveness.
                ER  -

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Downregulation of enhancer RNA EMX2OS is associated with poor prognosis in kidney renal clear cell carcinoma

Huiming Jiang, Haibin Chen, Pei Wan, Shengda Song, Nanhui Chen,

https://doi.org/10.18632/aging.202151 pp 25865—25877

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Jiang H, Chen H, Wan P, Song S, Chen N, . Downregulation of enhancer RNA EMX2OS is associated with poor prognosis in kidney renal clear cell carcinoma. . 12:25865-25877. https://doi.org/10.18632/aging.202151

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                TY  - JOUR
                AU  - Jiang, Huiming 
                AU  - Chen, Haibin 
                AU  - Wan, Pei 
                AU  - Song, Shengda 
                AU  - Chen, Nanhui 
                TI  - Downregulation of enhancer RNA EMX2OS is associated with poor prognosis in kidney renal clear cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202151
                DO  - 10.18632/aging.202151
                SP  - 25865
                EP  - 25877
                PY  - 
                AB  - Enhancer RNAs are a subclass of long non-coding RNAs transcribed from enhancer regions that play an important role in the transcriptional regulation of genes. However, their role in kidney renal clear cell carcinoma (KIRC) is largely unknown. Herein, we identified the key enhancer RNAs in KIRC via an integrated data analysis method. Gene expression profiles and clinical data of KIRC and 32 other cancer types were acquired using the University of California Santa Cruz Xena platform. Reported enhancer RNAs and genes regulated by them were selected as putative enhancer RNA-target pairs. Kaplan-Meier survival and correlation analyses were performed to identify the key enhancer RNAs. Finally, EMX2OS was identified as the enhancer RNA most associated with survival, with EMX2 as its target. EMX2OS downregulation was significantly associated with higher histological grade, advanced stage, and poorer prognosis. The results were validated in pan-cancer data from The Cancer Genome Atlas and RT-qPCR analysis of 12 pairs of KIRC and normal real-world samples. Functional enrichment analysis indicated that several metabolism-associated signaling pathways were enriched. This study demonstrated that EMX2OS is a key metabolism-associated enhancer RNA in KIRC with a favorable impact on survival and may be a novel therapeutic target in KIRC.
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Upregulation of KIF20A promotes tumor proliferation and invasion in renal clear cell carcinoma and is associated with adverse clinical outcome

Xiaohan Ren, Xinglin Chen, Yisheng Ji, Lin Li, Yunxin Li, Chao Qin, Kai Fang,

https://doi.org/10.18632/aging.202153 pp 25878—25894

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Ren X, Chen X, Ji Y, Li L, Li Y, Qin C, Fang K, . Upregulation of KIF20A promotes tumor proliferation and invasion in renal clear cell carcinoma and is associated with adverse clinical outcome. . 12:25878-25894. https://doi.org/10.18632/aging.202153

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                TY  - JOUR
                AU  - Ren, Xiaohan 
                AU  - Chen, Xinglin 
                AU  - Ji, Yisheng 
                AU  - Li, Lin 
                AU  - Li, Yunxin 
                AU  - Qin, Chao 
                AU  - Fang, Kai 
                TI  - Upregulation of KIF20A promotes tumor proliferation and invasion in renal clear cell carcinoma and is associated with adverse clinical outcome
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202153
                DO  - 10.18632/aging.202153
                SP  - 25878
                EP  - 25894
                PY  - 
                AB  - Extensive research has revealed the pivotal role of kinesin family member 20A (KIF20A) in cancer. However, its latent involvement in renal clear cell carcinoma (ccRCC) still remains unclear. Thus, here we explored the role of KIF20A in ccRCC. For this, a series of software including R (v. 3.6.1), SPSS (v. 23), ImageJ and FlowJo were used for the analyses. Open-access data were obtained from The Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC) and Gene Expression Omnibus (GEO) databases. Weighted Gene Co-expression Network Analysis (WGCNA) was used for module gene identification. In vitro results indicated that KIF20A expression is up-regulated in ccRCC tissue. KIF20A knockdown was able to inhibite cell proliferation and invasion of kidney A498 and Caki-1 cells. Meanwhile, KIF20A showed a strong association with immune infiltration. Particularly, KIF20A had a strong positive correlation with Th2 cells, Treg cells and Macrophages, but a negative correlation with Th17 cells, Mast cells and NK cells. These correlations may suggest the use of KIF20A as an underlying immunotherapy target in ccRCC. Our data indicated that KIF20A may promote cell invasion and proliferation in ccRCC, thus serving as an independent tumor marker and a putative therapeutic target.
                ER  -

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Effect of menopausal status on the survival and recurrence of sex-classified hepatocellular carcinoma after liver resection: a case-matched study with propensity score matching

Wenli Zhang, Fuchen Liu, Jian Huang, Xinggang Guo, Wei Dong, Shuxun Wei, Li Li, Xiuli Zhu, Weiping Zhou, Hui Liu,

https://doi.org/10.18632/aging.202155 pp 25895—25915

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Zhang W, Liu F, Huang J, Guo X, Dong W, Wei S, Li L, Zhu X, Zhou W, Liu H, . Effect of menopausal status on the survival and recurrence of sex-classified hepatocellular carcinoma after liver resection: a case-matched study with propensity score matching. . 12:25895-25915. https://doi.org/10.18632/aging.202155

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                TY  - JOUR
                AU  - Zhang, Wenli 
                AU  - Liu, Fuchen 
                AU  - Huang, Jian 
                AU  - Guo, Xinggang 
                AU  - Dong, Wei 
                AU  - Wei, Shuxun 
                AU  - Li, Li 
                AU  - Zhu, Xiuli 
                AU  - Zhou, Weiping 
                AU  - Liu, Hui 
                TI  - Effect of menopausal status on the survival and recurrence of sex-classified hepatocellular carcinoma after liver resection: a case-matched study with propensity score matching
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202155
                DO  - 10.18632/aging.202155
                SP  - 25895
                EP  - 25915
                PY  - 
                AB  - Objective: To investigate the impact of menopausal status on the prognosis for sex-classified Hepatocellular carcinoma (HCC) and to establish prognostic nomograms for patients after liver resection.
                Results: After propensity score matching (PSM), statistically significant differences in both overall survival (OS) and recurrence-free survival (RFS) were found between men and women HCC patients. Based on Cox regression analysis, these differences were evident in the normal menstruation (N) group expanded with male patients, but not in either the expanded postmenopausal (P) or intermediate (I) groups. Sex disparity was also apparent in the recurrence-free survival (RFS) of the total HCC patients. Integrated with independent factors, nomograms for the OS and RFS of the expanded N group showed higher C-indices of 0.773 and 0.724, respectively, than those of nomograms for the total patients and BCLC stage (P&lt;0.001).
                Conclusion: Sex disparity appears to affect both the survival and recurrence of HCC only in normal menstruation women and their matched men. For predicting survival, prognostic nomograms derived from the expanded N group of HCC patients were more accurate for patients with the same clinical conditions.
                Methods: The patients (390 females and 1920 males), who underwent curative liver resection for HCC during 2008 to 2012, were screened. The 390 women were divided into three groups: normal menstruation, intermediate, and postmenopausal. To overcome selection bias, the three groups of females were matched with males at a ratio of 1:2, using propensity score matching. Based on further Cox regression analysis, independent factors were integrated into nomograms for OS and RFS by R rms. The accuracy and discrimination of the nomograms were evaluated by the C-index, calibration curve, and decision curve analysis.
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Exploring diagnostic m6A regulators in endometriosis

Li Jiang, Mengmeng Zhang, Jingni Wu, Sixue Wang, Xiang Yang, Mingyu Yi, Xinyue Zhang, Xiaoling Fang,

https://doi.org/10.18632/aging.202163 pp 25916—25938

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Jiang L, Zhang M, Wu J, Wang S, Yang X, Yi M, Zhang X, Fang X, . Exploring diagnostic m6A regulators in endometriosis. . 12:25916-25938. https://doi.org/10.18632/aging.202163

