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        <title>Ageing Research Reviews via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Ageing Research Reviews' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Ageing+Research+Reviews&t=Ageing+Research+Reviews&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 15:46:54 +0100</lastBuildDate>
        <item>
            <title>Mechanistic Contribution of Carnitine Deficiency to Geriatric Frailty.</title>
            <link>http://www.medworm.com/index.php?rid=3359947&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20223299%26dopt%3DAbstract</link>
            <description>Authors: Crentsil V
    Frailty is a geriatric syndrome characterized by muscle weakness, sarcopenia, and fatigue, and is associated with several adverse health outcomes, including disability. Design of therapeutic interventions for geriatric frailty has been challenging and may be because of inadequate understanding of its biological underpinnings. Carnitine is important for energy production in skeletal muscles and there seems to be a negative correlation between advancing age and muscle carnitine levels. Carnitine deficiency may therefore result in geriatric frailty. Age-associated carnitine deficiency from a variety of etiologies, including organic cation transporter (OCTN2) mutation and carnitine palmitoyltransferase II (CPT) deficiency, may potentially explain the relationship betwee...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3359947</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Ketogenic diets: an historical antiepileptic therapy with promising potentialities for the aging brain.</title>
            <link>http://www.medworm.com/index.php?rid=3327760&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20188215%26dopt%3DAbstract</link>
            <description>Authors: Balietti M, Casoli T, Di Stefano G, Giorgetti B, Aicardi G, Fattoretti P
    Ketogenic diets (KDs), successfully used in the therapy of paediatric epilepsy for nearly a century, have recently shown beneficial effects also in cancer, obesity, diabetes, GLUT 1 deficiencies, hypoxia-ischemia, traumatic brain injuries, and neurodegeneration. The latter achievement designates aged individuals as optimal recipients, but concerns derive from possible age-dependent differences in KDs effectiveness. Indeed, the main factors influencing ketone bodies utilization by the brain (blood levels, transport mechanisms, catabolic enzymes) undergo developmental changes, although several reports indicate that KDs maintain some efficacy during adulthood and even advanced aging. Encouraging results obta...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3327760</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Protein kinase A signaling as an anti-aging target.</title>
            <link>http://www.medworm.com/index.php?rid=3327759&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20188216%26dopt%3DAbstract</link>
            <description>Authors: Enns LC, Ladiges W
    Protein kinase A (PKA) is a multi-unit protein kinase that mediates signal transduction of G-protein-coupled receptors through its activation by adenyl cyclase (AC)-mediated cAMP. The vital importance of PKA signaling to cellular function is reflected in the widespread expression of PKA subunit genes. As one of its many functions, PKA plays a key role in the regulation of metabolism and triglyceride storage. The PKA pathway has become of great interest to the study of aging, since mutations that cause a reduction in PKA signaling have been shown to extend lifespan in yeast, and to both delay the incidence and severity of age-related disease, and to promote leanness and longevity, in mice. There is increasing interest in the potential for the inhibition or re...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3327759</comments>
            <pubDate>Tue, 23 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3327759</guid>        </item>
        <item>
            <title>Rna surveillance- an emerging role for rna regulatory networks in aging.</title>
            <link>http://www.medworm.com/index.php?rid=3299797&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20170753%26dopt%3DAbstract</link>
            <description>We present data showing that transcriptional knockdown of RNA interference restores lifespan losses in the context of RNA editing defects, further suggesting that interaction between these two systems influences lifespan. Finally, we discuss the implications of RNA surveillance for sarcopenia and muscle maintenance, as frailty is a universal feature of aging. We end with a discussion of RNA surveillance as a robust regulatory system that can change in response to environmental stressors and represents a novel axis in aging science.
    PMID: 20170753 [PubMed - as supplied by publisher] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3299797</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Protein Homeostasis and Aging: the importance of exquisite quality control.</title>
            <link>http://www.medworm.com/index.php?rid=3276438&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20152936%26dopt%3DAbstract</link>
            <description>Authors: Koga H, Kaushik S, Cuervo AM
    All cells count on precise mechanisms that regulate protein homeostasis to maintain a stable and functional proteome. A progressive deterioration in the ability of cells to preserve the stability of their proteome occurs with age and contributes to the functional loss characteristic of old organisms. Molecular chaperones and the proteolytic systems are responsible for this cellular quality control by assuring continuous renewal of intracellular proteins. When protein damage occurs, such as during cellular stress, the coordinated action of these cellular surveillance systems allows detection and repair of the damaged structures or, in many instances, leads to the complete elimination of the altered proteins from inside cells. Dysfunction of the qual...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3276438</comments>
            <pubDate>Tue, 09 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3276438</guid>        </item>
        <item>
            <title>Metabolic and Endocrine Factors in Mild Cognitive Impairment.</title>
            <link>http://www.medworm.com/index.php?rid=3223753&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20109582%26dopt%3DAbstract</link>
            <description>Authors: Etgen T, Bickel H, F&amp;#xF6;rstl H
    Mild cognitive impairment (MCI) is a heterogeneous condition with cognitive changes between normal aging and dementia. Some forms of MCI are regarded as potential preclinical forms of dementia. The control of treatable somatic risk factors is of great relevance in patients with MCI, particularly as there is insufficient evidence for the efficacy of interventions targeting neurodegenerative processes, as used in manifest dementia. The etiology of MCI is varied including cerebrovascular risk factors and is also associated with metabolic and endocrine factors: Chronic kidney disease is a newly identified and independent risk factor for MCI. Testosterone substitution is useful if a low testosterone level is present but general screening for testost...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3223753</comments>
            <pubDate>Mon, 25 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3223753</guid>        </item>
        <item>
            <title>Comparative Cellular Biogerontology: Primer and Prospectus.</title>
            <link>http://www.medworm.com/index.php?rid=3223752&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20109583%26dopt%3DAbstract</link>
            <description>Authors: Miller RA, Williams JB, Kiklevich JV, Austad S, Harper JM
    Most prior work on the biological basis of aging has focused on describing differences between young and old individuals but provided only limited insight into the mechanisms controlling the rate of aging. Natural selection has produced a goldmine of experimental material, in the form of species of differing aging rate, whose longevity can vary by 10-fold or more within mammalian orders, but these resources remain largely unexplored at the cellular level. In this review article we focus on one approach to comparative biogerontology: the strategy of evaluating the properties of cultured cells from organisms of varying lifespan and aging rate. In addition, we discuss problems associated with the analysis and interpretatio...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3223752</comments>
            <pubDate>Mon, 25 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3223752</guid>        </item>
        <item>
            <title>Predicting whether dietary restriction would increase longevity in species not tested so far.</title>
            <link>http://www.medworm.com/index.php?rid=3223754&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20105461%26dopt%3DAbstract</link>
            <description>This article argues that whether DR will increase longevity is dependent on life-history strategies. Long-lived species are not expected to live much longer under DR, contrarily to short-lived ones. However, species able to cover long distances are not expected to live longer under DR, even if they are short-lived. Human beings are long-lived and can also cover long distances: thus, DR would probably not increase their lifespan. One may wonder whether DR mimetics would have some effects in human beings if DR does not increase longevity in this species.
    PMID: 20105461 [PubMed - as supplied by publisher] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3223754</comments>
            <pubDate>Sun, 24 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3223754</guid>        </item>
        <item>
            <title>Does Brown Fat Protect Against Diseases of Aging?</title>
            <link>http://www.medworm.com/index.php?rid=3072291&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19969105%26dopt%3DAbstract</link>
            <description>Authors: Mattson MP
    The most commonly studied laboratory rodents possess a specialized form of fat called brown adipose tissue (BAT) that generates heat to help maintain body temperature in cold environments. In humans, BAT is abundant during embryonic and early postnatal development, but is absent or present in relatively small amounts in adults where it is located in paracervical and supraclavicular regions. BAT cells can 'burn' fatty acid energy substrates to generate heat because they possess large numbers of mitochondria in which oxidative phosphorylation is uncoupled from ATP production as a result of a transmembrane proton leak mediated by uncoupling protein 1 (UCP1). Studies of rodents in which BAT levels are either increased or decreased have revealed a role for BAT in protect...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3072291</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3072291</guid>        </item>
        <item>
            <title>Age-Related Defects in the Cytoskeleton Signaling Pathways of CD4 T Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3036254&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19941976%26dopt%3DAbstract</link>
            <description>Authors: Garcia GG, Miller RA
    It has been postulated that the cytoskeleton controls many aspects of T cell function, including activation, proliferation and apoptosis. Recent advances in our understanding of F-actin polymerization and the Ezrin-Radixin-Moesin (ERM) family of cytoskeleton signal proteins have provided new insights into immunological synapse formation during T cell activation. During aging there is a significant decline of T cell function largely attributable to declines in activation of CD4 T cells and defects in the formation of the immunological synapse. Here we discuss recent progress in the understanding of how aging alters F-actin and ERM proteins in mouse CD4 T cells, and the implications of these changes for the T cell activation process.
    PMID: 19941976 [PubM...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3036254</comments>
            <pubDate>Mon, 23 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3036254</guid>        </item>
        <item>
            <title>Effect of aging on cellular mechanotransduction.</title>
            <link>http://www.medworm.com/index.php?rid=3030872&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19932197%26dopt%3DAbstract</link>
            <description>Authors: Wu M, Fannin J, Rice KM, Wang B, Blough ER
    Aging is becoming a critical heath care issue and a burgeoning economic burden on society. Mechanotransduction is the ability of the cell to sense, process, and respond to mechanical stimuli and is an important regulator of physiologic function that has been found to play a role in regulating gene expression, protein synthesis, cell differentiation, tissue growth, and most recently, the pathophysiology of disease. Here we will review some of the recent findings of this field and attempt, where possible, to present changes in mechanotransduction that are associated with the aging process in several selected physiological systems, including musculoskeletal, cardiovascular, neuronal, respiratory systems and skin.
    PMID: 19932197 [PubM...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3030872</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3030872</guid>        </item>
        <item>
            <title>Genetics vs. entropy: Longevity factors suppress the NF-kappaB-driven entropic aging process.</title>
            <link>http://www.medworm.com/index.php?rid=2982162&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19903538%26dopt%3DAbstract</link>
            <description>Authors: Salminen A, Kaarniranta K
    Molecular studies in model organisms have identified potent longevity genes which can delay the aging process and extend the lifespan. Longevity factors promote stress resistance and cellular survival. It seems that the aging process itself is not genetically programmed but a random process involving the loss of molecular fidelity and subsequent accumulation of waste products. This age-related increase in cellular entropy is compatible with the disposable soma theory of aging. A large array of host defence systems has been linked to the NF-kappaB system which is an ancient signaling pathway specialized to host defence, e.g. functioning in immune system. Emerging evidence demonstrates that the NF-kappaB system is activated during aging. Oxidative stres...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982162</comments>
            <pubDate>Sat, 07 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982162</guid>        </item>
        <item>
            <title>Perturbed Cellular Response to Brain Injury During Aging.</title>
            <link>http://www.medworm.com/index.php?rid=2982164&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900590%26dopt%3DAbstract</link>
            <description>Authors: Popa-Wagner A, Buga AM, Kokaia Z
    Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are only partly understood. Therefore, studying the basic mechanisms underlying structural and functional recovery after brain injury in aged subjects is of considerable clinical interest. Behavioral and cytological analyses of rodents that have undergone experimental injury show that: (a) behaviorally, aged rodents are more severely impaired by ischemia than are young animals, and older rodents also show diminished functional recovery; (b) compared to young animals, aged animals develop a larger infarct area, as well as a necrotic zone characterized by a higher rate of cellular degeneration ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982164</comments>
            <pubDate>Fri, 06 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982164</guid>        </item>
        <item>
            <title>Next-generation sequencing in aging research: emerging applications, problems, pitfalls and possible solutions.</title>
            <link>http://www.medworm.com/index.php?rid=2982163&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19900591%26dopt%3DAbstract</link>
            <description>Authors: Magalh&amp;#xE3;es JP, Finch CE, Janssens G
    Recent technological advances that allow faster and cheaper DNA sequencing are now driving biological and medical research. In this review, we provide an overview of state-of-the-art next-generation sequencing (NGS) platforms and their applications, including in genome sequencing and resequencing, transcriptional profiling (RNA-Seq) and high-throughput survey of DNA-protein interactions (ChIP-Seq) and of the epigenome. Particularly, we focus on how new methods made possible by NGS can help unravel the biological and genetic mechanisms of aging, longevity and age-related diseases. In the same way, however, NGS platforms open discovery not available before, they also give rise to new challenges, in particular in processing, analyzing and i...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2982163</comments>
            <pubDate>Fri, 06 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2982163</guid>        </item>
        <item>
            <title>Mechanical properties of cells and ageing.</title>
            <link>http://www.medworm.com/index.php?rid=2975854&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19897057%26dopt%3DAbstract</link>
            <description>Authors: Starodubtseva MN
    Mechanical properties are fundamental properties of the cells and tissues of living organisms. The mechanical properties of a single cell as a biocomposite are determined by the interdependent combination of cellular components mechanical properties. Quantitative estimate of the cell mechanical properties depends on a cell state, method of measurement, and used theoretical model. Predominant tendency for the majority of cells with ageing is an increase of cell stiffness and a decrease of cell ability to undergo reversible large deformations. The mechanical signal transduction in old cells becomes less effective than that in young cells, and with ageing, the cells lose the ability of the rapid functional rearrangements of cellular skeleton. The article reviews ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2975854</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2975854</guid>        </item>
        <item>
            <title>Will Targeting insulin growth factor help us or hurt us?: an oncologist's perspective.</title>
            <link>http://www.medworm.com/index.php?rid=2975855&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19896561%26dopt%3DAbstract</link>
            <description>Authors: Kamrava M, Gius D, Casagrande G, Kohn E
    The insulin/insulin growth factor (IGF) pathway is a critical mediator of longevity and aging. Efforts to extend longevity by altering the insulin/IGF pathway may have varying effects on other physiological processes. Reduced insulin/IGF levels may decrease the incidence of certain cancers as well as the risk of developing metastatic disease. However, it may also increase the risk of developing cardiovascular disease as well as cardiovascular related mortality. Pursuing the right insulin/IGF pathway targets will require striking a balance between inhibiting cancer cell development and progression and avoiding damage to tissues under normal insulin/IGF mediated control. This review will discuss the roles of the insulin/IGF pathway in agin...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2975855</comments>
            <pubDate>Wed, 04 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2975855</guid>        </item>
        <item>
            <title>Human intestinal microbiota and healthy ageing.</title>
            <link>http://www.medworm.com/index.php?rid=2947631&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19874918%26dopt%3DAbstract</link>
            <description>Authors: Tiihonen K, Ouwehand AC, Rautonen N
    Earlier studies have indicated a decrease in anaerobes and bifidobacteria and a concomitant increase in enterobacteria in the intestinal microbiota with ageing. However, new data obtained with molecular techniques suggests decreased stability and increased diversity of the gut microbiota with advancing age. Further, no simple marker change in microbiota composition can be identified. Except for the reduced immune function, ageing itself may have relatively little effect on overall gastrointestinal function. Concomitant changes in nutrition, increased incidence of disease and corresponding use of medication with advancing age modify the composition of the microbial community of the gastrointestinal tract. This minireview will focus on the rec...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2947631</comments>
            <pubDate>Mon, 26 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2947631</guid>        </item>
        <item>
            <title>Biological Effects of Calorie Restriction: From Soup to Nuts.</title>
            <link>http://www.medworm.com/index.php?rid=2934550&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19853062%26dopt%3DAbstract</link>
            <description>Authors: Spindler SR
    Caloric restriction (CR), reduced protein, methionine, or tryptophan diets; and reduced insulin and/or IGFI intracellular signaling can extend mean and/or maximum lifespan and delay deleterious age-related physiological changes in animals. Mice and flies can shift readily between the control and CR physiological states, even at older ages. Many health benefits are induced by even brief periods of CR in flies, rodents, monkeys, and humans. In humans and nonhuman primates, CR produces most of the physiologic, hematologic, hormonal, and biochemical changes it produces in other animals. In primates, CR provides protection from type 2 diabetes, cardiovascular and cerebral vascular diseases, immunological decline, malignancy, hepatotoxicity, liver fibrosis and failure, s...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2934550</comments>
            <pubDate>Tue, 20 Oct 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Hypothermia as a Cytoprotective Strategy in Ischemic Tissue Injury.</title>
