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Biomedical subjects

J C Alden

Publications and source records attributed to J C Alden.

4 recordsLinked to original sources

Osteoporosis--a review.

Osteoporosis is a major medical problem in older women. Although a variety of factors influence bone formation and resorption, ovarian failure and a reduction in adrenal androgen production are major causes of menopausal osteoporosis. The prevention of trabecular bone loss and vertebral fractures in menopausal patients is feasible. Women who are at risk, so-called "fast bone losers," can be identified by office and chemical laboratory techniques. Estrogen therapy reduces or halts osteoclastic resorption and preserves bone mass. Exercise and anabolic hormones, including progesterone, stimulate osteoblastic building of bone. The combination of estrogen and progesterone reduces the risk of uterine malignancy below that seen in patients who take estrogen alone and possibly below the incidence seen in women who take no hormones. An individual's doses of replacement hormones will vary, depending on the amount of endogenous bone-targeted hormones and the response to treatment. These doses can be determined by monitoring their effect on 24-hour hydroxyproline and calcium excretion. Another way to monitor dose effect is by observation of the FSH levels. The serum FSH levels should be reduced at least to that level considered to be diagnostic of menopause. It may be unnecessary, if not inappropriate, to strive to restore FSH levels to normal premenopausal levels. Age-associated osteoporosis is a potentially fatal disease. Osteomalacia, with the associated loss of cortical bone, is superimposed upon the trabecular bone loss due to ovarian and adrenal androgen hormone deficiencies. These hormone deficiencies continue to operate upon trabecular bone at this later stage in the continuum. In addition to estrogen therapy and progesterone replacement, patients who are fracture victims may benefit from androgen replacement to increase their bone mass. Replacing androgens using nandrolone decanoate in women may address the natural loss of their adrenal bone-targeted hormones. The identification and treatment of individuals who need vitamin D and calcium replacement will reverse this contribution to the loss of bone. Clinical experience demonstrates that monitored hormone, vitamin D, and calcium supplements reduce the frequency of fractures, especially hip fractures, which may be reduced as much as 40% to 60% over a three-year period with such treatment. Cautious fluoride supplements in addition to calcium, hormones, and appropriate amounts of vitamin D appear to reduce vertebral fracture rates. The associated suffering, disability, and death from osteoporosis-induced fractures can be dramatically altered.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗

Comparative dynamics of salmonella infection after primary and secondary challenge of mice exposed to 10 and 23 C.

Mortality of mice increased significantly as a result of cold exposure when the animals were challenged orally with Salmonella typhimurium, strain RIA. As reported earlier, cold exposure alone did not kill control animals nor did oral challenge at room temperature. No differences were apparent in the number of Salmonella per gram of liver-spleen, colon, or lung between groups of infected mice housed at 23 and 10 C. The number of bacteria increased equally in liver-spleen samples during the period of increasing mortality in the group housed at 10 C and the period of overt illness in those housed at 23 C. The ability to clear the bloodstream of a secondary intravenous challenge did not seem to be impaired by cold exposure. The bacterial load in the spleen and the rate of change in weight of that organ was equal in animals given a secondary challenge at 10 or 23 C. However, the absolute spleen weight was less in the cold-exposed group as was survival when the secondary challenge was administered 3 days after the primary oral challenge. The studies indicate that endotoxin from S. typhimurium may sensitize mice to the lethal effects of cold exposure. The increase in mortality observed in cold-exposed, infected mice is not due to greater bacterial proliferation in these animals. Rather, the combined stress effects of the bacterial agent(s) and cold may link lympholytic effects to impaired detoxification and increased energy demands, which often leads to lethal vascular collapse in cold-exposed, infected mice.

Administration, Oral↗