Volume 12, Issue 7

Sex differences in out-of-hospital cardiac arrest

Iris Oving, Marieke T. Blom, Hanno L. Tan,

https://doi.org/10.18632/aging.102980 pp 5588—5589

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Oving I, Blom MT, Tan HL, . Sex differences in out-of-hospital cardiac arrest. . 12:5588-5589. https://doi.org/10.18632/aging.102980

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Down-regulation of AMPK signaling pathway rescues hearing loss in TFB1 transgenic mice and delays age-related hearing loss

Jingjing Zhao, Gen Li, Xuan Zhao, Xin Lin, Yunge Gao, Nuno Raimundo, Geng-Lin Li, Wei Shang, Hao Wu, Lei Song,

https://doi.org/10.18632/aging.102977 pp 5590—5611

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Zhao J, Li G, Zhao X, Lin X, Gao Y, Raimundo N, Li G, Shang W, Wu H, Song L, . Down-regulation of AMPK signaling pathway rescues hearing loss in TFB1 transgenic mice and delays age-related hearing loss. . 12:5590-5611. https://doi.org/10.18632/aging.102977

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Provider: 
                TY  - JOUR
                AU  - Zhao, Jingjing 
                AU  - Li, Gen 
                AU  - Zhao, Xuan 
                AU  - Lin, Xin 
                AU  - Gao, Yunge 
                AU  - Raimundo, Nuno 
                AU  - Li, Geng-Lin 
                AU  - Shang, Wei 
                AU  - Wu, Hao 
                AU  - Song, Lei 
                TI  - Down-regulation of AMPK signaling pathway rescues hearing loss in TFB1 transgenic mice and delays age-related hearing loss
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102977
                DO  - 10.18632/aging.102977
                SP  - 5590
                EP  - 5611
                PY  - 
                AB  - AMP-activated protein kinase (AMPK) integrates the regulation of cell growth and metabolism. AMPK activation occurs in response to cellular energy decline and mitochondrial dysfunction triggered by reactive oxygen species (ROS). In aged Tg-mtTFB1 mice, a mitochondrial deafness mouse model, hearing loss is accompanied with cochlear pathology including reduced endocochlear potential (EP) and loss of spiral ganglion neurons (SGN), inner hair cell (IHC) synapses and outer hair cells (OHC). Accumulated ROS and increased apoptosis signaling were also detected in cochlear tissues, accompanied by activation of AMPK. To further explore the role of AMPK signaling in the auditory phenotype, we used genetically knocked out AMPK&#x3B1;1 as a rescue to Tg-mtTFB1 mice and observed: improved ABR wave I, EP and IHC function, normal SGNs, IHC synapses morphology and OHC survivals, with decreased ROS, reduced pro-apoptotic signaling (Bax) and increased anti-apoptotic signaling (Bcl-2) in the cochlear tissues, indicating that reduced AMPK attenuated apoptosis via ROS-AMPK-Bcl2 pathway in the cochlea. To conclude, AMPK hyperactivation causes accelerated presbycusis in Tg-mtTFB1 mice by redox imbalance and dysregulation of the apoptosis pathway. The effects of AMPK downregulation on pro-survival function and reduction of oxidative stress indicate AMPK serves as a target to rescue or relieve mitochondrial hearing loss.
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Supraphysiological protection from replication stress does not extend mammalian lifespan

Eliene Albers, Alexandra Avram, Mauro Sbroggio, Oscar Fernandez-Capetillo, Andres J. Lopez-Contreras,

https://doi.org/10.18632/aging.103039 pp 5612—5624

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Albers E, Avram A, Sbroggio M, Fernandez-Capetillo O, Lopez-Contreras AJ, . Supraphysiological protection from replication stress does not extend mammalian lifespan. . 12:5612-5624. https://doi.org/10.18632/aging.103039

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                TY  - JOUR
                AU  - Albers, Eliene 
                AU  - Avram, Alexandra 
                AU  - Sbroggio, Mauro 
                AU  - Fernandez-Capetillo, Oscar 
                AU  - Lopez-Contreras, Andres J. 
                TI  - Supraphysiological protection from replication stress does not extend mammalian lifespan
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103039
                DO  - 10.18632/aging.103039
                SP  - 5612
                EP  - 5624
                PY  - 
                AB  - Replication Stress (RS) is a type of DNA damage generated at the replication fork, characterized by single-stranded DNA (ssDNA) accumulation, and which can be caused by a variety of factors. Previous studies have reported elevated RS levels in aged cells. In addition, mouse models with a deficient RS response show accelerated aging. However, the relevance of endogenous or physiological RS, compared to other sources of genomic instability, for the normal onset of aging is unknown. We have performed long term survival studies of transgenic mice with extra copies of the Chk1 and/or Rrm2 genes, which we previously showed extend the lifespan of a progeroid ATR-hypomorphic model suffering from high levels of RS. In contrast to their effect in the context of progeria, the lifespan of Chk1, Rrm2 and Chk1/Rrm2 transgenic mice was similar to WT littermates in physiological settings. Most mice studied died due to tumors -mainly lymphomas- irrespective of their genetic background. Interestingly, a higher but not statistically significant percentage of transgenic mice developed tumors compared to WT mice. Our results indicate that supraphysiological protection from RS does not extend lifespan, indicating that RS may not be a relevant source of genomic instability on the onset of normal aging.
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LncRNA 2310043L19Rik inhibits differentiation and promotes proliferation of myoblast by sponging miR-125a-5p

Rongyang Li, Bojiang Li, Ming Shen, Yan Cao, Xuan Zhang, Weijian Li, Jingli Tao, Wangjun Wu, Honglin Liu,

https://doi.org/10.18632/aging.102905 pp 5625—5639

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Li R, Li B, Shen M, Cao Y, Zhang X, Li W, Tao J, Wu W, Liu H, . LncRNA 2310043L19Rik inhibits differentiation and promotes proliferation of myoblast by sponging miR-125a-5p. . 12:5625-5639. https://doi.org/10.18632/aging.102905

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                TY  - JOUR
                AU  - Li, Rongyang 
                AU  - Li, Bojiang 
                AU  - Shen, Ming 
                AU  - Cao, Yan 
                AU  - Zhang, Xuan 
                AU  - Li, Weijian 
                AU  - Tao, Jingli 
                AU  - Wu, Wangjun 
                AU  - Liu, Honglin 
                TI  - LncRNA 2310043L19Rik inhibits differentiation and promotes proliferation of myoblast by sponging miR-125a-5p
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102905
                DO  - 10.18632/aging.102905
                SP  - 5625
                EP  - 5639
                PY  - 
                AB  - Although many long non-coding RNAs (lncRNAs) have been identified in muscle, some of their physiological functions and regulatory mechanisms remain elusive. Here we report the functional identification and characterization of a novel lncRNA 2310043L19Rik (lnc-231), which is highly expressed in muscle. The expression level of lnc-231 in skeletal muscle of young mice is higher than that in aged mice. Functional analysis showed that overexpression of lnc-231 restrained differentiation and promoted proliferation of myoblast, while inhibition of lnc-231 revealed completely opposite effects in vitro. RNA molecules of lnc-231 acted mechanistically as competing endogenous RNAs (ceRNA) to target miR-125a-5p, whereas miR-125a-5p binds to the 3&#x2019;-UTR of E2F3 mRNA to inhibit its function. Collectively, lncRNA 2310043L19Rik promotes proliferation and inhibits differentiation of myoblast cells by attenuating the function of miR-125a-5p.
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Inhibition of miR-19a partially reversed the resistance of colorectal cancer to oxaliplatin via PTEN/PI3K/AKT pathway

Ye Zhang, Xinxin Liu, Junying Zhang, Yuanyuan Xu, Jie Shao, Yue Hu, Peng Shu, Haibo Cheng,

https://doi.org/10.18632/aging.102929 pp 5640—5650

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Zhang Y, Liu X, Zhang J, Xu Y, Shao J, Hu Y, Shu P, Cheng H, . Inhibition of miR-19a partially reversed the resistance of colorectal cancer to oxaliplatin via PTEN/PI3K/AKT pathway. . 12:5640-5650. https://doi.org/10.18632/aging.102929

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                TY  - JOUR
                AU  - Zhang, Ye 
                AU  - Liu, Xinxin 
                AU  - Zhang, Junying 
                AU  - Xu, Yuanyuan 
                AU  - Shao, Jie 
                AU  - Hu, Yue 
                AU  - Shu, Peng 
                AU  - Cheng, Haibo 
                TI  - Inhibition of miR-19a partially reversed the resistance of colorectal cancer to oxaliplatin via PTEN/PI3K/AKT pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102929
                DO  - 10.18632/aging.102929
                SP  - 5640
                EP  - 5650
                PY  - 
                AB  - Oxaliplatin is a platinum-based chemotherapeutic drug that is effective and commonly used in the treatment of colorectal cancer (CRC). However, long-term use of oxaliplatin usually induces significant drug resistance. It is urgent to develop strategies to reverse the oxaliplatin resistance to CRC cells. In the present study, we established the model of oxaliplatin-resistant CRC cell lines (SW480/R and HT29/R) through continuous treatment of SW480 and HT29 cells with oxaliplatin. Results of qRT-PCR analysis showed that expression of miR-19a was significantly increased in SW480/R and HT29/R compared to their parental SW480 and HT29. However, combination treatment with anti-miR-19a, an antisense oligonucleotide of miR-19a, was found to resensitize SW480/R and HT29/R cells to oxaliplatin treatment. In the mechanism research, we found that anti-miR-19a increased the expression of PTEN and thus inhibited the phosphorylation of PI3K and AKT in SW480/R and HT29/R cells. As a result, mitochondrial apoptosis induced by oxaliplatin was expanded. We demonstrated that PTEN was the target of miR-19a and inhibition of miR-19a partially reversed the resistance of colorectal cancer to oxaliplatin via PTEN/PI3K/AKT pathway.
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Intermedin_1-53 attenuates aging-associated vascular calcification in rats by upregulating sirtuin 1

Yao Chen, Lin-Shuang Zhang, Jin-Ling Ren, Ya-Rong Zhang, Ning Wu, Mo-Zhi Jia, Yan-Rong Yu, Zhong-Ping Ning, Chao-Shu Tang, Yong-Fen Qi,

https://doi.org/10.18632/aging.102934 pp 5651—5674

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Chen Y, Zhang L, Ren J, Zhang Y, Wu N, Jia M, Yu Y, Ning Z, Tang C, Qi Y, . Intermedin_1-53 attenuates aging-associated vascular calcification in rats by upregulating sirtuin 1. . 12:5651-5674. https://doi.org/10.18632/aging.102934

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                TY  - JOUR
                AU  - Chen, Yao 
                AU  - Zhang, Lin-Shuang 
                AU  - Ren, Jin-Ling 
                AU  - Zhang, Ya-Rong 
                AU  - Wu, Ning 
                AU  - Jia, Mo-Zhi 
                AU  - Yu, Yan-Rong 
                AU  - Ning, Zhong-Ping 
                AU  - Tang, Chao-Shu 
                AU  - Qi, Yong-Fen 
                TI  - Intermedin<sub>1-53</sub> attenuates aging-associated vascular calcification in rats by upregulating sirtuin 1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102934
                DO  - 10.18632/aging.102934
                SP  - 5651
                EP  - 5674
                PY  - 
                AB  - Vascular calcification is a common phenomenon in older adults. Intermedin (IMD) is a cardiovascular bioactive peptide inhibiting vascular calcification. In this study, we aimed to investigate whether IMD1-53 attenuates aging-associated vascular calcification. Vascular calcification was induced by vitamin D3 plus nicotine (VDN) in young and old rats. The calcification in aortas was more severe in old rats treated with VDN than young control rats, and IMD expression was lower. Exogenous administration of IMD1-53 significantly inhibited the calcium deposition in aortas and the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) in VDN-treated old rats. Moreover, levels of aging-related p16, p21 and &#x3B2;-galactosidase were all greatly decreased by IMD1-53. These results were further confirmed in rat and human VSMCs in vitro. In addition, IMD-deficient mouse VSMCs showed senescence features coinciding with osteogenic transition as compared with wild-type mouse VSMCs. Mechanistically, IMD1-53 significantly increased the expression of the anti-aging factor sirtuin 1 (sirt1); the inhibitory effects of IMD1-53 on calcification and senescence were blocked by sirt1 knockdown. Furthermore, preincubation with inhibitors of PI3K, AMPK or PKA efficiently blunted the upregulatory effect of IMD1-53 on sirt1. Consequently, IMD1-53 could attenuate aging-associated vascular calcification by upregulating sirt1 via activating PI3K/Akt, AMPK and cAMP/PKA signaling.
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STAT5A induced LINC01198 promotes proliferation of glioma cells through stabilizing DGCR8

Cheng Tan, Yimeng Dai, Xiaoyang Liu, Guifang Zhao, Weiyao Wang, Jia Li, Ling Qi,

https://doi.org/10.18632/aging.102938 pp 5675—5692

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Tan C, Dai Y, Liu X, Zhao G, Wang W, Li J, Qi L, . STAT5A induced LINC01198 promotes proliferation of glioma cells through stabilizing DGCR8. . 12:5675-5692. https://doi.org/10.18632/aging.102938

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                TY  - JOUR
                AU  - Tan, Cheng 
                AU  - Dai, Yimeng 
                AU  - Liu, Xiaoyang 
                AU  - Zhao, Guifang 
                AU  - Wang, Weiyao 
                AU  - Li, Jia 
                AU  - Qi, Ling 
                TI  - STAT5A induced LINC01198 promotes proliferation of glioma cells through stabilizing DGCR8
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102938
                DO  - 10.18632/aging.102938
                SP  - 5675
                EP  - 5692
                PY  - 
                AB  - Background: LINC01198 has been suggested to be able to predict overall prognosis for glioma; however, it has been little described in glioma.Results: It was shown that LINC01198 was markedly enriched in neoplasmic tissues relative to normal controls; and that elevated LINC01198 significantly correlated with unfavorable overall prognosis. Moreover, activation of STAT5A, identified as transcription factor (TF), can induce the expression of LINC01198. DGCR8, a kind of RNA-binding proteins (RBPs), was identified to be able to bind with LINC01198 that can stabilize the DGCR8. Five differential miRNAs with most significant difference, including miR-21-5p, miR-34-5p, miR-1246, miR-4488 and miR-494, were obtainable after silencing of DGCR8.Conclusions: Together, the data we presented here suggested that STAT5 induced LINC01198 promotes proliferation and motility of glioma cells through stabilizing DGCR8 in glioma cells.Methods: Expression of LINC01198 was appraised by quantitative PCR (qPCR) and in situ hybridization (ISH) in glioma clinical specimens, totaling 100 cases. Post hoc statistical analysis was conducted. In vitro, LINC01198 was stably silenced or re-expressed by transfection with lentiviral-based vectors. Chromatin-immunoprecipitation (CHIP) was applied to identify the relevant TFs that can bind with LINC01198, which was corroborated with electrophoretic mobility shift (EMSA) assay. RNA-immunoprecipitation (RIP) was used to identify the RNA-binding protein that can bind with LINC01198. Moreover, miRNA microarray was used to screen out differential miRNAs after silencing of DGCR8.
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Indian Hedgehog regulates senescence in bone marrow-derived mesenchymal stem cell through modulation of ROS/mTOR/4EBP1, p70S6K1/2 pathway

Mahmoud Al-Azab, Bing Wang, Abdalkhalig Elkhider, Williams Walana, Weiping Li, Bo Yuan, Yunshan Ye, Yawei Tang, Marwan Almoiliqy, Salah Adlat, Jing Wei, Yan Zhang, Xia Li,

https://doi.org/10.18632/aging.102958 pp 5693—5715

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Al-Azab M, Wang B, Elkhider A, Walana W, Li W, Yuan B, Ye Y, Tang Y, Almoiliqy M, Adlat S, Wei J, Zhang Y, Li X, . Indian Hedgehog regulates senescence in bone marrow-derived mesenchymal stem cell through modulation of ROS/mTOR/4EBP1, p70S6K1/2 pathway. . 12:5693-5715. https://doi.org/10.18632/aging.102958

