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Biomedical subjects

S Marshall

Publications and source records attributed to S Marshall.

At least 199 records · Page 11Linked to original sources
PubMed1980

Regulation of insulin receptors: evidence for involvement of an endocytotic internalization pathway.

Cultured human fibroblasts degrade insulin by a receptor-mediated process. When intracellular hormone degradation is inhibited by chloroquine, 125I-labeled insulin internalizes and accumulates intracellularly. In contrast, cultured IM-9 lymphocytes do not degrade receptor-bound insulin or accumulate 125I-labeled insulin in the presence of chloroquine. Insulin-induced receptor loss occurs in both cell types, and chloroquine inhibits this process in fibroblasts but not in IM-9 lymphocytes. Transglutaminase is a membrane-associated enzyme thought to mediate the process of ligand-induced receptor aggregation and internalization; levels of this enzyme were high in fibroblasts but barely detectable in IM-9 lymphocytes. Furthermore, dansylcadaverine--a potent inhibitor of transglutaminase--blocked insulin-induced receptor loss in fibroblasts but was without effect in IM-9 lymphocytes. These results support the concept that insulin receptor regulation is mediated via an endocytotic internalization pathway in human fibroblasts and that the mechanisms of this process differ among cell types.

Cadaverine↗
PubMed1980

Neoplasms of immunoregulatory T cells in clinical investigation.

Normal T cells play a critical role in the regulation of humoral immune responses by acting as potentiators (helper cells) or inhibitors (suppressor cells) of the process by which B cells differentiate into immunoglobulin-secreting plasma cells. Certain diseases in which malignant T cells appear to retain an immunoregulatory function are characterized by a propensity of a lymphomatous T-cell population to infiltrate skin. Some cutaneous T-cell lymphomas, as well as some T-cell neoplasms without dermatologic involvement, provide a homogeneous supply of T lymphocytes which act as immunoregulators. The availability of neoplastic T cells with immunoregulatory properties could accelerate the serologic and biochemical analysis of the cellular control of normal immunity in man.

Agammaglobulinemia↗
PubMed1980

Effects of insulin incubation on insulin binding, glucose transport, and insulin degradation by isolated rat adipocytes. Evidence for hormone-induced desensitization at the receptor and postreceptor level.

We have examined the effect of in vitro hyperinsulinemia on insulin binding, glucose transport, and insulin degradation in isolated rat adipocytes. When cells were incubated with insulin for 2 or 4 h at 37 degrees C, followed by washing in insulin-free buffer to remove extracellular and receptor-bound insulin, a time and dose-dependent decrease in insulin receptors was observed, which was accompanied by a reduced ability of cells to degrade insulin. Furthermore, the quantitatively predicted rightward shift in the insulin-glucose transport dose-response curve could be demonstrated. In addition to this reduction in insulin sensitivity, a striking decrease in maximal insulin-stimulated glucose transport was observed in the 4-h insulin-treated cells, indicating an abnormality distal to the insulin receptor. Thus, in vitro insulin-induced insulin resistance in adipocytes is caused by both receptor and postreceptor abnormalities. The post-receptor defect is most likely at the level of the glucose transport system per se because the insulinlike agents, spermine and antiinsulin receptor antibodies, also had a markedly reduced ability to stimulate glucose transport in 4-h insulin-treated cells. On the other hand, when cells were incubated with 100 ng/ml insulin for up to 4 h, after which time 2-deoxy glucose uptake was measured without removing buffer insulin or allowing receptor-bound insulin to dissociate, no decrease in maximal insulin-stimulated glucose transport was found. In conclusion, (a) insulin leads to a dose-dependent loss of insulin receptors in freshly isolated adipocytes accompanied by the predicted functional consequence of decreased receptors, i.e., a rightward shift in the insulin-glucose transport dose-response curve, (b) prolonged incubation with insulin causes a marked postreceptor defect in the glucose transport system, (c) maintenance of the activated state of the glucose transport system prevents the expression of the post-receptor defect, (d) the location of the postreceptor abnormality is most likely in the glucose transport system per se, and (e) insulin-induced receptor loss is accompanied by a decrease in insulin degradation.

Adipose Tissue↗
PubMed1979

Clinical experience with methylphenidate.

The indications for the use of methylphenidate in 250 children are reviewed, and the effect of the drug is examined. Concentration was improved or hyperactive behaviour diminished in 89% of the children with normal intelligence and with no gross physical defect, in 72% of the children with cerebral palsy, and 68% of the children with subnormal intelligence. In children with emotional disturbance, response to methylphenidate was seldom satisfactory. Significant side-effects occurred infrequently and only 2 children lost weight during the period of medication.

Adolescent↗
PubMed1979

Effects of hypophysectomy, thyroidectomy, and thyroxine on specific prolactin receptor sites in kidneys and adrenals of male rats.

The effect of T4 on specific PRL binding in the kidneys and adrenals was measured in intact, hypophysectomized, and thyroidectomized male rats. PRL binding in the kidneys was reduced from 12.1 +/- 1.1% in the intact group to 4.5 +/- 0.5% after hypophysectomy; 4-day replacement with T4 returned PRL binding to intact values. T4 administered to intact rats significantly increased PRL binding above intact values. Thyroidectomy reduced PRL binding in the kidneys from 14.9 +/- 1.2% to 7.0 +/- 0.6%, and T4 treatment restored PRL binding to intact values. PRL binding was measured at 2, 3, 5, 7, and 10 days after thyroidectomy in kidneys and found to decrease progressively from 8.2+/-0.5% in the intact rats to 2.3+/-0.3% on day 10. A single injection of T4 doubled PRL recetor binding in kidneys of thyroidectomized rats at 12 h and returned binding to intact levels at 24 h. In contrast to the effects of T4 on kidney PRL binding, adrenal PRL binding was only slightly altered by thyroidectomy and T4. These results suggest that T4 has a specific role in regulating PRL receptors in the kidneys but not in the adrenals. Since PRL receptors in the adrenals were only slightly altered by thyroid status, it is believed that the changes in kidney receptors represent a specific rather than a general metabolic effect of T4.

Adrenal Glands↗
PubMed1978

Effect of pesticides on testicular function.

Marked impairment of spermatogenesis was found in a group of men exposed to the pesticide 1,2-dibromo-3-chloropropane (DBCP), demonstrated by semen analyses, testicular biopsies, and hormone studies. The ramifications of the use of this pesticide are discussed.

Chemical Industry↗
PubMed1978

Transient fertility after vasovasostomy.

Sperm generally appear in the ejaculate within three weeks after vasovasostomy, but may soon disappear because of scarring of the anastomotic site. For this reason attempt at conception early after the operation should be encouraged.

Cicatrix↗
PubMed1978

Commercial fibrinogen, autogenous plasma, whole blood and cryoprecipitate for coagulum pyelolithotomy: a comparative study.

Coagulation pyelolithotomy provides an effective means to remove multiple calculi from the renal collecting system. The strength of the coagulum is directly proportional to the concentration of fibrinogen and inversely proportional to the concentration of thrombin. Because of the fear of hepatitis fibrinogen may soon be unavailable commercially. It will then become necessary to use plasma from the patient as the source of fibrinogen. By the process of cryoprecipitation fibrinogen levels can be increased about 10-fold, yielding clots of greater tensile strength than would be obtained from non-concentrated plasma.

Animals↗