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Biomedical subjects

K M Ostrom

Publications and source records attributed to K M Ostrom.

4 recordsLinked to original sources

A review of the hormone prolactin during lactation.

The principal lactogenic hormone, prolactin, secreted by the anterior pituitary is critical to the establishment of lactation, milk macronutrient content and milk production. The concentration of circulating prolactin increases during pregnancy so that by the end of gestation, levels are 10 to 20 times over normal amounts. However, prolactin is prevented from exerting its effect on milk secretion by elevated levels of progesterone. Following clearance of progesterone and estrogen at parturition, copious milk secretion begins. The minimal hormonal requirements for normal lactation to occur are prolactin, insulin and hydrocortisone. Prolactin stabilizes and promotes transcription of casein mRNA; may stimulate synthesis of alpha-lactalbumin, the regulatory protein of the lactose synthetase enzyme system; and increases lipoprotein lipase activity in the mammary gland. Prolactin levels decrease as lactation is established but nursing stimulates prolactin release from the pituitary which promotes continued milk production. Prolactin is secreted into milk at levels representative of the average circulating concentration. The physiological significance of milk prolactin to the infant is uncertain. Prolactin exists in three heterogenic forms which possess varying biological activity. The monomer with a molecular weight of 23 kDa is found in greatest quantity and is the principal biologically active form. The pattern of heterogeneity changes during pregnancy to favor even more monomer in proportion to the dimer. However, during lactation, the proportion of the monomer in circulation decreases in response to selective uptake of the monomer by the mammary gland. Over 90 percent of the prolactin in milk is present as the monomer. Prolactin may exert some of its biological effect by a shift in the ratio of active to less active forms of the molecule.

Animals

Quality-specific taste changes in multiple sclerosis.

Taste sensitivity in 79 patients with multiple sclerosis (MS) and 65 age- and sex-matched control subjects was measured with a sip-and-spit, suprathreshold scaling, magnitude estimation procedure using six concentrations each of sodium chloride, sucrose, citric acid, and quinine hydrochloride. Results were analyzed with a taste scoring system and by plotting psychophysical functions (log concentration versus log magnitude estimate) normalized to 1.0 M sucrose. Gender did not affect taste scores, but age was inversely related, so the results were analyzed by an analysis of covariance with age as the covariant. There was a significant alteration in taste sensitivity in the subjects with MS for sodium chloride and quinine hydrochloride stimuli but not for sucrose and citric acid; these results were confirmed by a separate analysis of the psychophysical functions. Some of the MS taste scores correlated with MS functional and physical disability scores. Taste sensitivity was not correlated with clinical history or presence of facial symptoms.

Humans

Zinc in multiple sclerosis.

Zinc profiles were examined in 68 patients with multiple sclerosis, 62 normal volunteers, and 13 patients with other neurological diseases. Plasma zinc levels were slightly increased in patients with multiple sclerosis and significantly increased in those with other neurological impairments (p less than 0.01), compared with control subjects. Albumin-bound as well as protein-bound zinc levels were normal in all groups tested. The alpha 2 macroglobulin-bound zinc level was significantly lower (p less than 0.01) in patients with multiple sclerosis than in control subjects. Erythrocyte-bound zinc levels were significantly increased (p less than 0.05) in patients with multiple sclerosis when compared with control subjects. Erythrocyte-bound zinc was normal in patients with other neurological impairments. Because erythrocyte-bound zinc levels are relatively independent of daily fluctuations in dietary zinc intake, an increase in these values may suggest alterations in the control mechanisms governing zinc compartmentalization in patients with multiple sclerosis.

Blood Proteins