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Relation of leptin cheap 160mg super viagra otc, adiponectin and insulin resistance to bone mineral density in type 2 diabetic postmenopausal women generic super viagra 160 mg with amex. Periodontitis and bone mineral density among pre and post menopausal women: A comparative study. The role of body mass index, insulin, and adiponectin in the relation between fat distribution and bone mineral density. Effects of the transition from premenopause to postmenopause on lipids and lipoproteins: quantification and related parameters. Estrogen-induced improvement in coronary flow responses during atrial pacing in relation to endothelin-1 levels in postmeno pausal women without coronary disease. Insulin resistance and management of the meno pause: a clinical hypothesis in practice. Association of sex hormones and sex hormone-binding globu lin with depressive symptoms in postmenopausal women: the Multiethnic Study of Atherosclerosis. Oxidative Profile of the Menopausal Woman: Estrogens Rol in the Prevention and Treatment of Diseases. Structural basis for an drogen specificity and oestrogen synthesis in human aromatase. Hyperhomocysteinemia, oxidative stress, endothelial dysfunction in postmenopausal women. Research into Specific Modulators of Vascular Sex Hormone Receptors in the Management of Post menopausal Cardiovascular Disease. Role of estrogens in pathogenesis of age-related disease in women of menopausal age. Neuroprotective effects of oestrogen against oxidative toxicity through activation of G-protein-cou pled receptor 30 receptor. Serum -glutamyltransfer ase as Oxidative Stress Marker in Pre-and Postmenopausal Iraqi Women. Correlation of increased oxidative stress to body weight in disease-free post menopausal women. Oxidative stress, body fat composition, and endocrine status in pre- and post menopausal women. Total antioxidant capacity and superoxide dismutase activity levels in serum and gingival crevicular fluid in post-menopausal women with chronic periodontitis. Behaviour of some indica tors of oxidative stress in postmenopausal and fertile women. Decreased oxidant profile and increased antioxidant capacity in naturally postmenopausal women. Estradiol levels and oxidative bal ance in a population of pre-, peri-, and post-menopausal women. Total antioxidant status correlates with cognitive impairment in patients with recurrent depressive disorder. Effect of Chronic Administration of Estradiol, Progesterone, and Tibolone on the Expression and Phosphorylation of Glycogen Synthase Kinase-3b and the Microtubule-Associat ed Protein Tau in the Hippocampus and Cerebellum of Female Rat. Lifetime History of Depression, Type 2 Diabetes, and Endothelial Reactivity to Acute Stress in Postmenopausal Women. Homocysteine oxidative stress and relation to bone mineral density in post-menopausal osteoporosis. Association of oxidative stress, iron, and centralized fat mass in healthy post menopausal women. Study of changes in antioxidant enzymes status in diabetic post menopausal group of women suffering from cardiovascular complications. Oxidative stress contributes to chronic leg vasoconstriction in estrogen-deficient postmenopausal women. Duration of menopause and behavior of malondialdehyde, lipids, lipoproteins and carotid wall artery intima-media thickness. Duration of estrogen deprivation, not chronological age, prevents estrogen s ability to enhance hippocampal synaptic physiology. Proceedings of National Academy of Science of United States of America, 107(45), 19543-19548. Women s use of hormone replacement therapy for relief of menopausal symptoms, for prevention of osteoporosis, and after hysterecto my. Updated clinical recommendations for the use of ti bolone in Asian women Climateric,13:, 317-327. Effect of short-term hormone ther apy on oxidative stress and endothelial function in African American and Caucasian postmenopausal women. Effects of hormonal replacement therapy on oxidative stress and total antioxidant capacity in postmenopausal hemodialysis patients. Oxidative stress measured by carbonyl groups level in postmenopausal women after oral and trans dermal hormone therapy. Hormone replacement therapy: relation to homocysteine and prooxidant-antioxidant status in healthy postmenopausal women Archives of Gynecology and Obstetretics,, 285(3), 733-9.

