越来越庞大的衰老抗衰老研究中国军团 —— 2016 杭州衰老及老年病大会 “ 生煎包 ” 杭州的 G20 刚刚落下帷幕， 2016.9.9 ，乱花迷人的西湖边，衰老抗衰老研究中国军团就在杭州师范大学的主持下开了个很 “ 洋气 ” 的大会。为了让国内衰老研究同行跟上衰老研究新时代混乱的步伐，这里把会议消息介绍如下，不懂 “ 鹰文 ” 的民科就请将就着猜两下。看不懂没有关系，科学前沿，特别是像衰老这样的 “ 科学航空母舰 ” 巨问题，世界上是没有几个大侠真的能雾里看出花来的。 下面先给出节选，想一口吃撑成胖子，或是想看看作报告的大侠的尊容的可看博文后面的附件： 衰老研究所 , 杭州师范大学 E-News ——2016 年 7-8 月期 2016 InternationalConference on Aging Research: Molecular Mechanismsand Associated Diseases Hangzhou, Zhejiang,China September 9-11, 2016 Table of Contents Conference Committees.................................................................................................1 Program..........................................................................................................................2 Plenary I Healthy aging andmetabolism .......................................................................6 Guang Ning............................................................................... 错误 ! 未定义书签。 Session 1: Mechanisms regulatingaging..................................................................... 7 Jing-Dong Jackie Han...............................................................................................7 Zhongjun Zhou..........................................................................................................8 Session 2: Stress signaling andmetabolic aging ....................................................... 10 Nick Musi................................................................................................................10 Feng Liu..................................................................................................................11 Yuying Zhang, Kaiyuan Wu, WentingSu, Chang Chen ......................................... 12 Session 3: Inflammation in agingand related disorders ............................................ 14 Bryan R. G.Williams, Afsar U.Ahmed ................................................................... 14 Matthew J Sweet.....................................................................................................15 Hui Y. Lan...............................................................................................................16 Session 4: Neural degenerativedisease in aging ....................................................... 19 Zhuohua Zhang.......................................................................................................19 Biao Chen................................................................................................................20 Jun-Ping Liu............................................................................................................21 Yanjiang Wang........................................................................................................22 Xiaotao Li ................................................................................................................23 Plenary II Telomere and agingdiseases....................................................................... 25 Jerry W. Shay ..........................................................................................................26 Session 5: Telomere and genomeinstability in aging (1) .......................................... 27 Peili Gu, Yang Wang, SusanBailey, et al. ...............................................................27 Ming Lei.................................................................................... 错误 ! 未定义书签。 Laetitia Maestroni, StéphaneCoulon, Vincent Géli ................................................ 29 Zhou Songyang.......................................................................................................30 Ning Liu, Deqiang Ding andYu-Sheng Cong ......................................................... 31 Session 6: Mitochondrialdysfunction in aging .........................................................32 Michael V Berridge.................................................................................................32 Quan Chen...............................................................................................................34 Justin St. John..........................................................................................................35 Session 7: Tissue stem cell aging..............................................................................37 Peter Lansdorp........................................................................................................37 Zhenyu Ju................................................................................................................38 Lin Liu, Jiao Yang...................................................................................................39 Guang-Hui Liu........................................................................................................41 Session 8: Cardiovascular andother aging-related diseases ..................................... 43 QiulunLu, YufengYao, QingKennethWang ............................................................ 