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61.
Protective effect of human granulocyte colony-stimulating factor on microbial infection in neutropenic mice. 总被引:6,自引:8,他引:6 下载免费PDF全文
M Matsumoto S Matsubara T Matsuno M Tamura K Hattori H Nomura M Ono T Yokota 《Infection and immunity》1987,55(11):2715-2720
A purified human granulocyte colony-stimulating factor (hG-CSF) was studied for its protective effect on the induction of neutropenia and enhanced susceptibility to microbial infections in mice receiving cyclophosphamide (CPA). A severe reduction in peripheral blood neutrophils was induced 4 days after injection with 200 mg of CPA per kg although the level normalized rapidly thereafter. When mice were injected subcutaneously once a day with 2.5 micrograms of hG-CSF beginning on the day after CPA injection, the reduction was prevented markedly, even 4 days later. On the other hand, in mice receiving CPA 4 days prior to infection, a weakened resistance to intraperitoneal challenge with a strain of Pseudomonas aeruginosa was induced. This weakened resistance was dose-dependently restored to normal by four daily injections with hG-CSF. A daily dose of 1.0 microgram was required for complete restoration, although hG-CSF did not directly inhibit bacterial growth in vitro. In hG-CSF-treated mice, morphologically mature neutrophils migrated rapidly into the peritoneal cavities where bacteria were inoculated, followed by a rapid elimination of bacteria from the locality as compared with controls. In addition, the same treatment with hG-CSF was able to protect significantly against systemic infections caused by Serratia marcescens, Escherichia coli, Staphylococcus aureus, and Candida albicans. These data show the possibility that prophylactic therapy with hG-CSF may augment the resistance of immunocompromised patients to infections. 相似文献
62.
Yoshida T Iwamoto T Adachi K Yokota T Miyake Y Hamaguchi M 《International journal of molecular medicine》2005,15(2):269-275
M1 mouse myeloid leukemia cells exhibit growth arrest and differentiation to monocytes/macrophages in response to leukemia inhibitory factor (LIF) stimulation. Although recent studies have demonstrated that STAT3 plays a central role in this process, it is unknown whether STAT3 activation alone is sufficient. To address this issue, we have established M1/STAT3ER cells, where STAT3 is selectively activated by 4-hydroxytamoxifen (4HT). 4HT stimulation did not have any effect on growth and morphology of M1/ STAT3ER cells, and did not induce the down-regulation of mRNA of c-myc and c-myb, which is necessary for M1 cell differentiation. On the other hand, mRNA of jun-B, IRF1 and p19 was increased by 4HT. DNA precipitation assay indicated that both stimulation of LIF and 4HT similarly activated STAT3ER. Introduction of a constitutive active MAP kinase kinase (MEK1) into M1/STAT3ER cells did not induce differentiation either. Together, our present data suggest that signaling other than the activation of STAT3 and MEK1 may be necessary for M1 cell-growth arrest and differentiation, while a set of early genes of LIF are induced by only STAT3 activation. 相似文献
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65.
M Hayashi C Abe R T Nozawa T Yokota T Iso Y Shiokawa 《International journal of immunopharmacology》1986,8(3):299-304
Macrophages which play an important role in host resistance against infections are considered to be a target for various immunomodulators. In order to examine the effects of selected immunomodulators on macrophage function, the effects of N-(2-mercapto-2-methylpropanoyl)-L-cysteine (SA96), levamisole (LMS) and D-penicillamine (D-Pc) on the candidacidal activity of the normal peritoneal cells (PC) were investigated. In the in vitro studies, SA96 increased the candidacidal activity of PC 4-fold, while D-Pc and LMS treatments did not increase this activity. In the ex vivo studies, PC obtained from the mice pre-treated with SA96, D-Pc and LMS showed a high candidacidal activity. Elevated candidacidal activity was not due to changes of cell types of PC populations. These results suggest that D-Pc and LMS activate the function of macrophage in vivo and SA96 activates the function both in vitro and in vivo. 相似文献
66.
Tokuhiro Ishihara Yoshimi Yamashita Yoshiko Okuzono Tadaaki Yokota Mutsuo Takahashi Toshiaki Kamei Fumiya Uchino Noboru Matsumoto Shiro Miwa Hisaichi Fuji Takeshi Kozaki 《Ultrastructural pathology》1985,8(1):13-23
By light and electron microscopy, we observed foamy cells in the spleens from a patient with hemolytic anemia due to red cell adenosine deaminase (ADA) overproduction, a patient with rheumatoid arthritis (RA) treated with gold, and patients with idiopathic thrombocytopenic purpura (ITP)
The foamy cells associated with red cell ADA overproduction were essentially similar to Gaucher-like cells described in patients with thalassemia, and it was suggested that the accelerated destruction of red cells was one of the factors responsible for the development of foamy cells. Foamy cells in ITP and RA were closely associated with an increased destruction of platelets in the spleen. Morphologic transitions between phagocytosed platelets and myelinlike materials were traced in these disorders. In RA, however, foamy cells were heterogeneous from an ultrastructural standpoint, with different cytoplasmic inclusions. In addition to myelinlike materials, dense bodies, vacuoles with flocculent materials, and gold were noted in most of foamy cells. As gold compounds are known to inhibit lysosomal enzymes, we surmise that an acquired disturbance in lysosomal digestion is partially responsible for the accumulation of intermediate metabolites.