It may be argued that oxidative damage is linked to aging in a universal manner and that changes in endo- crine function are secondary to changes in oxidant production in endocrine cells [64 cheap 160mg super viagra with mastercard, 65] generic super viagra 160mg with mastercard. Thus, similar cellular mechanisms (free radical production) may broadly affect aging and simultaneously contribute to the development of pain. Another example of the overlap in the biology of chronic pain, and aging is in the case of central pain resulting from spinal cord injury. Similar changes in neuronal function are commonly observed in uninjured older animals, suggesting an overlap in the cellular mechanisms responsible for neuronal changes in excitabil- ity resulting from injury and aging. Similarities in cellular mechanism(s) underlying pain and aging can also be found with the results of the drug rapamycin, initially developed as an antifungal agent and found to have immunosuppressive properties [68]. A rapamycin sensitive signaling pathway was also shown to be essential for the expression of persistent pain states [70], and rapamycin reduces clinical signs of neuropathic pain in a model of experimental autoimmune encephalomyeli- tis [71]. These examples of overlapping mechanisms reveal the need for collabora- tive efforts between the elds of pain and aging research to more fully explore the biological processes that contribute to both senescence and chronic pain. Age-related anatomi- cal and functional changes have been described in both human and non-human studies of the somatosensory system [74]. For example, peripheral nerves show an age-related reduction of both myelinated and unmyelinated bers [75, 76] as well as signs of Wallerian degeneration [77, 78]. In addition to peripheral changes, central changes in the expression of neu- rotransmitters and receptors may contribute to age-related alterations in somatosen- sation. A decrease in the number of opiate receptors and decreased efcacy of opiate-mediated antinociception may also contribute to age-related changes in the processing of nociceptive information [89 91]. Further, autonomic dysfunction can be instrumental in the generation and maintenance of chronic pain. Aging is associated with changes in the sympathetic nerve supply to a number of targets, and quantitative changes in sympathetic nerve bers result in changes in transmitter expression [97]. Although the exact relationship between pain and the sympathetic nervous system remains unclear, the sympathetic nervous system is known to be involved in maintaining protective body reactions associated with pain. Clinical and preclinical studies have documented that physiological activation of sympathetic neurons can enhance pain and blockade of sympathetic activity can relieve pain. The glial response to injury contributes to neuronal hypersensitivity leading to the production of inammatory mediators such as cytokines and chemokines. This glia cascade has been related to the regulation of synaptic strength and plasticity and the generation of central sensitization [101, 102]. However, the contribution of glia to the induction or main- tenance of chronic pain in aged rats is unknown. Stuesse and colleagues [103 ] found that ligation-induced hyperreexia was correlated with increased staining for acti- vated microglia regardless of age. Selective inhibition of acti- vated microglia can alleviate acute and chronic pain behaviors [105], though clini- cal evidence of a benecial effect of microglia inhibition in persistent pain conditions is lacking [106, 107 ]. The microglia-to-neuron signaling link has also been shown to involve a molecu- lar pathway in the spinal cord that includes Toll-like receptors, phosphorylated mitogen-activated protein kinase and purinergic P2X4 receptors on microglia [108, 109]. Thus, substantial evidence exists that immune responses elicit a well-orchestrated temporal pattern of activation of different immune cells, including microglia and astrocytes, which may contribute to chronic pain development. At present the involvement of glia in the induction or maintenance of chronic pain in aged rats is an evolving story. However, age-related morphological changes in microglia may reect an important mechanism mediating age-dependent increases in pain sensitivity. It is important to point out that the majority of these studies employed reex-based behavioral measures to determine changes in thermal and/or mechanical sensitivity. The execution of these reex-based mea- sures do not require cerebral processing for the conscious perception of sensory events and are subsequently thought to be less relevant to clinical pain [111]. In order to address these deciencies an operant escape task was developed to evaluate thermal nociceptive sensitivity in awake, unrestrained rats [112]. This test over- comes the limitations inherent with reexive responses by providing a measure of pain sensitivity and affective response to nociceptive stimuli. Use of operant (learned) tests provides a measure of pain involving neuronal pathways extending throughout the neuraxis. Importantly, reex-based and operant assays often yield substantively different results [113 115], and the ndings from operant assays are typically more consistent with predictions from available human reports than are the results from reex-based tests [111]. Using paw lick and tail ick latencies in young (2 3 months), adult (6 12 months), and aged (24 months) rats, Hess et al. These results correlated with a decrease in the number of opiate receptors in the frontal poles, striatum, and hippocampus. Another evaluation of thermal response latencies showed that young mice (6 8 weeks) had signicantly shorter latencies than animals 24 months of age [116]. The decreased sensitivity in older animals was greater for females and correlated with a decrease in the expres- sion of Nav1.

