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Volume 191 (2000)
- Issue 4 Pages 187-
- Issue 3 Pages 119-
- Issue 2 Pages 59-
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Volume 191, Issue 4
August
Displaying 1-7 of 7 articles from this issue
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Regular Contributions
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Yasumasa Iwasaki, Yutaka Oiso, Hidehiko Saito, Joseph A. Majzoub2000 Volume 191 Issue 4 Pages 187-202
Published: 2000
Released on J-STAGE: April 26, 2005
JOURNAL FREE ACCESSThe vasopressin gene encodes three polypeptides besides the signal peptide: vasopressin, neurophysin II (neurophysin), and the carboxy-terminal glycopeptide (glycopeptide). Although the function of vasopressin is well characterized, those of the latter two are not completely understood. In the present study, we investigated the effects of various mutations within the neurophysin/glycopeptide portion of the vasopressin gene on vasopressin secretion in vitro, to clarify the role of each peptide in vasopressin biosynthesis. Expression vectors containing the vasopressin gene, either wild-type or various mutants, were transiently transfected into AtT20 cells, which are known to have the enzymes necessary for the proper processing of the vasopressin precursor protein. The amount of vasopressin secreted into the culture medium was estimated by specific radioimmunoassay. Variable degrees of decreased vasopressin secretion were observed with mutant vasopressin genes harboring deletions or amino acid substitutions in neurophysin. The naturally-occurring frame-shift mutation in the hereditary diabetes insipidus (Brattleboro) rat completely eliminated vasopressin expression. In contrast, a missense mutation found in patients with familial neurogenic diabetes insipidus only partially decreased vasopressin secretion. Finally, the mutant vasopressin gene lacking the N-linked glycosylation site in glycopeptide had no effect on vasopressin expression. Our data suggest that 1) intact neurophysin is not indispensable for vasopressin expression, although an altered structure of neurophysin significantly affects the secretion of the hormone; 2) the pathogenesis of diabetes insipidus with the two naturally-occurring mutations found in the rat (Brattleboro rat) and human (familial central diabetes insipidus) seem to be different; and 3) glycosylation of the carboxy-terminal glycopeptide is not essential for the expression of vasopressin.View full abstractDownload PDF (1001K) -
Kenji Goto, Kohachiro Sugiyama, Toshihiro Ando, Fumihiko Mizutani, Koj ...2000 Volume 191 Issue 4 Pages 203-207
Published: 2000
Released on J-STAGE: April 26, 2005
JOURNAL FREE ACCESSTo date, the routes of mother-to-infant transmission of TT virus (TTV) have not been fully elucidated. The present study examines the detection rates of TTV DNA in the serum of pregnant Japanese women and in cord blood at the time of delivery, as well as in the saliva and breast milk of mothers one-month postpartum. Primers derived from the well-known translated region N22 (N22 system), as well as the untranslated region (UTR system) were used. The prevalence of TTV DNA in the serum of pregnant women was found to be 11.9% (19/160) using the N22 system and 72.4% (55/76) using the UTR system. No TTV DNA was detected in the cord blood samples (0/160) when the N22 system was used for detection but TTV DNA was detected in 11.8% (7/76) of samples studied with the UTR system. Using the N22 system, TTV DNA was not detected in breast milk, but was detected in saliva. However using the UTR system, TTV DNA was detected in both specimens. These results imply that some babies are vertically infected with TTV via cord blood at the time of delivery or via breast milk or saliva. However, further research is necessary to confirm this hypothesis.View full abstractDownload PDF (333K) -
Minoru Yoshida, Kyouko Iizuka, Atsushi Terada, Masayuki Hara, Hironori ...2000 Volume 191 Issue 4 Pages 209-220
Published: 2000
Released on J-STAGE: April 26, 2005
JOURNAL FREE ACCESSThe ability of ebselen, which exhibits glutathione peroxidase (GSH-Px)-like activity, to prevent cisplatin (CDDP)-induced nephrotoxicity was examined in rats. CDDP (6 mg/kg [20 μmol/kg] body weight) was injected intraperitoneally. In subgroups, daily ebselen doses of 2.75 (10 μmol), 5.5 (20 μmol), or 11.0 mg (40 μmol)/kg body weight were administrated orally 1 hour prior to CDDP treatment. Treatment with CDDP alone resulted in significantly increased plasma creatinine (Cr) and blood urea nitrogen (BUN) levels. Repeated administration of 5.5 and 11.0 mg/kg ebselen prevented the CDDP-induced elevation of plasma Cr and BUN levels and protected against kidney damage. Relative to controls, rat that received CDDP treatment displayed a decreased ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG), an indicator directly related to oxidative stress, and elevated malondialdehyde (MDA) levels in the kidney. In comparison with controls, activity of GSH-Px activity, which antioxidant enzyme, was also reduced in the kidney of rats treated with CDDP. Repeated administration of 5.5 or 11.0 mg/kg ebselen prevented CDDP-induced alteration of GSH/GSSG ratios, MDA levels, and GSH-Px activity; however, no protection against CDDP was observed with administration of 2.75 mg/kg ebselen. Effective protection of CDDP-induced nephrotoxicity with ebselen was observed only when the molar amount of each daily ebselen treatment equaled or exceeded the molar amount of CDDP administrated.View full abstractDownload PDF (1258K) -
Tagayasu Nishiyama, Shimpei Nishikawa, Hiroshi Tomita, Makoto Tamai2000 Volume 191 Issue 4 Pages 221-232
Published: 2000
Released on J-STAGE: April 26, 2005