            <link>http://www.medworm.com/index.php?rid=2900931&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19833233%26dopt%3DAbstract</link>
            <description>Authors: Tang XN, Yenari MA
    Hypothermia is a well established cytoprotectant, with remarkable and consistent effects demonstrated across multiple laboratories. At the clinical level, it has recently been shown to improve neurological outcome following cardiac arrest and neonatal hypoxia ischemia. It is increasingly being embraced by the medical community, and could be considered an effective neuroprotectant. Conditions such as brain injury, hepatic encephalopathy and cardiopulmonary bypass seem to benefit from this intervention. It's role in direct myocardial protection is also being explored. A review of the literature has demonstrated that in order to appreciate the maximum benefits of hypothermia, cooling needs to begin soon after the insult, and maintained for relatively long perio...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2900931</comments>
            <pubDate>Sun, 11 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2900931</guid>        </item>
        <item>
            <title>Anti-aging herbal medicine - How and why can they be used in aging-associated neurodegenerative diseases?</title>
            <link>http://www.medworm.com/index.php?rid=2900927&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19833234%26dopt%3DAbstract</link>
            <description>Authors: Ho YS, So KF, Chang RC
    Aging is a universal biological process that leads to progressive and deleterious changes in organisms. From ancient time, mankind has already interested in preventing and keeping ourselves young. Anti-aging study is certainly not a new research area. Nowadays, the meaning of anti-aging has been changed from simply prolonging lifespan to increasing health span, which emphasizes more on the quality of life. This is the concept of healthy aging and prevention of pathological aging, which is associated with diseases. Keeping our brain functions as in young age is an important task for neuroscientists to prevent aging-associated neurological disorders, such as Alzheimer's diseases (AD) and Parkinson's disease (PD). The causes of these diseases are not fully ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2900927</comments>
            <pubDate>Sun, 11 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2900927</guid>        </item>
        <item>
            <title>Powerful signals for weak muscles.</title>
            <link>http://www.medworm.com/index.php?rid=2748494&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19716529%26dopt%3DAbstract</link>
            <description>Authors: Saini A, Faulkner S, Al-Shanti N, Stewart C
    The aim of the present review is to summarise, evaluate and critique the different mechanisms involved in anabolic growth of skeletal muscle and the catabolic processes involved in cancer cachexia and sarcopenia of ageing. This is highly relevant, since they represent targets for future promising clinical investigations. Sarcopenia is an inevitable process associated with a gradual reduction in muscle mass and strength, associated with a reduction in motor unit number and atrophy of muscle fibres, especially the fast type IIa fibres. The loss of muscle mass with ageing is clinically important because it leads to diminished functional ability and associated complications. Cachexia is widely recognised as severe and rapid wasting accom...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2748494</comments>
            <pubDate>Tue, 01 Sep 2009 10:00:08 +0100</pubDate>
            <guid isPermaLink="false">2748494</guid>        </item>
        <item>
            <title>The role of epigenetics in aging and age-related diseases.</title>
            <link>http://www.medworm.com/index.php?rid=2748493&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19716530%26dopt%3DAbstract</link>
            <description>Authors: Calvanese V, Lara E, Kahn A, Fraga MF
    The role of epigenetics in aging and age-related diseases is a key issue in molecular physiology and medicine because certain epigenetic factors are thought to mediate, at least in part, the relationship between the genome and the environment. An active role for epigenetics in aging must meet two prior conditions: there must be specific epigenetic changes during aging and they must be functionally associated with the aged phenotype. Assuming that specific epigenetic modifications can have a direct functional outcome in aging, it is also essential to establish whether they depend on genetic, environmental or stochastic factors, and if they can be transmitted from one generation to the next. Here we discuss current knowledge about these matt...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2748493</comments>
            <pubDate>Tue, 01 Sep 2009 10:00:06 +0100</pubDate>
            <guid isPermaLink="false">2748493</guid>        </item>
        <item>
            <title>Energy Expenditure and Aging.</title>
            <link>http://www.medworm.com/index.php?rid=2734772&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19698803%26dopt%3DAbstract</link>
            <description>Authors: Manini TM
    The study of energy expenditure (EE) has deep roots in understanding aging and lifespan in all species. In humans, total EE decreases substantially in advanced age resulting from parallel changes in resting metabolic rate (RMR) and activity EE. For RMR, this reduction appears to be due to a reduction in organ mass and specific metabolic rates of individual tissues. However, these anatomical changes explain very little regarding the decline in activity EE, which is governed by both genetic and environmental sources. The biological control centers for activity EE are closely coupled with body mass fluctuations and seem to originate in the brain. Several candidate neuromodulators may be involved in the age-related reduction of activity EE that include: orexin, agouti-re...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734772</comments>
            <pubDate>Mon, 17 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2734772</guid>        </item>
        <item>
            <title>Impact of Ageing on Muscle Cell Regeneration.</title>
            <link>http://www.medworm.com/index.php?rid=2712464&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19683075%26dopt%3DAbstract</link>
            <description>Authors: Carosio S, Berardinelli MG, Aucello M, Musar&amp;#xF2; A
    Skeletal muscle regeneration is a coordinate process in which several factors are sequentially activated to maintain and preserve muscle structure and function. The major role in the growth, remodeling and regeneration is played by satellite cells, a quiescent population of myogenic cells that reside between the basal lamina and plasmalemma and are rapidly activated in response to appropriate stimuli. However, in several muscle conditions, including aging, the capacity of skeletal muscle to sustain an efficient regenerative pathway is severely compromised. Nevertheless, if skeletal muscle possesses a stem cell compartment it is not clear why the muscle fails to regenerate under pathological conditions. Either the resident mu...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2712464</comments>
            <pubDate>Tue, 11 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2712464</guid>        </item>
        <item>
            <title>Ageing and its Possible Impact on Mucosal Immune Responses.</title>
            <link>http://www.medworm.com/index.php?rid=2696354&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19664726%26dopt%3DAbstract</link>
            <description>Authors: Ogra PL
    
    PMID: 19664726 [PubMed - as supplied by publisher] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2696354</comments>
            <pubDate>Mon, 03 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2696354</guid>        </item>
        <item>
            <title>Bats and Birds: Exceptional Longevity despite High Metabolic Rates.</title>
            <link>http://www.medworm.com/index.php?rid=2662808&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19643206%26dopt%3DAbstract</link>
            <description>Authors: Munshi-South J, Wilkinson GS
    Bats and birds live substantially longer on average than non-flying mammals of similar body size. The combination of small body size, high metabolic rates, and long lifespan in bats and birds would not seem to support oxidative theories of ageing that view senescence as the gradual accumulation of damage from metabolic byproducts. However, large-scale comparative analyses and laboratory studies on a few emerging model species have identified multiple mechanisms for resisting oxidative damage to mitochondrial DNA and cellular structures in both bats and birds. Here we review these recent findings, and suggest areas in which additional progress on ageing mechanisms can be made using bats and birds as novel systems. New techniques for determining the ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2662808</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2662808</guid>        </item>
        <item>
            <title>Dietary Fatty Acids in Dementia and Predementia Syndromes: Epidemiological Evidence and Possible Underlying Mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=2662807&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19643207%26dopt%3DAbstract</link>
            <description>Authors: Solfrizzi V, Frisardi V, Capurso C, D'Introno A, Colacicco AM, Vendemiale G, Capurso A, Panza F
    Drugs currently used in the treatment of cognitive impairment and dementia have a very limited therapeutic value, suggesting the necessity to potentially individualize new strategies able to prevent and to slow down the progression of predementia and dementia syndromes. An increasing body of epidemiological evidence suggested that elevated saturated fatty acids (SFA) could have negative effects on age-related cognitive decline (ARCD) and mild cognitive impairment (MCI). Furthermore, a clear reduction of risk for cognitive decline has been found in population samples with elevated fish consumption, high intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUF...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2662807</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2662807</guid>        </item>
        <item>
            <title>Hypothalamic and dietary control of temperature-mediated longevity.</title>
            <link>http://www.medworm.com/index.php?rid=2650371&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19631766%26dopt%3DAbstract</link>
            <description>Authors: Tabarean I, Morrison B, Marcondes MC, Bartfai T, Conti B
    Temperature is an important modulator of longevity and aging in both poikilotherms and homeotherm animals. In homeotherms, temperature homeostasis is regulated primarily in the preoptic area (POA) of the hypothalamus. This region receives and integrates peripheral, central and environmental signals and maintains a nearly constant core body temperature (T(core)) by regulating the autonomic and hormonal control of heat production and heat dissipation. Temperature sensitive neurons found in the POA are considered key elements of the neuronal circuitry modulating these effects. Nutrient homeostasis is also a hypothalamically regulated modulator of aging as well as one of the signals that can influence T(core) in homeotherms....</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2650371</comments>
            <pubDate>Tue, 21 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2650371</guid>        </item>
        <item>
            <title>Endothelial dysfunction and aging: an update.</title>
            <link>http://www.medworm.com/index.php?rid=2626796&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19619671%26dopt%3DAbstract</link>
            <description>ENDOTHELIAL DYSFUNCTION AND AGING: AN UPDATE.
    Ageing Res Rev. 2009 Jul 17;
    Authors: Herrera MD, Mingorance C, Rodr&amp;#xED;guez-Rodr&amp;#xED;guez R, Sotomayor MA
    Aging is an important risk factor for the development of many cardiovascular diseases as atherosclerosis and hypertension with a common underlying circumstance: the progressive decline of endothelial function. Vascular endothelial dysfunction occurs during the human aging process and is accompanied by deterioration in the balance between vasodilator and vasoconstriction substances produced by the endothelium. This imbalance is mainly characterized by a progressive reduction of the bioavailability of nitric oxide (NO) and an increase in the production of cyclooxygenase (COX)-derived vasoconstrictor factors. Both circumstances...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626796</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2626796</guid>        </item>
        <item>
            <title>Circadian Temperature Variation and Ageing.</title>
            <link>http://www.medworm.com/index.php?rid=2626795&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19619672%26dopt%3DAbstract</link>
            <description>Authors: Weinert D
    In the present paper, an attempt is made to summarize current knowledge concerning the daily body temperature rhythm and its age-dependent alterations. Homeostatic and circadian control mechanisms are considered. Special attention is paid to the circadian system, as the mechanisms of autonomic control are the topic of another contribution to this special issue. Also, the interactions of the core body temperature rhythm with other circadian functions are discussed in detail as they constitute an essential part of the internal temporal order of living systems and thus guarantee their optimal functioning. In the second part of the paper, age-dependent changes in the circadian body temperature rhythm and their putative causes, considering circadian and homeostatic compon...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626795</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2626795</guid>        </item>
        <item>
            <title>Ischemic preconditioning in the aging heart: from bench to bedside.</title>
            <link>http://www.medworm.com/index.php?rid=2626798&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19615470%26dopt%3DAbstract</link>
            <description>Authors: Abete P, Cacciatore F, Testa G, Della-Morte D, Galizia G, de Santis D, Calabrese C, Cioppa A, Ferrara N, Rengo F
    Coronary artery disease is the leading cause of death in industrialized countries for people older than 65 years of age. The reasons are still unclear. A reduction of endogenous mechanisms against ischemic insults has been proposed to explain this phenomenon. Cardiac ischemic preconditioning represents the most powerful endogenous protective mechanism against ischemia. Brief episodes of ischemia are able to protect the heart against a following more prolonged ischemic period. This protective mechanism seems to be reduced with aging both in experimental and clinical studies. Alterations of mediators release and/or intracellular pathways may be responsible for age-rel...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2626798</comments>
            <pubDate>Mon, 13 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2626798</guid>        </item>
        <item>
            <title>Regulatory role of HIF-1alpha in the pathogenesis of age-related macular degeneration (AMD).</title>
            <link>http://www.medworm.com/index.php?rid=2591952&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19589398%26dopt%3DAbstract</link>
            <description>Authors: Arjamaa O, Nikinmaa M, Salminen A, Kaarniranta K
    Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the elderly throughout the world. AMD is attributed to a complex interaction of genetic and environmental factors. It is characterized by degeneration involving the retinal photoreceptors, retinal pigment epithelium (RPE), and Bruch's membrane, as well as alterations in choroidal capillaries. Aging and age-associated degenerative diseases, such as AMD, are intimately associated with decreased levels of tissue oxygenation and hypoxia that may induce accumulation of detrimental RPE -associated deposits, inflammation and neovascularization processes in retina. Hypoxia inducible factor (HIF) is the master regulator for hypoxia-induced cellular ada...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2591952</comments>
            <pubDate>Sun, 05 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2591952</guid>        </item>
        <item>
            <title>Aging: central role for autophagy and the lysosomal degradative system.</title>
            <link>http://www.medworm.com/index.php?rid=2543505&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19427410%26dopt%3DAbstract</link>
            <description>Authors: Rajawat YS, Hilioti Z, Bossis I
    The lysosomal network is the major intracellular proteolytic system accounting for more than 98% of long-lived bulk protein degradation and recycling particularly in tissues such as liver and muscles. Lysosomes are the final destination of intracellular damaged structures, identified and sequestered by the processes of macroautophagy and chaperone-mediated autophagy (CMA). In the process of macroautophagy, long-lived proteins and other macromolecular aggregates and damaged intracellular organelles are first engulfed by autophagosomes. Autophagosomes themselves have limited degrading capacity and rely on fusion with lysosomes. Unlike macroautophagy, CMA does not require intermediate vesicle formation and the cytosolic proteins recognized by this ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543505</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:28 +0100</pubDate>
            <guid isPermaLink="false">2543505</guid>        </item>
        <item>
            <title>The ER and ageing II: calcium homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=2543504&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19427411%26dopt%3DAbstract</link>
            <description>Authors: Puzianowska-Kuznicka M, Kuznicki J
    Increase in intracellular Ca(2+) concentration occurs by Ca(2+) influx through the plasma membrane and by Ca(2+) release from intracellular stores. The ER is the most important Ca(2+) store. Its stress, characterized by the impairment of Ca(2+) homeostasis and by the accumulation of misfolded proteins, can be induced by different factors. In turn, it induces defense mechanisms such as unfolded protein response, and when it is severe and prolonged, activation of the apoptotic pathway. Damage to the ER, impairment of its function, and a decreased level of its Ca(2+)-handling proteins might all play a role in physiological ageing by handicapping the ER stress response. Thus, healthy ageing is accompanied by subtle alterations of Ca(2+) homeostas...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543504</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:26 +0100</pubDate>
            <guid isPermaLink="false">2543504</guid>        </item>
        <item>
            <title>The ageing epigenome: damaged beyond repair?</title>
            <link>http://www.medworm.com/index.php?rid=2543503&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19439199%26dopt%3DAbstract</link>
            <description>Authors: Sinclair DA, Oberdoerffer P
    Of all the proposed causes of ageing, DNA damage remains a leading, though still debated theory. Unlike most other types of age-related cellular damage, which can hypothetically be reversed, mutations in DNA are permanent. Such errors result in the accumulation of changes to RNA and protein sequences with age, and are tightly linked to cellular senescence and overall organ dysfunction. Over the past few years, an additional, more global role has emerged for the contribution of DNA damage and genomic instability to the ageing process. We, and others have found that DNA damage and the concomitant repair process can induce genome-wide epigenetic changes, which may promote a variety of age-related transcriptional and functional changes. Here, we discuss...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543503</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:24 +0100</pubDate>
            <guid isPermaLink="false">2543503</guid>        </item>
        <item>
            <title>Clathrin-mediated endocytosis and Alzheimer's disease: an update.</title>
            <link>http://www.medworm.com/index.php?rid=2543500&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19491039%26dopt%3DAbstract</link>
            <description>Authors: Wu F, Yao PJ
    Thanks to new evidence we are now a step closer to understanding how neurons produce amyloid-beta peptide (Abeta)-the chief culprit of Alzheimer's disease. As importance of clathrin-mediated endocytosis to normal neurons has become clearer, so has its role in pathology of neurological disorders. Here we update recent evidence that endocytosis plays a central role in the production of Abeta in neurons.
    PMID: 19491039 [PubMed - in process] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543500</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:18 +0100</pubDate>
            <guid isPermaLink="false">2543500</guid>        </item>
        <item>
            <title>ER and aging-Protein folding and the ER stress response.</title>
            <link>http://www.medworm.com/index.php?rid=2543499&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19491040%26dopt%3DAbstract</link>
            <description>Authors: Naidoo N
    The endoplasmic reticulum (ER) is a multifunctional organelle which co-ordinates protein folding, lipid biosynthesis, calcium storage and release. Perturbations that disrupt ER homeostasis lead to the misfolding of proteins, ER stress and up-regulation of a signaling pathway called the ER stress response or the unfolded protein response (UPR). The UPR is characterized by the induction of chaperones, degradation of misfolded proteins and attenuation of protein translation. Age-related declines and activity in key molecular chaperones and folding enzymes compromise proper protein folding and the adaptive response of the UPR. This review will highlight age-related changes in the protein folding machinery and in the UPR.