43 Michal Berndt..........................................................................................................45 Jian Li........................................................................................ 错误 ! 未定义书签。 Xiangmei Chen........................................................................................................46 Plenary III Epigenetic regulationof longevity............................................................. 47 Vera Gorbunova ......................................................................................................48 Session 9: Longevity andmechanisms...................................................................... 49 Xiao-Li Tian............................................................................................................49 Yousin Suh..............................................................................................................51 Xiao-Ling Li, Ze Yang............................................................................................52 Ejun Huang..............................................................................................................53 Session 10: Telomere and genomeinstability in aging (2) ........................................ 54 Jing Peng, Qiong-Di Zhang,Jin-Qiu Zhou ............................................................. 54 Eric Gilson..............................................................................................................56 Jun Xing, Yiling Ying, Wai IanLeong, et al ........................................................... 57 Yong Zhao...............................................................................................................59 Session 11: Signaling defect inaging ........................................................................60 John Speakman........................................................................................................60 Yang Wang, Zhi-Xiong Jim Xiao............................................................................ 61 Jianfeng Liu.............................................................................................................62 Baohua Liu..............................................................................................................63 Session 12: Mechanisms of ovarianaging ................................................................ 64 Hui Chen, YechunRuan, XiaohuaJiang, Hsiao Chang Chan .................................. 64 Chao Yu, Yin-Li Zhang, Heng-YuFan .................................................................... 66 Plenary IV Signaling networks intissue stem cell aging ............................................. 68 Xinhua Feng............................................................................................................69 Poster Presentations.....................................................................................................70 I. Brain degenerative diseases...................................................................................71 Fei Dou....................................................................................................................71 Jian Fu, Zi Zhou, Ya Fang.......................................................................................72 Feijuan Huang, Xianxiang Tian,Guangshan Xie, et al. .......................................... 73 Wang-Sheng Jin, Yan-JiangWang...........................................................................75 Zhigang Liu, Yuwei Chen, QianLiu, et al .............................................................. 76 Lin-Lin Shen, Yan-Jiang Wang ...............................................................................77 Fei Wang, Guangming Chang, XinGeng................................................................ 78 Ping Wang, Zi Zhou, Ya Fang.................................................................................79 II. Cardiovascular diseases........................................................................................80 Shi-lian Hu, Xiang Fang, Shi Yin,Gan Shen .......................................................... 80 III. Cancer biology.....................................................................................................82 Yu-Sheng Guo, Hong-Guo Jiang,Shu-Ting Jia, Ying Luo ..................................... 82 Dongsheng Shang, Yanfang Wu,Zhigang Tu ......................................................... 84 Hang Yu, Xiaosun Liu, YanyunHong, et al ............................................................ 85 IV. Digestion, metabolism andendocrine diseases .................................................... 86 Yu-ning Chen, Meng-yun Cai, ShunXu, et al ........................................................ 86 Fangyuan Dong, Yan Zhang, YiqinHuang, et al ..................................................... 