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                TY  - JOUR
                AU  - Al-Azab, Mahmoud 
                AU  - Wang, Bing 
                AU  - Elkhider, Abdalkhalig 
                AU  - Walana, Williams 
                AU  - Li, Weiping 
                AU  - Yuan, Bo 
                AU  - Ye, Yunshan 
                AU  - Tang, Yawei 
                AU  - Almoiliqy, Marwan 
                AU  - Adlat, Salah 
                AU  - Wei, Jing 
                AU  - Zhang, Yan 
                AU  - Li, Xia 
                TI  - Indian Hedgehog regulates senescence in bone marrow-derived mesenchymal stem cell through modulation of ROS/mTOR/4EBP1, p70S6K1/2 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102958
                DO  - 10.18632/aging.102958
                SP  - 5693
                EP  - 5715
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Al-Azab, Mahmoud 
                AU  - Wang, Bing 
                AU  - Elkhider, Abdalkhalig 
                AU  - Walana, Williams 
                AU  - Li, Weiping 
                AU  - Yuan, Bo 
                AU  - Ye, Yunshan 
                AU  - Tang, Yawei 
                AU  - Almoiliqy, Marwan 
                AU  - Adlat, Salah 
                AU  - Wei, Jing 
                AU  - Zhang, Yan 
                AU  - Li, Xia 
                TI  - Indian Hedgehog regulates senescence in bone marrow-derived mesenchymal stem cell through modulation of ROS/mTOR/4EBP1, p70S6K1/2 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102958
                DO  - 10.18632/aging.102958
                SP  - 5693
                EP  - 5715
                PY  - 
                AB  - Premature senescence of bone marrow-derived mesenchymal stem cells (BMSC) remains a major concern for their application clinically. Hedgehog signaling has been reported to regulate aging-associated markers and MSC skewed differentiation. Indian Hedgehog (IHH) is a ligand of Hedgehog intracellular pathway considered as an inducer in chondrogenesis of human BMSC. However, the role of IHH in the aging of BMSC is still unclear. This study explored the role IHH in the senescence of BMSC obtained from human samples and senescent mice. Isolated BMSC were transfected with IHH siRNA or incubated with exogenous IHH protein and the mechanisms of aging and differentiation investigated. Moreover, the interactions between IHH, and mammalian target of rapamycin (mTOR) and reactive oxygen species (ROS) were evaluated using the corresponding inhibitors and antioxidants. BMSC transfected with IHH siRNA showed characteristics of senescence-associated features including increased senescence-associated &#x3B2;-galactosidase activity (SA-&#x3B2;-gal), induction of cell cycle inhibitors (p53/p16), development of senescence-associated secretory phenotype (SASP), activation of ROS and mTOR pathways as well as the promotion of skewed differentiation. Interestingly, BMSC treatment with IHH protein reversed the senescence markers and corrected biased differentiation. Moreover, IHH shortage-induced senescence signs were compromised after mTOR and ROS inhibition. Our findings presented anti-aging activity for IHH in BMSC through down-regulation of ROS/mTOR pathways. This discovery might contribute to increasing the therapeutic, immunomodulatory and regenerative potency of BMSC and introduce a novel remedy in the management of aging-related diseases.
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Ube2s-stabilized β-catenin protects against myocardial ischemia/reperfusion injury by activating HIF-1α signaling

Xi Chen, Chiyao Wang, Pei Yang, Lei Shi, Haiyan Wang,

https://doi.org/10.18632/aging.102960 pp 5716—5732

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Chen X, Wang C, Yang P, Shi L, Wang H, . Ube2s-stabilized β-catenin protects against myocardial ischemia/reperfusion injury by activating HIF-1α signaling. . 12:5716-5732. https://doi.org/10.18632/aging.102960

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                TY  - JOUR
                AU  - Chen, Xi 
                AU  - Wang, Chiyao 
                AU  - Yang, Pei 
                AU  - Shi, Lei 
                AU  - Wang, Haiyan 
                TI  - Ube2s-stabilized β-catenin protects against myocardial ischemia/reperfusion injury by activating HIF-1α signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102960
                DO  - 10.18632/aging.102960
                SP  - 5716
                EP  - 5732
                PY  - 
                AB  - The activation of hypoxia-inducible factor (HIF) is an important event for mediating the adaptive response to myocardial ischemia/reperfusion (MI/R) injury. The ubiquitin-conjugating enzyme E2S (Ube2s) catalyzes ubiquitin conjugation to target proteins. Here, we report the positive regulation of HIF-1&#x3B1; signaling by Ube2s via stabilizing &#x3B2;-catenin, by which Ube2s acts to protect against MI/R injury. We show that Ube2s expression is upregulated in the hearts of mice subjected to MI/R injury. Functionally, Ube2s depletion exacerbates and its overexpression ameliorates MI/R injury. In addition, Ube2s augments the activation of HIF-1&#x3B1; and reduces myocardial apoptosis. Moreover, Ube2s induces the accumulation of &#x3B2;-Catenin through increasing its stabilization. Importantly, &#x3B2;-Catenin knockdown abrogates Ube2s-augmented HIF-1&#x3B1; activation, and meanwhile, diminishes the protective effect of Ube2s on MI/R injury, thus establishing a causal link between Ube2s-stabilized &#x3B2;-catenin and HIF-1&#x3B1;-mediated myocardial protection. Altogether, this study identifies the Ube2s/&#x3B2;-catenin/HIF-1&#x3B1; axis as a novel protective regulator involved in MI/R injury, and also implies that it might represent a potential therapeutic target for ameliorating MI/R injury.
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Immune gene signature delineates a subclass of thyroid cancer with unfavorable clinical outcomes

Jingtai Zhi, Jiaoyu Yi, Mengran Tian, Huijuan Wang, Ning Kang, Xiangqian Zheng, Ming Gao,

https://doi.org/10.18632/aging.102963 pp 5733—5750

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Zhi J, Yi J, Tian M, Wang H, Kang N, Zheng X, Gao M, . Immune gene signature delineates a subclass of thyroid cancer with unfavorable clinical outcomes. . 12:5733-5750. https://doi.org/10.18632/aging.102963

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                TY  - JOUR
                AU  - Zhi, Jingtai 
                AU  - Yi, Jiaoyu 
                AU  - Tian, Mengran 
                AU  - Wang, Huijuan 
                AU  - Kang, Ning 
                AU  - Zheng, Xiangqian 
                AU  - Gao, Ming 
                TI  - Immune gene signature delineates a subclass of thyroid cancer with unfavorable clinical outcomes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102963
                DO  - 10.18632/aging.102963
                SP  - 5733
                EP  - 5750
                PY  - 
                AB  - Thyroid cancer (THCA) is a heterogeneous disease with multiple clinical outcomes Immune cells regulate its progression. Three immunomolecular subtypes (C1, C2, C3) were identified in gene expression data sets from TCGA and GEO databases. Among them, subtype C3 had highest frequency of BRAF mutations, lowest frequency of RAS mutations, highest mutation load and shorter progression-free survival. Functional enrichment analysis for the genes revealed that C1 was up-regulated in the ERK cascade pathway, C2 was up-regulated in cell migration and proliferation pathways, while C3 was enriched in body fluid, protein regulation and response to steroid hormones functions. Notably, the three molecular subtypes exhibit differences in immune microenvironments as shown by timer database and analysis of immune expression signatures. The abundance of B_cell, CD4_Tcell, Neutrophil, Macrophage and Dendritic cells in C2 subtype were lower than in C1 and C3 subtypes Leukocyte fraction, proliferation macrophage regulation, lymphocyte infiltration, IFN gamma response and TGF beta response scores were significantly higher in C3 compared with C1 and C2 subtypes. Unlike C3 subtype, it was observed that C1 and C2 subtypes were significantly negatively correlated with most immune checkpoint genes in two different cohorts. The characteristic genes were differentially expressed between cancer cells, adjacent tissues, and metastatic tissues in different cohorts. In summary, THCA can be subclassified into three molecular subtypes with distinct histological types, genetic and transcriptional phenotypes, all of which have potential clinical implications.
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Molecular anatomy of the subcellular localization and nuclear import mechanism of herpes simplex virus 1 UL6

Mingsheng Cai, Xiaowen Ou, Yiwen Li, Xingmei Zou, Zuo Xu, Yuanfang Wang, Hao Peng, Yangxi Deng, Yingjie Guo, Manjiao Lu, Weidong Gan, Tao Peng, Meili Li,

https://doi.org/10.18632/aging.102965 pp 5751—5763

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Cai M, Ou X, Li Y, Zou X, Xu Z, Wang Y, Peng H, Deng Y, Guo Y, Lu M, Gan W, Peng T, Li M, . Molecular anatomy of the subcellular localization and nuclear import mechanism of herpes simplex virus 1 UL6. . 12:5751-5763. https://doi.org/10.18632/aging.102965

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                TY  - JOUR
                AU  - Cai, Mingsheng 
                AU  - Ou, Xiaowen 
                AU  - Li, Yiwen 
                AU  - Zou, Xingmei 
                AU  - Xu, Zuo 
                AU  - Wang, Yuanfang 
                AU  - Peng, Hao 
                AU  - Deng, Yangxi 
                AU  - Guo, Yingjie 
                AU  - Lu, Manjiao 
                AU  - Gan, Weidong 
                AU  - Peng, Tao 
                AU  - Li, Meili 
                TI  - Molecular anatomy of the subcellular localization and nuclear import mechanism of herpes simplex virus 1 UL6
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102965
                DO  - 10.18632/aging.102965
                SP  - 5751
                EP  - 5763
                PY  - 
                AB  - As an indispensable structure protein, the herpes simplex virus 1 (HSV-1) UL6 has been described to exert numerous roles in viral proliferation. However, its exact subcellular localization and subcellular transport mechanism is not well known. In the present study, by utilizing confocal fluorescent microscopy, UL6 was shown to mainly locate in the nucleus in enhanced yellow fluorescent protein or Flag tag fused expression plasmid-transfected cells or HSV-1-infected cells, whereas its predicted nuclear localization signal was nonfunctional. In addition, by exploiting dominant negative mutant and inhibitor of different nuclear import receptors, as well as co-immunoprecipitation and RNA interference assays, UL6 was established to interact with importin &#x3B1;1, importin &#x3B1;7 and transportin-1 to mediate its nuclear translocation under the help of Ran-mediated GTP hydrolysis. Accordingly, these results will advance the knowledge of UL6-mediated biological significances in HSV-1 infection cycle.
                ER  -

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CK1δ as a potential therapeutic target to treat bladder cancer

Yu-Chen Lin, Mei-Chuan Chen, Tsung-Han Hsieh, Jing-Ping Liou, Chun-Han Chen,

https://doi.org/10.18632/aging.102966 pp 5764—5780

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Lin Y, Chen M, Hsieh T, Liou J, Chen C, . CK1δ as a potential therapeutic target to treat bladder cancer. . 12:5764-5780. https://doi.org/10.18632/aging.102966

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                TY  - JOUR
                AU  - Lin, Yu-Chen 
                AU  - Chen, Mei-Chuan 
                AU  - Hsieh, Tsung-Han 
                AU  - Liou, Jing-Ping 
                AU  - Chen, Chun-Han 
                TI  - CK1δ as a potential therapeutic target to treat bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102966
                DO  - 10.18632/aging.102966
                SP  - 5764
                EP  - 5780
                PY  - 
                AB  - Bladder cancer is the second most common genitourinary malignancy in the world. However, only immune-checkpoint inhibitors and erdafitinib are available to treat advanced bladder cancer. Our previous study reported that 4-((4-(4-ethylpiperazin-1-yl) phenyl)amino)-N-(3,4,5-trichlorophenyl)-7H-pyrrolo-[2, 3-d]pyrimidine-7-carboxamide hydrochloride (13i HCl) is a potent CK1&#x3B4; inhibitor showing significant anti-bladder cancer activity. In this study, we elucidated the pharmacological mechanisms underlying 13i HCl&#x2019;s inhibition of human bladder cancer. Our results demonstrate that expression of the CSNK1D gene, which codes for CK1&#x3B4;, is upregulated in superficial and infiltrating bladder cancer patients in two independent datasets. CK1&#x3B4; knockdown decreased &#x3B2;-catenin expression in bladder cancer cells and inhibited their growth. Additionally, 13i HCl suppressed bladder cancer cell proliferation and increased apoptosis. We also observed that inhibition of CK1&#x3B4; using 13i HCl or PF-670462 triggers necroptosis in bladder cancer cells. Finally, 13i HCl inhibited bladder cancer cell migration and reversed their mesenchymal characteristics. These findings suggest further development of 13i HCl as a potential therapeutic agent to treat bladder cancer is warranted.
                ER  -

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A novel germline gain-of-function HIF2A mutation in hepatocellular carcinoma with polycythemia

Jiong Yu, Xiaowei Shi, Chunzhang Yang, Petra Bullova, Christopher S. Hong, Cody L. Nesvick, Pauline Dmitriev, Karel Pacak, Zhengping Zhuang, Hongcui Cao, Lanjuan Li,

https://doi.org/10.18632/aging.102967 pp 5781—5791

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Yu J, Shi X, Yang C, Bullova P, Hong CS, Nesvick CL, Dmitriev P, Pacak K, Zhuang Z, Cao H, Li L, . A novel germline gain-of-function HIF2A mutation in hepatocellular carcinoma with polycythemia. . 12:5781-5791. https://doi.org/10.18632/aging.102967

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                TY  - JOUR
                AU  - Yu, Jiong 
                AU  - Shi, Xiaowei 
                AU  - Yang, Chunzhang 
                AU  - Bullova, Petra 
                AU  - Hong, Christopher S. 
                AU  - Nesvick, Cody L. 
                AU  - Dmitriev, Pauline 
                AU  - Pacak, Karel 
                AU  - Zhuang, Zhengping 
                AU  - Cao, Hongcui 
                AU  - Li, Lanjuan 
                TI  - A novel germline gain-of-function HIF2A mutation in hepatocellular carcinoma with polycythemia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102967
                DO  - 10.18632/aging.102967
                SP  - 5781
                EP  - 5791
                PY  - 
                AB  - Hypoxia-inducible factors (HIFs) regulate oxygen sensing and expression of genes involved in angiogenesis and erythropoiesis. Polycythemia has been observed in patients with hepatocellular carcinoma (HCC), but the underlying molecular basis remains unknown. Liver tissues from 302 HCC patients, including 104 with polycythemia, were sequenced for HIF2A mutations. A germline HIF2A mutation was detected in one HCC patient with concurrent polycythemia. Three additional family members carried this mutation, but none exhibited polycythemia or were diagnosed with HCC. The gain-of-function mutation resulted in a HIF-2&#x3B1; protein that was transcribed normally but resistant to degradation. HIF-2&#x3B1; target genes EDN1, EPO, GNA14, and VEGF were significantly upregulated in the tumor bed but not in the surrounding liver tissue. Polycythemia resolved upon total resection of the tumor tissue. This newly described HIF2A mutation may promote HCC oncogenesis.
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Decitabine in combination with low-dose cytarabine, aclarubicin and G-CSF tends to improve prognosis in elderly patients with high-risk AML

Ming Hong, Han Zhu, Qian Sun, Yu Zhu, Yi Miao, Hui Yang, Hai-Rong Qiu, Jian-Yong Li, Si-Xuan Qian,

https://doi.org/10.18632/aging.102973 pp 5792—5811

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Hong M, Zhu H, Sun Q, Zhu Y, Miao Y, Yang H, Qiu H, Li J, Qian S, . Decitabine in combination with low-dose cytarabine, aclarubicin and G-CSF tends to improve prognosis in elderly patients with high-risk AML. . 12:5792-5811. https://doi.org/10.18632/aging.102973

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                TY  - JOUR
                AU  - Hong, Ming 
                AU  - Zhu, Han 
                AU  - Sun, Qian 
                AU  - Zhu, Yu 
                AU  - Miao, Yi 
                AU  - Yang, Hui 
                AU  - Qiu, Hai-Rong 
                AU  - Li, Jian-Yong 
                AU  - Qian, Si-Xuan 
                TI  - Decitabine in combination with low-dose cytarabine, aclarubicin and G-CSF tends to improve prognosis in elderly patients with high-risk AML
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102973
                DO  - 10.18632/aging.102973
                SP  - 5792
                EP  - 5811
                PY  - 
                AB  - We evaluated the risk status and survival outcomes of 125 elderly acute myeloid leukemia (AML) patients treated with decitabine in combination with low-dose cytarabine, aclarubicin, and G-CSF (D-CAG). The risk status was evaluated by determining the frequency of recurring gene mutations using next-generation sequencing (NGS) analysis of 23 selected genes and cytogenetic profiling of bone marrow samples at diagnosis. After a median follow-up of 12 months (range: 2-82 months), 86 patients (68.8%) had achieved complete remission after one cycle of induction, and 94 patients (75.2%) had achieved it after two cycles. The median overall survival (OS) and disease-free survival (DFS) were 16 and 12 months, respectively. In 21 AML patients aged above 75 years, the median OS and DFS were longer in the low- and intermediate-risk group than the high-risk group, but the differences were not statistically significant. The median OS and DFS were similar in patients with or without TET2, DNMT3A, IDH2, TP53 and FLT3 mutations. Multivariate analysis showed that patient age above 75 years, high-risk status, and genetic anomalies, like deletions in chromosomes 5 and/or 7, were significant variables in predicting OS. D-CAG regimen tends to improve the prognosis of a subgroup of elderly patients with high-risk AML.
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Klotho antagonizes pulmonary fibrosis through suppressing pulmonary fibroblasts activation, migration, and extracellular matrix production: a therapeutic implication for idiopathic pulmonary fibrosis

Qiqing Huang, Yan Chen, Shaoran Shen, Yuanyuan Wang, Liya Liu, Shuangshuang Wu, Wei Xu, Weihong Zhao, Mingyan Lin, Jianqing Wu,

https://doi.org/10.18632/aging.102978 pp 5812—5831

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Huang Q, Chen Y, Shen S, Wang Y, Liu L, Wu S, Xu W, Zhao W, Lin M, Wu J, . Klotho antagonizes pulmonary fibrosis through suppressing pulmonary fibroblasts activation, migration, and extracellular matrix production: a therapeutic implication for idiopathic pulmonary fibrosis. . 12:5812-5831. https://doi.org/10.18632/aging.102978

