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In our mutation analyses of bilirubin UDP glycosyltransferase (UGT1A1) gene, we encountered six patients with Crigler-Najjar syndrome type II who were double homozygotes for G71R and Y486D, a patient with Gilbert's syndrome who was a single homozygote for G71R and six patients with Gilbert's syndrome who were single heterozygote for G71R. To clarify the(More)
OBJECTIVE The incidence of nonphysiologic neonatal hyperbilirubinemia is twice as high in East Asians as in whites. We studied whether the condition was associated with mutations in the gene for bilirubin uridine 5'-diphosphate-glucuronosyltransferase (UGT1A1), a key enzyme of bilirubin catabolism. DESIGN We analyzed the UGT1A1 gene in 25 Japanese(More)
We report a case of Gilbert syndrome caused by a homozygous missense mutation (Tyr486Asp) of the bilirubin UDP-glucuronosyltransferase gene. Homozygous missense mutations of the gene have previously been recognized as responsible for Crigler-Najjar syndrome type II. We conclude that Gilbert syndrome in some patients results from homozygous missense(More)
Ring chromosomes offer an opportunity to measure sister-chromatid exchange (SCE) frequencies without the use of an agent to differentiate sister chromatids: SCE frequencies can be determined from the number of dicentric rings formed in cells from a cell line carrying a monocentric ring chromosome. Ash is a pseudotetraploid Chinese hamster ovary cell line in(More)
Light and electron microscopy were performed in a study of the effects of electrical stimulation upon the reparative processes in flexor tendons cultured in vitro. After one or two weeks of incubation, the unstimulated control tendons were covered with fibroblastic surface cells, thought to have originated from the epitenon. In contrast, the tendons(More)
In-vitro V79 and L5178Y cells were exposed in a rotating test tube to continuous-wave (CW) 1 MHz 35 W/cm2 ultrasound (0-4 or 0-3 min, respectively) and subsequently assayed for mutation as evidenced by resistance to 6-thioguanine (6-TG). There was a modest but statistically significant increase in mutation frequency in both cell types with increase in(More)
We measured IgA1 and IgA2 subclass antibody levels against human type I, II, III and IV collagens in patients with ankylosing spondylitis (AS) by enzyme linked immunosorbent assay (ELISA). Significant elevations of IgA1 antibodies against type II collagen (p < 0.01) and IgA2 antibodies against type I (p < 0.001), III (p < 0.001), and IV (p < 0.01) collagens(More)