Volume 12, Issue 6

Nuclear protein export pathway in aging therapeutics

Bulmaro Cisneros, Ian García-Aguirre,

https://doi.org/10.18632/aging.102948 pp 4682—4684

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Cisneros B, García-Aguirre I, . Nuclear protein export pathway in aging therapeutics. . 12:4682-4684. https://doi.org/10.18632/aging.102948

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Prometheus revisited: liver homeostasis and repair

Tianliang Sun, Stefano Annunziato, Jan S. Tchorz,

https://doi.org/10.18632/aging.102957 pp 4685—4687

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ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging

Jing Zhao, Lei Zhang, Aiping Lu, Yingchao Han, Debora Colangelo, Christina Bukata, Alex Scibetta, Matthew J. Yousefzadeh, Xuesen Li, Aditi U. Gurkar, Sara J. McGowan, Luise Angelini, Ryan O’Kelly, Hongshuai Li, Lana Corbo, Tokio Sano, Heather Nick, Enrico Pola, Smitha P.S. Pilla, Warren C. Ladiges, Nam Vo, Johnny Huard, Laura J. Niedernhofer, Paul D. Robbins,

https://doi.org/10.18632/aging.102863 pp 4688—4710

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Zhao J, Zhang L, Lu A, Han Y, Colangelo D, Bukata C, Scibetta A, Yousefzadeh MJ, Li X, Gurkar AU, McGowan SJ, Angelini L, O’Kelly R, et al, . ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging. . 12:4688-4710. https://doi.org/10.18632/aging.102863

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Provider: 
                TY  - JOUR
                AU  - Zhao, Jing 
                AU  - Zhang, Lei 
                AU  - Lu, Aiping 
                AU  - Han, Yingchao 
                AU  - Colangelo, Debora 
                AU  - Bukata, Christina 
                AU  - Scibetta, Alex 
                AU  - Yousefzadeh, Matthew J. 
                AU  - Li, Xuesen 
                AU  - Gurkar, Aditi U. 
                AU  - McGowan, Sara J. 
                AU  - Angelini, Luise 
                AU  - O’Kelly, Ryan 
                AU  - Li, Hongshuai 
                AU  - Corbo, Lana 
                AU  - Sano, Tokio 
                AU  - Nick, Heather 
                AU  - Pola, Enrico 
                AU  - Pilla, Smitha P.S. 
                AU  - Ladiges, Warren C. 
                AU  - Vo, Nam 
                AU  - Huard, Johnny 
                AU  - Niedernhofer, Laura J. 
                AU  - Robbins, Paul D. 
                TI  - ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102863
                DO  - 10.18632/aging.102863
                SP  - 4688
                EP  - 4710
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhao, Jing 
                AU  - Zhang, Lei 
                AU  - Lu, Aiping 
                AU  - Han, Yingchao 
                AU  - Colangelo, Debora 
                AU  - Bukata, Christina 
                AU  - Scibetta, Alex 
                AU  - Yousefzadeh, Matthew J. 
                AU  - Li, Xuesen 
                AU  - Gurkar, Aditi U. 
                AU  - McGowan, Sara J. 
                AU  - Angelini, Luise 
                AU  - O’Kelly, Ryan 
                AU  - Li, Hongshuai 
                AU  - Corbo, Lana 
                AU  - Sano, Tokio 
                AU  - Nick, Heather 
                AU  - Pola, Enrico 
                AU  - Pilla, Smitha P.S. 
                AU  - Ladiges, Warren C. 
                AU  - Vo, Nam 
                AU  - Huard, Johnny 
                AU  - Niedernhofer, Laura J. 
                AU  - Robbins, Paul D. 
                TI  - ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102863
                DO  - 10.18632/aging.102863
                SP  - 4688
                EP  - 4710
                PY  - 
                AB  - NF-&#x3BA;B is a transcription factor activated in response to inflammatory, genotoxic and oxidative stress and important for driving senescence and aging. Ataxia-telangiectasia mutated (ATM) kinase, a core component of DNA damage response signaling, activates NF-&#x3BA;B in response to genotoxic and oxidative stress via post-translational modifications. Here we demonstrate that ATM is activated in senescent cells in culture and murine tissues from Ercc1-deficient mouse models of accelerated aging, as well as naturally aged mice. Genetic and pharmacologic inhibition of ATM reduced activation of NF-&#x3BA;B and markers of senescence and the senescence-associated secretory phenotype (SASP) in senescent Ercc1-/- MEFs. Ercc1-/&#x394; mice heterozygous for Atm have reduced NF-&#x3BA;B activity and cellular senescence, improved function of muscle-derived stem/progenetor cells (MDSPCs) and extended healthspan with reduced age-related pathology especially age-related bone and intervertebral disc pathologies. In addition, treatment of Ercc1-/&#x2206; mice with the ATM inhibitor KU-55933 suppressed markers of senescence and SASP. Taken together, these results demonstrate that the ATM kinase is a major mediator of DNA damage-induced, NF-&#x3BA;B-mediated cellular senescence, stem cell dysfunction and aging and thus represents a therapeutic target to slow the progression of aging.
                ER  -

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Silencing of lncRNA XIST inhibits non-small cell lung cancer growth and promotes chemosensitivity to cisplatin

Xiaohui Xu, Xiaoyun Zhou, Zhenju Chen, Chao Gao, Luo Zhao, Yushang Cui,

https://doi.org/10.18632/aging.102673 pp 4711—4726

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Xu X, Zhou X, Chen Z, Gao C, Zhao L, Cui Y, . Silencing of lncRNA XIST inhibits non-small cell lung cancer growth and promotes chemosensitivity to cisplatin. . 12:4711-4726. https://doi.org/10.18632/aging.102673

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                TY  - JOUR
                AU  - Xu, Xiaohui 
                AU  - Zhou, Xiaoyun 
                AU  - Chen, Zhenju 
                AU  - Gao, Chao 
                AU  - Zhao, Luo 
                AU  - Cui, Yushang 
                TI  - Silencing of lncRNA XIST inhibits non-small cell lung cancer growth and promotes chemosensitivity to cisplatin
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102673
                DO  - 10.18632/aging.102673
                SP  - 4711
                EP  - 4726
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) play critical roles in tumour progression and metastasis. Emerging evidence indicates that the lncRNA X inactive-specific transcript (XIST) is dysregulated in several tumor types, including non-small cell lung cancer (NSCLC). However, in NSCLC and other cancers the oncogenic mechanism of XIST remains incompletely understood. Here, we confirmed that XIST is upregulated in human NSCLC specimens, and is especially overexpressed in tumors previously treated with cisplatin (cis-diamminedichloroplatinum(II); DDP). In vitro, XIST knockdown inhibited NSCLC cell growth and promoted DDP chemosensitivity by stimulating apoptosis and pyroptosis. Moreover, XIST&#x2019;s oncogenic effects and ability to promote DDP chemoresistance were largely related to its binding to the TGF-&#x3B2; effector SMAD2, which inhibited its translocation to the nucleus and prevented the transcription of p53 and NLRP3, crucial regulators of apoptosis and pyroptosis, respectively. Using DDP-resistant NSCLC cells, mouse xenograft studies verified the oncogenic function of XIST and its ability to inhibit programmed cell death, thereby mediating DDP chemoresistance. These findings suggest that XIST expression may serve as a novel biomarker to predict DDP treatment efficacy, and may help in the design of new therapies to circumvent DDP chemoresistance in NSCLC and other tumor types.
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Metformin coordinates osteoblast/osteoclast differentiation associated with ischemic osteonecrosis

See-Hyoung Park, Mi-Ae Kang, Young Jae Moon, Kyu Yun Jang, Jung Ryul Kim,

https://doi.org/10.18632/aging.102796 pp 4727—4741

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Park S, Kang M, Moon YJ, Jang KY, Kim JR, . Metformin coordinates osteoblast/osteoclast differentiation associated with ischemic osteonecrosis. . 12:4727-4741. https://doi.org/10.18632/aging.102796

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                TY  - JOUR
                AU  - Park, See-Hyoung 
                AU  - Kang, Mi-Ae 
                AU  - Moon, Young Jae 
                AU  - Jang, Kyu Yun 
                AU  - Kim, Jung Ryul 
                TI  - Metformin coordinates osteoblast/osteoclast differentiation associated with ischemic osteonecrosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102796
                DO  - 10.18632/aging.102796
                SP  - 4727
                EP  - 4741
                PY  - 
                AB  - In this study, we aimed to identify a candidate drug that can activate endogenous Angiopoietin 1 (Ang1) expression via drug repositioning as a pharmacological treatment for avascular osteonecrosis. After incubation with 821 drugs from the Food and Drug Administration (FDA)-approved drug library, Ang1 expression in U2OS cell culture media was examined by ELISA. Metformin, the first-line medication for treatment of type 2 diabetes, was selected as a candidate for in vitro and in vivo experimental evaluation. Ang1 was induced, and alkaline phosphatase activity was increased by metformin treatment in U2OS and MG63 cells. Wound healing and migration assay showed increased osteoblastic cell mobility by metformin treatment in U2OS and MG63 cells. Metformin upregulated expression of protein markers for osteoblastic differentiation in U2OS and MG63 cells but inhibited osteoclastic differentiation in Raw264.7 cells. Metformin (25 mg/kg) protected against ischemic necrosis in the epiphysis of the rat femoral head by maintaining osteoblast/osteocyte function and vascular density but inhibiting osteoclast activity in the necrotic femoral head. These findings provide novel insight into the specific biomarkers that are targeted and regulated by metformin in osteoblast differentiation and contribute to understanding the effects of these FDA-approved small-molecule drugs as novel therapeutics for ischemic osteonecrosis.
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Genome-wide association study identifies genetic factors that modify age at onset in Machado-Joseph disease

Fulya Akçimen, Sandra Martins, Calwing Liao, Cynthia V. Bourassa, Hélène Catoire, Garth A. Nicholson, Olaf Riess, Mafalda Raposo, Marcondes C. França, João Vasconcelos, Manuela Lima, Iscia Lopes-Cendes, Maria Luiza Saraiva-Pereira, Laura B. Jardim, Jorge Sequeiros, Patrick A. Dion, Guy A. Rouleau,

https://doi.org/10.18632/aging.102825 pp 4742—4756

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Akçimen F, Martins S, Liao C, Bourassa CV, Catoire H, Nicholson GA, Riess O, Raposo M, França MC, Vasconcelos J, Lima M, Lopes-Cendes I, Saraiva-Pereira ML, et al, . Genome-wide association study identifies genetic factors that modify age at onset in Machado-Joseph disease. . 12:4742-4756. https://doi.org/10.18632/aging.102825

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                TY  - JOUR
                AU  - Akçimen, Fulya 
                AU  - Martins, Sandra 
                AU  - Liao, Calwing 
                AU  - Bourassa, Cynthia V. 
                AU  - Catoire, Hélène 
                AU  - Nicholson, Garth A. 
                AU  - Riess, Olaf 
                AU  - Raposo, Mafalda 
                AU  - França, Marcondes C. 
                AU  - Vasconcelos, João 
                AU  - Lima, Manuela 
                AU  - Lopes-Cendes, Iscia 
                AU  - Saraiva-Pereira, Maria Luiza 
                AU  - Jardim, Laura B. 
                AU  - Sequeiros, Jorge 
                AU  - Dion, Patrick A. 
                AU  - Rouleau, Guy A. 
                TI  - Genome-wide association study identifies genetic factors that modify age at onset in Machado-Joseph disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102825
                DO  - 10.18632/aging.102825
                SP  - 4742
                EP  - 4756
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Akçimen, Fulya 
                AU  - Martins, Sandra 
                AU  - Liao, Calwing 
                AU  - Bourassa, Cynthia V. 
                AU  - Catoire, Hélène 
                AU  - Nicholson, Garth A. 
                AU  - Riess, Olaf 
                AU  - Raposo, Mafalda 
                AU  - França, Marcondes C. 
                AU  - Vasconcelos, João 
                AU  - Lima, Manuela 
                AU  - Lopes-Cendes, Iscia 
                AU  - Saraiva-Pereira, Maria Luiza 
                AU  - Jardim, Laura B. 
                AU  - Sequeiros, Jorge 
                AU  - Dion, Patrick A. 
                AU  - Rouleau, Guy A. 
                TI  - Genome-wide association study identifies genetic factors that modify age at onset in Machado-Joseph disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102825
                DO  - 10.18632/aging.102825
                SP  - 4742
                EP  - 4756
                PY  - 
                AB  - Machado-Joseph disease (MJD/SCA3) is the most common form of dominantly inherited ataxia worldwide. The disorder is caused by an expanded CAG repeat in the ATXN3 gene. Past studies have revealed that the length of the expansion partly explains the disease age at onset (AO) variability of MJD, which is confirmed in this study (Pearson&#x2019;s correlation coefficient R2 = 0.62). Using a total of 786 MJD patients from five different geographical origins, a genome-wide association study (GWAS) was conducted to identify additional AO modifying factors that could explain some of the residual AO variability. We identified nine suggestively associated loci (P &lt; 1 &#xD7; 10&#x2212;5). These loci were enriched for genes involved in vesicle transport, olfactory signaling, and synaptic pathways. Furthermore, associations between AO and the TRIM29 and RAG genes suggests that DNA repair mechanisms might be implicated in MJD pathogenesis. Our study demonstrates the existence of several additional genetic factors, along with CAG expansion, that may lead to a better understanding of the genotype-phenotype correlation in MJD.
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Prognostic value of immune-related genes in the tumor microenvironment of lung adenocarcinoma and lung squamous cell carcinoma

Yan Qu, Bo Cheng, Na Shao, Yibin Jia, Qingxu Song, Bingxu Tan, Jianbo Wang,

https://doi.org/10.18632/aging.102871 pp 4757—4777

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Qu Y, Cheng B, Shao N, Jia Y, Song Q, Tan B, Wang J, . Prognostic value of immune-related genes in the tumor microenvironment of lung adenocarcinoma and lung squamous cell carcinoma. . 12:4757-4777. https://doi.org/10.18632/aging.102871

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                TY  - JOUR
                AU  - Qu, Yan 
                AU  - Cheng, Bo 
                AU  - Shao, Na 
                AU  - Jia, Yibin 
                AU  - Song, Qingxu 
                AU  - Tan, Bingxu 
                AU  - Wang, Jianbo 
                TI  - Prognostic value of immune-related genes in the tumor microenvironment of lung adenocarcinoma and lung squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102871
                DO  - 10.18632/aging.102871
                SP  - 4757
                EP  - 4777
                PY  - 
                AB  - Non-small cell lung cancer (NSCLC), which consists mainly of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), are the leading cause of cancer deaths worldwide. In this study, we performed a comprehensive analysis of the tumor microenvironmental and genetic factors to identify prognostic biomarkers for NSCLC. We evaluated the immune and stromal scores of patients with LUAD and LUSC using data from The Cancer Genome Atlas database with the ESTIMATE algorithm. Based on these scores, the differentially expressed genes were obtained and immune-related prognostic genes were identified. Functional analysis and protein-protein interaction network further revealed the immune-related biological processes in which these genes participated. Additionally, 22 subsets of tumor-infiltrating immune cells (TIICs) in the tumor microenvironment were analyzed with the CIBERSORT algorithm. Finally, we validated these valuable genes using an independent cohort from the Gene Expression Omnibus database. The associations of the immune and stromal scores with patients&#x2019; clinical characteristics and prognosis were positive in LUAD but negative in LUSC and the correlations of TIICs with clinical characteristics were clarified. Several differentially expressed genes were identified to be potential immune-related prognostic genes. This study comprehensively analyzed the tumor microenvironment and presented immune-related prognostic biomarkers for NSCLC.
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Transplant of microbiota from long-living people to mice reduces aging-related indices and transfers beneficial bacteria

Yinfeng Chen, Siyuan Zhang, Bo Zeng, Jiangchao Zhao, Mingyao Yang, Mingwang Zhang, Yan Li, Qingyong Ni, De Wu, Ying Li,

https://doi.org/10.18632/aging.102872 pp 4778—4793

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Chen Y, Zhang S, Zeng B, Zhao J, Yang M, Zhang M, Li Y, Ni Q, Wu D, Li Y, . Transplant of microbiota from long-living people to mice reduces aging-related indices and transfers beneficial bacteria. . 12:4778-4793. https://doi.org/10.18632/aging.102872

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                TY  - JOUR
                AU  - Chen, Yinfeng 
                AU  - Zhang, Siyuan 
                AU  - Zeng, Bo 
                AU  - Zhao, Jiangchao 
                AU  - Yang, Mingyao 
                AU  - Zhang, Mingwang 
                AU  - Li, Yan 
                AU  - Ni, Qingyong 
                AU  - Wu, De 
                AU  - Li, Ying 
                TI  - Transplant of microbiota from long-living people to mice reduces aging-related indices and transfers beneficial bacteria
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102872
                DO  - 10.18632/aging.102872
                SP  - 4778
                EP  - 4793
                PY  - 
                AB  - A close relationship between age and gut microbiota exists in invertebrates and vertebrates, including humans. Long-living people are a model for studying healthy aging; they also have a distinctive microbiota structure. The relationship between the microbiota of long-living people and aging phenotype remains largely unknown. Herein, the feces of long-living people were transplanted into mice, which were then examined for aging-related indices and beneficial bacteria. Mice transplanted with fecal matter from long-living people (L group) had greater &#x3B1; diversity, more probiotic genera (Lactobacillus and Bifidobacterium), and short-chain fatty acid producing genera (Roseburia, Faecalibacterium, Ruminococcus, Coprococcus) than the control group. L group mice also accumulated less lipofuscin and &#x3B2;-galactosidase and had longer intestinal villi. This study indicates the effects that the gut microbiota from long-living people have on healthy aging.
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The LSD1 inhibitor iadademstat (ORY-1001) targets SOX2-driven breast cancer stem cells: a potential epigenetic therapy in luminal-B and HER2-positive breast cancer subtypes