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                TY  - JOUR
                AU  - Huang, Qiqing 
                AU  - Chen, Yan 
                AU  - Shen, Shaoran 
                AU  - Wang, Yuanyuan 
                AU  - Liu, Liya 
                AU  - Wu, Shuangshuang 
                AU  - Xu, Wei 
                AU  - Zhao, Weihong 
                AU  - Lin, Mingyan 
                AU  - Wu, Jianqing 
                TI  - Klotho antagonizes pulmonary fibrosis through suppressing pulmonary fibroblasts activation, migration, and extracellular matrix production: a therapeutic implication for idiopathic pulmonary fibrosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102978
                DO  - 10.18632/aging.102978
                SP  - 5812
                EP  - 5831
                PY  - 
                AB  - Idiopathic pulmonary fibrosis (IPF) has been widely accepted as an aging-related fatal lung disease with a therapeutic impasse, largely a consequence of the complex and polygenic gene architecture underlying the molecular pathology of IPF. Here, by conducting an integrative network analysis on the largest IPF case-control RNA-seq dataset to date, we attributed the systems-level alteration in IPF to disruptions in a handful of biological processes including cell migration, transforming growth factor-&#x3B2; (TGF-&#x3B2;) signaling and extracellular matrix (ECM), and identified klotho (KL), a typical anti-aging molecule, as a potential master regulator of those disease-relevant processes. Following experiments showed reduced Kl in isolated pulmonary fibroblasts from bleomycin-exposed mice, and demonstrated that recombinant KL effectively mitigated pulmonary fibrosis in an ex vivo model and alleviated TGF-&#x3B2;-induced pulmonary fibroblasts activation, migration, and ECM production in vitro, which was partially ascribed to FOXF1 and CAV1, two highly co-expressed genes of KL in the IPF. Overall, KL appears to be a vital regulator during pulmonary fibrosis. Given that administration of exogenous KL is a feasible treatment strategy, our work highlighted a promising target gene that could be easily manipulated, leaving the field well placed to further explore the therapeutic potential of KL for IPF.
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Development of a prognostic index and screening of potential biomarkers based on immunogenomic landscape analysis of colorectal cancer

Kang Lin, Jun Huang, Hongliang Luo, Chen Luo, Xiaojian Zhu, Fanqin Bu, Han Xiao, Li Xiao, Zhengming Zhu,

https://doi.org/10.18632/aging.102979 pp 5832—5857

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Lin K, Huang J, Luo H, Luo C, Zhu X, Bu F, Xiao H, Xiao L, Zhu Z, . Development of a prognostic index and screening of potential biomarkers based on immunogenomic landscape analysis of colorectal cancer. . 12:5832-5857. https://doi.org/10.18632/aging.102979

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                TY  - JOUR
                AU  - Lin, Kang 
                AU  - Huang, Jun 
                AU  - Luo, Hongliang 
                AU  - Luo, Chen 
                AU  - Zhu, Xiaojian 
                AU  - Bu, Fanqin 
                AU  - Xiao, Han 
                AU  - Xiao, Li 
                AU  - Zhu, Zhengming 
                TI  - Development of a prognostic index and screening of potential biomarkers based on immunogenomic landscape analysis of colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102979
                DO  - 10.18632/aging.102979
                SP  - 5832
                EP  - 5857
                PY  - 
                AB  - Background: Colorectal cancer (CRC) accounts for the highest fatality rate among all malignant tumors. Immunotherapy has shown great promise in management of many malignant tumors, necessitating the need to explore its role in CRC.Results: Our analysis revealed a total of 71 differentially expressed IRGs, that were associated with prognosis of CRC patients. Ten IRGs (FABP4, IGKV1-33, IGKV2D-40, IGLV6-57, NGF, RETNLB, UCN, VIP, NGFR, and OXTR) showed high prognostic performance in predicting CRC outcomes, and were further associated with tumor burden, metastasis, tumor TNM stage, gender, age, and pathological stage. Interestingly, the IRG-based prognostic index (IRGPI) reflected infiltration of multiple immune cell types.Conclusions: This model provides an effective approach for stratification and characterization of patients using IRG-based immunolabeling tools to monitor prognosis of CRC.Methods: We performed a comprehensive analysis of expression profiles for immune-related genes (IRGs) and overall survival time in 437 CRC patients from the TCGA database. We employed computational algorithms and Cox regression analysis to estimate the relationship between differentially expressed IRGs and survival rates in CRC patients. Furthermore, we investigated the mechanisms of action of the IRGs involved in CRC, and established a novel prognostic index based on multivariate Cox models.
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Renin-angiotensin-aldosterone system blockade is associated with higher risk of contrast-induced acute kidney injury in patients with diabetes

Mengqing Ma, Xin Wan, Min Gao, Binbin Pan, Dawei Chen, Qing Sun, Mengyu Zhang, Changgao Zhou, Tao Li, Hanchao Pan, Wei Shao, Zhihe Liu, Yue Chen, Changchun Cao,

https://doi.org/10.18632/aging.102982 pp 5858—5877

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Ma M, Wan X, Gao M, Pan B, Chen D, Sun Q, Zhang M, Zhou C, Li T, Pan H, Shao W, Liu Z, Chen Y, et al, . Renin-angiotensin-aldosterone system blockade is associated with higher risk of contrast-induced acute kidney injury in patients with diabetes. . 12:5858-5877. https://doi.org/10.18632/aging.102982

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                TY  - JOUR
                AU  - Ma, Mengqing 
                AU  - Wan, Xin 
                AU  - Gao, Min 
                AU  - Pan, Binbin 
                AU  - Chen, Dawei 
                AU  - Sun, Qing 
                AU  - Zhang, Mengyu 
                AU  - Zhou, Changgao 
                AU  - Li, Tao 
                AU  - Pan, Hanchao 
                AU  - Shao, Wei 
                AU  - Liu, Zhihe 
                AU  - Chen, Yue 
                AU  - Cao, Changchun 
                TI  - Renin-angiotensin-aldosterone system blockade is associated with higher risk of contrast-induced acute kidney injury in patients with diabetes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102982
                DO  - 10.18632/aging.102982
                SP  - 5858
                EP  - 5877
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ma, Mengqing 
                AU  - Wan, Xin 
                AU  - Gao, Min 
                AU  - Pan, Binbin 
                AU  - Chen, Dawei 
                AU  - Sun, Qing 
                AU  - Zhang, Mengyu 
                AU  - Zhou, Changgao 
                AU  - Li, Tao 
                AU  - Pan, Hanchao 
                AU  - Shao, Wei 
                AU  - Liu, Zhihe 
                AU  - Chen, Yue 
                AU  - Cao, Changchun 
                TI  - Renin-angiotensin-aldosterone system blockade is associated with higher risk of contrast-induced acute kidney injury in patients with diabetes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102982
                DO  - 10.18632/aging.102982
                SP  - 5858
                EP  - 5877
                PY  - 
                AB  - As the incidence of diabetes and cardiovascular comorbidities continues to rise, driven by increased prevalence of obesity and an aging population, so does the demand for percutaneous coronary intervention (PCI) to restore cardiac blood flow. Renin-angiotensin-aldosterone system (RAAS) inhibitors are commonly prescribed to hypertensive diabetic patients to prevent diabetic nephropathy. However, evidence suggests that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) may increase the risk of contrast-induced acute kidney injury (CIAKI) following coronary angiography (CAG) and PCI. We therefore conducted a retrospective, multicenter study applying the propensity score matching method to evaluate the impact of RAAS inhibition on CIAKI in diabetic patients undergoing CAG/PCI. Among 2240 subjects that met the inclusion criteria, 704 patients in the ACEIs/ARBs group were successfully matched to eligible control patients. The incidence of CIAKI (serum creatinine increase &#x2265;0.5 mg/dl or &#x2265;25% from baseline within 72 h post-CAG/PCI) was significantly higher in the ACEIs/ARBs group than in the control group (26.6% vs. 16.2%, P&lt;0.001). However, control patients showed increased risk of overall adverse cardiovascular events (4.1% vs. 1.8% for ACEIs/ARBs; P=0.016). These data indicate that RAAS inhibition increases the risk of CIAKI in diabetic patients, but confers protection against early cardiovascular events.
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Survival-associated alternative splicing signatures in non-small cell lung cancer

Deze Zhao, Chuantao Zhang, Man Jiang, Yongjie Wang, Yu Liang, Li Wang, Kang Qin, Faisal UL Rehman, Xiaochun Zhang,

https://doi.org/10.18632/aging.102983 pp 5878—5893

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Zhao D, Zhang C, Jiang M, Wang Y, Liang Y, Wang L, Qin K, Rehman FU, Zhang X, . Survival-associated alternative splicing signatures in non-small cell lung cancer. . 12:5878-5893. https://doi.org/10.18632/aging.102983

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                TY  - JOUR
                AU  - Zhao, Deze 
                AU  - Zhang, Chuantao 
                AU  - Jiang, Man 
                AU  - Wang, Yongjie 
                AU  - Liang, Yu 
                AU  - Wang, Li 
                AU  - Qin, Kang 
                AU  - Rehman, Faisal UL 
                AU  - Zhang, Xiaochun 
                TI  - Survival-associated alternative splicing signatures in non-small cell lung cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102983
                DO  - 10.18632/aging.102983
                SP  - 5878
                EP  - 5893
                PY  - 
                AB  - Alternative splicing (AS) is fundamental to transcriptome and proteome richness, and data from recent studies suggested a critical association between AS and oncogenic processes. To date, no systematic analysis has been conducted on AS from the perspective of different sexes and subtypes in non-small-cell lung cancer (NSCLC). Thus, we integrated the information of NSCLC patients from The Cancer Genome Atlas (TCGA) and evaluated AS profiles from the perspectives of sex and subtype. Eventually, a total of 813 and 1020 AS events were found to be significantly related to the overall survival (OS) of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) patients. Four prognostic prediction models performed well at 1, 3, and 5 years, with an area under the receiver operating characteristic (ROC) curve (AUC) greater than 0.75. Notably, we explored the upstream splicing factors (SFs) and downstream regulatory mechanisms of the OS-associated AS events and verified four differentially expressed alternative splicing (DEAS) events via qPCR. These findings can provide important guidance for subsequent studies. In addition, we also constructed nomograms to facilitate early screening by clinicians and to determine patient outcomes in NSCLC.
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Risk of breast cancer-related death in women with a prior cancer

Fei Ji, Ci-Qiu Yang, Xiao-Ling Li, Liu-Lu Zhang, Mei Yang, Jie-Qing Li, Hong-Fei Gao, Teng Zhu, Min-Yi Cheng, Wei-Ping Li, Si-Yan Wu, Ai-Ling Zhong, Kun Wang,

https://doi.org/10.18632/aging.102984 pp 5894—5906

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Ji F, Yang C, Li X, Zhang L, Yang M, Li J, Gao H, Zhu T, Cheng M, Li W, Wu S, Zhong A, Wang K, . Risk of breast cancer-related death in women with a prior cancer. . 12:5894-5906. https://doi.org/10.18632/aging.102984

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                TY  - JOUR
                AU  - Ji, Fei 
                AU  - Yang, Ci-Qiu 
                AU  - Li, Xiao-Ling 
                AU  - Zhang, Liu-Lu 
                AU  - Yang, Mei 
                AU  - Li, Jie-Qing 
                AU  - Gao, Hong-Fei 
                AU  - Zhu, Teng 
                AU  - Cheng, Min-Yi 
                AU  - Li, Wei-Ping 
                AU  - Wu, Si-Yan 
                AU  - Zhong, Ai-Ling 
                AU  - Wang, Kun 
                TI  - Risk of breast cancer-related death in women with a prior cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102984
                DO  - 10.18632/aging.102984
                SP  - 5894
                EP  - 5906
                PY  - 
                AB  - The overall risk of developing a second primary cancer is increasing. The purpose of this study was to analyze the survival of patients with breast cancer diagnosed after a prior cancer and identify risk factors of breast cancer death in this population. Using the SEER database, we identified 1,310 woman diagnosed with breast cancer between 2010 and 2015 after a prior cancer as the primary cohort. Clinicopathological characteristics were compared using the Student t-test and chi-square test. Fine and Gray&#x2019;s regression was used to evaluate the effect of treatments on breast cancer death. After propensity score matching (PSM), 9,845 pairs of patients with breast cancer as the prior or second cancer diagnosed between 2010 and 2011 were included as a second cohort. PSM-adjusted Kaplan-Meier and Cox hazards models were used to evaluate the impact of prior cancer on survival. The results showed that survivors of gynecologic cancers (e.g., ovarian cancer) had a higher risk of developing breast cancer than survivors of gastrointestinal and urinary tract cancers. More patients died of breast cancer than of prior urinary cancer (53.3% vs. 40%, P &lt; 0.05) and melanoma (66.7% vs. 33.3%, P &lt; 0.05). The ratio of breast cancer deaths to prior cancer deaths was significantly higher in patients with diagnoses interval &#x2265; 3 years than in those with the interval &lt; 3 years (2.67 vs. 0.69, P &lt; 0.001). Breast cancer-specific survival and overall survival rates were significantly lower in women with breast cancer as the second primary cancer than in those with breast cancer as the prior cancer, especially among hormone receptor-positive women. However, breast cancer treatment decreased the risk of breast cancer -specific death (hazard ratio = 0.695, 95% confidence interval: 0.586&#x2013;0.725, P &lt; 0.001). Breast cancer patients with prior cancers must be carefully considered for clinical trials.
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Increased intrinsic default-mode network activity as a compensatory mechanism in aMCI: a resting-state functional connectivity MRI study

Jiali Liang, Yunfei Li, Hao Liu, Sisi Zhang, Meimei Wang, Yonghua Chu, Jianping Ye, Qian Xi, Xiaohu Zhao,

https://doi.org/10.18632/aging.102986 pp 5907—5919

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Liang J, Li Y, Liu H, Zhang S, Wang M, Chu Y, Ye J, Xi Q, Zhao X, . Increased intrinsic default-mode network activity as a compensatory mechanism in aMCI: a resting-state functional connectivity MRI study. . 12:5907-5919. https://doi.org/10.18632/aging.102986

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                TY  - JOUR
                AU  - Liang, Jiali 
                AU  - Li, Yunfei 
                AU  - Liu, Hao 
                AU  - Zhang, Sisi 
                AU  - Wang, Meimei 
                AU  - Chu, Yonghua 
                AU  - Ye, Jianping 
                AU  - Xi, Qian 
                AU  - Zhao, Xiaohu 
                TI  - Increased intrinsic default-mode network activity as a compensatory mechanism in aMCI: a resting-state functional connectivity MRI study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102986
                DO  - 10.18632/aging.102986
                SP  - 5907
                EP  - 5919
                PY  - 
                AB  - Numerous studies have investigated the differences in the mean functional connectivity (FC) strength between amnestic mild cognitive impairment (aMCI) patients and normal subjects using resting-state functional magnetic resonance imaging. However, whether the mean FC is increased, decreased or unchanged in aMCI patients compared to normal controls remains unclear. Two factors might lead to inconsistent results: the determination of regions of interest and the reliability of the FC.We explored differences in FC and the degree centrality (Dc) constructed by the bootstrap method, between and within networks (default-mode network (DN), frontoparietal control network (CN), dorsal attention network (AN)), and resulting from a hierarchical-clustering algorithm.The mean FC within the DN and CN was significantly increased (P &lt; 0.05, uncorrected) in patients. Significant increases (P &lt; 0.05, uncorrected) in the mean FC were found in patients between DN and CN and between DN and AN. Five pairs of FC (false discovery rate corrected) and the Dc of six regions (Bonferroni corrected) displayed a significant increase in patients. Lower cognitive ability was significantly associated with a greater increase in the Dc of the left superior temporal sulcus.Our results demonstrate that the early dysfunctions in aMCI disease are mainly compensatory impairments.
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Genetics of physiological dysregulation: findings from the long life family study using joint models

Konstantin G. Arbeev, Olivia Bagley, Svetlana V. Ukraintseva, Deqing Wu, Hongzhe Duan, Alexander M. Kulminski, Eric Stallard, Kaare Christensen, Joseph H. Lee, Bharat Thyagarajan, Joseph M. Zmuda, Anatoliy I. Yashin,

https://doi.org/10.18632/aging.102987 pp 5920—5947

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Arbeev KG, Bagley O, Ukraintseva SV, Wu D, Duan H, Kulminski AM, Stallard E, Christensen K, Lee JH, Thyagarajan B, Zmuda JM, Yashin AI, . Genetics of physiological dysregulation: findings from the long life family study using joint models. . 12:5920-5947. https://doi.org/10.18632/aging.102987

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                TY  - JOUR
                AU  - Arbeev, Konstantin G. 
                AU  - Bagley, Olivia 
                AU  - Ukraintseva, Svetlana V. 
                AU  - Wu, Deqing 
                AU  - Duan, Hongzhe 
                AU  - Kulminski, Alexander M. 
                AU  - Stallard, Eric 
                AU  - Christensen, Kaare 
                AU  - Lee, Joseph H. 
                AU  - Thyagarajan, Bharat 
                AU  - Zmuda, Joseph M. 
                AU  - Yashin, Anatoliy I. 
                TI  - Genetics of physiological dysregulation: findings from the long life family study using joint models
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102987
                DO  - 10.18632/aging.102987
                SP  - 5920
                EP  - 5947
                PY  - 
                AB  - Recently, Mahalanobis distance (DM) was suggested as a statistical measure of physiological dysregulation in aging individuals. We constructed DM variants using sets of biomarkers collected at the two visits of the Long Life Family Study (LLFS) and performed joint analyses of longitudinal observations of DM and follow-up mortality in LLFS using joint models. We found that DM is significantly associated with mortality (hazard ratio per standard deviation: 1.31 [1.16, 1.48] to 2.22 [1.84, 2.67]) after controlling for age and other covariates. GWAS of random intercepts and slopes of DM estimated from joint models found a genome-wide significant SNP (rs12652543, p=7.2&#xD7;10-9) in the TRIO gene associated with the slope of DM constructed from biomarkers declining in late life. Review of biological effects of genes corresponding to top SNPs from GWAS of DM slopes revealed that these genes are broadly involved in cancer prognosis and axon guidance/synapse function. Although axon growth is mainly observed during early development, the axon guidance genes can function in adults and contribute to maintenance of neural circuits and synaptic plasticity. Our results indicate that decline in axons&#x2019; ability to maintain complex regulatory networks may potentially play an important role in the increase in physiological dysregulation during aging.
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Overexpression of miR-10a-5p facilitates the progression of osteoarthritis

