The formation of biaryl compounds through the diazo reaction has been observed at various times by different investigators. These compounds are produced principally under the following conditions.Reduction of the Diazonium Salts.-When the reduction of the salt, accompanied by liberation of nitrogen, is only partial, then there ensues in addition to the formation of the hydrocarbon also a coupling of two aryl radicals: RN2X

A solution of 4.4 g. of A6-pregnene-3/3-ol-20one and 2.45 g. of p-toluenesulfonic acid in 500 cc. of acetic anhydride was boiled gently and the solvent allowed to distil. After about seven hours the residual dark solution (100-150 cc.) was poured into ice-water, and after a short interval the product was extracted with ether and the solution was washed with water, sodium carbonate solution, and again with water, dried and evaporated. The

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Type 1 diabetes is an autoimmune disorder in which the destruction of insulin-producing beta-cells can be detected years before the clinical manifestation of the disease [1]. Selective autoantibody assays and metabolic testing can now identify first degree relatives of Type I diabetic patients, in whom the risk of diabetes is over 80 % at 5 years [2,3]. The ability to identify subjects at risk makes the exploration of immune intervention strategies to halt or even prevent betacell destruction a major goal. Growing evidence in animal models of Type I diabetes mellitus suggests Diabetologia (1998) Summary The Schwabing Insulin Prophylaxis Trial is a randomised, controlled pilot study designed to examine whether insulin therapy can delay or prevent the clinical onset of Type I diabetes in high risk first degree relatives of people with the disease. First degree relatives of patients with Type I diabetes, who were aged 4 years or more, had an islet cell antibody (ICA) value more than 20 Junevile Diabetes Foundation Units (JDF-U), a reduced first phase insulin response (FPI) to an i. v. glucose tolerance test less than the 5th centile, and a normal oral glucose tolerance test were eligible for the trial. Between January 1989 and October 1995, 1736 relatives of patients with Type I diabetes were screened for ICA. We identified 64 cases (3.7 %) with ICA values more than 20 JDF-U. Of ICA positive relatives, 17 (27 %) had a low FPI and were eligible for enrolment. Of these 14 agreed to participate, of whom 7 were randomised to the treatment group and 7 to the control group. In the treatment group, human insulin was administered i. v. by continuous infusion for 7 days, followed by daily s. c. injections for 6 months. Intravenous insulin infusions were repeated every 12 months. In the treatment group 3 of the 7 individuals (follow-up from time of eligibility: 2.3 to 7.1 years) and in the control group 6 of the 7 untreated individuals (1.7 to 7.1 years) developed clinical diabetes. Life table analysis showed that clinical onset of Type I diabetes was delayed in insulin-treated subjects compared with control subjects (means ± SEM diabetes-free survival: 5.0 ± 0.9 years vs 2.3 ± 0.7 years, p < 0.03). Insulin levels after i. v. glucose increased in the first year of intervention therapy. Titres of ICA, and antibodies to glutamic acid decarboxylase, and tyrosine phosphatase-like protein IA2 remained unchanged. These data suggest that insulin prophylaxis can delay the onset of overt diabetes in high risk relatives. This is encouraging in view of 1) the continuing American Diabetes Prevention Trial, which is currently testing the effect of parenteral insulin in a large nation-wide study and 2) the initiation of pilot trials to determine whether new antigen-specific intervention is more effective in delaying the clinical onset of Type I diabetes. [Diabetologia (1998)

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