Elisabet Cuyàs, Juan Gumuzio, Sara Verdura, Joan Brunet, Joaquim Bosch-Barrera, Begoña Martin-Castillo, Tomás Alarcón, José Antonio Encinar, Ángel G. Martin, Javier A. Menendez,

https://doi.org/10.18632/aging.102887 pp 4794—4814

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Cuyàs E, Gumuzio J, Verdura S, Brunet J, Bosch-Barrera J, Martin-Castillo B, Alarcón T, Encinar JA, Martin ÁG, Menendez JA, . The LSD1 inhibitor iadademstat (ORY-1001) targets SOX2-driven breast cancer stem cells: a potential epigenetic therapy in luminal-B and HER2-positive breast cancer subtypes. . 12:4794-4814. https://doi.org/10.18632/aging.102887

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                TY  - JOUR
                AU  - Cuyàs, Elisabet 
                AU  - Gumuzio, Juan 
                AU  - Verdura, Sara 
                AU  - Brunet, Joan 
                AU  - Bosch-Barrera, Joaquim 
                AU  - Martin-Castillo, Begoña 
                AU  - Alarcón, Tomás 
                AU  - Encinar, José Antonio 
                AU  - Martin, Ángel G. 
                AU  - Menendez, Javier A. 
                TI  - The LSD1 inhibitor iadademstat (ORY-1001) targets SOX2-driven breast cancer stem cells: a potential epigenetic therapy in luminal-B and HER2-positive breast cancer subtypes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102887
                DO  - 10.18632/aging.102887
                SP  - 4794
                EP  - 4814
                PY  - 
                AB  - SOX2 is a core pluripotency-associated transcription factor causally related to cancer initiation, aggressiveness, and drug resistance by driving the self-renewal and seeding capacity of cancer stem cells (CSC). Here, we tested the ability of the clinically proven inhibitor of the lysine-specific demethylase 1 (LSD1/KDM1A) iadademstat (ORY-100) to target SOX2-driven CSC in breast cancer. Iadademstat blocked CSC-driven mammosphere formation in breast cancer cell lines that are dependent on SOX2 expression to maintain their CSC phenotype. Iadademstat prevented the activation of an LSD1-targeted stemness-specific SOX2 enhancer in CSC-enriched 3-dimensional spheroids. Using high-throughput transcriptional data available from the METABRIC dataset, high expression of SOX2 was significantly more common in luminal-B and HER2-enriched subtypes according to PAM50 classifier and in IntClust1 (high proliferating luminal-B) and IntClust 5 (luminal-B and HER2-amplified) according to integrative clustering. Iadademstat significantly reduced mammospheres formation by CSC-like cells from a multidrug-resistant luminal-B breast cancer patient-derived xenograft but not of those from a treatment-na&#xEF;ve luminal-A patient. Iadademstat reduced the expression of SOX2 in luminal-B but not in luminal-A mammospheres, likely indicating a selective targeting of SOX2-driven CSC. The therapeutic relevance of targeting SOX2-driven breast CSC suggests the potential clinical use of iadademstat as an epigenetic therapy in luminal-B and HER2-positive subtypes.
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Clinical significance of age at diagnosis among patients with thymic epithelial tumors: a population-based study

Mina Liu, Changlu Wang, Lanting Gao, Changxing Lv, Xiaolong Fu,

https://doi.org/10.18632/aging.102897 pp 4815—4821

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Liu M, Wang C, Gao L, Lv C, Fu X, . Clinical significance of age at diagnosis among patients with thymic epithelial tumors: a population-based study. . 12:4815-4821. https://doi.org/10.18632/aging.102897

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                TY  - JOUR
                AU  - Liu, Mina 
                AU  - Wang, Changlu 
                AU  - Gao, Lanting 
                AU  - Lv, Changxing 
                AU  - Fu, Xiaolong 
                TI  - Clinical significance of age at diagnosis among patients with thymic epithelial tumors: a population-based study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102897
                DO  - 10.18632/aging.102897
                SP  - 4815
                EP  - 4821
                PY  - 
                AB  - Background: To investigate the clinicopathologic characteristics and survival outcomes of patients with thymic epithelial tumors (TET) according to age at diagnosis.Results: A total of 4431 patients were analyzed. Gender, race, tumor histology and surgery were similar between different age groups. The 0-18 group was associated with a higher risk of distant metastasis. Compared to patients aged above 80, the hazard ratios (HR) for patients aged 0-18, 19-30, 31-40, 41-50, 51-60, 61-70, 71-80 were 1.079, 0.739, 0.614, 0.621, 0.633, 0.673, 0.861, respectively. From the subgroup analysis for the adult patients who were above 19 years old, we found that the 19-70 group had significant better cancer specific survival (CSS) and overall survival (OS) than the above 70 group.Conclusions: Age is a strong independent prognostic factor for survival in TET. Pediatric TET has a higher risk of distant metastasis and an inferior CSS. For the adults who were above 19, patients older than 70-year-old were associated with a shorter CSS.Methods: Information of 4431 TET patients was retrieved from the Surveillance, Epidemiology, and End Results (SEER) database. Demographic features, clinicopathologic characteristics and survival outcomes were compared between patients diagnosed at different age groups (0-18, 19-30, 31-40, 41-50, 51-60, 61-70, 71-80, above 80).
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Prediction of cognitive performance in old age from spatial probability maps of white matter lesions

Cui Zhao, Ying Liang, Ting Chen, Yihua Zhong, Xianglong Li, Jing Wei, Chunlin Li, Xu Zhang,

https://doi.org/10.18632/aging.102901 pp 4822—4835

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Zhao C, Liang Y, Chen T, Zhong Y, Li X, Wei J, Li C, Zhang X, . Prediction of cognitive performance in old age from spatial probability maps of white matter lesions. . 12:4822-4835. https://doi.org/10.18632/aging.102901

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                TY  - JOUR
                AU  - Zhao, Cui 
                AU  - Liang, Ying 
                AU  - Chen, Ting 
                AU  - Zhong, Yihua 
                AU  - Li, Xianglong 
                AU  - Wei, Jing 
                AU  - Li, Chunlin 
                AU  - Zhang, Xu 
                TI  - Prediction of cognitive performance in old age from spatial probability maps of white matter lesions
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102901
                DO  - 10.18632/aging.102901
                SP  - 4822
                EP  - 4835
                PY  - 
                AB  - The purposes of this study were to explore the association between cognitive performance and white matter lesions (WMLs), and to investigate whether it is possible to predict cognitive impairment using spatial maps of WMLs. These WML maps were produced for 263 elders from the OASIS-3 dataset, and a relevance vector regression (RVR) model was applied to predict neuropsychological performance based on the maps. The association between the spatial distribution of WMLs and cognitive function was examined using diffusion tensor imaging data. WML burden significantly associated with increasing age (r=0.318, p&lt;0.001) and cognitive decline. Eight of 15 neuropsychological measures could be accurately predicted, and the mini-mental state examination (MMSE) test achieved the highest predictive accuracy (CORR=0.28, p&lt;0.003). WMLs located in bilateral tapetum, posterior corona radiata, and thalamic radiation contributed the most prediction power. Diffusion indexes in these regions associated significantly with cognitive performance (axial diffusivity&gt;radial diffusivity&gt;mean diffusivity&gt;fractional anisotropy). These results show that the combination of the extent and location of WMLs exhibit great potential to serve as a generalizable marker of multidomain neurocognitive decline in the aging population. The results may also shed light on the mechanism underlying white matter changes during the progression of cognitive decline and aging.
                ER  -

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Nrf2 deficiency aggravates PM_2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder

Chenxu Ge, Linfeng Hu, Deshuai Lou, Qiang Li, Jing Feng, Yekuan Wu, Jun Tan, Minxuan Xu,

https://doi.org/10.18632/aging.102906 pp 4836—4865

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Ge C, Hu L, Lou D, Li Q, Feng J, Wu Y, Tan J, Xu M, . Nrf2 deficiency aggravates PM_2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder. . 12:4836-4865. https://doi.org/10.18632/aging.102906

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Provider: 
 TY - JOUR
 AU - Ge, Chenxu 
 AU - Hu, Linfeng 
 AU - Lou, Deshuai 
 AU - Li, Qiang 
 AU - Feng, Jing 
 AU - Wu, Yekuan 
 AU - Tan, Jun 
 AU - Xu, Minxuan 
 TI - Nrf2 deficiency aggravates PM2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder
 JO - 
 JA - 
 VL - 12
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102906
 DO - 10.18632/aging.102906
 SP - 4836
 EP - 4865
 PY - 
 AB - PM2.5 is a well-known air pollutant threatening public health, and long-term exposure to PM2.5 increases the risk of cardiovascular diseases. Nrf2 plays a pivotal role in the amelioration of PM2.5-induced lung injury. However, if Nrf2 is involved in PM2.5-induced heart injury, and the underlying molecular mechanisms have not been explored. In this study, wild type (Nrf2+/+) and Nrf2 knockout (Nrf2-/-) mice were exposed to PM2.5 for 6 months. After PM2.5 exposure, Nrf2-/- mice developed severe physiological changes, lung injury and cardiac dysfunction. In the PM2.5-exposed hearts, Nrf2 deficiency caused significant collagen accumulation through promoting the expression of fibrosis-associated signals. Additionally, Nrf2-/- mice exhibited greater oxidative stress in cardiac tissues after PM2.5 exposure. Furthermore, PM2.5-induced inflammation in heart samples were accelerated in Nrf2-/- mice through promoting inhibitor of &#x3B1;/nuclear factor &#x3BA;B (I&#x3BA;B&#x3B1;/NF-&#x3BA;B) signaling pathways. We also found that Nrf2-/- aggravated autophagy initiation and glucose metabolism disorder in hearts of mice with PM2.5 challenge. Cardiac receptor-interacting protein kinase 3 (RIPK3) expression triggered by PM2.5 was further enhanced in mice with the loss of Nrf2. Collectively, these results suggested that strategies for enhancing Nrf2 could be used to treat PM2.5-induced cardiovascular diseases.
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MiR-519d targets HER3 and can be used as a potential serum biomarker for non-small cell lung cancer

Aili Wang, Hongxia Zhang, Jinxiang Wang, Shuming Zhang, Zhenyang Xu,

https://doi.org/10.18632/aging.102908 pp 4866—4878

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Wang A, Zhang H, Wang J, Zhang S, Xu Z, . MiR-519d targets HER3 and can be used as a potential serum biomarker for non-small cell lung cancer. . 12:4866-4878. https://doi.org/10.18632/aging.102908

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                TY  - JOUR
                AU  - Wang, Aili 
                AU  - Zhang, Hongxia 
                AU  - Wang, Jinxiang 
                AU  - Zhang, Shuming 
                AU  - Xu, Zhenyang 
                TI  - MiR-519d targets HER3 and can be used as a potential serum biomarker for non-small cell lung cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102908
                DO  - 10.18632/aging.102908
                SP  - 4866
                EP  - 4878
                PY  - 
                AB  - Development of specific serum biomarkers is essential to improve diagnosis and prognosis of non-small cell lung cancer (NSCLC). Here, we show that serum and tissue levels of miR-519d are significantly decreased in NSCLC patients. The low expression of miR-519d is associated with lymph node metastases, clinical stage, and a poor prognosis in NSCLC patients. In addition, ROC analysis demonstrated that the serum miR-519d levels can distinguish NSCLC patients from healthy controls. MiR-519d inhibits proliferation, migration, and invasion by lung cancer cells, indicating that it may function as a tumor suppressor in lung cancer. Furthermore, our data demonstrate that HER3 is a target gene of miR-519d in lung cancer cells, and show that by targeting HER3, miR-519d inhibits the PI3K/Akt pathway. These findings demonstrate that the miR-519d levels are decreased in serum and tumor tissues of NSCLC patients, and indicate that miR-519d regulates NSCLC progression by targeting HER3. MiR-519d could potentially serve as a novel serum biomarker for NSCLC.
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A nine-gene signature related to tumor microenvironment predicts overall survival with ovarian cancer

Qi Ding, Shanshan Dong, Ranran Wang, Keqiang Zhang, Hui Wang, Xiao Zhou, Jing Wang, Kee Wong, Ying Long, Shuai Zhu, Weigang Wang, Huayi Ren, Yong Zeng,

https://doi.org/10.18632/aging.102914 pp 4879—4895

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Ding Q, Dong S, Wang R, Zhang K, Wang H, Zhou X, Wang J, Wong K, Long Y, Zhu S, Wang W, Ren H, Zeng Y, . A nine-gene signature related to tumor microenvironment predicts overall survival with ovarian cancer. . 12:4879-4895. https://doi.org/10.18632/aging.102914

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                TY  - JOUR
                AU  - Ding, Qi 
                AU  - Dong, Shanshan 
                AU  - Wang, Ranran 
                AU  - Zhang, Keqiang 
                AU  - Wang, Hui 
                AU  - Zhou, Xiao 
                AU  - Wang, Jing 
                AU  - Wong, Kee 
                AU  - Long, Ying 
                AU  - Zhu, Shuai 
                AU  - Wang, Weigang 
                AU  - Ren, Huayi 
                AU  - Zeng, Yong 
                TI  - A nine-gene signature related to tumor microenvironment predicts overall survival with ovarian cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102914
                DO  - 10.18632/aging.102914
                SP  - 4879
                EP  - 4895
                PY  - 
                AB  - Mounting evidence suggests that immune cell infiltration within the tumor microenvironment (TME) is a crucial regulator of carcinogenesis and therapeutic efficacy in ovarian cancer (OC). In this study, 593 OC patients from TCGA were divided into high and low score groups based on their immune/stromal scores resulting from analysis utilizing the ESTIMATE algorithm. Differential expression analysis revealed 294 intersecting genes that influencing both the immune and stromal scores. Further Cox regression analysis identified 34 differentially expressed genes (DEGs) as prognostic-related genes. Finally, the nine-gene signature was derived from the prognostic-related genes using a Least Absolute Shrinkage and Selection Operator (LASSO) and Cox regression. This nine-gene signature could effectively distinguish the high-risk patients in the training (TCGA database) and validation (GSE17260) cohorts (all p &lt; 0.01). A time-dependent receiver operating characteristic (ROC) analysis showed that the nine-gene signature had a reasonable predictive accuracy (AUC = 0.707, AUC =0.696) in both cohorts. In addition, this nine-gene signature is associated with immune infiltration in TME by Gene Set Variation Analysis (GSVA), and can be used to predict the survival of patients with OC.
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Development and validation of a nomogram for preoperative prediction of cervical lymph node involvement in thyroid microcarcinoma

Si Lu, Rongjie Zhao, Yeqin Ni, Jinwang Ding, Fuqiang Qiu, You Peng, Gang Pan, Fan Wu, Yu Zhang, Jingjing Shi, Tianhan Zhou, Dingcun Luo,

https://doi.org/10.18632/aging.102915 pp 4896—4906

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Lu S, Zhao R, Ni Y, Ding J, Qiu F, Peng Y, Pan G, Wu F, Zhang Y, Shi J, Zhou T, Luo D, . Development and validation of a nomogram for preoperative prediction of cervical lymph node involvement in thyroid microcarcinoma. . 12:4896-4906. https://doi.org/10.18632/aging.102915

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                TY  - JOUR
                AU  - Lu, Si 
                AU  - Zhao, Rongjie 
                AU  - Ni, Yeqin 
                AU  - Ding, Jinwang 
                AU  - Qiu, Fuqiang 
                AU  - Peng, You 
                AU  - Pan, Gang 
                AU  - Wu, Fan 
                AU  - Zhang, Yu 
                AU  - Shi, Jingjing 
                AU  - Zhou, Tianhan 
                AU  - Luo, Dingcun 
                TI  - Development and validation of a nomogram for preoperative prediction of cervical lymph node involvement in thyroid microcarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102915
                DO  - 10.18632/aging.102915
                SP  - 4896
                EP  - 4906
                PY  - 
                AB  - Cervical regional lymph node involvement (CRLNI) is common in papillary thyroid microcarcinoma (PTMC), but the way to deal with cervical lymph node involvement of clinically negative PTMC is controversial. We studied data of patients histologically confirmed PTMC in the Surveillance, Epidemiology, and End Results (SEER) Program and Department of Surgical Oncology in Hangzhou First People&#x2019;s Hospital (China). We screened 6 variables of demographic and clinicopathological characteristics as potential predictors and further constructed a lymph node involvement model based on the independent predictors including age, race, sex, extension, multifocality and tumor size. The model was validated by both the internal and the external testing sets, and the visual expression of the model was displayed by a nomogram. As a result, the C-index of this predictive model in the training set was 0.766, and the internal and external testing sets through cross-validation were 0.753 and 0.668, respectively. The area under the receiver operating characteristic curve (AUC) was 0.766 for the training set. We also performed a Decision Curve Analysis (DCA), which showed that predicting the cervical lymph node involvement risk applying this nomogram would be better than having all patients or none patients use this nomogram.
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The neurocognitive and BDNF changes of multicomponent exercise for community-dwelling older adults with mild cognitive impairment or dementia: a systematic review and meta-analysis

Xinyi Wang, Haiyun Wang, Zhenghui Ye, Guofei Ding, Fengli Li, Ji Ma, Wei Hua,

https://doi.org/10.18632/aging.102918 pp 4907—4917

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Wang X, Wang H, Ye Z, Ding G, Li F, Ma J, Hua W, . The neurocognitive and BDNF changes of multicomponent exercise for community-dwelling older adults with mild cognitive impairment or dementia: a systematic review and meta-analysis. . 12:4907-4917. https://doi.org/10.18632/aging.102918

