[A case of single coronary artery complicated with myocardial infarction].
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Biomedical subjects
Publications and source records attributed to T Oda.
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Protein species interacting with newly replicated DNA were analyzed using a photo cross-linking technique. Nascent DNA was labeled in vitro with [alpha-32P]dCTP and BrdUTP in SV40-infected CV-1 cells made permeable with saponin. The labeled cells were then irradiated with UV light (254 nm) and were treated extensively with DNase I. Proteins with radioactive DNA tags were separated by SDS-PAGE and visualized by autoradiography. Among 10-15 proteins which were cross-linked, the proteins with apparent molecular weights of 16.5 K, 44 K, 82 K and those in the 94-140 K region appeared to be associated with newly replicated SV40 DNA. A pulse-chase experiment showed that the 82 K and 94-140 K proteins interacted with new DNA in a relatively localized region close to the replication fork. The 44 K protein was identified as the major viral capsid protein, VP1, using antiserum to SV40 capsid proteins. It was suggested that VP1 binds to nascent DNA shortly after DNA synthesis and migrates into chromatin maturation regions.
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Localization of serine: pyruvate aminotransferase [EC 2.6.1.51]; SPT in rat eosinophile leukocytes was investigated by protein A-gold technique. Thin sections of rat intestine were incubated with anti-SPT, followed by protein A-gold complex. Labelling with gold particles was seen on the specific granules of eosinophile leukocytes, in which 78% of the gold particles were localized on their paracrystalline cores and 22% on matrix, indicating that the main intragranular sites of SPT are the core. Other cell organelles such as nucleus and mitochondria were not labelled specifically. Quantitative analysis of labelling density in the subcellular compartments also confirmed that SPT is present exclusively in the specific granules.
The protective efficacy of a hepatitis B vaccine against infections from transfusions of large volumes of highly infective blood in five immunized chimpanzees was assessed. Hepatitis B surface antigen (HBsAg) became positive and antibody to HBsAg (anti-HBs) disappeared soon after transfusion in the five chimpanzees. Two chimpanzees that had HBsAg only on the day of transfusion did not develop infection. However, the remaining three chimpanzees with persistent HBsAg antigenemia for three to four days developed serologic evidence of infection. Two chimpanzees did not have hepatitis and the third had a mild, transient case of acute hepatitis. The hepatitis B vaccine prevented the four immunized chimpanzees from developing illness. The remaining chimpanzee developed hepatitis, but a rapid booster response of anti-HBs owing to the previous vaccination appeared to lighten the severity of the disease and prevent chronicity.
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Isolated rat pancreatic islets, incubated in the presence of extracellular 32Pi to a state of steady 32P incorporation into cellular phosphopeptides, were exposed to glucagon, (Bu)2cAMP, or somatostatin for 10 min. In other experiments, homogenates of rat islets were phosphorylated using [gamma-32P]ATP with or without cAMP. Proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and phosphorylation of proteins was measured by liquid scintillation counting of gel slices. Glucagon (2.9 X 10(-7) M) stimulated the phosphorylation of 15 polypeptides (by approximately 20-50%) with major phosphorylation of proteins with mol wts of 138,000, 93,000, 53,000, 49,000, 35,000, 27,000 and 15,000 in intact rat islets and also stimulated insulin release by 202%. Somatostatin (6.6 X 10(-7) M) inhibited all the glucagon-stimulated phosphorylation by approximately 15-30% and also inhibited the glucagon-stimulated insulin release by 46%. (Bu)2cAMP (10(-3) M) stimulated 32P incorporation (by approximately 20-50%) into the same 15 peptides as did glucagon and also stimulated insulin release by 169%. When homogenates of rat islets were used. cAMP (10(-6) M) stimulated the phosphorylation of proteins (by approximately 25-60%) to an extent similar to that seen in the presence of glucagon or (Bu)2cAMP in intact islets. These findings indicate that the glucagon-stimulated phosphorylation of rat islet proteins may be mediated by cAMP-dependent protein kinase and that protein phosphorylation may be important in mediating the glucagon-stimulated insulin release.
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The susceptibility of Rous sarcoma virus (RSV) genomes integrated in mouse ascites sarcoma cells (SR-C3H/He cells) to DNase I and DNase II was investigated. Approximately half of the viral sequences were sensitive to DNase I and DNase II when 17% and 7.4% of the chromatin DNA was rendered acid soluble, respectively. The results suggest that newly acquired exogenous proviral sequences are integrated into both transcriptionally active and inactive regions of chromatin in cells lacking related endogenous viral sequences.
Electron microscopy of four human T-cell lines revealed the production of type C virus particles in two T-cell lines: one derived from acute lymphoblastic leukemia and the other from a leukemic T-lymphoid malignancy. Virus particles isolated from these cells had reverse transcriptase activity and the major internal structural protein of 30,000 daltons (p30). The indirect immunofluorescence test of these virus-producing cells with sera of patients with adult T-cell leukemia (ATL) was negative. The data indicate that these retroviruses are different from adult T-cell leukemia virus (ATLV).
Repair polymerases participating in unscheduled DNA synthesis in isolated liver nuclei, bleomycin-treated permeable cells and in ultraviolet-irradiated living cells were studied using two specific inhibitors of DNA polymerases, aphidicolin and 2', 3'-dideoxythymidine-5'-triphosphate. Unscheduled, i.e., repair, DNA synthesis in rat liver nuclei, and in bleomycin-treated permeable SR-C3H/He and XC cells was mostly attributed to DNA polymerase beta. Unscheduled DNA synthesis in human liver nuclei, bleomycin-treated permeable HeLa and HEp-2 cells, and in ultraviolet-irradiated HeLa, HEp-2 and XC cells was partially inhibited by the polymerase alpha-specific inhibitor, aphidicolin. The results suggested that both DNA polymerase alpha and beta participated in unscheduled DNA synthesis, though the respective degrees of participation differed depending on cell type and the nature and degree of DNA damage.
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Sixteen cases with ovarian immature teratoma received our managements have been reviewed. After exhaustive tissue examination, those neoplasms were graded histologically according to the criteria proposed by Thurlbeck and Scully, in addition, to exclude the mixed germ cell tumors, alfa fetoprotein stainings by PAP method were performed. Ten of all patients are alive without any signs of recurrence and none of grade 3 patients could survive. In our small series, the histologic grade seemed to correlate with the prognosis. Now-a-days the prognostic significance of the grading systems, however, still remains controversial, and it is discussed in this paper. Of particular interest is that the immature teratoma containing glioblastoma element took most fulminant clinical course. It was suggested that special attention should be paid to the histologic components of glioblastoma in the neoplasm. Serum alfa feto-protein level, elevated in two cases, was not associated with the clinical situation and AFP value appears to have questionable diagnostic importance as the tumor marker. Although we had no standard chemotherapeutic programs for immature teratomas, it is believed that the more aggressive surgery followed by good combination chemotherapy brings better prognosis.