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                TY  - JOUR
                AU  - Jiang, Li 
                AU  - Zhang, Mengmeng 
                AU  - Wu, Jingni 
                AU  - Wang, Sixue 
                AU  - Yang, Xiang 
                AU  - Yi, Mingyu 
                AU  - Zhang, Xinyue 
                AU  - Fang, Xiaoling 
                TI  - Exploring diagnostic m6A regulators in endometriosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202163
                DO  - 10.18632/aging.202163
                SP  - 25916
                EP  - 25938
                PY  - 
                AB  - Endometriosis is an estrogen-dependent inflammatory disorder, usually causing infertility, pelvic pain, and ovarian masses. This study intended to investigate the implication of N6-methyladenosine (m6A) regulators in endometriosis. We acquired 34 normal, 127 eutopic, and 46 ectopic, samples of endometrium from the Gene Expression Omnibus (GSE7305, GSE7307, GSE51981) database and the Array-express (E-MTAB-694) database. These samples were then used to profile the expression of 20 m6A regulators in endometriosis. The results indicated that most dysregulated (19/20) m6A regulators were significantly downregulated in eutopic vs. normal endometrium and also significantly downregulated in ectopic vs. eutopic endometrium. Several dysregulated m6A regulators were common to both contrast matrices: METTL3, YTHDF2, YTHDF3, HNRNPA2B1, HNRNPC, and FTO. Both HNRNPA2B1 and HNRNPC were associated with the severity of endometriosis in eutopic samples, and also exhibited diagnostic potential for endometriosis. HNRNPA2B1 and HNRNPC may influence immune pathways and the infiltration of immune cells in endometriosis. Abnormalities in the gene transcription factors network associated with endometriosis might affect the expression of HNRNPA2B1 and HNRNPC. In conclusion, we observed significant dysregulation of m6A regulators in endometriosis, and found that HNRNPA2B1 and HNRNPC might correlate with the immune response and serve as useful diagnostic biomarkers for endometriosis.
                ER  -

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Sexual dimorphism in aging hematopoiesis: an earlier decline of hematopoietic stem and progenitor cells in male than female mice

Eui-Young So, Euy-Myoung Jeong, Keith Q. Wu, Patrycja M. Dubielecka, Anthony M. Reginato, Peter J. Quesenberry, Olin D. Liang,

https://doi.org/10.18632/aging.202167 pp 25939—25955

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So E, Jeong E, Wu KQ, Dubielecka PM, Reginato AM, Quesenberry PJ, Liang OD, . Sexual dimorphism in aging hematopoiesis: an earlier decline of hematopoietic stem and progenitor cells in male than female mice. . 12:25939-25955. https://doi.org/10.18632/aging.202167

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                TY  - JOUR
                AU  - So, Eui-Young 
                AU  - Jeong, Euy-Myoung 
                AU  - Wu, Keith Q. 
                AU  - Dubielecka, Patrycja M. 
                AU  - Reginato, Anthony M. 
                AU  - Quesenberry, Peter J. 
                AU  - Liang, Olin D. 
                TI  - Sexual dimorphism in aging hematopoiesis: an earlier decline of hematopoietic stem and progenitor cells in male than female mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202167
                DO  - 10.18632/aging.202167
                SP  - 25939
                EP  - 25955
                PY  - 
                AB  - Adult hematopoietic stem and progenitor cells (HSPCs) reside in the bone marrow (BM) ensuring homeostasis of blood production and immune response throughout life. Sex differences in immunocompetence and mortality are well-documented in humans. However, whether HSPCs behave dimorphically between sexes during aging remains unknown. Here, we show that a significant expansion of BM-derived HSPCs occurs in the middle age of female but in the old age of male mice. We then show that a decline of HSPCs in male mice, as indicated by the expression levels of select hematopoietic genes, occurs much earlier in the aging process than that in female mice. Sex-mismatched heterochronic BM transplantations indicate that the middle-aged female BM microenvironment plays a pivotal role in sustaining hematopoietic gene expression during aging. Furthermore, a higher concentration of the pituitary sex hormone follicle-stimulating hormone (FSH) in the serum and a concomitant higher expression of its receptor on HSPCs in the middle-aged and old female mice than age-matched male mice, suggests that FSH may contribute to the sexual dimorphism in aging hematopoiesis. Our study reveals that HSPCs in the BM niches are possibly regulated in a sex-specific manner and influenced differently by sex hormones during aging hematopoiesis.
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Periodontitis in elderly patients with type 2 diabetes mellitus: impact on gut microbiota and systemic inflammation

Jinyou Li, Haifeng Lu, Huanwen Wu, Shunmei Huang, Lufang Chen, Qifeng Gui, Wenjing Zhou, Yichen Yang, Yue Wu, Hua Zhang, Qin Zhang, Yunmei Yang,

https://doi.org/10.18632/aging.202174 pp 25956—25980

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Li J, Lu H, Wu H, Huang S, Chen L, Gui Q, Zhou W, Yang Y, Wu Y, Zhang H, Zhang Q, Yang Y, . Periodontitis in elderly patients with type 2 diabetes mellitus: impact on gut microbiota and systemic inflammation. . 12:25956-25980. https://doi.org/10.18632/aging.202174

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                TY  - JOUR
                AU  - Li, Jinyou 
                AU  - Lu, Haifeng 
                AU  - Wu, Huanwen 
                AU  - Huang, Shunmei 
                AU  - Chen, Lufang 
                AU  - Gui, Qifeng 
                AU  - Zhou, Wenjing 
                AU  - Yang, Yichen 
                AU  - Wu, Yue 
                AU  - Zhang, Hua 
                AU  - Zhang, Qin 
                AU  - Yang, Yunmei 
                TI  - Periodontitis in elderly patients with type 2 diabetes mellitus: impact on gut microbiota and systemic inflammation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202174
                DO  - 10.18632/aging.202174
                SP  - 25956
                EP  - 25980
                PY  - 
                AB  - Elderly patients with type 2 diabetes mellitus (T2DM) exhibit considerable periodontitis frequency, which causes tooth loss and poor quality of life. To investigate the impact of periodontitis on gut microbiota, we used 16S rRNA amplicon sequencing to characterize the composition and structure of gut microbiota among elderly patients with T2DM and periodontitis (T2DM_P), elderly patients with T2DM alone (T2DM_NP), and healthy volunteers. We identified 34 key gut microbiota markers that distinguished participants with different periodontal conditions and investigated their connections to other gut bacteria, as well as their clinical correlates. The most striking differences in co-occurrence networks between the T2DM_P and T2DM_NP groups comprised interactions involving dominant genera in the oral cavity (i.e., Streptococcus and Veillonella). Of the 34 identified key gut microbiota markers that distinguished participants with different periodontal conditions, 25 taxa were correlated with duration of diabetes, dry mouth or the peripheral levels of pro-inflammatory cytokines (e.g., tumor necrosis factor-&#x3B1;, interferon-&#x3B3;, prostaglandin E2, interleukin-17, and interleukin-6) and metabolic parameters (e.g., hemoglobin A1c), respectively. Our findings suggest that gut microbial shifts driven by periodontitis may contribute to systemic inflammation and metabolic dysfunction during the progression of T2DM.
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Profilin 2 promotes growth, metastasis, and angiogenesis of small cell lung cancer through cancer-derived exosomes

Qi Cao, Yihan Liu, Ying Wu, Caijiao Hu, Lei Sun, Jinghui Wang, Changlong Li, Meng Guo, Xin Liu, Jianyi Lv, Xueyun Huo, Junming Yue, Xiaoyan Du, Zhenwen Chen,

https://doi.org/10.18632/aging.202213 pp 25981—25999

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Cao Q, Liu Y, Wu Y, Hu C, Sun L, Wang J, Li C, Guo M, Liu X, Lv J, Huo X, Yue J, Du X, et al, . Profilin 2 promotes growth, metastasis, and angiogenesis of small cell lung cancer through cancer-derived exosomes. . 12:25981-25999. https://doi.org/10.18632/aging.202213