    PMID: 19491040 [PubMed - in process] (Source: A...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543499</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:16 +0100</pubDate>
            <guid isPermaLink="false">2543499</guid>        </item>
        <item>
            <title>The coordination of nuclear and mitochondrial communication during aging and calorie restriction.</title>
            <link>http://www.medworm.com/index.php?rid=2543498&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19491041%26dopt%3DAbstract</link>
            <description>Authors: Finley LW, Haigis MC
    Mitochondria are dynamic organelles that integrate environmental signals to regulate energy production, apoptosis and Ca(2+) homeostasis. Not surprisingly, mitochondrial dysfunction is associated with aging and the pathologies observed in age-related diseases. The vast majority of mitochondrial proteins are encoded in the nuclear genome, and so communication between the nucleus and mitochondria is essential for maintenance of appropriate mitochondrial function. Several proteins have emerged as major regulators of mitochondrial gene expression, capable of increasing transcription of mitochondrial genes in response to the physiological demands of the cell. In this review, we will focus on PGC-1alpha, SIRT1, AMPK and mTOR and discuss how these proteins regula...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543498</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:14 +0100</pubDate>
            <guid isPermaLink="false">2543498</guid>        </item>
        <item>
            <title>Relation between replicative senescence of human fibroblasts and life history characteristics.</title>
            <link>http://www.medworm.com/index.php?rid=2543497&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19491042%26dopt%3DAbstract</link>
            <description>Authors: Maier AB, Westendorp RG
    Replicative ageing of fibroblasts in vitro has often been used as a model for organismal ageing. The general assumption that the ageing process is mirrored by cellular senescence in vitro is based on lower replicative capacity of human fibroblasts from patients with accelerated ageing syndromes, patients with age related diseases such as diabetes mellitus, and donors of higher chronological age, but these inverse relations have not been reported unequivocally. Therefore, we have performed a formal review on the replicative capacity of fibroblasts from patients suffering from accelerated ageing syndromes, age related diseases and donor age. Some 13 studies including 79 patients with accelerated ageing syndromes showed replicative capacity of fibroblasts ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543497</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:12 +0100</pubDate>
            <guid isPermaLink="false">2543497</guid>        </item>
        <item>
            <title>Can hematopoietic stem cells be an alternative source for skin regeneration?</title>
            <link>http://www.medworm.com/index.php?rid=2543496&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19491043%26dopt%3DAbstract</link>
            <description>Authors: Fu X, Sun X
    In the past few years, the plasticity of adult cells in several post-natal tissues has attracted special attention in regenerative medicine. Skin is the largest organ in the body. Adult skin consists of epidermis, dermis and appendages such as hair and glands that are linked to the epidermis but project deep into the dermal layer. Stem cell biology of skin has been a focus of increasing interest in current life science. Committed stem cells with a limited differentiation potential for regeneration and repair of epidermis have been known for decades. Recent studies further found that adult skin tissues contain cell populations with pluripotent characteristics. Multipotent stem cells from skin with and without hair follicles, both in epidermal and dermal tissues, can...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543496</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:10 +0100</pubDate>
            <guid isPermaLink="false">2543496</guid>        </item>
        <item>
            <title>Non-apolipoprotein E and apolipoprotein E genetics of sporadic Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=2543495&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19496238%26dopt%3DAbstract</link>
            <description>Authors: Seripa D, Panza F, Franceschi M, D'Onofrio G, Solfrizzi V, Dallapiccola B, Pilotto A
    The genetic epidemiology of sporadic Alzheimer's disease (SAD) remains a very active area of research,making it one of the most prolifically published areas in medicine and biology. Numerous putative candidate genes have been proposed. However, with the exception of apolipoprotein E (APOE), the only confirmed genetic risk factor for SAD, all the other data appear to be not consistent. Nevertheless, the genetic risk for SAD attributable to the APOE gene in the general population is 20-0%, providing a strong evidence for the existence of additional genetic risk factors. The first part of the present article was dedicated to non-APOE genetics of SAD, reviewing chromosomes-by-chromosomes the avail...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543495</comments>
            <pubDate>Sun, 28 Jun 2009 01:37:08 +0100</pubDate>
            <guid isPermaLink="false">2543495</guid>        </item>
        <item>
            <title>Cyanobacteria and ultraviolet radiation (UVR) stress: Mitigation strategies.</title>
            <link>http://www.medworm.com/index.php?rid=2543494&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19524071%26dopt%3DAbstract</link>
            <description>Authors: Singh SP, H&amp;#xE4;der DP, Sinha RP
    Cyanobacteria are primitive photosynthetic oxygen-evolving prokaryotes that appeared on the Earth when there was no ozone layer to protect them from damaging ultraviolet radiation (UVR). UVR has both direct and indirect effects on the cyanobacteria due to absorption by biomolecules and UVR-induced oxidative stress, respectively. However, these organisms have developed several lines of mitigation strategies/defense mechanisms such as avoidance, scavenging, screening, repair and programmed cell death to counteract the damaging effects of UVR. This review presents an update on the effects of UVR on cyanobacteria and the defense mechanisms employed by these prokaryotes to withstand UVR stress. In addition, recent developments in the field of molec...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543494</comments>
            <pubDate>Wed, 10 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2543494</guid>        </item>
        <item>
            <title>Chronic diseases and risk for depression in old age: A meta-analysis of published literature.</title>
            <link>http://www.medworm.com/index.php?rid=2543493&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19524072%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: We concluded here that in old age, the associations of depression with some chronic diseases were definite; among these chronic diseases, stroke, loss of hearing, loss of vision, cardiac disease and chronic lung disease were risk factors for increased depression, but it should be further investigated whether arthritis, hypertension and diabetes were risk factors for increased depression or not.
    PMID: 19524072 [PubMed - as supplied by publisher] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543493</comments>
            <pubDate>Wed, 10 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2543493</guid>        </item>
        <item>
            <title>The impact of sarcopenia and exercise training on skeletal muscle satellite cells.</title>
            <link>http://www.medworm.com/index.php?rid=2543502&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19464390%26dopt%3DAbstract</link>
            <description>Authors: Snijders T, Verdijk LB, van Loon LJ
    It has been well-established that the age-related loss of muscle mass and strength, or sarcopenia, impairs skeletal muscle function and reduces functional performance at a more advanced age. Skeletal muscle satellite cells (SC), as precursors of new myonuclei, have been suggested to be involved in the development of sarcopenia. In accordance with the type II muscle fiber atrophy observed in the elderly, recent studies report a concomitant fiber type specific reduction in SC content. Resistance type exercise interventions have proven effective to augment skeletal muscle mass and improve muscle function in the elderly. In accordance, recent work shows that resistance type exercise training can augment type II muscle fiber size and reverse the ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543502</comments>
            <pubDate>Wed, 20 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2543502</guid>        </item>
        <item>
            <title>Suicidal function of DNA methylation in age-related genome disintegration.</title>
            <link>http://www.medworm.com/index.php?rid=2543501&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19464391%26dopt%3DAbstract</link>
            <description>Authors: Mazin AL
    DNA cytosine methylation can affect genetic and epigenetic processes, works as a part of the genome-defense system and has mutagenic activity; however, the biological functions of this enzymatic modification are not well understood. This review will put forward the hypothesis that the host-defense role of DNA methylation in silencing and mutational destroying of retroviruses and other intragenomic parasites was extended during evolution to most host genes that have to be inactivated in differentiated somatic cells, where it acquired a new function in age-related self-destruction of the genome. The proposed model considers DNA methylation as the generator of 5mC&amp;gt;T transitions that induce most of the multiple classes of spontaneous mutations at CpG and CpNpG methylat...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543501</comments>
            <pubDate>Wed, 20 May 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2543501</guid>        </item>
        <item>
            <title>Endothelial dysfunction-An obstacle of therapeutic angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2543506&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19389489%26dopt%3DAbstract</link>
            <description>Authors: Sun L, Bai Y, Du G
    Due to ageing populations and improvements in survival, increasing numbers of patients suffering from ischemic cardiovascular disease are not amenable to revascularization. Hence, interests are currently focused on &quot;therapeutic angiogenesis&quot;, which is the clinical use of growth factors to enhance or promote the development of collateral blood vessels in ischemic tissue. Several growth factors (or genes encoding these growth factors) are now available for therapeutic vascular growth in normal and ischemic tissues. However, the successes of angiogenic therapy observed in pre-clinical studies have not been realized in clinical trials. Most animal studies demonstrating the physiologic effectiveness of angiogenic therapies have been performed in normal young anim...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543506</comments>
            <pubDate>Mon, 20 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2543506</guid>        </item>
        <item>
            <title>Biomarkers of oxidative and nitrosative damage in Alzheimer's disease and mild cognitive impairment.</title>
            <link>http://www.medworm.com/index.php?rid=2543508&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19376275%26dopt%3DAbstract</link>
            <description>Authors: Mangialasche F, Polidori MC, Monastero R, Ercolani S, Camarda C, Cecchetti R, Mecocci P
    Alzheimer's disease (AD) is the most common type of dementia in the elderly. Products of oxidative and nitrosative stress (OS and NS, respectively) accumulate with aging, which is the main risk factor for AD. This provides the basis for the involvement of OS and NS in AD pathogenesis. OS and NS occur in biological systems due to the dysregulation of the redox balance, caused by a deficiency of antioxidants and/or the overproduction of free radicals. Free radical attack against lipids, proteins, sugars and nucleic acids leads to the formation of bioproducts whose detection in fluids and tissues represents the currently available method for assessing oxidative/nitrosative damage. Post-mortem ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543508</comments>
            <pubDate>Thu, 16 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2543508</guid>        </item>
        <item>
            <title>PON1 is a longevity gene: Results of a meta-analysis.</title>
            <link>http://www.medworm.com/index.php?rid=2543507&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19376276%26dopt%3DAbstract</link>
            <description>Authors: Lescai F, Marchegiani F, Franceschi C
    Paraoxonase 1 (PON1) is one of the most studied genes regarding cardiovascular risk, oxidative stress and inflammation. Several lines of evidence suggests that PON1 promotes an atheroprotective effect. Patients carrying PON1 codon 192 QQ genotype display a higher risk of cardiovascular events, the major cause of mortality in the elderly: it can be predicted that gene variants increasing the risk of mortality will be under-represented in long-living individuals. We first reported that PON1 R allele (R+) carriers are significantly more represented in Italian centenarians; subsequently this topic has been addressed by many other groups, and here we report a meta-analysis on 11 studies in different populations selected by a review of the liter...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2543507</comments>
            <pubDate>Thu, 16 Apr 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2543507</guid>        </item>
        <item>
            <title>Viewpoint: dried plum, an emerging functional food that may effectively improve bone health.</title>
            <link>http://www.medworm.com/index.php?rid=2255667&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19274852%26dopt%3DAbstract</link>
            <description>Authors: Hooshmand S, Arjmandi BH
    Osteoporosis is a debilitating disorder that affects both female and male, albeit to a greater extent in women than men. As the demographic shift to a more aged population continues, a growing number of men and women will be afflicted with osteoporosis and a search for potential non-pharmacological alternative therapies for osteoporosis is of prime interest. Aside from existing drug therapies, certain lifestyle and nutritional factors are known to reduce the risk of osteoporosis. Among nutritional factors, recent observations suggest that dried plum, or prunes (Prunus domestica L.) is the most effective fruit in both preventing and reversing bone loss. Animal studies and a 3-month clinical trial conducted in our laboratories have shown that dried plum ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2255667</comments>
            <pubDate>Thu, 12 Mar 2009 17:30:58 +0100</pubDate>
            <guid isPermaLink="false">2255667</guid>        </item>
        <item>
            <title>Heat shock proteins as gatekeepers of proteolytic pathways-Implications for age-related macular degeneration (AMD).</title>
            <link>http://www.medworm.com/index.php?rid=2255666&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19274853%26dopt%3DAbstract</link>
            <description>Authors: Kaarniranta K, Salminen A, Eskelinen EL, Kopitz J
    Age-related macular degeneration (AMD) is the major diagnosis for severe and irreversible central loss of vision in elderly people in the developed countries. The loss of vision involves primarily a progressive degeneration and cell death of postmitotic retinal pigment epithelial cells (RPE), which secondarily evokes adverse effects on photoreceptor cells. The RPE cells are exposed to chronic oxidative stress from three sources: their high levels of oxygen consumption, their exposure to the high levels of lipid peroxidation derived from the photoreceptor outer segments and their exposure to constant light stimuli. Cells increase the expression of heat shock proteins (HSPs) in order to normalize their growth conditions in respon...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2255666</comments>
            <pubDate>Thu, 12 Mar 2009 17:30:32 +0100</pubDate>
            <guid isPermaLink="false">2255666</guid>        </item>
        <item>
            <title>Biological changes associated with healthy versus pathological aging: a symposium review.</title>
            <link>http://www.medworm.com/index.php?rid=2255664&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19274854%26dopt%3DAbstract</link>
            <description>Authors: Rajah MN, Bastianetto S, Bromley-Brits K, Cools R, D'Esposito M, Grady CL, Poirier J, Quirion R, Raz N, Rogaeva E, Song W, Pruessner J
    The Douglas Mental Health University Institute, in collaboration with the McGill Centre for Studies in Aging, organized a 2-day symposium entitled &quot;Biological Changes Associated with Healthy Versus Pathological Aging&quot; that was held in 13 and 14 December 2007 on the Douglas campus. The symposium involved presentations on current trends in aging and dementia research across several sub-disciplines: genetics, neurochemistry, structural and functional neuroimaging and clinical treatment and rehabilitation. The goal of this symposium was to provide a forum for knowledge-transfer between scientists and clinicians with different specializations in ord...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2255664</comments>
            <pubDate>Thu, 12 Mar 2009 17:30:11 +0100</pubDate>
            <guid isPermaLink="false">2255664</guid>        </item>
        <item>
            <title>Signaling mechanisms of angiotensin II in regulating vascular senescence.</title>
            <link>http://www.medworm.com/index.php?rid=2131203&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19162241%26dopt%3DAbstract</link>
            <description>Authors: Min LJ, Mogi M, Iwai M, Horiuchi M
    Angiotensin (Ang) II, the major effector of the rennin-angiotensin-aldosterone system (RAAS), has multiple functions in regulating cardiovascular hemodynamics and structure. Recent evidence strongly supports that Ang II promotes the onset and progression of vascular senescence, which is associated with vascular functional and structural changes, contributing to age-related vascular diseases. The vast majority of the cardiovascular actions of Ang II, including vascular senescence, are mediated by the Ang II type-1 (AT(1)) receptor. Similar to its growth-promoting process, the signaling mechanisms of AT(1) receptor-mediated vascular senescence-promoting effects involve activation of small G-protein Ras such as Ki-ras2A, mitogen-activated protei...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2131203</comments>
            <pubDate>Wed, 31 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2131203</guid>        </item>
        <item>
            <title>Recent insights into the molecular mechanisms involved in aging and the malignant transformation of adult stem/progenitor cells and their therapeutic implications.</title>
            <link>http://www.medworm.com/index.php?rid=2073672&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19114129%26dopt%3DAbstract</link>
            <description>Authors: Mimeault M, Batra SK
    Recent advancements in tissue-resident adult stem/progenitor cell research have revealed that enhanced telomere attrition, oxidative stress, ultraviolet radiation exposure and oncogenic events leading to severe DNA damages and genomic instability may occur in these immature and regenerative cells during chronological aging. Particularly, the alterations in key signaling components controlling their self-renewal capacity and an up-regulation of tumor suppressor gene products such as p16(INK4A), p19(ARF), ataxia-telangiectasia mutated (ATM) kinase, p53 and/or the forkhead box O (FOXOs) family of transcription factors may result in their dysfunctions, growth arrest and senescence or apoptotic death during the aging process. These molecular events may culminat...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2073672</comments>
            <pubDate>Tue, 09 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2073672</guid>        </item>
        <item>
            <title>Endothelial progenitor cell therapy in atherosclerosis: A double-edged sword?</title>
            <link>http://www.medworm.com/index.php?rid=2065128&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19103308%26dopt%3DAbstract</link>
            <description>Authors: Liu P, Zhou B, Gu D, Zhang L, Han Z
    Atherosclerosis, an inflammatory process that selectively affects arteries, is highly prevalent in human. Thrombo-occlusive complications of atherosclerosis, including stroke and myocardial infarction, are becoming major causes of morbidity and mortality in the industrialized world. Atherosclerosis develops in response to local endothelial injuries. Endothelial dysfunction and cell loss are prominent features in atherosclerosis. Restoring the endothelial lining to normal is critical for slowing or reversing the progression of atherosclerosis. Increasing data suggest that endothelial progenitor cells (EPCs) play a significant role in reendothelialization of the injured blood vessels. This review focuses on the effects of EPC mobilization and ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2065128</comments>
            <pubDate>Wed, 03 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2065128</guid>        </item>
        <item>
            <title>Blood pressure and the risk for dementia-A double edged sword.</title>
            <link>http://www.medworm.com/index.php?rid=2026684&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19063999%26dopt%3DAbstract</link>
            <description>Authors: Kennelly SP, Lawlor BA, Kenny RA
