Annals of the New York Academy of Sciences
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Ann. N. Y. Acad. Sci. · Nov 1998
ReviewOxidative damage and mutation to mitochondrial DNA and age-dependent decline of mitochondrial respiratory function.
Mitochondrial respiration and oxidative phosphorylation are gradually uncoupled, and the activities of the respiratory enzymes are concomitantly decreased in various human tissues upon aging. An immediate consequence of such gradual impairment of the respiratory function is the increase in the production of the reactive oxygen species (ROS) and free radicals in the mitochondria through the increased electron leak of the electron transport chain. Moreover, the intracellular levels of antioxidants and free radical scavenging enzymes are gradually altered. ⋯ The respiratory enzymes containing the mutant mtDNA-encoded defective protein subunits inevitably exhibit impaired respiratory function and thereby increase electron leak and ROS production, which in turn elevates the oxidative stress and oxidative damage of the mitochondria. This vicious cycle operates in different tissue cells at different rates and thereby leads to the differential accumulation of mutation and oxidative damage to mtDNA in human aging. This may also play some role in the pathogenesis of degenerative diseases and the age-dependent progression of the clinical course of mitochondrial diseases.
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Loss of bone is an almost universal accompaniment of aging that proceeds at an average rate of 0.5-1% per annum from midlife onwards. There are at least four nutrients involved in this process: calcium, salt, protein, and vitamin D, at least in women. The pathogenesis of osteoporosis in men is more obscure. ⋯ Low protein intakes in third world countries may partially protect against osteoporosis. Vitamin D (sometimes called a nutrient and sometimes a hormone) is important because age-related vitamin D deficiency leads to malabsorption of calcium, accelerated bone loss, and increased risk of hip fracture. Vitamin D supplementation has been shown to retard bone loss and reduce hip fracture incidence in elderly women.
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Infection, trauma, and injury result in a stereotypical response that includes loss of food appetite, increased sleepiness, muscle aches, and fever. For thousands of years fever was considered a protective response, and fevers were induced by physicians to combat certain infections. But with the advent of antipyretic drugs, physicians started to reduce fevers, and fever therapy was virtually abandoned. ⋯ However, data indicate that not all fevers are protective and that high fevers are maladaptive. These issues are discussed in the context of the evolution of host defense responses versus modern medical technology. In short, we speculate that patients who would not have survived severe sepsis in the past are now being kept alive and that the occasionally high fevers seen in these patients may be maladaptive.
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Ann. N. Y. Acad. Sci. · Jun 1998
Animal disease regionalization and its impact on tropical countries.
This paper reviews progress that has been made around the world in animal disease regionalization. Signatory countries of the Uruguay Round of the General Agreement on Tariffs and Trade (GATT) and other free-trade associations are currently implementing regionalization, one of the cornerstone provisions of the Uruguay Round of the GATT and the World Trade Organization's (WTO) Sanitary and Phytosanitary Agreement. ⋯ The implementation of regionalization by importing countries affects export markets of tropical nations. Veterinary officials of tropical countries must give regionalization due priority such that import and export trade in animals and animal products is not hindered, and the public and animal herd health are protected.
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Aging is associated with the loss of brain neurotransmitter function, which apparently is the substrate for an adverse constellation of age-associated symptoms. In particular, cholinergic deficits have been associated with cognitive impairment in aging. ⋯ In addition to correcting cholinergic neurochemistry, it improves spatial learning and memory impairment, and restores the number and the size of the cholinergic neurons in the basal forebrain and striatum. The induced neuronal recovery by GM1 is long-lasting.