Journal of the American Aging Association最新文献

{"title":"Stem cells from birth to death: The history and the future.","authors":"Gerald de Haan, Gary Van Zant","doi":"10.1007/s11357-002-0006-z","DOIUrl":"10.1007/s11357-002-0006-z","url":null,"abstract":"<p><p>The concept that adult stem cells, despite their impressive proliferative potential, are immortal has been challenged by experimental studies of hematopoietic stem cells. In this review, we discuss the properties that characterize a stem cell, the growing list of tissues in which stem cells are found, how they can be identified and isolated, how stem cells may transdifferentiate, and the findings that illustrate how age affects the hematopoietic stem cell population. We propose that an aging stem cell population affects tissue and organ homeostasis, particularly in response to environmental stresses, and we hypothesize that through this mechanism the functional status of stem cells affects the longevity of the organism.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 2","pages":"79-86"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3455756/pdf/11357_2002_Article_6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31374149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lasofoxifene (CP-336,156), a novel selective estrogen receptor modulator, in preclinical studies.","authors":"H Z Ke,&nbsp;T A Brown,&nbsp;D D Thompson","doi":"10.1007/s11357-002-0007-y","DOIUrl":"https://doi.org/10.1007/s11357-002-0007-y","url":null,"abstract":"<p><p>Estrogen replacement therapy is reported to reduce the incidence of vertebral fractures in postmenopausal women, however, its compliance is limited because of side effects and safety concerns. Estrogen's side effects on breast and uterine tissues leading to the potential increased risk of uterine and breast cancer limit widespread estrogen usage. Thus, there is a significant medical need for a therapy that protects against postmenopausal bone loss but is free of estrogen's negative effects on reproductive tissues. Selective estrogen receptor modulators (SERMs) have been investigated as an alternative to hormone replacement therapy. One such compound, raloxifene, has been approved for the prevention and treatment of osteoporosis. Lasofoxifene (LAS), a new, nonsteroidal, and potent SERM, is an estrogen antagonist or agonist depending on the target tissue. LAS selectively binds with high affinity to human estrogen receptors. In ovariectomized (OVX) rat studies, LAS prevented the decrease in femoral bone mineral density, tibial and lumbar vertebral trabecular bone mass at an ED100 of about 60 μg/kg/day. LAS inhibited the activation of trabecular and endocortical bone resorption and bone turnover in tibial metaphyses and diaphyses, and lumbar vertebral body in OVX rats. In addition, LAS decreased total serum cholesterol, inhibited body weight gain and increased soleus muscle weight in OVX rats. Similarly, LAS prevented bone loss induced by orchidectomy or aging in male rats by decreasing bone resorption and bone turnover while it had no effect in the prostate. Further, LAS decreased total serum cholesterol in intact aged male rats or in orchidectomized male rats. Synergestic skeletal effects were found with LAS in combination with bone anabolic agents such as prostaglandin E2 (PGE2), parathyroid hormone (PTH) or a growth hormone secretagoue (GHS) in OVX rats. In combination with estrogen, LAS inhibited the uterine stimulating effects of estrogen but did not block the bone protective effects of estrogen. In immature and aged female rats, LAS did not affect the uterine weight and uterine histology. In OVX adult female rats, LAS slightly but significantly increased uterine weight. These results demonstrated that LAS produced effects on the skeleton indistinguishable from estrogen in female and male rats. However, unlike estrogen, LAS had little effect on uterine weight and cellular proliferation of uterus in female rats. In preclinical anti-tumor studies, LAS inhibited human breast cancer growth in mice bearing MCF7 tumors, prevented NMU-induced mammary carcinomas and possessed chemotherapeutic effects in NMU-induced carcinomas in rats. Therefore, we conclude that LAS possesses the antiestrogenic effects in breast tissue and estrogenic effects in bone and serum cholesterol, but lacks estrogen's side effects on uterine tissue. These data support the therapeutic potential of LAS for the prevention and treatment of postmenopausal bone loss and mammary","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 2","pages":"87-99"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0007-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31374150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A morphometric study on human muscle mitochondria in aging.","authors":"Carlo Bertoni-Freddari,&nbsp;Patrizia Fattoretti,&nbsp;Ugo Caselli,&nbsp;Belinda Giorgetti,&nbsp;Stefano Albanelli,&nbsp;Francesco Torelli,&nbsp;Giorgio Felzani,&nbsp;Jacopo Vecchiet","doi":"10.1007/s11357-002-0008-x","DOIUrl":"https://doi.org/10.1007/s11357-002-0008-x","url":null,"abstract":"<p><p>Mitochondria