87 Fengyi Gao, Guoping Li, Chao Liu,et al ................................................................ 88 Weiquan Li..............................................................................................................89 Zhen Li....................................................................................................................90 Zhongchi Li,Kang Xu, Sen Zhao, etal ................................................................... 91 Fuzhi Lian, Jinquan Wang, YuchaoLiu, et al .......................................................... 92 Yang Liu, Zhang Rui, Alex.....................................................................................94 Zhigang Liu, Qinglian Qiao, YaliSun, et al ............................................................ 95 Guoliang Lv, Yiting Guan, Wei Tao........................................................................ 96 Chi-Hao Shao, Kun Wu, Hai-Li Li,et al ................................................................. 98 Xue-qing Zhang, Yi Yu, Fang Pang,et al ................................................................ 99 Ru-Yi Zhang, Kang Gao, Dan Zhao,et al ............................................................. 100 Yin-Li Zhang, Jue Zhang, Long-WenZhao, Heng-Yu Fan ................................... 101 Zepeng Zhang, Tianpeng Zhang,Haiying Liu, et al ............................................. 102 Mushi Chen...........................................................................................................103 V. Virus infection and immunerelated diseases ...................................................... 104 Yang Xiang, Yuyan Zhang, YunZhang ................................................................. 104 VI. Cell therapy and stem cellbiology ....................................................................106 Hong-Jing Cui, Xin-Gang Cui, WeiZhao, et al .................................................... 106 Zhi-Wen Jiang, Hui-Ling Zheng,Wei-Chun Chen, et al ....................................... 107 Jianfeng Liu...........................................................................................................108 Shun Xu, Hai-Jiao Huang, BingZhang, et al ........................................................ 109 Wei Zhao, Hua-zhen Zheng, TaoZhou, et al ........................................................ 110 VII. Traditional Chinesemedicine, drug development and clinical trials ............... 111 Lei Peng, Jing Liu, Wen-HuiHuang, et al ............................................................ 111 Ling Xiao..............................................................................................................113 Cheng-Kui Xiu, Yan Lei.......................................................................................114 Jing Yang, Yan Lei.................................................................................................115 List of Participants.....................................................................................................116 Plenary I Healthy aging and metabolism Session 1: Mechanisms regulatingaging A systems approach to reverseengineer lifespan extension by dietary restriction Jing-Dong Jackie Han Dietary restriction (DR) is themost powerful natural means to extend lifespan. Although several genes can mediate responses to alternate DR regimens, no single genetic intervention has recapitulated the full effects of DR, and nounified system is known for different DR regimens. Here we obtain temporally resolved transcriptomes during chronic DR and intermittent fasting (IF) in Caenorhabditis elegans, and find that early and late responses involve metabolisms, and cell cycle/DNA damage, respectively. We uncover three network modules of regulators by target specificity. By genetic manipulations of nodes representing discrete modules, we induce transcriptomes that progressively resemble DR as multiple nodes are perturbed. Targeting all three nodes simultaneously results in extremely long-lived animals that that are refractory to DR. These results and dynamic simulations demonstrate that extensive feedback controls among regulators may be leveraged todrive the regulatory circuitry to a younger steady state, recapitulating thefull effect of DR. Genetics and epigenetics: fromaccelerated aging to human aging Zhongjun Zhou Faculty of Medicine, TheUniversity of Hong Kong Abnormal splicing of LMNA genegives rise to a truncated prelamin A termed as progerin which is accumulated inpatients suffering from Hutchinson-Gilford progeria Syndrome. Lamin A interacts with and activates a variety of nuclear factors including histone modifying enzymes such as MOF, SUV39H1, SIRT1 and SIRT6. The presence of progerin compromises the proper association of these important nuclear proteins with nuclear matrix,leading to defective chromatin remodeling in response to DNA damage. The nuclear lamin A also serves as activators for SIRT1 and SIRT6 that are critical in stem cell maintenance and DNA damage repair. Targeting the