A mathematical model predicting chromosome loss in cultured cells of young adults.
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Biomedical subjects
Publications and source records attributed to J M Martin.
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Using the chicken red blood cell assay, the human Chang liver cell assay, and a lymphoblastoid cell assay, mononuclear cells from asthmatics and normals were tested for antibody-dependent cellular cytotoxicity (ADCC) capacity. Mononuclear cell preparations from perennial nonallergic asthmatics with a history of asthma associated with viral infections had a reduced ADCC capacity in the chicken red blood cell assay, an increased ADCC capacity in the Chang liver cell assay, and normal ADCC capacity in the lymphoblastoid cell assay. The data also suggested that perennial nonallergic asthmatics had increased percentages of surface IgG-negative lymphocytes in the peripheral blood when compared to normals.
This study was undertaken to assess whether a hypothalamic extract has any direct metabolic action on adipose and muscle tissues. An acid bovine hypothalamic extract (HE) was tested for its effect on the utilization of D[U-14C]glucose by isolated rat adipocytes and rat hemidiaphragms. The HE was ineffective in stimulating the conversion of labeled glucose into CO2 and glycogen by rat hemidiaphragm. However, in isolated adipocytes, the HE had significant lipogenic activity. This lipogenic effect was independent of insulin and nonsuppressible by insulin antibodies. The dose-response curve was linear and saturable. That insulin and the HE were not additive at maximal concentrations suggests that they act through a common rate-limiting step, possibly a receptor site. Other hypothalamic substances tested (thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, and substance P) showed no lipogenic activity. Somatostatin (6 microgram/ml) was an insulin potentiator but only when preincubated with the fat cells. It is concluded that the hypothalamic regulation of body weight may be mediated by a neurohumoral mechanism affecting adipose tissue stores.
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Using a 51Cr-labeled, antibody-coated chicken red blood cell assay system, mononuclear cell and granulocyte preparations from infectious asthmatics, noinfectious asthmatics, and normal controls were tested for antibody-dependent cellular cytotoxicity (ADCC) capacity. The corrected cytotoxic indices of mononuclear cell preparations from infectious asthmatics were reduced (34 +/- 10 SD) as compared to noninfectious asthmatiics (47 +/- 7 SD) or normal controls (47 +/- 6 SD). Granulocyte preparations from infectious asthmatics and normal controls had a severity of the disease or in vivo drug treatment.
Evidence of a neurohumoral factor capable of stimulating insulin and glucagon secretion was found in perfusates from ventrolateral hypothalamus (VLH) of rhesus monkeys. The perfusates from the VLH were collected via push-pull cannulas and injected into the peripheral circulation. Increase in portal insulin and glucagon was observed following the injection of six different perfusates. The amount of insulin released from isolated rat islets incubated with perfusates was significantly increased at glucose concentrations greater than 5 mM. The perfusates from the VLH appear to have effects on insulin and glucagon secretion that are opposite those of somatostatin.
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Highly inbred male rats were made diabetic by subtotal pancreatectomy. After diabetes developed, the animals were transplanted with an average of 500 isolated islets, obtained from donors of the same sex and strain, into the portal vein. Groups of islet-transplanted diabetic rats were followed for periods of 3, 6, and 14 months, during which time the performance of the transplanted islets was investigated. Control animals were followed for similar period of time. The findings obtained from each experimental group were integrated so as to provide a continuous picture of the transplanted islet's behaviour from 2 weeks to 14 months post transplantation. To assess islet performance, normal, untreated diabetic, and transplanted animals were subjected to three stimulatory tests of insulin secretion: (1) oral glucose tolerance, (2) intravenous sulfonylurea, and (3) intraperitoneal L-arginine. Normal and transplanted rats were additionally subjected to one inhibitory test of insulin secretion, diazoxide (given orally). At the end of the study, control and experimental animals were killed, and morphological investigations were performed on liver and pancreas. Isotransplantation of islets in partially depancreatized diabetic rats resulted in the reversal of the condition. The transplanted islets were found to respond to physiologic and pharmacologic controls, although the characteristics of the responses were not identical with that of the normal intact islet. The results of this study have suggested that a functional development of the transplanted islets occurs.
The effects of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, substance P, somatostatin, and a partially purified hypothalamic extract on insulin secretion were tested both in vitro and in vivo. Only somatostatin and the hypothalamic extract affected insulin secretion. In vitro, somatostatin decreased glucose-stimulated insulin secretion by isolated islets and in vivo significantly reduced the rate of insulin output into the portal vein. The hypothalamic extract significantly stimulated insulin secretion in both systems. These effects in vivo were independent of glucose concentration. Islets preincubated for four hours responded better in vitro to the hypothalamic extract stimulation and the somatostatin inhibition.
This article deals with an attempt at evaluating the success of a drug-free narcotic treatment program in New York City through a follow-up study of 300 ex-clients of the program. Two hundred ex-clients out of the 300 target population were actually interviewed. The number of months the clients had remained in the treatment program was found to be a key factor in the outcome of the program. The length of time in the program was itself highly dependent upon the client's background: the higher the pretreatment pathology the lower the chance of treatment success.
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