Hui-Zi Li, Xiang-He Xu, Nan Lin, Da-Wei Wang, Yi-Ming Lin, Zhong-Zhen Su, Hua-Ding Lu,

https://doi.org/10.18632/aging.102989 pp 5948—5976

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Li H, Xu X, Lin N, Wang D, Lin Y, Su Z, Lu H, . Overexpression of miR-10a-5p facilitates the progression of osteoarthritis. . 12:5948-5976. https://doi.org/10.18632/aging.102989

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                TY  - JOUR
                AU  - Li, Hui-Zi 
                AU  - Xu, Xiang-He 
                AU  - Lin, Nan 
                AU  - Wang, Da-Wei 
                AU  - Lin, Yi-Ming 
                AU  - Su, Zhong-Zhen 
                AU  - Lu, Hua-Ding 
                TI  - Overexpression of miR-10a-5p facilitates the progression of osteoarthritis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102989
                DO  - 10.18632/aging.102989
                SP  - 5948
                EP  - 5976
                PY  - 
                AB  - The current study was aimed at exploring the potential roles and possible mechanisms of miR-10a-5p in osteoarthritis (OA). We performed RT-qPCR, Western blot, CCK8, EdU Assay, and flow cytometry assay to clarify the roles of miR-10a-5p in OA. Furthermore, the whole transcriptome sequencing together with integrated bioinformatics analyses were conducted to elucidate the underlying mechanisms of miR-10a-5p involving in OA. Our results demonstrated that miR-10a-5p was upregulated in OA and acted as a significant contributing factor for OA. A large number of circRNAs, lncRNAs, miRNAs, and mRNAs were identified by overexpressing miR-10a-5p. Functional enrichment analyses indicated that these differentially-expressed genes were enriched in some important terms including PPAR signaling pathway, PI3K-Akt signaling pathway, and p53 signaling pathway. A total of 42 hub genes were identified in the protein-protein interaction network including SERPINA1, TTR, APOA1, and A2M. Also, we constructed the network regulatory interactions across coding and noncoding RNAs triggered by miR-10a-5p, which revealed the powerful regulating effects of miR-10a-5p. Moreover, we found that HOXA3 acted as the targeted genes of miR-10a-5p and miR-10a-5p contributed to the progression of OA by suppressing HOXA3 expression. Our findings shed insight on regulatory mechanisms of miR-10a-5p, which might provide novel therapeutic targets for OA.
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Nrf2 deficiency promotes the increasing trend of autophagy during aging in skeletal muscle: a potential mechanism for the development of sarcopenia

Dong-Dong Huang, Xia-Lin Yan, Sheng-Dong Fan, Xi-Yi Chen, Jing-Yi Yan, Qian-Tong Dong, Wei-Zhe Chen, Na-Xin Liu, Xiao-Lei Chen, Zhen Yu,

https://doi.org/10.18632/aging.102990 pp 5977—5991

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Huang D, Yan X, Fan S, Chen X, Yan J, Dong Q, Chen W, Liu N, Chen X, Yu Z, . Nrf2 deficiency promotes the increasing trend of autophagy during aging in skeletal muscle: a potential mechanism for the development of sarcopenia. . 12:5977-5991. https://doi.org/10.18632/aging.102990

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                TY  - JOUR
                AU  - Huang, Dong-Dong 
                AU  - Yan, Xia-Lin 
                AU  - Fan, Sheng-Dong 
                AU  - Chen, Xi-Yi 
                AU  - Yan, Jing-Yi 
                AU  - Dong, Qian-Tong 
                AU  - Chen, Wei-Zhe 
                AU  - Liu, Na-Xin 
                AU  - Chen, Xiao-Lei 
                AU  - Yu, Zhen 
                TI  - Nrf2 deficiency promotes the increasing trend of autophagy during aging in skeletal muscle: a potential mechanism for the development of sarcopenia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102990
                DO  - 10.18632/aging.102990
                SP  - 5977
                EP  - 5991
                PY  - 
                AB  - This study aims to explore the impact of nuclear factor erythroid 2-related factor 2 (Nrf2) deficiency on skeletal muscle autophagy and the development of sarcopenia. LC3b, P62, Bnip3, Lamp-1, and AMPK protein levels were measured in muscle from young, middle-aged, old Nrf2&#x2212;/&#x2212; (knockout, KO) mice and age-matched wild-type (WT) C57/BL6 mice. Autophagy flux was measured in young WT, young KO, old WT, old KO mice, using colchicine as autophagy inhibitor. There was a trend of higher accumulation of LC3b-II, P62, Bnip3, Lamp-1 induced by colchicine in old WT mice compared with young WT mice. Colchicine induced a significantly higher accumulation of LC3b-II, P62, Bnip3, Lamp-1 in KO mice compared with WT mice, both in the young and old groups. AMPK and reactive oxygen species (ROS) were unregulated following Nrf2 KO and increasing age, which was consistent with the increasing trend of autophagy flux following Nrf2 KO and increasing age. Nrf2 KO and increasing age caused decreased cross-sectional area of extensor digitorum longus and soleus muscles. We concluded that Nrf2 deficiency and increasing age may activate AMPK and ROS signals to cause excessive autophagy activation in skeletal muscle, which can be a potential mechanism for the development of sarcopenia.
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PCNA-associated factor KIAA0101 transcriptionally induced by ELK1 controls cell proliferation and apoptosis in nasopharyngeal carcinoma: an integrated bioinformatics and experimental study

Hu Zhao, Miaosheng Chen, Jie Wang, Gang Cao, Wei Chen, Jinke Xu,

https://doi.org/10.18632/aging.102991 pp 5992—6017

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Zhao H, Chen M, Wang J, Cao G, Chen W, Xu J, . PCNA-associated factor KIAA0101 transcriptionally induced by ELK1 controls cell proliferation and apoptosis in nasopharyngeal carcinoma: an integrated bioinformatics and experimental study. . 12:5992-6017. https://doi.org/10.18632/aging.102991

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                TY  - JOUR
                AU  - Zhao, Hu 
                AU  - Chen, Miaosheng 
                AU  - Wang, Jie 
                AU  - Cao, Gang 
                AU  - Chen, Wei 
                AU  - Xu, Jinke 
                TI  - PCNA-associated factor KIAA0101 transcriptionally induced by ELK1 controls cell proliferation and apoptosis in nasopharyngeal carcinoma: an integrated bioinformatics and experimental study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102991
                DO  - 10.18632/aging.102991
                SP  - 5992
                EP  - 6017
                PY  - 
                AB  - KIAA0101, previously identified as PCNA-associated factor, is overexpressed among almost majority of human cancers and has emerged as an important regulator of cancer progression; however, its function in human nasopharyngeal carcinoma (NPC) remain unknown. Integrated bioinformatics approaches were employed to determine the KIAA0101 expressions in the NPC samples. Lentiviral vectors carrying KIAA0101 shRNA were constructed and stable transfected cells were validated by qRT-PCR and western blot. Cellular functions were then evaluated by MTT, colony formation, Brdu staining, and flow cytometry. Mechanistic studies were systematically investigated by UCSC Genome Browser, GEO, UALCAN, QIAGEN, PROMO and JASPAR, ChIP, and the cBioPortal, et al. The results showed that KIAA0101 ranked top overexpressed gene lists in GSE6631 dataset. KIAA0101 was highly expressed in NPC tissues and cell lines. Furthermore, knockdown of KIAA0101 significantly inhibited cell proliferation and DNA replication, promoted apoptosis and cell cycle arrest in vitro. Meanwhile, the mechanistic study revealed that MAP kinase phosphorylation-dependent activation of ELK1 may enhance neighbor gene expressions of KIAA0101 and TRIP4 by binding both promotor regions in the NPC cells. Taken together, our findings indicate that overexpression of KIAA0101 activated by MAP kinase phosphorylation-dependent activation of ELK1 may play an important role in NPC progression.
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Reversal of multidrug resistance in leukemia cells using a transferrin-modified nanomicelle encapsulating both doxorubicin and psoralen

He-Wen Wang, Ke-Ling Ma, Hua Liu, Jia-Yun Zhou,

https://doi.org/10.18632/aging.102992 pp 6018—6029

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Wang H, Ma K, Liu H, Zhou J, . Reversal of multidrug resistance in leukemia cells using a transferrin-modified nanomicelle encapsulating both doxorubicin and psoralen. . 12:6018-6029. https://doi.org/10.18632/aging.102992

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                TY  - JOUR
                AU  - Wang, He-Wen 
                AU  - Ma, Ke-Ling 
                AU  - Liu, Hua 
                AU  - Zhou, Jia-Yun 
                TI  - Reversal of multidrug resistance in leukemia cells using a transferrin-modified nanomicelle encapsulating both doxorubicin and psoralen
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102992
                DO  - 10.18632/aging.102992
                SP  - 6018
                EP  - 6029
                PY  - 
                AB  - To ameliorate multidrug resistance (MDR) observed in leukemia cells, nanomicelles modified by transferrin (Tf-M-DOX/PSO), coencapsulating doxorubicin (DOX) and psoralen (PSO), were designed, synthesized and tested in K562 and doxorubicin-resistant K562 (K562/DOX) cells. In vitro drug release kinetics for constructed nanomicelles were measured using high-performance liquid chromatography. Characterization of the produced nanomicelles was completed using transmission electron microscopy and dynamic light scattering. Uptake of the nanomicelles in K562 cells was investigated using both confocal microscopy and flow cytometry. Apoptosis levels as well as the expression of glycoprotein (P-gp) were analyzing by western blotting and flow cytometry. Cellular cytotoxicity resulting from the exposure of nanomicelles was evaluated using MTT assays. The nanomicelles all showed mild release of DOX in PBS solution. In K562/DOX cells, Tf-M-Dox/PSO exhibited higher uptake compared to the other nanomicelles observed. Furthermore, cellular cytotoxicity when exposed to Tf-M-Dox/PSO was 2.8 and 1.6-fold greater than observed in the unmodified DOX and Tf-nanomicelles loaded with DOX alone, respectively. Tf-M-Dox/PSO strongly increased apoptosis of K562/DOX cells. Finally, the reversal of the drug resistance when cells are exposed to Tf-M-DOX/PSO was associated with P-gp expression inhibition. The Tf-M-Dox/PSO nanomicelle showed a reversal of MDR, with enhanced cellular uptake and delivery release.
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Elevated p38MAPK activity promotes neural stem cell aging

Leire Moreno-Cugnon, Olatz Arrizabalaga, Irantzu Llarena, Ander Matheu,

https://doi.org/10.18632/aging.102994 pp 6030—6036

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Moreno-Cugnon L, Arrizabalaga O, Llarena I, Matheu A, . Elevated p38MAPK activity promotes neural stem cell aging. . 12:6030-6036. https://doi.org/10.18632/aging.102994

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                TY  - JOUR
                AU  - Moreno-Cugnon, Leire 
                AU  - Arrizabalaga, Olatz 
                AU  - Llarena, Irantzu 
                AU  - Matheu, Ander 
                TI  - Elevated p38MAPK activity promotes neural stem cell aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102994
                DO  - 10.18632/aging.102994
                SP  - 6030
                EP  - 6036
                PY  - 
                AB  - Age-progressive neural stem cell (NSC) dysfunction leads to impaired neurogenesis, cognitive decline and the onset of age-related neurodegenerative pathologies. p38MAPK signalling pathway limits stem cell activity during aging in several tissues. Its role in NSCs remains controversial. In this work, we show that p38MAPK activity increases in NSCs with age in the subventricular zone (SVZ) and its pharmacological inhibition is sufficient to rejuvenate their activity in vitro. These data reveal a cell-autonomous role for p38MAPK increase in decreasing NSC homeostasis with age. This information shed light in the role of p38MAPK in NSC aging.
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COVID-19
Predictors for imaging progression on chest CT from coronavirus disease 2019 (COVID-19) patients

Zongguo Yang, Jia Shi, Zhang He, Ying Lü, Qingnian Xu, Chen Ye, Shishi Chen, Bozong Tang, Keshan Yin, Yunfei Lu, Xiaorong Chen,

https://doi.org/10.18632/aging.102999 pp 6037—6048

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Yang Z, Shi J, He Z, Lü Y, Xu Q, Ye C, Chen S, Tang B, Yin K, Lu Y, Chen X, . Predictors for imaging progression on chest CT from coronavirus disease 2019 (COVID-19) patients. . 12:6037-6048. https://doi.org/10.18632/aging.102999

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                TY  - JOUR
                AU  - Yang, Zongguo 
                AU  - Shi, Jia 
                AU  - He, Zhang 
                AU  - Lü, Ying 
                AU  - Xu, Qingnian 
                AU  - Ye, Chen 
                AU  - Chen, Shishi 
                AU  - Tang, Bozong 
                AU  - Yin, Keshan 
                AU  - Lu, Yunfei 
                AU  - Chen, Xiaorong 
                TI  - Predictors for imaging progression on chest CT from coronavirus disease 2019 (COVID-19) patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102999
                DO  - 10.18632/aging.102999
                SP  - 6037
                EP  - 6048
                PY  - 
                AB  - Objective: This study aimed to investigate the potential parameters associated with imaging progression on chest CT from coronavirus disease 19 (COVID-19) patients.Results: The average age of 273 COVID-19 patients enrolled with imaging progression were older than those without imaging progression (p = 0.006). The white blood cells, platelets, neutrophils and acid glycoprotein were all decreased in imaging progression patients (all p &lt; 0.05), and monocytes were increased (p = 0.025). The parameters including homocysteine, urea, creatinine and serum cystatin C were significantly higher in imaging progression patients (all p &lt; 0.05), while eGFR decreased (p &lt; 0.001). Monocyte-lymphocyte ratio (MLR) was significantly higher in imaging progression patients compared to that in imaging progression-free ones (p &lt; 0.001). Logistic models revealed that age, MLR, homocysteine and period from onset to admission were factors for predicting imaging progression on chest CT at first week from COVID-19 patients (all p &lt; 0.05).Conclusion: Age, MLR, homocysteine and period from onset to admission could predict imaging progression on chest CT from COVID-19 patients.Methods: The primary outcome was imaging progression on chest CT. Baseline parameters were collected at the first day of admission. Imaging manifestations on chest CT were followed-up at (6&#xB1;1) days.
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COVID-19
Does comorbidity increase the risk of patients with COVID-19: evidence from meta-analysis

Bolin Wang, Ruobao Li, Zhong Lu, Yan Huang,

https://doi.org/10.18632/aging.103000 pp 6049—6057

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Wang B, Li R, Lu Z, Huang Y, . Does comorbidity increase the risk of patients with COVID-19: evidence from meta-analysis. . 12:6049-6057. https://doi.org/10.18632/aging.103000

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                TY  - JOUR
                AU  - Wang, Bolin 
                AU  - Li, Ruobao 
                AU  - Lu, Zhong 
                AU  - Huang, Yan 
                TI  - Does comorbidity increase the risk of patients with COVID-19: evidence from meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103000
                DO  - 10.18632/aging.103000
                SP  - 6049
                EP  - 6057
                PY  - 
                AB  - Currently, the number of patients with coronavirus disease 2019 (COVID-19) has increased rapidly, but relationship between comorbidity and patients with COVID-19 still not clear. The aim was to explore whether the presence of common comorbidities increases COVID-19 patients&#x2019; risk. A literature search was performed using the electronic platforms (PubMed, Cochrane Library, Embase, and other databases) to obtain relevant research studies published up to March 1, 2020. Relevant data of research endpoints in each study were extracted and merged. All data analysis was performed using Stata12.0 software. A total of 1558 patients with COVID-19 in 6 studies were enrolled in our meta-analysis eventually. Hypertension (OR: 2.29, P&lt;0.001), diabetes (OR: 2.47, P&lt;0.001), chronic obstructive pulmonary disease (COPD) (OR: 5.97, P&lt;0.001), cardiovascular disease (OR: 2.93, P&lt;0.001), and cerebrovascular disease (OR:3.89, P=0.002)were independent risk factors associated with COVID-19 patients. The meta-analysis revealed no correlation between increased risk of COVID-19 and liver disease, malignancy, or renal disease. Hypertension, diabetes, COPD, cardiovascular disease, and cerebrovascular disease are major risk factors for patients with COVID-19. Knowledge of these risk factors can be a resource for clinicians in the early appropriate medical management of patients with COVID-19.
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Aspirin alleviates hepatic fibrosis by suppressing hepatic stellate cells activation via the TLR4/NF-κB pathway

Yan Liu, Li Nong, Yuxian Jia, Aihua Tan, Lixia Duan, Yongkui Lu, Jinmin Zhao,

https://doi.org/10.18632/aging.103002 pp 6058—6066

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Liu Y, Nong L, Jia Y, Tan A, Duan L, Lu Y, Zhao J, . Aspirin alleviates hepatic fibrosis by suppressing hepatic stellate cells activation via the TLR4/NF-κB pathway. . 12:6058-6066. https://doi.org/10.18632/aging.103002

