No association between islet cell antibodies and coxsackie B, mumps, rubella and cytomegalovirus antibodies in non-diabetic individuals aged 7–19 years

Viral antibodies were tested in a cohort of 44 isletcell antibody-positive individuals age 7–19 years, and 44 of their islet cell antibody-negative age and sex-matched classmates selected from a population study of 4208 pupils who had been screened for islet cell antibodies. Anti-coxsackie B1-5 IgM responses were detected in 14 of 44 (32%) of the islet cell antibody-positive subjects and in 7 of 44 (16%) control subjects. This difference did not reach the level of statistical significance. None of the islet cell antibody-positive subjects had specific IgM antibodies to mumps, rubella, or cytomegalovirus. There was also no increase in the prevalence or the mean titres of anti-mumps-IgG or IgA and anti-cytomegalovirus-IgG in islet cell antibody-positive subjects compared to control subjects. These results do not suggest any association between islet cell antibodies, and possibly insulitis, with recent mumps, rubella or cytomegalo virus infection. Further studies are required to clarify the relationship between islet cell antibodies and coxsackie B virus infections

Use of the artificial B-cell (Biostator) in improving insulin therapy in unstable insulin-dependent diabetes

The present study was designed to improve the conventional subcutaneous insulin treatment of labile insulin-dependent diabetic patients by means of the artificial B-cell (Biostator) during a combination of conventional treatment and a glucose-controlled insulin infusion. Eleven patients with no residual B-cell function and poor metabolic control were studied. All patients were treated as effectively as possible by conventional methods using a combination of regular and intermediate insulin under clinical conditions. In order to determine the inadequacy of previous insulin treatment, all patients were connected to the Biostator, and the profile of daily physical activity was simulated using a bicycle ergometer. Metabolic control was compared during a 6-day period before and after a 30-50-h connection to the artificial B-cell. Using a preselected blood glucose level of 80 mg/dl (4.44 mmol/L), the additional insulin requirement amounted to 45.5 +/- 11.1 U/24 h (N = 6). The day after connection to the artificial B-cell, the patients received a new insulin regimen according to the additional insulin delivery determined by the Biostator. No better metabolic control was achieved and frequent hypoglycemic episodes occurred in this group. Another group (N = 5) was therefore studied at a preselected blood glucose level of 130 mg/dl (7.22 mmol/L). The mean additional insulin delivery by the Biostator was lower (17.2 +/- 2.1 U/24 h; P less than 0.05) and all patients were significantly better equilibrated after the new insulin regimen derived from data given by the Biostator. The ratio of short-acting to intermediate-acting insulin was 3:1; 40% of the total dosage was given in the morning. This study demonstrates that using the Biostator in addition to subcutaneous insulin allows determination of the amount of additional regular insulin that should be administered to improve glycemic control in labile diabetes

Effects of Dehydroepiandrosterone Sulfate on the Evoked Cortical Activity of Controls and of Brain-Injured Rats

Dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) are sex hormone precursors which exert marked neurotrophic and/or neuroprotective activity in the central nervous system (CNS). In the present electrophysiological experiments, we studied the effects of peripherally administered DHEAS on responses of the primary somatosensory (SSI) and motor cortices (MI) of (i) anesthetized controls and (ii) MI focal cold-lesioned rats. (iii) The effects of DHEAS on the field excitatory postsynaptic potentials (fEPSPs) were also studied in vitro brain slices. DHEAS (50 mg/kg) was injected subcutaneously 12 h before and immediately after cold lesion induction. The anesthetized rats were fixed in a stereotaxic frame, the SSI and MI were exposed, and control SSI and MI responses were evoked by contralateral whisker pad stimulation. After registration of the evoked responses for a 35-min period, a copper cylinder (2 mm in diameter) cooled with a mixture of acetone and dry ice (-78 degrees C) was applied to produce a lesion in the MI and the registration of the evoked responses was then continued for an additional 360 min. In the controls, DHEAS administration resulted in slight increases in amplitude of both the SSI and the MI responses. After focal cold lesion induction, the most significant reduction in amplitude was observed at the focus of the lesion in the primary MI, but the amplitudes of the SSI responses were also decreased. After 3-5 h of lesion induction, the amplitudes started to increase around the injury in the primary MI, while the SSI response had already started to recover 2 h after induction of the MI lesion. In the course of the postlesion recovery period, the MI responses peripherally to the center of the lesion frequently exhibited extremely high and low amplitudes. The paired-pulse paradigm revealed changing, but basically high levels of disinhibition and facilitation in extended cortical areas after focal cortical cold lesion induction. The deviations (e.g., the extremely augmented responses) in cortical functioning of the anesthetized rats were unambiguously diminished by DHEAS administration, and the period required for the cortical responses to recover was significantly shorter after the steroid treatment. In the in vitro studies, however, DHEAS administration resulted in an enhanced level of disinhibition in extended cortical areas of both the hemispheres. This observation draws attention to the possible differences between the results obtained in different models (in vitro vs. in situ). Nevertheless, all the presented data suggest that DHEAS treatment might have neuroprotective effect on the neocortex at least at a short-time scale