    Alzheimer's disease (AD) and vascular dementia (VaD) are important causes of cognitive decline in the elderly. As a result of the aging population, the incidence of dementia is expected to increase substantially over the coming decades. Many studies have identified that vascular risk factors are implicated in the pathogenesis of both AD and VaD. Longitudinal studies have suggested that high blood pressure in midlife is associated with a higher incidence of both AD and VaD in later life. The association appears weaker for hypertension in later life. Some studies also suggest that hypotension; especially low diastolic blood pressure in late-life is also associated with an increased risk of AD. Long-standing hypertension may lead to severe atheros...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2026684</comments>
            <pubDate>Fri, 21 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2026684</guid>        </item>
        <item>
            <title>Current understanding of klotho.</title>
            <link>http://www.medworm.com/index.php?rid=1980426&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19022406%26dopt%3DAbstract</link>
            <description>Authors: Wang Y, Sun Z
    Klotho is a new anti-aging gene. Genetic mutation of klotho causes multiple premature aging-like phenotypes and strikingly shortens lifespan. Overexpression of the klotho gene in mice suppresses aging and extends lifespan which may involve the mechanism of suppression of insulin signaling and oxidant stress. Klotho functions as a cofactor/coreceptor regulating fibroblast growth factor (FGF) 23 signaling. Klotho acts as a glucuronidase and activates ion channel TRPV5. Klotho protects against endothelial dysfunction and regulates the production of nitric oxide. Klotho also influences intracellular signaling pathways including p53/p21, cAMP, protein kinase C (PKC) and Wnt signaling pathways. The discovery of klotho has a great impact on aging research. The purpose o...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1980426</comments>
            <pubDate>Fri, 31 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1980426</guid>        </item>
        <item>
            <title>Heart rate, lifespan, and mortality risk.</title>
            <link>http://www.medworm.com/index.php?rid=1980427&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19022405%26dopt%3DAbstract</link>
            <description>Authors: Zhang GQ, Zhang W
    An increasing body of research and evidence indicates that resting heart rate (HR) is inversely related to the lifespan among homeothermic mammals and within individual species. In numerous human studies with patients stratified by resting HR, increased HR is universally associated with greater risk of death. The correlation between HR and maximum lifespan seems to be due to both basal metabolic rate and cardiovascular-related mortality risk. Both intrinsic and extrinsic factors are already postulated to determine how the biological clock works, through regulating and modulating the processes such as protein oxidation, free radical production, inflammation and telomere shortening. Given the remarkable correlation between HR and lifespan, resting HR should be ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1980427</comments>
            <pubDate>Thu, 30 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1980427</guid>        </item>
        <item>
            <title>Effect of interleukin-6 polymorphisms on human longevity: A systematic review and meta-analysis.</title>
            <link>http://www.medworm.com/index.php?rid=1894703&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18930842%26dopt%3DAbstract</link>
            <description>Authors: Di Bona D, Vasto S, Capurso C, Christiansen L, Deiana L, Franceschi C, Hurme M, Mocchegiani E, Rea M, Lio D, Candore G, Caruso C
    Several studies have assessed changes in frequency of -174 interleukin (IL)-6 single nucleotide polymorphism (SNP) with age. If IL-6 tracks with disability and age-related diseases, then there should be reduction, in the oldest old, of the frequency of homozgyous GG subjects, who produce higher IL-6 levels. However, discordant results have been obtained. To explore the relationship between this polymorphism and longevity, we analyzed individual data on long-living subjects and controls from eight case-control studies conducted in Europeans, using meta-analysis. There was no significant difference in the IL-6 genotype between the oldest old and contro...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1894703</comments>
            <pubDate>Sat, 27 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1894703</guid>        </item>
        <item>
            <title>Inflammatory response is associated with aortic dissection.</title>
            <link>http://www.medworm.com/index.php?rid=1797915&amp;cid=s_34430_50_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18789403%26dopt%3DAbstract</link>
            <description>Authors: Luo F, Zhou XL, Li JJ, Hui RT
    Aortic dissection is an age-dependent life-threatening cardiovascular disease with high mortality rates. Recent research has shown that inflammation plays an important role in aortic dissection. Inflammatory cells, such as lymphocytes and macrophages, not only increase the expression of proteases and cell adhesion molecules but also release reactive oxygen species. These cells also contribute to apoptosis of smooth muscle cells in the aortic artery, and finally lead to medial degradation. This process has been considered to be the principal mechanism for aortic dissection. Furthermore, changes in systemic inflammatory biomarkers are associated with acute-phase reactions and complications in aortic dissection. These biomarkers are also used to pred...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1797915</comments>
            <pubDate>Fri, 22 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1797915</guid>        </item>
        <item>
            <title>Effects of whole body vibration on the skeleton and other organ systems in man and animal models: What we know and what we need to know.</title>
            <link>http://www.medworm.com/index.php?rid=1759725&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18762281%26dopt%3DAbstract</link>
            <description>Authors: Prisby RD, Lafage-Proust MH, Malaval L, Belli A, Vico L
    Previous investigations reported enhanced osseous parameters subsequent to administration of whole body vibration (WBV). While the efficacy of WBV continues to be explored, scientific inquiries should consider several key factors. Bone remodeling patterns differ according to age and hormonal status. Therefore, WBV protocols should be designed specifically for the subject population investigated. Further, administration of WBV to individuals at greatest risk for osteoporosis may elicit secondary physiological benefits (e.g., improved balance and mobility). Secondly, there is a paucity of data in the literature regarding the physiological modulation of WBV on other organ systems and tissues. Vibration-induced modulation of ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1759725</comments>
            <pubDate>Tue, 12 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1759725</guid>        </item>
        <item>
            <title>Proteomics in animal models of Alzheimer's and Parkinson's diseases.</title>
            <link>http://www.medworm.com/index.php?rid=1708787&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18703168%26dopt%3DAbstract</link>
            <description>Authors: Sowell RA, Owen JB, Allan Butterfield D
    The risk of developing neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD) increases with age. AD and PD are the two most common neurodegenerative diseases that currently affect millions of persons within the United States population. While many clues about the mechanisms of these disorders have been uncovered, to date, the molecular mechanisms associated with the cause of these diseases are not completely understood. Furthermore, there are no available cures or preventive treatments for either disorder. Animal models of AD and PD, though not perfect, offer a means to gain knowledge of the basic biochemistry associated with these disorders and with drug efficacy. The field of proteomics which focuses...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1708787</comments>
            <pubDate>Fri, 18 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1708787</guid>        </item>
        <item>
            <title>Molecular inflammation: Underpinnings of aging and age-related diseases.</title>
            <link>http://www.medworm.com/index.php?rid=1700480&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18692159%26dopt%3DAbstract</link>
            <description>Authors: Chung HY, Cesari M, Anton S, Marzetti E, Giovannini S, Seo AY, Carter C, Yu BP, Leeuwenburgh C
    Recent scientific studies have advanced the notion of chronic inflammation as a major risk factor underlying aging and age-related diseases. In this review, low-grade, unresolved, molecular inflammation is described as an underlying mechanism of aging and age-related diseases, which may serve as a bridge between normal aging and age-related pathological processes. Accumulated data strongly suggest that continuous (chronic) upregulation of pro-inflammatory mediators (e.g., TNF-alpha, IL-1beta, 6, COX-2, iNOS) are induced during the aging process due to an age-related redox imbalance that activates many pro-inflammatory signaling pathways, including the NF-kappaB signaling pathway. The...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1700480</comments>
            <pubDate>Fri, 18 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1700480</guid>        </item>
        <item>
            <title>Role of neuroendocrine pathways in cognitive decline during aging.</title>
            <link>http://www.medworm.com/index.php?rid=1674729&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18672097%26dopt%3DAbstract</link>
            <description>Authors: Ferrari E, Magri F
    The pineal and pituitary-adrenocortical secretions play an important role in adaptive responses of the organism acting as coordinating signals for both several biological rhythms and multiple neuroendocrine and metabolic functions. The more relevant neuroendocrine changes occurring with ageing affect the secretion of melatonin and of corticosteroids. These changes may be clearly appreciated by the study of their circadian rhythmicity. The circadian profile of plasma melatonin was clearly flattened in elderly subjects and even more in old individuals with dementia. Indeed, the impairment of melatonin signal occurring in aging was related either to age itself or to the cognitive performances of subjects. The biosynthetic dissociation between glucocorticoids an...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1674729</comments>
            <pubDate>Thu, 10 Jul 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1674729</guid>        </item>
        <item>
            <title>Pro-inflammatory genetic background and zinc status in old atherosclerotic subjects.</title>
            <link>http://www.medworm.com/index.php?rid=1605784&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18611449%26dopt%3DAbstract</link>
            <description>Authors: Giacconi R, Caruso C, Malavolta M, Lio D, Balistreri CR, Scola L, Candore G, Muti E, Mocchegiani E
    Inflammation and genetics are prominent mechanisms in the pathogenesis of atherosclerosis (AT) and its complications. In this review we discuss the possible impact on AT development of several genetic determinants involved in inflammation, oxidative stress and cytoprotection (IL-6, TNF-alpha, IL-10, CD14, TLR4, MT, HSP70). Genetic polymorphisms of these genes may affect a differential inflammatory response predisposing to AT. However, allelic polymorphisms of genes which increase the risk of AT frequently occur in the general population but, only adequate gene-environment-polymorphism interactions promote the onset of the disease. Zinc deficiency has been suggested as an environm...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1605784</comments>
            <pubDate>Thu, 19 Jun 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1605784</guid>        </item>
        <item>
            <title>On high-frequency insulin oscillations.</title>
            <link>http://www.medworm.com/index.php?rid=1551198&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18583199%26dopt%3DAbstract</link>
            <description>Authors: Schmitz O, Rungby J, Edge L, Juhl CB
    Insulin is released in a pulsatile manner, which results in oscillatory concentrations in blood. The oscillatory secretion improves release control and enhances the hormonal action. Insulin oscillates with a slow ultradian periodicity ( approximately 140min) and a high-frequency periodicity ( approximately 6-10min). Only the latter is reviewed in this article. At least 75% of the insulin secretion is released in a pulsatile manner. Individuals prone to developing diabetes or with overt type 2 diabetes are characterized by irregular oscillations of plasma insulin. Many factors have impact on insulin pulsatility such as age, insulin resistance and glycemic level. In addition, tiny glucose oscillations are capable of entraining insulin oscilla...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1551198</comments>
            <pubDate>Sat, 03 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1551198</guid>        </item>
        <item>
            <title>Detoxification reactions: Relevance to aging.</title>
            <link>http://www.medworm.com/index.php?rid=1516349&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18547875%26dopt%3DAbstract</link>
            <description>Authors: Zimniak P
    It is widely (although not universally) accepted that organismal aging is the result of two opposing forces: (i) processes that destabilize the organism and increase the probability of death, and (ii) longevity assurance mechanisms that prevent, repair, or contain damage. Processes of the first group are often chemical and physico-chemical in nature, and are either inevitable or only under marginal biological control. In contrast, protective mechanisms are genetically determined and are subject to natural selection. Life span is therefore largely dependent on the investment into protective mechanisms which evolve to optimize reproductive fitness. Recent data indicate that toxicants, both environmental and generated endogenously by metabolism, are major contributors t...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1516349</comments>
            <pubDate>Fri, 02 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1516349</guid>        </item>
        <item>
            <title>A multi-hit endocrine model of intrinsic adult-onset asthma.</title>
            <link>http://www.medworm.com/index.php?rid=1340426&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18373959%26dopt%3DAbstract</link>
            <description>Authors: Atwood CS, Bowen RL
    Epidemiological studies indicate that adult-onset asthma is initiated by stress (anxiety and depression), obesity and menopause. Ironically, despite our understanding of the various stressors that promote chronic adult-onset asthma, most of which are known to elevate cortisol production via the hypothalamic-pituitary-adrenal (HPA) axis, inhaled and systemic corticosteroids are the mainstay for the treatment of chronic asthma. This implicates other endocrine or cellular changes independent of cortisol synthesis in non-allergic adult-onset asthma. The mechanism by which corticosteroids are thought to modulate bronchial tone in relieving asthma is via corticosteroid-responsive genes that increase PGE(2) and cAMP production which promote muscle relaxation. Ther...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1340426</comments>
            <pubDate>Tue, 01 Apr 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1340426</guid>        </item>
        <item>
            <title>Cyclin-dependent kinase inhibitor p16(INK4a) and telomerase may co-modulate endothelial progenitor cells senescence.</title>
            <link>http://www.medworm.com/index.php?rid=1310853&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18343732%26dopt%3DAbstract</link>
            <description>Authors: Yang DG, Liu L, Zheng XY
    Endothelial cells (ECs) damage is an initial and pivotal step in the formation of atherosclerosis. Endothelial progenitor cells (EPCs), which have been considered as the precursor of ECs, can migrate and home to the site of injured ECs to divide into mature ECs and keep the integrity of the endothelial monolayer. It has been shown that the number and function of EPCs are negatively correlated with various atherosclerotic risk factors. This finding may be explained partly by accelerated senescence of EPCs induced by telomere attrition or shortening owning to oxidative stress and accumulative ROS. However, elevated telomerase activity which extends the telomere cannot lead to cellular immortal in the presence of the cyclin-dependent kinase inhibitor p16(...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1310853</comments>
            <pubDate>Tue, 12 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1310853</guid>        </item>
        <item>
            <title>Caloric restriction: Impact upon pituitary function and reproduction.</title>
            <link>http://www.medworm.com/index.php?rid=1294198&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18329344%26dopt%3DAbstract</link>
            <description>Authors: Martin B, Golden E, Carlson OD, Egan JM, Mattson MP, Maudsley S
    Reduced energy intake, or caloric restriction (CR), is known to extend life span and to retard age-related health decline in a number of different species, including worms, flies, fish, mice and rats. CR has been shown to reduce oxidative stress, improve insulin sensitivity, and alter neuroendocrine responses and central nervous system (CNS) function in animals. CR has particularly profound and complex actions upon reproductive health. At the reductionist level the most crucial physiological function of any organism is its capacity to reproduce. For a successful species to thrive, the balance between available energy (food) and the energy expenditure required for reproduction must be tightly linked. An ability to ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1294198</comments>
            <pubDate>Thu, 07 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1294198</guid>        </item>
        <item>
            <title>Dysregulation of pulsatility in aging IV. Pulsatile signaling and cardiovascular aging: Functions and regulation of natriuretic peptide signaling.</title>
            <link>http://www.medworm.com/index.php?rid=1207075&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18243818%26dopt%3DAbstract</link>
            <description>Authors: Charloux A, Brandenberger G, Piquard F, Geny B
    Atrial and brain natriuretic peptides (ANP and BNP) are cardiac hormones connecting heart and kidney and playing a key role in hydromineral and hemodynamic homeostasis. In contrast with the renin-angiotensin-aldosterone system, circulating ANP and BNP are not temporally related with rapid eye movement (REM)-nonREM sleep cycles, autonomic activity, or blood pressure. Cardiac natriuretic peptides are secreted in a pulsatile manner, with short periods of 20-48min, in normal as well as in pathological conditions. The frequency of pulses seems to be unchanged with aging, whereas the absolute amplitude of the oscillations seems to increase, most likely as a result of an increase in the plasma hormone levels observed in elderly. Enhanced...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1207075</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1207075</guid>        </item>
        <item>
            <title>Hormesis defined.</title>
            <link>http://www.medworm.com/index.php?rid=1121647&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18162444%26dopt%3DAbstract</link>
            <description>Authors: Mattson MP
    Hormesis is a term used by toxicologists to refer to a biphasic dose-response to an environmental agent characterized by a low dose stimulation or beneficial effect and a high dose inhibitory or toxic effect. In the fields of biology and medicine hormesis is defined as an adaptive response of cells and organisms to a moderate (usually intermittent) stress. Examples include ischemic preconditioning, exercise, dietary energy restriction and exposures to low doses of certain phytochemicals. Recent findings have elucidated the cellular signaling pathways and molecular mechanisms that mediate hormetic responses which typically involve enzymes such as kinases and deacetylases, and transcription factors such as Nrf-2 and NF-kappaB. As a result, cells increase their product...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1121647</comments>
            <pubDate>Wed, 05 Dec 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1121647</guid>        </item>
        <item>
            <title>Stem cells for tissue engineering of myocardial constructs.</title>
            <link>http://www.medworm.com/index.php?rid=1052154&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981518%26dopt%3DAbstract</link>
            <description>Authors: Wu KH, Mo XM, Liu YL, Zhang YS, Han ZC
    Cardiovascular diseases are the leading cause of morbidity and mortality. Tissue engineering offers new option in the myocardial repair techniques. The cellular component of this regenerative approach will play a key role in bringing these tissue engineered constructs from the laboratory bench to the clinical bedside. However, the ideal source of cells still remains unclear and may differ depending upon the application. Current research for many applications is focused on the use of stem cells. The combination of stem cell technology and tissue engineering has been investigated and offers promising avenues for myocardial tissue regeneration, and this shows great promise in future reconstructive surgery. We explore the basic concepts and m...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1052154</comments>
            <pubDate>Tue, 27 Nov 2007 14:11:12 +0100</pubDate>
            <guid isPermaLink="false">1052154</guid>        </item>
        <item>
            <title>Activation of innate immunity system during aging: NF-kB signaling is the molecular culprit of inflamm-aging.</title>
            <link>http://www.medworm.com/index.php?rid=989546&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17964225%26dopt%3DAbstract</link>
            <description>Authors: Salminen A, Huuskonen J, Ojala J, Kauppinen A, Kaarniranta K, Suuronen T
