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Red cell ferritin--its biochemical and clinicopathological characterization. 红细胞铁蛋白——其生化和临床病理特征。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-12-01
H Yamada
{"title":"Red cell ferritin--its biochemical and clinicopathological characterization.","authors":"H Yamada","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1302-9"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13838550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Interactions via eicosanoids between vascular and blood cells. 血管细胞和血细胞之间通过类二十烷的相互作用。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-12-01
H Takayama
{"title":"Interactions via eicosanoids between vascular and blood cells.","authors":"H Takayama","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1322-9"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13838551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cytosolic calcium levels in vascular smooth muscle. 血管平滑肌细胞质钙水平。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-12-01
H Karaki
{"title":"Cytosolic calcium levels in vascular smooth muscle.","authors":"H Karaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Increase in cytosolic Ca2+ level ([Ca2+] cyt) is prerequisite for smooth muscle contraction. Simultaneous measurements of [Ca2+] cyt and muscle tension give direct information for the Ca2(+)-regulation of smooth muscle. A fluorescent Ca2+ indicator, fura-2, is used for this purpose. Comparison between [Ca2+] cyt and muscle tension in vascular smooth muscle indicates that, although high K+ and receptor-agonists such as norepinephrine and prostaglandin F2 alpha induce sustained contraction by the sustained increase in [Ca2+] cyt, greater contraction is produced by receptor-agonists than high K+ at a given [Ca2+]cyt. Phorbol ester show similar effects as receptor-agonists, and it potentiates a high K(+)-induced contraction with little effect on [Ca2+]cyt. These results suggest that the contraction of smooth muscle is due to the increase in [Ca2+]cyt. Furthermore, receptor-agonists stimulate phosphatidylinositol turnover and generates diacyl glycerol which activates protein kinase C and may consequently increase the Ca2+ sensitivity of contractile elements. The [Ca2+]cyt -dependent portion of these contractions is inhibited by Ca2+ channel blockers such as verapamil by the decrease in [Ca2+]cyt. By contrast, increase in cyclic AMP by isoproterenol and forskolin inhibits smooth muscle contraction by the decrease in [Ca2+]cyt also by the decrease in the Ca2+ sensitivity of contractile elements. Increase in the cyclic GMP level by sodium nitroprusside show effects quite similar to those of cyclic AMP. Thus, contractility of vascular smooth muscle seems to be regulated by [Ca2+]cyt and also by Ca2+ sensitivity of the contractile elements. Furthermore, at least part of the receptor-mediated changes may be due to activation of protein kinase C.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1506-15"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13840147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Flow cytometric studies of anti-granulocyte antibodies]. [流式细胞术研究抗粒细胞抗体]。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-11-01
M Ohnishi
{"title":"[Flow cytometric studies of anti-granulocyte antibodies].","authors":"M Ohnishi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>An indirect immunofluorescence test using anti-granulocyte antibodies was developed to examine many sera samples in a one-step procedure by flow cytometry. Granulocytes obtained from several random donors were fixed with 0.5% paraformaldehyde solution on the first day, and the fluorescence intensity of granulocytes that had reacted with sera was measured on the following day. Non-specific reactions with isoantibodies, i.e., anti-A, anti-B, or serum IgG had no influence on the fluorescence intensity. Therefore, anti-granulocyte antibodies from a patient with immune neutropenia and patients with febrile transfusion reactions can be studied using this method. The results suggest that the IgG-antibody from a patient with immune neutropenia is granulocyte-specific and its subclass is IgG2.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 7","pages":"1147-54"},"PeriodicalIF":0.0,"publicationDate":"1989-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13759891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Genetic markers and thrombin reaction in a family of Bernard-Soulier syndrome]. [遗传标记与Bernard-Soulier综合征家族的凝血酶反应]。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-11-01
Y Shimamoto, H Kaneoka, M Matsuzaki, Y Katsuki, K Ono, M Sano, T Kariya, M Yamaguchi