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                TY  - JOUR
                AU  - Cao, Qi 
                AU  - Liu, Yihan 
                AU  - Wu, Ying 
                AU  - Hu, Caijiao 
                AU  - Sun, Lei 
                AU  - Wang, Jinghui 
                AU  - Li, Changlong 
                AU  - Guo, Meng 
                AU  - Liu, Xin 
                AU  - Lv, Jianyi 
                AU  - Huo, Xueyun 
                AU  - Yue, Junming 
                AU  - Du, Xiaoyan 
                AU  - Chen, Zhenwen 
                TI  - Profilin 2 promotes growth, metastasis, and angiogenesis of small cell lung cancer through cancer-derived exosomes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202213
                DO  - 10.18632/aging.202213
                SP  - 25981
                EP  - 25999
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cao, Qi 
                AU  - Liu, Yihan 
                AU  - Wu, Ying 
                AU  - Hu, Caijiao 
                AU  - Sun, Lei 
                AU  - Wang, Jinghui 
                AU  - Li, Changlong 
                AU  - Guo, Meng 
                AU  - Liu, Xin 
                AU  - Lv, Jianyi 
                AU  - Huo, Xueyun 
                AU  - Yue, Junming 
                AU  - Du, Xiaoyan 
                AU  - Chen, Zhenwen 
                TI  - Profilin 2 promotes growth, metastasis, and angiogenesis of small cell lung cancer through cancer-derived exosomes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202213
                DO  - 10.18632/aging.202213
                SP  - 25981
                EP  - 25999
                PY  - 
                AB  - Small cell lung cancer (SCLC) is highly aggressive and prone to hypervascular metastases. Recently, we found profilin 2 (PFN2) expression in SCLC but not in normal tissues. Furthermore, PFN2 expression had been shown to promote angiogenesis through exosomes. However, it remains unclear whether PFN2 contributes to the progression and metastasis of SCLC through angiogenesis. We report here that overexpression (OE) of PFN2 increased, whereas its knockdown (KD) decreased the proliferation, migration, and invasion of SCLC cell H446. The exosomes from OE-H446 (SCLC-OE-exo) exhibited similar effects on H446 properties. Culturing of endothelial cells (ECs) in SCLC-OE conditioned medium (CM) or SCLC-OE-exo increased the migration and tube formation ability of ECs, whereas SCLC-KD-CM and SCLC-KD-exo had inhibitory effects. Interestingly, both SCLC- and EC-derived exosomes were internalized in H446 more rapidly than in ECs. More importantly, OE-PFN2 dramatically elevated SCLC growth and vasculature formation as well as lung metastasis in tumor xenograft models. Finally, we found that PFN2 activated Smad2/3 in H446 and pERK in ECs, respectively. Taken together, our study revealed the role of PFN2 in SCLC development and metastasis, as well as tumor angiogenesis through exosomes, providing a new molecular target for SCLC treatment.
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Suppression of long noncoding RNA LINC00324 restricts cell proliferation and invasion of papillary thyroid carcinoma through downregulation of TRIM29 via upregulating microRNA-195-5p

Jinkai Xu, Zongyu Li, Qinghua Su, Jun Zhao, Jiancang Ma,

https://doi.org/10.18632/aging.202219 pp 26000—26011

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Xu J, Li Z, Su Q, Zhao J, Ma J, . Suppression of long noncoding RNA LINC00324 restricts cell proliferation and invasion of papillary thyroid carcinoma through downregulation of TRIM29 via upregulating microRNA-195-5p. . 12:26000-26011. https://doi.org/10.18632/aging.202219

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                TY  - JOUR
                AU  - Xu, Jinkai 
                AU  - Li, Zongyu 
                AU  - Su, Qinghua 
                AU  - Zhao, Jun 
                AU  - Ma, Jiancang 
                TI  - Suppression of long noncoding RNA LINC00324 restricts cell proliferation and invasion of papillary thyroid carcinoma through downregulation of TRIM29 via upregulating microRNA-195-5p
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202219
                DO  - 10.18632/aging.202219
                SP  - 26000
                EP  - 26011
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) are identified as novel regulators of carcinogenesis. To date, the precise functions of lncRNAs in papillary thyroid carcinoma (PTC) remains poorly understood. The purposes of this work were to explore the potential relevance of lncRNA 00324 (LINC00324) in PTC. Levels of LINC00324 were markedly up-regulated in PTC. Silencing of LINC00324 significantly repressed the proliferation and invasion of PTC cells. LINC00324 was documented as a sponge of microRNA-195-5p (miR-195-5p). Decreased levels of miR-195-5p were detected in PTC. The up-regulation of miR-195-5p suppressed PTC cellular proliferation and invasion. Suppression of miR-195-5p partially reversed the LINC00324-knockdown-mediated effects in PTC cells. We identified tripartite motif-containing 29 (TRIM29) as a target gene of miR-195-5p. TRIM29 overexpression partially reversed the LINC00324-knockdown- or miR-195-5p-overexpression-mediated effects in PTC cells. In short, this work demonstrates that LINC00324 knockdown inhibits the proliferation and invasion of PTC cells by decreasing TRIM29 expression via up-regulating miR-195-5p expression.
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Decreased testosterone secretion index and free testosterone level with multiple symptoms for late-onset hypogonadism identification: a nationwide multicenter study with 5980 aging males in China

Honggang Li, Yiqun Gu, Xuejun Shang, Yuanzhong Zhou, Huiping Zhang, Liandong Zuo, Guangan Mei, Wei Xia, Huangtao Guan, Wenpei Xiang, Shanjie Zhou, Changchun Wan, Baojin Hao, Xubo Shen, Linguo Tang, Weixiong Wu, Ying Qi, Na Yu, Xiangbin Kong, Yaoping Chen, Yihong Yang, Xingrong Qing, Chengliang Xiong,

https://doi.org/10.18632/aging.202227 pp 26012—26028

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Li H, Gu Y, Shang X, Zhou Y, Zhang H, Zuo L, Mei G, Xia W, Guan H, Xiang W, Zhou S, Wan C, Hao B, et al, . Decreased testosterone secretion index and free testosterone level with multiple symptoms for late-onset hypogonadism identification: a nationwide multicenter study with 5980 aging males in China. . 12:26012-26028. https://doi.org/10.18632/aging.202227