    Innate and adaptive immunity are the major defence mechanisms of higher organisms against inherent and environmental threats. Innate immunity is present already in unicellular organisms but evolution has added novel adaptive immune mechanisms to the defence armament. Interestingly, during aging, adaptive immunity significantly declines, a phenomenon called immunosenescence, whereas innate immunity seems to be activated which induces a characteristic pro-inflammatory profile. This process is called inflamm-aging. The recognition and signaling mechanisms involved in innate immunity have been conserved during evolution. The master regulator of the innate immunity is the NF-kB system, an ancient signaling pat...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=989546</comments>
            <pubDate>Thu, 20 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">989546</guid>        </item>
        <item>
            <title>The role of inflammation in coronary artery calcification.</title>
            <link>http://www.medworm.com/index.php?rid=989545&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17964226%26dopt%3DAbstract</link>
            <description>Authors: Li JJ, Zhu CG, Yu B, Liu YX, Yu MY
    Vascular calcification is an age-dependent, common finding in human coronary arteries and begins as early as the second decade of life, just after fatty streak formation. Previous studies have showed that the severity of coronary calcification is closely related to atherosclerotic plaque burden and cardiac event rate. In the past few decades, coronary calcification has been considered passive and degenerative. With recent clinical and basic research, however, there is increasing recognition that coronary calcification is an active, regulated process. Current diagnostic methods for coronary artery calcification (CAC) are usually traditional coronary angiography, intravascular ultrasound (IVUS), electron beam computed tomography (EBCT) and mult...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=989545</comments>
            <pubDate>Fri, 14 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">989545</guid>        </item>
        <item>
            <title>Dietary factors, hormesis and health.</title>
            <link>http://www.medworm.com/index.php?rid=936629&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17920340%26dopt%3DAbstract</link>
            <description>Authors: Mattson MP
    The impact of dietary factors on health and longevity is increasingly appreciated. The most prominent dietary factor that affects the risk of many different chronic diseases is energy intake-excessive calorie intake increases the risk. Reducing energy intake by controlled caloric restriction or intermittent fasting increases lifespan and protects various tissues against disease, in part, by hormesis mechanisms that increase cellular stress resistance. Some specific dietary components may also exert health benefits by inducing adaptive cellular stress responses. Indeed, recent findings suggest that several heavily studied phytochemicals exhibit biphasic dose responses on cells with low doses activating signaling pathways that result in increased expression of genes e...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=936629</comments>
            <pubDate>Tue, 04 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">936629</guid>        </item>
        <item>
            <title>Dietary factors, hormesis and health.</title>
            <link>http://www.medworm.com/index.php?rid=930993&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17913594%26dopt%3DAbstract</link>
            <description>Authors: Mattson MP
    The impact of dietary factors on health and longevity is increasingly appreciated. The most prominent dietary factor that affects the risk of many different chronic diseases is energy intake - excessive calorie intake increases the risk. Reducing energy intake by controlled caloric restriction or intermittent fasting increases lifespan and protects various tissues against disease, in part, by hormesis mechanisms that increase cellular stress resistance. Some specific dietary components may also exert health benefits by inducing adaptive cellular stress responses. Indeed, recent findings suggest that several heavily studied phytochemicals exhibit biphasic dose responses on cells with low doses activating signaling pathways that result in increased expression of genes...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=930993</comments>
            <pubDate>Sat, 01 Sep 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">930993</guid>        </item>
        <item>
            <title>Hormesis: A promising strategy to sustain endogenous neuronal survival pathways against neurodegenerative disorders.</title>
            <link>http://www.medworm.com/index.php?rid=903112&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17889623%26dopt%3DAbstract</link>
            <description>Authors: Marini AM, Jiang H, Pan H, Wu X, Lipsky RH
    The brain developed adaptive mechanisms in the face of changing environments and stresses imposed on the nervous system. The addition of glutamate as the major excitatory amino acid neurotransmitter to the brain's complement of amino acids and peptides dictated a coordinated transcriptional and translational program to meet the demands of excitatory neurotransmission. One such program is the ability of neurons to sustain and maintain their survival given the nature of glutamate-mediated receptor activation. The unique development of endogenous neuronal pathways activated by glutamate receptors transformed neurons and allowed them to survive under conditions of high energy demands. These same endogenous survival pathways also mediate p...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=903112</comments>
            <pubDate>Fri, 24 Aug 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">903112</guid>        </item>
        <item>
            <title>The cell biology of intervertebral disc aging and degeneration.</title>
            <link>http://www.medworm.com/index.php?rid=882419&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17870673%26dopt%3DAbstract</link>
            <description>Authors: Zhao CQ, Wang LM, Jiang LS, Dai LY
    Intervertebral disc degeneration, which mimics disc aging but occurs at an accelerated rate, is considered to be related to neck or low back pain and disc herniation. Degenerated discs show breakdown of the extracellular matrix and thus fail to bear the daily loadings exerted on the spine. Rather than a passive process of wear and tear, disc degeneration is an aberrant, cell-mediated response to progressive structural failure due to aging and other environmental factors such as abnormal mechanical stress. With aging and degeneration, disc cells undergo substantially biologic changes, including alternation of cell type in the nucleus pulposus, increased cell density but decreased number of viable cells as a result of increased cell death and i...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882419</comments>
            <pubDate>Fri, 10 Aug 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">882419</guid>        </item>
        <item>
            <title>Exercise, oxidative stress and hormesis.</title>
            <link>http://www.medworm.com/index.php?rid=882421&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869589%26dopt%3DAbstract</link>
            <description>Authors: Radak Z, Chung HY, Koltai E, Taylor AW, Goto S
    Physical inactivity leads to increased incidence of a variety of diseases and it can be regarded as one of the end points of the exercise-associated hormesis curve. On the other hand, regular exercise, with moderate intensity and duration, has a wide range of beneficial effects on the body including the fact that it improves cardio-vascular function, partly by a nitric oxide-mediated adaptation, and may reduce the incidence of Alzheimer's disease by enhanced concentration of neurotrophins and by the modulation of redox homeostasis. Mechanical damage-mediated adaptation results in increased muscle mass and increased resistance to stressors. Physical inactivity or strenuous exercise bouts increase the risk of infection, while modera...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882421</comments>
            <pubDate>Thu, 02 Aug 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">882421</guid>        </item>
        <item>
            <title>Review of ICT-based services for identified unmet needs in people with dementia.</title>
            <link>http://www.medworm.com/index.php?rid=882420&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869590%26dopt%3DAbstract</link>
            <description>Authors: Lauriks S, Reinersmann A, Van der Roest HG, Meiland FJ, Davies RJ, Moelaert F, Mulvenna MD, Nugent CD, Dr&amp;#xF6;es RM
    Some of the needs that people with dementia and their informal carers currently perceive as insufficiently met by regular care and support services might be alleviated, or even be met, using modern Information and Communication Technology (ICT). The study described in this paper was designed to provide an insight into the state of the art in ICT solutions that could contribute to meet the most frequently mentioned unmet needs by people with dementia and their informal carers. These needs can be summarized as (1) the need for general and personalized information; (2) the need for support with regard to symptoms of dementia; (3) the need for social contact and com...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882420</comments>
            <pubDate>Thu, 02 Aug 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">882420</guid>        </item>
        <item>
            <title>Converging concepts: Adaptive response, preconditioning, and the Yerkes-Dodson Law are manifestations of hormesis.</title>
            <link>http://www.medworm.com/index.php?rid=843627&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17768095%26dopt%3DAbstract</link>
            <description>Authors: Calabrese EJ
    The adaptive response in toxicology and environmental mutagenesis, preconditioning in biomedicine and the Yerkes-Dodson Law in psychology have dominating research themes with widespread and significant scientific and societal implications. This paper suggests that these apparently independent biological dose-response phenomena are manifestations of the common and more general biphasic dose-response relationship concept called hormesis. These three types of dose-response, as well as the hormesis concept, may represent the same general type of adaptation, which were discovered independently in different biological disciplines, amongst which there has been little communication. This intellectual isolation, due principally to progressively greater disciplinary special...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=843627</comments>
            <pubDate>Tue, 31 Jul 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">843627</guid>        </item>
        <item>
            <title>Highly resistant macromolecular components and low rate of generation of endogenous damage: Two key traits of longevity.</title>
            <link>http://www.medworm.com/index.php?rid=808444&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17702671%26dopt%3DAbstract</link>
            <description>Authors: Pamplona R, Barja G
    Key characteristics relating oxidative damage to aging and longevity are reviewed. Available information indicates that the specific composition of tissue macromolecules (proteins, lipids and mitochondrial DNA) in long-lived animal species gives them an intrinsically high resistance to modification that likely contributes to the superior longevity of these species. This is obtained in the case of lipids by decreasing fatty acid unsaturation, and in the proteins by lowering their methionine content. Long-lived animals also show low rates of reactive oxygen species (ROS) generation and oxidative damage at their mitochondria. On the other hand, dietary restriction decreases mitochondrial ROS production and oxidative damage to mitochondrial DNA and proteins. Th...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=808444</comments>
            <pubDate>Fri, 13 Jul 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">808444</guid>        </item>
        <item>
            <title>Does renal ageing affect survival?</title>
            <link>http://www.medworm.com/index.php?rid=768820&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17662672%26dopt%3DAbstract</link>
            <description>Authors: Razzaque MS
    The effects of ageing on progressive deterioration of renal function, both in human and experimental animals, are described elsewhere, but the effect of renal damage on overall survival and longevity is not yet clearly established. The wild-type animals of various genetic backgrounds, fed with regular diet, overtime develop severe age-associated nephropathy, that include but not limited to inflammatory cell infiltration, glomerulosclerosis, and tubulointerstitial fibrosis. Such renal damage significantly reduces their survival. Reducing renal damage, either by caloric restriction or by suppressing growth hormone (GH)/insulin-like growth factor-1 (IGF-1) activity could significantly enhance the longevity of these animals. Available survival studies using experimenta...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=768820</comments>
            <pubDate>Fri, 29 Jun 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">768820</guid>        </item>
        <item>
            <title>Isoflavones-Safe food additives or dangerous drugs?</title>
            <link>http://www.medworm.com/index.php?rid=711495&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17604235%26dopt%3DAbstract</link>
            <description>Authors: Wuttke W, Jarry H, Seidlová-Wuttke D
    The sales volume of products containing isoflavone has increased since the publication of the Women's Health Initiative. The many apparently contradictory results published on the effects of isoflavones on a variety of estrogen-regulated organs point to both beneficial as well as adverse effects on human health. It is of particular importance that psychovegetative climacteric complaints such as hot flushes are, if at all, only slightly influenced by isoflavones. The substances appear to have weak anti-osteoporotic effect. Their anti-atherosclerotic action is debatable, as not all authors find any beneficial effect on lipids. Most importantly, there is dispute as to whether isoflavones derived from soy or red clover have negative, positive ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=711495</comments>
            <pubDate>Wed, 16 May 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">711495</guid>        </item>
        <item>
            <title>The influences of diet and exercise on mental health through hormesis.</title>
            <link>http://www.medworm.com/index.php?rid=711494&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17604236%26dopt%3DAbstract</link>
            <description>Authors: Gomez-Pinilla F
    It is likely that the capacity of the brain to remain healthy during aging depends upon its ability to adapt and nurture in response to environmental challenges. In these terms, main principles involved in hormesis can be also applied to understand relationships at a higher level of complexity such as those existing between the CNS and the environment. This review emphasizes the ability of diet, exercise, and other lifestyle adaptations to modulate brain function. Exercise and diet are discussed in relationship to their aptitude to impact systems that sustain synaptic plasticity and mental health, and are therefore important for combating the effects of aging. Mechanisms that interface energy metabolism and synaptic plasticity are discussed, as these are the fr...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=711494</comments>
            <pubDate>Sat, 05 May 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">711494</guid>        </item>
        <item>
            <title>Does reproduction decrease longevity in human beings?</title>
            <link>http://www.medworm.com/index.php?rid=650374&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17532269%26dopt%3DAbstract</link>
            <description>Authors: Le Bourg E
    According to the disposable soma theory, a cost for reproduction could exist in human beings and other species and, thus, longevity could decrease when women have a higher number of children. The purpose of this article is to review the evidence in populations living or not living under natural fertility conditions, i.e. when fertility is near its biological maximum. The results indicate that in natural fertility conditions longevity does not decrease when the number of children increases but, in modern populations, mortality could slightly increase when women have more than ca 5 children. Complete data for these modern cohorts will tell us, one day, whether these results are still observed when the variable of interest is longevity and not only mortality.
    PMID:...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=650374</comments>
            <pubDate>Tue, 01 May 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">650374</guid>        </item>
        <item>
            <title>Sir2 and calorie restriction in yeast: A skeptical perspective.</title>
            <link>http://www.medworm.com/index.php?rid=628667&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17512264%26dopt%3DAbstract</link>
            <description>We present here a historical perspective and critical evaluation of the model that CR acts through Sir2 in yeast, and interpret prior reports in light of more recent discoveries. Several specific cases where the Sir2 model of CR is inconsistent with experimental data are noted. These shortcomings must be considered along with evidence supporting a role for Sir2 in CR in order to fully evaluate the validity of this model.
    PMID: 17512264 [PubMed - as supplied by publisher] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=628667</comments>
            <pubDate>Thu, 19 Apr 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">628667</guid>        </item>
        <item>
            <title>Small laboratory fish as models for aging research.</title>
            <link>http://www.medworm.com/index.php?rid=510636&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17392037%26dopt%3DAbstract</link>
            <description>Authors: Gerhard GS
    Fish represent approximately half of all vertebrate species, yet have received little attention as models for aging research relative to invertebrate organisms or rodents. However, the basic gerontological characteristics of several fish species have been studied and provide compelling data for further investigation. In particular, guppies have proved to be an invaluable model for evolutionary analyses of aging, killifish are short-lived and may be exploitable for life span manipulation studies, and zebrafish come with a formidable armament of associated biological tools from their widespread use as a model of vertebrate development. These fish are well suited for the investigation of basic processes implicated in aging, such as insulin signaling, oxidative stress, ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=510636</comments>
            <pubDate>Sat, 03 Mar 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">510636</guid>        </item>
        <item>
            <title>A role of the circadian system and circadian proteins in aging.</title>
            <link>http://www.medworm.com/index.php?rid=486901&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17369106%26dopt%3DAbstract</link>
            <description>Authors: Kondratov RV
    Circadian rhythms are genetically determined biological rhythms that are considered an important adaptive mechanism to the cyclical light/dark alterations in the Earth environment. Age-related changes in the circadian time-keeping mechanism are well known, and seemingly contribute to various pathologies of aging. Recent findings demonstrate that the circadian system and circadian proteins play direct roles in many physiological processes, including those associated with aging. The core circadian proteins BMAL1 and PERIODs, in addition to their known functions in the circadian oscillator, play essential non-redundant roles in the control of tissue homeostasis and aging. Although the exact mechanisms are unknown, the involvement of circadian proteins in the regulati...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=486901</comments>
            <pubDate>Wed, 21 Feb 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">486901</guid>        </item>
        <item>
            <title>Premature aging in klotho mutant mice: Cause or consequence?</title>
            <link>http://www.medworm.com/index.php?rid=471128&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17353153%26dopt%3DAbstract</link>
            <description>Authors: Lanske B, Razzaque MS
    Suitable mammalian models for aging with a wide range of age-associated pathology are desirable to study molecular mechanisms of human aging. Recent studies have identified that fibroblast growth factor 23 (Fgf-23) null mice and klotho hypomorphs could generate multiple premature aging-like features, including shortened lifespan, infertility, kyphosis, atherosclerosis, extensive soft tissue calcifications, skin atrophy, muscle wasting, T cell dysregulation, pulmonary emphysema, osteoporosis/osteopenia, abnormal mineral ion metabolism, and impaired vitamin-D homeostasis. The strikingly similar in vivo phenotypes of two separate genetically altered mouse lines implicate that the premature aging-like features may be partly regulated through a common signalin...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=471128</comments>
            <pubDate>Tue, 20 Feb 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">471128</guid>        </item>
        <item>
            <title>The role of vascular stem cells in atherogenesis and post-angioplasty restenosis.</title>
            <link>http://www.medworm.com/index.php?rid=442313&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17324640%26dopt%3DAbstract</link>
            <description>This article will mainly review the role of VPCs in atherogenesis, thus providing a novel understanding about the pathophysiology of atherosclerosis.
