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Islet cell cytoplasmic and cell surface antibodies along with other autogenic tissue antibodies were determined prospectively from the day of diagnosis of insulin-dependent diabetes in a group of children and adolescents. Prior to the initiation of insulin therapy 30 out of 33 were antibody-positive, 67% having islet cytoplasmic antibodies and 67% islet cell surface antibodies. Among 74 age- and s

Diabetic A.TL and A.TH mice, congenic inbred strains differing only in the I and S (non-K, non-D) regions of the major histocompatibility (H-2) complex, received intrasplenic allogeneic and isogeneic pancreatic islet transplants. The isografts were uniformly accepted, while approximately 60% of the recipients receiving allografts rejected the islets, most within 4 weeks of transplantation. With ei

Dispersed rat pancreatic islet cells were mixed into a short column of Bio-Gel P-2 polyacrylamide beads and perifused with an antiserum containing islet cell surface antibodies. The release of radioactive chromium from prelabeled cells, as a measure of cell membrane permeability, was not affected by cell surface antibodies alone, but increased dramatically in the presence of complement. While ther

Streptozotocin (SZ) given in five low doses causes diabetes and an associated lymphocytic infiltration of the pancreatic islets. Using C57BL/KsJ-mice, we demonstrate a reduction in islet number (-38%) and volume (-64%) within 1 day following the last injection of SZ. A substantial fall of insulin secretory capacity (-84%) in the in vitro perfused pancreas matches the reduction in islet cell volume

Genetic susceptibility, environmental factors and immune mechanisms are implicated in the pathogenesis and etiology of insulindependent diabetes mellitus. The onset of the disease is associated with a major loss of beta cells, and inflammatory cells may be seen in and around the islets of Langerhans. Insulin-dependent diabetes is often associated with autoimmune endocrinopathies. Antipancreatic ce

Recent observations have shown the presence of thyrotropin-releasing hormone-like material (TRH-LM) in rat pancreatic islets and in retina. Its immunological and biological properties are identical to those of synthetic thyrotropin-releasing hormone (thyroliberin). This communication deals with the ontogenesis of TRH-LM in rat pancreas and retina as compared to that of rat hypothalamus. Effects of

Dispersed islet cells were prepared from collagenase-isolated lean mouse pancreatic islets by Dispase-II and subsequent mechanical treatment in calcium depleted media. An average yield of 600 cells per islet was obtained, 84% of the cells being β-cells. Cells were incubated with radioactive chromium as a marker of cell viability. Optimal labelling of 1-2 cpm per cell was obtained by incubating 10

Pancreatic islets from rats or ob/ob mice were homogenized and fractionated either by a two-step or one-step sucrose gradient centrifugation. A plasma membrane enriched fraction was obtained at a sucrose density of about 1.10. The distribution of the plasma membrane probe 125I-wheat germ agglutinin was parallel to that of other plasma membrane markers. Hydrolysis of Mg-ATP-gamma-3Pp in rat islet m

Rabbits were immunised with suspensions of viable, insulin-producing islet cells prepared from collagenase-isolated rat or ob/ob mouse pancreatic islets. Antibodies reactive with the surface of dispersed rat islet cells were present in both the rabbit anti-rat and the rabbit anti -ob/ob mouse islet sera as revealed by indirect immunofluorescence or by a radioligandassay using 125 I-Protein A as

There is evidence that the destruction of the pancreatic B cell in insulin-dependent diabetes mellitus is due to autoimmune reactions. Transplantation of islet cell tissue might then provoke 'reimmunization', and this could presumably lead to destruction of the transplanted B cells. The authors have looked for signs of recurrence of autoimmunity following pancreatic transplantation.

Building on empirical material from 6 months ethnographically inspired fieldwork in Málaga Común, a mutual credit community currency in Southern Spain, the paper uses Ostrom’s (1991) theoretical framework on common-pool resources to look deeper into the provision and appropriation dynamics in the currency scheme. Particular attention is put into the sources of inequality in members’ provision and

Sweden went back to gold at the pre‐war parity, whereas Finland returned at the existing rate, accepting the depreciation of the markka that had occurred over the war and early post‐war years. The authors use a quantity‐theory framework to investigate the results of the divergent exchange rate and monetary policies followed by the two countries. The Swedish economy was forced to undergo a severe c