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Biomedical subjects

J Krug

Publications and source records attributed to J Krug.

At least 55 records · Page 3Linked to original sources
PubMed1992

Intraocular pressure determination in infants with severe retinopathy of prematurity.

We determined intraocular pressure (IOP) in 55 premature infants (122 determinations) with stage V retinopathy of prematurity (ROP) by applanation and indentation tonometry corrected for scleral rigidity and found a modest correlation of r = 0.52 between readings. Chronologic age and the scleral rigidity coefficient were the most significant factors affecting the closeness in readings. Our findings suggest that the applanation method of obtaining IOP values is preferable in infants with ROP because this method is less affected by technical error and the variable nature of premature infant sclera. Frequent examination may be necessary to detect an early IOP increase, especially in infants who have had successful retinal reattachment through vitreoretinal techniques.

Child, Preschool↗
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↗
PubMed1991

Identification of cells responsible for the suppression of anti-beta-cell cytotoxicity in type I (insulin-dependent) diabetes mellitus.

Peripheral blood mononuclear cells (PBMC) from newly diagnosed type I diabetic patients induced a significantly higher cytotoxic insulin leakage from isolated rat islets during a 20-h incubation. compared with PBMC from healthy controls (13.9 +/- 7.7 versus 2.6 +/- 3.2 ng insulin/islet/20 h). The addition of PBMC from healthy subjects in a ratio of 1:4 suppressed the cytotoxic effect (13.9 +/- 7.7 to 6.7 +/- 4.4 ng insulin/islet/20 h). Depletion of CD8+ T lymphocytes from the PBMC of healthy subjects abolished their suppressive capacity, while depletion of CD4+ T lymphocytes and pre-incubation with CD3 monoclonal antibodies had no effect.

Adolescent↗
PubMed1991

Parathyroiditis in the non-obese diabetic mouse--a new finding.

Autoimmune reactions to parathyroid cells have been observed in human autoimmune polyendocrinopathy, but such findings have not been described in animal models of polyendocrine autoimmunity. We report here three cases of lymphocytic infiltrations in 12 parathyroid glands identified in a total of 18 thyroid glands studied in the non-obese diabetic (NOD) mouse. The majority of parathyroid-infiltrating lymphocytes possessed the helper/inducer phenotype as defined by the L3T4 monoclonal antibody. Parathyroiditis was accompanied by lymphocytic thyroiditis only on one occasion, whereas in other cases of thyroiditis, lymphocytic infiltration of the parathyroid was undetectable. We conclude that parathyroiditis in the NOD mouse is part of the wide spectrum of autoimmunity observed in this animal model of diabetes.

Animals↗
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↗
PubMed1990

Lymphocyte transfusion in recent onset type I diabetes mellitus--a one-year follow-up of cell-mediated anti-islet cytotoxicity and C-peptide secretion.

In 19 patients with newly diagnosed Type I diabetes mellitus a single transfusion of 1.9 x 10(9) to 1.5 x 10(10) lymphocytes was performed. Fifteen Type I diabetic patients who did not receive a transfusion were used as controls. Anti-beta-cell cell-mediated cytotoxicity was measured using an insulin release assay. Stimulated C-peptide secretion (100 g glucose orally, 1 mg glucagon i.v.) was used to estimate residual beta-cell function. Both parameters were measured prior to transfusion and after 12 months. The transfusions were followed by a fall of cytotoxicity below the 95% confidence limit of the controls in 11 of the 19 patients ('responders') (15.7 +/- 1.7 ng insulin/islet/20 h vs 6.7 +/- 1.3 P less than 0.001), while the other eight transfused patients ('non-responders') (13.5 +/- 1.9 vs 17.1 +/- 2.9, ns) and the non-transfused control patients (11.6 +/- 1.1 vs 14.2 +/- 2.4, ns) displayed persistently high cytotoxicity levels. In the responder group a slight improvement in stimulated C-peptide secretion was observed (136 +/- 43 pmol/dl vs 148 +/- 38, ns) whereas in the non-responder (127 +/- 28 vs 106 +/- 25, ns) and in the control group (130 +/- 17 vs 97 +/- 19, P less than 0.05) the stimulated C-peptide responses declined during the 12-month follow-up. Thus, lymphocyte transfusion may have beneficial effects by suppressing anti-beta-cell cytotoxicity and preserving C-peptide secretion.

Adolescent↗