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Prior reviews have discussed the sig- nicance of multimorbidity in the context of aging [11 17 ] safe 160mg super viagra. The development of multiple diseases in the same person occurs buy super viagra 160 mg free shipping, in part, by chance alone, as a result of the length of exposure and cumulative development of the resulting pathophysiologic alterations. However, recent data suggest that the development of multi-morbidity is not merely the result of multiple independent, disease-specic pathophysiological processes. Their development can derive from shared etiologic factors, which predict many different chronic diseases that are age- related. Further, a number of studies have recently suggested that this is only part of the story. A land- mark paper that tested the hypothesis that certain diseases tend to appear in clusters in some specic individuals was published by van den Akker and colleagues in 1998 [15]. Working in a large general practice, they used data on disease prevalence and co-prevalence to calculate the expected prevalence of multi-morbidity under the assumption of association by pure chance. The authors found that more people than expected did not have any disease or had four or more diseases, while less than expected had one or two diseases. This suggests that some individuals develop a global susceptibility to multiple diseases, while others appear to be unusually resis- tant, and that the co-occurrence of some specic diseases is not due to chance alone. These authors and others have suggested that the force of aging is different in different individuals and makes them more or less susceptible to multi-morbidity. Compromising this research is the absence of standardization of methods, which has resulted in high variability among studies and inconsistency in results, making it difcult to compare them. Interestingly, chronological aging appears to be a strong predictor of mortality even in analyses that take into account the contribu- tions of multiple diseases and risk factors [18, 19]. While this is not a surprising nding to clinicians, it clearly underlines the fact that that the parameters that are usually observed and considered in medical care do not exhaust all of the changes in health status that occur with aging. In other words, there are biological processes that occur with aging that are not revealed by clinically evident disease. It is quite possible that the excess mortality associated purely with old age may be due to Etiological Role of Aging in Chronic Diseases: From Epidemiological Evidence 45 subclinical disease, unobserved confounding and/or measurement error in assessing the full effect of diseases on prognosis. However, an alternative hypothesis is that some fundamental biological processes essential for life across cells, tissue and the entire organism deteriorate with the aging process and facilitate the emergence of both diseases and a general decline in health status that is not classied as disease but increase the risk of mortality. A number of studies have found that aging is associated with loss of mitochondrial function; the mitochondrion being the key organelle responsible for cellular energy production in tissues and organs. In addition, impairment in mitochondria may affect apoptosis as well as autophagy mechanisms. When mitochondria are not functioning properly, tissues that have high energy demands suffer rst. This is manifest in genetic mitochondrial disorders, which mostly affect the nervous system, heart and skeletal muscle [21]. It is notable that inadequate energy support, excessive and unopposed oxidative stress as well as chronic inammation have all been associated with the syndrome of frailty and with almost all chronic diseases whose incidence and preva- lence increase with aging as well as with sarcopenia, gait disorders, and brain dys- function. The translation of these biological events into both multi-morbidity and frailty is direct and intuitive. Further, it is easy to see how age-associated mitochondrial dysfunction can produce a number of vicious cycles that further impair mitochondrial physiology, for example, by causing ischemia or metabolic derangement. There are now many other examples implicating a single biological mechanism that, while driving the development of aging as a phenotype and aging- related frailty, also causes multi-morbidity. What is important here is that the trian- gle of aging-multimorbidity-and frailty may derive from the same root cause and, plausibly, they may all respond to the same interventions. We develop further here the concept and the evidence that underlying mechanism(s) of aging as exemplied 46 L. Ferrucci above by the example of mitochondrial changes - may lead to this syndrome of frailty. Frailty is associated with a dysregulation of the complex adaptive mecha- nisms that support organismal resilience; the dysregulation leading to loss of homeostatic capabilities and increased susceptibility to stress. The net result is the emergence of a distinct clinical syndrome with a characteristic phenotype that is predictive of a range of adverse clinical outcomes. We will rst describe frailty as a prototypical constellation of signs and symp- toms that allows a clinical diagnosis and then, working backwards in the causal pathway to etiology, we will consider how what we currently know about frailty informs understanding of aging and accelerated aging. When a critical number of such signs and symptoms occur in the same individual they identify the frailty syn- drome [23]. It is noteworthy that studies have demonstrated that the phenotypic criteria of frailty co-occur in ways that are consistent with the denition of a medi- cal syndrome [24]. That they predict the clinical outcomes associated with being frail provides criterion validity.

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