Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society最新文献

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Ca2+ influx and platelet membrane glycoproteins. Ca2+内流与血小板膜糖蛋白。
A Yamaguchi, K Tanoue, H Yamazaki
{"title":"Ca2+ influx and platelet membrane glycoproteins.","authors":"A Yamaguchi,&nbsp;K Tanoue,&nbsp;H Yamazaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>When aequorin-loaded platelets were stimulated with thrombin, the luminescence of aequorin showed two peaks. From experiments with 1 mM external Ca2+ or 1 mM EGTA, both one-half of the first peak and the entire second peak reflected the influx of Ca2+ from the external medium, and the remaining half of the first peak reflected the mobilization of Ca2+ from its storage site. A monoclonal antibody (TM83), that recognizes the GPIIb/IIIa complex which has binding sites for fibrinogen, and synthetic peptide GRGDSP are known to inhibit fibrinogen binding and platelet aggregation. Both of them eliminated the second peak of intracellular free calcium. Similar effects were observed during activation by collagen, but not by TPA. Also dihydrocytochalasin B inhibited the second peak of Ca2+ influx by thrombin, suggesting that the signal, which was caused by fibrinogen-binding to GPIIb/IIIa (aggregation) in thrombin-activated platelets, is transferred to the inner sites of GPIIb/IIIa complex and induces the cytoskeletal reorganization such as actin polymerization. This in turn, induces the secondary increase in [Ca2+] i of platelets. It is interesting that ticlopidine inhibited the Ca2+ influx through the GPIIb/IIIa complex. This result suggests the importance of such kinds of antiplatelet drugs to prevent thrombus formation.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1480-8"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13772386","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 anemia. Immunosuppressive therapy in a multi center trial in Japan. 再生障碍性贫血。免疫抑制疗法在日本的多中心试验。
K Kitamura, A Urabe
{"title":"Aplastic anemia. Immunosuppressive therapy in a multi center trial in Japan.","authors":"K Kitamura,&nbsp;A Urabe","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We evaluated the biologic characteristics and effectiveness of immunosuppressive agents in patients with a severe form of aplastic anemia in a multicenter study. Treatment with a bolus of methylprednisolone (mPSL) was associated with a good response and a partial response in 19.4% and 1.4% of the patients, respectively. In contrast, two kinds of antilymphocyte globulin (ALG) were effective for 9.4% and 15.6% of the severe form of aplastic anemia, and two kinds of antithymocytoglobulin (ATG) were effective in 30.8% and 37.2% of the patients, although the difference between ALG and ATG was not statistically significant. We recommend that patients diagnosed as having severe aplastic anemia should be referred as soon as possible for treatment with immunosuppressive agents or bone marrow transplantation, the latter depending on disease severity, age, and potential availability of an HLA-identical sibling donor.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1361-9"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13840142","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
A mechanism for cross-lineage gene rearrangements in B-cell neoplasm. b细胞肿瘤中跨谱系基因重排的机制。
H Miwa, K Kita, T Nosaka, K Kawakami, T Ikeda, S Shirakawa
{"title":"A mechanism for cross-lineage gene rearrangements in B-cell neoplasm.","authors":"H Miwa,&nbsp;K Kita,&nbsp;T Nosaka,&nbsp;K Kawakami,&nbsp;T Ikeda,&nbsp;S Shirakawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The organization of immunoglobulin heavy chain (IgH) gene of B precursor cell acute lymphoblastic leukemia (ALL) was examined in order to elucidate the mechanism causing simultaneous TCR gene rearrangements. Study using a 5'D probe lying 20 kb upstream of IgH D region genes was useful to distinguish diversity(D)-joining(J) recombination(DJ) from variable(V)-DJ recombination(VDJ). Indeed, IgH gene structures determined by 5'D study well correlated to those recognized by DJ or VDJ transcripts. IgH gene rearrangements of B precursor cell ALL showed developmentally restricted gene recombination; DJ/DJ genotype in the most immature stage and VDJ/VDJ genotype in the relatively mature stage. B precursor cell ALL with simultaneous rearrangements were frequently found in relatively mature cells, i.e., CD20 expressing cells on their surface. Furthermore, most of such dual genotypic ALL showed that at least one allele of IgH genes was VDJ recombination. This finding suggests that dual genotype was the incidental product by a putative common recombinase during the process of VH gene rearrangements. Moreover, since IgH gene rearrangements of acute unclassified leukemia with dual genotype were DQ52 genotype, which indicates abortive gene rearrangements, it was also thought that dual genotype occurred due to the pluripotentiality of the stem cell.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1442-50"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13664941","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
