start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=105 end-page=114 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A cytogenetic study of nonpolymalformed patients with mental retardation of clinically undefined etiology: application of a high resolution banding technique. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

We performed a cytogenetic study on 140 nonpolymalformed patients with mental retardation of clinically undefined origin, using a high resolution banding technique, to determine how much chromosome abnormalities contribute to the etiology of this condition. A total of 15 patients (10.7%) were found to have autosomal or sex chromosomal abnormalities. Autosomal abnormalities included partial monosomy (5 cases), reciprocal translocation (one case), 13/14 robertsonian translocation (3 cases), unbalanced translocation (one case), inverted duplication of 15q (one case) and mosaic trisomy 21 (one case). Sex chromosomal abnormalities comprised structural rearrangement of the short arm of the X chromosome (one case) and 47, XXY in a pure or mosaic form (two cases). It should be noted that four out of the 5 cases of partial monosomy had subtle interstitial deletions, which might have been unidentified by the conventional G-banding method alone. In one case of the robertsonian translocation 46,XY,t(13;14)/45,XY,t(13;14), a small deletion was thought to have occurred in the cells with a chromosome number of 45. Comparison of clinical features of the 15 chromosomally abnormal patients with those of patients with normal karyotypes did not show any clinical parameter indicative of chromosome imbalance. These results suggest that a subtle chromosomal deletion is specific to mental retardation associated with few malformations. We believe that diagnostic evaluation of mentally retarded patients, even if nonmalformed, should include chromosome analysis using a high resolution banding technique.

en-copyright= kn-copyright= en-aut-name=KikkawaKiyoshi en-aut-sei=Kikkawa en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=NaraharaKouji en-aut-sei=Narahara en-aut-mei=Kouji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KimotoHiroshi en-aut-sei=Kimoto en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=chromosomes kn-keyword=chromosomes en-keyword=high resolution banding technique kn-keyword=high resolution banding technique en-keyword=subtle interstitial deletion kn-keyword=subtle interstitial deletion en-keyword=mental retardation kn-keyword=mental retardation END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=131 end-page=134 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A case of ovarian leiomyoma. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

A case of ovarian leiomyoma is reported, together with histologic, immunohistologic and electron microscopic findings. A solid firm tumor, measuring 6.5 X 5 X 5 cm, was found in the right ovary of a 65-year-old woman. The tumor had an obvious whorled pattern on the cut-surface. Well-differentiated, long spindle-shaped neoplastic cells revealed positive immunoreactivity for anti-desmin. Ultrastructural observations included numerous microfilaments with dense patches in the cytoplasm, micropinocytotic vesicles beneath plasma membranes and continuous basal laminae around neoplastic cells. These findings were compatible with leiomyoma. The possible histogenesis of ovarian leiomyoma was discussed.

en-copyright= kn-copyright= en-aut-name=SonobeHiroshi en-aut-sei=Sonobe en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKazuhiko en-aut-sei=Hayashi en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakahashiKiyoshi en-aut-sei=Takahashi en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Kochi Medecal Scool affil-num=2 en-affil= kn-affil=Kochi Medecal Scool affil-num=3 en-affil= kn-affil=Kochi Medecal Scool en-keyword=leiomyoma kn-keyword=leiomyoma en-keyword=ovary kn-keyword=ovary en-keyword=immunohistochemistry kn-keyword=immunohistochemistry en-keyword=ultrastructure kn-keyword=ultrastructure END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=73 end-page=80 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A cell-free system for studying a priming factor involved in repair of bleomycin-damaged DNA. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

A simple cell-free system for studying a priming factor involved in the repair of bleomycin-damaged DNA was established. The template-primer used for the repair DNA synthesis was prepared by treating the closed circular, superhelical form of pUC19 plasmid DNA with 2.2 microM bleomycin and 20 microM ferrous ions. Single-strand breaks were introduced into pUC19 DNA by the bleomycin treatment, and the DNA was consequently converted largely into the open circular form. A system for repair of this bleomycin-damaged DNA was constructed with a priming factor, DNA polymerase (DNA polymerase beta or Klenow fragment of DNA polymerase I), ATP, T4 DNA ligase and four deoxynucleoside triphosphates. After incubation, the conformation of the DNA was analyzed by agarose gel electrophoresis and electron microscopy. The open circular DNA was largely converted to the closed circular DNA, indicating that the single-strand breaks of DNA were repaired. When the priming factor was omitted, DNA repair did not occur. The present system seemed to be applicable to the study of priming factors involved in the repair of DNA with single-strand breaks caused not only by bleomycin but also by ionizing radiation or active oxygen.

