The Tohoku Journal of Experimental Medicine
Online ISSN : 1349-3329
Print ISSN : 0040-8727
ISSN-L : 0040-8727
Volume 179, Issue 1
May
Displaying 1-7 of 7 articles from this issue
Regular Contributions
  • Adnan Menevse, Melahat Ülküer, Nedim Sultan
    1996 Volume 179 Issue 1 Pages 1-9
    Published: 1996
    Released on J-STAGE: September 19, 2006
    JOURNAL FREE ACCESS
    A polymerase chain reaction for the rapid and specific detection of Mycobacterium tuberculosis has been used and evaluated for clinical applicability. Two oligonucleotide primers derived from the nucleotide sequence of a immunogenic protein MPB 64 amplified DNA from M. tuberculosis and M. bovis. No amplification was observed from any of ten different mycobacterial strains. A total of 126 clinical samples were amplified and tested by both dot blot hybridization and restriction enzyme analysis. M. tuberculosis was detected by PCR in 38 smear and 42 culture positive cases. An additional 16 culture negative specimens were PCR positive yielding an overall M. tuberculosis positivity rate of 46.0% (58/126) compared to 33.3% (42/126) by culture. The superior sensitivity of PCR to culture was more evident in non-pulmonary cases where PCR picked up 10 cases in addition to 6 culture positives out of 46 specimens. On the other hand, out of 80 pulmonary specimens only 6 cases in addition to 36 culture positives were picked up by PCR. The specificity of PCR was confirmed with dot blot hybridization and restriction enzyme analysis. This study corroborates that PCR offers a more sensitive and rapid alternative for the detection of M. tuberculosis to culture, and that it can be used in uncultured clinical specicimens.
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  • Ippei Nakagawa, Masahiko Satoh, Akira Naganuma, Nobumasa Imura
    1996 Volume 179 Issue 1 Pages 11-21
    Published: 1996
    Released on J-STAGE: September 19, 2006
    JOURNAL FREE ACCESS
    The protective role of metallothionein (MT) against renal lipid peroxidation caused by administration of cis-diamminedichloroplatinum (II) (cis-DDP) was examined in glutathione (GSH)-depleted mice. Pretreatment with DL-buthionine-SR-sulfoximine (BSO), an inhibitor of GHS synthesis, 4 hr prior to injection of a subtoxic dose of cis-DDP (45 μmol/kg) significantly induced renal toxicity of this anticancer drug evaluated by an increase in blood urea nitrogen (BUN) levels. Renal levels of thiobarbituratereactive substances (TBA-RS), determined as an indicator for lipid peroxidation, were also significantly increased in BSO-treated mice by cis-DDP in advance of the increase in BUN values. The BSO-enhanced renal lipid peroxidation induced by cis-DDP was found to be attenuated by pre-administration of zinc chloride, an inducer of MT synthesis. Binding of platinum to MT in the kidneys of mice after cis-DDP administration was not increased by pretreatment with zinc chloride. A significant decrease in concentration of preinduced-MT was observed after administration of cis-DDP. This result suggests that MT may prevent the lipid peroxidation by scavenging free radicals generated by cis-DDP, but not by binding directly to cis-DDP or its metabolites, in GSH-depleted mice. The present findings support the view that MT may substitute for GSH as a scavenger of radicals produced by cis-DDP.