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                TY  - JOUR
                AU  - Liu, Yan 
                AU  - Nong, Li 
                AU  - Jia, Yuxian 
                AU  - Tan, Aihua 
                AU  - Duan, Lixia 
                AU  - Lu, Yongkui 
                AU  - Zhao, Jinmin 
                TI  - Aspirin alleviates hepatic fibrosis by suppressing hepatic stellate cells activation via the TLR4/NF-κB pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103002
                DO  - 10.18632/aging.103002
                SP  - 6058
                EP  - 6066
                PY  - 
                AB  - Hepatic fibrosis arises from a sustained wound-healing response to chronic liver injury. Because the occurrence and development of hepatic fibrosis is always associated with chronic inflammation, controlling inflammation within the liver may be an effective means of controlling the development and progression of hepatic fibrosis. Aspirin is a non-steroidal anti-inflammatory drug used to relieve both inflammatory symptoms and pain. The results of our study showed that aspirin significantly attenuated hepatic inflammation and fibrosis. Aspirin effectively inhibited the activation and proliferation of hepatic stellate cells (HSCs), which led to downregulation of inflammatory factors, including IL-6 and TNF-&#x3B1; in those cells. Aspirin also downregulated expression of Toll-like receptor-4 (TLR4) on HSCs, as well as its downstream mediators, MyD88 and NF-&#x3BA;B. The results of our study demonstrate aspirin&#x2019;s potential to inhibit the development of hepatic fibrosis and the molecular mechanism by which it acts. They suggest aspirin may be an effective therapeutic agent for the treatment of hepatic fibrosis.
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Identification of an exosomal long non-coding RNAs panel for predicting recurrence risk in patients with colorectal cancer

Yanli Zhang, Hui Liu, Xinfeng Liu, Yulian Guo, Yanlei Wang, Yonggang Dai, Jinhua Zhuo, Bing Wu, Hongchun Wang, Xin Zhang,

https://doi.org/10.18632/aging.103006 pp 6067—6088

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Zhang Y, Liu H, Liu X, Guo Y, Wang Y, Dai Y, Zhuo J, Wu B, Wang H, Zhang X, . Identification of an exosomal long non-coding RNAs panel for predicting recurrence risk in patients with colorectal cancer. . 12:6067-6088. https://doi.org/10.18632/aging.103006

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                TY  - JOUR
                AU  - Zhang, Yanli 
                AU  - Liu, Hui 
                AU  - Liu, Xinfeng 
                AU  - Guo, Yulian 
                AU  - Wang, Yanlei 
                AU  - Dai, Yonggang 
                AU  - Zhuo, Jinhua 
                AU  - Wu, Bing 
                AU  - Wang, Hongchun 
                AU  - Zhang, Xin 
                TI  - Identification of an exosomal long non-coding RNAs panel for predicting recurrence risk in patients with colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103006
                DO  - 10.18632/aging.103006
                SP  - 6067
                EP  - 6088
                PY  - 
                AB  - Recurrence is a major cause of cancer-related deaths in colorectal cancer (CRC) patients, but the current strategies are limited to predict this clinical behavior. Our aim is to develop a recurrence prediction model based on long non-coding RNAs (lncRNAs) in exosomes of serum to improve the prediction accuracy. In discovery phase, 11 lncRNAs were found to be associated with CRC recurrence in tissues using high-throughput lncRNAs microarray and reverse transcription quantitative real-time PCR. And, 9 of them were correlated with their expression levels of serum exosomes. In training phase, a model based on 5-exosomal lncRNAs (exolncRNAs) panel was constructed, and showed high distinguish capability for recurrent CRC patients. ROC showed the panel was superior to serum CEA and CA19-9 in prediction of CRC recurrence. In both training and test sets, high-risk patients defined by the 5-exolncRNAs panel had poor recurrence free and overall survival. And, COX model showed it was an independent factor for CRC prognosis. Moreover, there was a significant relationship in detection of 5-exolncRNAs between plasma samples and paired serum samples. In summary, the 5-exolncRNAs panel robustly stratifies CRC patients&#x2019; risk of recurrence, enabling more accurate prediction of prognosis.
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Estradiol-induced senescence of hypothalamic astrocytes contributes to aging-related reproductive function declines in female mice

Xiaoman Dai, Luyan Hong, Hui Shen, Qiang Du, Qinyong Ye, Xiaochun Chen, Jing Zhang,

https://doi.org/10.18632/aging.103008 pp 6089—6108

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Dai X, Hong L, Shen H, Du Q, Ye Q, Chen X, Zhang J, . Estradiol-induced senescence of hypothalamic astrocytes contributes to aging-related reproductive function declines in female mice. . 12:6089-6108. https://doi.org/10.18632/aging.103008

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                TY  - JOUR
                AU  - Dai, Xiaoman 
                AU  - Hong, Luyan 
                AU  - Shen, Hui 
                AU  - Du, Qiang 
                AU  - Ye, Qinyong 
                AU  - Chen, Xiaochun 
                AU  - Zhang, Jing 
                TI  - Estradiol-induced senescence of hypothalamic astrocytes contributes to aging-related reproductive function declines in female mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103008
                DO  - 10.18632/aging.103008
                SP  - 6089
                EP  - 6108
                PY  - 
                AB  - Hypothalamic astrocytes are important contributors that activate gonadotropin-releasing hormone (GnRH) neurons and promote GnRH/LH (luteinizing hormone) surge. However, the potential roles and mechanisms of astrocytes during the early reproductive decline remain obscure. The current study reported that, in intact middle-aged female mice, astrocytes within the hypothalamic RP3V accumulated senescence-related markers with increasing age. It employed an ovariectomized animal model and a cell model receiving estrogen intervention to confirm the estrogen-induced senescence of hypothalamic astrocytes. It found that estrogen metabolites may be an important factor for the estrogen-induced astrocyte senescence. In vitro molecular analysis revealed that ovarian estradiol activated PKA and up-regulated CYPs expression, metabolizing estradiol into 2-OHE2 and 4-OHE2. Of note, in middle-aged mice, the progesterone synthesis and the ability to promote GnRH release were significantly reduced. Besides, the expression of growth factors decreased and the mRNA levels of proinflammatory cytokines significantly increased in the aging astrocytes. The findings confirm that ovarian estradiol induces the senescence of hypothalamic astrocytes and that the senescent astrocytes compromise the regulation of progesterone synthesis and GnRH secretion, which may contribute to the aging-related declines in female reproductive function.
                ER  -

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Ginsenoside Rh3 activates Nrf2 signaling and protects endometrial cells from oxygen and glucose deprivation-reoxygenation

Xiu-mei Wang, Chang She, Quan Li, Di Zhang, Jin-xia Xu, Min-hui Li, Ping Li, Hong-bin Xu,

https://doi.org/10.18632/aging.103009 pp 6109—6119

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Wang X, She C, Li Q, Zhang D, Xu J, Li M, Li P, Xu H, . Ginsenoside Rh3 activates Nrf2 signaling and protects endometrial cells from oxygen and glucose deprivation-reoxygenation. . 12:6109-6119. https://doi.org/10.18632/aging.103009

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                TY  - JOUR
                AU  - Wang, Xiu-mei 
                AU  - She, Chang 
                AU  - Li, Quan 
                AU  - Zhang, Di 
                AU  - Xu, Jin-xia 
                AU  - Li, Min-hui 
                AU  - Li, Ping 
                AU  - Xu, Hong-bin 
                TI  - Ginsenoside Rh3 activates Nrf2 signaling and protects endometrial cells from oxygen and glucose deprivation-reoxygenation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103009
                DO  - 10.18632/aging.103009
                SP  - 6109
                EP  - 6119
                PY  - 
                AB  - Oxygen and glucose deprivation (OGD)-reoxygenation (OGDR) induces oxidative injury to endometrial cells in vitro. We tested the potential effect of ginsenoside Rh3 (GRh3) in the process. Our results show that GRh3 activated Nrf2 signaling in T-HESC cells and primary murine endometrial cells. GRh3 induced Nrf2 Ser-40 phosphorylation and Keap1-Nrf2 disassociation, causing Nrf2 protein stabilization and nuclear translocation, which led to transcription and expression of antioxidant response element-dependent genes (HO1, NQO1 and GCLC). In T-HESC cells and primary murine endometrial cells, GRh3 potently attenuated OGDR-induced reactive oxygen species production, lipid peroxidation and mitochondrial depolarization, as well as cell viability reduction and necrosis. Activation of Nrf2 is required for GRh3-induced anti-OGDR actions in endometrial cells. Nrf2 inhibition, by Nrf2 shRNA, knockout (through CRISPR-Cas9-editing) or S40T mutation, abolished GRh3-induced endometrial cell protection against OGDR. Additionally, forced activation of Nrf2, by Keap1 knockout, mimicked and nullified GRh3-induced anti-OGDR actions in T-HESC cells. Together, we conclude that GRh3 protects endometrial cells from OGDR via activation of Nrf2 signaling.
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Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury

Cong Ye, Huiting Li, Minwei Bao, Ran Zhuo, Gening Jiang, Weixi Wang,

https://doi.org/10.18632/aging.103010 pp 6120—6128

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Ye C, Li H, Bao M, Zhuo R, Jiang G, Wang W, . Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury. . 12:6120-6128. https://doi.org/10.18632/aging.103010

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                TY  - JOUR
                AU  - Ye, Cong 
                AU  - Li, Huiting 
                AU  - Bao, Minwei 
                AU  - Zhuo, Ran 
                AU  - Jiang, Gening 
                AU  - Wang, Weixi 
                TI  - Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103010
                DO  - 10.18632/aging.103010
                SP  - 6120
                EP  - 6128
                PY  - 
                AB  - Severe acute lung injury (ALI) can cause death, and the survivals may develop acute respiratory distress syndrome (ARDS) due to fibrotic repair of the lung. Alveolar macrophages play a demonstrative role during the pathogenesis of ALI, and the timing and degree of differentially polarization of macrophages determine the severity of disease and outcome. Exosomes are important mediators of cellular communication and play critical roles during macrophage differentiation, proliferation and function. Nevertheless, the exact effects of alveolar macrophage - derived exosomes on ALI remain unknow. Here, we used lipopolysaccharide (LPS) to induce ALI in mice and analyzed the exosome population in bronchoalveolar lavage fluid (BALF) from macrophages, neutrophils and epithelial cells at different time points after treatment. Our data showed that macrophages were the major secretors for early secreted pro-inflammatory cytokines in the BALF-exosomes, which likely activated neutrophils to produce a variety of pro-inflammatory cytokines and IL-10. IL-10 by neutrophils in BALF-exosomes likely in turn polarized macrophages to M2c, which may be responsible for post-ALI fibrosis. Our study thus reveals a previous non-acknowledged role of BALF-exosomes as a mediator of inflammatory response and cell crosstalk during ALI.
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Inhibiting Forkhead box K1 induces autophagy to reverse epithelial-mesenchymal transition and metastasis in gastric cancer by regulating Myc-associated zinc finger protein in an acidic microenvironment

Yixuan Wang, Libin Sun, Wensheng Qiu, Weiwei Qi, Yaoyue Qi, Zhao Liu, Shihai Liu, Jing Lv,

https://doi.org/10.18632/aging.103013 pp 6129—6150

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Wang Y, Sun L, Qiu W, Qi W, Qi Y, Liu Z, Liu S, Lv J, . Inhibiting Forkhead box K1 induces autophagy to reverse epithelial-mesenchymal transition and metastasis in gastric cancer by regulating Myc-associated zinc finger protein in an acidic microenvironment. . 12:6129-6150. https://doi.org/10.18632/aging.103013

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                TY  - JOUR
                AU  - Wang, Yixuan 
                AU  - Sun, Libin 
                AU  - Qiu, Wensheng 
                AU  - Qi, Weiwei 
                AU  - Qi, Yaoyue 
                AU  - Liu, Zhao 
                AU  - Liu, Shihai 
                AU  - Lv, Jing 
                TI  - Inhibiting Forkhead box K1 induces autophagy to reverse epithelial-mesenchymal transition and metastasis in gastric cancer by regulating Myc-associated zinc finger protein in an acidic microenvironment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103013
                DO  - 10.18632/aging.103013
                SP  - 6129
                EP  - 6150
                PY  - 
                AB  - Background: Forkhead box K1 (FOXK1) is a transcription factor belonging to the Forkhead box (FOX) family and is closely related to the development of various cancers, but the functional mechanism through which FOXK1 regulates autophagy and epithelial-mesenchymal transition (EMT) in the acidic microenvironment of gastric cancer (GC) remains unclear.Results: Our results indicated that the inhibition of FOXK1 induced autophagy and thus exerted antimetastatic effects in an acidic microenvironment. The dual inhibition of mammalian target of rapamycin (mTOR) and FOXK1 enhanced autophagy and reversed EMT of acidic GC cells. In addition, FOXK1 activated transcription in conjunction with the MAZ promoter.Conclusion: Together, our results suggest that FOXK1 can be used as an independent prognostic indicator for GC patients. We also revealed a new strategy involving the cotargeting of FOXK1 and autophagy to reverse the effects of EMT. MAZ is involved in the development and progression of GC as a downstream target of FOXK1.Methods: Here, the cellular responses to the inhibition of FOXK1 in GC were studied in vivo and in vitro through wound healing assays, transwell assays, Western blotting, laser confocal microscopy and transmission electron microscopy. The molecular mechanisms of FOXK1 and Myc-associated zinc finger protein (MAZ) were studied via chromatin immunoprecipitation sequencing (ChIP-seq), bioinformatics, Western blotting, and quantitative real-time PCR (q-PCR).
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Systemic administration of the di-apocarotenoid norbixin (BIO201) is neuroprotective, preserves photoreceptor function and inhibits A2E and lipofuscin accumulation in animal models of age-related macular degeneration and Stargardt disease

Valérie Fontaine, Elodie Monteiro, Mylène Fournié, Elena Brazhnikova, Thinhinane Boumedine, Cécile Vidal, Christine Balducci, Louis Guibout, Mathilde Latil, Pierre J. Dilda, Stanislas Veillet, José-Alain Sahel, René Lafont, Serge Camelo,

https://doi.org/10.18632/aging.103014 pp 6151—6171

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Fontaine V, Monteiro E, Fournié M, Brazhnikova E, Boumedine T, Vidal C, Balducci C, Guibout L, Latil M, Dilda PJ, Veillet S, Sahel J, Lafont R, et al, . Systemic administration of the di-apocarotenoid norbixin (BIO201) is neuroprotective, preserves photoreceptor function and inhibits A2E and lipofuscin accumulation in animal models of age-related macular degeneration and Stargardt disease. . 12:6151-6171. https://doi.org/10.18632/aging.103014

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                TY  - JOUR
                AU  - Fontaine, Valérie 
                AU  - Monteiro, Elodie 
                AU  - Fournié, Mylène 
                AU  - Brazhnikova, Elena 
                AU  - Boumedine, Thinhinane 
                AU  - Vidal, Cécile 
                AU  - Balducci, Christine 
                AU  - Guibout, Louis 
                AU  - Latil, Mathilde 
                AU  - Dilda, Pierre J. 
                AU  - Veillet, Stanislas 
                AU  - Sahel, José-Alain 
                AU  - Lafont, René 
                AU  - Camelo, Serge 
                TI  - Systemic administration of the di-apocarotenoid norbixin (BIO201) is neuroprotective, preserves photoreceptor function and inhibits A2E and lipofuscin accumulation in animal models of age-related macular degeneration and Stargardt disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103014
                DO  - 10.18632/aging.103014
                SP  - 6151
                EP  - 6171
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Fontaine, Valérie 
                AU  - Monteiro, Elodie 
                AU  - Fournié, Mylène 
                AU  - Brazhnikova, Elena 
                AU  - Boumedine, Thinhinane 
                AU  - Vidal, Cécile 
                AU  - Balducci, Christine 
                AU  - Guibout, Louis 
                AU  - Latil, Mathilde 
                AU  - Dilda, Pierre J. 
                AU  - Veillet, Stanislas 
                AU  - Sahel, José-Alain 
                AU  - Lafont, René 
                AU  - Camelo, Serge 
                TI  - Systemic administration of the di-apocarotenoid norbixin (BIO201) is neuroprotective, preserves photoreceptor function and inhibits A2E and lipofuscin accumulation in animal models of age-related macular degeneration and Stargardt disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103014
                DO  - 10.18632/aging.103014
                SP  - 6151
                EP  - 6171
                PY  - 
                AB  - Atrophic A\age-related macular degeneration (AMD) and Stargardt disease (STGD) are major blinding diseases affecting millions of patients worldwide, but no treatment is available. In dry AMD and STGD oxidative stress and subretinal accumulation of N-retinylidene-N-retinylethanolamine (A2E), a toxic by-product of the visual cycle, causes retinal pigment epithelium (RPE) and photoreceptor degeneration leading to visual impairment. Acute and chronic retinal degeneration following blue light damage (BLD) in BALB/c mice and aging of Abca4-/- Rdh8-/- mice, respectively, reproduce features of AMD and STGD. Efficacy of systemic administrations of 9&apos;-cis-norbixin (norbixin), a natural di-apocarotenoid, prepared from Bixa orellana seeds with anti-oxidative properties, was evaluated during BLD in BALB/c mice, and in Abca4-/- Rdh8-/- mice of different ages, following three experimental designs: &#x201C;preventive&#x201D;, &#x201C;early curative&#x201D; and &#x201C;late curative&#x201D; supplementations. Norbixin injected intraperitoneally in BALB/c mice, maintained scotopic and photopic electroretinogram amplitude and was neuroprotective. Norbixin chronic oral administration for 6 months in Abca4-/- Rdh8-/- mice following the &#x201C;early curative&#x201D; supplementation showed optimal neuroprotection and maintenance of photoreceptor function and reduced ocular A2E accumulation. Thus, norbixin appears promising as a systemic drug candidate for both AMD and STGD treatment.
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USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis

