This searchable list includes the abstracts of all presentations given at a conference organised as part of the SENS series. We regret that the videos recorded at SENS3 and SENS4 are currently unavailable.
The cerebellum is a vital organ for postural control, equilibrium, and motor coordination; its increasing dysfunction as a result of normal aging can lead to life threatening accidents. The objective of this study was to identify and quantify all expressed cerebellar genes in the adolescent, adult, and aging mouse cerebellum using SAGE, a powerful tool for assessing the absolute expression levels of multiple genes simultaneously. The SAGE method is based on the isolation of short nucleotide sequence tags from a defined position within a transcript, followed by serial concatenation of tags.Keywords: SAGE, Gene expression
Ultrasound in determining pleural effusion nature as an alternative way for aspiration specialy in old age people
As you know many diseases causes pleural effusion such as cardiac diseases, nephrotic syndromes, malignancies and so on.
Its important for a physician to know the nature of pleural effusion . Is it transudate or exudates? The answer determines the differential diagnosis and treatment.
For years there has been no way except aspiration of the pleural fluid to discover what kind of effusion we have encountered.
Organ failure is placing enormous burdens on our health care systems yet the medical capacity to treat disease is frustrated by the limited availability of donated organs. Many could benefit from a transplant were there an unlimited supply of organs and no waiting lists for a transplant. Perhaps more importantly, the population is aging rapidly leading to a substantial increase in the demand for technologies that will improve morbidity, mortality and productivity.Keywords: tissue engineering, organs, angiogenesis , ,
Age-associated accumulation of post-translational oxidative modifications on skeletal muscle phosphorylase B in fisher 344 rats
Post-translational modification of proteins has been implicated in the loss of physiological functions in aging. The accumulation of modified proteins is species and tissue specific and depends on many processes including elevated oxidant levels, decline in antioxidant protection systems, protein repair and turnover systems.Keywords: protein oxidation, aging, phosphorylase b, mass spectrometry,
Functional telomeres are essential for continued cell proliferation. Induction of telomere-based replicative senescence is caused by the lack of sufficient telomerase activity, and this leads to progressive telomere erosion with each replication (end-replication problem). Telomere shortening occurs as part of normal aging and this is enhanced in chronic diseases associated with increased cellular turnover. There is mounting correlative evidence that telomere shortening may be an important aspect of tissue dysfunction.Keywords: telomeres, telomerase, tissue engineering, senescence, aging
Advanced glycation endproducts (AGEs) are the result of a non-enzymatic reaction of reducing sugars and primary amino-groups of proteins (Maillard reaction). They accumulate in various tissues in the course of ageing and induce protein crosslinks as well as oxidative stress (radicals) within cells and tissues.Keywords: glycation, oxidative stress, remodelling, heart, tumor
Cancer is a disease of aging. Progressive decline in the mitochondrial function plays a significant role in the aging process. Recent studies have demonstrated that a decline in mitochondrial function is due to the accumulation of mutations in mitochondrial DNA (mtDNA) during the aging process. Strikingly, mitochondrial dysfunction is also one of the most common and profound phenotypes of cancer cells. Another hallmark of cancer cells is the rapid accumulation of mutations in the nuclear genome that drive tumor development.Keywords: aging, cancer, mitochondria, mutator phenotype, mutation
Evidence supporting a proximal role for oxidative stress in the pathogenesis Alzheimer disease (AD) led us to investigate the causes and consequences of oxidative stress, which, along the way, led to a number of surprising findings concerning disease pathogenesis.
