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The rate constants were estimated by phosphorus NMR spectroscopy for the reactions of alcohols (Tr-dT, 2-cyanoethanol) in pyridine with the main types of the reactive phosphorylating intermediates formed by treatment of pdT-Ac, pdTpdT-Ac, Tr-dTpdT-Ac, Tr-dTpdTpdT-Ac with 2, 4, 6-triisopropylbenzene-sulfonyl chloride (TPS): 1) B type derivatives with phosphomono ester (PME) group converted to a phosphoryl pyridinium residue; 2) C type derivatives with PME and phosphodiester (PDE) groups converted to trisubstituted pyrophosphate; 3) D type derivatives with PDE groups converted to tetrasubstituted pyrophosphate. The two latter types are partially present as cyclic intramolecular pyrophosphates Ci and Di. The reactivity of the intermediates decrease in the series B greater than Ci approximately Di greater than C approximately D. The Ci derivative of pdTpdT-Ac when obtained in dimethylformamide was found to be rather stable to hydrolysis and could be separated from the other dinucleotide derivatives by ion-exchange chromatography. The Arrhenius parameters of all steps of the conversion of PME group of pdT-Ac to B derivative and of the reaction of TPS with PDE group of dinucleoside phosphate Tr-dTpdT-Ac were measured.

A genetically restricted allogeneic effect factor (AEF) derived from a mixed lymphocyte culture reaction between Ia-negative activated responder cells and irradiated T-cell-depleted stimulator cells was characterized. Restricted AEF is a B-cell-derived soluble helper factor which consists in part of Ia antigens controlled by the I-A subregion of the stimulator haplotype; additional control by the I-B, I-E, and I-C subregions, although unlikely, could not be excluded. This factor helps B cells of only its own haplotype or of haplotypes which carry an I-A and/or I-B subregion identity. Unprimed as well as hapten-primed Ia-positive B cells express a receptor for restricted AEF. The results indicate that the B-cell receptor for AEF is determined by the I-A subregion. Both restricted AEF and its receptor may therefore be products of the same I-region gene(s). The data are compatible with the hypothesis that the AEF Ia antigens serve as a second signal required for B-cell activation to IgG antibody production.

A rational diagnostic procedure has to be not only scientifically should but also economically reasonable. One has always to ask to what purpose the diagnosis shall serve. The diagnosis is mainly necessary for the treatment of a patient. This includes aiming at a causal therapy, informing the patient about cause and meaning of his symptoms, and also considering prognosis and, if necessary, prophylaxis. In liver disease the following investigations are obligatory: history, signs and symptoms and a minimal set of tests (SGPT, SGOT, gamma-GT, serum bilirubin, urobilinogen in the urine). The next level of diagnostic measures evolves out of several questions: in case of acute disease: etiology (infections; toxic?); evidence of chronic liver disease; differentiation between intra- and extrahepatic cholestasis; evidence of a circumscript lesion of the liver; associated reaction of the liver in connection with other extrahepatic diseases. Serum bilirubin is of relatively little importance except for disturbances of the bilirubin metabolism. The same is true for serum iron except for the diagnosis of hemochromatosis. Blood coagulation tests are of great value for the diagnosis and evaluation of acute and chronic liver disease as are immunologic and serologic investigations (HBsAg, HBcAg, Anti-HBeAg, Anti-HVA, ANF, SMA).

Three patients with a severe bleeding disorder and disseminated intravascular coagulation were effectively treated with human antithrombin-III concentrates. This treatment, followed by administration of prothrombin complex and platelet suspensions, resulted in a normal haemostasis, which was maintained during clinical investigations and surgery.

A new lymphocyte-activating determinant (Lad) locus expressed on T cells was identified, mapping in the I-C subregions of H-2k and H-2d haplotypes. The mixed lymphocyte reaction stimulation could be inhibited by anti-Ia sera made in strains incompatible for this chromosomal segment. Experiments with purified lymphocyte cell populations suggested that this Lad locus was expressed on T cells. Further, only purified T cells were able to remove the inhibiting activity from the anti-Ia sera. I-C subregion gene(s) seem to code for products selectively expressed on a subpopulation of T cells.