Guojun Wei, Tianwei Zhang, Zongguang Li, Naichun Yu, Xiang Xue, Daguo Zhou, Yongjie Chen, Linlin Zhang, Xiaoli Yao, Guangrong Ji,

https://doi.org/10.18632/aging.103015 pp 6172—6190

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Wei G, Zhang T, Li Z, Yu N, Xue X, Zhou D, Chen Y, Zhang L, Yao X, Ji G, . USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis. . 12:6172-6190. https://doi.org/10.18632/aging.103015

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                TY  - JOUR
                AU  - Wei, Guojun 
                AU  - Zhang, Tianwei 
                AU  - Li, Zongguang 
                AU  - Yu, Naichun 
                AU  - Xue, Xiang 
                AU  - Zhou, Daguo 
                AU  - Chen, Yongjie 
                AU  - Zhang, Linlin 
                AU  - Yao, Xiaoli 
                AU  - Ji, Guangrong 
                TI  - USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103015
                DO  - 10.18632/aging.103015
                SP  - 6172
                EP  - 6190
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) have been certified as important regulators in tumorigenesis. LncRNA GAS6-AS2 (GAS6-AS2) was a newly identified tumor-related lncRNA, and its dysregulation and oncogenic effects in melanoma and bladder cancer had been reported in previous studies. However, the expression pattern and potential function of GAS6-AS2 in osteosarcoma (OS) have not been investigated. In this study, we identified a novel OS-related lncRNA GAS6-AS2. We found that GAS6-AS2 was distinctly upregulated in both OS specimens and cell lines. Distinct up-regulation of GAS6-AS2 in OS was correlated with advanced clinical stages and shorter survivals. In addition, USF1 could directly bind to the GAS6-AS2 promoter and contribute to its overexpression. Furthermore, GAS6-AS2 knockdown caused tumor suppressive effects via reducing cellular proliferation, migration and invasion, and promoting OS cell apoptosis. Besides, GAS6-AS2 directly bound to miR-934 and downregulated its expression. Mechanistically, GAS6-AS2 positively regulated the expression of BCAT1 through sponging miR-934. Taken together, our data illustrated how GAS6-AS2 played an oncogenic role in OS and might offer a potential therapeutic target for treating OS.
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Long non-coding RNA TPT1-AS1 promotes angiogenesis and metastasis of colorectal cancer through TPT1-AS1/NF90/VEGFA signaling pathway

Yiyun Zhang, Jiangyun Sun, Yuan Qi, Yimin Wang, Yu Ding, Kun Wang, Qingxin Zhou, Jingxuan Wang, Fei Ma, Jianguo Zhang, Baoliang Guo,

https://doi.org/10.18632/aging.103016 pp 6191—6205

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Zhang Y, Sun J, Qi Y, Wang Y, Ding Y, Wang K, Zhou Q, Wang J, Ma F, Zhang J, Guo B, . Long non-coding RNA TPT1-AS1 promotes angiogenesis and metastasis of colorectal cancer through TPT1-AS1/NF90/VEGFA signaling pathway. . 12:6191-6205. https://doi.org/10.18632/aging.103016

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                TY  - JOUR
                AU  - Zhang, Yiyun 
                AU  - Sun, Jiangyun 
                AU  - Qi, Yuan 
                AU  - Wang, Yimin 
                AU  - Ding, Yu 
                AU  - Wang, Kun 
                AU  - Zhou, Qingxin 
                AU  - Wang, Jingxuan 
                AU  - Ma, Fei 
                AU  - Zhang, Jianguo 
                AU  - Guo, Baoliang 
                TI  - Long non-coding RNA TPT1-AS1 promotes angiogenesis and metastasis of colorectal cancer through TPT1-AS1/NF90/VEGFA signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103016
                DO  - 10.18632/aging.103016
                SP  - 6191
                EP  - 6205
                PY  - 
                AB  - LncRNAs have been proven closely correlated to tumor progression. A recent study identified LncRNA TPT1-AS1 (TPT1-AS1) as one of the liver-metastasis associated LncRNAs in colorectal cancer (CRC). In this study, we report that TPT1-AS1 is upregulated in CRC tissues, which is associated with poor prognosis. Functional assays unravel a pro-angiogenesis and metastasis role of TPT1-AS1. Mechanistically, Flexmap 3D assays reveal that TPT1-AS1 upregulates the VEGFA secretion in CRC cells. RNA immunoprecipitation and mRNA stability assays further show that TPT1-AS1 interacts with nuclear factor 90 (NF90) and subsequently promotes the association between NF90 and VEGFA mRNA, which leads to the upregulation of VEGFA mRNA stability. Therefore, we elucidate a new regulatory mechanism of TPT1-AS1 in CRC angiogenesis and targeting the TPT1-AS1/NF90/VEGFA axis may provide a useful strategy for diagnosis and treatment for colorectal cancer patients.
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Application of Generalized Split Linearized Bregman Iteration algorithm for Alzheimer's disease prediction

Weimin Zheng, Bin Cui, Zeyu Sun, Xiuli Li, Xu Han, Yu Yang, Kuncheng Li, Lingjing Hu, Zhiqun Wang, Alzheimer's Disease Neuroimaging Initiative,

https://doi.org/10.18632/aging.103017 pp 6206—6224

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Zheng W, Cui B, Sun Z, Li X, Han X, Yang Y, Li K, Hu L, Wang Z, , . Application of Generalized Split Linearized Bregman Iteration algorithm for Alzheimer's disease prediction. . 12:6206-6224. https://doi.org/10.18632/aging.103017

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                TY  - JOUR
                AU  - Zheng, Weimin 
                AU  - Cui, Bin 
                AU  - Sun, Zeyu 
                AU  - Li, Xiuli 
                AU  - Han, Xu 
                AU  - Yang, Yu 
                AU  - Li, Kuncheng 
                AU  - Hu, Lingjing 
                AU  - Wang, Zhiqun 
                AU  - ,  
                TI  - Application of Generalized Split Linearized Bregman Iteration algorithm for Alzheimer's disease prediction
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103017
                DO  - 10.18632/aging.103017
                SP  - 6206
                EP  - 6224
                PY  - 
                AB  - In this paper, we applied a novel method for the detection of Alzheimer&#x2019;s disease (AD) based on a structural magnetic resonance imaging (sMRI) dataset. Specifically, the method involved a new classification algorithm of machine learning, named Generalized Split Linearized Bregman Iteration (GSplit LBI). It combines logistic regression and structural sparsity regularizations. In the study, 57 AD patients and 47 normal controls (NCs) were enrolled. We first extracted the entire brain gray matter volume values of all subjects and then used GSplit LBI to build a predictive classification model with a 10-fold full cross-validation method. The model accuracy achieved 90.44%. To further verify which voxels in the dataset have greater impact on the prediction results, we ranked the weight parameters and obtained the top 6% of the model parameters. To verify the generalization of model prediction and the stability of feature selection, we performed a cross-test on the Alzheimer&apos;s Disease Neuroimaging Initiative (ADNI) and a Chinese dataset and achieved good performances on different cohorts. Conclusively, based on the sMRI dataset, our algorithm not only had good performance in a local cohort with high accuracy but also had good generalization of model prediction and stability of feature selection in different cohorts.
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Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17

Tianying Zhan, Xiaomei Wang, Zijun Ouyang, Youli Yao, Jiangyao Xu, Shikang Liu, Kan Liu, Qiyu Deng, Yushu Wang, Yingying Zhao,

https://doi.org/10.18632/aging.103018 pp 6225—6239

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Zhan T, Wang X, Ouyang Z, Yao Y, Xu J, Liu S, Liu K, Deng Q, Wang Y, Zhao Y, . Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17. . 12:6225-6239. https://doi.org/10.18632/aging.103018

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                TY  - JOUR
                AU  - Zhan, Tianying 
                AU  - Wang, Xiaomei 
                AU  - Ouyang, Zijun 
                AU  - Yao, Youli 
                AU  - Xu, Jiangyao 
                AU  - Liu, Shikang 
                AU  - Liu, Kan 
                AU  - Deng, Qiyu 
                AU  - Wang, Yushu 
                AU  - Zhao, Yingying 
                TI  - Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103018
                DO  - 10.18632/aging.103018
                SP  - 6225
                EP  - 6239
                PY  - 
                AB  - Multiple sclerosis (MS) is an autoimmune disease characterized by T cell infiltration and demyelination of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is a classical preclinical animal model of MS. In this study, we found that rotating magnetic field (RMF) treatment exerts potential preventive effects on the discovery of EAE, including reducing the severity of the disease and delaying the onset of the disease. The results indicated that RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes by downregulating the expression of CCL-2, CCL-3 and CCL-5, but has no significant effect on myelin oligodendrocyte glycoprotein (MOG) specific T cell responses. Simultaneously, RMF treatment adjusted the imbalance between regulatory T (Treg) cell and T helper 1 (Th1) cells or T helper 17 (Th17) cells by increasing the proportion of Treg cells and inhibiting the ratio of Th1 and Th17 cell subsets. These findings suggest that exposure to RMF may improve EAE disease by promoting CD4+ cell accumulation into peripheral lymphoid tissue, improving the imbalance between Treg and Th1/Th17 cells. Therefore, as a mild physical therapy approach, RMF, is likely to be a potential way to alter the development of EAE.
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Inhibition of esophageal-carcinoma cell proliferation by genistein via suppression of JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways

Jing Gao, Rongmu Xia, Jianbo Chen, Jing Gao, Xianyang Luo, Chunlin Ke, Caihong Ren, Jiayi Li, Yanjun Mi,

https://doi.org/10.18632/aging.103019 pp 6240—6259

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Gao J, Xia R, Chen J, Gao J, Luo X, Ke C, Ren C, Li J, Mi Y, . Inhibition of esophageal-carcinoma cell proliferation by genistein via suppression of JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways. . 12:6240-6259. https://doi.org/10.18632/aging.103019

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                TY  - JOUR
                AU  - Gao, Jing 
                AU  - Xia, Rongmu 
                AU  - Chen, Jianbo 
                AU  - Gao, Jing 
                AU  - Luo, Xianyang 
                AU  - Ke, Chunlin 
                AU  - Ren, Caihong 
                AU  - Li, Jiayi 
                AU  - Mi, Yanjun 
                TI  - Inhibition of esophageal-carcinoma cell proliferation by genistein via suppression of JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103019
                DO  - 10.18632/aging.103019
                SP  - 6240
                EP  - 6259
                PY  - 
                AB  - Esophageal carcinoma (EsC) is a clinically challenging neoplastic disease. Genistein, a natural isoflavone product, has anti-tumor properties. Through in vitro and in vivo studies, we found that genistein suppressed EsC cell proliferation in a time- and concentration-dependent manner. In addition, genistein markedly promoted apoptosis and arrested cell cycle at the G0/G1 phase in a concentration-dependent manner. Furthermore, high concentrations of genistein have no adverse effect on normal esophageal epithelial cells. Mechanistically, genistein treatment strikingly reduced the expression of cell cycle-associated genes, and up-regulated the expression of cell apoptosis-related genes in EsC cells. Additionally, genistein dramatically decreased epidermal growth factor receptor (EGFR) expression and attenuated its down-stream signaling molecules STAT3, MDM2, Akt and JAK1/2 phosphorylation, resulting in inhibited nuclear translocation of STAT3 and MDM2, thereby inhibiting the JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways. In xenograft nude mice, genistein administration strikingly impaired tumor growth in a dose-dependent manner. Moreover, similar disturbances in molecular mechanisms were observed in vivo. Taken together, genistein suppressed the JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways by decreasing EGFR expression, leading to cell apoptosis, cell cycle arrest, and proliferation inhibition in EsC cells. Our findings suggest that genistein may be a promising alternative adjuvant therapy for patients with EsC.
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Myotonic Dystrophy type 1 cells display impaired metabolism and mitochondrial dysfunction that are reversed by metformin

Mikel García-Puga, Ander Saenz-Antoñanzas, Roberto Fernández-Torrón, Adolfo Lopez de Munain, Ander Matheu,

https://doi.org/10.18632/aging.103022 pp 6260—6275

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García-Puga M, Saenz-Antoñanzas A, Fernández-Torrón R, Munain ALd, Matheu A, . Myotonic Dystrophy type 1 cells display impaired metabolism and mitochondrial dysfunction that are reversed by metformin. . 12:6260-6275. https://doi.org/10.18632/aging.103022

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                TY  - JOUR
                AU  - García-Puga, Mikel 
                AU  - Saenz-Antoñanzas, Ander 
                AU  - Fernández-Torrón, Roberto 
                AU  - Munain, Adolfo Lopez de 
                AU  - Matheu, Ander 
                TI  - Myotonic Dystrophy type 1 cells display impaired metabolism and mitochondrial dysfunction that are reversed by metformin
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103022
                DO  - 10.18632/aging.103022
                SP  - 6260
                EP  - 6275
                PY  - 
                AB  - Myotonic dystrophy type 1 (DM1; MIM #160900) is an autosomal dominant disorder, clinically characterized by progressive muscular weakness and multisystem degeneration. The broad phenotypes observed in patients with DM1 resemble the appearance of a multisystem accelerated aging process. However, the molecular mechanisms underlying these phenotypes remain largely unknown. In this study, we characterized the impact of metabolism and mitochondria on fibroblasts and peripheral blood mononuclear cells (PBMCs) derived from patients with DM1 and healthy individuals. Our results revealed a decrease in oxidative phosphorylation system (OXPHOS) activity, oxygen consumption rate (OCR), ATP production, energy metabolism, and mitochondrial dynamics in DM1 fibroblasts, as well as increased accumulation of reactive oxygen species (ROS). PBMCs of DM1 patients also displayed reduced mitochondrial dynamics and energy metabolism. Moreover, treatment with metformin reversed the metabolic and mitochondrial defects as well as additional accelerated aging phenotypes, such as impaired proliferation, in DM1-derived fibroblasts. Our results identify impaired cell metabolism and mitochondrial dysfunction as important drivers of DM1 pathophysiology and, therefore, reveal the efficacy of metformin treatment in a pre-clinical setting.
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DNA N⁶-methyladenine modification in hypertension

Ye Guo, Yuqing Pei, Kexin Li, Wei Cui, Donghong Zhang,

https://doi.org/10.18632/aging.103023 pp 6276—6291

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Guo Y, Pei Y, Li K, Cui W, Zhang D, . DNA N⁶-methyladenine modification in hypertension. . 12:6276-6291. https://doi.org/10.18632/aging.103023

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                TY  - JOUR
                AU  - Guo, Ye 
                AU  - Pei, Yuqing 
                AU  - Li, Kexin 
                AU  - Cui, Wei 
                AU  - Zhang, Donghong 
                TI  - DNA N<sup>6</sup>-methyladenine modification in hypertension
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103023
                DO  - 10.18632/aging.103023
                SP  - 6276
                EP  - 6291
                PY  - 
                AB  - DNA methylation has a role in the pathogenesis of essential hypertension. DNA N6-methyladenine (6mA) modification as a novel adenine methylation exists in human tissues, but whether it plays a role in hypertension development remains unclear. Here, we reported that the global 6mA DNA level in leukocytes was significantly reduced in patients with hypertension and was reversed with successful treatment. Age, systolic blood pressure, and serum total cholesterol and high-density lipoprotein levels were associated with decreased leukocyte 6mA DNA level. Elevated ALKBH1 (AlkB homolog 1), a demethylase of 6mA, level mediated this dynamic change in 6mA level in leukocytes and vascular smooth muscle cells in hypertension mouse and rat models. Knockdown of ALKBH1 suppressed angiotensin II-induced vascular smooth muscle phenotype transformation, proliferation and migration. ALKBH1-6mA directly and negatively regulated hypoxia inducible factor 1 &#x3B1; (HIF1&#x3B1;), which responded to angiotensin II-induced vascular remodeling. Collectively, our results demonstrate a potential epigenetic role for ALKBH1-6mA regulation in hypertension development, diagnosis and treatment.
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Systematic analysis of bacteriostatic mechanism of flavonoids using transcriptome and its therapeutic effect on vaginitis

Zeyan Lin, Yanyan Lin, Zhengbing Zhang, Jinxing Shen, Caimei Yang, Meijiao Jiang, Youming Hou,

https://doi.org/10.18632/aging.103024 pp 6292—6305

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Lin Z, Lin Y, Zhang Z, Shen J, Yang C, Jiang M, Hou Y, . Systematic analysis of bacteriostatic mechanism of flavonoids using transcriptome and its therapeutic effect on vaginitis. . 12:6292-6305. https://doi.org/10.18632/aging.103024

