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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。
H Yamada
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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。
H Takayama
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引用次数: 0
Cytosolic calcium levels in vascular smooth muscle. 血管平滑肌细胞质钙水平。
H Karaki

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.

增加细胞质Ca2+水平([Ca2+] cyt)是平滑肌收缩的先决条件。同时测量[Ca2+] cyt和肌肉张力为平滑肌的Ca2(+)调节提供直接信息。荧光Ca2+指示剂fura-2用于此目的。[Ca2+]细胞和血管平滑肌肌张力之间的比较表明,尽管高K+和受体激动剂如去甲肾上腺素和前列腺素F2 α通过持续增加[Ca2+]细胞诱导持续收缩,但在给定的[Ca2+]细胞中,受体激动剂比高K+产生更大的收缩。佛波酯表现出与受体激动剂相似的作用,它增强了高K(+)诱导的收缩,而对[Ca2+]细胞的影响很小。这些结果表明,平滑肌的收缩是由于[Ca2+]cyt的增加。此外,受体激动剂刺激磷脂酰肌醇周转并产生二酰基甘油,其激活蛋白激酶C并可能因此增加收缩元件的Ca2+敏感性。这些收缩的[Ca2+]细胞依赖部分被Ca2+通道阻滞剂如维拉帕米通过[Ca2+]细胞减少而抑制。相比之下,异丙肾上腺素和福斯克林增加环AMP抑制平滑肌收缩,通过减少[Ca2+]cyt,也通过减少Ca2+收缩元件的敏感性。硝普钠增加环GMP水平的作用与环AMP非常相似。因此,血管平滑肌的收缩性似乎是由[Ca2+]cyt和收缩元件的Ca2+敏感性调节的。此外,至少部分受体介导的变化可能是由于蛋白激酶C的激活。
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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]。
M Ohnishi

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.

一种使用抗粒细胞抗体的间接免疫荧光试验被开发出来,通过流式细胞术一步检测许多血清样本。随机取几个供者的粒细胞,第一天用0.5%多聚甲醛溶液固定,第二天测定与血清反应的粒细胞的荧光强度。与抗a、抗b或血清IgG等等抗体的非特异性反应对荧光强度无影响。因此,免疫中性粒细胞减少患者和发热性输血反应患者的抗粒细胞抗体可以用这种方法进行研究。结果提示免疫中性粒细胞减少症患者的igg抗体是粒细胞特异性的,其亚类为IgG2。
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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]。
Y Shimamoto, H Kaneoka, M Matsuzaki, Y Katsuki, K Ono, M Sano, T Kariya, M Yamaguchi

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.

参考遗传标记和凝血酶反应对1例Bernard-Soulier综合征(BSS)家族进行了调查。先证者为24岁男性,终身有鼻出血和牙龈出血史。他的父母是表兄妹;此外,他的父亲是由表亲所生。父亲也有出血倾向,也被诊断为BSS。然而,他的母亲和哥哥都很正常。家族成员间的遗传标记分析表明,第16染色体与BSS的发生有关,因为在先证者及其父亲中,只有第16染色体上编码的触珠蛋白基因型是标记。此外,它们在低剂量时都表现出凝血酶诱导的血小板聚集减少,但在高剂量时几乎是正常的反应。
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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]。
T Harano, K Harano, S Ueda, T Nagao, T Mori

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.

血红蛋白H病通常是由四个α -珠蛋白基因(基因型:-/- α)中的三个缺失引起的。我们研究了一名日本女孩,她患有小细胞性低色素贫血,α / β珠蛋白合成比例下降,新鲜溶血中Hb H约为8%,采用zeta和α特异性探针对α样基因复合物(5'- ζ - φ ζ - α α 2- α α 1- α 2- α 1- α -3')进行限制性内切酶定位。结果发现,其中一条染色体的缺陷与约18 kb的DNA缺失相关,称为-SEA型α -地中海贫血-1,包括phi α 2、α α 1、α 2、α 1和θ珠蛋白部分的缺失,而另一条染色体的缺陷与3.7 kb的DNA缺失相关,称为右向缺失型α -地中海贫血-2。家庭研究结果表明,缺失单倍型-SEA遗传自父亲一方,而另一方- α 3.7遗传自母亲一方。
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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]。
K Nibu, I Matsumoto, F Yanai, T Nunoue

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.