Molecular genetic approach to the analysis of clonal proliferation in hematologic disorders. 血液病克隆增殖的分子遗传学分析。
K Morita, N Tsukamoto, M Karasawa, M Omine
{"title":"Molecular genetic approach to the analysis of clonal proliferation in hematologic disorders.","authors":"K Morita,&nbsp;N Tsukamoto,&nbsp;M Karasawa,&nbsp;M Omine","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The clonal composition of each cell population was determined from the characteristic methylation pattern of DNA and the restriction fragment length polymorphism (RFLP) of the hypoxanthine phosphoribosyltransferase (HPRT) and phosphoglycerate kinase (PGK) genes, both located on the X chromosome. About 71% of Japanese females are heterozygous in terms of the RFLP of either HPRT or PGK genes, which was demonstrated by using 5' genomic DNA or cDNA probes for these genes. All 3 cases of chronic myeloproliferative disorders showed monoclonal patterns. AML or ALL cases demonstrated either monoclonal or polyclonal patterns depending upon the percentage of blastic cells. Monoclonal patterns were seen in 3 of 4 cases of myelodysplastic syndromes and both PNH cases.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1414-22"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13718905","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
Bone marrow transplantation for patients with severe aplastic anemia and myelodysplastic syndrome. 骨髓移植治疗严重再生障碍性贫血和骨髓增生异常综合征。
S Kai, Y Shinohara
{"title":"Bone marrow transplantation for patients with severe aplastic anemia and myelodysplastic syndrome.","authors":"S Kai,&nbsp;Y Shinohara","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A survey of the results of marrow transplantation for severe aplastic anemia (SAA) and myelodysplastic syndrome (MDS) in Japan is reported. Of the 152 patients with SAA, 109 were alive between 2 and 132 months following transplantation and the probability of survival at 5 years was 70% (for the patients with grafts from HLA-matched siblings) and 100% (for the patients with grafts from monozygous twins). Survival rate at 3 years for the patients with grafts from family members other than HLA-matched siblings was 46%. The chance of survival was influenced by conditioning regimen and recipient's age. Recipients with sustained engraftment had a significantly higher survival rate than those with graft failure (83% vs 11%, p less than 0.001). Since 1985, the results of transplantation from HLA-matched siblings have improved and the 3-year survival is more than 90% for patients under 20 years old. For MDS, the actuarial survival at 3 years was 42%. The chance of survival was not influenced by the FAB classification, patient's age, patient's sex, interval from diagnosis to transplant, karyotype anomaly or graft versus host disease.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1402-11"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13772381","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
Prognosis of chronic thrombocytopenic purpura. 慢性血小板减少性紫癜的预后。
S Kuriya, T Nomura
{"title":"Prognosis of chronic thrombocytopenic purpura.","authors":"S Kuriya,&nbsp;T Nomura","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A multicenter prospective study on the treatment of chronic idiopathic thrombocytopenic purpura (ITP), conducted by the Idiopathic Disorders of Hematopoietic Organ Research Committee, the Ministry of Health and Welfare of Japan, is currently in progress. In this study we analyzed the clinical records of 256 patients with chronic ITP in order to define the prognostic factors. As of November, 1988 after a median observation period of 34 months, 174 of the 256 patients (68%) were alive, 11 (4%) dead and 71 (28%) lost to follow-up. Bleeding was a direct cause of death in only one patient. Assessment of the status of patients based on platelet count at the final observation revealed that 48% of patients were in remission, 21% showed improvement, and 31% remained unchanged or worsened. Univariate analyses identified 4 parameters associated with favorable prognosis: presenting platelet count less than 2 x 10(4)/microliters, platelet count greater than 10 X 10(4)/microliters after one-year follow-up, maximal platelet count greater than 10 X 10(4)/microliters during administration of the initial dose of corticosteroids and splenectomy.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1379-85"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13840145","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
Analysis of gene amplification in human tumor cells by in-gel DNA renaturation assay. 凝胶DNA再生法分析人肿瘤细胞基因扩增。
M Fukumoto, H Tashiro, I B Roninson