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                TY  - JOUR
                AU  - Lin, Zeyan 
                AU  - Lin, Yanyan 
                AU  - Zhang, Zhengbing 
                AU  - Shen, Jinxing 
                AU  - Yang, Caimei 
                AU  - Jiang, Meijiao 
                AU  - Hou, Youming 
                TI  - Systematic analysis of bacteriostatic mechanism of flavonoids using transcriptome and its therapeutic effect on vaginitis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103024
                DO  - 10.18632/aging.103024
                SP  - 6292
                EP  - 6305
                PY  - 
                AB  - The flavonoids in Ageratum conyzoides L. have been used in traditional medicine due to its anti-inflammatory and antibacterial properties. However, the specific mechanism of its antibacterial effect, and the potential therapeutic effect on vaginitis have not been well explained. The growth curves of E. coli, S. aurues, and P. aeruginosa after treatment with flavonoids were measured. The influences of flavonoids on the conductivity of bacterial culture medium and exudation of bacterial nucleic acid were also detected. Transcriptomics analysis was applied to analyze the potential mechanism of flavonoids. Flavonoids significantly suppressed the growth curves of E. coli, S. aurues, and P. aeruginosa, and increased the conductivity of bacteria and nucleic acid exudation. Transcriptomics analysis indicated that flavonoids could suppress bacteria by affecting the transcription and metabolism pathways. The obvious therapeutic effect of flavonoids on bacterial vaginitis was also observed. This study systematically analyzed the bacteriostatic mechanism of flavonoids, which should be helpful to develop new drugs based on the bacteriostatic effect of flavonoids.
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Bone marrow mesenchymal stem cells transplantation alleviates brain injury after intracerebral hemorrhage in mice through the Hippo signaling pathway

Xiao Chen, Can-Xin Xu, Huaibin Liang, Zhiyu Xi, Jiaji Pan, Yong Yang, Qingfang Sun, Guoyuan Yang, Yuhao Sun, Liuguan Bian,

https://doi.org/10.18632/aging.103025 pp 6306—6323

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Chen X, Xu C, Liang H, Xi Z, Pan J, Yang Y, Sun Q, Yang G, Sun Y, Bian L, . Bone marrow mesenchymal stem cells transplantation alleviates brain injury after intracerebral hemorrhage in mice through the Hippo signaling pathway. . 12:6306-6323. https://doi.org/10.18632/aging.103025

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                TY  - JOUR
                AU  - Chen, Xiao 
                AU  - Xu, Can-Xin 
                AU  - Liang, Huaibin 
                AU  - Xi, Zhiyu 
                AU  - Pan, Jiaji 
                AU  - Yang, Yong 
                AU  - Sun, Qingfang 
                AU  - Yang, Guoyuan 
                AU  - Sun, Yuhao 
                AU  - Bian, Liuguan 
                TI  - Bone marrow mesenchymal stem cells transplantation alleviates brain injury after intracerebral hemorrhage in mice through the Hippo signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103025
                DO  - 10.18632/aging.103025
                SP  - 6306
                EP  - 6323
                PY  - 
                AB  - Intracerebral hemorrhage (ICH) is a common acute nervous system disease with high mortality and severe disability. Mesenchymal stem cells (MSCs) have been reported to promote neurogenesis and to alleviate side effects in areas of brain injury areas. The Hippo pathway regulates diverse cellular processes, including cell survival, proliferation, differentiation, and organ size. Here, we found that transplantation of bone marrow MSCs (BM-MSCs) into the brains of mice could alleviate ICH-mediated injury and protect astrocytes from apoptosis by regulating mammalian sterile 20-like kinase (MST)1 and Yes-associated protein (YAP). Knocking down of MST1 by si-RNA triggered YAP nuclear translocation. We further demonstrated that astrocytes undergo astroglial-mesenchymal phenotype switching and become capable of proliferating after BM-MSC transplantation via the Hippo signaling pathway. Together, our identification of the Hippo pathway in mediating the beneficial effects of BM-MSCs may provide a novel therapeutic target in the treatment and management of ICH.
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Anterior thalamic nucleus stimulation protects hippocampal neurons by activating autophagy in epileptic monkeys

Ting-Ting Du, Guanyu Zhu, Yingchuan Chen, Lin Shi, Defeng Liu, Yuye Liu, Xin Zhang, Jianguo Zhang,

https://doi.org/10.18632/aging.103026 pp 6324—6339

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Du T, Zhu G, Chen Y, Shi L, Liu D, Liu Y, Zhang X, Zhang J, . Anterior thalamic nucleus stimulation protects hippocampal neurons by activating autophagy in epileptic monkeys. . 12:6324-6339. https://doi.org/10.18632/aging.103026

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                TY  - JOUR
                AU  - Du, Ting-Ting 
                AU  - Zhu, Guanyu 
                AU  - Chen, Yingchuan 
                AU  - Shi, Lin 
                AU  - Liu, Defeng 
                AU  - Liu, Yuye 
                AU  - Zhang, Xin 
                AU  - Zhang, Jianguo 
                TI  - Anterior thalamic nucleus stimulation protects hippocampal neurons by activating autophagy in epileptic monkeys
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103026
                DO  - 10.18632/aging.103026
                SP  - 6324
                EP  - 6339
                PY  - 
                AB  - Deep brain stimulation of the anterior nucleus of the thalamus (ANT-DBS) is effective in treating temporal lobe epilepsy (TLE) and protects hippocampal neurons. Autophagy plays an essential role in epileptogenesis; however, the underlying effect of autophagy on ANT-DBS-mediated neuroprotection remains unclear. A monkey model of epilepsy was established by injecting kainic acid into the hippocampus and amygdala using a robot-assisted system. ANT-DBS was delivered in the chronic stage of the epileptic model and continued for 8 weeks. We found that ANT-DBS reduced the frequency of seizures and exerted neuroprotective effects via activating autophagy in hippocampal neurons. ANT-DBS increased light chain 3 (LC3) II level and co-localization of LC3 and lysosomal-associated membrane protein-1, accompanied by decreased expression of the autophagy substrate ubiquitin-binding protein p62, suggesting increased autophagosome formation. Most importantly, brain-derived neurotrophic factor (BDNF) &#x2013;tropomyosin-related kinase type B (TrkB) pathway were involved in the regulation of autophagy. Both protein levels were reduced by ANT-DBS, and there was less phosphorylation of downstream regulators, extracellular signal-regulated kinase and Akt, followed by inactivation of mammalian target of rapamycin complex 1. Taken together, chronic ANT-DBS exerts neuroprotective effects on hippocampal neurons through inducing autophagy via suppressing the BDNF&#x2013;TrkB pathway in a TLE monkey model.
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Leptin acts on mesenchymal stem cells to promote chemoresistance in osteosarcoma cells

Helin Feng, Qianqian Zhang, Yi Zhao, Lili Zhao, Baoen Shan,

https://doi.org/10.18632/aging.103027 pp 6340—6351

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Feng H, Zhang Q, Zhao Y, Zhao L, Shan B, . Leptin acts on mesenchymal stem cells to promote chemoresistance in osteosarcoma cells. . 12:6340-6351. https://doi.org/10.18632/aging.103027

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                TY  - JOUR
                AU  - Feng, Helin 
                AU  - Zhang, Qianqian 
                AU  - Zhao, Yi 
                AU  - Zhao, Lili 
                AU  - Shan, Baoen 
                TI  - Leptin acts on mesenchymal stem cells to promote chemoresistance in osteosarcoma cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103027
                DO  - 10.18632/aging.103027
                SP  - 6340
                EP  - 6351
                PY  - 
                AB  - Leptin signaling influences osteoblastogenesis and modulates the fate of mesenchymal stem cells (MSCs) during bone and cartilage regeneration. Although MSCs abound in the osteosarcoma (OS) microenvironment, and leptin exhibits pro-tumorigenic properties, leptin&#x2019;s influence on OS progression and chemoresistant signaling in MSCs remains unclear. Using cell viability and apoptosis assays, we showed that medium conditioned by leptin-treated human MSCs promotes cisplatin resistance in cultured human OS cells. Moreover, GFP-LC3 expression and chloroquine treatment experiments showed that this effect is mediated by stimulation of autophagy in OS cells. TGF-&#x3B2; expression in MSCs was upregulated by leptin and suppressed by leptin receptor knockdown. Silencing TGF-&#x3B2; in MSCs also abolished OS cell chemoresistance induced by leptin-conditioned medium. Cisplatin resistance was also induced when leptin-conditioned MSCs were co-injected with MG-63 OS cells to generate subcutaneous xenografts in nude mice. Finally, we observed a significant correlation between autophagy-associated gene expression in OS clinical samples and patient prognosis. We conclude that leptin upregulates TGF-&#x3B2; in MSCs, which promotes autophagy-mediated chemoresistance in OS cells.
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FAM46C inhibits cell proliferation and cell cycle progression and promotes apoptosis through PTEN/AKT signaling pathway and is associated with chemosensitivity in prostate cancer

Libin Ma, Huadong He, Kang Jiang, Peiwu Jiang, Han He, Shengjia Feng, Kean Chen, Jia Shao, Gang Deng,

https://doi.org/10.18632/aging.103030 pp 6352—6369

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Ma L, He H, Jiang K, Jiang P, He H, Feng S, Chen K, Shao J, Deng G, . FAM46C inhibits cell proliferation and cell cycle progression and promotes apoptosis through PTEN/AKT signaling pathway and is associated with chemosensitivity in prostate cancer. . 12:6352-6369. https://doi.org/10.18632/aging.103030

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                TY  - JOUR
                AU  - Ma, Libin 
                AU  - He, Huadong 
                AU  - Jiang, Kang 
                AU  - Jiang, Peiwu 
                AU  - He, Han 
                AU  - Feng, Shengjia 
                AU  - Chen, Kean 
                AU  - Shao, Jia 
                AU  - Deng, Gang 
                TI  - FAM46C inhibits cell proliferation and cell cycle progression and promotes apoptosis through PTEN/AKT signaling pathway and is associated with chemosensitivity in prostate cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103030
                DO  - 10.18632/aging.103030
                SP  - 6352
                EP  - 6369
                PY  - 
                AB  - Family with sequence similarity 46 member C (FAM46C) is a non-canonical poly(A) polymerase that is associated with tumorigenesis. However, its role in prostate cancer development is not fully understood. Herein, we determined expression pattern of FAM46C in prostate cancer and further identified its effect on the tumorigenesis and chemosensitivity. FAM46C expression was decreased in prostate cancer tissues and cell lines compared with corresponding controls. FAM46C expression was significantly associated with the Gleason score, tumor size and overall survival. FAM46C knockdown in 22RV1 and DU145 cells significantly inhibited apoptosis and promoted cell proliferation and cell cycle progression as well as activation of AKT. FAM46C overexpression had an inverse effect in DU145 cells and inhibited tumor growth in vivo. FAM46C inhibited cell proliferation and cell cycle progression and induced apoptosis via the PTEN/AKT signaling pathway. FAM46C promoted PTEN expression through inhibiting PTEN ubiquitination. The prostate cancer cells and patient-derived xenograft (PDX) mice with high-FAM46C-expressing demonstrated an enhanced chemosensitivity to docetaxel. These findings suggest that FAM46C control cell proliferation, cell cycle and apoptosis through PTEN/AKT signaling pathway and is associated with chemosensitivity of prostate cancer. Modulation of their levels may offer a new approach for improving anti-tumor efficacy for chemotherapeutic agents in prostate cancer.
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NO up-regulates migraine-related CGRP via activation of an Akt/GSK-3β/NF-κB signaling cascade in trigeminal ganglion neurons

Gang Yao, Yu-Hong Man, An-Ran Li, Yu Guo, Yun Dai, Ping Wang, Yi-Fa Zhou,

https://doi.org/10.18632/aging.103031 pp 6370—6384

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Yao G, Man Y, Li A, Guo Y, Dai Y, Wang P, Zhou Y, . NO up-regulates migraine-related CGRP via activation of an Akt/GSK-3β/NF-κB signaling cascade in trigeminal ganglion neurons. . 12:6370-6384. https://doi.org/10.18632/aging.103031

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                TY  - JOUR
                AU  - Yao, Gang 
                AU  - Man, Yu-Hong 
                AU  - Li, An-Ran 
                AU  - Guo, Yu 
                AU  - Dai, Yun 
                AU  - Wang, Ping 
                AU  - Zhou, Yi-Fa 
                TI  - NO up-regulates migraine-related CGRP via activation of an Akt/GSK-3β/NF-κB signaling cascade in trigeminal ganglion neurons
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103031
                DO  - 10.18632/aging.103031
                SP  - 6370
                EP  - 6384
                PY  - 
                AB  - The release of the neuropeptide CGRP from the trigeminal ganglion neurons (TGNs) plays a central role in migraine. Whereas CGRP can activate NO release from ganglionic glial cells, NO in turn enhances CGRP release. However, it remains unclear how NO promotes CGRP release. Here, we report that the NO donor SNAP triggered CGRP release from cultured primary TGNs. This event was associated with GSK-3&#x3B2; activation and Akt inactivation. Immunofluorescent staining revealed that GSK-3&#x3B2; primarily located in neurons. Furthermore, GSK-3&#x3B2; inhibition resulted in a marked reduction in expression of CGRP as well as other migraine-related factors, including substance P, cholecystokinin, and prostaglandin E2. Last, exposure to SNAP also activated NF-&#x3BA;B, while NF-&#x3BA;B inhibition prevented the induction of CGRP by SNAP. Interestingly, this event was blocked by GSK-3&#x3B2; inhibition, in association with inhibition of NF-&#x3BA;B/p65 expression and nuclear translocation. Together, these findings argue that NO could stimulate TGNs to release of CGRP as well as other migraine-related factors, likely by activating GSK-3&#x3B2;, providing a novel mechanism underlying a potential feed-forward loop between NO and CGRP in migraine. They also raise a possibility that GSK-3&#x3B2; might act to trigger migraine through activation of NF-&#x3BA;B, suggesting a link between neuroinflammation and migraine.
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Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis

Weihua Bian, Xiaohong Jing, Zhiyu Yang, Zhen Shi, Ruiyao Chen, Aili Xu, Na Wang, Jing Jiang, Cheng Yang, Daolai Zhang, Lan Li, Haiyan Wang, Juan Wang, Yeying Sun, Chunxiang Zhang,

https://doi.org/10.18632/aging.103034 pp 6385—6400

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Bian W, Jing X, Yang Z, Shi Z, Chen R, Xu A, Wang N, Jiang J, Yang C, Zhang D, Li L, Wang H, Wang J, et al, . Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis. . 12:6385-6400. https://doi.org/10.18632/aging.103034

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                TY  - JOUR
                AU  - Bian, Weihua 
                AU  - Jing, Xiaohong 
                AU  - Yang, Zhiyu 
                AU  - Shi, Zhen 
                AU  - Chen, Ruiyao 
                AU  - Xu, Aili 
                AU  - Wang, Na 
                AU  - Jiang, Jing 
                AU  - Yang, Cheng 
                AU  - Zhang, Daolai 
                AU  - Li, Lan 
                AU  - Wang, Haiyan 
                AU  - Wang, Juan 
                AU  - Sun, Yeying 
                AU  - Zhang, Chunxiang 
                TI  - Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103034
                DO  - 10.18632/aging.103034
                SP  - 6385
                EP  - 6400
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Bian, Weihua 
                AU  - Jing, Xiaohong 
                AU  - Yang, Zhiyu 
                AU  - Shi, Zhen 
                AU  - Chen, Ruiyao 
                AU  - Xu, Aili 
                AU  - Wang, Na 
                AU  - Jiang, Jing 
                AU  - Yang, Cheng 
                AU  - Zhang, Daolai 
                AU  - Li, Lan 
                AU  - Wang, Haiyan 
                AU  - Wang, Juan 
                AU  - Sun, Yeying 
                AU  - Zhang, Chunxiang 
                TI  - Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103034
                DO  - 10.18632/aging.103034
                SP  - 6385
                EP  - 6400
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) play important roles in the development of vascular diseases. However, the effect of lncRNA NORAD on atherosclerosis remains unknown. This study aimed to investigate the effect NORAD on endothelial cell injury and atherosclerosis. Ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and high-fat-diet (HFD)-fed ApoE&#x2212;/&#x2212; mice were used as in vitro and in vivo models. Results showed that NORAD-knockdown induced cell cycle arrest in G0/G1 phase, aggravated ox-LDL-induced cell viability reduction, cell apoptosis, and cell senescence along with the increased expression of Bax, P53, P21 and cleaved caspase-3 and the decreased expression of Bcl-2. The effect of NORAD on cell viability was further verified via NORAD-overexpression. NORAD- knockdown increased ox-LDL-induced reactive oxygen species, malondialdehyde, p-IKB&#x3B1; expression levels and NF-&#x3BA;B nuclear translocation. Proinflammatory molecules ICAM, VCAM, and IL-8 were also increased by NORAD- knockdown. Additionally, we identified the strong interaction of NORAD and IL-8 transcription repressor SFPQ in HUVECs. In ApoE&#x2212;/&#x2212; mice, NORAD-knockdown increased the lipid disorder and atherosclerotic lesions. The results have suggested that lncRNA NORAD attenuates endothelial cell senescence, endothelial cell apoptosis, and atherosclerosis via NF-&#x3BA;B and p53&#x2013;p21 signaling pathways and IL-8, in which NORAD-mediated effect on IL-8 might through the direct interaction with SFPQ.
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Spermidine and spermine delay brain aging by inducing autophagy in SAMP8 mice