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                TY  - JOUR
                AU  - Wang, Xinyi 
                AU  - Wang, Haiyun 
                AU  - Ye, Zhenghui 
                AU  - Ding, Guofei 
                AU  - Li, Fengli 
                AU  - Ma, Ji 
                AU  - Hua, Wei 
                TI  - The neurocognitive and BDNF changes of multicomponent exercise for community-dwelling older adults with mild cognitive impairment or dementia: a systematic review and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102918
                DO  - 10.18632/aging.102918
                SP  - 4907
                EP  - 4917
                PY  - 
                AB  - Our goal was to examine whether multicomponent exercise performed by older adults with mild cognitive impairment or dementia as group-based exercise in community have beneficial effects on cognition and brain-derived neurotrophic factor. Eight studies were identified through Emabase, Medline, PubMed. Searches combined terms for neurocognitive and biochemical changes with those for MCI and dementia. Data were extracted and checked by a second reviewer, systematically reviewed, and meta analyzed where appropriate. There was significant difference in favor of multicomponent exercise in cognition (WMD:0.18; 95%CI:0.02-0.34), attention (SMD=2.16; 95%CI:1.2to3.12) and executive function (SMD =0.80; 95%CI: 0.28to1.31), but not in memory. However, there was limited reporting of the effects of multicomponent exercise on depression and brain-derived neurotrophic factor for this group of people. In conclusion, this meta-analysis indicated that group exercises improve cognition, attention and executive function in community-dwelling older adults with mild cognitive impairment or Alzheimer&apos;s disease.
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Efficacy and safety of recombinant human follicle-stimulating hormone in patients undergoing in vitro fertilization-embryo transfer

Linli Hu, Songying Zhang, Song Quan, Jieqiang Lv, Weiping Qian, Yuanhua Huang, Weiying Lu, Yingpu Sun,

https://doi.org/10.18632/aging.102919 pp 4918—4930

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Hu L, Zhang S, Quan S, Lv J, Qian W, Huang Y, Lu W, Sun Y, . Efficacy and safety of recombinant human follicle-stimulating hormone in patients undergoing in vitro fertilization-embryo transfer. . 12:4918-4930. https://doi.org/10.18632/aging.102919

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Provider: 
 TY - JOUR
 AU - Hu, Linli 
 AU - Zhang, Songying 
 AU - Quan, Song 
 AU - Lv, Jieqiang 
 AU - Qian, Weiping 
 AU - Huang, Yuanhua 
 AU - Lu, Weiying 
 AU - Sun, Yingpu 
 TI - Efficacy and safety of recombinant human follicle-stimulating hormone in patients undergoing in vitro fertilization-embryo transfer
 JO - 
 JA - 
 VL - 12
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102919
 DO - 10.18632/aging.102919
 SP - 4918
 EP - 4930
 PY - 
 AB - To compare the ovarian responses after administration of two recombinant follicle-stimulating hormone (r-FSH) preparations under gonadotropin-releasing hormone (GnRH) analogue downregulation, we conducted a phase 3, randomized, multicenter, assessor-blind, active-controlled, parallel group study. The primary outcome was the number of oocytes retrieved. The secondary outcomes included total dose and duration of r-FSH administered, oocyte quality, blood estradiol levels, follicular development, fertilization rates, implantation rates, and pregnancy rates (biochemical, clinical, and ongoing). A total of 451 patients with infertility were randomized to receive either Follitrope&#x2122; Prefilled Syringe or Gonal-F&#xAE; Pen for ovarian stimulation. The mean number of oocytes retrieved was 14.9 in the FollitropeTM Prefilled Syringe group, and 12.8 in the Gonal-F&#xAE; Pen group. The 95% confidence interval in the oocyte number difference between the groups was [&#x2013;0.1, 4.2], demonstrating that FollitropeTM Prefilled Syringe was not inferior to Gonal-F&#xAE; Pen. The clinical pregnancy rates (FollitropeTM Prefilled Syringe vs. Gonal-F&#xAE; Pen: 55.4% vs. 51.9%) and ongoing pregnancy rates (44.1% vs. 43.0%) were similar between the groups. No clinically significant adverse events were observed in either group. In summary, our study indicates that FollitropeTM Prefilled Syringe is safe and efficacious for ovarian stimulation.
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Optimal cumulative cisplatin dose in nasopharyngeal carcinoma patients based on plasma Epstein–Barr virus DNA level after induction chemotherapy

Sai-Lan Liu, Xue-Song Sun, Li-Ting Liu, Rui Sun, Dong-Hua Luo, Qiu-Yan Chen, Huan-Xin Lin, Li Yuan, Lin-Quan Tang, Ling Guo, Hai-Qiang Mai,

https://doi.org/10.18632/aging.102920 pp 4931—4944

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Liu S, Sun X, Liu L, Sun R, Luo D, Chen Q, Lin H, Yuan L, Tang L, Guo L, Mai H, . Optimal cumulative cisplatin dose in nasopharyngeal carcinoma patients based on plasma Epstein–Barr virus DNA level after induction chemotherapy. . 12:4931-4944. https://doi.org/10.18632/aging.102920

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                TY  - JOUR
                AU  - Liu, Sai-Lan 
                AU  - Sun, Xue-Song 
                AU  - Liu, Li-Ting 
                AU  - Sun, Rui 
                AU  - Luo, Dong-Hua 
                AU  - Chen, Qiu-Yan 
                AU  - Lin, Huan-Xin 
                AU  - Yuan, Li 
                AU  - Tang, Lin-Quan 
                AU  - Guo, Ling 
                AU  - Mai, Hai-Qiang 
                TI  - Optimal cumulative cisplatin dose in nasopharyngeal carcinoma patients based on plasma Epstein–Barr virus DNA level after induction chemotherapy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102920
                DO  - 10.18632/aging.102920
                SP  - 4931
                EP  - 4944
                PY  - 
                AB  - Purpose: This study aimed to elucidate the optimal cumulative cisplatin dose (CCD) for concurrent chemoradiotherapy (CCRT) according to the post-induction chemotherapy (IC) plasma Epstein&#x2013;Barr virus (EBV) DNA level.Results: EBV DNA was detected and undetected in 179 and 370 patients, respectively. Of the entire cohort, 73/549 (13.3%) patients received a total CCD &#x2265; 160 mg/m2 and 476/549 (86.7%) patients, &lt;160 mg/m2. CCD enhancement was not associated with a survival benefit in patients with undetected EBV DNA after IC. However, among patients with post-IC detectable EBV DNA, higher 3-year PFS and locoregional relapse-free survival (LRFS) rates were observed in those who received a CCD &#x2265; 160 mg/m2. Multivariate analysis also showed CCD was an independent prognostic factor for PFS and LRFS in patients with post-IC detectable EBV DNA.Conclusions: CCD enhancement was not associated with a survival benefit in patients with undetected EBV DNA after IC. However, among patients with post-IC detectable EBV DNA, those receiving &#x2265;160 mg/m2 CCD showed significantly improved 3-year PFS and LRFS.Methods: NPC patients (549) treated with IC and CCRT were included. Prognosis was assessed using a multivariate Cox proportional hazards model. Furthermore, grade 1&#x2013;4 toxicities were compared between different CCD groups.
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Fasting blood glucose and cerebrospinal fluid Alzheimer’s biomarkers in non-diabetic cognitively normal elders: the CABLE study

Ya-Nan Ou, Xue-Ning Shen, He-Ying Hu, Hao Hu, Zuo-Teng Wang, Wei Xu, Qiang Dong, Lan Tan, Jin-Tai Yu,

https://doi.org/10.18632/aging.102921 pp 4945—4952

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Ou Y, Shen X, Hu H, Hu H, Wang Z, Xu W, Dong Q, Tan L, Yu J, . Fasting blood glucose and cerebrospinal fluid Alzheimer’s biomarkers in non-diabetic cognitively normal elders: the CABLE study. . 12:4945-4952. https://doi.org/10.18632/aging.102921

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                TY  - JOUR
                AU  - Ou, Ya-Nan 
                AU  - Shen, Xue-Ning 
                AU  - Hu, He-Ying 
                AU  - Hu, Hao 
                AU  - Wang, Zuo-Teng 
                AU  - Xu, Wei 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - Yu, Jin-Tai 
                TI  - Fasting blood glucose and cerebrospinal fluid Alzheimer’s biomarkers in non-diabetic cognitively normal elders: the CABLE study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102921
                DO  - 10.18632/aging.102921
                SP  - 4945
                EP  - 4952
                PY  - 
                AB  - It is unclear how blood glucose levels mediate the pathology of Alzheimer&apos;s disease (AD). This study aimed to investigate whether fasting blood glucose (FBG) levels are associated with cerebrospinal fluid (CSF) biomarkers preferentially affected by AD in non-diabetic cognitively normal elders. A total of 499 non-diabetic cognitively normal elders were from the Chinese Alzheimer&#x2019;s Biomarker and LifestyLE (CABLE) study. We detected the associations of FBG with individual CSF measures using multiple linear regression models controlling for age, sex, educational level, and apolipoprotein E (APOE) &#x3B5;4 genotype. Fasting blood glucose level was positively correlated with CSF A&#x3B2;42 level (&#x3B2; = 0.045, p = 0.010), CSF A&#x3B2;42/A&#x3B2;40 ratio (&#x3B2; = 0.005, p &lt; 0.001), A&#x3B2;42/P-tau ratio (&#x3B2; = 0.282, p = 0.013), and A&#x3B2;42/T-tau ratio (&#x3B2; = 0.050, p = 0.040). Interaction analysis indicated that gender affected the correlations of FBG level with CSF A&#x3B2;40 (p &lt; 0.001) and A&#x3B2;42/A&#x3B2;40 ratio (p &lt; 0.001). This study raises additional questions about the role of blood glucose in the predisposition to AD and supports the possibility of targeting these processes in pre-symptomatic AD trials in non-diabetic elders.
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RNA sequencing analysis of monocrotaline-induced PAH reveals dysregulated chemokine and neuroactive ligand receptor pathways

Genfa Xiao, Tingjun Wang, Wei Zhuang, Chaoyi Ye, Li Luo, Huajun Wang, Guili Lian, Liangdi Xie,

https://doi.org/10.18632/aging.102922 pp 4953—4969

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Xiao G, Wang T, Zhuang W, Ye C, Luo L, Wang H, Lian G, Xie L, . RNA sequencing analysis of monocrotaline-induced PAH reveals dysregulated chemokine and neuroactive ligand receptor pathways. . 12:4953-4969. https://doi.org/10.18632/aging.102922

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                TY  - JOUR
                AU  - Xiao, Genfa 
                AU  - Wang, Tingjun 
                AU  - Zhuang, Wei 
                AU  - Ye, Chaoyi 
                AU  - Luo, Li 
                AU  - Wang, Huajun 
                AU  - Lian, Guili 
                AU  - Xie, Liangdi 
                TI  - RNA sequencing analysis of monocrotaline-induced PAH reveals dysregulated chemokine and neuroactive ligand receptor pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102922
                DO  - 10.18632/aging.102922
                SP  - 4953
                EP  - 4969
                PY  - 
                AB  - Pulmonary arterial hypertension (PAH) is a serious disease characterized by elevated pulmonary artery pressure, inflammatory cell infiltration and pulmonary vascular remodeling. However, little is known about the pathogenic mechanisms underlying the disease onset and progression. RNA sequencing (RNA-seq) was used to identify the transcriptional profiling in control and rats injected with monocrotaline (MCT) for 1, 2, 3 and 4 weeks. A total of 23200 transcripts and 280, 1342, 908 and 3155 differentially expressed genes (DEGs) were identified at the end of week 1, 2, 3 and 4, of which Svop was the common top 10 DEGs over the course of PAH progression. Functional enrichment analysis of DEGs showed inflammatory/immune response occurred in the early stage of PAH development. KEGG pathway enrichment analysis of DEGs showed that cytokine-cytokine receptor interaction and neuroactive ligand-receptor interaction were in the initiation and progression of PAH. Further analysis revealed impaired expression of cholinergic receptors, adrenergic receptors including alpha1, beta1 and beta2 receptor, and dysregulated expression of &#x3B3;-aminobutyric acid receptors. In summary, the dysregulated inflammation/immunity and neuroactive ligand receptor signaling pathways may be involved in the onset and progression of PAH.
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Integrative analysis of DNA methylation and gene expression reveals distinct hepatocellular carcinoma subtypes with therapeutic implications

Xiaowen Huang, Chen Yang, Jilin Wang, Tiantian Sun, Hua Xiong,

https://doi.org/10.18632/aging.102923 pp 4970—4995

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Huang X, Yang C, Wang J, Sun T, Xiong H, . Integrative analysis of DNA methylation and gene expression reveals distinct hepatocellular carcinoma subtypes with therapeutic implications. . 12:4970-4995. https://doi.org/10.18632/aging.102923

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                TY  - JOUR
                AU  - Huang, Xiaowen 
                AU  - Yang, Chen 
                AU  - Wang, Jilin 
                AU  - Sun, Tiantian 
                AU  - Xiong, Hua 
                TI  - Integrative analysis of DNA methylation and gene expression reveals distinct hepatocellular carcinoma subtypes with therapeutic implications
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102923
                DO  - 10.18632/aging.102923
                SP  - 4970
                EP  - 4995
                PY  - 
                AB  - We aimed to develop an HCC classification model based on the integrated gene expression and methylation data of methylation-driven genes. Genome, methylome, transcriptome, proteomics and clinical data of 369 HCC patients from The Cancer Genome Atlas Network were retrieved and analyzed. Consensus clustering of the integrated gene expression and methylation data from methylation-driven genes identified 4 HCC subclasses with significant prognosis difference. HS1 was well differentiated with a favorable prognosis. HS2 had high serum &#x3B1;-fetoprotein level that was correlated with its poor outcome. High percentage of CTNNB1 mutations corresponded with its activation in WNT signaling pathway. HS3 was well differentiated with low serum &#x3B1;-fetoprotein level and enriched in metabolism signatures, but was barely involved in immune signatures. HS3 also had high percentage of CTNNB1 mutations and therefore enriched in WNT activation signature. HS4 was poorly differentiated with the worst prognosis and enriched in immune-related signatures, but was barely involved in metabolism signatures. Subsequently, a prediction model was developed. The prediction model had high sensitivity and specificity in distributing potential HCC samples into groups identical with the training cohort. In conclusion, this work sheds light on HCC patient prognostication and prediction of response to targeted therapy.
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Identification of survival-associated alternative splicing events and signatures in adrenocortical carcinoma based on TCGA SpliceSeq data

Ning Xu, Zhi-Bin Ke, Xiao-Dan Lin, Fei Lin, Shao-Hao Chen, Yu-Peng Wu, Ye-Hui Chen, Yong Wei, Qing-Shui Zheng,

https://doi.org/10.18632/aging.102924 pp 4996—5009

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Xu N, Ke Z, Lin X, Lin F, Chen S, Wu Y, Chen Y, Wei Y, Zheng Q, . Identification of survival-associated alternative splicing events and signatures in adrenocortical carcinoma based on TCGA SpliceSeq data. . 12:4996-5009. https://doi.org/10.18632/aging.102924

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                TY  - JOUR
                AU  - Xu, Ning 
                AU  - Ke, Zhi-Bin 
                AU  - Lin, Xiao-Dan 
                AU  - Lin, Fei 
                AU  - Chen, Shao-Hao 
                AU  - Wu, Yu-Peng 
                AU  - Chen, Ye-Hui 
                AU  - Wei, Yong 
                AU  - Zheng, Qing-Shui 
                TI  - Identification of survival-associated alternative splicing events and signatures in adrenocortical carcinoma based on TCGA SpliceSeq data
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102924
                DO  - 10.18632/aging.102924
                SP  - 4996
                EP  - 5009
                PY  - 
                AB  - Objective: To explore the correlations among alternative splicing (AS), splicing factors (SF) and survival outcome in adrenocortical carcinoma (ACC) patients.Results: A total of 92 ACC patients were included. Univariate analysis identified 3919 AS events significantly associated with overall survival. Lasso method followed by multivariate analysis revealed that the prognostic capacity of these survival-related AS events is satisfactory. Interestingly, we found that the area under the curve (AUC) of AA, AD, AP and RI were more than 0.9, indicating that these four types of AS were of great significance. Independent prognostic analysis showed that only the risk score was the independent risk factor of ACC survival. Finally, we constructed an interesting interaction network between AS and SF.Conclusions: This is the first and most comprehensive study to explore the aberrant AS variants in ACC, which might provide novel insights into molecular mechanism of ACC.Methods: The transcriptome data, clinical information and Percent Spliced In (PSI) values of the ACC were obtained from TCGA database and TCGA SpliceSeq data portal. Lasso method and uni/multivariate Cox regression analysis were used to identify survival-related AS events and develop multi-AS-based signatures. The relationship between AS events and SFs was also investigated.
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Development of an immune-related prognostic index associated with hepatocellular carcinoma

Bo Hu, Xiao-Bo Yang, Xin-Ting Sang,

https://doi.org/10.18632/aging.102926 pp 5010—5030

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Hu B, Yang X, Sang X, . Development of an immune-related prognostic index associated with hepatocellular carcinoma. . 12:5010-5030. https://doi.org/10.18632/aging.102926