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                TY  - JOUR
                AU  - Li, Honggang 
                AU  - Gu, Yiqun 
                AU  - Shang, Xuejun 
                AU  - Zhou, Yuanzhong 
                AU  - Zhang, Huiping 
                AU  - Zuo, Liandong 
                AU  - Mei, Guangan 
                AU  - Xia, Wei 
                AU  - Guan, Huangtao 
                AU  - Xiang, Wenpei 
                AU  - Zhou, Shanjie 
                AU  - Wan, Changchun 
                AU  - Hao, Baojin 
                AU  - Shen, Xubo 
                AU  - Tang, Linguo 
                AU  - Wu, Weixiong 
                AU  - Qi, Ying 
                AU  - Yu, Na 
                AU  - Kong, Xiangbin 
                AU  - Chen, Yaoping 
                AU  - Yang, Yihong 
                AU  - Qing, Xingrong 
                AU  - Xiong, Chengliang 
                TI  - Decreased testosterone secretion index and free testosterone level with multiple symptoms for late-onset hypogonadism identification: a nationwide multicenter study with 5980 aging males in China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202227
                DO  - 10.18632/aging.202227
                SP  - 26012
                EP  - 26028
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Honggang 
                AU  - Gu, Yiqun 
                AU  - Shang, Xuejun 
                AU  - Zhou, Yuanzhong 
                AU  - Zhang, Huiping 
                AU  - Zuo, Liandong 
                AU  - Mei, Guangan 
                AU  - Xia, Wei 
                AU  - Guan, Huangtao 
                AU  - Xiang, Wenpei 
                AU  - Zhou, Shanjie 
                AU  - Wan, Changchun 
                AU  - Hao, Baojin 
                AU  - Shen, Xubo 
                AU  - Tang, Linguo 
                AU  - Wu, Weixiong 
                AU  - Qi, Ying 
                AU  - Yu, Na 
                AU  - Kong, Xiangbin 
                AU  - Chen, Yaoping 
                AU  - Yang, Yihong 
                AU  - Qing, Xingrong 
                AU  - Xiong, Chengliang 
                TI  - Decreased testosterone secretion index and free testosterone level with multiple symptoms for late-onset hypogonadism identification: a nationwide multicenter study with 5980 aging males in China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202227
                DO  - 10.18632/aging.202227
                SP  - 26012
                EP  - 26028
                PY  - 
                AB  - Late-onset hypogonadism (LOH) is a syndrome in middle-aged and elderly men caused by age-related testosterone deficiency. Age-related change of total testosterone (TT) of Asian males is different from Caucasian population, suggesting difference for LOH identification in Asians. A nationwide cross-sectional study involving six centers in China was conducted. Totally 6296 men aged 40-79 were recruited. After exclusions 5980 men were left for analyses. The serum TT level, was neither decreased with aging nor correlated with most hypogonadal symptoms. Instead, ten hypogonadal symptoms were found to be significantly correlated with free testosterone and testosterone secretion index, thus were chosen to form a concise scale. Further analysis identified a level of free testosterone &lt;210 pmol/L, testosterone secretion index &lt;1.8, and the concise scale score &#x2267;17 could be diagnosed as having significantly aggravated LOH. This study developed an evidence-based criteria for LOH identification in Chinese population and may be adopted in other Asians. It includes the impaired testosterone secretion ability and deficiency of bioavailable testosterone, which should be the main cause in LOH pathogenesis despite normal TT levels, as well as correlated multiple hypogonadal symptoms. Our results may guide the LOH treatment to increase testicular function of testosterone secretion and bioavailable testosterone.
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DUSP5 suppresses interleukin-1β-induced chondrocyte inflammation and ameliorates osteoarthritis in rats

Zhipeng Wu, Langhai Xu, Yuzhe He, Kai Xu, Zhonggai Chen, Safwat Adel Abdo Moqbel, Chiyuan Ma, Lifeng Jiang, Jisheng Ran, Lidong Wu, Ying Zhong,

https://doi.org/10.18632/aging.202252 pp 26029—26046

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Wu Z, Xu L, He Y, Xu K, Chen Z, Moqbel SAA, Ma C, Jiang L, Ran J, Wu L, Zhong Y, . DUSP5 suppresses interleukin-1β-induced chondrocyte inflammation and ameliorates osteoarthritis in rats. . 12:26029-26046. https://doi.org/10.18632/aging.202252

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                TY  - JOUR
                AU  - Wu, Zhipeng 
                AU  - Xu, Langhai 
                AU  - He, Yuzhe 
                AU  - Xu, Kai 
                AU  - Chen, Zhonggai 
                AU  - Moqbel, Safwat Adel Abdo 
                AU  - Ma, Chiyuan 
                AU  - Jiang, Lifeng 
                AU  - Ran, Jisheng 
                AU  - Wu, Lidong 
                AU  - Zhong, Ying 
                TI  - DUSP5 suppresses interleukin-1β-induced chondrocyte inflammation and ameliorates osteoarthritis in rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202252
                DO  - 10.18632/aging.202252
                SP  - 26029
                EP  - 26046
                PY  - 
                AB  - Osteoarthritis (OA) is a chronic degenerative joint disease characterized by deterioration of articular cartilage. Dual specificity phosphatase 5 (DUSP5), a member of the DUSP subfamily, is known to regulate cellular inflammation. Here, we studied the relationship between DUSP5 and OA by knockdown and overexpression DUSP5, respectively. Results from in vitro experiments demonstrated that the knockdown of DUSP5 increased interleukin-1&#x3B2; (IL-1&#x3B2;)-induced expression of inflammatory genes, such as inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX2), and matrix metalloproteinases (MMPs) in chondrocytes, whereas it decreased the expression of anti-inflammatory genes, such as tissue inhibitor of metalloproteinase 3 (TIMP3) and IL-10. Conversely, the overexpression of DUSP5 suppressed the IL-1&#x3B2;-induced expression of iNOS, COX-2, and MMPs, and upregulated the expression of TIMP3 and IL-10. Moreover, knockdown of DUSP5 enhanced the IL-1&#x3B2;-induced activation of NF-&#x3BA;B and ERK pathways, whereas its overexpression inhibited these pathways. DUSP5 overexpression prevented cartilage degeneration in a rat OA model, while its knockdown reversed that effect. Our findings reveal that DUSP5 suppresses IL-1&#x3B2;-induced chondrocyte inflammation by inhibiting the NF-&#x3BA;B and ERK signaling pathways and ameliorates OA.
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6-Bromoindirubin-3’-oxime (6BIO) prevents myocardium from aging by inducing autophagy

Donghao Guo, Lizhen Cheng, Yun Shen, Wei Li, Qinjie Li, Yuan Zhong, Ya Miao,

https://doi.org/10.18632/aging.202253 pp 26047—26062

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Guo D, Cheng L, Shen Y, Li W, Li Q, Zhong Y, Miao Y, . 6-Bromoindirubin-3’-oxime (6BIO) prevents myocardium from aging by inducing autophagy. . 12:26047-26062. https://doi.org/10.18632/aging.202253

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                TY  - JOUR
                AU  - Guo, Donghao 
                AU  - Cheng, Lizhen 
                AU  - Shen, Yun 
                AU  - Li, Wei 
                AU  - Li, Qinjie 
                AU  - Zhong, Yuan 
                AU  - Miao, Ya 
                TI  - 6-Bromoindirubin-3’-oxime (6BIO) prevents myocardium from aging by inducing autophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202253
                DO  - 10.18632/aging.202253
                SP  - 26047
                EP  - 26062
                PY  - 
                AB  - 6-Bromoindirubin-3&#x2019;-oxime (6BIO) is a novel small molecule that exerts positive effects on several age-related alterations. However, the anti-aging effects of 6BIO on the aging heart remain unknown. Herein, we aim to investigate the effects of 6BIO on the myocardium and its underlying mechanism in vivo and vitro. Following 6BIO treatment, an increased p53 contents, a reduced p16 and &#x3B2;-gal levels, and attenuation of cardiac fibrosis were observed, suggesting 6BIO retarded aging of cardiomyocytes. As observed, 6BIO reduced p62 contents, elevated the levels of Beclin-1 and the ratio of LC3II/I, indicating the induction of autophagy, while the reduction of the accumulation of ROS indicated 6BIO alleviated oxidative stress. In addition, 6BIO treatment inhibited both GSK3&#x3B2; signaling and mTOR signaling. 6BIO might be a promising agent for preventing myocardium from aging.
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An Immuno-Clinic score model for evaluating T cell immunity and predicting early antiviral therapy effectiveness in chronic hepatitis B

Yurong Gu, Xiaoyan Li, Lin Gu, Yifan Lian, Ke Wang, Youming Chen, Jing Lai, Yongyu Mei, Jing Liu, Zexuan Huang, Min Zhang, Lubiao Chen, Yuehua Huang,

https://doi.org/10.18632/aging.202274 pp 26063—26079

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Gu Y, Li X, Gu L, Lian Y, Wang K, Chen Y, Lai J, Mei Y, Liu J, Huang Z, Zhang M, Chen L, Huang Y, . An Immuno-Clinic score model for evaluating T cell immunity and predicting early antiviral therapy effectiveness in chronic hepatitis B. . 12:26063-26079. https://doi.org/10.18632/aging.202274