are dynamic organelles capable of significant changes of their ultrastructural features according to the tissue-specific energy demands. In human biopsies of vastus lateralis and anterior tibialis muscles from young (25.0 ± 4.4 years), middle-aged (50.4 ± 7.5 years) and old (75.5±3.9 years) healthy volunteers, we carried out a morphometric study on subsarcolemmal and intermyofibrillar mitochondria to assess whether age-related alterations of the morphology of these organelles contribute to the muscle performance decay in aging. By computer-assisted methods, we measured: the average area (MAA), the longer diameter (Dmax) and the ratio perimeter to area (pleomorphic index: Plei) of mitochondria. No significant age-related ultrastructural differences were found either in subsarcolemmal or intermyofibrillar organelles. However, in middle-aged as well as in the old group of patients vs. the young one, MAA and Dmax showed a clear trend to decrease, while Plei showed a marked, age-related tendency to increase. Higher percentages of less pleomorphic organelles were found in the youngest group of patients and this was particularly evident in the subsarcolemmal mitochondrial population. In addition to reporting on discrete aspects of mitochondrial ultrastructure, MAA, Dmax and Plei are closely related to each other and provide a reliable index of the muscle mitochondria adaptive response to age. Thus, we interpret our results as indicating a substantial preservation of muscle mitochondrial ultrastructure during aging.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 2","pages":"101-5"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0008-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31374151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of aging and resistance exercise on determinants of muscle strength.","authors":"Charles P Lambert,&nbsp;William J Evans","doi":"10.1007/s11357-002-0005-0","DOIUrl":"https://doi.org/10.1007/s11357-002-0005-0","url":null,"abstract":"<p><p>Although the loss of muscle strength with aging is multifactorial, the primary factor is the loss of muscle mass. A preferential loss of Type II (fast-twitch) muscle fibers which produce more force than Type I fibers is also observed. The loss of muscle mass may be related to a reduction in the rate of muscle protein synthesis in the old versus the young. Changes in muscle quality and the ability to activate muscle appear to play a minor role in the loss of strength with age. However, co-activation of antagonist muscle groups does appear to reduce muscle force generating capacity in the elderly. Strength gains in response to resistance exercise training in the elderly, although substantial, may be less than in young individuals. Increases in muscle mass appear to be similar in elderly and young individuals as does the muscle protein synthetic response to resistance exercise. Muscle co-activation appears to be substantially and similarly reduced (improved) in young and elderly individuals as a result of resistance training.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 2","pages":"73-8"},"PeriodicalIF":0.0,"publicationDate":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0005-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31373654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Survival and cell mediated immunity after burn injury in aged mice.","authors":"Elizabeth J Kovacs,&nbsp;Kristy A Grabowski,&nbsp;Lisa A Duffner,&nbsp;Timothy P Plackett,&nbsp;Meredith S Gregory","doi":"10.1007/s11357-002-0001-4","DOIUrl":"https://doi.org/10.1007/s11357-002-0001-4","url":null,"abstract":"<p><p>The elderly are less able to survive burn injury than young healthy individuals. Regardless of age, burn victims often succumb to secondary infections rather than the primary injury. Since immune responses diminish with age, it is likely that aged individuals are predisposed to a poor outcome by virtue of their weak immune system. Elevated production of macrophage-derived mediators, including interleukin-6 (IL-6), may lead to post-injury immunosuppression in young adults. Healthy aged individuals produce high circulating levels of these mediators; therefore, the combination of the age and burn trauma could further suppress immune responses and contribute to the rapid demise of aged burn patients. Herein, the effects of age and burn trauma using a murine scald injury model were examined. After injury, aged mice are less likely to survive, are unable to mount immune responses, and produce more IL-6 when compared to young adult mice given the same size injuries. Enhancing our understanding of the mechanisms responsible for regulating cell-mediated immune responses after injury could lead to the development of therapies designed to treat aged burn patients.