epigenetic changes significantly rescue the cellular senescence and extend lifespan in progeroid mice.Our studies suggest a profound role forlamin A in regulating nuclear architecture, chromatin dynamics and stem cellpotency that all contribute to the aging processes Acknowledgements These works are supported bygrants from Research Grant Council (CRF/GRF) of Hong Kong and Natural ScienceFoundation of China. Session 2: Stress signaling andmetabolic aging Pros and cons of suppressinginflammation in aging Nick Musi Adipose mTORC1 signaling andfunction in metabolic homeostasis Feng Liu Metabolic Syndrome ResearchCenter, the Second Xiangya Hospital, Central South University Mammalian/Mechanistic target of rapamycin (mTOR) is a key energy sensor and its dysregulation is associated with various aging-associated diseases. Studies have shown that inhibition of themTOR signaling pathway extends lifespan in experimental animals. However, chronic and whole-body suppression of this signaling pathway may lead to serious side effects, suggesting that tissue-specific inhibition of this signaling pathway may promote healthy aging. Adipose tissue synthesizes and secretes numerous hormones or cytokines (adipokines) that play a major role in the maintenance of energy homeostasis in our body. In this presentation, I will briefly summarize our recent studies on the roles of adipose tissue mTOR complex I (mTORC1) signaling in regulating beige fat development and energy homeostasis. Comprehensive analysis of key signaling pathways involved in the regulation of adipocytebiology and function should shed newlight on the development of novel therapeutic treatments for variousaging-associated diseases. Say NO to aging: the key enzymeof S-nitrosation GSNOR in age related cognitive impairment Yuying Zhang, Kaiyuan Wu, WentingSu, Chang Chen National Laboratory of Biomacromolecules,Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Chaoyang District,Beijing 100101, China. The free radical theory of aging proposed by Harman in 1956 had been paid widely attention, whichsuggests that free radicals damage cellular macromolecules cause aging. However,more and more studies show the other side of free radicals in signaling and physiological function. Here we foundthat S-nitrosoglutathione reductase (GSNOR), the key enzyme metabolizing the intracellular nitric oxide (NO) and S-nitrosation, significantly increased in the hippocampus of both aging human and mice. Neuronal specific overexpression of GSNOR leads tocognitive impairment, long-term potentiation (LTP) defect and lower dendritespine density. While knock out GSNOR rescued the age related cognitive impairment. We then performed liquid chromatography-tandem mass spectrometry (LC-MS/MS)-basedquantitative proteomic analysis of protein S-nitrosation and foundS-nitrosation of CamKIIα was significantly decreased in the hippocampus of aging mice and GSNOR transgenic mice. In consistant with the change of CamKIIα S-nitrosation, the accumulation of CamKIIα in hippocampal synaptosomal and its downstream signaling p-GLUR1 and CREB/c-fos were also significantly decreased, which can all be rescued in GSNOR knock out mice. We further verified that the S-nitrosationof CamKIIα is responsible for the CamKIIα synaptosomal accumulation by CamKIIαS-nitrosated sites (C280/289) mutant experiment. The cognitive impairment in GSNORtransgenic mice can be rescued by up-regulation of the NO signaling pathway or CamKIIα/CREB signaling pathway. In summary, our research demonstrated that GSNOR impaired cognitive function in aging through de-nitrosation of CamkIIα. GSNOR is a new potential target for treatment of the agerelated cognitive impairment. In contrast to the free radical theory of aging,NO signaling deficiency may be the main cause to induce age-related cognitive impairment. In addition, we explored the physiological function of S-nitrosation of CamKIIα for the firsttime. Session 3: Inflammation in agingand related disorders The role of Integrin-linkedkinase in aging, innate immunity and cancer Bryan R. G.Williams and Afsar U.Ahmed Centre for Cancer Research,Hudson Institute of Medical Research, Clayton, Victoria 3164, Australia Integrin-Linked Kinase (ILK) is aubiquitously expressed protein that forms an important component of cell matrix adhesions to regulate integrin function in response to a wide variety of extracellularstimuli. ILK dysregulation is a feature of different human diseases including cancer and cardiovascular disease. Although deletion of ILK is embryonic lethal, reduced levels of ILK havebeen associated with extended lifespans in C. elegans and Drosophila. Reduced ILK levels also lessen the effects of normal cardiac aging in Drosophila. In primary cardiac myocytes reduced ILK expression prevents the phenotypic changes associated with senescence seen in aging cells. Conversely an increase in ILK expression can induce premature senescence. Overexpression of ILK is also a feature of different