    PMID: 17324640 [PubMed - as supplied by publisher] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=442313</comments>
            <pubDate>Thu, 25 Jan 2007 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">442313</guid>        </item>
        <item>
            <title>Apolipoprotein E polymorphism, age and coronary heart disease.</title>
            <link>http://www.medworm.com/index.php?rid=393855&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17224309%26dopt%3DAbstract</link>
            <description>Authors: Kolovou GD, Anagnostopoulou KK
    Plasma concentrations of lipids, lipoproteins, and apolipoproteins (apo) are established risk factors for coronary heart disease (CHD). The knowledge of lipid profile may predict the potential victims of cardiovascular disease before its initiation and progression and offer the opportunity for primary prevention. The most common apo E polymorphism has been found to influence blood lipid concentrations and its correlation with CHD has been extensively investigated in the last decade. At younger ages, death from CHD is influenced by genetic factors, while the genetic effect decreases at older ages where environmental factors may play a more prominent role. If apo E polymorphism is an important genetic factor in the pathogenesis of atherosclerosis, ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393855</comments>
            <pubDate>Wed, 20 Dec 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393855</guid>        </item>
        <item>
            <title>Age-related impairment of GM-CSF-induced signalling in neutrophils: Role of SHP-1 and SOCS proteins.</title>
            <link>http://www.medworm.com/index.php?rid=393857&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17142110%26dopt%3DAbstract</link>
            <description>Authors: Tortorella C, Simone O, Piazzolla G, Stella I, Antonaci S
    Functional activities of mature human neutrophils are strongly influenced by the pro-inflammatory cytokine granulocyte macrophage-colony stimulating factor (GM-CSF). Accordingly, a defective response to GM-CSF might have dramatic consequences for neutrophil functions and the host defence against infections. Such an event is most likely to occur in senescence. A number of studies have, in fact, reported an impairment of the GM-CSF capacity to prime and/or to activate respiratory burst, as well as to delay apoptotic events, in neutrophils from elderly individuals. In the last 2 decades many efforts have been made to explore at molecular levels the mechanism underlying these defects. Recent studies let us depict a scenario...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393857</comments>
            <pubDate>Fri, 01 Dec 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393857</guid>        </item>
        <item>
            <title>Design and analysis in genetic studies of human ageing and longevity.</title>
            <link>http://www.medworm.com/index.php?rid=393893&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16337437%26dopt%3DAbstract</link>
            <description>Authors: Tan Q, Kruse TA, Christensen K
    With the success of the Human Genome Project and taking advantage of the recent developments in high-throughput genotyping techniques as well as in functional genomics, it is now feasible to collect vast quantities of genetic data with the aim of deciphering the genetics of human complex traits. As a result, the amount of research on human ageing and longevity has been growing rapidly in recent years. The situation raises questions concerning efficient choice of study population, sampling schemes, and methods of data analysis. In this article, we summarize the key issues in genetic studies of human ageing and longevity ranging from research design to statistical analyses. We discuss the virtues and drawbacks of the multidisciplinary approaches in...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393893</comments>
            <pubDate>Wed, 01 Nov 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393893</guid>        </item>
        <item>
            <title>Alzheimer's disease and endocytic dysfunction: clues from the Down syndrome-related proteins, DSCR1 and ITSN1.</title>
            <link>http://www.medworm.com/index.php?rid=393891&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16442855%26dopt%3DAbstract</link>
            <description>Authors: Keating DJ, Chen C, Pritchard MA
    Down syndrome (DS) is a genetically-based disorder which results in multiple conditions for sufferers. Amongst these is a common early incidence of Alzheimer's disease (AD) which usually affects DS individuals by their mid 40s. This fact provides a clue that one or more of the genes located on chromosome 21 may be involved in the onset of AD. Current evidence suggests that endosomal disorders may underlie the earliest pathology of AD, preceding the classical pathological markers of beta-amyloid plaque deposition and neurofibrillary tangles. Therefore, any genes involved in endocytosis and vesicle trafficking which are over-expressed in DS are novel candidates in the pathogenesis of AD. Intersectin-1 (ITSN1) and Down syndrome candidate region 1 ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393891</comments>
            <pubDate>Wed, 01 Nov 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393891</guid>        </item>
        <item>
            <title>Oxidative phosphorylation and aging.</title>
            <link>http://www.medworm.com/index.php?rid=393877&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16831573%26dopt%3DAbstract</link>
            <description>Authors: Lesnefsky EJ, Hoppel CL
    This review addresses the data that support the presence and contribution of decreased mitochondrial oxidative phosphorylation during aging to impaired cellular metabolism. Aging impairs substrate oxidation, decreases cellular energy production and increases the production of reactive intermediates that are toxic to the cell. First, the basic principles of mitochondrial oxidative physiology are briefly reviewed. Second, the focus on the relationship of altered mitochondrial respiration to the increased production of reactive oxygen species that are employed by the &quot;rate of living&quot; and the &quot;uncoupling to survive&quot; theories of aging are discussed. Third, the impairment of function of respiration in aging is reviewed using an organ-based approach in mammali...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393877</comments>
            <pubDate>Wed, 01 Nov 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393877</guid>        </item>
        <item>
            <title>Systems approaches to the networks of aging.</title>
            <link>http://www.medworm.com/index.php?rid=393871&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16904954%26dopt%3DAbstract</link>
            <description>Authors: Kriete A, Sokhansanj BA, Coppock DL, West GB
    The aging of an organism is the result of complex changes in structure and function of molecules, cells, tissues, and whole body systems. To increase our understanding of how aging works, we have to analyze and integrate quantitative evidence from multiple levels of biological organization. Here, we define a broader conceptual framework for a quantitative, computational systems biology approach to aging. Initially, we consider fractal supply networks that give rise to scaling laws relating body mass, metabolism and lifespan. This approach provides a top-down view of constrained cellular processes. Concomitantly, multi-omics data generation build such a framework from the bottom-up, using modeling strategies to identify key pathways ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393871</comments>
            <pubDate>Wed, 01 Nov 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393871</guid>        </item>
        <item>
            <title>Epigenetics, disease, and therapeutic interventions.</title>
            <link>http://www.medworm.com/index.php?rid=393859&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16965942%26dopt%3DAbstract</link>
            <description>Authors: Lu Q, Qiu X, Hu N, Wen H, Su Y, Richardson BC
    Heritable changes in gene expression that do not involve coding sequence modifications are referred to as &quot;epigenetic&quot;. Epigenetic mechanisms principally include DNA methylation and a variety of histone modifications, of which the best characterized is acetylation. DNA hypermethylation and histone hypoacetylation are hallmarks of gene silencing, while DNA hypomethylation and acetylated histones promote active transcription. Aberrant DNA methylation and histone acetylation have been linked to a number of age related disorders including cancer, autoimmune disorders and others. Since epigenetic alterations are reversible, modifying epigenetic marks contributing to disease development may provide an approach to designing new therapies....</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393859</comments>
            <pubDate>Wed, 01 Nov 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393859</guid>        </item>
        <item>
            <title>Caloric restriction and intermittent fasting: two potential diets for successful brain aging.</title>
            <link>http://www.medworm.com/index.php?rid=393875&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16899414%26dopt%3DAbstract</link>
            <description>Authors: Martin B, Mattson MP, Maudsley S
    The vulnerability of the nervous system to advancing age is all too often manifest in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. In this review article we describe evidence suggesting that two dietary interventions, caloric restriction (CR) and intermittent fasting (IF), can prolong the health-span of the nervous system by impinging upon fundamental metabolic and cellular signaling pathways that regulate life-span. CR and IF affect energy and oxygen radical metabolism, and cellular stress response systems, in ways that protect neurons against genetic and environmental factors to which they would otherwise succumb during aging. There are multiple interactive pathways and molecular mechanisms by which CR and IF bene...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393875</comments>
            <pubDate>Tue, 01 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393875</guid>        </item>
        <item>
            <title>Plasticity of neuroendocrine-thymus interactions during ontogeny and ageing: role of zinc and arginine.</title>
            <link>http://www.medworm.com/index.php?rid=393873&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16904953%26dopt%3DAbstract</link>
            <description>Authors: Mocchegiani E, Santarelli L, Costarelli L, Cipriano C, Muti E, Giacconi R, Malavolta M
    Thymic re-growth and reactivation of thymic functions may be achieved in old animals by different endocrinological or nutritional manipulations such as, (a) treatment with melatonin, (b) implantation of a growth hormone (GH) secreting tumour cell line (GH3 cells) or treatment with exogenous GH, (c) castration or treatment with exogenous luteinizing hormone-releasing hormone (LHRH), (d) treatment with exogenous thyroxin or triiodothyronine, and (e) nutritional interventions such as arginine or zinc supplementation. These data strongly suggest that thymic involution is a phenomenon secondary to age-related alterations in neuroendocrine-thymus interactions and that it is the disruption of these...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393873</comments>
            <pubDate>Tue, 01 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393873</guid>        </item>
        <item>
            <title>Compensatory mechanisms in the aging motor system.</title>
            <link>http://www.medworm.com/index.php?rid=393869&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16905372%26dopt%3DAbstract</link>
            <description>Authors: Ward NS
    Motor functions decline with age due to a number of factors. There is interest in whether these changes are reflected in the organisation of the cerebral motor system in older subjects and whether such changes might be in some way compensatory. Most studies in humans have used functional brain imaging techniques to compare motor system activation in younger and older subjects. Interpretation of these results is made more difficult by potential neurovascular changes in older subjects. However, in general, there appears to be greater motor task-related brain activity in a wider network of brain regions in older compared to younger subjects. The evidence that these changes are compensatory in nature is less clear. Incorporation of behavioural and anatomical data will be r...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393869</comments>
            <pubDate>Tue, 01 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393869</guid>        </item>
        <item>
            <title>Synaptic plasticity in early aging.</title>
            <link>http://www.medworm.com/index.php?rid=393867&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16935034%26dopt%3DAbstract</link>
            <description>Authors: Lynch G, Rex CS, Gall CM
    Studies of how aging affects brain plasticity have largely focused on old animals. However, deterioration of memory begins well in advance of old age in animals, including humans; the present review is concerned with the possibility that changes in synaptic plasticity, as found in the long-term potentiation (LTP) effect, are responsible for this. Recent results indicate that impairments to LTP are in fact present by early middle age in rats but only in certain dendritic domains. The search for the origins of these early aging effects necessarily involves ongoing analyses of how LTP is induced, expressed, and stabilized. Such work points to the conclusion that cellular mechanisms responsible for LTP are redundant and modulated both positively and negati...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393867</comments>
            <pubDate>Tue, 01 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393867</guid>        </item>
        <item>
            <title>Resistance training, and IGF involvement in the maintenance of muscle mass during the aging process.</title>
            <link>http://www.medworm.com/index.php?rid=393865&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16949353%26dopt%3DAbstract</link>
            <description>Authors: Adamo ML, Farrar RP
    Sarcopenia is the decline of muscle mass and strength with age. Sarcopenia leads to significant impairment in the ability to carry out normal daily function and thus there is a great need for interventions that will lead to muscle regeneration and repair in the aging population. Age-related sarcopenia in humans, characterized by loss of type I and type II muscle fibers and a decrease in fiber cross-sectional area primarily in type II fibers, can be attenuated by mechanical load on the muscle, which increases cross-sectional area of the remaining fibers, but does not restore fiber numbers characteristic of young muscle. Considerable evidence also implicates age-related declines in muscle insulin-like growth factor action in sarcopenia. IGF-I promotes myoblas...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393865</comments>
            <pubDate>Tue, 01 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393865</guid>        </item>
        <item>
            <title>Neuroprotective effects of cognitive enrichment.</title>
            <link>http://www.medworm.com/index.php?rid=393863&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16949888%26dopt%3DAbstract</link>
            <description>Authors: Milgram NW, Siwak-Tapp CT, Araujo J, Head E
    Cognitive enrichment early in life, as indicated by level of education, complexity of work environment or nature of leisure activities, appears to protect against the development of age-associated cognitive decline and also dementia. These effects are more robust for measures of crystallized intelligence than for measures of fluid intelligence and depend on the ability of the brain to compensate for pathological changes associated with aging. This compensatory ability is referred to as cognitive reserve. The cognitive reserve hypothesis suggests that cognitive enrichment promotes utilization of available functions. Alternatively, late life cognitive changes in cognition may be linked to a factor, such as cholinergic dysfunction, that...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393863</comments>
            <pubDate>Tue, 01 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393863</guid>        </item>
        <item>
            <title>The adversities of aging.</title>
            <link>http://www.medworm.com/index.php?rid=393861&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16950665%26dopt%3DAbstract</link>
            <description>Authors: Cutler RG, Mattson MP
    The aging process is evolutionarily conserved and subject to quantitative modification by both genetic and environmental factors. Fundamental mechanisms of aging result in progressive deficits in the function of cells and organs, often leading to diseases that ultimately kill the organism such as cancers, cardiovascular disease and neurodegenerative disorders. Oxidative stress and damage to all of the major classes of molecules in cells are involved in aging and age-related diseases. The widely pursued approach of targeting disease-specific processes to develop therapeutic interventions has not had a major impact on healthspan. A more productive approach would be to target the fundamental mechanisms of aging throughout adult life so as to extend healthspa...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393861</comments>
            <pubDate>Tue, 01 Aug 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393861</guid>        </item>
        <item>
            <title>Lipotoxicity, overnutrition and energy metabolism in aging.</title>
            <link>http://www.medworm.com/index.php?rid=393889&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16630750%26dopt%3DAbstract</link>
            <description>Authors: Slawik M, Vidal-Puig AJ
    The safest place to store lipids is the white adipose tissue, but its storage capacity may become saturated resulting in excess of fat &quot;overspilled&quot; to non-adipose tissues. This overspill of fat occurs in apparently opposite pathological states such as lipodistrophy or obesity. When the excess of energy is redirected towards peripheral organs, their initial response is to facilitate the storage of the surplus in the form of triacylglycerol, but the limited triacylglycerol buffer capacity becomes saturated soon. Under these conditions excess of lipids enter alternative non-oxidative pathways that result in production of toxic reactive lipid species that induce organ-specific toxic responses leading to apoptosis. Reactive lipids can accumulate in non-adip...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393889</comments>
            <pubDate>Mon, 01 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393889</guid>        </item>
        <item>
            <title>Bioenergetics of aging and calorie restriction.</title>
            <link>http://www.medworm.com/index.php?rid=393887&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16644290%26dopt%3DAbstract</link>
            <description>Authors: Hunt ND, Hyun DH, Allard JS, Minor RK, Mattson MP, Ingram DK, de Cabo R
    Aging is a physiological process that involves a multi-factorial set of deleterious changes. These alterations are caused by an exponential increase in damage to macromolecules. This process is likely due to the cumulative effects of oxidative stress over time. One area of ongoing research in gerontology has focused on determining why there is an age-dependent decrease in cellular bioenergetics. The aim of this review is to summarize the recent findings on the effects of aging and calorie restriction on energy metabolism. The effect of calorie restriction on age-associated changes in bioenergetic parameters will be examined.
    PMID: 16644290 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393887</comments>
            <pubDate>Mon, 01 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393887</guid>        </item>
        <item>
            <title>Mitochondrial DNA mutations, energy metabolism and apoptosis in aging muscle.</title>
            <link>http://www.medworm.com/index.php?rid=393885&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16647308%26dopt%3DAbstract</link>
            <description>Authors: Dirks AJ, Hofer T, Marzetti E, Pahor M, Leeuwenburgh C
    Locomotor functional decline and loss in muscle mass with age is virtually a universal characteristic that has been documented in several species, including worms, fruit flies, rodents, non-human primates and humans. The age-related loss of muscle mass and strength (sarcopenia) represents an important risk factor for disability and mortality in older subjects and has been linked with cellular energy deficit and increased apoptosis at old age. Many key theories on aging describing the mechanisms underlying sarcopenia are now focused on the mitochondria because of their dichotomous role in controlling life and death processes within myocytes. Mitochondria represent the main producers of cellular energy in the form of adenosi...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393885</comments>
            <pubDate>Mon, 01 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393885</guid>        </item>
        <item>
            <title>Hormesis/preconditioning mechanisms, the nervous system and aging.</title>
            <link>http://www.medworm.com/index.php?rid=393883&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682262%26dopt%3DAbstract</link>
            <description>Authors: Arumugam TV, Gleichmann M, Tang SC, Mattson MP
    Throughout life, organisms and their cells are subjected to various stressors which they must respond to adaptively in order to avoid disease and death. Accordingly, cells possess a variety of stress-responsive signaling pathways that are coupled to kinase cascades and transcription factors that induce the expression of genes that encode cytoprotective proteins such as protein chaperones (PC), growth factors and antioxidant enzymes. Emerging findings suggest that many of the environmental factors that improve health and so prolong lifespan (for example, dietary restriction, exercise and cognitive stimulation) exert their beneficial effects through a hormesis-like mechanism. Here we describe data supporting the hormesis hypothesis ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393883</comments>
            <pubDate>Mon, 01 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393883</guid>        </item>
        <item>
            <title>The plasma membrane redox system in aging.</title>
            <link>http://www.medworm.com/index.php?rid=393881&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16697277%26dopt%3DAbstract</link>
            <description>Authors: Hyun DH, Hernandez JO, Mattson MP, de Cabo R
    Oxidative stress over time leads to the accumulation of damaged macromolecules and to profound physiological changes that are associated with several age-related diseases. The plasma membrane redox system (PMRS) appears to attenuate oxidative stress acting as a compensatory mechanism during the aging process. The PMRS appears to play a protective role during mitochondrial dysfunction to provide cells with a survival mechanism by lowering oxidative stress. The PMRS accomplishes this by producing more NAD(+) for glycolytic ATP production via transfer of electrons from intracellular reducing equivalents to extracelluar acceptors. Ubiquinone and alpha-tocopherol are key antioxidant molecules in the plasma membrane that are affected by a...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393881</comments>
            <pubDate>Mon, 01 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393881</guid>        </item>
        <item>
            <title>Uncoupling protein homologs may provide a link between mitochondria, metabolism and lifespan.</title>
            <link>http://www.medworm.com/index.php?rid=393879&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16707280%26dopt%3DAbstract</link>
            <description>Authors: Wolkow CA, Iser WB
    Uncoupling proteins (UCPs), which dissipate the mitochondrial proton gradient, have the ability to decouple mitochodrial respiration from ATP production. Since mitochondrial electron transport is a major source of free radical production, it is possible that UCP activity might impact free radical production. Free radicals can react with and damage cellular proteins, DNA and lipids. Accumulated damage from oxidative stress is believed to be a major contributor to cellular decline during aging. If UCP function were to impact mitochondrial free radical production, then one would expect to find a link between UCP activity and aging. This theory has recently been tested in a handful of organisms whose genomes contain UCP1 homologs. Interestingly, these experiment...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393879</comments>
            <pubDate>Mon, 01 May 2006 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393879</guid>        </item>
        <item>
            <title>Age-related neuropathology, cognitive decline, and Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=393915&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16084778%26dopt%3DAbstract</link>
            <description>Authors: Keller JN
    In the last 20 years, there have been tremendous strides made in the understanding of the molecular and cellular processes that occur during brain aging, as well as our understanding of age-related disorders of the central nervous system (CNS). Aging is associated with a decline in cognitive performance, and is the biggest risk factor for the development of Alzheimer's disease (AD), although the underlying basis for both of these observations is poorly defined. Both normal aging and AD are associated with overlapping and increased levels of pathology. Numerous reports have now linked elevations in pathology as potential mediators of cognitive decline in the elderly, with most studies focusing on the role of AD-related pathology. However, it is important to point out ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393915</comments>
            <pubDate>Wed, 01 Feb 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393915</guid>        </item>
        <item>
            <title>The evolution of late life.</title>
            <link>http://www.medworm.com/index.php?rid=393914&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16085467%26dopt%3DAbstract</link>
            <description>Authors: Rauser CL, Mueller LD, Rose MR
    Late life is a distinct phase of life characterized by a cessation in the deterioration of survivorship and fecundity characteristic of normal aging. Several theories have been proposed to explain non-aging at late ages, specifically with regards to late-life mortality-rate plateaus. All such theories must be compatible with formal evolutionary theory and experimental findings. Here, we develop a critique of theories of late life based on evolutionary biology.