Ting-Ting Xu, Han Li, Zhao Dai, George K. Lau, Ben-Yue Li, Wen-Li Zhu, Xiao-Qi Liu, Hao-Fei Liu, Wei-Wu Cai, Shui-Qing Huang, Qi Wang, Shi-Jie Zhang,

https://doi.org/10.18632/aging.103035 pp 6401—6414

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Xu T, Li H, Dai Z, Lau GK, Li B, Zhu W, Liu X, Liu H, Cai W, Huang S, Wang Q, Zhang S, . Spermidine and spermine delay brain aging by inducing autophagy in SAMP8 mice. . 12:6401-6414. https://doi.org/10.18632/aging.103035

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                TY  - JOUR
                AU  - Xu, Ting-Ting 
                AU  - Li, Han 
                AU  - Dai, Zhao 
                AU  - Lau, George K. 
                AU  - Li, Ben-Yue 
                AU  - Zhu, Wen-Li 
                AU  - Liu, Xiao-Qi 
                AU  - Liu, Hao-Fei 
                AU  - Cai, Wei-Wu 
                AU  - Huang, Shui-Qing 
                AU  - Wang, Qi 
                AU  - Zhang, Shi-Jie 
                TI  - Spermidine and spermine delay brain aging by inducing autophagy in SAMP8 mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103035
                DO  - 10.18632/aging.103035
                SP  - 6401
                EP  - 6414
                PY  - 
                AB  - The natural polyamine spermidine and spermine have been reported to ameliorate aging and aging-induced dementia. However, the mechanism is still confused. An aging model, the senescence accelerated mouse-8 (SAMP8), was used in this study. Novel object recognition and the open field test results showed that oral administration of spermidine, spermine and rapamycin increased discrimination index, modified number, inner squares distance and times. Spermidine and spermine increased the activity of SOD, and decreased the level of MDA in the aging brain. Spermidine and spermine phosphorylate AMPK and regulate autophagy proteins (LC3, Beclin 1 and p62). Spermidine and spermine balanced mitochondrial and maintain energy for neuron, with the regulation of MFN1, MFN2, DRP1, COX IV and ATP. In addition, western blot results (Bcl-2, Bax and Caspase-3, NLRP3, IL-18, IL-1&#x3B2;) showed that spermidine and spermine prevented apoptosis and inflammation, and elevate the expression of neurotrophic factors, including NGF, PSD95and PSD93 and BDNF in neurons of SAMP8 mice. These results indicated that the effect of spermidine and spermine on anti-aging is related with improving autophagy and mitochondrial function.
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Electrical stimulation inhibits Val-boroPro-induced pyroptosis in THP-1 macrophages via sirtuin3 activation to promote autophagy and inhibit ROS generation

Lin Cong, Ziyu Gao, Yinghong Zheng, Ting Ye, Zitong Wang, Pengyu Wang, Manman Li, Bowen Dong, Wei Yang, Quanfeng Li, Shupei Qiao, Cao Wang, Yijun Shen, Hong Li, Weiming Tian, Liming Yang,

https://doi.org/10.18632/aging.103038 pp 6415—6435

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Cong L, Gao Z, Zheng Y, Ye T, Wang Z, Wang P, Li M, Dong B, Yang W, Li Q, Qiao S, Wang C, Shen Y, et al, . Electrical stimulation inhibits Val-boroPro-induced pyroptosis in THP-1 macrophages via sirtuin3 activation to promote autophagy and inhibit ROS generation. . 12:6415-6435. https://doi.org/10.18632/aging.103038

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                TY  - JOUR
                AU  - Cong, Lin 
                AU  - Gao, Ziyu 
                AU  - Zheng, Yinghong 
                AU  - Ye, Ting 
                AU  - Wang, Zitong 
                AU  - Wang, Pengyu 
                AU  - Li, Manman 
                AU  - Dong, Bowen 
                AU  - Yang, Wei 
                AU  - Li, Quanfeng 
                AU  - Qiao, Shupei 
                AU  - Wang, Cao 
                AU  - Shen, Yijun 
                AU  - Li, Hong 
                AU  - Tian, Weiming 
                AU  - Yang, Liming 
                TI  - Electrical stimulation inhibits Val-boroPro-induced pyroptosis in THP-1 macrophages via sirtuin3 activation to promote autophagy and inhibit ROS generation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103038
                DO  - 10.18632/aging.103038
                SP  - 6415
                EP  - 6435
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cong, Lin 
                AU  - Gao, Ziyu 
                AU  - Zheng, Yinghong 
                AU  - Ye, Ting 
                AU  - Wang, Zitong 
                AU  - Wang, Pengyu 
                AU  - Li, Manman 
                AU  - Dong, Bowen 
                AU  - Yang, Wei 
                AU  - Li, Quanfeng 
                AU  - Qiao, Shupei 
                AU  - Wang, Cao 
                AU  - Shen, Yijun 
                AU  - Li, Hong 
                AU  - Tian, Weiming 
                AU  - Yang, Liming 
                TI  - Electrical stimulation inhibits Val-boroPro-induced pyroptosis in THP-1 macrophages via sirtuin3 activation to promote autophagy and inhibit ROS generation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103038
                DO  - 10.18632/aging.103038
                SP  - 6415
                EP  - 6435
                PY  - 
                AB  - The incidence of atherosclerosis (AS), a major contributor to cardiovascular disease, is steadily rising along with an increasingly older population worldwide. Pyroptosis, a form of inflammatory programmed cell death, determines the release of pro-inflammatory mediators by endothelial cells, smooth muscle cells, and atheroma-associated macrophages and foam cells, thereby playing a critical role in AS progression. Canonical pyroptosis is mediated by inflammasome formation, activation of caspase-1, and maturation and release of proinflammatory cytokines. Electrical stimulation (ES) is a noninvasive, safe therapy that has been shown to alleviate symptoms in several health conditions. Here, we investigated the anti-inflammatory and anti-pyroptotic effects of ES in human THP-1 macrophages treated with the dipeptidyl peptidase inhibitor Val-boroPro (VbP). We found that ES downregulated NOD-like receptor family protein 3 (NLRP3) inflammasome, ASC, and caspase-1 expression and abrogated the release of Interleukin-1&#x3B2; (IL-1&#x3B2;) and Interleukin-18 (IL-18), indicating effective pyroptosis inhibition. These changes were paralleled by a reduction in reactive oxygen species (ROS) production, reversal of VbP-induced sirtuin3 (Sirt3) downregulation, deacetylation of ATG5, and induction of autophagy. These findings suggest that ES may be a viable strategy to counteract pyroptosis-mediated inflammation in AS by raising Sirt3 to promote autophagy and inhibit ROS generation.
                ER  -

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Sevoflurane inhibits neuronal migration and axon growth in the developing mouse cerebral cortex

Dongdong Chai, Jia Yan, Chunzhu Li, Yu Sun, Hong Jiang,

https://doi.org/10.18632/aging.103041 pp 6436—6455

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Chai D, Yan J, Li C, Sun Y, Jiang H, . Sevoflurane inhibits neuronal migration and axon growth in the developing mouse cerebral cortex. . 12:6436-6455. https://doi.org/10.18632/aging.103041

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                TY  - JOUR
                AU  - Chai, Dongdong 
                AU  - Yan, Jia 
                AU  - Li, Chunzhu 
                AU  - Sun, Yu 
                AU  - Jiang, Hong 
                TI  - Sevoflurane inhibits neuronal migration and axon growth in the developing mouse cerebral cortex
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103041
                DO  - 10.18632/aging.103041
                SP  - 6436
                EP  - 6455
                PY  - 
                AB  - The highly organized laminar structure of the mammalian brain is dependent on successful neuronal migration, and migration deficits can cause lissencephaly and behavioral and cognitive defects. Here, we investigated the contribution of neuronal migration dysregulation to anesthesia-induced neurotoxicity in the fetal brain. Pregnant C57BL/6 mice at embryonic day 14.5 received 2.5% sevoflurane daily for two days. Cortical neuron migration and axon lengths were evaluated using GFP immunostaining. Morris water maze tests were performed to assess the effects of sevoflurane exposure on spatial memory in offspring. We found that sevoflurane exposure decreased axon length and caused cognitive defects in young mice. RNA sequencing revealed that these defects were associated with reduced neuro-oncological ventral antigen 2 (Nova2) expression. In utero electroporation experiments using Nova2 shRNA recapitulated this finding. Nova2 shRNA inhibited neuronal migration and decreased axon lengths. Finally, we found that Netrin-1/Deleted in Colorectal Cancer (Dcc) proteins acted downstream of Nova2 to suppresses neuronal migration. These findings describe a novel mechanism by which prenatal anesthesia exposure affects embryonic neural development and postnatal behavior.
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FGF22 promotes generation of ribbon synapses through downregulating MEF2D

Shuna Li, Jingchun He, Yupeng Liu, Jun Yang,

https://doi.org/10.18632/aging.103042 pp 6456—6466

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Li S, He J, Liu Y, Yang J, . FGF22 promotes generation of ribbon synapses through downregulating MEF2D. . 12:6456-6466. https://doi.org/10.18632/aging.103042

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                TY  - JOUR
                AU  - Li, Shuna 
                AU  - He, Jingchun 
                AU  - Liu, Yupeng 
                AU  - Yang, Jun 
                TI  - FGF22 promotes generation of ribbon synapses through downregulating MEF2D
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103042
                DO  - 10.18632/aging.103042
                SP  - 6456
                EP  - 6466
                PY  - 
                AB  - Cochlear ribbon synapses play a pivotal role in the prompt and precise acoustic signal transmission from inner hair cells (IHCs) to the spiral ganglion neurons, while noise and aging can damage ribbon synapses, resulting in sensorineural hearing loss. Recently, we described reduced fibroblast growth factor 22 (FGF22) and augmented myocyte enhancer factor 2D (MEF2D) in an ototoxicity mouse model with impaired ribbon synapses. Here, we investigated the mechanisms that underlie the FGF22/MEF2D- regulated impairment of ribbon synapses. We generated adeno-associated virus (AAV) carrying FGF22, shFGF22, MEF2D, shMEF2D, calcineurin (CalN), shCalN or corresponding scramble controls for transduction of cultured mouse hair cells. We found that FGF22 was a suppressor for MEF2D, but not vice versa. Moreover, FGF22 likely induced increases in the calcium influx into IHCs to activate CalN, which subsequently inhibited MEF2D. Cochlear infusion of AAV-shFGF22 activated MEF2D, reduced ribbon synapse number and impaired hearing function, which were all abolished by co-infusion of AAV-shMEF2D. Hence, our data suggest that the ribbon synapses may be regulated by FGF22/calcium/CalN/MEF2D signaling, which implied novel therapeutic targets for hearing loss.
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Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease

Ruibing Li, Sam Toan, Hao Zhou,

https://doi.org/10.18632/aging.102972 pp 6467—6485

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Li R, Toan S, Zhou H, . Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease. . 12:6467-6485. https://doi.org/10.18632/aging.102972

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                TY  - JOUR
                AU  - Li, Ruibing 
                AU  - Toan, Sam 
                AU  - Zhou, Hao 
                TI  - Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102972
                DO  - 10.18632/aging.102972
                SP  - 6467
                EP  - 6485
                PY  - 
                AB  - Nutrient oversupply and mitochondrial dysfunction play central roles in nonalcoholic fatty liver disease (NAFLD). The mitochondria are the major sites of &#x3B2;-oxidation, a catabolic process by which fatty acids are broken down. The mitochondrial quality control (MQC) system includes mitochondrial fission, fusion, mitophagy and mitochondrial redox regulation, and is essential for the maintenance of the functionality and structural integrity of the mitochondria. Excessive and uncontrolled production of reactive oxygen species (ROS) in the mitochondria damages mitochondrial components, including membranes, proteins and mitochondrial DNA (mtDNA), and triggers the mitochondrial pathway of apoptosis. The functionality of some damaged mitochondria can be restored by fusion with normally functioning mitochondria, but when severely damaged, mitochondria are segregated from the remaining functional mitochondrial network through fission and are eventually degraded via mitochondrial autophagy, also called as mitophagy. In this review, we describe the functions and mechanisms of mitochondrial fission, fusion, oxidative stress and mitophagy in the development and progression of NAFLD.
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Correction for: Rapamycin doses sufficient to extend lifespan do not compromise muscle mitochondrial content or endurance

Lan Ye, Anne L. Widlund, Carrie A. Sims, Dudley W. Lamming, Yuxia Guan, James G. Davis, David M. Sabatini, David E. Harrison, Ole Vang, Joseph A. Baur,

https://doi.org/10.18632/aging.102976 pp 6486—6487

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Ye L, Widlund AL, Sims CA, Lamming DW, Guan Y, Davis JG, Sabatini DM, Harrison DE, Vang O, Baur JA, . Correction for: Rapamycin doses sufficient to extend lifespan do not compromise muscle mitochondrial content or endurance. . 12:6486-6487. https://doi.org/10.18632/aging.102976

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Correction for: Lycorine induces autophagy-associated apoptosis by targeting MEK2 and enhances vemurafenib activity in colorectal cancer

Man Hu, Zhaomin Yu, Peiyuan Mei, Jinxiao Li, Dan Luo, Haiming Zhang, Minfeng Zhou, Fengxia Liang, Rui Chen,

https://doi.org/10.18632/aging.103011 pp 6488—6489

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Hu M, Yu Z, Mei P, Li J, Luo D, Zhang H, Zhou M, Liang F, Chen R, . Correction for: Lycorine induces autophagy-associated apoptosis by targeting MEK2 and enhances vemurafenib activity in colorectal cancer. . 12:6488-6489. https://doi.org/10.18632/aging.103011

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Volume 12, Issue 7

About the Cover

Editorial

Iris Oving, Marieke T. Blom, Hanno L. Tan,

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Priority Research Papers

Jingjing Zhao, Gen Li, Xuan Zhao, Xin Lin, Yunge Gao, Nuno Raimundo, Geng-Lin Li, Wei Shang, Hao Wu, Lei Song,

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Eliene Albers, Alexandra Avram, Mauro Sbroggio, Oscar Fernandez-Capetillo, Andres J. Lopez-Contreras,

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Rongyang Li, Bojiang Li, Ming Shen, Yan Cao, Xuan Zhang, Weijian Li, Jingli Tao, Wangjun Wu, Honglin Liu,

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Ye Zhang, Xinxin Liu, Junying Zhang, Yuanyuan Xu, Jie Shao, Yue Hu, Peng Shu, Haibo Cheng,

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Yao Chen, Lin-Shuang Zhang, Jin-Ling Ren, Ya-Rong Zhang, Ning Wu, Mo-Zhi Jia, Yan-Rong Yu, Zhong-Ping Ning, Chao-Shu Tang, Yong-Fen Qi,

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Cheng Tan, Yimeng Dai, Xiaoyang Liu, Guifang Zhao, Weiyao Wang, Jia Li, Ling Qi,

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Mahmoud Al-Azab, Bing Wang, Abdalkhalig Elkhider, Williams Walana, Weiping Li, Bo Yuan, Yunshan Ye, Yawei Tang, Marwan Almoiliqy, Salah Adlat, Jing Wei, Yan Zhang, Xia Li,

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Xi Chen, Chiyao Wang, Pei Yang, Lei Shi, Haiyan Wang,

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Jingtai Zhi, Jiaoyu Yi, Mengran Tian, Huijuan Wang, Ning Kang, Xiangqian Zheng, Ming Gao,

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Mingsheng Cai, Xiaowen Ou, Yiwen Li, Xingmei Zou, Zuo Xu, Yuanfang Wang, Hao Peng, Yangxi Deng, Yingjie Guo, Manjiao Lu, Weidong Gan, Tao Peng, Meili Li,

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Yu-Chen Lin, Mei-Chuan Chen, Tsung-Han Hsieh, Jing-Ping Liou, Chun-Han Chen,

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Jiong Yu, Xiaowei Shi, Chunzhang Yang, Petra Bullova, Christopher S. Hong, Cody L. Nesvick, Pauline Dmitriev, Karel Pacak, Zhengping Zhuang, Hongcui Cao, Lanjuan Li,

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Ming Hong, Han Zhu, Qian Sun, Yu Zhu, Yi Miao, Hui Yang, Hai-Rong Qiu, Jian-Yong Li, Si-Xuan Qian,

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Qiqing Huang, Yan Chen, Shaoran Shen, Yuanyuan Wang, Liya Liu, Shuangshuang Wu, Wei Xu, Weihong Zhao, Mingyan Lin, Jianqing Wu,

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Kang Lin, Jun Huang, Hongliang Luo, Chen Luo, Xiaojian Zhu, Fanqin Bu, Han Xiao, Li Xiao, Zhengming Zhu,

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Mengqing Ma, Xin Wan, Min Gao, Binbin Pan, Dawei Chen, Qing Sun, Mengyu Zhang, Changgao Zhou, Tao Li, Hanchao Pan, Wei Shao, Zhihe Liu, Yue Chen, Changchun Cao,

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Deze Zhao, Chuantao Zhang, Man Jiang, Yongjie Wang, Yu Liang, Li Wang, Kang Qin, Faisal UL Rehman, Xiaochun Zhang,

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Fei Ji, Ci-Qiu Yang, Xiao-Ling Li, Liu-Lu Zhang, Mei Yang, Jie-Qing Li, Hong-Fei Gao, Teng Zhu, Min-Yi Cheng, Wei-Ping Li, Si-Yan Wu, Ai-Ling Zhong, Kun Wang,

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