cancers. Impaired innate immune responses are a feature of aging but whether ILK is implicated has not been determined. However, we have shown that there is a role for ILK in regulating the innate immunesystem. Pharmacologic or genetic inhibition of ILK in mouse embryo fibroblasts and macrophages selectively blocks LPS-induced production of the pro-inflammatory cytokinesILK is required for TLR-induced NF-B activation and transcriptional induction of TNF-, through an ILK-PI3K axis. The modulation of LPS-induced TNF- synthesis by ILK does not involve the classical NF-B pathway since IkB degradation and p65 nuclear translocation are both unaffected by ILK inhibition. Instead, ILK is involved in a non-classical activation of NF-B signalingby modulating the phosphorylation of p65 at ser536. Furthermore, ILK-mediated non-classical NF-Bactivation through p65 ser536 phosphorylation also exists in a host-pathogen interaction in Helicobacter pyroli infection. Thus ILK as a critical regulatory molecule for NF-B- mediated proinflammatory signaling pathwayand regulation of innate immune responses. Innate immune pattern recognitionreceptors and pathological inflammatory responses Matthew J Sweet Institute for MolecularBioscience, University of Queensland, Brisbane, Qld, 4072, Australia Aging populations areparticularly susceptible to a range of chronic inflammation-related diseases, as well as infectious diseases. Innate immune cells such as macrophages are central mediators of host defence against invading pathogens, and also coordinate inflammatory responses. These cells detect and respond to danger through several families of pattern recognition receptors, of which the Toll-like receptors (TLRs) and inflammasome-forming Nod-like Receptors(NLRs) are the most widely studied. Histone deacetylases (HDACs), a family of enzymes most widely studied in the context of epigenetic control of gene expression, are key regulators of lifespan, inflammation and host defence. Inhibitors of these enzymeshave also been developed as anti-cancer drugs, but applications in other disease areas require more detailed knowledge of the role of individual HDACs in inflammation and host defence. We have been studying specific molecular mechanisms by which individual HDAC enzymes regulate macrophage-mediated inflammation and anti-bacterial responses,including via control of TLR-inducible mitochondrial reactive oxygen species production. These studies have revealed specific HDAC enzymes as new candidate targets for anti-inflammatory and anti-infective drug development. TGF-beta signaling in tissuerepair: role of Smad3 Hui Y. Lan Department of Medicine Therapeutics, Li Ka Shing Institute of Health Sciences, and Shenzhen Research Institute,The Chinese University of Hong Kong, Hong Kong, China Increasing evidence shows thatTGF- plays a critical role in cell repair or tissue fibrosis in both physiological and pathological conditions. It is now well accepted that TGF-βcauses cell cycle arrest at the G1 phase and thereby potently inhibits cell proliferation. However, the signaling mechanism of TGF- thatregulates these processes remains unknown. In the kidney, tubular epithelial cells (TECs) play a determinant rolein the tissue repair or fibrosis in response to acute injury and the degree of TEC regeneration or repair largely determines the progression or repair of acute kidney injury. We found that in a mouse model of ischemia-induced acute kidney injury, deletion of Smad3, a key downstream mediator of TGF-/Smad signaling, can protect kidney from the acute kidney injury by largely suppressing p27, thereby promoting CKD2/cyclin E-dependent TEC proliferation. In contract, enhanced Smad3 signaling by deleting Smad7, an inhibitor of Smad signaling, results in more severe acute kidneyinjury by impairing TEC regeneration via the Smad3-p27-dependent mechanism. We also found that activated Smad3 can bind directly to p27 to suppress CKD2/cyclinE-dependent TEC proliferation, which is inhibited by a Smad3 inhibitor, identifying activation of the Smad3-p27 pathway as a key mechanism bywhich TGF-1 induces the cell growth arrest at the G1 phase. More importantly,we also find that deletion of Smad7 promotes Smad3-mediated tissue fibrosisafter acute renal injury, suggesting that Smad3 palys a dual role intissue repair and fibrosis. In conclusion, TGF- may impair the tissue repair and cause renal fibrosis via the Smad3-dependent mechanism. Thus, targeting Smad3may represent as a novel and effective therapy for both acute and chronic kidney diseases, including aging-related kidney disorders. Session 4: Neural degenerativedisease in aging Molecular dissection of Parkinson disease Zhuohua Zhang Aging, alpha-Synuclein andParkinson's disease Biao Chen Lysosomal homeostasis, motor andnon-motor behavioral defects in Parkinson’s disease Jun-Ping Liu Institute of Aging Research,Hangzhou Normal University, Hangzhou, Zhejiang Province, China The lysosomes of various sizedintracellular