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                TY  - JOUR
                AU  - Hu, Bo 
                AU  - Yang, Xiao-Bo 
                AU  - Sang, Xin-Ting 
                TI  - Development of an immune-related prognostic index associated with hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102926
                DO  - 10.18632/aging.102926
                SP  - 5010
                EP  - 5030
                PY  - 
                AB  - Liver hepatocellular carcinoma (LIHC), an inflammation-associated cancer induced by a variety of etiological factors, is still one of the most prevalent and lethal cancers in human population. In this study, the expression profiles of immune-related genes (IRGs) were integrated with the overall survival (OS) of 378 LIHC patients based on the Cancer Genome Atlas (TCGA) dataset. Moreover, the differentially expressed and survival related IRGs among LIHC patients were predicted through the computational difference algorithm and COX regression analysis. As a result, 7 genes, including HSPA4, S100A10, FABP6, CACYBP, HDAC1, FCGR2B and SHC1, were retrieved to construct a predictive model associated with the overall survival (OS) of LIHC patients. Typically, the as-constructed model performed moderately in predicting prognosis, which was also correlated with tumor grade. Functional enrichment analysis revealed that the genes of high-risk group were actively involved in mRNA binding and the spliceosome pathway. Intriguingly, the prognostic index established based on IRGs reflected infiltration by multiple types of immunocytes. Our findings screen several IRGs with clinical significance, reveal the drivers of immune repertoire, and illustrate the importance of a personalized, IRG-based immune signature in LIHC recognition, surveillance, and prognosis prediction.
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Expression and prognosis analysis of TET family in acute myeloid leukemia

Tingjuan Zhang, Yangli Zhao, Yangjing Zhao, Jingdong Zhou,

https://doi.org/10.18632/aging.102928 pp 5031—5047

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Zhang T, Zhao Y, Zhao Y, Zhou J, . Expression and prognosis analysis of TET family in acute myeloid leukemia. . 12:5031-5047. https://doi.org/10.18632/aging.102928

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Provider: 
 TY - JOUR
 AU - Zhang, Tingjuan 
 AU - Zhao, Yangli 
 AU - Zhao, Yangjing 
 AU - Zhou, Jingdong 
 TI - Expression and prognosis analysis of TET family in acute myeloid leukemia
 JO - 
 JA - 
 VL - 12
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102928
 DO - 10.18632/aging.102928
 SP - 5031
 EP - 5047
 PY - 
 AB - TET family members (TETs) encode proteins that represent crucial factors in the active DNA demethylation pathway. Evidence has proved that TET2 mutation is associated with leukemogenesis, drug response, and prognosis in acute myeloid leukemia (AML). However, few studies revealed the TETs expression and its clinical significance in AML. We conducted a detailed expression and prognosis analysis of TETs expression in human AML cell lines and patients by using public databases. We observed that TETs expression especially TET2 and TET3 was closely associated with AML among various human cancers. TET1 expression was significantly reduced in AML patients, whereas TET2 and TET3 expression was significantly increased. Kaplan-Meier analysis showed that only TET3 expression was associated with overall survival (OS) and disease-free survival (DFS) among both total AML as well as non-M3 AML, and was confirmed by another independent cohort. Moreover, Cox regression analysis revealed that TET3 expression may act as an independent prognostic factor for OS and DFS in total AML. Interestingly, patients that received hematopoietic stem cell transplantation (HSCT) did not show significantly longer OS and DFS than those who did not receive HSCT in TET3 high-expressed groups; whereas, in TET3 low-expressed groups, patients that accepted HSCT showed significantly longer OS and DFS than those who did not accept HSCT. By bioinformatics analysis, TET3 expression was found positively correlated with tumor suppressor gene including CDKN2B, ZIC2, miR-196a, and negatively correlated with oncogenes such as PAX2 and IL2RA. Our study demonstrated that TETs showed significant expression differences in AML, and TET3 expression acted as a potential prognostic biomarker in AML, which may guide treatment choice between chemotherapy and HSCT.
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Using ESTIMATE algorithm to establish an 8-mRNA signature prognosis prediction system and identify immunocyte infiltration-related genes in Pancreatic adenocarcinoma

Zibo Meng, Dianyun Ren, Kun Zhang, Jingyuan Zhao, Xin Jin, Heshui Wu,

https://doi.org/10.18632/aging.102931 pp 5048—5070

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Meng Z, Ren D, Zhang K, Zhao J, Jin X, Wu H, . Using ESTIMATE algorithm to establish an 8-mRNA signature prognosis prediction system and identify immunocyte infiltration-related genes in Pancreatic adenocarcinoma. . 12:5048-5070. https://doi.org/10.18632/aging.102931

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                TY  - JOUR
                AU  - Meng, Zibo 
                AU  - Ren, Dianyun 
                AU  - Zhang, Kun 
                AU  - Zhao, Jingyuan 
                AU  - Jin, Xin 
                AU  - Wu, Heshui 
                TI  - Using ESTIMATE algorithm to establish an 8-mRNA signature prognosis prediction system and identify immunocyte infiltration-related genes in Pancreatic adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102931
                DO  - 10.18632/aging.102931
                SP  - 5048
                EP  - 5070
                PY  - 
                AB  - Objective: The tumour microenvironment is one of the significant factors driving the carcinogenesis of Pancreatic adenocarcinoma (PAAD). However, the underlying mechanism of how the tumour microenvironment impacts the prognosis of PAAD is not completely clear.Results: The transcriptome and clinical data of 182 PAAD program cases were downloaded from the TCGA database. Three hundred thirty-three differentially expressed genes (DEGs) between high and low stromal groups and 314 DEGs between high and low immune score groups were identified using ESTIMATE score. Based on the 203 genes differentially expressed simultaneously in two score-related comparisons, we established an 8-mRNA signature to evaluate the prognosis of PAAD patients. Kaplan-Meier curves showed significantly worse survival for patients with high-risk scores in both the training and validation groups. The risk score was an independent prognostic factor and had a high predictive value for the prognosis of patients with PAAD. By searching the TCGA database, we showed that CA9, CXCL9, and GIMAP7 from the 8-mRNA signature were associated with the infiltration levels of immunocytes by regulating FOXO1 expression in PAAD.Conclusions: Unlike traditional methods of screening for differential genes in cancer and healthy tissues, we constructed a novel 8-mRNA signature to predict the prognosis of PAAD patients by applying ESTIMATE scoring to RNA-seq-based transcriptome data. Most importantly, we identified CA9, CXCL9, and GIMAP7 from the above eight genes as regulators of immunocyte infiltration by adjusting the expression of FOXO1 in PAAD. Thus, CA9, CXCL9, and GIMAP7 might be the ideal targets of immune therapy of PAAD.Methods: ESTIMATE scoring was used to determine the stromal and immune scores of transcriptome datasets downloaded from the TCGA database. An mRNA-based prognostic signature was built for the training cohort via the LASSO Cox regression model. The signature was verified using a validation cohort. Kaplan-Meier curves and log-rank analysis were used to identify survival differences. Western blot analysis and RT-qPCR analysis were carried out to analyze the expression of specific proteins and mRNAs. IHC was performed to assess the protein levels of Forkhead box-O 1 (FOXO1), Carbonic anhydrase 9 (CA9), C-X-C motif chemokine ligand 9 (CXCL9), and GTPase, IMAP family member 7 (GIMAP7) in the tissue microarray of PAAD.
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Comprehensive analysis of circular RNA profiles in skeletal muscles of aging mice and after aerobic exercise intervention

Mingwei Guo, Jin Qiu, Fei Shen, Sainan Wang, Jian Yu, Hui Zuo, Jing Yao, Sainan Xu, Tianhui Hu, Dongmei Wang, Yu Zhao, Yepeng Hu, Feixia Shen, Xinran Ma, Jian Lu, Xuejiang Gu, Lingyan Xu,

https://doi.org/10.18632/aging.102932 pp 5071—5090

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Guo M, Qiu J, Shen F, Wang S, Yu J, Zuo H, Yao J, Xu S, Hu T, Wang D, Zhao Y, Hu Y, Shen F, et al, . Comprehensive analysis of circular RNA profiles in skeletal muscles of aging mice and after aerobic exercise intervention. . 12:5071-5090. https://doi.org/10.18632/aging.102932

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                TY  - JOUR
                AU  - Guo, Mingwei 
                AU  - Qiu, Jin 
                AU  - Shen, Fei 
                AU  - Wang, Sainan 
                AU  - Yu, Jian 
                AU  - Zuo, Hui 
                AU  - Yao, Jing 
                AU  - Xu, Sainan 
                AU  - Hu, Tianhui 
                AU  - Wang, Dongmei 
                AU  - Zhao, Yu 
                AU  - Hu, Yepeng 
                AU  - Shen, Feixia 
                AU  - Ma, Xinran 
                AU  - Lu, Jian 
                AU  - Gu, Xuejiang 
                AU  - Xu, Lingyan 
                TI  - Comprehensive analysis of circular RNA profiles in skeletal muscles of aging mice and after aerobic exercise intervention
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102932
                DO  - 10.18632/aging.102932
                SP  - 5071
                EP  - 5090
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Guo, Mingwei 
                AU  - Qiu, Jin 
                AU  - Shen, Fei 
                AU  - Wang, Sainan 
                AU  - Yu, Jian 
                AU  - Zuo, Hui 
                AU  - Yao, Jing 
                AU  - Xu, Sainan 
                AU  - Hu, Tianhui 
                AU  - Wang, Dongmei 
                AU  - Zhao, Yu 
                AU  - Hu, Yepeng 
                AU  - Shen, Feixia 
                AU  - Ma, Xinran 
                AU  - Lu, Jian 
                AU  - Gu, Xuejiang 
                AU  - Xu, Lingyan 
                TI  - Comprehensive analysis of circular RNA profiles in skeletal muscles of aging mice and after aerobic exercise intervention
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102932
                DO  - 10.18632/aging.102932
                SP  - 5071
                EP  - 5090
                PY  - 
                AB  - Aging induces gradual accumulation of damages in cells and tissues, which leads to physiological dysfunctions. Aging-associated muscle dysfunction is commonly seen in aged population and severely affects their physical activity and life quality, against which aerobic training has been shown to exert antagonizing or alleviating effects. Circular RNAs (circRNAs) play important roles in various physiological processes, yet their involvement in aging-associated muscle dysfunction is not well understood. In this study, we performed comprehensive analysis of circRNAs profiles in quadriceps muscles in sedentary young and aging mice, as well as aging mice with aerobic exercise using RNA sequencing. Our results identified circRNAs altered by factors of aging and aerobic exercise. Their host genes were then predicted and analyzed by gene ontology enrichment analysis. Importantly, we found that circBBS9 featured decreased levels in aging compared to young mice and elevated expression in exercise versus sedentary aging mice. Besides, we performed GO and KEGG analysis on circBBS9 target genes, as well as established the circBBS9-miRNA-mRNAs interaction network. Our results indicate that circBBS9 may play active roles in muscle aging by mediating the benefits of aerobic training intervention, thus may serve as a novel therapeutic target combating aging-associated muscle dysfunction.
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Time-dependent interactions of blood platelets and cancer cells, accompanied by extramedullary hematopoiesis, lead to increased platelet activation and reactivity in a mouse orthotopic model of breast cancer – implications for pulmonary and liver metastasis

Hassan Kassassir, Kamil Karolczak, Karolina M. Siewiera, Dagmara W. Wojkowska, Marcin Braun, Cezary W. Watala,

https://doi.org/10.18632/aging.102933 pp 5091—5120

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Kassassir H, Karolczak K, Siewiera KM, Wojkowska DW, Braun M, Watala CW, . Time-dependent interactions of blood platelets and cancer cells, accompanied by extramedullary hematopoiesis, lead to increased platelet activation and reactivity in a mouse orthotopic model of breast cancer – implications for pulmonary and liver metastasis. . 12:5091-5120. https://doi.org/10.18632/aging.102933

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                TY  - JOUR
                AU  - Kassassir, Hassan 
                AU  - Karolczak, Kamil 
                AU  - Siewiera, Karolina M. 
                AU  - Wojkowska, Dagmara W. 
                AU  - Braun, Marcin 
                AU  - Watala, Cezary W. 
                TI  - Time-dependent interactions of blood platelets and cancer cells, accompanied by extramedullary hematopoiesis, lead to increased platelet activation and reactivity in a mouse orthotopic model of breast cancer – implications for pulmonary and liver metastasis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102933
                DO  - 10.18632/aging.102933
                SP  - 5091
                EP  - 5120
                PY  - 
                AB  - Aging has become a significant risk factor for several diseases, including breast cancer.Platelet activation and platelet-cancer cell aggregate fractions were found to increase with tumor progression in a mouse model of breast cancer. At advanced stages of tumor development, platelets from mice with breast cancer were hyperreactive to low agonist concentrations and hyporeactive to high ones. Platelet activation and reactivity were strongly associated with breast cancer metastasis in the lungs and extramedullary hematopoiesis in the liver. A greater fraction of platelet aggregates was observed in 4T1-injected mice at the advanced stages of breast cancer. In vitro, platelet activation was elevated after incubation with 4T1 cells, and thrombin-stimulated platelets formed aggregates with 4T1 cells. Neither GPIb&#x3B1;, nor GPIIb/IIIa blocking antibodies, were able to affect platelet-cancer cell aggregation in vitro.The primed circulating platelets became more sensitive to subthreshold stimuli at advanced stages of tumor development, and the formation of platelet-cancer cell aggregates increased with cancer progression. Our findings demonstrate that the age-associated progression of breast cancer cells is connected with increased platelet functioning, and that it can be manifested by the increased number of metastases and extramedullary hematopoiesis in a time-dependent-manner.
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EMMPRIN/CD147 plays a detrimental role in clinical and experimental ischemic stroke

Anthony Patrizz, Sarah J. Doran, Anjali Chauhan, Hilda Ahnstedt, Meaghan Roy-O’Reilly, Yun-Ju Lai, Gillian Weston, Sami Tarabishy, Anita R. Patel, Rajkumar Verma, Ilene Staff, Julia K. Kofler, Jun Li, Fudong Liu, Rodney M. Ritzel, Louise D. McCullough,

https://doi.org/10.18632/aging.102935 pp 5121—5139

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Patrizz A, Doran SJ, Chauhan A, Ahnstedt H, Roy-O’Reilly M, Lai Y, Weston G, Tarabishy S, Patel AR, Verma R, Staff I, Kofler JK, Li J, et al, . EMMPRIN/CD147 plays a detrimental role in clinical and experimental ischemic stroke. . 12:5121-5139. https://doi.org/10.18632/aging.102935

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                TY  - JOUR
                AU  - Patrizz, Anthony 
                AU  - Doran, Sarah J. 
                AU  - Chauhan, Anjali 
                AU  - Ahnstedt, Hilda 
                AU  - Roy-O’Reilly, Meaghan 
                AU  - Lai, Yun-Ju 
                AU  - Weston, Gillian 
                AU  - Tarabishy, Sami 
                AU  - Patel, Anita R. 
                AU  - Verma, Rajkumar 
                AU  - Staff, Ilene 
                AU  - Kofler, Julia K. 
                AU  - Li, Jun 
                AU  - Liu, Fudong 
                AU  - Ritzel, Rodney M. 
                AU  - McCullough, Louise D. 
                TI  - EMMPRIN/CD147 plays a detrimental role in clinical and experimental ischemic stroke
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102935
                DO  - 10.18632/aging.102935
                SP  - 5121
                EP  - 5139
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Patrizz, Anthony 
                AU  - Doran, Sarah J. 
                AU  - Chauhan, Anjali 
                AU  - Ahnstedt, Hilda 
                AU  - Roy-O’Reilly, Meaghan 
                AU  - Lai, Yun-Ju 
                AU  - Weston, Gillian 
                AU  - Tarabishy, Sami 
                AU  - Patel, Anita R. 
                AU  - Verma, Rajkumar 
                AU  - Staff, Ilene 
                AU  - Kofler, Julia K. 
                AU  - Li, Jun 
                AU  - Liu, Fudong 
                AU  - Ritzel, Rodney M. 
                AU  - McCullough, Louise D. 
                TI  - EMMPRIN/CD147 plays a detrimental role in clinical and experimental ischemic stroke
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102935
                DO  - 10.18632/aging.102935
                SP  - 5121
                EP  - 5139
                PY  - 
                AB  - Background: Ischemic stroke is a devastating disease, often resulting in death or permanent neurological deficits. EMMPRIN/CD147 is a plasma membrane protein that induces the production of matrix metalloproteinases (MMPs), which contribute to secondary damage after stroke by disrupting the blood brain barrier (BBB) and facilitating peripheral leukocyte infiltration into the brain.Results: CD147 surface expression increased significantly after stroke on infiltrating leukocytes, astrocytes and endothelial cells, but not on resident microglia. Inhibition of CD147 reduced MMP levels, decreased ischemic damage, and improved functional, cognitive and histological outcomes after experimental ischemic stroke in both young and aged mice. In stroke patients, high levels of serum CD147 24 hours after stroke predicted poor functional outcome at 12 months. Brain CD147 levels were correlated with MMP-9 and secondary hemorrhage in post-mortem samples from stroke patients.Conclusions: Acute inhibition of CD147 decreases levels of MMP-9, limits tissue loss, and improves long-term cognitive outcomes following experimental stroke in aged mice. High serum CD147 correlates with poor outcomes in stroke patients. This study identifies CD147 as a novel, clinically relevant target in ischemic stroke.
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Association between serum angiopoietin-2 concentrations and periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention

Wen Jian, Jia-Hui Guan, Wen-Bo Zheng, Chang-Hua Mo, Yu-Tao Xu, Qi-Li Huang, Chun-Mei Wei, Can Wang, Zhi-Jie Yang, Guo-Liang Yang, Chun Gui,

https://doi.org/10.18632/aging.102936 pp 5140—5151

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Jian W, Guan J, Zheng W, Mo C, Xu Y, Huang Q, Wei C, Wang C, Yang Z, Yang G, Gui C, . Association between serum angiopoietin-2 concentrations and periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention. . 12:5140-5151. https://doi.org/10.18632/aging.102936