JOURNAL FREE ACCESSThe role of Müller cells in the preconditioned retinal ischemic injury rat was investigated. In anesthetized Sprague Dawley rats, retinal ischemia for 5 minutes constituted the preconditioning stimulus for the left eye. After 24 hours, both eyes were clamped for 60 minutes. In 30, 60, 90, and 120, minutes and 1 day, 3 days, and 7 days after ischemia, electroretinograms were recorded, and the eyeballs were enucleated. After fixation with 4% paraformaldehyde, the avidin-biotin-peroxidase technique was applied to show glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP). Furthermore, for the solubilized retinas, Western blot analysis and enzyme-linked immunosorbent assay were performed to detect GS and GFAP in the extracts. Preconditioning performed 24 hours before ischemia significantly improved the recovery of the a-, and b-waves 1 day after 60 minute ischemia. In the 30, 60, 90, and 120 minutes after ischemia, the recovery of the a-wave only was observed. There was a nonsignificant trend toward greater recovery in the first 120 minutes after 60 minute ischemia, especially in the b-wave. GS immunoreactivity had no significant difference between non-preconditioned and preconditioned groups 30, 60, 90, and 120 minutes after ischemia. In 1 day after ischemia, GS immunoreactivity decreased in both groups. In 3 and 7 days after ischemia, GS immunoreactivity recovered only in the preconditioned group. The retinas at 3 and 7 days after 1 hour of ischemia showed increased GFAP immunoreactivity in the non-preconditioned group. In the preconditioned group, only slight GFAP immunoreactivity was observed. These results suggested that the mechanism of preconditioned retinal ischemia may be related to Müller cells in the retina.View full abstractDownload PDF (1417K) -
Kohachiro Sugiyama, Kenji Goto, Toshihiro Ando, Fumihiko Mizutani, Koj ...2000 Volume 191 Issue 4 Pages 233-239
Published: 2000
Released on J-STAGE: April 26, 2005
JOURNAL FREE ACCESSThe pathogenecity of the TT virus (TTV) especially during childhood remains obscure. We investigated the prevalence of TTV in 40 patients with non-A to C hepatic dysfunction (non-A to C hepatic dysfunction group). Five patients with fulminant hepatitis of unknown etiology were enrolled in this group. We also examined 380 children without a history of transfusion or liver disease (control group). Subsequently, the genotypes of TTV strains isolated were analyzed in terms of their nucleotide sequences including 222 bp in the open reading frame 1 region. The prevalence of serum TTV DNA was 10/40 (25%) in the non-A to C hepatic dysfunction group and 25/380 (7%) in the control group. Sixty-six percent (23/35) of all examined cases exhibited either genotype 1 or 2. However, assessment of genotype in the non-A to C hepatic dysfunction group (10 cases) revealed a higher prevalence of genotype 1 than of all other genotypes (80% vs. 20%). This result differed significantly from that of the control group (25 cases; 32% vs. 68%). Such overrepresentation of genotype 1 suggests that this type of TTV strain is associated with the development of hepatic dysfunction of unknown etiology in Japanese children.View full abstractDownload PDF (466K) -
Choong-Yong Kim, Kunihiko Nakai, Satomi Kameo, Naoyuki Kurokawa, Zhang ...2000 Volume 191 Issue 4 Pages 241-246
Published: 2000
Released on J-STAGE: April 26, 2005
JOURNAL FREE ACCESSEffect of melatonin on the mortality in methylmercury chloride (MMC)-intoxicated mice was evaluated. Mice were given MMC in the diet (40 mgHg/g) with or without melatonin in drinking water (20 mg/ml) for 5 weeks. In the control group, given MMC alone, 4 of 10 mice began to show neurological signs (e.g., abnormal righting reflex, staggering gaitfallen and posture on its side) concomitant with loss of body weight 4-7 days before death. This group also showed 60% of survival rate on the 35th day. However, the treated group, concomitantly given melatonin, showed a 100% of survival rate on the 35th day, although 1 of 10 mice began to show the neurological signs on the 33rd day. The level of thiobarbituric acid reactive substance in the brain, as an indication of oxidative damage, showed a significant decrease in the treated group compared with the control group. Thus, the 100% survival rate in the treated group may be partly due to antioxidative effect of melatonin on the MMC induced neurotoxicity.View full abstractDownload PDF (315K)
Case Report
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Yuki Terui, Takafumi Saito, Hisayoshi Watanabe, Masanori Aoki, Hiroko ...2000 Volume 191 Issue 4 Pages 247-253
Published: 2000
Released on J-STAGE: April 26, 2005
JOURNAL FREE ACCESSA 27-year-old man who had been diagnosed as having chronic hepatitis B suffered disease exacerbation with marked reactivation of hepatitis B virus (HBV). Treatment with interferon (IFN) did not improve his condition, and his serum HBV DNA level increased to over 10 000 pg/ml during IFN administration. Following replacement with lamivudine, there was a substantial reduction in HBV DNA to an undetectable level, and liver function parameters subsequently improved to within the normal range. Quantitative analysis of the precore mutant HBV DNA, which is a variant that cannot express hepatitis B e antigen due to a G-to-A point mutation in the precore region of the viral genome, revealed that the amount present was greater than for the precore wild-type HBV DNA in the serum taken before IFN treatment. This case suggests that lamivudine would be an appropriate alternative to IFN, particularly in patients infected with HBV containing an excess of precore mutants resistant to IFN therapy.View full abstractDownload PDF (445K)
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