    PMID: 16085467 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393914</comments>
            <pubDate>Wed, 01 Feb 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393914</guid>        </item>
        <item>
            <title>Living by the clock: the circadian pacemaker in older people.</title>
            <link>http://www.medworm.com/index.php?rid=393913&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16126012%26dopt%3DAbstract</link>
            <description>Authors: Hofman MA, Swaab DF
    The suprachiasmatic nucleus (SCN) of the hypothalamus is considered to be a critical component of a neural oscillator system implicated in the timing of a wide variety of biological processes. The circadian cycles established by this biological clock occur throughout nature and have a period of approximately 24 h. With advancing age, however, these daily fluctuations deteriorate, leading to disrupted cycles with a reduced amplitude. In humans, age-related changes have been described for hormonal rhythms, body core temperature, sleep-wakefulness and several other behavioral cycles. It appears that the disruption of circadian rhythms and the increased incidence of disturbed sleep during aging are paralleled by age-related alterations in the neural and tempora...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393913</comments>
            <pubDate>Wed, 01 Feb 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393913</guid>        </item>
        <item>
            <title>How should we assess the impact of genetic changes on ageing in model species?</title>
            <link>http://www.medworm.com/index.php?rid=393912&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16203179%26dopt%3DAbstract</link>
            <description>Authors: Minois N
    One of the most active branches of genetic research is the quest for the genetic determinants of ageing. The ultimate goal of much of this effort is to understand ageing in humans. In addition to work on human genetics, many researchers look to model organisms in order to find genetic variation that can affect ageing. The fly Drosophila, the worm Caenorhabditis elegans, rodents, and yeast are among the most widely studied species. However, while great care is given to the genetic aspects of this form of research, the methods used to assess the impact of the genetic changes on the organism in question do not always provide as complete a picture as possible of ageing's multi-facetted nature. In this commentary, I propose a systematic and rigorous approach, and draw atte...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393912</comments>
            <pubDate>Wed, 01 Feb 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393912</guid>        </item>
        <item>
            <title>Aging of mesenchymal stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=393897&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16310414%26dopt%3DAbstract</link>
            <description>Authors: Sethe S, Scutt A, Stolzing A
    The role of adult mesenchymal stem cells (MSC) in tissue maintenance and regeneration has received significant attention of late. Questions arise to what extent these cells are either subject to, or causes of aging; whether age-related changes in these cells are due to intrinsic factors or induced by the somatic environment. This review collates and examines recent data in support of these different theories. By means of introduction, a brief overview is given of current MSC definitions and their basic role in tissue regeneration followed by a comparative analysis of gerontological studies involving MSC. Evidence for extrinsic aging and various aging markers relating to morphology, proliferation, signalling, senescence markers, telomeres and telome...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393897</comments>
            <pubDate>Wed, 01 Feb 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393897</guid>        </item>
        <item>
            <title>The ubiquitin-proteasome system at the crossroads of stress-response and ageing pathways: a handle for skin care?</title>
            <link>http://www.medworm.com/index.php?rid=393895&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16330259%26dopt%3DAbstract</link>
            <description>Authors: Brégégère F, Milner Y, Friguet B
    The regulation of gene expression at the transcriptional level has been considered for long as the main mechanism of cellular adaptive responses. Since the turn of the century, however, it is becoming clear that higher organisms developed a complex, sensitive and maybe equally important network of regulatory pathways, relying largely on protein interactions, post-translational modifications and proteolysis. Here we review the involvement of the ubiquitin-proteasome pathway of protein degradation at different levels of cellular life in relation with ageing, and with a special focus on skin. It comes out that the ubiquitin system plays a major role in signal transduction associated with stress and ageing, in skin in particular through the cont...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393895</comments>
            <pubDate>Wed, 01 Feb 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393895</guid>        </item>
        <item>
            <title>Discovering causes and cures for cancer from gene expression analysis.</title>
            <link>http://www.medworm.com/index.php?rid=393911&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16243590%26dopt%3DAbstract</link>
            <description>Authors: Weeraratna AT
    Tumorigenesis is governed by a series of complex genetic and epigenetic changes. Both mechanisms can result in either the silencing or aberrant expression of messages in a cell. Gene expression profiling techniques such as the serial analysis of gene expression (SAGE) or microarray analysis can provide global overviews of these changes, as well identify key genes and pathways involved in this process. This review outlines the current roles of these techniques in cancer research, and how they may contribute to finding not only mechanisms of this disease, but potential targets for therapy.
    PMID: 16243590 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393911</comments>
            <pubDate>Tue, 01 Nov 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393911</guid>        </item>
        <item>
            <title>Gene expression and DNA repair in progeroid syndromes and human aging.</title>
            <link>http://www.medworm.com/index.php?rid=393909&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16246641%26dopt%3DAbstract</link>
            <description>Authors: Kyng KJ, Bohr VA
    Human progeroid syndromes are caused by mutations in single genes accelerating some but not all features of normal aging. Most progeroid disorders are linked to defects in genome maintenance, and while it remains unknown if similar processes underlie normal and premature aging, they provide useful models for the study of aging. Altered transcription is speculated to play a causative role in aging, and is involved in the pathology of most if not all progeroid syndromes. Previous studies demonstrate that there is a similar pattern of gene expression changes in primary cells from old and Werner syndrome compared to young suggesting a presence of common cellular aging mechanisms in old and progeria. Here we review the role of transcription in progeroid syndromes a...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393909</comments>
            <pubDate>Tue, 01 Nov 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393909</guid>        </item>
        <item>
            <title>Expression profiling in the aging brain: a perspective.</title>
            <link>http://www.medworm.com/index.php?rid=393907&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16249125%26dopt%3DAbstract</link>
            <description>Authors: Galvin JE, Ginsberg SD
    To evaluate molecular events associated with the aging process in animal models and human tissues, microarray analysis is performed at the regional and cellular levels to define transcriptional patterns or mosaics that may lead to better understanding of the mechanism(s) that drive senescence. In this review, we outline the experimental and analytical issues associated with high-throughput genomic analyses in aging brain and other tissues for a comprehensive evaluation of the current state of microarray analysis in aging paradigms. Ultimately, the goal of these studies is to apply functional genomics and proteomics approaches to aging research to develop new tools to assess age in cell- and tissue-specific manners in order to develop aging biomarkers for...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393907</comments>
            <pubDate>Tue, 01 Nov 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393907</guid>        </item>
        <item>
            <title>Harnessing the power of gene microarrays for the study of brain aging and Alzheimer's disease: statistical reliability and functional correlation.</title>
            <link>http://www.medworm.com/index.php?rid=393905&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16257272%26dopt%3DAbstract</link>
            <description>Authors: Blalock EM, Chen KC, Stromberg AJ, Norris CM, Kadish I, Kraner SD, Porter NM, Landfield PW
    During normal brain aging, numerous alterations develop in the physiology, biochemistry and structure of neurons and glia. Aging changes occur in most brain regions and, in the hippocampus, have been linked to declining cognitive performance in both humans and animals. Age-related changes in hippocampal regions also may be harbingers of more severe decrements to come from neurodegenerative disorders such as Alzheimer's disease (AD). However, unraveling the mechanisms underlying brain aging, AD and impaired function has been difficult because of the complexity of the networks that drive these aging-related changes. Gene microarray technology allows massively parallel analysis of most gene...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393905</comments>
            <pubDate>Tue, 01 Nov 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393905</guid>        </item>
        <item>
            <title>mRNA methods used in dissecting gene expression of the brain.</title>
            <link>http://www.medworm.com/index.php?rid=393903&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16257586%26dopt%3DAbstract</link>
            <description>Authors: Kannanayakal TJ, Eberwine J
    
    PMID: 16257586 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393903</comments>
            <pubDate>Tue, 01 Nov 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393903</guid>        </item>
        <item>
            <title>Gene expression changes reveal patterns of aging in the rat digestive tract.</title>
            <link>http://www.medworm.com/index.php?rid=393901&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16260189%26dopt%3DAbstract</link>
            <description>Authors: Englander EW
    Similarly to other organs, the human digestive system is adversely affected by aging presenting physiologic manifestations that include compromised absorption and secretion, decreased motility, weakened mucosal barrier and as well as a high incidence of colon cancer. As biomedical advances enable the population to live longer, our understanding of molecular events that govern aging and disease states is enhanced through methodical analyses of temporal tissue-specific gene expression profiles. Recently, DNA microarray analyses have been employed to examine age-associated transcriptional profiles in the mammalian digestive tract. Gene expression patterns revealed that the magnitude and trend of age-associated changes differ in the rat colon and duodenum. Interesting...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393901</comments>
            <pubDate>Tue, 01 Nov 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393901</guid>        </item>
        <item>
            <title>Flies and their golden apples: the effect of dietary restriction on Drosophila aging and age-dependent gene expression.</title>
            <link>http://www.medworm.com/index.php?rid=393899&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16263339%26dopt%3DAbstract</link>
            <description>Authors: Pletcher SD, Libert S, Skorupa D
    Reduced nutrient availability (dietary restriction) extends lifespan in species as diverse as yeast, nematode worms, Daphnia, Drosophila, and mammals. Recent demographic experiments have shown that moderate nutrient manipulation in adult Drosophila affects current mortality rate in a completely reversible manner, which suggests that dietary restriction in Drosophila increases lifespan through a reduction of the current risk of death rather than a slowing of aging-related damage. When examined in the light of the new demographic data, age-dependent changes in gene expression in normal and diet-restricted flies can provide unique insight into the biological processes affected by aging and may help identify molecular pathways that regulate it.
   ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393899</comments>
            <pubDate>Tue, 01 Nov 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393899</guid>        </item>
        <item>
            <title>Functional senescence in Drosophila melanogaster.</title>
            <link>http://www.medworm.com/index.php?rid=393923&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16024299%26dopt%3DAbstract</link>
            <description>Authors: Grotewiel MS, Martin I, Bhandari P, Cook-Wiens E
    The fruit fly Drosophila melanogaster is one of the principal model organisms used for studying the biology of aging. Flies are well suited for such studies for a number of reasons. Flies develop to adulthood quickly, have a relatively short life span, and are inexpensive to house. Most of the fly genome has been sequenced, powerful genetic tools are available to manipulate it, and most fly genes have obvious homologues in mammals. While the majority of aging studies in flies have focused on regulation of life span, the fly is emerging as a powerful model system for investigating the biology that underlies age-related functional decline. Key to the use of flies in this way is the striking number of parallels between functional s...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393923</comments>
            <pubDate>Mon, 01 Aug 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393923</guid>        </item>
        <item>
            <title>Intergenerational transfers may have decoupled physiological and chronological age in a eusocial insect.</title>
            <link>http://www.medworm.com/index.php?rid=393922&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16039913%26dopt%3DAbstract</link>
            <description>Authors: Amdam GV, Page RE
    Life-history theory generally predicts that there should be no selection for longevity beyond the limit of reproductive capacity. However, the capacity to increase fitness may not end when individuals reach a state of functional sterility. Recent studies show that intergenerational transfers of resources from post-reproductive parents can increase the offspring's fitness, and analytical theory shows that age-trajectories of transfers may shape the course of senescence in social organisms. In eusocial insects, female roles are partitioned so that one phenotype or &quot;caste&quot; reproduces while another is responsible for resource transfers: the reproductive &quot;queens&quot; are arrested in a continuous reproductive mode, while transfer-activities such as hygienic behaviors, ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393922</comments>
            <pubDate>Mon, 01 Aug 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393922</guid>        </item>
        <item>
            <title>Medical bioremediation: prospects for the application of microbial catabolic diversity to aging and several major age-related diseases.</title>
            <link>http://www.medworm.com/index.php?rid=393921&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16040282%26dopt%3DAbstract</link>
            <description>Authors: de Grey AD, Alvarez PJ, Brady RO, Cuervo AM, Jerome WG, McCarty PL, Nixon RA, Rittmann BE, Sparrow JR
    Several major diseases of old age, including atherosclerosis, macular degeneration and neurodegenerative diseases are associated with the intracellular accumulation of substances that impair cellular function and viability. Moreover, the accumulation of lipofuscin, a substance that may have similarly deleterious effects, is one of the most universal markers of aging in postmitotic cells. Reversing this accumulation may thus be valuable, but has proven challenging, doubtless because substances resistant to cellular catabolism are inherently hard to degrade. We suggest a radically new approach: augmenting humans' natural catabolic machinery with microbial enzymes. Many recalcitr...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393921</comments>
            <pubDate>Mon, 01 Aug 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393921</guid>        </item>
        <item>
            <title>Why dietary restriction substantially increases longevity in animal models but won't in humans.</title>
            <link>http://www.medworm.com/index.php?rid=393920&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16046282%26dopt%3DAbstract</link>
            <description>Authors: Phelan JP, Rose MR
    Caloric restriction (CR) extends maximum longevity and slows aging in mice, rats, and numerous non-mammalian taxa. The apparent generality of the longevity-increasing effects of CR has prompted speculation that similar results could be obtained in humans. Longevity, however, is not a trait that exists in a vacuum; it evolves as part of a life history and the physiological mechanisms that determine longevity are undoubtedly complex. Longevity is intertwined with reproduction and there is a cost to reproduction. The impact of this cost on longevity can be age-independent or age-dependent. Given the complexity of the physiology underlying reproductive costs and other mechanisms affecting life history, it is difficult to construct a simple model for the relation...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393920</comments>
            <pubDate>Mon, 01 Aug 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393920</guid>        </item>
        <item>
            <title>Does dietary restriction really increase longevity in Drosophila melanogaster?</title>
            <link>http://www.medworm.com/index.php?rid=393918&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16051527%26dopt%3DAbstract</link>
            <description>Authors: Le Bourg E, Minois N
    It is often accepted that dietary restriction (DR) increases longevity in most species so far tested. Showing the same result in the fruit fly Drosophila melanogaster would be of interest, because this species is widely used in aging research. Some studies have shown that dietary restriction decreases longevity in this species while the opposite result has also been reported. However, some recent results appear to be flawed due to the use of not optimal control rearing conditions. It is argued that, for the time being, it cannot be concluded that dietary restriction increases longevity in D. melanogaster. It has also been shown in other fly species that dietary restriction does not increase longevity.
    PMID: 16051527 [PubMed - indexed for MEDLINE] (Sour...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393918</comments>
            <pubDate>Mon, 01 Aug 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393918</guid>        </item>
        <item>
            <title>C. elegans DAF-12, Nuclear Hormone Receptors and human longevity and disease at old age.</title>
            <link>http://www.medworm.com/index.php?rid=393917&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16051528%26dopt%3DAbstract</link>
            <description>Authors: Mooijaart SP, Brandt BW, Baldal EA, Pijpe J, Kuningas M, Beekman M, Zwaan BJ, Slagboom PE, Westendorp RG, van Heemst D
    In Caenorhabditis elegans, DAF-12 appears to be a decisive checkpoint for many life history traits including longevity. The daf-12 gene encodes a Nuclear Hormone Receptor (NHR) and is member of a superfamily that is abundantly represented throughout the animal kingdom, including humans. It is, however, unclear which of the human receptor representatives are most similar to DAF-12, and what their role is in determining human longevity and disease at old age. Using a sequence similarity search, we identified human NHRs similar to C. elegans DAF-12 and found that, based on sequence similarity, Liver X Receptor A and B are most similar to C. elegans DAF-12, follow...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393917</comments>
            <pubDate>Mon, 01 Aug 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393917</guid>        </item>
        <item>
            <title>Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis.</title>
            <link>http://www.medworm.com/index.php?rid=393916&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16081325%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: This systematic review shows enteral nutritional support, particularly high protein ONS, can significantly reduce the risk of developing pressure ulcers (by 25%). Although studies suggest ONS and ETF may improve healing of PU, further research to confirm this trend is required.