人细小病毒B19由于感染红细胞祖细胞的细胞毒性作用,已知可引起溶血性贫血患者的再生危机。我们在此报告第一例由B19引起再生危机的患者葡萄糖-6-磷酸脱氢酶缺乏症。一名5岁男孩因严重贫血、发烧和黄疸入院。入院后4周,患者出现感染性红斑。采用逆流免疫电泳、Southern blotting和杂交法及B19特异性IgM放射免疫分析证实B19感染。用间接免疫荧光法在骨髓中无颗粒的大单核细胞的细胞质和细胞核中检测B19病毒抗原。入院时血红蛋白为3.1 g/dl,外周血涂片未检出网织红细胞。骨髓检查显示骨髓正常细胞伴红细胞发育不全,M/E比值为7.38。大嗜碱性红母细胞含有空泡。间接胆红素和血红蛋白尿升高提示血管内溶血。观察到短暂性轻度血小板减少与PAIgG升高相关。B19病毒感染可能导致溶血,从而导致严重贫血。
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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]。
K Tanaka, M Takechi, J Hong, C Shigeta, N Oguma, N Kamada, Y Takimoto, A Kuramoto, H Okita

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.

我们报告了两例双分钟(DMs)染色体白血病患者。两例患者均被诊断为急性髓细胞白血病(AML) FAB M2。细胞遗传学分析显示,1例患者染色体核型正常,1-53条DMs染色体;2例患者在白血病发生前8年有喉癌广泛放疗史,8号染色体8q24区缺失,1-84条DMs染色体复杂畸变。对两名患者的DNA分析显示,癌基因c-myc在白血病细胞中扩增了约5至10倍。c-myc的其他14个致癌基因为c-myb、c-abl和N-myc,基因含量没有增加。此外,通过体内选择法在第一例患者中检测到一种转化基因N-ras。这是关于c-myc基因扩增和DMs染色体的AML患者的第二篇报道。
{"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]。
K Okajima, S Koga, T Nakagaki, H Okabe, A Funatsu, K Takatsuki

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.

为了阐明蛋白C (PC)在内皮细胞释放纤溶酶原激活物抑制剂(PAI)中的作用,我们观察了蛋白C和活化蛋白C (APC)对内毒素(ET)处理大鼠血浆PAI水平的影响。当被蛇毒激活时,人PC显著延长了人和大鼠血浆样品的活化部分凝血活素时间(APTT)。APC的加入也延长了人和大鼠血浆样品的APTT。APC可中和败血症患者和et治疗大鼠血浆中的PAI活性。小剂量ET(0.1微克/千克)逐渐使血浆PAI活性升高,并在ET处理后3h达到最大值。在et治疗前施用APC, PC降低了PAI活性,但在et治疗后施用APC,没有发现这种抑制作用。败血症患者血浆中PC浓度与PAI活性呈显著负相关。提示内皮细胞表面PC的活化对PAI的释放具有调节作用,内毒素可能抑制了PC的表面活化。
{"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]。
F Inoue, R Matsuyama, S Yoneyama

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.

用聚丙烯酰胺凝胶电泳分析了冲绳一个遗传性球形红细胞增多症家族9人的红细胞膜蛋白。电泳结果显示膜蛋白组分条带4.2(分子量72 kDa)出现异常。在家族中有三个兄弟姐妹中发现了带4.2缺陷,其他三个成员的带4.2缺陷虽小但显著减少。然而,在其他家庭成员或正常受试者中没有发现这一成分的变化。
{"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
期刊
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society
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