Causes: Considering that oxidative damage in the brains of AD-affected individuals occurs predominantly within the neuronal cell bodies, we investigated abnormalities that may initiate and promote neuronal oxidative damage. We found a synergistic interplay between mitochondrial abnormalities and redox metal imbalance.Keywords: , , , ,
Quantitative changes in the activity of genes can control the rate of aging and the development of age-related diseases in invertebrates and mammals. Caloric restriction (CR) is the most robust environmental method known for decelerating aging and the development of age-related diseases. CR is widely viewed as acting slowly and incrementally to prevent the accumulation of deleterious age-related physiological changes. CR is also widely thought to be less effective in older animals.Keywords: caloric restriction, mimetics, short-term, life span, metformin
As we begin to understand the biology of aging, it will be ever more tempting to try to plan for the social consequences of the coming biomedical interventions in this arena. But this will remain a daunting task, because the larger consequences of the arrival of anti-aging interventions will greatly depend on the relative character and timing of the specific procedures that emerge. Three basic classes of interventions are likely: ones that slow aspects of aging in adults, ones that reverse aspects of aging in adults, and embryonic interventions that modify the trajectory of human aging.Keywords: social, political, demography, anti-aging, ethics
The effect of vitamin E on the protein homeostase in adult microglia - counteracting the age-related decline of protein degradation
Introduction: Common symptoms of different neurodegenerative diseases start in the second half of the human life. Several of theses diseases, including Alzheimer’s and Parkinsons disease, are accompanied by severe disturbances of protein metabolism and homeostasis in the brain. Since microglial cells are to some extend responsible for the maintenance of this homeostasis, age related functional changes of the microglia are significant as is the possible restoration of normal function of adult microgilal cells.Keywords: Aging, Microglia, Proteasome, Vitamin E ,
Stem cells have been suggested as a possible fountain of youth for replacing tissues lost during aging. In the brain, replacing lost neurons may be possible, but is a challenge, as they have to then be re-connected with their appropriate targets. Furthermore, during aging memories are stored in specific circuits that might not be fully replaced by new neurons. Perhaps a more realistic and practical strategy for affecting the aging process would be to prevent the loss of neurons from occurring, thus retaining intact circuitry.Keywords: stem cell, GDNF, Parkinson's Disease, Brain,
Altered proteins accumulate in various tissues with age. Both constitutive and inducible heat shock proteins (HSPs) play an important role in the renaturation of conformationally altered proteins. Decrease in the expression of HSPs might contribute to an increase in the amount of altered proteins in cells. In this study, we investigated the effect of aging on the expression of hsp25 and hsp70 genes in the brain, liver and heart of unstressed rats (F344/DuCrj).Keywords: heat shock protein, hsp70, hsp25, liver, brain
Morbidity and mortality from heart diseases are highly represented in geriatric-aged patients, but also they have supporting diseases. Acute coronary syndrome includes unstable angina and acute myocardial infarction with and without ST-elevation.
The aim of this study is to make a retrospective analysis of morbidity of emergency entered patients.Keywords: geriatry, acute coronary syndrome, morbidity, co-morbidity, mortality
Correlation between lipofuscin accumulation, oxidative stress and mitochondrial damage in cultured rat cardiac myocytes
Oxidant-induced macromolecular damage is believed to be an important contributor to aging, which mainly affects postmitotic cells, such as cardiac myocytes and neurons (1). Neonatal rat cardiac myocytes maintained in culture develop progressive senescent-like alterations, similar to those observed in the aging heart in vivo. These changes include the accumulation of functionally effete, often mutant and enlarged mitochondria, as well as the deposition of lipofuscin (age pigment) within the lysosomal compartment.Keywords: Aging, lipofuscin, lysosomes, mitochondria, oxidative stress
We hypothesized that the children of centenarians (c-children) age more slowly and delay, if not escape, age-related diseases. We compared 177 c-children and 166 controls -- offspring of parents who were born in the same years as the centenarians but at least one of whom died at age 73, the average life expectancy for that cohort.Keywords: longevity, centenarian, cardiovascular disease , ,
Loss of muscle mass (sarcopenia) is a predictable occurrence during aging that reduces the quality of life, and can contribute to functional defects in other systems that are associated with reduced physical activity. Mechanical loading of muscle can slow sarcopenia, but the mechanisms through which the mechanical environment can influence muscle mass are not well-understood. Our current work is directed toward examining the role of neuronal nitric oxide synthase (nNOS) as a mechanical signal transducer that functions as a positive regulator of muscle mass.Keywords: muscle, nitric oxide, calpain, sarcopenia ,
Normal brain ageing is associated with a degree of functional impairment of neuronal activity that results in a reduction in memory and cognitive functions. One hypothesis proposed to explain these age-dependent changes in neuronal activity is the "Ca2+ hypothesis of ageing". However, recent experiments using cerebellar brain slices  show that in resting conditions there are few differences in the main parameters of Ca2+ homeostasis between young, mature and aged neurones.Keywords: , , , ,
Transcriptional control of telomerase reverse transcriptase in normal endothelial cells. Differences between stimulation by fibroblast growth factor-2 and vascular endothelial growth factor
