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By: Cynthia K. Kirkwood, PharmD, BCPP Executive Associate Dean for Academic Affairs; Professor, Department of Pharmacotherapy & Outcomes Science, School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia

Signicant architectural changes occur during the slow but inexorable process of uncoupled bone turnover buy zenegra 100 mg free shipping erectile dysfunction my age is 24. Aging and the Bone-Muscle Interface 265 20 years 60 years 90 years Female Male Periosteum Cortical bone Endosteum Marrow cavity Fig generic zenegra 100 mg visa erectile dysfunction operations. A cross sec- tional view of a typical long bone (femur) showing different features which dynamically change with age and sex Paradoxically buy generic zenegra 100mg line erectile dysfunction at 30, the periosteal surface of the cortex is not subject to loss and in fact expands at the same time as there is endocortical resorption [37] proven super cialis 80mg. Remarkably generic viagra sublingual 100 mg with visa, those mice with the greatest cortical thickness had the highest survival rate. Not surprisingly, the authors also noted that the endosteal envelope expanded by nearly 20 % due to increased bone resorption with age. Importantly, the increase in cortical area with age from 4 to 24 months was predominantly related to the increase in periosteal circumference (from 4. How periosteal expansion is related to lifespan remains to be deter- mined in mice but may reect the health of connective tissue or the pool of progenitors that are necessary for this compensation. The expansion of the medullary diameter with a simultaneous increase in the periosteal diameter was directly correlated (r = 0. The strength index decreased as might be expected but might have been more severe had periosteal expansion not occurred. The factors that regulate this expansion are not clear, but interestingly, estradiol levels were inversely related to the periosteal expansion rate. In summary, aging is associated with progressive increases in med- ullary diameter accompanied by periosteal expansion The structural implications of this compensatory response and their relationship to progressive age-related muscle loss need further exploration. The factors that permit the periosteum to resist age- related changes in metabolism and buildup of reactive oxygen species are also unknown. But the periosteum also contains signicant num- bers of progenitors and mesenchymal stem cells and it is the balance between mature and progenitor cells that ultimately dene the function of the periosteum [37, 31 ]. If one of the determinants of unhealthy aging is reduced stem cell pools or reduced stem cell function, the periosteum may be at least partially protected. Alternatively it is possible that adult periosteal cells may undergo senescence and thereby be resis- tant to autocrine, paracrine or endocrine signals such as inammatory cytokines. O Keefe and col- leagues recently reported that reduced fracture healing in aging involves decreased proliferation and differentiation of stem cells lining the bone surface. Another mechanism whereby periosteal expansion may be limited during aging is through the impairment of progenitor cell recruitment from muscles. Recent stud- ies have established that muscle-derived stem cells are able to differentiate into cartilage and bone and can directly participate in fracture healing. The role of muscle-derived stem cells is particularly important in fractures associated with more severe injury to the periosteum. Muscle anabolic agents may improve function Aging and the Bone-Muscle Interface 267 and reduce the incidence of fracture with aging as well as maintaining the muscle- bone interface [42]. A new model for predicting periosteal appo- sition rate for men and women was developed by Jepsen et al. Periosteal apposition rate varied up to eightfold across bone sizes, and this depended on the relationship between cortical area and total area, which varies with external size and among anatomical sites.

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Only recently has substantial effort gone into assessing the health consequences of some of the many longevity- enhancing mutations found in C buy discount zenegra 100mg line erectile dysfunction bp meds. A recent examination of four differ- ent worm longevity mutations cheap zenegra amex impotence of organic origin icd 9, including the most robust of the known mutations zenegra 100mg otc erectile dysfunction joke, daf-2(e1370) buy viagra 100mg with amex, employing four carefully thought out metrics of worm health (heat and oxidative stress resistance plus activity in liquid or solid media) found that none of the mutations compressed morbidity (dened as a loss of 50 % the capacity of a young adult) relative to wild-type by any metric cheap viagra plus uk. Moreover, in only 5 of 16 pos- sible cases (4 longevity mutations 4 health measures) was healthy life extended, and in all of these the unhealthy period of life was also extended. In 7 of 16 possible cases, the period of healthy life was actually shortened compared to wild-type and the unhealthy period extended. Research into laboratory rodent health has a much longer history, is considerably easier to assess, and is undoubtedly more relevant to what we might expect in humans. Moreover, what is known about the health consequences of life-extending interventions in mice is considerably more promising than evidence to date from the invertebrates (see below). However, functional metrics are performed (or at least reported) haphazardly and it is never clear whether all investigated metrics have been reported or there was a selection for reporting those that improved. What is needed in rodent aging research is a widely-agreed upon panel of functional indica- 22 S. Although various drugs and supplements have been reported to extend the lives of laboratory rodents at least since the early 1960s [128 132], until recently none had withstood the test of inde- pendent replication. A difcult problem with rodent longevity studies is that the cost and time involved in doing them makes replication rare. However, this is essential, so that scientists do not spend years pursuing dead ends arising from anomalous experimental results. A recent example is the 1999 report that a targeted mutation in the mouse p66shc gene increased lifespan by 30 % [133], a nding that was never independently validated until 15 years later when it could not be replicated [134 ]. Some of the compounds have been tested at several doses and/or initiated at several different ages. One major result is that none of the compounds tested to date has signicantly shortened mouse lifespan. Another rather astonishing result is that so far 5 of the 16 compounds have signicantly extended life in either males alone or in both sexes. Aspirin is a familiar nonsteroidal anti-inammatory drug with anti-thrombotic and antioxidant proper- ties. At the single dose tested, there was a small (8 %) but statistically signicant lengthening of median lifespan in males but no signicant effect in females and no effect on maximum longevity (last surviving 10 %) in either sex [135]. Further investigation indicated that females had less bioactive plasma levels of aspirin and its metabolites. Austad male survival of those getting the drug is 8 10 % greater than controls and at no dose do females appear to be living longer [138 ]. A nonfeminizing estrogen with little or no afnity for the classical estrogen receptors, 17-estradiol has been repeatedly reported to have neuroprotective and antioxidant properties [139].