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Polymorphism of the glycogen synthase gene is associated with non-insulin-dependent diabetes mellitus (NIDDM) and insulin resistance. NIDDM is characterized by defective glycogen synthesis and insulin resistance and is thought to be a genetic disease. Impairment or inactivation of the gene for glycogen synthase, an enzyme involved in glycogen synthesis, might explain this defect. DNA probes of 107 patients with NIDDM and 164 non-diabetic individuals with no family history of NIDDM revealed two polymorphic alleles for the glycogen synthase gene, labelled A1 and A2. Thirty percent of the patients with NIDDM had either the A1A2 or A2A2 genotype compared with only 8% of patients without NIDDM. Diabetics with the A2 allele had a significantly greater incidence of high blood pressure and insulin resistance and had an extensive family history of NIDDM. The presence of the A2 allele could be considered an indicator of NIDDM.

HLA antigens were examined in 118 unrelated patients of whom 49 had definite severe systemic lupus erythematosus (SLE). HLA A1 was found in 45% of the 49 SLE patients and in 20% of the controls, which consisted of 900 blood donors. HLA B8 was found in 47% of the patients and in 20% of the controls (relative risk=3.5, P=0.000017), while HLA B7 was found in 22% of the patients and in 24% of the controls. Of the 118 patients 69 had chronic biologically false-positive (CBFP) seroreactions for syphilis. In 32 of these 69 patients definite or probable SLE was diagnosed during the observation time, which varied from 3 to 16 years. HLA B7 was found in 38% of these 32 patients, while HLA B8 was found in 25%. When the occurrence of these antigens was correlated to the length of the observation time it was found that 53% of the patients in whom the disease manifested first after 10 years follow-up were carriers of HLA B7 ( P=0.0005) and only 12% had HLA B8 (relative risk=0.5). In patients with a faster development of the disease both of these antigens were found in about the same frequency as in severe SLE patients. In 37 of the 69 patients no definite diagnosis could be established even it 19 of them had clinical and serological manifestations compatible with SLE. HLA B7 was found in 46% and HLA B8 in 14% of these patients. Moreover it was found that 72% of the 18 patients who had only antilipoidal antibodies in their serum were carriers of HLA B7, while 21% of the 19 patients with other circulating auto-antibodies had HLA B7. D-locus antigens were examined in 35 patients. HLA D w3 was found in 54% of the patients and in 24% of the controls. Twelve of the patients with D w3 had severe SLE and nine of them had also HLA B8. [ABSTRACT FROM AUTHOR]

Children with newly diagnosed insulin-dependent diabetes mellitus (IDDM) bad increased numbers of CD25 positive lymphocytes in peripheral blood and peripheral blood mononuclear cells responded to insulin antigens by proliferation. The CD25 positivity and insulin proliferation were associated to the duration of symptoms before the diagnosis of IDDM. Thus increased numbers of CD25 positive cells were found in 89%, and insulin induced proliferation in 100% of patients with symptoms of diabetes of less than 1 week's duration before diagnosis, while CD25 positivity and insulin-induced proliferation were observed in 36% and 29% of children who had had symptoms for 4 weeks or more before diagnosis. Children with IDDM also bad increased numbers of CD4 positive T cells in peripheral blood. The frequency of HLA-DR4 and HLA-DR3/4 in diabetic children was higher and that of HLA-DR2 lower than In the normal population. Insulin, islet cell, gastric-parietal cell, thyroid and antinuclear antibodies did not correlate to the duration of symptoms before diagnosis. [ABSTRACT FROM AUTHOR]

We coupled bacteriophage T4 with standard (0.16%) or low (0.005%) concentrations of NIP-azide. The low concentration produced haptenated phage (type B) that was inactivated by the IgG anti-NIP of some rabbits but not by that of other rabbits similarly immunized. The most active IgG fraction at an anti-NIP concentration of 100 µg/ml inactivated the type B phage with a titre of 2400, while the same anti-NIP concentration of the least active IgG fraction from another rabbit had a titre of 0.3. With the standard haptenated phage titres only varied within a 20-fold range. IgM fractions of a few rabbits tested did not appear to exhibit a great variation with the type B phage. The IgG fractions with high titres against the type B phage bound more NIP-hapten at low (≈ 10-10M) hapten concentrations than those with a low titre, but this superiority was greatly reduced by an increase of hapten concentration to 10-8M. The same phenomenon could be demonstrated by an inhibition technique, lnactivation of type B phage appeared to detect exclusively antibodies with association constants considerably higher than 108. Its affinity threshold seems to be higher than the threshold of two other methods employed, haemagglutination of haptenated erythrocytes and inactivation of the standard haptenated phage. [ABSTRACT FROM AUTHOR]