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                TY  - JOUR
                AU  - Jian, Wen 
                AU  - Guan, Jia-Hui 
                AU  - Zheng, Wen-Bo 
                AU  - Mo, Chang-Hua 
                AU  - Xu, Yu-Tao 
                AU  - Huang, Qi-Li 
                AU  - Wei, Chun-Mei 
                AU  - Wang, Can 
                AU  - Yang, Zhi-Jie 
                AU  - Yang, Guo-Liang 
                AU  - Gui, Chun 
                TI  - Association between serum angiopoietin-2 concentrations and periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102936
                DO  - 10.18632/aging.102936
                SP  - 5140
                EP  - 5151
                PY  - 
                AB  - Angiopoietin-2 (Ang-2) is a proangiogenic factor that mediates inflammation and atherosclerosis. We evaluated the predictive value of circulating Ang-2 levels for periprocedural myocardial injury (PMI) in 145 patients undergoing elective percutaneous coronary intervention (PCI), and investigated whether post-PCI Ang-2 levels are influenced by PMI. PMI was defined as a post-procedural troponin elevation above the 5&#xD7;99th percentile upper reference limit. Blood samples for Ang-2 analysis were collected at admission and on postoperative days 1 and 3. PMI occurred in 40 patients (28%). At baseline, there was no difference in Ang-2 levels between PMI and non-PMI patients (P=0.554). However, a significant interaction effect between PMI occurrence and time on Ang-2 levels was observed (interaction P=0.036). Although serum Ang-2 levels in non-PMI patients gradually decreased, Ang-2 levels in PMI patients did not change between different time-points. Multiple logistic regression analysis revealed that age, total stent length, and serum levels of N-terminal pro-brain natriuretic peptide were independent PMI predictors. These findings indicate that pre-procedural Ang-2 levels do not impact PMI occurrence after elective PCI. However, changes in Ang-2 levels after the procedure are closely related to PMI.
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Rapamycin protects chondrocytes against IL-18-induced apoptosis and ameliorates rat osteoarthritis

Jiapeng Bao, Zhonggai Chen, Langhai Xu, Lidong Wu, Yan Xiong,

https://doi.org/10.18632/aging.102937 pp 5152—5167

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Bao J, Chen Z, Xu L, Wu L, Xiong Y, . Rapamycin protects chondrocytes against IL-18-induced apoptosis and ameliorates rat osteoarthritis. . 12:5152-5167. https://doi.org/10.18632/aging.102937

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                TY  - JOUR
                AU  - Bao, Jiapeng 
                AU  - Chen, Zhonggai 
                AU  - Xu, Langhai 
                AU  - Wu, Lidong 
                AU  - Xiong, Yan 
                TI  - Rapamycin protects chondrocytes against IL-18-induced apoptosis and ameliorates rat osteoarthritis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102937
                DO  - 10.18632/aging.102937
                SP  - 5152
                EP  - 5167
                PY  - 
                AB  - Interleukin 18 (IL-18) promotes inflammation and apoptosis in chondrocytes, thereby contributing to the development and progression of osteoarthritis (OA). Here, we investigated the effects of IL-18 treatment and inhibition in rat chondrocytes in vitro and in vivo. We used RT-PCR and Western blotting to measure the mRNA and protein levels of the chondrocyte-specific genes Collagen II and Aggrecan as well as the protein levels of apoptosis-related (Bax, Bcl2, Caspase3/9), autophagy-related (Atg5, Atg7, Beclin1, LC3), and mTOR pathway-related genes (PI3K, Akt, mTOR). We observed a decrease in Collagen II and Aggrecan mRNA and protein levels, upregulation of chondrocyte apoptosis, downregulation of chondrocyte autophagy, and activation of the PI3K/Akt/mTOR pathway upon IL-18 treatment. PI3K/Akt/mTOR pathway activation and inhibition tests using rat 740Y-P (PI3K activator), SC79 (AKT activator), 3BDO (mTOR activator), or LY294002 (PI3K inhibitor) revealed that activation of the PI3K/Akt/mTOR pathway enhances chondrocyte-specific gene degradation induced by IL-18, while its inhibition has protective effects on chondrocytes. We also found that treatment with rapamycin (a selective mTOR inhibitor) also exerts chondro-protective effects that ameliorate OA by promoting autophagy. These results suggest that inhibition of the mTOR pathway could be exploited for therapeutic benefits in the treatment of OA.
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Impaired brain network architecture in Cushing’s disease based on graph theoretical analysis

Can-Xin Xu, Hong Jiang, Rui-Zhe Zheng, Yu-Hao Sun, Qing-Fang Sun, Liu-Guan Bian,

https://doi.org/10.18632/aging.102939 pp 5168—5182

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Xu C, Jiang H, Zheng R, Sun Y, Sun Q, Bian L, . Impaired brain network architecture in Cushing’s disease based on graph theoretical analysis. . 12:5168-5182. https://doi.org/10.18632/aging.102939

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                TY  - JOUR
                AU  - Xu, Can-Xin 
                AU  - Jiang, Hong 
                AU  - Zheng, Rui-Zhe 
                AU  - Sun, Yu-Hao 
                AU  - Sun, Qing-Fang 
                AU  - Bian, Liu-Guan 
                TI  - Impaired brain network architecture in Cushing’s disease based on graph theoretical analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102939
                DO  - 10.18632/aging.102939
                SP  - 5168
                EP  - 5182
                PY  - 
                AB  - To investigate the whole functional brain networks of active Cushing disease (CD) patients about topological parameters (small world and rich club et al.) and compared with healthy control (NC). Nineteen active CD patients and twenty-two healthy control subjects, matched in age, gender, and education, underwent resting-state fMRI. Graph theoretical analysis was used to calculate the functional brain network organizations for all participants, and those for active CD patients were compared for and NCs. Active CD patients revealed higher global efficiency, shortest path length and reduced cluster efficiency compared with healthy control. Additionally, small world organization was present in active CD patients but higher than healthy control. Moreover, rich club connections, feeder connections and local connections were significantly decreased in active CD patients. Functional network properties appeared to be disrupted in active CD patients compared with healthy control. Analyzing the changes that lead to abnormal network metrics will improve our understanding of the pathophysiological mechanisms underlying CD.
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LncRNA AGAP2-AS1 augments cell viability and mobility, and confers gemcitabine resistance by inhibiting miR-497 in colorectal cancer

Sen Hong, Zhenkun Yan, YuMei Song, MiaoMiao Bi, Shiquan Li,

https://doi.org/10.18632/aging.102940 pp 5183—5194

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Hong S, Yan Z, Song Y, Bi M, Li S, . LncRNA AGAP2-AS1 augments cell viability and mobility, and confers gemcitabine resistance by inhibiting miR-497 in colorectal cancer. . 12:5183-5194. https://doi.org/10.18632/aging.102940

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                TY  - JOUR
                AU  - Hong, Sen 
                AU  - Yan, Zhenkun 
                AU  - Song, YuMei 
                AU  - Bi, MiaoMiao 
                AU  - Li, Shiquan 
                TI  - LncRNA AGAP2-AS1 augments cell viability and mobility, and confers gemcitabine resistance by inhibiting miR-497 in colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102940
                DO  - 10.18632/aging.102940
                SP  - 5183
                EP  - 5194
                PY  - 
                AB  - Background: Most recently, long non-coding RNAs (lncRNAs) emerge as crucial modulators in many biological processes, such as embryonic development, cell growth, and tumorigenesis. However, the correlations between lncRNAs and colorectal cancer (CRC) cell proliferation, metastasis, and gemcitabine resistance are not well understood.Results: The expression of AGAP2-AS1 was overexpressed in CRC tissues and negatively correlated with the survival of patients with CRC. AGAP2-AS1 promoted CRC cell proliferation and inhibited apoptosis. Moreover, AGAP2-AS1 enhanced the chemoresistance of CRC cells to gemcitabine. In addition, AGAP2-AS1 enhanced the migration and invasion of CRC cells. Mechanistic studies showed that AGAP2-AS1 regulated fibroblast growth factor receptor 1 (FGFR1) expression by sponging miR-497 in CRC progression.Conclusion: We identified an oncogenic role of AGAP2-AS1 in the development and progression of CRC.Methods: qRT-PCR was used to measure the expression of AGAP2 Antisense RNA 1 (AGAP2-AS1) in 116 cases of CRC and adjacent normal tissues. Luciferase reporter assays was used to detect the interaction between AGAP2-AS1 and miR-497. The xenograft tumor experiment was used to study the in vivo function of AGAP2-AS1.
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Peroxisomal abnormalities and catalase deficiency in Hutchinson-Gilford Progeria Syndrome

Xiaojing Mao, Pratima Bharti, Abhirami Thaivalappil, Kan Cao,

https://doi.org/10.18632/aging.102941 pp 5195—5208

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Mao X, Bharti P, Thaivalappil A, Cao K, . Peroxisomal abnormalities and catalase deficiency in Hutchinson-Gilford Progeria Syndrome. . 12:5195-5208. https://doi.org/10.18632/aging.102941

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                TY  - JOUR
                AU  - Mao, Xiaojing 
                AU  - Bharti, Pratima 
                AU  - Thaivalappil, Abhirami 
                AU  - Cao, Kan 
                TI  - Peroxisomal abnormalities and catalase deficiency in Hutchinson-Gilford Progeria Syndrome
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102941
                DO  - 10.18632/aging.102941
                SP  - 5195
                EP  - 5208
                PY  - 
                AB  - Peroxisomes are small, membrane-enclosed eukaryotic organelles that house various enzymes with metabolic functions. One important feature in both Hutchinson-Gilford Progeria Syndrome (HGPS) and normal aging is the elevated levels of Reactive Oxygen Species (ROS), which are generated from metabolic pathways with the capacity to cause oxidative damage to macromolecules within the cells. Although peroxisomal bioreactions can generate free radicals as their byproducts, many metabolic enzymes within the peroxisomes play critical roles as ROS scavengers, in particular, catalase. Here, we observed impaired peroxisomes-targeting protein trafficking, which suggested that the poorly assembled peroxisomes might cause high oxidative stress, contributing to the premature senescent phenotype in HGPS. We then investigated the ROS clearance efficiency by peroxisomal enzymes and found a significantly decreased expression of catalase in HGPS. Furthermore, we evaluated the effects of two promising HGPS-treatment drugs Methylene Blue and RAD001 (Everolimus, a rapamycin analog) on catalase in HGPS fibroblasts. We found that both drugs effectively reduced cellular ROS levels. MB, as a well-known antioxidant, did not affect catalase expression or activity. Interestingly, RAD001 treatment significantly upregulated catalase activity in HGPS cells. Our study presents the first characterization of peroxisomal function in HGPS and provides new insights into the cellular aspects of HGPS and the ongoing clinical trial.
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MicroRNA-325-3p prevents sevoflurane-induced learning and memory impairment by inhibiting Nupr1 and C/EBPβ/IGFBP5 signaling in rats

Lili Xu, Qi Xu, Fang Xu, Wenxin Zhang, Qing Chen, Hui Wu, Xinzhong Chen,

https://doi.org/10.18632/aging.102942 pp 5209—5220

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Xu L, Xu Q, Xu F, Zhang W, Chen Q, Wu H, Chen X, . MicroRNA-325-3p prevents sevoflurane-induced learning and memory impairment by inhibiting Nupr1 and C/EBPβ/IGFBP5 signaling in rats. . 12:5209-5220. https://doi.org/10.18632/aging.102942

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                TY  - JOUR
                AU  - Xu, Lili 
                AU  - Xu, Qi 
                AU  - Xu, Fang 
                AU  - Zhang, Wenxin 
                AU  - Chen, Qing 
                AU  - Wu, Hui 
                AU  - Chen, Xinzhong 
                TI  - MicroRNA-325-3p prevents sevoflurane-induced learning and memory impairment by inhibiting Nupr1 and C/EBPβ/IGFBP5 signaling in rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102942
                DO  - 10.18632/aging.102942
                SP  - 5209
                EP  - 5220
                PY  - 
                AB  - Endoplasmic reticulum stress-induced neuronal apoptosis contributes to neurotoxicity observed after sevoflurane exposure. However, the molecular mechanism underlying the resulting learning and memory impairments remains unknown. Here, we investigated the roles of miR-325-3p and Nupr1 in sevoflurane-induced learning and memory impairments in neonatal rats and HCN-2 human cortical neuronal cells. We found that in both neonatal rats and HCN-2 cells, sevoflurane exposure impairs learning and memory in neonatal rats and increases expression of Nupr1, the endoplasmic reticulum stress marker proteins C/EBP&#x3B2; and IGFBP5, and the apoptosis-related protein markers cleaved-Caspase-3 and Bax. Using bioinformatics tools to identify microRNAs that bind to Nupr1, we found that miR-325-3p is downregulated in hippocampal neurons exposed to sevoflurane. Moreover, Nupr1 knockdown and miR-325-3p overexpression improved the rats&#x2019; performance in learning and memory tests and reduced sevoflurane-induced apoptosis in vitro and in vivo. These results suggest that miR-325-3p blocks sevoflurane-induced learning and memory impairments by inhibiting Nupr1 and the downstream C/EBP&#x3B2;/IGFBP5 signaling axis in neonatal rats. MiR-325-3p may therefore be a useful therapeutic target in sevoflurane-induced neurotoxicity.
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Genetic networks in Parkinson’s and Alzheimer’s disease

Jack Kelly, Rana Moyeed, Camille Carroll, Shouqing Luo, Xinzhong Li,

https://doi.org/10.18632/aging.102943 pp 5221—5243

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Kelly J, Moyeed R, Carroll C, Luo S, Li X, . Genetic networks in Parkinson’s and Alzheimer’s disease. . 12:5221-5243. https://doi.org/10.18632/aging.102943

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                TY  - JOUR
                AU  - Kelly, Jack 
                AU  - Moyeed, Rana 
                AU  - Carroll, Camille 
                AU  - Luo, Shouqing 
                AU  - Li, Xinzhong 
                TI  - Genetic networks in Parkinson’s and Alzheimer’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102943
                DO  - 10.18632/aging.102943
                SP  - 5221
                EP  - 5243
                PY  - 
                AB  - Parkinson&#x2019;s disease (PD) and Alzheimer&#x2019;s disease (AD) are the most common neurodegenerative diseases and there is increasing evidence that they share common physiological and pathological links. Here we have conducted the largest network analysis of PD and AD based on their gene expressions in blood to date. We identified modules that were not preserved between disease and healthy control (HC) networks, and important hub genes and transcription factors (TFs) in these modules. We highlighted that the PD module not preserved in HCs was associated with insulin resistance, and HDAC6 was identified as a hub gene in this module which may have the role of influencing tau phosphorylation and autophagic flux in neurodegenerative disease. The AD module associated with regulation of lipolysis in adipocytes and neuroactive ligand-receptor interaction was not preserved in healthy and mild cognitive impairment networks and the key hubs TRPC5 and BRAP identified as potential targets for therapeutic treatments of AD. Our study demonstrated that PD and AD share common disrupted genetics and identified novel pathways, hub genes and TFs that may be new areas for mechanistic study and important targets in both diseases.
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Increased expression of the mitochondrial derived peptide, MOTS-c, in skeletal muscle of healthy aging men is associated with myofiber composition

Randall F. D’Souza, Jonathan S. T. Woodhead, Christopher P. Hedges, Nina Zeng, Junxiang Wan, Hiroshi Kumagai, Changhan Lee, Pinchas Cohen, David Cameron-Smith, Cameron J. Mitchell, Troy L. Merry,

https://doi.org/10.18632/aging.102944 pp 5244—5258

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D’Souza RF, Woodhead JST, Hedges CP, Zeng N, Wan J, Kumagai H, Lee C, Cohen P, Cameron-Smith D, Mitchell CJ, Merry TL, . Increased expression of the mitochondrial derived peptide, MOTS-c, in skeletal muscle of healthy aging men is associated with myofiber composition. . 12:5244-5258. https://doi.org/10.18632/aging.102944

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                TY  - JOUR
                AU  - D’Souza, Randall F. 
                AU  - Woodhead, Jonathan S. T. 
                AU  - Hedges, Christopher P. 
                AU  - Zeng, Nina 
                AU  - Wan, Junxiang 
                AU  - Kumagai, Hiroshi 
                AU  - Lee, Changhan 
                AU  - Cohen, Pinchas 
                AU  - Cameron-Smith, David 
                AU  - Mitchell, Cameron J. 
                AU  - Merry, Troy L. 
                TI  - Increased expression of the mitochondrial derived peptide, MOTS-c, in skeletal muscle of healthy aging men is associated with myofiber composition
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102944
                DO  - 10.18632/aging.102944
                SP  - 5244
                EP  - 5258
                PY  - 
                AB  - Mitochondria putatively regulate the aging process, in part, through the small regulatory peptide, mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) that is encoded by the mitochondrial genome. Here we investigated the regulation of MOTS-c in the plasma and skeletal muscle of healthy aging men. Circulating MOTS-c reduced with age, but older (70-81 y) and middle-aged (45-55 y) men had ~1.5-fold higher skeletal muscle MOTS-c expression than young (18-30 y). Plasma MOTS-c levels only correlated with plasma in young men, was associated with markers of slow-type muscle, and associated with improved muscle quality in the older group (maximal leg-press load relative to thigh cross-sectional area). Using small mRNA assays we provide evidence that MOTS-c transcription may be regulated independently of the full length 12S rRNA gene in which it is encoded, and expression is not associated with antioxidant response element (ARE)-related genes as previously seen in culture. Our results suggest that plasma and muscle MOTS-c are differentially regulated with aging, and the increase in muscle MOTS-c expression with age is consistent with fast-to-slow type muscle fiber transition. Further research is required to determine the molecular targets of endogenous MOTS-c in human muscle but they may relate to factors that maintain muscle quality.
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Whole-transcriptome analysis reveals a potential hsa_circ_0001955/hsa_circ_0000977-mediated miRNA-mRNA regulatory sub-network in colorectal cancer