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  • Hiroko Abe, Mayumi Abe, Katsuhiro Tanaka, Chika Iwasaka, Yasufumi Sato
    1996 Volume 179 Issue 1 Pages 23-34
    Published: 1996
    Released on J-STAGE: September 19, 2006
    JOURNAL FREE ACCESS
    Latent transforming growth factor-β (TGF-β) is activated when endothelial cells (ECs) and smooth muscle cells (SMCs) are in contact. This activation requires plasminogen activator (PA) activity on ECs and the binding of latent TGF-β to SMCs. Since SMCs are not always in contact with ECs in the vascular wall, a mechanism for the activation of latent TGE-β in homotypic SMCs needs to be elucidated. A low-dose of TGF-β1 (10∼100 pg/ml) stimulated the proliferation of porcine aortic SMCs (PASMCs), while a high-dose of TGF-β1 (1,000 pg/ml) inhibited proliferation. Exogenous urokinase-type PA (uPA) enhanced the proliferation of PASMCs, and the stimulatory effect of uPA was comparable with that of low-dose TGF-β1. The effect of uPA on the proliferation of PASMCs was blocked by a co-administration of either neutralizing anti-TGF-β antibody or α2 plasmin inhibitor, suggesting that exogenous uPA generates active TGF-β via plasmin activity. A binding experiment using 125I-uPA showed that PASMCs expressed specific receptors for uPA. The 2 hr incubation of PASMCs with uPA increased the cell-associated uPA activity. When PASMCs were washed after incubation under the same conditions, the stimulatory effect of uPA on the proliferation of PASMCs persisted. Thus, receptor-bound uPA has been found to be involved in this reaction. The stimulatory effect of uPA on the proliferation of PASMCs was abrogated by the monoclonal antibody against latency-associated peptide, which inhibits the binding of latent TGF-β to PASMCs. These results indicate that the simultaneous bindings of uPA and latent TGF-β generates active TGF-β in homotypic SMCs.
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  • Hideaki Suzuki, Yoshihisa Tomioka, Shunji Ishiwata, Takahumi Yamaguchi ...
    1996 Volume 179 Issue 1 Pages 35-45
    Published: 1996
    Released on J-STAGE: September 19, 2006
    JOURNAL FREE ACCESS
    We established two monoclonal antibodies (MAbs, A6-1-E4, 1gM; κ and BC-D1, IgG1, λ), that specifically recognize different epitopes of rat Δ3, Δ2-enoyl-CoA isomerase (ECI). We then developed a specific and reliable sandwich enzyme-linked immunosorbent assay (sandwich ELISA) using a capture monoclonal antibody and an indicator polyclonal antibody to evaluate ECI. The amounts of ECI were linearly determined in the ranges from 15 to 250 ng/well by this method. This assay can detect the amount of ECI in tissue homogenates without subfractionation. The ECI levels were 0.13 ng/μg homogenate in normal rat liver and 1.50 ng/μg homogenate in clofibrate-treated rat liver.
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  • Meral Asçioglu, Çigdem Özesmi, Pakize Dogan, Figen ...
    1996 Volume 179 Issue 1 Pages 47-53
    Published: 1996
    Released on J-STAGE: September 19, 2006
    JOURNAL FREE ACCESS
    Effects of chronic grayanotoxin-I (GTX-I) administration have been investigated on hepatic and renal functions in rats. Fourtyfive 12-15 week old Swiss Albino male rats, weighing 170-300 g were housed at 23-25°C and fed with standard diet for a period of 3 months. The rats were divided into 3 groups of 15 animals each. Animals in group 1 received i.p. GTX-I at a dose of 0.075 mg/kg daily for 3 months. Group 2 received i.p. GTX-I at a dose of 0.15 mg/kg daily and control rats received i.p. saline solution (0.9%) only, for 3 months. At the end of the 3 month experimental duration, urine analysis (leukocytes, urobilinogen, protein, pH, blood, ketone, glucose, nitrites), was performed. Then the animals were sacrified and serum was obtained for the following determinations: the activities of glutamic pyruvic transaminase (GPT), γ-glutamyl transferase (γ-GT), isoenzymes of lactate dehydrogenase (LDH) (as a percentage of total LDH) and transferrin, ceruloplasmin, total protein concentrations. In addition histopathologic changes in liver, kidney and heart were examined. Findings of urine analysis showed that the chronic GTX-I administration produced proteinuria and hematuria and decrease in level of urine ketone bodies. It was also observed that there were increases in serum GPT and LDH4 activities, but decrease in serum total protein levels occured in a dose releated manner. There was no significant histopathologic alterations, detectable by light microscopy, in examined tissues.
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