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                TY  - JOUR
                AU  - Gu, Yurong 
                AU  - Li, Xiaoyan 
                AU  - Gu, Lin 
                AU  - Lian, Yifan 
                AU  - Wang, Ke 
                AU  - Chen, Youming 
                AU  - Lai, Jing 
                AU  - Mei, Yongyu 
                AU  - Liu, Jing 
                AU  - Huang, Zexuan 
                AU  - Zhang, Min 
                AU  - Chen, Lubiao 
                AU  - Huang, Yuehua 
                TI  - An Immuno-Clinic score model for evaluating T cell immunity and predicting early antiviral therapy effectiveness in chronic hepatitis B
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202274
                DO  - 10.18632/aging.202274
                SP  - 26063
                EP  - 26079
                PY  - 
                AB  - We generated an Immuno-Clinic score (ICS) model to evaluate T cell immunity based on the clustering of antiviral cytokines and inhibitory molecules in 229 na&#xEF;ve chronic hepatitis B (CHB) patients. 126 patients receiving antiviral therapy were used to validate the model for predicting antiviral therapy effectiveness. Through receiver-operator characteristic curve analysis, the area under the curve, sensitivity, and specificity of the ICS model were 0.801 (95%CI 0.703-0.900), 0.727, and 0.722, respectively. The cut-off value was 0.442. Re-evaluation of T cell immunity in different phases of CHB showed that patients in the immune tolerant phase had the lowest percentage of ICS-high (15%), while patients in the inactive carrier phase had the highest percentage of ICS-high (92%). Patients in the immune active and gray zone phases had 17% and 56% ICS-high, respectively. Elevation of ICS as early as four weeks after treatment could predict the effectiveness of hepatitis B virus (HBV) DNA loss and normalization of alanine aminotransferase, while eight weeks after treatment could predict HBV surface antigen decline. Thus, this ICS model helps clinicians choose an optimal time for initiating antiviral therapy and predicting its efficacy.
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Postprandial triglyceride-rich lipoproteins-induced premature senescence of adipose-derived mesenchymal stem cells via the SIRT1/p53/Ac-p53/p21 axis through oxidative mechanism

Qun-yan Xiang, Feng Tian, Xiao Du, Jin Xu, Li-yuan Zhu, Li-ling Guo, Tie Wen, You-shuo Liu, Ling Liu,

https://doi.org/10.18632/aging.202298 pp 26080—26094

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Xiang Q, Tian F, Du X, Xu J, Zhu L, Guo L, Wen T, Liu Y, Liu L, . Postprandial triglyceride-rich lipoproteins-induced premature senescence of adipose-derived mesenchymal stem cells via the SIRT1/p53/Ac-p53/p21 axis through oxidative mechanism. . 12:26080-26094. https://doi.org/10.18632/aging.202298

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                TY  - JOUR
                AU  - Xiang, Qun-yan 
                AU  - Tian, Feng 
                AU  - Du, Xiao 
                AU  - Xu, Jin 
                AU  - Zhu, Li-yuan 
                AU  - Guo, Li-ling 
                AU  - Wen, Tie 
                AU  - Liu, You-shuo 
                AU  - Liu, Ling 
                TI  - Postprandial triglyceride-rich lipoproteins-induced premature senescence of adipose-derived mesenchymal stem cells via the SIRT1/p53/Ac-p53/p21 axis through oxidative mechanism
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202298
                DO  - 10.18632/aging.202298
                SP  - 26080
                EP  - 26094
                PY  - 
                AB  - The accumulation of senescent adipose-derived mesenchymal stem cells (AMSCs) in subcutaneous white adipose tissue (WAT) is the main cause for the deterioration of WAT and the subsequent age-related disorders in obesity. The number of AMSCs staining positively for senescence-associated-&#x3B2;-galactosidase (SA-&#x3B2;-Gal) increased significantly after incubation with postprandial triglyceride-rich lipoproteins (TRL), accompanied by an impaired cell proliferation capacity and increased expression of inflammatory factors. Besides, the expression of anti-aging protein, silent mating-type information regulation 2 homolog 1 (SIRT1), was downregulated significantly, while those of acetylated p53 (Ac-p53), total p53, and p21 proteins were upregulated significantly during postprandial TRL-induced premature senescence of AMSCs. Furthermore, the production of intracellular reactive oxygen species (ROS) in the TRL group increased significantly, while pretreatment with the ROS scavenger N-acetyl-L-cysteine effectively attenuated the premature senescence of AMSCs by decreasing ROS production and upregulating SIRT1 level. Thus, postprandial TRL induced premature senescence of AMSCs through the SIRT1/p53/Ac-p53/p21 axis, partly through increased oxidative stress.
                ER  -

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Identification and validation of an immune-related gene signature predictive of overall survival in colon cancer

Xuening Zhang, Hao Zhao, Xuezhong Shi, Xiaocan Jia, Yongli Yang,

https://doi.org/10.18632/aging.202317 pp 26095—26120

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Zhang X, Zhao H, Shi X, Jia X, Yang Y, . Identification and validation of an immune-related gene signature predictive of overall survival in colon cancer. . 12:26095-26120. https://doi.org/10.18632/aging.202317

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                TY  - JOUR
                AU  - Zhang, Xuening 
                AU  - Zhao, Hao 
                AU  - Shi, Xuezhong 
                AU  - Jia, Xiaocan 
                AU  - Yang, Yongli 
                TI  - Identification and validation of an immune-related gene signature predictive of overall survival in colon cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202317
                DO  - 10.18632/aging.202317
                SP  - 26095
                EP  - 26120
                PY  - 
                AB  - The heterogeneity and complexity of tumor-immune microenvironments lead to diverse immunotherapy effects among colon cancer patients. It is crucial to identify immune microenvironment-related biomarkers and construct prognostic risk models. In this study, the immune and stromal scores of 415 cases from TCGA were calculated using the ESTIMATE algorithm. AXIN2, CCL22, CLEC10A, CRIP2, RUNX3, and TRPM5 were screened and established a prognostic immune-related gene (IRG) signature using by univariate, LASSO, and multivariate Cox regression models. The predicted performance of IRG signature was external validated by GSE39582 (n=519). Stratified survival analysis showed IRG signature was an effective predictor of survival in patients with different clinical characteristics. The protein expression level of six genes was validated by immunohistochemistry analysis. Difference analysis indicated the mutation rate, immune cell of resting NK cells and regulatory T cells infiltration and four immune checkpoints of PD-1, PD-L1, LAG3 and VSIR expression levels in the high-risk group were significantly higher than those in the low-risk group. A nomogram incorporating the gene signatures and clinical factors was demonstrated had a good accuracy (1-, 3-, and 5-year AUC= 0.799, 0.791, 0.738). Our study identified a novel IRG signature, which may provide some references for the clinical precision immunotherapy of patients.
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Subanesthetic isoflurane abates ROS-activated MAPK/NF-κB signaling to repress ischemia-induced microglia inflammation and brain injury

Zhiqiang Yao, Ningning Liu, Xiaoshan Zhu, Ling Wang, Yali Zhao, Qinqin Liu, Chunfang Gao, Juntang Li,

https://doi.org/10.18632/aging.202349 pp 26121—26139

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Yao Z, Liu N, Zhu X, Wang L, Zhao Y, Liu Q, Gao C, Li J, . Subanesthetic isoflurane abates ROS-activated MAPK/NF-κB signaling to repress ischemia-induced microglia inflammation and brain injury. . 12:26121-26139. https://doi.org/10.18632/aging.202349

