We treated 19 Japanese patients with acute urticaria presumably caused by infection during the five years from 1994 to 1998. The patients' ages ranged from 2 to 66 years (8 males and 11 females). Most of them had urticaria, angioedema, high fever, neutrophilia, and high serum levels of C reactive protein (CRP). The skin rash lasted more than 24 hours. In four patients, a flow cytometric analysis revealed that the percentage of circulating T cells bearing T-cell receptor V beta 3 was decreased during the active stage and that this decrease was sustained for at least 2 to 3 weeks. This suggests that certain T-cell populations were numerically altered in association with the occurrence of the disease. A retrospective review indicated that the combination therapy with corticosteroid and antibiotics was more effective than the single use of either agent.

(2-O-hexadecyl)PI], were tested as substrates or inhibitors of glycosylphosphatidylinositol (GPI) bio-synthetic pathways using cell-free systems of the proto-zoan parasite Trypanosoma brucei (the causative agent of human African sleeping sickness) and human HeLa cells. Neither these compounds nor their N-acetyl derivatives are substrates or inhibitors of GPI bio-synthetic enzymes in the HeLa cell-free system but are potent inhibitors of GPI biosynthesis in the T.brucei cell-free system. GlcN-(2-O-hexadecyl)PI was shown to inhibit the first α-mannosyltransferase of the trypano-somal GPI pathway. The N-acetylated derivative GlcNAc-(2-O-octyl)PI is a substrate for the trypano-somal GlcNAc-PI deN -acetylase and this compound, like GlcN-(2-O-octyl)PI, is processed predominantly to Man 2 GlcN-(2-O-octyl)PI by the T.brucei cell-free system. Both GlcN-(2-O-octyl)PI and GlcNAc-(2-O-octyl)PI also inhibit inositol acylation of Man 1-3 GlcN-PI and, consequently, the addition of the ethanolamine phosphate bridge in the T.brucei cell-free system. The data establish these substrate analogues as the first generation of in vitro parasite GPI pathway-specific inhibitors.

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A family was found which indicated the existence of a silent allele (BF*QO) at the locus for complement factor B. Three generations with eight members were studied. Four individuals were considered to be heterozygous for B deficiency because of unusual segregation patterns of the BF electrophoretic variants and low levels of B. Haplotype study on the other HLA-linked markers supported the presumption. No unusual products were detected by immunoblotting after sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).