Bisha Ding, Minya Yao, Weimin Fan, Weiyang Lou,

https://doi.org/10.18632/aging.102945 pp 5259—5279

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Ding B, Yao M, Fan W, Lou W, . Whole-transcriptome analysis reveals a potential hsa_circ_0001955/hsa_circ_0000977-mediated miRNA-mRNA regulatory sub-network in colorectal cancer. . 12:5259-5279. https://doi.org/10.18632/aging.102945

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                TY  - JOUR
                AU  - Ding, Bisha 
                AU  - Yao, Minya 
                AU  - Fan, Weimin 
                AU  - Lou, Weiyang 
                TI  - Whole-transcriptome analysis reveals a potential hsa_circ_0001955/hsa_circ_0000977-mediated miRNA-mRNA regulatory sub-network in colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102945
                DO  - 10.18632/aging.102945
                SP  - 5259
                EP  - 5279
                PY  - 
                AB  - Background: Circular RNAs (circRNAs), a novel class of non-coding RNAs, have been found to act as microRNA (miRNA) sponges and thus play key roles in biological processes and pathogenesis. However, studies regarding circRNAs in colorectal cancer (CRC) remain inadequate.Results: By differential expression analysis, 10 candidate circRNAs (6 upregulated and 4 downregulated circRNAs) were chosen. 9 of 10 circRNAs were available on CSCD and their structure showed the binding potential of miRNA. Intersection analysis revealed that miR-145-5p, miR-3127-5p, miR-761, miR-4766-3p, miR-135a-5p, miR-135b-5p, miR-374a-3p and miR-330-3p were 8 miRNAs with the most potential in binding circRNAs. Further expression validation and correlation analysis demonstrated hsa_circ_0001955/miR-145-5p and hsa_circ_0000977/miR-135b-5p axes as key pathways in CRC. Subsequently, target gene prediction, differential expression analysis, intersection analysis and correlation analysis showed that CDK6, MMP12 and RAB3IP were the three potential downstream targets of hsa_circ_0001955/miR-145-5p axis and FOXO1, MBNL1, MEF2C, RECK, PPM1E, TTLL7 and PCP4L1 were the seven potential downstream targets of hsa_circ_0000977/miR-135b-5p axis in CRC. Finally, we also confirmed that expression of hsa_circ_0001955 or hsa_circ_0000977 was significantly positively correlated with their individual targets in CRC.Conclusions: In the present work, we constructed a potential hsa_circ_0001955/hsa_circ_0000977-mediated circRNA-miRNA-mRNA regulatory network in CRC by a series of in silico analysis and experimental validation.Methods: Whole-transcriptome microarrays from CRC and matched normal samples were obtained from GEO. The structure of circRNA was identified by CSCD. starBase and miRNet were successively used to predict miRNA of circRNA and target gene of miRNA. Expression correlation between RNA-RNA interactions was assessed using GEO and TCGA data. Finally, a potential circRNA-miRNA-mRNA network was established based on competing endogenous RNA (ceRNA) hypothesis.
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m⁶A-induced lncRNA MALAT1 aggravates renal fibrogenesis in obstructive nephropathy through the miR-145/FAK pathway

Peihua Liu, Bo Zhang, Zhi Chen, Yao He, Yongchao Du, Yuhang Liu, Xiang Chen,

https://doi.org/10.18632/aging.102950 pp 5280—5299

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Liu P, Zhang B, Chen Z, He Y, Du Y, Liu Y, Chen X, . m⁶A-induced lncRNA MALAT1 aggravates renal fibrogenesis in obstructive nephropathy through the miR-145/FAK pathway. . 12:5280-5299. https://doi.org/10.18632/aging.102950

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 TY - JOUR
 AU - Liu, Peihua 
 AU - Zhang, Bo 
 AU - Chen, Zhi 
 AU - He, Yao 
 AU - Du, Yongchao 
 AU - Liu, Yuhang 
 AU - Chen, Xiang 
 TI - m6A-induced lncRNA MALAT1 aggravates renal fibrogenesis in obstructive nephropathy through the miR-145/FAK pathway
 JO - 
 JA - 
 VL - 12
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102950
 DO - 10.18632/aging.102950
 SP - 5280
 EP - 5299
 PY - 
 AB - Renal fibrosis is a key factor in chronic kidney disease (CKD). Long non-coding RNAs (lncRNAs) play important roles in the physiological and pathological progression of human diseases. However, the roles and underlying mechanisms of lncRNAs in renal fibrosis still need to be discovered. In this study, we first displayed the increased lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression in renal fibrosis in patients with obstructive nephropathy (ON). Then we found that transforming growth factor beta 1 (TGF-&#x3B2;1) induced epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) protein deposition, which promoted the viability, proliferation and migration of human renal proximal tubular epithelial (HK2) cells. Next, MALAT1/miR-145/focal adhesion kinase (FAK) pathway was confirmed to play an importment role in TGF-&#x3B2;1-induced renal fibrosis. In addition, the MALAT1/miR-145/FAK pathway was involved in the effect of dihydroartemisinin (DHA) on TGF-&#x3B2;1-induced renal fibrosis in vitro and in vivo. Furthermore, m6A methyltransferase methyltransferase-like 3 (METTL3) was shown to be the main methyltransferase of m6A modification on MALAT1.
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Verapamil extends lifespan in Caenorhabditis elegans by inhibiting calcineurin activity and promoting autophagy

Wenwen Liu, Huiling Lin, Zhifan Mao, Lanxin Zhang, Keting Bao, Bei Jiang, Conglong Xia, Wenjun Li, Zelan Hu, Jian Li,

https://doi.org/10.18632/aging.102951 pp 5300—5317

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Liu W, Lin H, Mao Z, Zhang L, Bao K, Jiang B, Xia C, Li W, Hu Z, Li J, . Verapamil extends lifespan in Caenorhabditis elegans by inhibiting calcineurin activity and promoting autophagy. . 12:5300-5317. https://doi.org/10.18632/aging.102951

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Provider: 
 TY - JOUR
 AU - Liu, Wenwen 
 AU - Lin, Huiling 
 AU - Mao, Zhifan 
 AU - Zhang, Lanxin 
 AU - Bao, Keting 
 AU - Jiang, Bei 
 AU - Xia, Conglong 
 AU - Li, Wenjun 
 AU - Hu, Zelan 
 AU - Li, Jian 
 TI - Verapamil extends lifespan in Caenorhabditis elegans by inhibiting calcineurin activity and promoting autophagy
 JO - 
 JA - 
 VL - 12
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102951
 DO - 10.18632/aging.102951
 SP - 5300
 EP - 5317
 PY - 
 AB - Previous evidence has revealed that increase in intracellular levels of calcium promotes cellular senescence. However, whether calcium channel blockers (CCBs) can slow aging and extend lifespan is still unknown. In this study, we showed that verapamil, an L-type calcium channel blocker, extended the Caenorhabditis elegans (C. elegans) lifespan and delayed senescence in human lung fibroblasts. Verapamil treatment also improved healthspan in C. elegans as reflected by several age-related physiological parameters, including locomotion, thrashing, age-associated vulval integrity, and osmotic stress resistance. We also found that verapamil acted on the &#x3B1;1 subunit of an L-type calcium channel in C. elegans. Moreover, verapamil extended worm lifespan by inhibiting calcineurin activity. Furthermore, verapamil significantly promoted autophagy as reflected by the expression levels of LGG-1/LC3 and the mRNA levels of autophagy-related genes. In addition, verapamil could not further induce autophagy when tax-6, calcineurin gene, was knocked down, indicating that verapamil-induced lifespan extension is mediated via promoting autophagy processes downstream of calcineurin. In summary, our study provided mechanistic insights into the anti-aging effect of verapamil in C. elegans.
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Dexmedetomidine alleviates sleep-restriction-mediated exaggeration of postoperative immunosuppression via splenic TFF2 in aged mice

Guangzhi Wang, Xiaoying Wu, Guosong Zhu, Shuangyin Han, Jiaqiang Zhang,

https://doi.org/10.18632/aging.102952 pp 5318—5335

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Wang G, Wu X, Zhu G, Han S, Zhang J, . Dexmedetomidine alleviates sleep-restriction-mediated exaggeration of postoperative immunosuppression via splenic TFF2 in aged mice. . 12:5318-5335. https://doi.org/10.18632/aging.102952

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                TY  - JOUR
                AU  - Wang, Guangzhi 
                AU  - Wu, Xiaoying 
                AU  - Zhu, Guosong 
                AU  - Han, Shuangyin 
                AU  - Zhang, Jiaqiang 
                TI  - Dexmedetomidine alleviates sleep-restriction-mediated exaggeration of postoperative immunosuppression via splenic TFF2 in aged mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102952
                DO  - 10.18632/aging.102952
                SP  - 5318
                EP  - 5335
                PY  - 
                AB  - Major abdominal procedures could induce dysfunction in the immune system and lead to postoperative immunosuppression. Sleep dysfunction is associated with impaired immune activity. However, the effects of postoperative sleep dysfunction on postoperative immune function remain unclear. In this study, we found that sleep-restriction (SR) after surgery increased the spleen weight and the percentage of myeloid-derived suppressor cells (MDSCs) in the spleen, and inhibited splenic CD8+ T cells activity, which was via inhibiting subdiaphragmatic vagus nerve (SVN)-mediated trefoil factor 2 (TFF2) expression in the spleen of aged mice. Dexmedetomidine could alleviate SR-induced these changes via modulating gut microbiota, which acted through SVN. Moreover, we showed essential roles of splenic TFF2 in attenuating SR-induced reduced protective ability against Escherichia coli (E. coli) pneumonia, increased expression of IL-4 and IL-13 in the lung and M2 polarization of alveolar macrophages (AMs), and decreased phagocytic activity of AMs. Dexmedetomidine improved SR-induced reduced protective ability against E. coli pneumonia via splenic TFF2, and subsequently decreasing IL-4 and IL-13 expression in the lung via modulating gut microbiota/SVN, increasing the compromised phagocytic activity of AMs, and ultimately decreasing M2 polarization of AMs. Taken together, dexmedetomidine-induced increase in splenic TFF2 expresssion could alleviate SR-induced exaggeration of postoperative immunosuppression.
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Overexpressed ITGA2 contributes to paclitaxel resistance by ovarian cancer cells through the activation of the AKT/FoxO1 pathway

Linlin Ma, Yan Sun, Dan Li, Hansong Li, Xin Jin, Dianyun Ren,

https://doi.org/10.18632/aging.102954 pp 5336—5351

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Ma L, Sun Y, Li D, Li H, Jin X, Ren D, . Overexpressed ITGA2 contributes to paclitaxel resistance by ovarian cancer cells through the activation of the AKT/FoxO1 pathway. . 12:5336-5351. https://doi.org/10.18632/aging.102954

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                TY  - JOUR
                AU  - Ma, Linlin 
                AU  - Sun, Yan 
                AU  - Li, Dan 
                AU  - Li, Hansong 
                AU  - Jin, Xin 
                AU  - Ren, Dianyun 
                TI  - Overexpressed ITGA2 contributes to paclitaxel resistance by ovarian cancer cells through the activation of the AKT/FoxO1 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102954
                DO  - 10.18632/aging.102954
                SP  - 5336
                EP  - 5351
                PY  - 
                AB  - Ovarian cancer is one of the most malignant tumors of the female reproductive system, with high invasiveness. The disease is a severe threat to women&apos;s health. The ITGA2 gene, which codes for integrin subunit &#x3B1;2, is involved in the proliferation, invasion, and metastasis of cancer cells. Although previous studies have shown that ITGA2 increases in ovarian cancer, the specific molecular mechanism of how ITGA2 promotes ovarian cancer proliferation and metastasis is still unclear. In this study, we confirmed that ITGA2 was elevated in ovarian cancer, which led to poor prognosis and survival. Overexpressed ITGA2 promoted the proliferation of ovarian cancer cells. We also found that ITGA2 regulated the phosphorylation of forkhead box O1 (FoxO1) by mediating AKT phosphorylation, which provided a reasonable explanation for ITGA2&#x2019;s role in ovarian cancer&#x2019;s resistance to albumin paclitaxel. In summary, ITGA2 could be used as a new therapeutic target and prognostic indicator in ovarian cancer.
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Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration

Dong-Ming Zhou, Feng Ran, Hai-Zhen Ni, Li-Li Sun, Lun Xiao, Xiao-Qiang Li, Wen-Dong Li,

https://doi.org/10.18632/aging.102955 pp 5352—5361

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Zhou D, Ran F, Ni H, Sun L, Xiao L, Li X, Li W, . Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration. . 12:5352-5361. https://doi.org/10.18632/aging.102955

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                TY  - JOUR
                AU  - Zhou, Dong-Ming 
                AU  - Ran, Feng 
                AU  - Ni, Hai-Zhen 
                AU  - Sun, Li-Li 
                AU  - Xiao, Lun 
                AU  - Li, Xiao-Qiang 
                AU  - Li, Wen-Dong 
                TI  - Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102955
                DO  - 10.18632/aging.102955
                SP  - 5352
                EP  - 5361
                PY  - 
                AB  - We investigated the protective effects and mechanism of action of metformin on high glucose-induced smooth muscle cell proliferation and migration. Vascular smooth muscle cells (VSMCs) were subjected to a series of concentrations (0-10 mM) of metformin. CCK-8, wound healing, and transwell assays were performed. Correlations between metformin concentration and high-mobility group box 1 (HMGB1) and miR-142-3p levels were assessed. In addition, miR-142-3p mimic and siRNA were used to investigate VSMC migration in the presence or absence of metformin. In the high-glucose condition, metformin decreased cell growth and inhibited cell migration. HMGB1 gene expression correlated negatively with metformin concentration, whereas miR-142-3p expression correlated positively with metformin concentration. In addition, mimic-induced miR-142-3p elevation resulted in decreased HMGB1 and LC3II levels and elevated p62 levels in the high-glucose condition, whereas miR-142-3p knockdown had the reverse effects, and metformin abolished those effects. Metformin inhibits high glucose&#x2013;induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway.
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Delphinidin attenuates pathological cardiac hypertrophy via the AMPK/NOX/MAPK signaling pathway

Youming Chen, Zhuowang Ge, Shixing Huang, Lei Zhou, Changlin Zhai, Yuhan Chen, Qiuyue Hu, Wei Cao, Yuteng Weng, Yanyan Li,

https://doi.org/10.18632/aging.102956 pp 5362—5383

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Chen Y, Ge Z, Huang S, Zhou L, Zhai C, Chen Y, Hu Q, Cao W, Weng Y, Li Y, . Delphinidin attenuates pathological cardiac hypertrophy via the AMPK/NOX/MAPK signaling pathway. . 12:5362-5383. https://doi.org/10.18632/aging.102956

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                TY  - JOUR
                AU  - Chen, Youming 
                AU  - Ge, Zhuowang 
                AU  - Huang, Shixing 
                AU  - Zhou, Lei 
                AU  - Zhai, Changlin 
                AU  - Chen, Yuhan 
                AU  - Hu, Qiuyue 
                AU  - Cao, Wei 
                AU  - Weng, Yuteng 
                AU  - Li, Yanyan 
                TI  - Delphinidin attenuates pathological cardiac hypertrophy via the AMPK/NOX/MAPK signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102956
                DO  - 10.18632/aging.102956
                SP  - 5362
                EP  - 5383
                PY  - 
                AB  - Reactive oxygen species (ROS) play a pivotal role in the development of pathological cardiac hypertrophy. Delphinidin, a natural flavonoid, was reported to exert marked antioxidative effects. Therefore, we investigated whether delphinidin ameliorates pathological cardiac hypertrophy via inhibiting oxidative stress. In this study, male C57BL/6 mice were treated with DMSO or delphinidin after surgery. Neonatal rat cardiomyocytes (NRCMs) were treated with angiotensin II (Ang II) and delphinidin in vitro. Eighteen-month-old mice were administered delphinidin to investigate the effect of delphinidin on aging-related cardiac hypertrophy. Through analyses of hypertrophic cardiomyocyte growth, fibrosis and cardiac function, delphinidin was demonstrated to confer resistance to aging- and transverse aortic constriction (TAC)-induced cardiac hypertrophy in vivo and attenuate Ang II-induced cardiomyocyte hypertrophy in vitro by significantly suppressing hypertrophic growth and the deposition of fibrosis. Mechanistically, delphinidin reduced ROS accumulation upon Ang II stimulation through the direct activation of AMP-activated protein kinase (AMPK) and subsequent inhibition of the activity of Rac1 and expression of p47phox. In addition, excessive levels of ERK1/2, P38 and JNK1/2 phosphorylation induced by oxidative stress were abrogated by delphinidin. Delphinidin was conclusively shown to repress pathological cardiac hypertrophy by modulating oxidative stress through the AMPK/NADPH oxidase (NOX)/mitogen-activated protein kinase (MAPK) signaling pathway.
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N-Propargyl caffeate amide (PACA) prevents cardiac fibrosis in experimental myocardial infarction by promoting pro-resolving macrophage polarization

Yuanyuan Cheng, Dan Luo, Yingke Zhao, Jianhui Rong,

https://doi.org/10.18632/aging.102959 pp 5384—5398

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Cheng Y, Luo D, Zhao Y, Rong J, . N-Propargyl caffeate amide (PACA) prevents cardiac fibrosis in experimental myocardial infarction by promoting pro-resolving macrophage polarization. . 12:5384-5398. https://doi.org/10.18632/aging.102959