organelles act as the waste disposal system by sequesteringunwanted materials transported from the cytoplasm and taken-up through endocytosis.With 50 different enzyme types including 50 cysteine, serine and aspartate proteases responsible for more than 30 different human genetic diseases, lysosomes require optimal homeostasis of pH, lipidic composition and ionic specificity for functionality. The lysosomal storage diseases aremonogenic disorders resulting from an accumulation of specific substratesowning to the inability to dispose them. Occurring at a frequency of 1 in 5,000live births, the diseases are genetically susceptive to inherited defects in genes that mainly encode lysosomal proteins and involved in aging-related diseases such as neurodegenerative disorders, cancer, cardiovascular diseases . ATP13A2 (PARK9) is a lysosomalintegral membrane ATPase enriched in the brain and mutated in early-onset Parkinsonism and dementia in man. To investigate the roles of ATP13A2 in the etiology of Parkinson disease (PD), we mapped ATP13A2 gene expression and intracellular localization, inactivated the ATP13A2gene, and determined its roles in trans-lysosomal membrane transport. Furthermore, we investigated the cellular basis of ATP13A2 mutation in PD phenotypes. We found thatthe orbital frontal, basal ganglia and hypothalamic regional aging is involvedin the behavioral compulsivity associated with anxiety and motor deficit,recapitulating PD impulse control disorder in a novel lysosomal setting. References: 1 Platt, F. M. Sphingolipid lysosomal storage disorders. Nature 510, 68-75, doi:10.1038/nature13476 (2014). 2 Platt, F. M., Boland, B. van der Spoel, A. C. The cell biology ofdisease: lysosomal storage disorders: the cellular impact of lysosomal dysfunction. The Journal of cell biology 199, 723-734, Peripheral therapeutic approachfor Alzheimer's disease Yanjiang Wang Potential role of the REGgammaproteasome in aging brain disorder Xiaotao Li Shanghai Key Laboratory ofRegulatory Biology, Institute of Biomedical Sciences, School of Life Sciences; Key Laboratory of Brain Functional Genomics, Ministry of Education,East China Normal University, Shanghai, 200062, China REGγ, an important proteasomeactivator to promote ubiquitin–independent protein degradation, has beendemonstrated to degrade numerous intact proteins and is involved in the regulation of importantbiological and pathological processes. We have previously shown that REGγ deficiencyresults in premature aging. Here we demonstrate that REGγ knockout (REGγ -/-) mice exhibitbrain disorders, including decreased working memories, defective prepulseinhibition (PPI), and disability in nest building, at the age of 8 months, reminiscent of brainaging. Mechanistically, REGγ promoted the degradation of GSK3β protein, akinase involved in phosphorylation of tau. Consistently, REGγ-depletion significantlyaugmented phosphorylated tau. Inhibition of GSK3β rescued the compromised PPIphenotypes in the REGγ -/- mice. Also, we found an age-dependent decrease in thetrypsin-like proteasomal activity in REGγ -/- mice brains. Our data provide new indicationsthat REGγ-proteasome dysfunction may be involved in brain degenerative diseases. Plenary II Telomere and aging diseases Role of telomeres and telomerasein aging and cancer Jerry W. Shay Department of Cell Biology,University of Texas Southwestern Medical Center, Dallas, TX USA Human telomeres progressively shorten throughout life. A hallmark of advanced malignancies is the ability forcontinuous cell divisions that almost universally correlates with the stabilization oftelomere length by the reactivation of telomerase. The repression of telomerase and shorter telomeres in humans may have evolved in part as an anti-cancer protection mechanism. Whilethere is still much we do not understand about the regulation of telomerase, it remains a very attractive and novel target for cancer therapeutics. This presentation will focus on the current state of advances in the telomerase area, identifies outstanding questions, and addresses areas and methods that need refinement. Session 5: Telomere and genomeinstability in aging (1) mPOT1a and mPOT1b play distinctroles in telomere end protection Peili Gu Aging is associated with progressive telomere shortening, resulting in the formation of dysfunctional telomeres that compromise tissue proliferation. However, dysfunctional telomeres also limit tumorigenesis by activating p53-dependent cellular senescence and apoptosis. Protection of Telomere 1 (POT1) is an essential component of the shelterin complex and functions to maintain chromosome stability byrepressing the activation of aberrant DNA damage and repair responses attelomeres. Humans have one hPOT1 gene, while mice possess two POT1 proteins, mPOT1a and mPOT1b. Sporadic and familial mutations in the oligosaccharide-oligonucleotide (OB) folds of hPOT1 have been identified in many cancers, but themechanism underlying how hPOT1 mutations initiate