en-copyright= kn-copyright= en-aut-name=SekiShuji en-aut-sei=Seki en-aut-mei=Shuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ArakakiYusei en-aut-sei=Arakaki en-aut-mei=Yusei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OdaTakuzo en-aut-sei=Oda en-aut-mei=Takuzo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=priming factor kn-keyword=priming factor en-keyword=exonuclease kn-keyword=exonuclease en-keyword=DNA repair kn-keyword=DNA repair en-keyword=bleomycin kn-keyword=bleomycin en-keyword=pUC19 DNA kn-keyword=pUC19 DNA en-keyword=agarosegel electrophoresis kn-keyword=agarosegel electrophoresis END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=97 end-page=103 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Composition of culture media for steroid hormone secretion by murine adrenal tumor cells, Y-1 clone. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Murine adrenal tumor cells (Y-1 clone) were stimulated by adrenocorticotropic hormone (ACTH) and cyclic adenosine 3',5'-monophosphate (cyclic AMP) to produce steroid hormone (delta 4, 3-keto steroids). The steroids were secreted into the medium immediately after synthesis. The optimum concentrations of ACTH and cyclic AMP for stimulation of steroid production were 10(-2) U/ml and 1.0 mM, respectively. In serum-free medium, ACTH and cyclic AMP stimulated steroidogenesis in Y-1 cells, but the amount of steroid hormone in the culture medium was low. However, a high level of steroid production was maintained with medium containing 10 mg/ml bovine serum albumin (BSA). In culture medium containing a higher concentration of BSA, Y-1 cells did not become spherical as is usually the case when steroid production is stimulated by ACTH or cyclic AMP. The morphological changes did not always correlate with steroid secretion by Y-1 cells.

en-copyright= kn-copyright= en-aut-name=IchikawaYoshiko en-aut-sei=Ichikawa en-aut-mei=Yoshiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University en-keyword=Y-1 clone kn-keyword=Y-1 clone en-keyword=steroid hormone kn-keyword=steroid hormone en-keyword=ACTH kn-keyword=ACTH en-keyword=cyclic AMP kn-keyword=cyclic AMP END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=89 end-page=95 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Reduction of 3-mercaptopyruvate in rat liver is catalyzed by lactate dehydrogenase. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

It has been assumed that the in vivo reduction of 3-mercaptopyruvate, an intermediate of cysteine metabolism, to 3-mercaptolactate is catalyzed by lactate dehydrogenase (EC 1.1.1.27) though no definitive evidence has been presented. In order to examine this assumption, reduction of 3-mercaptopyruvate and its inhibition were studied using rat liver homogenate, lactate dehydrogenase purified from rat liver and anti-lactate dehydrogenase antiserum. Reduction of 3-mercaptopyruvate was actively catalyzed by rat liver homogenate and by the purified lactate dehydrogenase. This reducing activity was completely inhibited by anti-lactate dehydrogenase antiserum. These results indicate that the reduction of 3-mercaptopyruvate to 3-mercaptolactate in rat liver is catalyzed by lactate dehydrogenase.

en-copyright= kn-copyright= en-aut-name=OhtaJun en-aut-sei=Ohta en-aut-mei=Jun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UbukaToshihiko en-aut-sei=Ubuka en-aut-mei=Toshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University en-keyword=3-mercaptopyruvate kn-keyword=3-mercaptopyruvate en-keyword=3-mercaptolactate kn-keyword=3-mercaptolactate en-keyword=lactate dehydrogenase kn-keyword=lactate dehydrogenase en-keyword=antiserum kn-keyword=antiserum en-keyword=cysteine metabolism kn-keyword=cysteine metabolism END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=81 end-page=88 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Studies on bleomycin-induced repair DNA synthesis in permeable mouse ascites sarcoma cells. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