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                TY  - JOUR
                AU  - Yao, Zhiqiang 
                AU  - Liu, Ningning 
                AU  - Zhu, Xiaoshan 
                AU  - Wang, Ling 
                AU  - Zhao, Yali 
                AU  - Liu, Qinqin 
                AU  - Gao, Chunfang 
                AU  - Li, Juntang 
                TI  - Subanesthetic isoflurane abates ROS-activated MAPK/NF-κB signaling to repress ischemia-induced microglia inflammation and brain injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202349
                DO  - 10.18632/aging.202349
                SP  - 26121
                EP  - 26139
                PY  - 
                AB  - Isoflurane (ISO) elicits protective effects on ischemia-induced brain injury. We investigated whether sub-anesthetic (0.7%) ISO post-conditioning attenuates the inflammation and apoptosis in oxygen-glucose deprivation (OGD)-insulted co-cultures (microglia and neurons) in vitro and the brain injury of the middle cerebral arterial occlusion (MCAO) rat. We demonstrated that ISO augmented the viability of OGD-treated microglia and neurons. ISO reduced the expression and activation of COX2 and iNOS in OGD-challenged microglia. ISO repressed the production of tumor necrosis factor-&#x3B1;, interleukin (IL)-1&#x3B2;, IL-6, IL-8, and monocyte chemoattractant protein-1 in OGD-exposed microglia. ISO also decreased nucleosomal fragmentation and caspase-3 activity but increased mitochondrial membrane potential in OGD-stimulated microglia and neurons. Mechanistically, ISO suppressed OGD-induced microglial inflammation by blocking ROS-regulated p38 MAPK/NF-&#x3BA;B signaling pathway and hampered OGD-triggered microglial apoptosis in a ROS- or NO-dependent fashion. In vivo results with MCAO rats were partly consistent with the in vitro observation. These findings indicate that sub-anesthetic ISO post-conditioning abates the inflammation and apoptosis in OGD-stimulated rat microglia and the apoptosis of OGD-exposed neurons and the brain injuries of MCAO rats, suggesting it as a potentially effective therapeutic approach for ischemic brain damages.
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Role of electrocardiographic early repolarization pattern in long-term outcomes of a community-based middle-aged and geriatric ambulatory population: a prospective cohort study

Jyh-Ming Jimmy Juang, Yu-Jyun Huang, I-Shou Chang, Ching-Yu Julius Chen, I-Chien Wu, Chih-Cheng Hsu, Tzu-Yu Chen, Wei-Ting Tseng, Shih-Fan Sherri Yeh, Chao Agnes Hsiung,

https://doi.org/10.18632/aging.202369 pp 26140—26187

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Juang JJ, Huang Y, Chang I, Chen CJ, Wu I, Hsu C, Chen T, Tseng W, Yeh SS, Hsiung CA, . Role of electrocardiographic early repolarization pattern in long-term outcomes of a community-based middle-aged and geriatric ambulatory population: a prospective cohort study. . 12:26140-26187. https://doi.org/10.18632/aging.202369

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                TY  - JOUR
                AU  - Juang, Jyh-Ming Jimmy 
                AU  - Huang, Yu-Jyun 
                AU  - Chang, I-Shou 
                AU  - Chen, Ching-Yu Julius 
                AU  - Wu, I-Chien 
                AU  - Hsu, Chih-Cheng 
                AU  - Chen, Tzu-Yu 
                AU  - Tseng, Wei-Ting 
                AU  - Yeh, Shih-Fan Sherri 
                AU  - Hsiung, Chao Agnes 
                TI  - Role of electrocardiographic early repolarization pattern in long-term outcomes of a community-based middle-aged and geriatric ambulatory population: a prospective cohort study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202369
                DO  - 10.18632/aging.202369
                SP  - 26140
                EP  - 26187
                PY  - 
                AB  - In some studies, electrocardiographic early repolarization pattern (ERP) has been associated with an increased risk of death from cardiac causes. However, little is known about the prognostic significance of ERP in the middle-aged and geriatric general populations. We investigated the prevalence and long-term prognostic significance of early repolarization pattern (ERP) on electrocardiograms (ECGs) in the Healthy Aging Longitudinal Study (HALST) cohort of 4615 middle-aged and geriatric community-dwelling Han Chinese adults from Taiwan. The study subjects were followed-up for 95&#xB1;22 months. A positive ERP of &#x2265;0.1 mV was observed in 889 (19.3%) of the subjects. Kaplan-Meier survival curve analysis showed that ERP was not associated with all-cause and cardiovascular mortality (log-rank test, P=0.13 and 0.84, respectively). Cox regression analysis after adjusting for covariables revealed that age, blood pressure, smoking, diabetes, stroke, chronic kidney disease, and corrected QT interval (QTc) were associated with increased risk of all-cause mortality (P&lt;0.05). Age, and stroke were risk factors associated with increased risk of cardiovascular mortality (P&lt;0.05). However, ERP alone was not associated with all-cause or cardiovascular mortality. These findings show that ERP is common in the middle-aged and geriatric Han-Chinese individuals from the HALST cohort and is not associated with all-cause or cardiovascular mortality.
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MiR-223/NFAT5 signaling suppresses arterial smooth muscle cell proliferation and motility in vitro

Feifei Su, Miaoqian Shi, Jian Zhang, Qiangsun Zheng, Haichang Wang, Xue Li, Jianghong Chen,

https://doi.org/10.18632/aging.202395 pp 26188—26198

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Su F, Shi M, Zhang J, Zheng Q, Wang H, Li X, Chen J, . MiR-223/NFAT5 signaling suppresses arterial smooth muscle cell proliferation and motility in vitro. . 12:26188-26198. https://doi.org/10.18632/aging.202395

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Provider: 
 TY - JOUR
 AU - Su, Feifei 
 AU - Shi, Miaoqian 
 AU - Zhang, Jian 
 AU - Zheng, Qiangsun 
 AU - Wang, Haichang 
 AU - Li, Xue 
 AU - Chen, Jianghong 
 TI - MiR-223/NFAT5 signaling suppresses arterial smooth muscle cell proliferation and motility in vitro
 JO - 
 JA - 
 VL - 12
 IS - 24
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.202395
 DO - 10.18632/aging.202395
 SP - 26188
 EP - 26198
 PY - 
 AB - Aberrant proliferation and migration of vascular smooth muscle cells contributes to cardiovascular diseases (CVDs), including atherosclerosis. MicroRNA-223 (miR-223) protects against atherosclerotic CVDs. We investigated the contribution of miR-223 to platelet-derived growth factor-BB (PDGF-BB)-induced proliferation and migration of human aortic smooth muscle cells (HASMCs). We found that miR-223 was downregulated in PDGF-BB-treated HASMCs in a dose- and time-dependent manner, while nuclear factor of activated T cells 5 (NFAT5) was upregulated. Gain- and loss-of-function studies demonstrated that miR-223 treatment reduced PDGF-BB-induced HASMC proliferation and motility, whereas miR-223 inhibitor enhanced these processes. Moreover, NFAT5 was identified as a direct target of miR-223 in HASMC. The inhibitory effects of miR-223 on HASMC proliferation and migration were partly rescued by NFAT5 restoration. Overall, these findings suggest that miR-223 inhibits the PDGF-BB-induced proliferation and motility of HASMCs by targeting NFAT5 and that miR-223 and NFAT5 may be potential therapeutic targets for atherosclerosis.
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Ring finger protein 2 promotes colorectal cancer progression by suppressing early growth response 1

Feilong Wei, Haoren Jing, Ming Wei, Lei Liu, Jieheng Wu, Meng Wang, Donghui Han, Fa Yang, Bo Yang, Dian Jiao, Guoxu Zheng, Lingling Zhang, Wenjin Xi, Zhangyan Guo, An-Gang Yang, Weijun Qin, Yi Zhou, Weihong Wen,

https://doi.org/10.18632/aging.202396 pp 26199—26220

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Wei F, Jing H, Wei M, Liu L, Wu J, Wang M, Han D, Yang F, Yang B, Jiao D, Zheng G, Zhang L, Xi W, et al, . Ring finger protein 2 promotes colorectal cancer progression by suppressing early growth response 1. . 12:26199-26220. https://doi.org/10.18632/aging.202396

