preoperatively) increased to 169 +_ 86 pg. kg -I and 436 +_ 143 pg. kg -t at 60 rain after declamping of the aorta (P < 0.001, P < 0.001). The increases were greater than those fron, P < 0.001). 7"he levels of S-ICAM-I correlated with those of lL-8 (r = 0.5, P < 0.001).Key words ANAESTHESIA: cardiac, cardiopulmonary bypass; DRUG: ulinastatin, protease inhibitor; HEART: reperfusion injury; IMMtJNOLOGV: cytokines, adhesion molecules (S-ICAM-I, S-ELAM-I). Our previous studies showed L2 that the production of IL-8 and IL-6 increased after declarnping the aorta in patients who had undergone cardiac surgery with CPB, and that the increase in these factors correlated with CK-MB concentration, suggesting that IL-8 and IL-6 contributed to reperfusion injury following ischaemia. These intlammatory cytokines are known to potentiate the expression of various adhesion molecules on neutrophils and vascular endothelial cells 3.4 and, as a result, CAN J ANAESTH 1996 /43:5 /pp456-60

SummaryBiotin production and the growth of the strains of Bifido bacterium adolescentis, B. bifidum, B. breve, B, infantis, and B. longum were studied. These five strains showed heavy growth on BL medium. But when yeast extract medium (carbon source, glucose) was used, the extent of their growth was significantly decreased, one-half or less than that of the growth on BL medium. B. bifidum grew well on yeast extract medium containing oligosaccharides, such as isomaltooligosaccharide, and produced biotin extracellularly. The utilization of oligosaccharides in biotin production by these five strains was investigated.

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The case of a 27-year-old woman who simultaneously presented with SLE and severe refractory thrombotic microangiopathic hemolytic anemia (TMHA) is reported. She had extremely high levels of platelet-associated IgG (PAIgG), and her TMHA was refractory to plasma exchange and corticosteroid therapy. However, the TMHA was effectively controlled by i.v. cyclophosphamide therapy. ITP and TTP are generally considered distinct diseases; however, TMHA may occur secondary to platelet aggregation via autoimmune mechanisms in certain cases. Immunosuppressive therapy at an early stage of the disease may be beneficial in refractory cases of TMHA with autoimmune features.