{"title":"[Genetic markers and thrombin reaction in a family of Bernard-Soulier syndrome].","authors":"Y Shimamoto,&nbsp;H Kaneoka,&nbsp;M Matsuzaki,&nbsp;Y Katsuki,&nbsp;K Ono,&nbsp;M Sano,&nbsp;T Kariya,&nbsp;M Yamaguchi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A family with Bernard-Soulier syndrome (BSS) was investigated with reference to the genetic markers and thrombin reactions. The proband was a 24-year-old man with a life-long history of epistaxis and gingival bleeding. His parents were first cousins; furthermore, his father was born to parents of second cousins. His father also had bleeding tendency and was also diagnosed as having BSS. However, his mother and elder brother were normal. Genetic marker analysis among the family members suggested that the 16th chromosome was associated with the development of BSS, because only the haptoglobin genotype coded on the 16th chromosome was the marker in both the proband and his father. In addition, they both exhibited decreased thrombin-induced platelet aggregation at a low dose, but an almost normal reaction at a high dose of thrombin.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 7","pages":"1155-8"},"PeriodicalIF":0.0,"publicationDate":"1989-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13759892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[The molecular basis of HbH disease in a Japanese girl]. [一名日本女孩HbH疾病的分子基础]。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-11-01
T Harano, K Harano, S Ueda, T Nagao, T Mori
{"title":"[The molecular basis of HbH disease in a Japanese girl].","authors":"T Harano,&nbsp;K Harano,&nbsp;S Ueda,&nbsp;T Nagao,&nbsp;T Mori","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hemoglobin H disease is often caused by deletion of three of the four alpha-globin genes (genotype: --/-alpha). We studied a Japanese girl who had microcytic hypochromic anemia, a decreased alpha/beta globin synthetic ratio and about 8% Hb H in her fresh hemolysate, by means of restriction endonuclease mapping of the alpha-like gene complex (5'-zeta-phi zeta-phi alpha 2-phi alpha 1-alpha 2-alpha 1-theta-3') with zeta- and alpha-specific probes. It was found that the defect of one chromosome was associated with the removal of about 18 kb of DNA, known as --SEA type alpha-thalassemia-1, including the deletion of the part of phi alpha 2, phi alpha 1, alpha 2, alpha 1, and theta globin genes, while the other one was associated with the removal of 3.7 kb of DNA, known as rightward deletion type alpha-thalassemia-2. The results of a family study demonstrated that the deletion haplotype --SEA was inherited from her father's side and the other -alpha 3.7 from her mother's side.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 7","pages":"1128-36"},"PeriodicalIF":0.0,"publicationDate":"1989-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13759890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Aplastic crisis due to human parvovirus B19 infection in glucose-6-phosphate dehydrogenase deficiency]. [葡萄糖-6-磷酸脱氢酶缺乏症患者细小病毒B19感染所致再生危机]。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-11-01
K Nibu, I Matsumoto, F Yanai, T Nunoue
{"title":"[Aplastic crisis due to human parvovirus B19 infection in glucose-6-phosphate dehydrogenase deficiency].","authors":"K Nibu,&nbsp;I Matsumoto,&nbsp;F Yanai,&nbsp;T Nunoue","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Human parvovirus B19 is known to cause aplastic crisis in patients with hemolytic anemias due to cytotoxic effect of the infection to erythroid progenitor cells. We report here the first case of aplastic crisis by B19 in a patient with glucose-6-phosphate dehydrogenase deficiency. A five-year-old boy was admitted to the hospital because of severe anemia, fever and jaundice. Four weeks after admission, he developed erythema infectiosum. B19 infection was confirmed using countercurrent immunoelectrophoresis, Southern blotting and hybridization method, and radioimmunoassay for B19 specific IgM. B19 virus antigen was detected by an indirect immunofluorescent method in both the cytoplasm and nucleus of large mononuclear cells that had no granules in bone marrow. On admission, the hemoglobin was 3.1 g/dl and no reticulocytes were detected in the peripheral blood smear. Bone marrow examination revealed a normocellular marrow with erythroid hypoplasia and M/E ratio of 7.38. Large basophilic erythroblasts containing vacuoles were also noticed. Elevation of indirect bilirubin and hemoglobinuria suggested intravascular hemolysis. Transient mild thrombocytopenia associated with increased PAIgG was observed. It is likely that B19 virus infection caused hemolysis which contributed to severe anemia.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 7","pages":"1117-21"},"PeriodicalIF":0.0,"publicationDate":"1989-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13702496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[c-myc gene amplification and N-ras transforming gene in two cases of acute myelocytic leukemia with double minute chromosomes]. [c-myc基因扩增和N-ras转化基因在2例急性髓细胞白血病伴双微小染色体中的应用]。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-11-01
