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Biomedical subjects

J M Martin

Publications and source records attributed to J M Martin.

At least 163 records · Page 9Linked to original sources
PubMed1985

Cloned neoplastic cells from a chemically-induced rat glioma: immunocytochemical characterization.

A cell clone--A15 A5--derived from an N-ethyl-N-nitrosourea (ENU)-induced glioma in a BDIX rat has been maintained in vitro for over 50 passages. These cells, which produce tumours when injected intracerebrally into syngeneic rats, possess several features of neoplastic astrocytes. In the present study A15 A5 cells were found to express both glial fibrillary acidic protein and glutamine synthetase, thus confirming their astrocytic nature.

Animals↗
PubMed1985

Malignant fibrous histiocytoma in rats at sites of implanted millipore filters.

Soft-tissue tumors developing in rats at the site of implanted Millipore filters showed the structural, cytochemical, and biologic characteristics of the malignant fibrous histiocytomas occurring in man. Evidence from this tumor model suggests that malignant fibrous histiocytomas can arise from pluripotential mesenchymal stem cells which are not derived from the mononuclear/phagocytic system and that chronic inflammation and scarring may predispose to their development.

Animals↗
PubMed1984

A quantitative comparison of T-cell subsets in Hodgkin's disease and reactive hyperplasia. Frozen section immunohistochemistry.

Cryostat sections of lymph nodes from patients with Hodgkin's disease were stained with monoclonal antibodies reactive with T-cells including T-cell subsets. Lymph nodes showing reactive hyperplasia were used as controls. Using an eyepiece grid, the stained cells were counted and subset ratios determined. The ratio of helper T-cells to cytotoxic/suppressor T-cells, i.e., (formula; see text) in Hodgkin's disease was found to be significantly different from ratios obtained from reactive nodes. This difference may be explained by a relative increase in cytotoxic/suppressor T-cells and/or a decrease in helper T-cells. This finding may relate to the previously reported increase in suppressor cell activity in patients with Hodgkin's disease and may also correlate with diminished delayed-type hypersensitivity in such patients.

Adolescent↗
PubMed1984

Dietary protein: a trigger of insulin-dependent diabetes in the BB rat?

Animals from a colony of spontaneously diabetic insulin-dependent BB rats were fed from weaning with semi-synthetic diets in which natural proteins were replaced by l-amino acids with or without the addition of either milk or wheat proteins. The normal 50% incidence of diabetes in the colony was reduced to 15% in rats fed the basic semi-synthetic diet, while it was 35% and 52% when supplemented with gluten or milk, respectively. Thus, dietary factors might precipitate the expression of the disease.

Age Factors↗
PubMed1984

Hepoxilin, a new family of insulin secretagogues formed by intact rat pancreatic islets.

Isolated Krebs perifused rat pancreatic islets in the presence of 10 mM glucose convert 12S-HPETE into two hydroxy-epoxides, 8H-11,12-EPETE and 10H-11,12-EPETE for which we propose the name Hepoxilin A and B respectively. Hepoxilin A was investigated for its capacity to release insulin by this preparation. Insulin secretion by these cells, measured in the perifusate by radioimmunoassay, was dependent on the glucose concentration in the perifusing medium. Hepoxilin A dose dependently enhanced further the release of insulin during glucose (10 mM) stimulation (120 +/- 51% at 0.5 x 10(-6) M (n = 3) and 282 +/- 58% at 2.1 x 10(-6) M (n = 3) above control). These results suggest that Hepoxilin A (and possibly also Hepoxilin B) could be the active intermediate(s) involved in the potentiation of glucose dependent insulin secretion by both arachidonic acid and 12-HPETE.

8,11,14-Eicosatrienoic Acid↗
PubMed1984

Starvation-induced changes in insulin binding to hypothalamic receptors in the rat.

In order to determine whether insulin binding to receptors in the central nervous system can be modified by changes in energy balance, hypothalami from 48 h food deprived and 14 day food restricted (8 or 4 g chow/day) rats were removed and insulin binding to partially purified membranes from both medial and lateral hypothalamic regions was studied. Hypothalamic insulin concentration was measured in similarly treated animals. Although hypothalamic insulin concentration did not vary, insulin binding to lateral receptors was significantly lower than that obtained from the medial region. After prolonged food restriction, binding to medial receptors was significantly reduced in comparison to controls, whereas binding in the lateral region remained unchanged; differences were most pronounced at near-physiological insulin concentrations. Changes in per cent specific [125I]insulin binding were associated with corresponding changes in maximal insulin-binding capacity, the latter being inversely related to receptor affinity for this hormone. These results are consistent with the hypothesis that insulin, acting via hypothalamic receptors, may serve as a metabolic feedback signal linking the periphery with central body weight regulatory mechanisms.

Animals↗
PubMed1984

Failure of chronic experimental hyperinsulinism to alter insulin binding to hypothalamic receptors in the rat.