{"title":"Analysis of gene amplification in human tumor cells by in-gel DNA renaturation assay.","authors":"M Fukumoto,&nbsp;H Tashiro,&nbsp;I B Roninson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The incidence of gene amplification in leukemia/lymphoma is significantly lower than that in solid tumors. For understanding the biological characteristics of leukemia/lymphoma, it is necessary to clarify whether the incidence of gene amplification is actually lower or gene amplification specific to hemopoietic malignancies has not yet been found. We describe a new version of in-gel DNA renaturation technique for general screening of gene amplification that allows detection and cloning of amplified genes of unknown nature as few as 7- to 8-fold amplification.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1463-70"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13772385","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 signal transduction systems and intracellular Ca2+ dynamics in arachidonate-induced platelet activation. 花生四烯酸盐诱导血小板活化的信号转导系统和细胞内Ca2+动力学。
M Nishikawa, F Komada, Y Uemura, H Hidaka, S Shirakawa
{"title":"The signal transduction systems and intracellular Ca2+ dynamics in arachidonate-induced platelet activation.","authors":"M Nishikawa,&nbsp;F Komada,&nbsp;Y Uemura,&nbsp;H Hidaka,&nbsp;S Shirakawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Types II and III protein kinase C were expressed in human platelets and showed slightly different modes of activation and kinetic properties. Type III isozyme was more sensitive than type II for the activation of each isozyme with arachidonate (AA) although both isozymes were activated by diacylglycerol and phosphatidylserine in a similar manner. When human platelets were stimulated by AA, two types of platelet activation, a low level of AA (0.1-2.5 micrograms/ml)- and a high level of AA (10-50 micrograms/ml)-induced activations, were observed. These activations were associated with the phosphorylation of 40K and 20K proteins. Although a low level of AA (0.45-10.0 micrograms/ml) induced the formation of [32P] phosphatidate in intact platelets prelabeled with [32P] Pi, AA at high concentrations (20-50 micrograms/ml) did not stimulate phospholipase C. The incubation of fura 2 loaded platelets with a low level of AA evoked a rapid and transient elevation in [Ca2+] i. In contrast, a high level of AA induced an irreversible increase in [Ca2+] i but this [Ca2+] i elevation alone was not associated with platelet activation. These results suggest that the signal transduction system by a high level of AA on human platelets is different from that seen with a low level of AA. A high level of AA induces platelet activation, without phospholipase C stimulation, and therefore, the ability of AA to directly activate protein kinase C (pre-dominantly type III isozyme) may contribute toward the activation of platelets by a high level of AA.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1489-97"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13663340","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 role of complex formation and epidermal growth factor-like domains in the regulation of blood coagulation by the thrombomodulin-protein C system. 复合物的形成和表皮生长因子样结构域在凝血调节蛋白C系统中的作用。
S Kurosawa
{"title":"The role of complex formation and epidermal growth factor-like domains in the regulation of blood coagulation by the thrombomodulin-protein C system.","authors":"S Kurosawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The explosive nature of the coagulation cascade led many scientists to investigate how it is regulated. Proteinase inhibitors such as antithrombin III inhibit active proteases of the coagulation cascade. Cofactors such as factor Va and factor VIIIa are proteolytically inactivated by activated protein C. Protein C is activated by the thrombin-thrombomodulin complex on the endothelial cell surface. Thus, the independent actions of the proteinase inhibitor system and the thrombomodulin-protein C system complement each other to maintain regulation of blood coagulation. The thrombin binding site of thrombomodulin was identified to be the fifth and sixth repeats of the epidermal growth factor-like domain. The same binding template contains sufficient information to block the functions of thrombin as a procoagulant. However, additional repeats are required for the activation of protein C. Thrombomodulin is the first example which illustrates that the epidermal growth factor-like domain functions as a binding template for thrombin and as a switch to turn off the procoagulant activity of thrombin as well as to trigger the protein C anticoagulant pathway. Epidermal growth factor-like structures are found in many of the coagulation factors. Complex formation is a repeated theme not only in the blood coagulation cascade but also in the thrombomodulin-protein C anticoagulant pathway.</p>","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1343-9"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13703353","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
Chronic B cell lymphocytic leukemias: diagnosis and cytologic characteristics of their cells. 慢性B细胞淋巴细胞白血病的诊断及其细胞的细胞学特征。
T Kitani
{"title":"Chronic B cell lymphocytic leukemias: diagnosis and cytologic characteristics of their cells.","authors":"T Kitani","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76233,"journal":{"name":"Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society","volume":"52 8","pages":"1279-86"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13838549","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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