1,721,323 research outputs found
Role of the IGF/insulin system in longevity
Full text linkHuman life expectancy is influenced by multiple determinants, including various environmental and genetic factors. Though the non-genetic factors are important, it is estimated that approximately 25-32% of the overall difference in human lifespan for survival after the age of 60 years depends on for by genetic polymorphisms among individuals. In addition, there are human homologues to many genes that affect lifespan in model organisms. In people, longevity genes might slow the rate of age-related changes in cells, increase resistance to environmental stresses like infection and injury, and reduce the risk of many age-related conditions. The best studied longevity pathway is probably the one involving insulin/IGF-1 signaling. The important role of IGF and insulin-related signaling pathways in the control of longevity of worms and insects is very well documented. In the mouse, several spontaneous or experimentally induced mutations that interfere with GH/IGF axis modulation lead to extended longevity. Increases in the average life span in these mutants range from approximately 20-70% depending on the nature of the endocrine defect, gender, diet, and/or genetic background. All the data in animals models and in the population studies support the evidence that this pathway drives an evolutionarily conserved network that regulates lifespan and affects longevity across species. Results obtained in humans are still controversial and further extensive studies are required to firmly establish a role of the IGF1 axis in modulation of human longevity. A better knowledge of the role of this pathway in humans may assist in the design of improved treatment methods for age-related diseases, delay the aging process and prolong the human lifespa
Physiology and nosography of antiplatelet drug
No full textThe place of antiplatelet drugs in clinical medicine has been firmly established by experience with aspirin. Antiplatelet Trialists' Collaboration demonstrated that some antiplatelet therapy offers worthwile protection against myocardial infarction, stroke and death. Significant benefit is evident also among many other categories of high risk patients (such as those having vascular procedures and those with unstable angina or peripheral vascular disease). More potent platelet inhibitors have been developed and the challenge of the coming years is if they can be used practically and safety at effective doses in humans. Large scale randomized trials are now ongoing to provide reliable data on secondary prevention of vascular and cerebrovascular events of new interesting drugs
Andrologic problems and internal pathology in the elderly
No full textPopulation aging is continuously increasing in Italy and in the World. Individuals aged 60 years or more are currently 10,500,000 and will be 13,000,000 in 2015. Life quality in geriatric ages includes the maintenance of sexual power: according to recent data (Carrol et al., 1992), 80% of impotence cases are due to organic causes. In addition, the use of drugs can cause impotence. Among them tiazidic diuretics may cause an increase of sexual disturbances. Other drugs with this potential are digitalis, antihypertensive drugs (particularly beta blockers), major and minor tranquillizers, antidepressant, H2 receptor antagonists, antiparkinsonian cholinergic drugs and estrogens employed in the treatment of prostate tumors. Diseases of geriatric age that can alter sexual power are diabetes mellitus, ischemic heart disease for the accompanying depression and for the use of antidepressants; severe hypertension is complicated by impotence in 15% of cases. Among neurological diseases Parkinson's disease and multiple sclerosis can be causes of sexual dysfunctions. Patients on hemodialysis can be impotent, with recent data (Soloh et al 1992) showing that erythropoietin treatment of anemia also improve sexual dysfunctions. Prevention from a geriatric standpoint should be base on action on known risk factor as smoking, alcohol abuse and dislipidemias and with the activation of a close drug vigilance
Fundamental solution of the Cauchy problem for a Schrödinger pseudo-differenrial operator
No full textFibrinolytic and defibrinogenation therapy
No full textPlasma fibrinogen is one of the main determinants of blood viscosity and is known to play an important role in the pathogenesis of venous and arterial thromboembolism. The pharmacological intervention on these factors can be achieved by lowering fibrinogen. Plasma fibrinogen concentrations can be lowered by fast-acting and slow-acting drugs. Among fast-acting drugs, fibrinolytic agents (such as streptokinase, urokinase, brinase and plasmin) act by cleaving FGN directly or indirectly through the formation of the proteolytic enzyme plasmin. Defibrinogenating agents (ancrod and batroxobin) are thrombin-like enzymes which induce the in vivo formation of fibrin microclots characterized by a peculiar physicochemical structure rendering them more easily cleared by the reticuloendothelial system. There is a clear-cut evidence for the clinical efficacy of fast-acting FGN-lowering drugs in the prevention and treatment of a number of clinical conditions associated with thromboembolic manifestations. However, it is not well established to which extent the effectiveness is due to their action on blood viscosity rather than to their fibrinolytic and anticoagulant properties. Slow-acting drugs (such as anabolic steroids, clofibrate, ticlopidine and pentoxifylline) decrease plasma FGN less rapidly and to a smaller extent than fast-acting drugs. Unlike these, they can be employed in long-term treatments. Clinical trials have clearly shown their clinical efficacy in a number of conditions associated with an altered microcirculation (Raynaud's syndrome, liposclerosis and postphlebitic syndrome). Their effect on blood viscosity is likely to be an important determinant of the clinical efficacy of these drugs
Methods of studying platelet function research on the aggregation of circulating platelets
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Hemostasis and liver disease
No full textWe reviewed the main disturbances of hemostasis (coagulation, platelet, fibrinolysis) occurring in acute and chronic liver disease and during cholestasis. The significance of coagulation testing in the evaluation of hepatocytic synthetic function and the value of these tests in predicting bleeding episodes are also discussed in detail. Finally the role of replacement therapy with fresh-frozen plasma and prothrombin complex concentrates is evaluated for the treatment of bleeding occurring during various types of liver disease
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