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Biomedical subjects

M H Snow

Publications and source records attributed to M H Snow.

At least 73 records · Page 4Linked to original sources
PubMed1977

Evidence for dopaminergic control of thyrotrophin secretion in man.

After administration of the dopamine-receptor-blocking drug, metoclopramide (10 mg orally), there is significant release of thyrotrophin (T.S.H.) in hypothyroid patients which is not evident in euthyroid subjects. This is not due to spontaneous fluctuation in basal T.S.H. levels, and it indicates inhibitory dopaminergic control of T.S.H. release in man. The lack of significant T.S.H. release in euthyroid subjects may be due to the inhibitory effects of normal circulating levels of T3 and T4 on T.S.H. release. The T.S.H. response in hypothyroidism is significantly correlated with both T3 and T4 levels, suggesting suppression of this inhibitory pathway in increasingly severe hypothyroidism.

Administration, Oral↗
PubMed1977

Myogenic cell formation in regenerating rat skeletal muscle injured by mincing. I. A fine structural study.

The degenerative and early regenerative events following mincing and autotransplantation of rat skeletal muscle were examined at the ultrastructural level. During the first eight hours after injury, myonuclei undergo pyknosis, mitochondria become enlarged and vesiculated, myofilaments appear less distinct than normal and the sarcolemmata either disappear or become extensively fragmented. Further degeneration of the myofibers progresses slowly until macrophages and polymorphonuclear neutrophils invade the degenerating sarcoplasm between one to four days after mincing. Scattered throughout the minced muscle implant during the first 24 hours after injury are small, viable-appearing, undifferentiated cells located between the external lamina and degenerating sarcoplasm. Such cells, which are structurally similar to satellite cells seen in uninjured muscle, are believed to be regenerating presumptive myoblasts due to their mesenchymal-like morphology and sublaminar position. External laminae of the injured muscle fibers do not undergo immediate degenerative changes, but rather persist during the first three to six days as laminar tubes within which spindle-shaped myoblasts and newly formed myotubes are frequently observed. Examples of regenerating myoblasts in the process of budding-off from damaged muscle fibers were not observed in this study. Therefore, the evidence suggests that satellite cells are the major source of regenerating myoblasts in skeletal muscle of the rat.

Animals↗
PubMed1977

Myogenic cell formation in regenerating rat skeletal muscle injured by mincing. II. An autoradiographic study.

Myonuclei and satellite cell nuclei were differentially labelled with 3H-thymidine in uninjured skeletal muscle of young rats and then traced autoradiographically at intervals after mincing the radioactive hindlimb muscles to determine the source of regenerating presumptive myoblasts. Labelled nuclei were detected by light microscopic examination of 1-micron thick autoradiographs and identified by electron microscopic examination of an adjacent section. Repeated injections of 3H-thymidine during fetal and neonatal development, followed by a 4- to 5-week maturation period, resulted in labelling of 20% of the myonuclei. Satellite cells were not observed to be labelled in this series. Eight to sixteen hours after mincing, 20% of the pyknotic myonuclei were labelled, whereas none of the regenerating presumptive myoblasts appeared labelled. A single injection of 3H-thymidine administered to 18-day-old rats, followed by sacrifice within ten hours, resulted in labelling of 23% of the satellite cell nuclei. Myonuclei were not observed to be labelled in this series. Eight to sixteen hours after mincing, silver grains were detected over both pyknotic and regenerating cell nuclei. These experiments indicate that many satellite cells survive muscle injury and transplantation to become regenerating myogenic cells at a time when most, if not all, myonuclei are undergoing pyknosis.

Animals↗
PubMed1977

An investigation into the pathogenesis of hypertension in acromegaly.

1. In 29 patients with acromegaly, plasma renin activity and growth hormone were measured during fasting and recumbency on free diet. Exchangeable sodium was measured in all cases and expressed as a percentage of the expected value on the basis of lean body mass. 2. Twenty-two control subjects without evidence of cardiovascular, renal or endocrine disease were studied in the same way. 3. There was a significant increase in exchangeable sodium and suppression of plasma renin activity in the acromegalic patients in comparison with control subjects. 4. There was a significant positive correlation between exchangeable sodium and plasma growth hormone. 5. Hypertensive acromegalic patients (diastolic blood pressure larger than or equal to 100 mmHg) tend to have a lower (although not significantly so) exchangeable sodium than normotensive subjects. 6. We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly.

Acromegaly↗
PubMed1976

Actions of growth hormone-release inhibiting hormone (somatostatin) on the renin aldosterone system.

Administration of growth hormone-release inhibiting hormone (GH-RIH, somatostatin), as a 90 minute infusion (10 mug/min), to 3 healthy young men under conditons of active renin secretion acheived by pretreatment with furosemide (80 mg daily for 5 days), caused a mean 30% fall in plasma renin activity, which returned to basal levels immediately after stopping the GH-RIH infusion. Plasma aldosterone levels were not affected during the course of this experiment.

Adult↗
PubMed1976

The immediate postimplantation development of tetraploid mouse blastocysts.

The development during and immediately after the implantation period of 143 tetraploid blastocysts was studied both in vitro and in vivo; 58-7% in vitro and 38-8% in vivo were found to exhibit the changes associated with the early implanting blastocyst, i.e. giant cell transformation of the trophoblast and induction of the decidual cell reaction in the uterus. Of these 38-7% in vitro and 19-4% in vivo showed evidence of inner cell mass function during this time but only two in each system could be claimed as showing normal development. Examination of the developing blastocyst leads to the conclusion that lack of cell numbers in the inner cell mass is the most likely reason for the poor development of tetraploid embryos and suggests that the minimum number of ICM cells required to fulfil its role in embryogenesis is between four and eight.

Animals↗
PubMed1975

The development of trophoblast in vitro from blastocysts containing varying amounts of inner cell mass.

When intact mouse blastocysts are cultured in vitro in medium supplemented with foetal calf serum, trophoblast cells proliferate and undergo giant cell transformation such as occurs in vivo. If the amount of inner cell mass in the blastocyst is decreased by culture with [3H]-thymidine then giant cell transformation occurs normally but proliferation is reduced. In the absence of inner cell mass no proliferation occurs, and giant cell transformation is more rapid than in undamaged blastocysts.

Animals↗
PubMed1975

Embryonic development of tetraploid mice during the second half of gestation.

A small proportion (about 17%) of experimentally produced tetraploid blastocysts are capable of postimplantation development in the randomly bred Q strain of mice. Four newborn mice, three of which were confirmed as tetraploid, were produced but all were eaten by their mother within a few hours of birth. Studies on the embryonic development of tetraploid mice reveal a variety of developmental abnormalities, especially during the later stages of gestation. At 14 1/2 and 16 1/2 days, tetraploid embryos weigh significantly less than corresponding stage diploids, especially so if litter size is taken into account. Histologically, aberrations are found in many different tissues with a clear hierarchy of susceptibility shown among the organs. For instance, yolk-sac-derived blood, and gonads, are invariably affected and the anterior end of the neural tube also seems to be particularly at risk. Possible explanations for the aberrant development are discussed and it is concluded that strictly genetic reasons can be ruled out and that physiological difficulties imposed by the increased size of tetraploid cells and/or problems produced by lack of cell numbers are instrumental in causing abnormal development. Using weight as a guide it is estimated that tetraploid embryos at 14 1/2 and 16 1/2 days gestation contain about one-quarter as many cells as similar stage diploids.

Abnormalities, Multiple↗