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"3-9"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0001-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31466778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Journal of the American Aging Association","authors":"A. Balin, D. L. Busbee, R. Alfin-slater, V. Allfrey, Donald Armstrong, K. Brizzee, H. Fudenberg, S. Hendricks, L. Jarvik, J. Johnson, L. Mays, James Mead, A. Miller, J. Miquel, K. Moldave, M. Ordy, S. Podolsky, William M. Pryor, B. Sacktor, T. Samorajski, Edward Schneider, Klaus Schwartz, Marott F. Sinex, R. Walford, Gerald Weissman, Vernon Young, B. Zuckerman, L. Birnbaum, Barbara B. Bowman, P. Coleman, V. Cristofalo, J. Fleming, J. Johnson","doi":"10.1007/s11357-002-0024-x","DOIUrl":"https://doi.org/10.1007/s11357-002-0024-x","url":null,"abstract":"","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"221-250"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0024-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52978815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fellows/trustees and honorary members","authors":"A. Balin, P. Bickford, David Busbee, R. Cutler, S. Gambert, Denham Harman, H. Johnson, Martin L. Katz, Donald Kleinsek, R. Lippman, Harold R. Massie, J. McClaren, R. Mervis, M. Ordy, S. Podolsky, Elizabeth Steinhaben-Thiessen, Panaylotis D. Tsitouras, R. Walford, R. Weindruch, R. Young, Leslie A. Bailey, W. Baron, Paul Glenn, H. Boynton, Wilford Niedringhaus","doi":"10.1007/s11357-002-0020-1","DOIUrl":"https://doi.org/10.1007/s11357-002-0020-1","url":null,"abstract":"","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"211"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0020-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52978724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adverse effects of unconventional therapies in the elderly: A systematic review of the recent literature.","authors":"E Ernst","doi":"10.1007/s11357-002-0002-3","DOIUrl":"10.1007/s11357-002-0002-3","url":null,"abstract":"<p><p>Unconventional therapies are increasingly popular, not least in populations of elderly individuals. This review summarizes the evidence regarding the risk unconventional therapies may entail for the elderly. Computerized literature searches were performed to locate all reports with original data on this topic. Most of the evidence found was anecdotal by nature and thus has obvious limitations. The results show that elderly patients can suffer harm from unconventional therapies. Herbal treatments are associated most frequently with adverse events. They can cause both direct toxicity and unwanted herb-drug interactions. Acupuncture, spinal manipulation and even massage therapy have also been implicated. Indirect risks exist if unconventional therapies are employed as a substitute for conventional treatments. It is concluded that unconventional therapies are not risk-free for elderly patients. All parties involved ought to be educated with a view of minimizing this risk, and more research is needed to increase our understanding of this area.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"11-20"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3455291/pdf/11357_2002_Article_2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31373642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"International Association of Biomedical Gerontology 9th Congress","authors":"E. Porta","doi":"10.1007/s11357-002-0004-1","DOIUrl":"https://doi.org/10.1007/s11357-002-0004-1","url":null,"abstract":"","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"41-61"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0004-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52978610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabditis elegans; studies of mutation in the age-1, PI3 kinase homologue and short-term exposure to hyperoxia.","authors":"Y Honda,&nbsp;S Honda","doi":"10.1007/s11357-002-0003-2","DOIUrl":"https://doi.org/10.1007/s11357-002-0003-2","url":null,"abstract":"<p><p>Life span could be modified by genetic or environmental perturbations in Caenorhabditis elegans. Here we show that two extensions of life span are associated with oxidative stress resistance and upregulation of the gene expression of antioxidant enzymes. First, mutations in age-1 gene (PI3 kinase homologue)that confer life span extension, display oxidative stress resistance and increase in the gene expression of sod-3, one of two Mn-superoxide dismutases (SOD) and ctl-1, cytosolic catalase. In this study, these traits appear to be regulated by the following genetic pathway: daf-2 (insulin receptor family)-> daf-18 (PTEN homologue)-> age-1-> daf-16 (Fork head transcription factor family), similar to the genetic pathway for the life span extension. Second, we show that short-term exposure to hyperoxia extends life span slightly but significantly. This treatment increases oxidative stress resistance and the gene expression of three types of SOD isoforms. These results suggest that both of these two life span extensions are closely related with increase in the antioxidant defense function.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"21-8"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0003-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31373643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}