Objective: Telomerase plays a major role in the control of replicative capacity, a property critical to successful angiogenesis and maintenance of endothelial integrity. We have previously demonstrated that in normal human endothelial cells telomerase is differentially regulated by fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), two major pro-angiogenic growth factors.Keywords: telomerase, regulation, senescence, FGF-2, endothelium
Functional analysis of the senescence biomarker Clusterin/Apolipoprotein J in human osteosarcoma cells reveals both a pro- and anti-apoptotic function
Clusterin/Apolipoprotein J (CLU) is a secreted heterodimeric glycoprotein. We recently cloned CLU as a gene induced during cellular senescence and showed that apart from being up-regulated following cell exposure to various types of stress it also accumulates in the human serum during several age related diseases. Moreover, CLU is reportedly up regulated during tumorigenesis, as well as during cell injury or death. Nevertheless, despite extensive effort CLU function remains largely elusive.Keywords: apoptosis, Clusterin/Apolipoprotein J, DNA damage, senescence,
There is curious divergence between achievements of practical geriatrics and experimental gerontology. On the one hand, the consumption of brain protective, stimulative and regenerative drugs is expanding in elderly population. During last 30 years physicians in many developed countries have successfully prescribed a number of medicines to cure various symptoms of senescence. Most common of relevant medicines are nootropic piracetam and gamma-aminobutyric acid (GABA), selegiline, ginkgo biloba, cerebrolysin, solcoseryl, ergoloid, vinpocetin, sertraline, and some others.Keywords: legal anti-aging medicines, human longevity, , ,
The phenotypes of cancer and aging are in many instances contrary. Cancer cells do not "age", their metabolic, proliferative, growth and signalling characteristics are opposite to those observed with cellular aging (both replicative and functional). That is, cancer manifests itself as local uncontrolled "rejuvenation" in an organism. Available data suggest that the opposite phenotypic features of aging and cancer arise from the alternative regulation of the same genes particularly related to apoptotic and growth signal transduction pathways.Keywords: cancer, anti-aging phenotype, common genes, ,
Pleiotropic activities of TGF-b cytokines on human prostate basal cells: Increased SA-beta-galactosidase activity due to differentiation processes, not as a consequence of premature senescence
The family of transforming growth factors betas (TGF-bs) comprises pleiotropic molecules involved in growth inhibition, stress-induced premature senescence, epithelial mesenchymal transition and lumenal differentiation. The aim of this study was to clarify the effect of long time exposure of TGF-bs- which can be found in high concentrations in seminal fluid and areas of benign prostatic hyperplasia (BPH)- to human prostate basal cells.Keywords: prostate, cellular senescence, SA-beta-galactosidase, TGF-beta,
Effect of Aging and Caloric Restriction on the 24-hour Release Patterns of DHEAS and Cortisol in Male Rhesus Macaques
It is well established that dietary caloric restriction (CR) can retard aging in mice, but it is less clear whether CR can exert similar effects in long-lived species, such as primates. To examine this possibility, we tested the effect of CR on dehydroepiandrosterone sulfate (DHEAS), a reliable endocrine marker of aging in both human and nonhuman primates. Because DHEAS is known to decline markedly during aging, we predicted that the plasma concentrations of this adrenal steroid would be significantly higher in the CR animals than in the age-matched controls.Keywords: dehydroepiandrosterone sulfate, adrenal gland, , ,
Tumour suppressor protein TP53 (p53) mediated induction of apoptosis and senescence plays a key role in protection against cancer. Mice deficient for p53 are highly susceptible to cancer, while mice with overactive p53 (p53 +/m) are almost cancerfree. However, despite their cancer resistance, the longevity of p53 +/m mice is reduced and accompanied by early tissue and organ atrophy, hinting at accelerated depletion of adult stem cell reserves (Nature 415, 45-53).Keywords: longevity, cancer, p53 , ,
My objectives are first to critically review what is known about the effects of aging on stem cells in general, and hematopoietic stem cells in particular. Secondly, evidence is marshaled in support of the hypothesis that aging stem cells play a critical role in determining the effects of aging on organ function, and ultimately on the lifespan of a mammal. Aging has both quantitative and qualitative effects on stem cells.Keywords: , , , ,
Somatic mutations have been implicated as a major cause of both cancer and aging. Using a transgenic mouse model with a chromosomally integrated lacZ mutational target gene, mutations were found to accumulate with age in an organ-specific manner. Depending on the organ, many of the accumulated mutations were genome rearrangements rather than point mutations, some of them involving millions of basepairs (Dolle and Vijg, Genome Research 2002;12:1732-1738). Such large rearrangements could find their origin in misannealing of DNA double-strand breaks during error-prone repair.Keywords: somatic mutations, genome instability, DNA repair, aging,
Human Embyryonic Stem (ES) cells are unique in two important aspects. First, they are totipotent (capable of differentiating into any somatic cell type). Second, they are immortal germ-line cells and are, therefore, able to make young cells in vitro for therapy in age-related disease. An important problem to be resolved is how tolerance is to be achieved in transplants made from ES-derived cells.Keywords: , , , ,
Caloric restriction (CR) is the only intervention shown to extend lifespan and retard age-related declines in function in mammals. Mutations that extend lifespan in C. elegans suggest that insulin/IGF-1 signaling (IS) pathway may play a key role in retarding aging and extending the lifespan by CR. To evaluate this hypothesis, we subjected male F-344 rats to 2 mo or 25 mo CR (starting at 28 days old, 40% of control level) and then assessed the effects of CR on early events in the IS pathway in liver and muscle.Keywords: Caloric Restriction, Insulin Receptor, Phosphorylation, PTP-1B, PPARs