To study the mechanism of DNA excision repair, a DNA repair system employing permeable mouse sarcoma (SR-C3H/He) cells was established and characterized. SR-C3H/He cells were permeabilized with a 0.0175% Triton X-100 solution. The permeable cells were treated with 1 mM ATP and 0.11 mM bleomycin, and then washed thoroughly to remove ATP and bleomycin. Repair DNA synthesis occurred in the bleomycin-damaged, permeable SR-C3H/He cells when incubated with ATP and four deoxyribonucleoside triphosphates. The repair nature of the DNA synthesis was confirmed by the BrdUMP density shift technique, and by the reduced sensitivity of the newly synthesized DNA to Escherichia coli exonuclease III. The DNA synthesis was optimally enhanced by addition of 0.08 M NaCl. Studies using selective inhibitors of DNA synthesis showed that aphidicolin-sensitive DNA polymerase (DNA polymerase alpha and/or delta) and DNA polymerase beta were involved in the repair process. The present DNA repair system is thought to be useful to study nuclear DNA damage by bleomycin, removal of the damaged ends by an exonuclease, repair DNA synthesis by DNA polymerases and repair patch ligation by DNA ligase(s).

en-copyright= kn-copyright= en-aut-name=MoriShigeru en-aut-sei=Mori en-aut-mei=Shigeru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SekiShuji en-aut-sei=Seki en-aut-mei=Shuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OdaTakuzo en-aut-sei=Oda en-aut-mei=Takuzo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=DNA repair kn-keyword=DNA repair en-keyword=bleomycin kn-keyword=bleomycin en-keyword=DNA polymerases kn-keyword=DNA polymerases en-keyword=permeable cells kn-keyword=permeable cells en-keyword=mouse ascites cells kn-keyword=mouse ascites cells END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=127 end-page=129 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Rapid purification of squirrel monkey retrovirus-H major gag protein by high performance liquid chromatography. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

The major gag protein (p34) of squirrel monkey retrovirus-H was purified in one chromatographic step by anion-exchange high performance liquid chromatography. The virus in a crude fraction was disrupted with Brij 35 in the presence of three kinds of protease inhibitors. The soluble virus lysate was injected into a Polyanion SI column, and p34 was eluted with a linear salt gradient. The recovery of the protein was about 60%. The purified p34 was nearly homogenous as judged by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and silver staining.

en-copyright= kn-copyright= en-aut-name=IkedaShogo en-aut-sei=Ikeda en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TsutsuiKen en-aut-sei=Tsutsui en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HatsushikaMasao en-aut-sei=Hatsushika en-aut-mei=Masao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=WatanabeSekiko en-aut-sei=Watanabe en-aut-mei=Sekiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=OdaTakuzo en-aut-sei=Oda en-aut-mei=Takuzo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=retrovirus kn-keyword=retrovirus en-keyword=gag protein kn-keyword=gag protein en-keyword=protein purification kn-keyword=protein purification en-keyword=high performance liquid chromatography kn-keyword=high performance liquid chromatography END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=115 end-page=126 dt-received= dt-revised= dt-accepted= dt-pub-year=1989 dt-pub=198904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Initiation and recovery processes of endotoxin induced disseminated intravascular coagulation (DIC): scanning and transmission electron microscopic observations of rat renal tissues. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

To clarify the initiation, development and recovery processes of disseminated intravascular coagulation (DIC), rat glomerular capillaries and fibrin thrombi were examined under transmission and scanning electron microscopes. DIC was induced in rats by a single intraperitoneal injection of endotoxin (Et., 7.5 mg/kg lipopolysaccharide:B, E. coli 026:B6). At 2 h after Et. injection, the endothelial surface of the glomerular capillary became irregular with projections like a sea anemone. At 4 h after Et. injection, agglomerated fibrin thrombi composed of fibrin fiber bundles with fine cross-striated fibriform structures were observed in the capillary lumen. The fibrin thrombi gradually changed into fine reticular systems suggesting a degradation process by 6 h after Et. injection, and formed a coarse granular agglomerate by 8 h after Et. injection. These fibrin thrombi disappeared within 12 h of Et. injection, but the endothelial surface remained edematous. At 24 h after Et. injection, the microstructure of the glomerular capillaries returned normal. Based on these observations, we concluded that DIC was primarily initiated by injury to the capillary endothelium, and that changes on the endothelial surface contributed to the development of DIC.

en-copyright= kn-copyright= en-aut-name=MiyashimaTakanao en-aut-sei=Miyashima en-aut-mei=Takanao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKeiki en-aut-sei=Hayashi en-aut-mei=Keiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AwaiMichiyasu en-aut-sei=Awai en-aut-mei=Michiyasu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=disseminated intravascular coagulation kn-keyword=disseminated intravascular coagulation en-keyword=renal tissue kn-keyword=renal tissue en-keyword=electron microscope kn-keyword=electron microscope en-keyword=rat kn-keyword=rat END