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                TY  - JOUR
                AU  - Cheng, Yuanyuan 
                AU  - Luo, Dan 
                AU  - Zhao, Yingke 
                AU  - Rong, Jianhui 
                TI  - N-Propargyl caffeate amide (PACA) prevents cardiac fibrosis in experimental myocardial infarction by promoting pro-resolving macrophage polarization
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102959
                DO  - 10.18632/aging.102959
                SP  - 5384
                EP  - 5398
                PY  - 
                AB  - Macrophages control the initiation and resolution of cardiac fibrosis in post-infarction cardiac remodeling. The aim of the present study was to investigate whether N-propargyl caffeate amide (PACA) could suppress myocardial fibrosis via regulating macrophage polarization. By using rat model of isoproterenol-induced myocardial fibrosis, we discovered that PACA could reduce cardiac fibrosis in a dose-dependent manner. To elucidate the anti-fibrotic mechanisms, we examined whether PACA affected pro-inflammatory M1 and pro-resolving macrophage biomarkers in macrophage polarization. As result, PACA reduced the expression of pro-inflammatory M1 biomarkers (e.g., iNOS, TNF-&#x3B1;, CXCL10, IL-6, CCL2 and CD80) while increased the expression of pro-resolving M2a biomarkers (e.g., IL-10, arginase-1, FZZ1, YM-1 and CD163) in LPS-stimulated RAW264.7 macrophages. PACA also suppressed the elevation of M1 biomarker ED1 in the early phase but up-regulated the expression of pro-resolving biomarker ED2 in the later phase. Moreover, PACA reduced the expression of pro-fibrotic TGF-&#x3B2;1 and PDGF-&#x3B1; while maintained or even increased the production of pro-apoptotic MMP-13, MMP-9 and TRAIL. Importantly, mechanistic studies revealed that PACA might promote the switch of macrophage polarization towards a pro-resolving macrophage phenotype via activating PPAR-&#x3B3; pathway. Taken together, this study suggested that PACA might be a drug candidate for preventing cardiac fibrosis in myocardial infarction.
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The therapeutic value of the SphK1-targeting microRNA-3677 in human osteosarcoma cells

Chen Yao, Jian-Wei Ruan, Yun-Rong Zhu, Fei Liu, Hui-ming Wu, Yan Zhang, Qing Jiang,

https://doi.org/10.18632/aging.102961 pp 5399—5410

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Yao C, Ruan J, Zhu Y, Liu F, Wu H, Zhang Y, Jiang Q, . The therapeutic value of the SphK1-targeting microRNA-3677 in human osteosarcoma cells. . 12:5399-5410. https://doi.org/10.18632/aging.102961

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                TY  - JOUR
                AU  - Yao, Chen 
                AU  - Ruan, Jian-Wei 
                AU  - Zhu, Yun-Rong 
                AU  - Liu, Fei 
                AU  - Wu, Hui-ming 
                AU  - Zhang, Yan 
                AU  - Jiang, Qing 
                TI  - The therapeutic value of the SphK1-targeting microRNA-3677 in human osteosarcoma cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102961
                DO  - 10.18632/aging.102961
                SP  - 5399
                EP  - 5410
                PY  - 
                AB  - Sphingosine kinase 1 (SphK1) is a potential therapeutic target for human osteosarcoma (OS). SphK1-targeting microRNAs (miRNAs) could have important therapeutic value for OS. We discovered that micorRNA-3677 (miR-3677) is a SphK1-targeting miRNA, inhibiting OS cell progression. The results of RNA-Pull down assay confirmed direct binding between biotinylated-miR-3677 and SphK1 mRNA in primary human OS cells. In established and primary human OS cells forced overexpression of miR-3677, by a lentiviral construct, decreased SphK1 3&#x2019;-UTR (untranslated region) activity and downregulated SphK1 expression. Both were however enhanced with miR-3677 inhibition in OS cells. Function studies demonstrated that OS cell growth, proliferation and migration were inhibited with miR-3677 overexpression, but augmented with miR-3677 inhibition. MiR-3677 overexpression-induced anti-OS cell activity was reversed with re-expression of the 3&#x2019;-UTR-depleted SphK1. Additionally, in SphK1 knockout OS cells (by CRISPR/Cas9 strategy), altering miR-3677 expression failed to further alter cell functions. Finally, we show that miR-3677 expression was significantly downregulated in primary human OS tissues, correlating with SphK1 mRNA upregulation. We conclude that targeting SphK1 by miR-3677 inhibits human OS cell progression.
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HDAC6 promotes sepsis development by impairing PHB1-mediated mitochondrial respiratory chain function

Shi-dong Guo, Sheng-tao Yan, Wen Li, Hong Zhou, Jian-ping Yang, Yao Yao, Mei-jia Shen, Liu-wei Zhang, Hong-Bo Zhang, Li-Chao Sun,

https://doi.org/10.18632/aging.102964 pp 5411—5422

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Guo S, Yan S, Li W, Zhou H, Yang J, Yao Y, Shen M, Zhang L, Zhang H, Sun L, . HDAC6 promotes sepsis development by impairing PHB1-mediated mitochondrial respiratory chain function. . 12:5411-5422. https://doi.org/10.18632/aging.102964

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                TY  - JOUR
                AU  - Guo, Shi-dong 
                AU  - Yan, Sheng-tao 
                AU  - Li, Wen 
                AU  - Zhou, Hong 
                AU  - Yang, Jian-ping 
                AU  - Yao, Yao 
                AU  - Shen, Mei-jia 
                AU  - Zhang, Liu-wei 
                AU  - Zhang, Hong-Bo 
                AU  - Sun, Li-Chao 
                TI  - HDAC6 promotes sepsis development by impairing PHB1-mediated mitochondrial respiratory chain function
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102964
                DO  - 10.18632/aging.102964
                SP  - 5411
                EP  - 5422
                PY  - 
                AB  - Objective: This study was aimed at investigating the regulation of mitochondrial function by histone deacetylase 6 (HDAC6) and the role of HDAC6 in the development and progression of sepsis.Results: HDAC6 downregulated PHB1 and subsequently promoted the development of CLP-induced sepsis. Inhibition of HDAC6 significantly attenuated CLP-induced sepsis through inhibition of mitochondrial dysfunction and reduced oxidant production, thus protecting the rats from oxidative injury.Conclusions: In this sepsis model, HDAC6 inhibits the expression and function of PHB1 and alters the function of the mitochondrial respiratory chain mediated by PHB1, thus enhancing the production of oxidants and increasing oxidative stress and thereby leading to severe oxidative injury in multiple organs.Methods: The expression of HDAC6 and prohibitin 1 (PHB1) in humans and in a rat model of sepsis was measured by quantitative reverse-transcription PCR and western blotting. Sepsis induction by cecal ligation and puncture (CLP) was confirmed by histological analysis. Concentrations of different sepsis markers were measured by an enzyme-linked immunosorbent assay, and mitochondrial function was assessed via the mitochondrial respiratory control rate.
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Melatonin reverses nasopharyngeal carcinoma cisplatin chemoresistance by inhibiting the Wnt/β-catenin signaling pathway

Jian Zhang, Tao Xie, Xi Zhong, Hua-Li Jiang, Rong Li, Bai-Yao Wang, Xiao-Ting Huang, Bo-Hong Cen, Ya-Wei Yuan,

https://doi.org/10.18632/aging.102968 pp 5423—5438

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Zhang J, Xie T, Zhong X, Jiang H, Li R, Wang B, Huang X, Cen B, Yuan Y, . Melatonin reverses nasopharyngeal carcinoma cisplatin chemoresistance by inhibiting the Wnt/β-catenin signaling pathway. . 12:5423-5438. https://doi.org/10.18632/aging.102968

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                TY  - JOUR
                AU  - Zhang, Jian 
                AU  - Xie, Tao 
                AU  - Zhong, Xi 
                AU  - Jiang, Hua-Li 
                AU  - Li, Rong 
                AU  - Wang, Bai-Yao 
                AU  - Huang, Xiao-Ting 
                AU  - Cen, Bo-Hong 
                AU  - Yuan, Ya-Wei 
                TI  - Melatonin reverses nasopharyngeal carcinoma cisplatin chemoresistance by inhibiting the Wnt/β-catenin signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102968
                DO  - 10.18632/aging.102968
                SP  - 5423
                EP  - 5438
                PY  - 
                AB  - Cisplatin (DDP)-based concurrent chemo-radiotherapy is a standard approach to treat locoregionally advanced nasopharyngeal carcinoma (NPC). However, many patients eventually develop recurrence and/or distant metastasis due to chemoresistance. In this study, we aimed to elucidate the effects of melatonin on DDP chemoresistance in NPC cell lines in vitro and vivo, and we explored potential chemoresistance mechanisms. We found that DDP chemoresistance in NPC cells is mediated through the Wnt/&#x3B2;-catenin signaling pathway. Melatonin not only reversed DDP chemoresistance, but also enhanced DDP antitumor activity by suppressing the nuclear translocation of &#x3B2;-catenin, and reducing expression of Wnt/&#x3B2;-catenin response genes in NPC cells. In vivo, combined treatment with DDP and melatonin reduced tumor burden to a greater extent than single drug-treatments in an orthotopic xenograft mouse model. Our findings provide novel evidence that melatonin inhibits the Wnt/&#x3B2;-catenin pathway in NPC, and suggest that melatonin could be applied in combination with DDP to treat NPC.
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Identification of hub genes in hepatocellular carcinoma using integrated bioinformatic analysis

Shengni Hua, Zhonghua Ji, Yingyao Quan, Meixiao Zhan, Hao Wang, Wei Li, Yong Li, Xu He, Ligong Lu,

https://doi.org/10.18632/aging.102969 pp 5439—5468

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Hua S, Ji Z, Quan Y, Zhan M, Wang H, Li W, Li Y, He X, Lu L, . Identification of hub genes in hepatocellular carcinoma using integrated bioinformatic analysis. . 12:5439-5468. https://doi.org/10.18632/aging.102969

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                TY  - JOUR
                AU  - Hua, Shengni 
                AU  - Ji, Zhonghua 
                AU  - Quan, Yingyao 
                AU  - Zhan, Meixiao 
                AU  - Wang, Hao 
                AU  - Li, Wei 
                AU  - Li, Yong 
                AU  - He, Xu 
                AU  - Lu, Ligong 
                TI  - Identification of hub genes in hepatocellular carcinoma using integrated bioinformatic analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102969
                DO  - 10.18632/aging.102969
                SP  - 5439
                EP  - 5468
                PY  - 
                AB  - The molecular mechanisms underlying hepatocellular carcinoma (HCC) progression remain largely undefined. Here, we identified 176 commonly upregulated genes in HCC tissues based on three Gene Expression Omnibus datasets and The Cancer Genome Atlas (TCGA) cohort. We integrated survival and methylation analyses to further obtain 12 upregulated genes for validation. These genes were overexpressed in HCC tissues at the transcription and protein levels, and increased mRNA levels were related to higher tumor grades and cancer stages. The expression of all markers was negatively associated with overall and disease-free survival in HCC patients. Most of these hub genes can promote HCC proliferation and/or metastasis. These 12 hub genes were also overexpressed and had strong prognostic value in many other cancer types. Methylation and gene copy number analyses indicated that the upregulation of these hub genes was probably due to hypomethylation or increased gene copy numbers. Further, the methylation levels of three genes, KPNA2, MCM3, and LRRC1, were associated with HCC clinical features. Moreover, the levels of most hub genes were related to immune cell infiltration in HCC microenvironments. Finally, we identified three upregulated genes (KPNA2, TARBP1, and RNASEH2A) that could comprehensively and accurately provide diagnostic and prognostic value for HCC patients.
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Intranasal delivery of 9-cis retinoic acid reduces beta-amyloid deposition via inhibiting astrocyte-mediated inflammation

Hong Zhao, Shuo Li, Zhuo Li, Shuo Yang, Dandan Li, Jiaolin Zheng, Hongmei Gao, Ling Yun, YingLi Gu, Longxuan Li, Jing Zhao, Yuan Fu,

https://doi.org/10.18632/aging.102970 pp 5469—5478

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Zhao H, Li S, Li Z, Yang S, Li D, Zheng J, Gao H, Yun L, Gu Y, Li L, Zhao J, Fu Y, . Intranasal delivery of 9-cis retinoic acid reduces beta-amyloid deposition via inhibiting astrocyte-mediated inflammation. . 12:5469-5478. https://doi.org/10.18632/aging.102970

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                TY  - JOUR
                AU  - Zhao, Hong 
                AU  - Li, Shuo 
                AU  - Li, Zhuo 
                AU  - Yang, Shuo 
                AU  - Li, Dandan 
                AU  - Zheng, Jiaolin 
                AU  - Gao, Hongmei 
                AU  - Yun, Ling 
                AU  - Gu, YingLi 
                AU  - Li, Longxuan 
                AU  - Zhao, Jing 
                AU  - Fu, Yuan 
                TI  - Intranasal delivery of 9-cis retinoic acid reduces beta-amyloid deposition via inhibiting astrocyte-mediated inflammation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102970
                DO  - 10.18632/aging.102970
                SP  - 5469
                EP  - 5478
                PY  - 
                AB  - Alzheimer&apos;s disease (AD) is associated with the accumulation and deposition of a beta-amyloid (&#x391;&#x3B2;) peptide in the brain, resulting in increased neuroinflammation and synaptic dysfunction. Intranasal delivery of targeted drugs to the brain represents a noninvasive pathway that bypasses the blood-brain barrier and minimizes systemic exposure. The aim of this study was to evaluate the therapeutic effect of intranasally delivered 9-cis retinoic acid (RA) on the neuropathology of an AD mouse model. Herein, we observed dramatically decreased &#x391;&#x3B2; deposition in the brains of amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice (APP/PS1) treated intranasally with 9-cis RA for 4 weeks compared to that in the brains of vehicle-treated mice. Importantly, intranasal delivery of 9-cis RA suppressed &#x391;&#x3B2;-associated astrocyte activation and neuroinflammation and ultimately restored synaptic deficits in APP/PS1 transgenic mice. These results support the critical roles of &#x391;&#x3B2;-associated neuroinflammation responses to synaptic deficits, particularly during the deposition of &#x391;&#x3B2;. Our findings provide strong evidence that intranasally delivered 9-cis RA attenuates neuronal dysfunction in an AD mouse model and is a promising therapeutic strategy for the prevention and treatment of AD.
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Prognostic values of immune scores and immune microenvironment-related genes for hepatocellular carcinoma

Peng-lei Ge, Shi-fang Li, Wei-wei Wang, Chun-bo Li, Yu-bin Fu, Zheng-kai Feng, Lin Li, Gong Zhang, Zhi-qiang Gao, Xiao-wei Dang, Yang Wu,

https://doi.org/10.18632/aging.102971 pp 5479—5499

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Ge P, Li S, Wang W, Li C, Fu Y, Feng Z, Li L, Zhang G, Gao Z, Dang X, Wu Y, . Prognostic values of immune scores and immune microenvironment-related genes for hepatocellular carcinoma. . 12:5479-5499. https://doi.org/10.18632/aging.102971

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                TY  - JOUR
                AU  - Ge, Peng-lei 
                AU  - Li, Shi-fang 
                AU  - Wang, Wei-wei 
                AU  - Li, Chun-bo 
                AU  - Fu, Yu-bin 
                AU  - Feng, Zheng-kai 
                AU  - Li, Lin 
                AU  - Zhang, Gong 
                AU  - Gao, Zhi-qiang 
                AU  - Dang, Xiao-wei 
                AU  - Wu, Yang 
                TI  - Prognostic values of immune scores and immune microenvironment-related genes for hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102971
                DO  - 10.18632/aging.102971
                SP  - 5479
                EP  - 5499
                PY  - 
                AB  - It is crucial to grasp the characteristics of tumour immune microenvironment to improve effects of immunotherapy. In this study, the immune and stromal scores of 371 cases were calculated for quantitative analysis of immune and stromal cell infiltration in the tumour microenvironment of hepatocellular carcinoma (HCC). The weighted gene co-expression network analysis and protein&#x2013;protein interaction network were analysed to identify immune microenvironment-related genes. The results showed that patients with high immune scores had a higher 4-year recurrence-free rate. TP53, CTNNB1, and AXIN1 mutations significantly varied with immune scores. In immune score-related modules analysis, Kyoto encyclopaedia of genes and genomes pathways and gene ontology terms were closely related to immune processes, tumorigenesis, and metastasis. Twelve new immune microenvironment-related genes were identified and had significantly positive correlations with seven immune checkpoint genes. In prognostic analysis, eleven immune microenvironment-related genes exhibited high expression, nine of which were validated in the GSE62232 dataset and were significantly associated with a good prognosis. Our findings suggest that calculating immune score and stromal score could help to determine tumour purity and immune cell infiltration in the tumour microenvironment. Nine immune microenvironment-related genes identified in this study had potential as prognostic markers for HCC.
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The association of calcium intake with osteoporotic vertebral fractures in a large Chinese cohort

Ling Wang, Lu Yin, Xiaoguang Cheng, Kai Li, Yuebo Wang, Yong Zhang, Yang-yang Duanmu, Xiaoyun Liu, Guijuan Deng, Yang Wang, Nicola Veronese, Wei Li, Wei Tian, PURE China CASH study team,

https://doi.org/10.18632/aging.102974 pp 5500—5515

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Wang L, Yin L, Cheng X, Li K, Wang Y, Zhang Y, Duanmu Y, Liu X, Deng G, Wang Y, Veronese N, Li W, Tian W, et al, . The association of calcium intake with osteoporotic vertebral fractures in a large Chinese cohort. . 12:5500-5515. https://doi.org/10.18632/aging.102974