K Tanaka, M Takechi, J Hong, C Shigeta, N Oguma, N Kamada, Y Takimoto, A Kuramoto, H Okita
{"title":"[c-myc gene amplification and N-ras transforming gene in two cases of acute myelocytic leukemia with double minute chromosomes].","authors":"K Tanaka,&nbsp;M Takechi,&nbsp;J Hong,&nbsp;C Shigeta,&nbsp;N Oguma,&nbsp;N Kamada,&nbsp;Y Takimoto,&nbsp;A Kuramoto,&nbsp;H Okita","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We report two leukemia patients with double minutes (DMs) chromosomes. Both patients were diagnosed as having acute myelocytic leukemia (AML) FAB M2. Cytogenetic analysis showed normal chromosome karyotype with 1-53 DMs chromosomes in the first patient, and complex chromosome aberrations including deletion of chromosome 8 at 8q24 region and 1-84 DMs chromosomes in the second patient who had a history of extensive radiotherapy for laryngeal cancer 8 years prior to the development of leukemia. Analysis of DNA from the two patients revealed that oncogene of c-myc was amplified about 5 to 10 folds in the leukemic cells. The other fourteen oncogene of c-myc was c-myb, c-abl and N-myc, showed no increases of gene content. Furthermore, a transforming gene, N-ras was detected in the first patient by in vivo selection assay method. This is the second report on AML patients with c-myc gene amplification and DMs chromosomes.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 7","pages":"1137-46"},"PeriodicalIF":0.0,"publicationDate":"1989-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13834505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Role of protein C in endotoxin-induced release of plasminogen activator inhibitor from endothelial cell]. [蛋白C在内毒素诱导的纤溶酶原激活物抑制剂从内皮细胞释放中的作用]。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-11-01
K Okajima, S Koga, T Nakagaki, H Okabe, A Funatsu, K Takatsuki
{"title":"[Role of protein C in endotoxin-induced release of plasminogen activator inhibitor from endothelial cell].","authors":"K Okajima,&nbsp;S Koga,&nbsp;T Nakagaki,&nbsp;H Okabe,&nbsp;A Funatsu,&nbsp;K Takatsuki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To elucidate the role of protein C (PC) in the release of plasminogen activator inhibitor (PAI) from endothelial cells, the effect of PC and activated protein C (APC) on plasma levels of PAI in endotoxin (ET)-treated rats was examined. When activated by snake venom, human PC significantly prolonged the activated partial thromboplastin time (APTT) of both human and rat plasma samples. Addition of APC also prolonged the APTT of both human and rat plasma samples. PAI activity in plasma from septicemic patients and ET-treated rats was neutralized by APC. A small dose of ET (0.1 microgram/kg) gradually increased plasma PAI activity, which became maximum 3h after ET-treatment. APC administered prior to ET-treatment, PC decreased PAI activity, however, no such inhibition was seen when administered after ET-treatment. A significant negative correlation between PC concentrations and PAI activities was observed in plasma from septicemic patients. These findings indicated that activation of PC on endothelial surface plays a regulatory role in releasing PAI and that endotoxin might inhibit the surface activation of PC.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 7","pages":"1159-64"},"PeriodicalIF":0.0,"publicationDate":"1989-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13759893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Alteration of erythrocyte membrane proteins in a family with hereditary spherocytosis]. [遗传性球形红细胞增多症家族中红细胞膜蛋白的改变]。
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society Pub Date : 1989-11-01
F Inoue, R Matsuyama, S Yoneyama
{"title":"[Alteration of erythrocyte membrane proteins in a family with hereditary spherocytosis].","authors":"F Inoue,&nbsp;R Matsuyama,&nbsp;S Yoneyama","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Erythrocyte membrane proteins in a family of nine with hereditary spherocytosis in Okinawa were analyzed by polyacrylamide gel electrophoresis in the presence of 0.1% SDS. An abnormality in the membrane protein component band 4.2 (MW 72 kDa) on the electrophoresis was observed. Deficiency in band 4.2 was found in three sibling in the family and a small but significant decrease was noted in three other members. However, change of this component was not found in the remaining members of the family or in normal subjects.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 7","pages":"1122-7"},"PeriodicalIF":0.0,"publicationDate":"1989-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13759889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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