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                TY  - JOUR
                AU  - Wei, Feilong 
                AU  - Jing, Haoren 
                AU  - Wei, Ming 
                AU  - Liu, Lei 
                AU  - Wu, Jieheng 
                AU  - Wang, Meng 
                AU  - Han, Donghui 
                AU  - Yang, Fa 
                AU  - Yang, Bo 
                AU  - Jiao, Dian 
                AU  - Zheng, Guoxu 
                AU  - Zhang, Lingling 
                AU  - Xi, Wenjin 
                AU  - Guo, Zhangyan 
                AU  - Yang, An-Gang 
                AU  - Qin, Weijun 
                AU  - Zhou, Yi 
                AU  - Wen, Weihong 
                TI  - Ring finger protein 2 promotes colorectal cancer progression by suppressing early growth response 1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202396
                DO  - 10.18632/aging.202396
                SP  - 26199
                EP  - 26220
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wei, Feilong 
                AU  - Jing, Haoren 
                AU  - Wei, Ming 
                AU  - Liu, Lei 
                AU  - Wu, Jieheng 
                AU  - Wang, Meng 
                AU  - Han, Donghui 
                AU  - Yang, Fa 
                AU  - Yang, Bo 
                AU  - Jiao, Dian 
                AU  - Zheng, Guoxu 
                AU  - Zhang, Lingling 
                AU  - Xi, Wenjin 
                AU  - Guo, Zhangyan 
                AU  - Yang, An-Gang 
                AU  - Qin, Weijun 
                AU  - Zhou, Yi 
                AU  - Wen, Weihong 
                TI  - Ring finger protein 2 promotes colorectal cancer progression by suppressing early growth response 1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202396
                DO  - 10.18632/aging.202396
                SP  - 26199
                EP  - 26220
                PY  - 
                AB  - Ring finger protein 2 (RNF2) is an important component of polycomb repressive complex 1. RNF2 is upregulated in many kinds of tumors, and elevated RNF2 expression is associated with a poor prognosis in certain cancers. To assess the function of RNF2 in colorectal cancer, we examined RNF2 protein levels in 313 paired colorectal cancer tissues and adjacent normal tissues. We then analyzed the association of RNF2 expression with the patients&#x2019; clinicopathologic features and prognoses. RNF2 expression was upregulated in colorectal cancer tissues and was associated with the tumor differentiation status, tumor stage and prognosis. In colorectal cancer cell lines, downregulation of RNF2 inhibited cell proliferation and induced apoptosis. Gene microarray analysis revealed that early growth response 1 (EGR1) was upregulated in RNF2-knockdown cells. Knocking down EGR1 partially reversed the inhibition of cell proliferation and the induction of apoptosis in RNF2-knockdown cells. RNF2 was enriched at the EGR1 promoter, where it mono-ubiquitinated histone H2A, thereby inhibiting EGR1 expression. These results indicate that RNF2 is oncogenic in colorectal cancer and may promote disease progression by inhibiting EGR1 expression. RNF2 is thus a potential prognostic marker and therapeutic target in colorectal cancer.
                ER  -

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Construction and analysis of a joint diagnosis model of random forest and artificial neural network for heart failure

Yuqing Tian, Jiefu Yang, Ming Lan, Tong Zou,

https://doi.org/10.18632/aging.202405 pp 26221—26235

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Tian Y, Yang J, Lan M, Zou T, . Construction and analysis of a joint diagnosis model of random forest and artificial neural network for heart failure. . 12:26221-26235. https://doi.org/10.18632/aging.202405

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                TY  - JOUR
                AU  - Tian, Yuqing 
                AU  - Yang, Jiefu 
                AU  - Lan, Ming 
                AU  - Zou, Tong 
                TI  - Construction and analysis of a joint diagnosis model of random forest and artificial neural network for heart failure
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202405
                DO  - 10.18632/aging.202405
                SP  - 26221
                EP  - 26235
                PY  - 
                AB  - Heart failure is a global health problem that affects approximately 26 million people worldwide. As conventional diagnostic techniques for heart failure have been in practice with various limitations, it is necessary to develop novel diagnostic models to supplement existing methods. With advances and improvements in gene sequencing technology in recent years, more heart failure-related genes have been identified. Using existing gene expression data in the Gene Expression Omnibus (GEO) database, we screened differentially expressed genes (DEGs) of heart failure and identified six key genes (HMOX2, SERPINA3, LCN6, CSDC2, FREM1, and ZMAT1) by random forest classifier. Of these genes, CSDC2, FREM1, and ZMAT1 have never been associated with heart failure. We also successfully constructed a new diagnostic model of heart failure using an artificial neural network and verified its diagnostic efficacy in public datasets.
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Exosomal linc-FAM138B from cancer cells alleviates hepatocellular carcinoma progression via regulating miR-765

Chenyi Zhuo, Tingzhuang Yi, Jian Pu, Xiaoning Cen, Yang Zhou, Shi Feng, Cheng Wei, Pengyu Chen, Wei Wang, Chongchan Bao, Jianchu Wang, Qianli Tang,

https://doi.org/10.18632/aging.202430 pp 26236—26247

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Zhuo C, Yi T, Pu J, Cen X, Zhou Y, Feng S, Wei C, Chen P, Wang W, Bao C, Wang J, Tang Q, . Exosomal linc-FAM138B from cancer cells alleviates hepatocellular carcinoma progression via regulating miR-765. . 12:26236-26247. https://doi.org/10.18632/aging.202430

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                TY  - JOUR
                AU  - Zhuo, Chenyi 
                AU  - Yi, Tingzhuang 
                AU  - Pu, Jian 
                AU  - Cen, Xiaoning 
                AU  - Zhou, Yang 
                AU  - Feng, Shi 
                AU  - Wei, Cheng 
                AU  - Chen, Pengyu 
                AU  - Wang, Wei 
                AU  - Bao, Chongchan 
                AU  - Wang, Jianchu 
                AU  - Tang, Qianli 
                TI  - Exosomal linc-FAM138B from cancer cells alleviates hepatocellular carcinoma progression via regulating miR-765
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202430
                DO  - 10.18632/aging.202430
                SP  - 26236
                EP  - 26247
                PY  - 
                AB  - Exosomes are small vesicles with a diameter of 30-150 nm secreted by cells, which can be used as signal carriers to transfer nucleic acids, proteins, lipids and other functional substances to the recipient cells and play a role in cell communication. Hepatocellular carcinoma is the fourth most common cause of cancer-related death worldwide. Studies have shown that long non-coding RNAs (lncRNAs) are involved in the development and progression of many types of tumors. Our present study found that linc-FAM138B was reduced in HCC tissues and cell lines, low expression of linc-FAM138B indicated a poor prognosis in HCC patients. Interestingly, linc-FAM138B could be packaged into cancer cells. And exo-FAM138B inhibited the proliferation, migration and invasion of HCC cells. Furthermore, linc-FAM138B sponged miR-765 levels. And exo-si-FAM138B promoted HCC progression, while deletion of miR-765 reversed the role of exo-si-FAM138B. In vivo tumorigenesis experiments showed that exo-FAM138B suppressed HCC growth via modulating miR-765. In conclusion, exo-linc-FAM138B secreted by cancer cells inhibited HCC development via targeting miR-765, which provided a new idea and perspective for in-depth understanding of the complex signal regulation in HCC process.
                ER  -

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COVID-19
Influence of aging on deterioration of patients with COVID-19

Limin Pang, Yi Liu, Maoze Shen, Jujian Ye, Ruirong Chen, Zhien Lan, Zhijian Wu, Yang Guo, Peidong Zhang,

https://doi.org/10.18632/aging.202136 pp 26248—26262

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Pang L, Liu Y, Shen M, Ye J, Chen R, Lan Z, Wu Z, Guo Y, Zhang P, . Influence of aging on deterioration of patients with COVID-19. . 12:26248-26262. https://doi.org/10.18632/aging.202136