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                TY  - JOUR
                AU  - Wang, Ling 
                AU  - Yin, Lu 
                AU  - Cheng, Xiaoguang 
                AU  - Li, Kai 
                AU  - Wang, Yuebo 
                AU  - Zhang, Yong 
                AU  - Duanmu, Yang-yang 
                AU  - Liu, Xiaoyun 
                AU  - Deng, Guijuan 
                AU  - Wang, Yang 
                AU  - Veronese, Nicola 
                AU  - Li, Wei 
                AU  - Tian, Wei 
                AU  - ,  
                TI  - The association of calcium intake with osteoporotic vertebral fractures in a large Chinese cohort
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102974
                DO  - 10.18632/aging.102974
                SP  - 5500
                EP  - 5515
                PY  - 
                AB  - The effect of calcium on prevention of osteoporosis and related fracture which are aging issues is unclear. The aim of this study is to explore the association of calcium intake with vertebral fracture. This study enrolled 3,457 participants from China Action on Spine and Hip Status (CASH) study from 2013 and 2017. Dietary calcium intake was collected using validated food frequency questionnaires (FFQ). Vertebral fracture of CT images was defined as the primary outcome. The mean calcium intake of men and women were 522.75mg/day and 507.21mg/day, respectively. 6% reduction in the odds of fracture risk was observed per 100 unit increase of calcium intake from food among females (OR, 0.94; 95% CI, 0.89-0.99), but results among males were not significant. We divided calcium intake into quintiles when modelling its associations with fracture risk, negative associations of fracture risk with calcium intake were found among females. In a population with low usual calcium intake, higher dietary calcium intake was associated with fewer vertebral fracture in women and that no such association was seen in men.
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Microarray analysis of verbenalin-treated human amniotic epithelial cells reveals therapeutic potential for Alzheimer’s Disease

Farhana Ferdousi, Shinji Kondo, Kazunori Sasaki, Yoshiaki Uchida, Nobuhiro Ohkohchi, Yun-Wen Zheng, Hiroko Isoda,

https://doi.org/10.18632/aging.102985 pp 5516—5538

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Ferdousi F, Kondo S, Sasaki K, Uchida Y, Ohkohchi N, Zheng Y, Isoda H, . Microarray analysis of verbenalin-treated human amniotic epithelial cells reveals therapeutic potential for Alzheimer’s Disease. . 12:5516-5538. https://doi.org/10.18632/aging.102985

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                TY  - JOUR
                AU  - Ferdousi, Farhana 
                AU  - Kondo, Shinji 
                AU  - Sasaki, Kazunori 
                AU  - Uchida, Yoshiaki 
                AU  - Ohkohchi, Nobuhiro 
                AU  - Zheng, Yun-Wen 
                AU  - Isoda, Hiroko 
                TI  - Microarray analysis of verbenalin-treated human amniotic epithelial cells reveals therapeutic potential for Alzheimer’s Disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102985
                DO  - 10.18632/aging.102985
                SP  - 5516
                EP  - 5538
                PY  - 
                AB  - Alzheimer&#x2019;s disease (AD) has become a major world health problem as the population ages. There is still no available treatment that can stop or reverse the progression of AD. Human amnion epithelial cells (hAECs), an alternative source for stem cells, have shown neuroprotective and neurorestorative potentials when transplanted in vivo. Besides, studies have suggested that stem cell priming with plant-derived bioactive compounds can enhance stem cell proliferation and differentiation and improve the disease-treating capability of stem cells. Verbenalin is an iridoid glucoside found in medicinal herbs of Verbenaceae family. In the present study, we have conducted microarray gene expression profiling of verbenalin-treated hAECs to explore its therapeutic potential for AD. Gene set enrichment analysis revealed verbenalin treatment significantly enriched AD-associated gene sets. Genes associated with lysosomal dysfunction, pathologic angiogenesis, pathologic protein aggregation, circadian rhythm, age-related neurometabolism, and neurogenesis were differentially expressed in the verbenalin-treated hAECs compared to control cells. Additionally, the neuroprotective effect of verbenalin was confirmed against amyloid beta-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Our present study is the first to report the therapeutic potential of verbenalin for AD; however, further in-depth research in the in vitro and in vivo models are required to confirm our preliminary findings.
                ER  -

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Gut microbiota and pro/prebiotics in Alzheimer’s disease

Ryszard Pluta, Marzena Ułamek-Kozioł, Sławomir Januszewski, Stanisław J. Czuczwar,

https://doi.org/10.18632/aging.102930 pp 5539—5550

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Pluta R, Ułamek-Kozioł M, Januszewski S, Czuczwar SJ, . Gut microbiota and pro/prebiotics in Alzheimer’s disease. . 12:5539-5550. https://doi.org/10.18632/aging.102930

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                TY  - JOUR
                AU  - Pluta, Ryszard 
                AU  - Ułamek-Kozioł, Marzena 
                AU  - Januszewski, Sławomir 
                AU  - Czuczwar, Stanisław J. 
                TI  - Gut microbiota and pro/prebiotics in Alzheimer’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102930
                DO  - 10.18632/aging.102930
                SP  - 5539
                EP  - 5550
                PY  - 
                AB  - Alzheimer&#x2019;s disease is characterized by the accumulation of amyloid and dysfunctional tau protein in the brain along with the final development of dementia. Accumulation of amyloid in the brain was observed 10-20 years before the onset of clinical symptoms by diagnostic methods based on image analysis. This is a serious public health problem, incidence and prevalence being expected to reach epidemic proportions over the next few decades if the disease cannot be prevented or slowed down. Recently, in addition to the strongly developing ischemic etiology of Alzheimer&#x2019;s disease, it is suggested that the gut microbiota may also participate in the development of this disease. The brain and gut are thought to form a network called the &#x201C;gut-brain-microbiota axis&#x201D;, and it is strongly supported idea that the intestinal microflora can be involved in Alzheimer&#x2019;s disease. Lately, many new studies have been conducted that draw attention to the relationship between Alzheimer&#x2019;s disease and gut microbiota. This review presents a possible relationship between Alzheimer&#x2019;s disease and a microbiome. It is a promising idea for prevention or therapeutic intervention. Modulation of the gut microbiota through a personalized diet or beneficial microflora intervention like pro/prebiotics, changing microbiological partners and their products, including amyloid protein, can become a new treatment for Alzheimer&#x2019;s disease.
                ER  -

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Aging-associated alterations in epidermal function and their clinical significance

Zhen Wang, Mao-Qiang Man, Tienan Li, Peter M. Elias, Theodora M. Mauro,

https://doi.org/10.18632/aging.102946 pp 5551—5565

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Wang Z, Man M, Li T, Elias PM, Mauro TM, . Aging-associated alterations in epidermal function and their clinical significance. . 12:5551-5565. https://doi.org/10.18632/aging.102946

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                TY  - JOUR
                AU  - Wang, Zhen 
                AU  - Man, Mao-Qiang 
                AU  - Li, Tienan 
                AU  - Elias, Peter M. 
                AU  - Mauro, Theodora M. 
                TI  - Aging-associated alterations in epidermal function and their clinical significance
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102946
                DO  - 10.18632/aging.102946
                SP  - 5551
                EP  - 5565
                PY  - 
                AB  - Chronologically-aged skin displays multiple functional changes in both the dermis and the epidermis. It appears that epidermal dysfunction, compromised permeability homeostasis, reduced stratum corneum hydration and elevated skin surface pH predispose to the development of aging-associated cutaneous and extracutaneous disorders. Improvements in epidermal function have been shown to be an effective alternative therapy in the prevention and treatment of some aging-associated cutaneous disorders, including eczematous dermatitis, pruritus, and xerosis. Recent studies demonstrated that epidermal dysfunction leads to the development of chronic, low-grade systemic inflammation, termed &#x2018;inflammaging,&#x2019; which is linked to the development of aging-associated systemic disorders. Thus, correction of epidermal dysfunction could comprise a novel strategy in the prevention and treatment of aging-associated systemic disorders as well. In this review, we summarize aging-associated alterations in epidermal function, their underlying mechanisms, and their clinical significance. Regimens to improve epidermal function in the elderly are also discussed.
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Perspectives of Homo sapiens lifespan extension: focus on external or internal resources?

Vladimir P. Skulachev, Gregory A. Shilovsky, Tatyana S. Putyatina, Nikita A. Popov, Alexander V. Markov, Maxim V. Skulachev, Victor A. Sadovnichii,

https://doi.org/10.18632/aging.102981 pp 5566—5584

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Skulachev VP, Shilovsky GA, Putyatina TS, Popov NA, Markov AV, Skulachev MV, Sadovnichii VA, . Perspectives of Homo sapiens lifespan extension: focus on external or internal resources?. . 12:5566-5584. https://doi.org/10.18632/aging.102981

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 TY - JOUR
 AU - Skulachev, Vladimir P. 
 AU - Shilovsky, Gregory A. 
 AU - Putyatina, Tatyana S. 
 AU - Popov, Nikita A. 
 AU - Markov, Alexander V. 
 AU - Skulachev, Maxim V. 
 AU - Sadovnichii, Victor A. 
 TI - Perspectives of Homo sapiens lifespan extension: focus on external or internal resources?
 JO - 
 JA - 
 VL - 12
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102981
 DO - 10.18632/aging.102981
 SP - 5566
 EP - 5584
 PY - 
 AB - Homo sapiens and naked mole rats (Heterocephalus glaber) are vivid examples of social mammals that differ from their relatives in particular by an increased lifespan and a large number of neotenic features. An important fact for biogerontology is that the mortality rate of H. glaber (a maximal lifespan of more than 32 years, which is very large for such a small rodent) negligibly grows with age. The same is true for modern people in developed countries below the age of 60. It is important that the juvenilization of traits that separate humans from chimpanzees evolved over thousands of generations and millions of years. Rapid advances in technology resulted in a sharp increase in the life expectancy of human beings during the past 100 years. Currently, the human life expectancy has exceeded 80 years in developed countries. It cannot be excluded that the potential for increasing life expectancy by an improvement in living conditions will be exhausted after a certain period of time. New types of geroprotectors should be developed that protect not only from chronic phenoptosis gradual poisoning of the body with reactive oxygen species (ROS) but also from acute phenoptosis, where strong increase in the level of ROS immediately kills an already aged individual. Geroprotectors might be another anti-aging strategy along with neoteny (a natural physiological phenomenon) and technical progress.
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Correction for: Mitochondria and aging in older individuals: an analysis of DNA methylation age metrics, leukocyte telomere length, and mitochondrial DNA copy number in the VA normative aging study

Jacopo Dolcini, Haotian Wu, Jamaji C. Nwanaji-Enwerem, Marianthi-Anna Kioumourtozlogu, Akin Cayir, Marco Sanchez-Guerra, Pantel Vokonas, Joel Schwarz, Andrea A. Baccarelli,

https://doi.org/10.18632/aging.102962 pp 5585—5586

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Dolcini J, Wu H, Nwanaji-Enwerem JC, Kioumourtozlogu M, Cayir A, Sanchez-Guerra M, Vokonas P, Schwarz J, Baccarelli AA, . Correction for: Mitochondria and aging in older individuals: an analysis of DNA methylation age metrics, leukocyte telomere length, and mitochondrial DNA copy number in the VA normative aging study. . 12:5585-5586. https://doi.org/10.18632/aging.102962

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                TY  - JOUR
                AU  - Dolcini, Jacopo 
                AU  - Wu, Haotian 
                AU  - Nwanaji-Enwerem, Jamaji C. 
                AU  - Kioumourtozlogu, Marianthi-Anna 
                AU  - Cayir, Akin 
                AU  - Sanchez-Guerra, Marco 
                AU  - Vokonas, Pantel 
                AU  - Schwarz, Joel 
                AU  - Baccarelli, Andrea A. 
                TI  - Correction for: Mitochondria and aging in older individuals: an analysis of DNA methylation age metrics, leukocyte telomere length, and mitochondrial DNA copy number in the VA normative aging study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102962
                DO  - 10.18632/aging.102962
                SP  - 5585
                EP  - 5586
                PY  - 
                AB  - 
                ER  -

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Correction for: Ligustilide improves aging-induced memory deficit by regulating mitochondrial related inflammation in SAMP8 mice

Wen-Li Zhu, Jia-Yi Zheng, Wei-Wu Cai, Zhao Dai, Ben-Yue Li, Ting-Ting Xu, Hao-Fei Liu, Xiao-Qi Liu, Su-Fen Wei, Yi Luo, Hong Wang, Hua-Feng Pan, Qi Wang, Shi-Jie Zhang,

https://doi.org/10.18632/aging.102998 pp 5587

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Zhu W, Zheng J, Cai W, Dai Z, Li B, Xu T, Liu H, Liu X, Wei S, Luo Y, Wang H, Pan H, Wang Q, et al, . Correction for: Ligustilide improves aging-induced memory deficit by regulating mitochondrial related inflammation in SAMP8 mice. . 12:5587-5587. https://doi.org/10.18632/aging.102998

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                TY  - JOUR
                AU  - Zhu, Wen-Li 
                AU  - Zheng, Jia-Yi 
                AU  - Cai, Wei-Wu 
                AU  - Dai, Zhao 
                AU  - Li, Ben-Yue 
                AU  - Xu, Ting-Ting 
                AU  - Liu, Hao-Fei 
                AU  - Liu, Xiao-Qi 
                AU  - Wei, Su-Fen 
                AU  - Luo, Yi 
                AU  - Wang, Hong 
                AU  - Pan, Hua-Feng 
                AU  - Wang, Qi 
                AU  - Zhang, Shi-Jie 
                TI  - Correction for: Ligustilide improves aging-induced memory deficit by regulating mitochondrial related inflammation in SAMP8 mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102998
                DO  - 10.18632/aging.102998
                SP  - 5587
                EP  - 5587
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhu, Wen-Li 
                AU  - Zheng, Jia-Yi 
                AU  - Cai, Wei-Wu 
                AU  - Dai, Zhao 
                AU  - Li, Ben-Yue 
                AU  - Xu, Ting-Ting 
                AU  - Liu, Hao-Fei 
                AU  - Liu, Xiao-Qi 
                AU  - Wei, Su-Fen 
                AU  - Luo, Yi 
                AU  - Wang, Hong 
                AU  - Pan, Hua-Feng 
                AU  - Wang, Qi 
                AU  - Zhang, Shi-Jie 
                TI  - Correction for: Ligustilide improves aging-induced memory deficit by regulating mitochondrial related inflammation in SAMP8 mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102998
                DO  - 10.18632/aging.102998
                SP  - 5587
                EP  - 5587
                PY  - 
                AB  - 
                ER  -

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Volume 12, Issue 6

About the Cover

Editorials

Bulmaro Cisneros, Ian García-Aguirre,

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Tianliang Sun, Stefano Annunziato, Jan S. Tchorz,

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Priority Research Paper

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Research Papers

Xiaohui Xu, Xiaoyun Zhou, Zhenju Chen, Chao Gao, Luo Zhao, Yushang Cui,

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See-Hyoung Park, Mi-Ae Kang, Young Jae Moon, Kyu Yun Jang, Jung Ryul Kim,

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Yan Qu, Bo Cheng, Na Shao, Yibin Jia, Qingxu Song, Bingxu Tan, Jianbo Wang,

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Yinfeng Chen, Siyuan Zhang, Bo Zeng, Jiangchao Zhao, Mingyao Yang, Mingwang Zhang, Yan Li, Qingyong Ni, De Wu, Ying Li,

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Elisabet Cuyàs, Juan Gumuzio, Sara Verdura, Joan Brunet, Joaquim Bosch-Barrera, Begoña Martin-Castillo, Tomás Alarcón, José Antonio Encinar, Ángel G. Martin, Javier A. Menendez,

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Mina Liu, Changlu Wang, Lanting Gao, Changxing Lv, Xiaolong Fu,

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Cui Zhao, Ying Liang, Ting Chen, Yihua Zhong, Xianglong Li, Jing Wei, Chunlin Li, Xu Zhang,

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Chenxu Ge, Linfeng Hu, Deshuai Lou, Qiang Li, Jing Feng, Yekuan Wu, Jun Tan, Minxuan Xu,

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Aili Wang, Hongxia Zhang, Jinxiang Wang, Shuming Zhang, Zhenyang Xu,

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Qi Ding, Shanshan Dong, Ranran Wang, Keqiang Zhang, Hui Wang, Xiao Zhou, Jing Wang, Kee Wong, Ying Long, Shuai Zhu, Weigang Wang, Huayi Ren, Yong Zeng,

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Si Lu, Rongjie Zhao, Yeqin Ni, Jinwang Ding, Fuqiang Qiu, You Peng, Gang Pan, Fan Wu, Yu Zhang, Jingjing Shi, Tianhan Zhou, Dingcun Luo,

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Xinyi Wang, Haiyun Wang, Zhenghui Ye, Guofei Ding, Fengli Li, Ji Ma, Wei Hua,

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Linli Hu, Songying Zhang, Song Quan, Jieqiang Lv, Weiping Qian, Yuanhua Huang, Weiying Lu, Yingpu Sun,

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Sai-Lan Liu, Xue-Song Sun, Li-Ting Liu, Rui Sun, Dong-Hua Luo, Qiu-Yan Chen, Huan-Xin Lin, Li Yuan, Lin-Quan Tang, Ling Guo, Hai-Qiang Mai,

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Ya-Nan Ou, Xue-Ning Shen, He-Ying Hu, Hao Hu, Zuo-Teng Wang, Wei Xu, Qiang Dong, Lan Tan, Jin-Tai Yu,

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Genfa Xiao, Tingjun Wang, Wei Zhuang, Chaoyi Ye, Li Luo, Huajun Wang, Guili Lian, Liangdi Xie,