    PMID: 16081325 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393916</comments>
            <pubDate>Mon, 01 Aug 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393916</guid>        </item>
        <item>
            <title>The effects of stress and aging on glutathione metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=393930&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15936251%26dopt%3DAbstract</link>
            <description>Authors: Maher P
    Glutathione plays a critical role in many biological processes both directly as a co-factor in enzymatic reactions and indirectly as the major thiol-disulfide redox buffer in mammalian cells. Glutathione also provides a critical defense system for the protection of cells from many forms of stress. However, mild stress generally increases glutathione levels, often but not exclusively through effects on glutamate cysteine ligase, the rate-limiting enzyme for glutathione biosynthesis. This upregulation in glutathione provides protection from more severe stress and may be a critical feature of preconditioning and tolerance. In contrast, during aging, glutathione levels appear to decline in a number of tissues, thereby putting cells at increased risk of succumbing to stress...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393930</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393930</guid>        </item>
        <item>
            <title>Glucose metabolism and Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=393929&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15950548%26dopt%3DAbstract</link>
            <description>Authors: Schubert D
    The brain is the organ with the highest basal rate of glucose consumption. Most of the energy generated by the oxidation of glucose is used for the work necessary to maintain the ionic balances associated with synaptic transmission. When the nervous system is subjected to the oxidative stress of age-associated disease, there is a redistribution of glucose breakdown to pathways that more efficiently produce molecules involved in antioxidant metabolism. This shift is at least in part mediated by the transcription factor HIF-1. The clinical implications of this change in glucose metabolism are discussed in the context of aging and Alzheimer's disease.
    PMID: 15950548 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393929</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393929</guid>        </item>
        <item>
            <title>Aging, stress and the hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=393928&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15964248%26dopt%3DAbstract</link>
            <description>Authors: Miller DB, O'Callaghan JP
    Functional loss often occurs in many body systems (e.g., endocrine, cognitive, motor) with the passage of years, but there is great individual variation in the degree of compromise shown. The current focus on brain aging will continue because demographic trends indicate that the average lifespan will show a continued increase. There is increasing emphasis on understanding how aging contributes to a decline in brain functions, cognition being a prime example. This is due in part to the fact that dementias and other losses in brain function that sometimes accompany aging cause an obvious decline in the quality of life and these deficits are of more concern as the number of elderly increase. Stress also is a ubiquitous aspect of life and there is now a g...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393928</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393928</guid>        </item>
        <item>
            <title>Repeated stress and structural plasticity in the brain.</title>
            <link>http://www.medworm.com/index.php?rid=393927&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15993654%26dopt%3DAbstract</link>
            <description>Authors: Radley JJ, Morrison JH
    Although adrenal steroid receptors are distributed widely throughout the central nervous system, specific limbic and cortical regions targeted by stress hormones play a key role in integrating behavioral and physiological responses during stress and adaptation to subsequent stressors. When the stressor is of a sufficient magnitude or prolonged, it may result in abnormal changes in brain plasticity that, paradoxically, may impair the ability of the brain to appropriately regulate and respond to subsequent stressors. Here we review how repeated stress produces alterations in brain plasticity in animal models, and discuss its relevance to behavioral changes associated with these regions. Interestingly, prolonged stress produces opposing effects on structura...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393927</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393927</guid>        </item>
        <item>
            <title>The stress system in the human brain in depression and neurodegeneration.</title>
            <link>http://www.medworm.com/index.php?rid=393926&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15996533%26dopt%3DAbstract</link>
            <description>Authors: Swaab DF, Bao AM, Lucassen PJ
    Corticotropin-releasing hormone (CRH) plays a central role in the regulation of the hypothalamic-pituitary-adrenal (HPA)-axis, i.e., the final common pathway in the stress response. The action of CRH on ACTH release is strongly potentiated by vasopressin, that is co-produced in increasing amounts when the hypothalamic paraventricular neurons are chronically activated. Whereas vasopressin stimulates ACTH release in humans, oxytocin inhibits it. ACTH release results in the release of corticosteroids from the adrenal that, subsequently, through mineralocorticoid and glucocorticoid receptors, exert negative feedback on, among other things, the hippocampus, the pituitary and the hypothalamus. The most important glucocorticoid in humans is cortisol, pre...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393926</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393926</guid>        </item>
        <item>
            <title>Corticotropin-releasing factor-binding protein, stress and major depression.</title>
            <link>http://www.medworm.com/index.php?rid=393925&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15996902%26dopt%3DAbstract</link>
            <description>Authors: Van Den Eede F, Van Broeckhoven C, Claes SJ
    Major depressive disorder (MDD) is characterized by a dysregulation of the stress response system. A corticotropin-releasing factor (CRF) hyperdrive is a consistent and well-documented finding. CRF-binding protein (CRF-BP) may play a role in the pathogenesis of MDD. CRF-BP reduces the availability of CRF by binding free CRF and inhibits CRF function at the pituitary level. Moreover, CRF-BP expression increases in the pituitary and amygdala in response to acute stress, providing an additional feedback mechanism to maintain the homeostasis of the stress response. There are different regulatory elements of the expression of CRF-BP gene that are implicated in the pathophysiology of MDD, including CRF, glucocorticoids, cytokines and estro...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393925</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393925</guid>        </item>
        <item>
            <title>Growth hormone and insulin-like growth factor-1 (IGF-1) and their influence on cognitive aging.</title>
            <link>http://www.medworm.com/index.php?rid=393924&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16024298%26dopt%3DAbstract</link>
            <description>Authors: Sonntag WE, Ramsey M, Carter CS
    The concept that growth hormone and IGF-1 are required for normal development of the mammalian body and, more recently the brain, is supported by a vast experimental literature. IGF-1 crosses the blood-brain barrier and in recent years, much attention has focused on age-related decreases in serum growth hormone and IGF-1 as potential mechanisms that may influence cognitive function in the elderly. However, interventional studies are needed to establish a definite link between these hormones and function of the aging brain. In rodents, long-term growth hormone/IGF-1 replacement improves learning and memory in aged rats. While the exact mechanism underlying these cognitive improvements is unknown, growth hormone and IGF-1 replacement to aged anima...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393924</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393924</guid>        </item>
        <item>
            <title>The neuroprotective actions of corticotropin releasing hormone.</title>
            <link>http://www.medworm.com/index.php?rid=393919&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16046283%26dopt%3DAbstract</link>
            <description>Authors: Bayatti N, Behl C
    Corticotropin-releasing hormone (CRH) modulates the activity of the hypothalamic-pituitary-adrenal (HPA) axis, and has a key role in mediating neuroendocrine effects that occur in response to stressful stimuli. Disruption of the CRH system however has been shown to be closely associated with the progression of Alzheimer's disease (AD), and these observations prompted an investigation into the potential neuroprotective effects of the hormone. In addition to its regulatory affects on the molecular processes that underlie AD i.e., amyloid precursor protein (APP) processing and potentially tau phosphorylation, evidence is provided that the neuroprotective effects of CRH are mediated by a number of diverse mechanisms. These stem from activation of its high affinit...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393919</comments>
            <pubDate>Sun, 01 May 2005 06:00:00 +0100</pubDate>
            <guid isPermaLink="false">393919</guid>        </item>
        <item>
            <title>Open-minded scepticism: inferring the causal mechanisms of human ageing from genetic perturbations.</title>
            <link>http://www.medworm.com/index.php?rid=393937&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15619467%26dopt%3DAbstract</link>
            <description>Authors: de Magalhães JP
    Given the myriad of age-related changes and the many proposed mechanistic theories of ageing, a major problem in gerontology is distinguishing causes from effects. This review aims to identify and evaluate those mechanisms which have gathered experimental support in favour of seeing them as a cause rather than an effect of ageing. Recent results related to energy metabolism and ageing, the free radical and the DNA damage theories of ageing are reviewed and their predictions evaluated through a systems biology rationale. Crucial in this approach are genetic manipulations in animal models that enable researchers to discriminate causes from effects of ageing and focus on the causal structure of human ageing. Based on a system-level interpretation, the GH/IGF-1 ax...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393937</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393937</guid>        </item>
        <item>
            <title>Insights into age-related locomotor declines from studies of insects.</title>
            <link>http://www.medworm.com/index.php?rid=393936&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15619468%26dopt%3DAbstract</link>
            <description>Authors: Ridgel AL, Ritzmann RE
    Locomotor deficits frequently accompany aging in animals. These deficits are often caused by degeneration in the nervous and musculoskeletal systems. Insects are an excellent model for age-related behavior studies because they are short-lived and have a reduced nervous system with fewer cells than vertebrates. Furthermore, they are highly mobile and display a complex set of locomotor behaviors. This review presents research that has examined age-related locomotor deficits in insects and discusses the value of these studies to understand aging processes in all animals.
    PMID: 15619468 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393936</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393936</guid>        </item>
        <item>
            <title>The role of ubiquinone in Caenorhabditis elegans longevity.</title>
            <link>http://www.medworm.com/index.php?rid=393935&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15619469%26dopt%3DAbstract</link>
            <description>Authors: Rodríguez-Aguilera JC, Gavilán A, Asencio C, Navas P
    Aging is an irreversible physiological process that affects all living organisms. Different mutations in the insulin signaling pathway and caloric restriction have been shown to retard aging in Caenorhabditis elegans. In addition, mutations or RNAi silencing of components of the respiratory chain results in the modification of adult life span. Another class of genes that affect life span in C. elegans is the clock (clk) genes. Particularly interesting is clk-1, which encodes an enzyme required for ubiquinone (coenzyme Q, CoQ) biosynthesis. Down-regulation by RNAi silencing of the genes required for ubiquinone biosynthesis also extends life span in C. elegans, and CoQ supplied in the diet also affects nematode longevity in ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393935</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393935</guid>        </item>
        <item>
            <title>Lessons learned from gene expression profile studies of aging and caloric restriction.</title>
            <link>http://www.medworm.com/index.php?rid=393934&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15619470%26dopt%3DAbstract</link>
            <description>Authors: Park SK, Prolla TA
    To examine molecular events associated with aging and its retardation by caloric restriction (CR), we have employed high-density oligonucleotide microarrays to define transcriptional patterns in mouse tissues, including skeletal muscle, brain, heart, and adipose. Aging results in a differential gene expression pattern specific to each tissue, and most alterations can be completely or partially prevented by CR. Transcriptional patterns of tissues from calorie-restricted animals suggest that CR retards the aging process by reducing endogenous damage and by inducing metabolic shifts associated with specific transcriptional profiles. These studies demonstrate that DNA microarrays can be used in aging research to generate panels of hundreds of transcriptional bio...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393934</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393934</guid>        </item>
        <item>
            <title>Achieving immortality in the C. elegans germline.</title>
            <link>http://www.medworm.com/index.php?rid=393933&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15619471%26dopt%3DAbstract</link>
            <description>Authors: Smelick C, Ahmed S
    Germline immortality is a topic that has intrigued theoretical biologists interested in aging for over a century. The germ cell lineage can be passed from one generation to the next, indefinitely. In contrast, somatic cells are typically only needed for a single generation and are then discarded. Germ cells may, therefore, harbor rejuvenation mechanisms that enable them to proliferate for eons. Such processes are thought to be either absent from or down-regulated in somatic cells, although cell non-autonomous forms of rejuvenation are formally possible. A thorough description of mechanisms that foster eternal youth in germ cells is lacking. The mysteries of germline immortality are being addressed in the nematode Caenorhabditis elegans by studying mutants th...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393933</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393933</guid>        </item>
        <item>
            <title>Can flies shed light on our own age-related memory impairment?</title>
            <link>http://www.medworm.com/index.php?rid=393932&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15619472%26dopt%3DAbstract</link>
            <description>Authors: Horiuchi J, Saitoe M
    As organisms age, they suffer a progressive decline in cognitive function often referred to as age-related memory impairment (AMI). Currently, many advances have been made in elucidating pathways and mechanisms involved in the aging process. In addition, much is known about processes involved in memory formation. However, it is not yet clear how aging and memory interact such that memory declines upon age. Here, we review possible connections between the two processes and discuss how Drosophila may be used as a model organism to study this interaction.
    PMID: 15619472 [PubMed - indexed for MEDLINE] (Source: Ageing Research Reviews)</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393932</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393932</guid>        </item>
        <item>
            <title>Aging and enhanced hepatocarcinogenicity by peroxisome proliferator-activated receptor alpha agonists.</title>
            <link>http://www.medworm.com/index.php?rid=393931&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15619473%26dopt%3DAbstract</link>
            <description>Authors: Youssef JA, Badr MZ
    The hepatocarcinogenic effect of PPARalpha agonists is enhanced by aging. Exposure to these chemicals produces a five- to seven-fold higher yield of grossly visible hepatic tumors in old relative to young animals. This review presents current experimental evidence, which supports a mechanism involving enhanced exposure to oxidative stress, and diminished apoptosis in this age-related difference in sensitivity. In the aged liver, a decrease in hepatic antioxidant activity, coupled with a PPARalpha agonist-induced increase in the activities of various oxidases, may expose these livers to oxidative stress. Additionally, livers of senescent animals appeared more sensitive to the anti-apoptotic effect of PPARalpha agonists. Since apoptosis safeguards cells with ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393931</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393931</guid>        </item>
        <item>
            <title>Cognitive reserve and the neurobiology of cognitive aging.</title>
            <link>http://www.medworm.com/index.php?rid=393943&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15541707%26dopt%3DAbstract</link>
            <description>We describe the neurobiology of cognitive aging and conclude that perturbations of neural health attributable to oxidative stress and inflammatory processes alone are insufficient to distinguish cognitive aging from Alzheimer's disease. We introduce the concept of cognitive reserve and illustrate its utility in explaining individual differences in cognitive aging. Structural and functional brain imaging studies suggest plausible neural substrates of cognitive reserve, probably involving processes that support neuroplasticity in the aging brain. The cognitive reserve hypothesis conforms with reported associations between early and mid life lifestyle choices, early education, lifelong dietary habit, leisure pursuits and the retention of late life mental ability.
    PMID: 15541707 [PubMed - ...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393943</comments>
            <pubDate>Mon, 01 Nov 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393943</guid>        </item>
        <item>
            <title>Biophysical alterations of hippocampal pyramidal neurons in learning, ageing and Alzheimer's disease.</title>
            <link>http://www.medworm.com/index.php?rid=393942&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15541708%26dopt%3DAbstract</link>
            <description>Authors: Disterhoft JF, Wu WW, Ohno M
    A series of behavioral, electrophysiological, and molecular biochemical experiments are reviewed indicating that when animals learn hippocampus-dependent tasks, output neurons in the CA1 and CA3 hippocampal subfields show reductions in the slow, post-burst afterhyperpolarization (AHP). The slow AHP is mediated by an apamin-insensitive calcium-activated potassium current. A reduction in the slow AHP makes hippocampal neurons more excitable and facilitates NMDA receptor-mediated response and temporal summation. During normal aging and in a mouse model of Alzheimer's disease (AD), the slow AHP is increased, making neurons less excitable and making learning more difficult. The subgroup of aging animals that are able to learn demonstrates the capacity t...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393942</comments>
            <pubDate>Mon, 01 Nov 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">393942</guid>        </item>
        <item>
            <title>Regulation of late-phase LTP and long-term memory in normal and aging hippocampus: role of secreted proteins tPA and BDNF.</title>
            <link>http://www.medworm.com/index.php?rid=393941&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15541709%26dopt%3DAbstract</link>
            <description>We describe experiments that reveal the critical role of cAMP/protein kinase A and MAP kinase pathways, and the downstream transcription factor CREB. Because transcription-dependent long-term changes are input specific, we also discuss the role of &quot;local protein synthesis&quot; and &quot;synaptic tagging&quot; mechanisms that may confer synapse specificity. We then focus on brain-derived neurotrophic factor (BDNF) and tissue plasminogen activator (tPA), two secreted proteins that have been repeatedly implicated in L-LTP. Biochemical and molecular biology experiments indicate that the expression and secretion of both factors are enhanced by strong tetanic stimulation that induces L-LTP as well as by training in hippocampal-dependent memory tasks. Inhibition of either tPA or BDNF by gene knockout and speci...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393941</comments>
            <pubDate>Mon, 01 Nov 2004 07:00:00 +0100</pubDate>
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        <item>
            <title>Reactive oxygen species and synaptic plasticity in the aging hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=393940&amp;cid=s_34430_176_f&amp;fid=34430&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15541710%26dopt%3DAbstract</link>
            <description>Authors: Serrano F, Klann E
    Aging is associated with a general decline in physiological functions including cognitive functions. Given that the hippocampus is known to be critical for certain forms of learning and memory, it is not surprising that a number of neuronal processes in this brain area appear to be particularly vulnerable to the aging process. Long-term potentiation (LTP), a form of synaptic plasticity that has been proposed as a biological substrate for learning and memory, has been used to examine age-related changes in hippocampal synaptic plasticity. A current hypothesis states that oxidative stress contributes to age-related impairment in learning and memory. This is supported by a correlation between age, memory impairment, and the accumulation of oxidative damage to c...</description>
            <author>Ageing Research Reviews</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=393940</comments>
            <pubDate>Mon, 01 Nov 2004 07:00:00 +0100</pubDate>
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