Zur entstehung der immun-insulitis bei rinder-a-komponente und rinder-monokomponente-insulin-sensibilisierten mausen

Es wurde Untersuchungen an Mausen mit dem Rinder-Monokomponente-Insulin und der Rinder-a-Komponente durchgefGhrt, urn den Nachweis zu erbringen, ob das Monokomponente. Insulin oder die a-Komponente als ein Insulitis-erzeugendes Antigen dienen kann. Dabei wurden die Tiere mit den Substanzen, die jeweils mit Freund's complete adjuvant wiederholt verabreicht wurden, aktiv immunisiert und weiterhin untersucht auf eine dadurch bewirkte Insulitis. (1) Bei den mit dem Rinder-MonokomponenteInsulin sensibilisierten Gruppen kam die Insulitis bei 1 von 8 Fallen in der 20. Woche nach der ersten Sensibilisierung und bei 5 von 10 Fallen in der 28. Woche zur Erscheinung. (2) Bei den mit der a-Komponente behandelten Gruppen liet3 sich die Insulitis bei 0 von 9 Fallen in der 20. Woche nach dem Sensibilisierungsbeginn und auch bei 1 von 10 Fallen in der 28. Woche nachweisen. Diese Ergebnisse zeigen, dat3 das Monokomponente-Insulin als ein Insulitis-erzeugendes Antigen wirken kann. Dagegen war nur ein Fall von Insulitis befallen unter 19 Tieren, die mit der a-Komponente behandelt wurden.</p

Experimentelle erzeugung der immun. Insulitis bei mausen

Experimentelle Produktion der Immun-Insu1itis wurde aufgrund der aktiven Immunisierung der Mause vom dd-Stamm durch wiederholte Gabe vom rekristallisierten Rinderinsulin im Abstand von 4 Wochen unternommen. Wahrend der Zeitdauer vom 3. Tag bis zur 28. Woche nach der ersten Sensibilisierung wurden serologische sowie histo1ogische Untersuchungen an diesen Tieren vorgenommen. Dabei ergaben sich fo1gende Befunde: (1) Die Immunlnsulitis kam bei allen von 58 Fallen bis zu 16 Wochen nach dem Sensibilisierungsbeginn nicht zur Erscheinung, und trat bei 2 von 8 Fallen erst in der 20. Woche und dann bei 3 von 8 Fallen in der 28. Woche in die Erscheinung. (2) Kein signifikanter Unterschied bestand in Hinsicht des insulinverbindenden Antikorpertiters im Blut zwischen den Fallen mit und ohne Immun-Insulitis in der 20. Woche sowie in der 28. Woche. (3) 1m Zeitlauf gab es aber eine gute Koinzidenz zwischen der Entstehung der Immun-Insulitis und der Herabsetzung des Antikorpertiters im Blut. (4) Untersuchungen des Pankreas mit Hi1fe der direkten Fluoreszenz-Antikorpermethode ergaben keine erkennbare spezifische Fluoreszenz innerhalb der Langerhansschen Inseln. Diese Untersuchungsergebnisse liefern der Ansicht einen Beweis, da~ die Insulitis, die fUr den mensch1ichen Diabetes mellitus spezifisch ist, mindestens zum Teil durch einen immuno1ogischen Mechanismus entstehen konnte.</p

Pancreatic islet lesions of autoimmune origin, and ICA and ICSA.

CHBB male rats, 120-150 g in weight, were used both as animals to be sensitized and as donors of homologous islets as antigen. At no time did sensitized animals give a positive reaction for islet-cell antibodies or islet-cell surface bound antibodies at any of the dilutions tested. None of the frozen sections of the pancreas were positive for fluorescence specific for IgG or C3. Marked fibrosis and cell infiltration of pancreatic islets, a high degree of pyknosis of parenchymatous cells of islets, phagocytosis of fragmented islet cell nuclei by histiocytes, and a marked reduction in the number of beta cells were noted.</p

[Glucose tolerance abnormalities in mice actively immunized with components of bovine pancreatic hormones (author's transl)]

The relationship between immune insulitis and glucose tolerance was investigated in three groups of mice following active immunization with different components of bovine pancreatic hormone. An abnormal blood glucose level was observed in the three groups ranging from 33.3% to 87.5% of sensitized mice. A relationship was not present between the glucose tolerance response and the presence of insulitis or anti-insulin antibody in the blood of sensitized mice. However, all sensitized mice with a marked decrease in glucose tolerance were found to have insulitis. In animals without established insulitis and with no demonstrable anti-insulin antibody, abnormal glucose tolerance was noted. This latter condition occurred more frequently with recrystallized insulin than with a-component and did not occur with monocomponent insulin. These findings seemed to indicate that two distinct processes involving some circulating antibodies with anti-insulin antibody and insulitis might be involved in the development of the observed glucose tolerance abnormality.</p

Influence of an antianxiety drug on hyperemesis diabeticorum.

The patient was a 37-year-old female teacher with hyperemesis diabeticorum and juvenile Type-I diabetes. At the age of 29 years, nausea and vomiting developed and secured at nearly weekly intervals. She was started on clotiazepam (15 mg/day). The vomiting was cured and psychological improvement was evident; her anxiety about diabetes was markedly reduced. An X-ray examination after the administration of clotiazepam showed that she was entirely free from marked hypoperistalsis and the severe retention of gastric contents which had been present before this treatment. The present case is a clear example of stress closely related to the pathogenesis of hyperemesis diabeticorum.</p

Complement activation pathways associated with islet cell surface antibody (ICSA) derived from child patients with insulin-dependent diabetes mellitus (IDDM).

We studied the pathways of complement activation associated with the islet cell surface antibody (ICSA) obtained from sera of 7 patients (age less than 15 years) with insulin dependent diabetes mellitus (IDDM). The target cells were 51CR labelled rat islet cells and the complement source was human AB serum. Complement-dependent antibody mediated cytotoxicity (CAMC activity) was obtained using the percentage of cytotoxicity. CAMC activity of untreated sera was significantly inhibited by treating with EGTA or EDTA (p less than 0.001). The CAMC activity of EDTA-treated sera was significantly lower than that of EGTA-treated sera (p less than 0.001). In the inactivated human AB serum, it was lower than that of EGTA-treated sera (p less than 0.05), but not different from that of EDTA-treated sera. These results show that the complement activation associated with ICSA in patients occurred not only via the classical pathway but also via the alternative pathway.</p

What Factors are Involved in the Knowledge Necessary for the Self-Management of Diabetic Patients?

The aim of this study is to obtain data for improving a training program for patients with diabetes mellitus. One hundred eighty-seven patients with non-insulin dependent diabetes mellitus were tested with 20 questions about their knowledge for self-management of diabetes mellitus. Then to draw out factors in their personal backgrounds relating to their correct answers, multiple regression analyses were conducted. As a result, four factors showed significant differences in the following order: Educational careers &#62; ages &#62; duration of disease &#62; socioeconomic strata. The results of the present study have shown for the first time, that these four factors closely concern patients to acquire the necessary knowledge for their self-management of the disease. In addition, this study has raised some fundamental problems regarding the training program for patients: how education should be given to patients.</p