tumorigenesis has remained unclear. Here we show that the hPOT1 ‟ s OB-folds are essential for the protection of newly replicated telomeres. Oncogenic mutations in hPOT1 OB-fold fail to bind to ss telomeric DNA, eliciting a DNA damage response at telomeres thatpromote inappropriate chromosome fusionsvia the mutagenic alternative non-homologous end joining (A-NHEJ) pathway. hPOT1 mutations also result in telomere elongation and the formation of transplantable hematopoietic malignancies. Strikingly, conditional deletionof both mPot1a and p53 in mouse mammary epithelium resulted in development ofhighly invasive breast carcinomas and the formation of whole chromosomescontaining massive arrays of telomeric fusions. In contrast, we found that -Chk1 dependent DNA damage response to initiate a robust p53-independent, p73-dependent apoptotic pathway that limited stem cell proliferation but suppressed B-cell lymphomagenesis. Our results demonstrate that mPOT1a and mPOT1b play distinct roles in telomere end protection. Rearrangement of eroded telomeresin quiescent fission yeast cells Laetitia Maestroni, StéphaneCoulon, and Vincent Géli Cancer Research Centre ofMarseille, 27 boulevard Lei Roure, 13273, Marseille, France Telomere length is highlyvariable between tissues and organs and inversely related to chronological age. While the mechanisms of telomere maintenance have been investigated individing cells, little is known about the stability of telomeres in quiescent cellsand how dysfunctional telomeres are processed in non-proliferating cells. Totackle this issue we examined the stability of telomeres in quiescent cells using fission yeast cells that can be maintained for weeks in quiescence by nitrogen starvation. We have investigated how eroded telomeres are processed during quiescence and the fate of quiescent cells harboring these short telomeres. By deleting the RNA component of telomerase, we havefirst monitored the progressive telomere shortening after successive divisions. Then cells with short telomeres were placed under conditions in which they enter into quiescence. While WT telomeres are stable in quiescence, strikingly we observed that short telomeres were highly rearranged. We have determined that these rearrangements depended on homologous recombination and corresponded to the expansion of subtelomeric regions (named STEEx). We have identified a homologous sequenceof 226 bp within subtelomeric regions that might be used as a seed to promote recombination.We have further monitored the impact of STEEx on cell mortality during quiescenceand at the exit of quiescence. We first observed that the mortality of cells inthe absence of telomerase is correlated with the shortening of telomeres and the time spent in quiescence.Second, STEEx were not maintained when cells exit quiescence to re-enter into the cell cycle. We thus describe in fission yeast a new mode of telomere maintenance in theabsence of telomerase that is promoted in quiescence. This discovery highlightshow non-dividing cells that harbor eroded telomeres may circumvent the lack ofa functional telomere protection in the absence of replication. Mechanisms of telomere protectionin human cells Zhou Songyang ……… E-News 2016年7-8月期.pdf
老年人生活质量引起全球科学家的关注， 2016 年 3 月 ESI 高被引论文 80 篇、热点论文 1 篇主题涉及老年人生活质量（详细 ESI 高被引论文请看附件）。老年人的生活质量是指老年人物质生活、精神文化生活、老年人生命（生存）质量，即老年人的身心健康、老年人的生活环境、老年人口的素质和老年人充分享有权利的总和。 2005-2016 年 5月 SCI 、 SSCI 收录了主题涉及老年人生活质量（ Older Adult* and Quality ofLife ）论文 6595 篇（论文 5766 篇、综述 829 篇），学科涉及老年病学、老年学、公共环境与职业健康、精神病学、护理学、康复、健康科学、临床神经病学、运动科学等学科，发文主要国家与地区有美国 3166 篇、加拿大 656 篇、澳大利亚 552 篇、英国 459 篇、荷兰 312 篇、德国 276 篇、西班牙 275 篇、中国 200 篇等。涉及 1426 种期刊如： Journalof the American Geriatrics Society 《美国老年病学会志》 148 篇、 Qualityof Life Research 《生命质量研究》 100 篇、 Aging Mental Health 《衰老心理健康》 91 篇、 Archives of Gerontology and Geriatrics 《老年医学与老年病学集刊》 91 篇、 BMC Public Health 《 BMC 公共健康》 72 篇、 PLOSONE 《公共图书馆网络版》 72 篇、 Journalof Gerontological Nursing 《老年病护理杂志》 67 篇、 American Journal of Geriatric Psychiatry 《美国老年精神病学杂志》 64 篇。 中国学者发表的 老年人生活质量 论文 200 篇，其中香港中文大学 35 篇、香港大学 33 篇、香港理工大学 21 篇、北京大学 9 篇、复旦大学 8 篇、香港城市大学 7 篇、上海交通大学 7 篇、中山大学 7 篇、安徽医科大学 6 篇。 6595 篇 SCI 、 SSCI 老年人生活质量 论文其中 ESI 高被引论文 80 篇、热点论文 1 篇， 发文主要国家与地区有美国 49 篇、加拿大 14 篇、英国 10 篇、澳大利亚 9 篇、德国 4 篇、中国 2 篇等，涉及 49 种期刊如： Annals of Internal Medicine 《内科学纪事》 8 篇、 Journal of the American GeriatricsSociety 《美国老年病学会志》 6 篇、 JAMAJournal of the American Medical Association 《美国医学会志》 5 篇、 Circulation 《循环》 4 篇 等。 