We have previously shown that [125I]insulin binding to medial hypothalamic receptors is attenuated following 14 days of food restriction. Such rats are characterized by considerably reduced circulating insulin levels with unchanged hypothalamic insulin concentration. The present data demonstrate that, in contrast to the effects of starvation, [125I]insulin binding to hypothalamic receptors from rats made hyperinsulinaemic by daily injections of protamine zinc insulin (4-6 U/rat/day for 14 days) is unaffected by this manipulation, even though hypothalamic insulin concentration in insulin-injected animals was significantly higher than in saline-injected controls. Insulin binding to partially purified membranes from the medial hypothalamic region was significantly greater than that from the lateral area, confirming a finding in our earlier study. Insulin treatment was associated with slight reductions in maximal insulin-binding capacity of medial hypothalamic receptors, a tendency which appeared to be compensated by reciprocal changes in receptor affinity for this hormone. The data indicate that hypothalamic insulin receptors are not regulated by peripheral or even central insulin levels per se; it appears, rather, that some other, as yet unidentified, correlate(s) of significantly altered food intake and/or body weight can modify hypothalamic insulin receptor function. Perhaps such modifications could, in turn, participate in the activation of regulatory mechanisms involved in correcting energy imbalance.

Animals↗
PubMed1984

Fetal deformation caused by uterine malformation.

Two fetuses are described in whom deformation was caused by uterine malformation (bicornuate uterus). It is necessary to distinguish between fetal malformation and deformation, since the latter type of anomaly indicates that the uterine environment is distorted. Correction of this uterine malformation can significantly improve the prospects for future pregnancies.

Adult↗
PubMed1983

Partial purification of an insulin-releasing activity in human serum.

An activity that enhances insulin release from perifused rat pancreatic islets has recently been isolated from human serum fractions (molecular weight 1,000-5,000 daltons). To characterize this activity we have studied the insulin-releasing effect of serum subfractions from obese and non-obese children obtained by reversed-phase high-performance liquid chromatography (HPLC). The serum insulin-releasing activity eluted in the HPLC system at 12-13 minutes, which corresponded to the retention time of the tridecapeptide insulin-glucagon liberin isolated from bovine hypothalamus. Insulin-releasing activity was found in serum subfractions from both obese and normal-weight children. The relative insulin-releasing potency of the active subfractions was higher than that of the original total serum fractions, indicating the presence of some substance(s) which inhibit insulin secretion in the total serum fractions. Oral glucose loading increased the relative insulin-releasing activity in the HPLC subfractions from obese children. This study suggests that the insulin secretagogue in human serum might be identical to hypothalamic insulin-glucagon liberin as these substances behave similarly on reversed-phase HPLC and have parallel insulin-releasing properties.

Animals↗
PubMed1983

[Articular manifestations in leprosy].

Articular manifestations occur in approximately 1% of cases of leprosy, sometimes at onset. They consist in a highly inflammatory polyarthritis, fairly similar to that seen in rheumatoid polyarthritis. They often herald a reactive leprous exacerbation and are dependent upon immunologic disturbances in brittle leprosy (mainly lepromatous). Joint pain should be differentiated from neurologic pain resulting from peripheral neuropathy which is often concomitant. Leprosy should be considered among the causes of polyarthritis, especially in immigrants, but also in residents who have travelled to areas where leprosy is endemic.

Adult↗
PubMed1983

Lipolytic activity in brown adipocytes during spontaneous weight cycles in dormice.

In vitro release of glycerol from isolated brown adipocytes into incubation medium was measured using axillary brown adipose tissue (BAT) removed from dormice during various phases of the infradian body weight cycle. Lipolytic activity in BAT was reduced during the weight loss phase in comparison to the weight gain phase. In the absence of deep and prolonged torpor, BAT does not appear to act as an effector of weight loss for hibernators undergoing large cyclical fluctuations in body energy content.

Adipose Tissue, Brown↗
PubMed1983

Spontaneous obesity and weight loss: insulin action in the dormouse.

Dormice (Glis glis) undergo spontaneous cyclic changes in food intake and body weight. These infradian cycles with a periodicity of about 2 mo are endogenously controlled, since they persist in conditions of constant temperature and photoperiod. To evaluate the role of insulin as an effector of hyperphagia and fattening in dormice, experiments were conducted to study pancreatic function and adipose tissue metabolism during several phases of the infradian cycle. During the weight loss phase, peripheral insulin resistance occurs in the absence of hyperinsulinism. This resistance is not corrected by weight loss. Weight loss phase animals showed poor glucose tolerance and an impaired in vitro glucose-stimulated insulin secretion; these were not attributable to reduced pancreatic insulin content. Although basal glucose transport and basal, as well as insulin-stimulated, glucose utilization in isolated adipocytes were depressed during the weight loss phase, insulin-stimulated transport was significant. The data offer no evidence that insulin has a direct causal role in the development of spontaneous obesity in this species.

Adipose Tissue↗
PubMed1983

Spontaneous obesity and weight loss: insulin binding and lipogenesis in the dormouse.

Obese dormice (Glis glis) become anorexic during the weight loss phase of the 2-mo (infradian) body weight cycle. We have shown previously that this phase is characterized by severe insulin resistance, manifested by impaired insulin-stimulated glucose utilization in isolated adipocytes. Contrary to other obesity models, the insulin resistance was not accompanied by hyperinsulinism. In the present study, impaired lipogenesis was associated with decreased maximal insulin-binding capacity (due to a reduction in receptor concentration) and a postreceptor defect, which were exacerbated rather than attenuated during weight loss.

Adipose Tissue↗