In the pathogenesis of foamy cells associated with blood cell dyscrasia, the accelerated destruction of blood cells and/or acquired disorders in catabolic pathways within the macrophages are suggested to be the underlying mechanism of an intralysosomal accumulation of incompletely degraded cellular debris. 相似文献
The foamy cells associated with red cell ADA overproduction were essentially similar to Gaucher-like cells described in patients with thalassemia, and it was suggested that the accelerated destruction of red cells was one of the factors responsible for the development of foamy cells. Foamy cells in ITP and RA were closely associated with an increased destruction of platelets in the spleen. Morphologic transitions between phagocytosed platelets and myelinlike materials were traced in these disorders. In RA, however, foamy cells were heterogeneous from an ultrastructural standpoint, with different cytoplasmic inclusions. In addition to myelinlike materials, dense bodies, vacuoles with flocculent materials, and gold were noted in most of foamy cells. As gold compounds are known to inhibit lysosomal enzymes, we surmise that an acquired disturbance in lysosomal digestion is partially responsible for the accumulation of intermediate metabolites.
In the pathogenesis of foamy cells associated with blood cell dyscrasia, the accelerated destruction of blood cells and/or acquired disorders in catabolic pathways within the macrophages are suggested to be the underlying mechanism of an intralysosomal accumulation of incompletely degraded cellular debris. 相似文献
67.
Tadaaki Yokota Yoshimi Yamashita Yoshiko Okuzono Mutsuo Takahashi Shigeyoshi Fujihara Shin'ichiro Akizuki Tokuhiro Ishihara Fumiya Uchino Takako Iwata 《Pathology international》1984,34(3):663-668
A case of malignant cystosarcoma phyllodes of the prostate is reported in a 45-year-old male. This tumor was composed of benign columnar or squamous cystic folds and sarcomatous stroma including rhabdomyomatous elements. The prostatic origin of the tumor was clearly proved by the unlabeled immunoperoxidase method. ACTA PATHOL. JPN. 34: 663–668, 1984. 相似文献
68.
Tissue factor pathway inhibitor can interact with platelets 总被引:3,自引:0,他引:3
Nishioka T Yokota M Hino M Tsuda I Tatsumi N 《Journal of immunological methods》2002,266(1-2):181-184
Tissue factor pathway inhibitor (TFPI) regulates the extrinsic pathway of blood coagulation. However, there is no report on interaction between TFPI and platelets other than that by Tsuji, who found that whole blood anticoagulated with TFPI exhibited remarkable decrease in platelet count. Our study revealed that washed platelets suspended in modified Tyrode's buffer (8 mM CaCl2) containing TFPI exhibit platelet aggregation. However, platelets aggregation was observed without TFPI, but its increase and intensity were slow and weak, compared to that in the presence of TFPI. This aggregation was inhibited by anti-CD41 (anti-GPIIb) antibody. This finding suggested that TFPI promotes platelet aggregation. 相似文献
69.
Kimura K Nakano T Park YB Tani M Tsuda H Beppu Y Moriya H Yokota J 《Clinical & experimental metastasis》2002,19(6):477-486
Relevant animal models for metastasis of osteosarcoma is needed to understand the biology and to develop the treatment modality
of metastasis of human osteosarcoma. Therefore, we screened six human osteosarcoma cell lines for metastatic ability in nude
mice. The HuO9 cell line was identified as being metastatic to the lung after intravenous injection. We established two sublines,
HuO9-M112 and HuO9-M132, with high metastatic potential to the lung from the parental HuO9 cells by in vivo selection. There were no differences between these two sublines and the parental cells in the growth rate in vitro and the tumorigenicity after subcutaneous injection in nude mice, however, mice injected with the metastatic sublines became
moribund earlier than mice injected with the parental HuO9 cells did. Thus, adriamycin (ADR) and recombinant interleukin-12
(IL-12) were administered to mice injected with the HuO9-M112 subline to suppress experimental lung metastases. Production
of lung colonies was significantly suppressed and the prognoses of mice were significantly improved by both ADR and IL-12
treatments. These results indicate that both ADR and IL-12 are effective agents against pulmonary metastatic osteosarcoma,
and that these sublines are useful for studies on the biological behavior and treatment of pulmonary metastatic osteosarcoma.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
70.
Jun-Ichi Adachi Masayuki Shiseki Tomoko Okazaki Gosei Ishimaru Masayuki Noguchi Setsuo Hirohashi Jun Yokota 《Genes, chromosomes & cancer》1995,14(4):301-306
Fifty-seven primary lung carcinomas and 35 metastatic lung carcinomas were analyzed for microsatellite instability at 11 different chromosomal loci. Although no instability was detected in 37 small cell lung carcinomas (SCLC), it was frequently detected in non-small cell lung carcinomas (NSCLC) (16/55, 29%). In NSCLC, the incidence of replication errors (RERs) in metastatic tumors (12/22, 55%) was significantly higher than that in primary tumors (4/33, 12%) (P = 0.0021). Among 10 pairs of primary tumors and corresponding metastases, there were 4 cases which manifested the identical RER phenotypes in both primary and metastatic tumors. In two cases, RER phenotypes were detected in metastatic but not in primary tumors. Never was an RER phenotype found only in a primary tumor but not in the metastases. RERs were detected more frequently in stage III or IV tumors (3/8, 38%) than stage I or II tumors (1/25, 4%) (P = 0.0359). Tumor cells with allelic losses on chromosome arm 3p or 18q tended to have RER phenotypes (P = 0.0432 and P = 0.0187, respectively). The data suggest that microsatellite instability is common in NSCLC but not in SCLC, and that genomic instability appears late in tumor progression and plays an important role in the acquisition of more malignant phenotypes in NSCLC. 相似文献