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Biomedical subjects

C E Finch

Publications and source records attributed to C E Finch.

At least 217 records · Page 12Linked to original sources
PubMed1976

The regulation of physiological changes during mammalian aging.

Much evidence suggests that intrinsic molecular or cellular aging mechanisms need not be invoked to explain most age-related cellular changes and pathologcical conditions. Analysis of a widely scattered literature indicates that hormones and neural factors regulate a great number of cellular aging phenomena of mammals. It is proposed that age-related changes after maturation result from an extension of the neural and endocrine mechanisms that control earlier development and that produce a regulatory cascade of changing neural, endocrine, and target-tissue interactions.

Aging↗
PubMed1976

Hepatic glucocorticoid binders in mature and senescent C57BL/6J male mice.

Because of prominent age-related changes in the responses to stress and in steroid metabolism and excretion, the effect of age on fractionated liver glucocorticoid-binding proteins was studied in C57BL/6J male mice. When cytosol, pre-labeled with [3H]corticosterone, was chromatographed on Sephadex G-100, 4 peaks were obtained. Peak 1 (excluded), peak 2 (corresponding to plasma transcortin), and peak 3 corresponding to glucocorticoid receptors isolated from nuclei) showed no significant age differences. This finding is consistent with reports that glucocorticoid-mediated induction of hepatic tyrosine aminotransferase is not altered by aging in rodents. However, there was a striking age-related decrease (80%) in peak 4 (apparent MW 29,000). Competition studies imply that peak 4 binds aldosterone, testosterone, progesterone, and corticosterone (delta4-3-keto steroids), but not estradiol or dt a plasma component. Although the function of peak 4 is not identified, the pattern of highest competition with delta4-3-keto steroids suggests that it is a steroid ring "A" reductase.

Adrenalectomy↗
PubMed1975

Ageing and dopamine uptake by subcellular fractions of the C57BL/6J male mouse brain.

The uptake of dopamine (DA) by synaptosomes from the hypothalamus and striatum was reduced in healthy ageing mice at DA concentrations below 10(-7) M. Kinectic analysis indicates that ageing increases the Km of high affinity DA uptake processes by about 35%, but does not alter alter Vmax. l-Tyrosine and serotonin uptake at low concentrations was unaltered by ageing in the striatum and hypothalamus; no changes of L-norepinephrine uptake were found in the hypothalamus. We conclude that ageing may selectively affect DA uptake processes by neuronal membranes.

Aging↗
PubMed1975

The use of ammonium acetate in the precipitation of ribonucleic acid.

Ammonium acetate (0.24M) in combination with cold 66% (v/v) ethanol quantitatively precipitated RNA from very dilute solutions (greater than or equal to mug/ml) after centrifugation for 2.5 X 10(6)g-min. There was also less co-precipitation of detergents with ammonium acetate than NaCl.

Animals↗
PubMed1975

Aging and the passage of L-tyrosine, L-DOPA, and inulin into mouse brain slices in vitro.

The effect of age on active transport of catecholamine precursors was studied in a healthy population of mature (12-mo.-old) and senescent (30-mo.-old) C57BL/6J male mice. No age differences were observed in uptake of L-(3H)-tyrosine IN VITRO by slices of hypothalamus, brain stem, and striatum at external concentrations equal to or greater than blood levels. However, age-related reductions were observed intermittently in the hypothalamus, brain stem, and striatum at very low concentrations of tyrosine (less than 10 pg/ml). No age differences were observed in incorporation of L-(3H)-tyrosine into hypothalamic proteins when corrected for intracellular uptake of L-(3H)-tyrosine. No age differences were observed in uptake of L-(3H)-DOPA. The possible contribution of age-related changes in extra-cellular space to decreased uptake was determined to be negligible by wash-out studies of tyrosine and by the uptake of inulin. A significant age-related increase of inulin uptake IN VITRO was observed under ionic conditions which minimize tissue swelling.

Aging↗
PubMed1975

Norepinephrine uptake by the mycoardium of the senescent mouse in vitro.

Age-related delays in the uptake of norepinephrine (NE) by the rat myocardium were observed after subcutaneous injection of NE (Gey, Burkard, and Pletscher, 1965). We report here that in vitro uptake of 3H-NE by myocardial slices from healthy C57BL/6J male mice is not impaired by aging (8-28 mo.) at 0.1 ng/ml, 2.0 ng/ml, 1000 ng/ml of NE. Additionally, no age-related changes of inulin space in myocardial slices were observed. Hence, the delayed uptake observed in vivo by Gey et al. may be attributed to age-related changes in the absorption from the subcutaneous site.

Aging↗
PubMed1975

Plasma testosterone levels in C57BL/6J male mice: effects of age and disease.

Plasma testosterone (T) was measured by radioimmunoassay in both healthy and diseased, mature (8-11 months) and senescent (29-31 months) C57BL/6J male mice. Pathological lesions in diseased mice included reticulum cell sarcoma and enlarged mesenteric lymph nodes. In healthy mice neither plasma T nor testicular weight differed between age groups. Median levels and 95 percentiles of plasma T in ng/ml were 1.12 (0.19-12.18) in mature mice and 1.17 (0-7.31) in senescent mice. In diseased mice testicular weight and the range of values of plasma T were significantly reduced. The marked decreased in plasma T and testicular weight in diseased senescent mice illustrates the importance of distinguishing between disease-related changes and effects of aging, per se.

Aging↗