Biomedical subjects

E F Lampeter

Publications and source records attributed to E F Lampeter.

25 records · Page 2Linked to original sources

PubMed1992

Immunotherapy with ciamexon in the non obese diabetic (NOD) mouse.

Ciamexon (CMX), a new immunomodulatory compound acting mainly on B-lymphocytes was given orally to 42 NOD mice divided into three sex and litter matched groups (A: 0.3 mg/mouse/day CMX, B: 1.5 mg/mouse/day CMX, C: control) from 7 weeks of age. Animals were followed up for evaluation of diabetes incidence up to 32 weeks of age. There was a tendency for a delayed onset of hyperglycemia in mice of group B up to 26 weeks of age; however no significant difference in the cumulative incidence of diabetes at 32 weeks of age was observed (A: 57.5%, B: 38.5%, C: 38.5%). No differences were found in the number of infiltrated islets in animals culled at 10 weeks of age treated with CMX from 4 weeks of age. We conclude that CMX does not modify the course of insulitis and diabetes incidence in NOD mice although though the appearance of glycosuria was delayed by this treatment.

Adjuvants, Immunologic↗

PubMed1990

Raised temperature reduces the incidence of diabetes in the NOD mouse.

An association between the incidence of childhood Type 1 (insulin-dependent) diabetes mellitus and the average yearly temperature in different countries has been reported, the incidence being higher in countries with a lower mean temperature. We have studied the effect of environmental temperature on the incidence of diabetes in an animal model of Type 1 diabetes, the non-obese diabetic (NOD) mouse. Female NOD mice were divided at weaning, with one group placed at a higher temperature (mean 23.7 +/- 1.7 degrees C) and the other at a lower temperature (21.0 +/- 1.8 degrees C). At 20 weeks of age 6 of 16 mice at lower temperature and 1 of 17 mice at higher temperature had developed diabetes (p less than 0.02); at 30 weeks 10 of 16 and 5 of 17 mice had developed diabetes (p less than 0.05). Non-diabetic animals in the low temperature group had a higher food intake than those in the high temperature group between 13-15 weeks of age (28.0 +/- 1.2 g/week vs 24.8 +/- 0.7 g/week, p less than 0.05). In a parallel experiment, histological examination showed that there were similar degrees of insulitis in the high and low temperature groups at seven weeks of age. We conclude that environmental temperature can affect the incidence of diabetes in the NOD mouse and that this may be related to alterations in food intake.

Animals↗

PubMed1989

Lessons from the NOD mouse for the pathogenesis and immunotherapy of human type 1 (insulin-dependent) diabetes mellitus.

Suitable animal models of human Type 1 (insulin-dependent) diabetes mellitus have long been sought, in particular a model that would permit detailed histological and immunological investigation of changes in the islet preceding the metabolic disorder. This would allow hypotheses as to pathogenesis of the condition to be examined and interventions such as immunotherapy to be tested. The most widely studied models include the low-dose streptozotocin induced diabetic mouse and the BB rat, but both differ in important respects from the human disease. In this review we describe one highly successful model, the non obese diabetic mouse. Selected aspects of pathogenesis and immunotherapy are presented and analogies with human Type 1 diabetes discussed.

Animals↗

PubMed1987

A follow-up study of cell-mediated cytotoxicity and beta cell function in type I diabetes.

In 20 patients with a newly diagnosed type I diabetes mellitus a cytotoxic effect of blood lymphocytes against beta cells of the pancreas of neonatal rats could be demonstrated. This effect remained nearly unchanged during the first 12 months of control. During the course up to 18 months, the cytotoxicity decreased significantly. After stimulation with glucose and glucagon, a C-peptide secretion was demonstrated in all patients during the first 12 months but it decreased thereafter. The follow-up study showed cell-mediated immune reactions against beta cells in type I diabetics as long as the existence of beta cells can be assumed on the basis of functional tests. Thus the immune process seems to depend on the presence of the specific antigen.

Adolescent↗

PubMed1987

Ultrastructure of lymphocyte subsets and of activated lymphocytes in type 1 diabetes as defined by monoclonal antibodies and the immunogold technique.

The ultrastructure of peripheral blood lymphocyte subsets and activated lymphocytes from 5 patients with recent onset insulin-dependent diabetes as identified by monoclonal antibodies (CD4, CD8 and 4F2) and labelled with gold coupled goat anti-mouse IgG are described and depicted. Electron microscopy revealed no differences in appearance between investigated lymphocyte subsets at the single cell level. Activated lymphocytes as defined by an early activation antigen (4F2) do not always have a characteristic appearance nor do they show morphological signs of activation in all cases. We would conclude that it is not possible to recognize different lymphocyte subsets based only on their ultrastructure.

Antibodies, Monoclonal↗

PubMed1986

Cell-mediated immune reactions against B cells and defect of suppressor cell activity in type 1 (insulin-dependent) diabetes mellitus.

A cytotoxic effect of peripheral blood mononuclear cells from 22 out of 23 newly diagnosed Type 1 (insulin-dependent) diabetic patients against B cells of isolated rat islets was demonstrated. The addition of peripheral blood mononuclear cells from healthy subjects reduced the cytotoxic effect in 9 out of 10 patients. The addition of peripheral blood mononuclear cells from other diabetic patients was without significant effect in 14 out of 16 cases. The results indicate functional abnormalities of peripheral blood mononuclear cells in newly diagnosed Type 1 diabetes. Beside cytotoxic effects against B cells, a defect in the suppressor function seems to exist. The activation of T-lymphocytes might be a consequence of such a defect.

Adolescent↗

PubMed1984

Simultaneous biochemical and morphological investigations on the effect of leukocytes from type I diabetics on isolated rat islets.

The first morphological and biochemical findings on the effect of leukocytes from a newly diagnosed type I diabetic patient on isolated rat islets are presented. Leukocytes from venous blood were co-incubated with isolated neonatal rat islets for 22 h. According to the biochemical and electron-microscopical findings, beta cells localized in the periphery of the islets and a few single beta cells show lytic alterations (single cell necroses). The electron micrographs suggest that the beta cells were lysed after contact with lymphocytes or lymphoid cells from the diabetic patient (target cell reaction). The simultaneous biochemical and morphological investigations reveal that after beta cell lysis, insulin released in a granular state can be phagocytosed by granulocytes and thus escape the estimation of insulin concentration in the medium.

Animals↗