老年人生活质量80篇ESI高被引论文、1篇热点论文.doc 中国学者 2 篇 ESI 高被引论文如下： 第 1 条，共 2 条 标题 : Socio-economic factors related with the subjective well-being of the rural elderly people living independently in China 作者 : Zhou, YC (Zhou, Yicheng); Zhou, LY (Zhou, Linyi); Fu, CL (Fu, Changluan); Wang, Y (Wang, You); Liu, QL (Liu, Qingle); Wu, HT (Wu, Hongtao); Zhang, RJ (Zhang, Rongjun); Zheng, LF (Zheng, Linfeng) 来源出版物 : INTERNATIONAL JOURNAL FOR EQUITY IN HEALTH 卷 : 14 文献号 : 5 DOI: 10.1186/s12939-015-0136-4 出版年 : JAN 17 2015 Web of Science 核心合集中的 被引频次 : 4 被引频次合计 : 4 引用的参考文献数 : 46 摘要 : Background: Many Chinese elderly increasingly face the serious problem of the empty nest phenomenon. The elderly living independently, also called empty-nest elderly, refers to elderly people living alone whose children left home. However few studies concerned about the subjective well-being (SWB) of the elderly living independently. Methods: This study employs The Memorial University of Newfoundland Scale of Happiness (MUNSH) to explore the SWB of the elderly living independently in rural areas of Wenzhou, a relatively developed region in China . 536 sampled are randomly selected. Results: The results indicate that participants obtained low scores in positive affect, positive experience, and the total SWB score, but high scores in negative affect and negative experience. Age, low education, poor health condition and little income were found to be negatively correlated with SWB. The SWB score of the elderly living with a spouse is higher than those who divorced or lost their spouse and the score of women is lower than that of men. In addition, the survey revealed that children's support has a positive influence on the SWB of the rural elderly living independently. Conclusions: The elderly living independently in rural Wenzhou, China have unfavorable SWB. Poor socio-economic statuses are negative impact factors. But the children's support can help to improve. Special attention is needed to those with lower socio-economic status and less children's support. 文献类型 : Article 作者关键词 : MUNSH; SWB; The elderly living independently; Wenzhou; China KeyWords Plus: QUALITY-OF-LIFE; MOUNTAINOUS COUNTY; OLDER-ADULTS; AREA; CARE; SATISFACTION; LONELINESS; HAPPINESS; SAMPLE; SCALE 地址 : Soochow Univ, Sch Polit Publ Adm, Collaborat Innovat Ctr New Type Urbanizat Socia, Suzhou, Peoples R China. Yunnan Univ Finance Econ, Sch Stastist Mathemet, Kunming, Peoples R China . Zhejiang Int Studies Univ, Sch Management, Hangzhou, Zhejiang, Peoples R China . NW Univ Xian, Sch Philosophy Sociol, Xian 710069, Peoples R China . Cent Univ Finance Econ, Sch Govt, Beijing, Peoples R China . Soochow Univ, Affiliated Hosp 1, Suzhou, Peoples R China . Nanjing Univ Sci Technol, Nanjing, Jiangsu, Peoples R China . Chinese Acad Sci, Nanjing, Jiangsu, Peoples R China . 通讯作者地址 : Zhang, RJ ( 通讯作者 ),Nanjing Univ Sci Technol, Nanjing, Jiangsu, Peoples R China. 电子邮件地址 : zhangrj1973@sohu.com; linfengzh@126.com 来源出版物页码计数 : 9 第 2 条，共 2 条 标题 : Physical activity in older people: a systematic review 作者 : Sun, F (Sun, Fei); Norman, IJ (Norman, Ian J.); While, AE (While, Alison E.) 来源出版物 : BMC PUBLIC HEALTH 卷 : 13 文献号 : 449 DOI: 10.1186/1471-2458-13-449 出版年 : MAY 6 2013 Web of Science 核心合集中的 被引频次 : 44 被引频次合计 : 45 引用的参考文献数 : 73 摘要 : Background: Physical activity (PA) in older people is critically important in the prevention of disease, maintenance of independence and improvement of quality of life. Little is known about the physical activity of the older adults or their compliance with current physical activity guidelines. Methods: A systematic literature search of the published literature was conducted. Included were published reports of original research that independently reported: the PA level of non-institutional older adults (aged 60 years and over); and the proportion of older adults in the different samples who met PA recommendations or guidelines. The review was restricted to studies published since 2000 to provide a current picture of older adults' PA levels. Results: Fifty three papers were included in the review. The percentage of older adults meeting recommended physical activity ranged from 2.4 - 83.0% across the studies. Definitions of recommended physical activity in older adults varied across the studies as did approaches to measurement which posed methodological challenges to data analysis. Older age groups were less likely than the reference group to be regularly active, and women were less likely than men to achieve regular physical activity, especially leisure time physical activity, when measured by both subjective and objective criteria. Conclusion: The review highlights the need for studies which recruit representative random samples of community based older people and employ validated measurement methods consistently to enable comparison of PA levels over time and between countries. 文献类型 : Review 作者关键词 : Physical activity; Exercise; Older people; Older adults KeyWords Plus: FACTOR SURVEILLANCE SYSTEM; BRITISH WOMENS HEART; UNITED-STATES; ACTIVITY GUIDELINES; BUILT ENVIRONMENT; ACTIVITY PATTERNS; BRAZILIAN ADULTS; HEALTH BEHAVIORS; TEMPORAL TRENDS; LIFE EXPECTANCY 地址 : Second Mil Med Univ, Sch Nursing, Shanghai 200433, Peoples R China. Kings Coll London, Florence Nightingale Sch Nursing Midwifery, London SE1 8WA, England . 通讯作者地址 : While, AE ( 通讯作者 ),Kings Coll London, Florence Nightingale Sch Nursing Midwifery, 57 Waterloo Rd, London SE1 8WA, England. 电子邮件地址 : alison.while@kcl.ac.uk 来源出版物页码计数 : 17
标签: 老年病