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                TY  - JOUR
                AU  - Pang, Limin 
                AU  - Liu, Yi 
                AU  - Shen, Maoze 
                AU  - Ye, Jujian 
                AU  - Chen, Ruirong 
                AU  - Lan, Zhien 
                AU  - Wu, Zhijian 
                AU  - Guo, Yang 
                AU  - Zhang, Peidong 
                TI  - Influence of aging on deterioration of patients with COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202136
                DO  - 10.18632/aging.202136
                SP  - 26248
                EP  - 26262
                PY  - 
                AB  - Aging is an important factor affecting the deterioration of patients with coronavirus disease 2019 (COVID-19). The aging and degeneration of various tissues and organs in the elderly lead to impaired organ function. Underlying conditions such as chronic lung disease, cardiovascular disease, and diabetes in aged patients are associated with higher mortality. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily interacts with the cell surface receptor angiotensin-converting enzyme (ACE) 2 and other accessory proteins such as 78 kDa glucose-regulated protein 78 (GRP78) and CD147. Thus, altered receptor signals in aging and chronic disease play a role in SARS-CoV-2 infection, and are associated with a higher risk of deterioration in different organs. In this review, after a brief introduction to the link between aging and receptors for SARS-CoV-2, we focus on the risk of deterioration in different organs of COVID-19 patients considering aging as the main factor. We further discuss the structural and/or physiological changes in the immune system and organs (lung, heart, kidney, vessels, nerve system), as well as those associated with diabetes, in aging patients, and speculate on the most likely mechanisms underlying the deterioration of COVID-19 patients.
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COVID-19
Immunometabolism at the cornerstone of inflammaging, immunosenescence, and autoimmunity in COVID-19

Loukman Omarjee, Frédérique Perrot, Olivier Meilhac, Guillaume Mahe, Guilhem Bousquet, Anne Janin,

https://doi.org/10.18632/aging.202422 pp 26263—26278

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Omarjee L, Perrot F, Meilhac O, Mahe G, Bousquet G, Janin A, . Immunometabolism at the cornerstone of inflammaging, immunosenescence, and autoimmunity in COVID-19. . 12:26263-26278. https://doi.org/10.18632/aging.202422

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                TY  - JOUR
                AU  - Omarjee, Loukman 
                AU  - Perrot, Frédérique 
                AU  - Meilhac, Olivier 
                AU  - Mahe, Guillaume 
                AU  - Bousquet, Guilhem 
                AU  - Janin, Anne 
                TI  - Immunometabolism at the cornerstone of inflammaging, immunosenescence, and autoimmunity in COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 24
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202422
                DO  - 10.18632/aging.202422
                SP  - 26263
                EP  - 26278
                PY  - 
                AB  - Inflammaging constitutes the common factor for comorbidities predisposing to severe COVID-19. Inflammaging leads to T-cell senescence, and immunosenescence is linked to autoimmune manifestations in COVID-19. As in SLE, metabolic dysregulation occurs in T-cells. Targeting this T-cell dysfunction opens the field for new therapeutic strategies to prevent severe COVID-19. Immunometabolism-mediated approaches such as rapamycin, metformin and dimethyl fumarate, may optimize COVID-19 treatment of the elderly and patients at risk for severe disease.
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Correction for: Long non-coding RNA RNF7 promotes the cardiac fibrosis in rat model via miR-543/THBS1 axis and TGFβ1 activation

Fan Ouyang, Xiangyang Liu, Guoan Liu, Haihua Qiu, Yi He, Hongyu Hu, Ping Jiang,

https://doi.org/10.18632/aging.104222 pp 26279

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Ouyang F, Liu X, Liu G, Qiu H, He Y, Hu H, Jiang P, . Correction for: Long non-coding RNA RNF7 promotes the cardiac fibrosis in rat model via miR-543/THBS1 axis and TGFβ1 activation. . 12:26279-26279. https://doi.org/10.18632/aging.104222

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Volume 12, Issue 24

About the Cover

Editorials

Mario Kassmann, Gang Fan, Maik Gollasch,

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Claudia Lennicke, Eliano dos Santos, Helena M. Cochemé,

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Research Perspective

Alec Wong, Tra Kieu, Paul D. Robbins,

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Meeting Report

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Priority Research Paper

Xiaohong Chen, João A. Amorim, Giannis A. Moustafa, Jong-Jer Lee, Zhen Yu, Kenji Ishihara, Yasuhiro Iesato, Paulo Barbisan, Takashi Ueta, Konstantina A. Togka, Lin Lu, David A. Sinclair, Demetrios G. Vavvas,

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Research Papers

COVID-19 Mortality in an Italian nursing home during COVID-19 pandemic: correlation with gender, age, ADL, vitamin D supplementation, and limitations of the diagnostic tests

Biagio Cangiano, Letizia Maria Fatti, Leila Danesi, Giacomo Gazzano, Marina Croci, Giovanni Vitale, Luisa Gilardini, Stefania Bonadonna, Iacopo Chiodini, Chiara Francesca Caparello, Antonio Conti, Luca Persani, Marco Stramba-Badiale, Marco Bonomi,

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COVID-19 Coagulopathy in patients with COVID-19: a systematic review and meta-analysis

Xiaolin Zhang, Xue Yang, Hongmei Jiao, Xinmin Liu,

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COVID-19 Clinical outcomes of patients hospitalized for COVID-19 versus SARS: a meta-analysis

Po-Cheng Chang, Chien-Chang Yang, Kuo-Chin Kao, Ming-Shien Wen,

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COVID-19 Association between ageing population, median age, life expectancy and mortality in coronavirus disease (COVID-19)

Xue-Qiang Wang, Ge Song, Zheng Yang, Ren-Jie Chen, Yi-Li Zheng, Hao-Yu Hu, Xuan Su, Pei-Jie Chen,

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COVID-19 Characteristics of mortal COVID-19 cases compared to the survivors

Xianghui Zhou, Zhipeng Cheng, Dan Shu, Wenyi Lin, Zhangyin Ming, Wei Chen, Yu Hu,

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COVID-19 Dynamic monitoring of immune function indexes in COVID-19 patients

Yaohui Song, Huixiu Zhong, Lin Li, Minggang Yin, Yi Yin, Xiaolong Guo, Bo Zhang, Weiping Liu,

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Sinan Khor, Dongsheng Cai,

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Emmanuel Navarro-Flores, Ricardo Becerro de Bengoa Vallejo, Marta Elena Losa-Iglesias, Patricia Palomo-López, César Calvo-Lobo, Daniel López-López, Eva Maria Martínez-Jiménez, Carlos Romero-Morales,

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Krissy K. Moehling, Bo Zhai, William E. Schwarzmann, Uma R. Chandran, Marianna Ortiz, Mary Patricia Nowalk, David Nace, Chyongchiou J. Lin, Michael Susick, Min Z. Levine, John F. Alcorn, Richard K. Zimmerman,

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Javier A. Menendez, Susan K. Peirce, Adriana Papadimitropoulou, Elisabet Cuyàs, Travis Vander Steen, Sara Verdura, Luciano Vellon, Wen Y. Chen, Ruth Lupu,

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Lisa Harber-Aschan, Amaia Calderón-Larrañaga, Alexander Darin-Mattson, Xiaonan Hu, Laura Fratiglioni, Serhiy Dekhtyar,

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Rossella Gioco, Lidia Puzzo, Marco Patanè, Daniela Corona, Giuseppe Trama, Pierfrancesco Veroux, Massimiliano Veroux,

COVID-19
Mortality in an Italian nursing home during COVID-19 pandemic: correlation with gender, age, ADL, vitamin D supplementation, and limitations of the diagnostic tests

COVID-19
Coagulopathy in patients with COVID-19: a systematic review and meta-analysis

COVID-19
Clinical outcomes of patients hospitalized for COVID-19 versus SARS: a meta-analysis

COVID-19
Association between ageing population, median age, life expectancy and mortality in coronavirus disease (COVID-19)

COVID-19
Characteristics of mortal COVID-19 cases compared to the survivors

COVID-19
Dynamic monitoring of immune function indexes in COVID-19 patients