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51.
Takashi Sekine Keiko Fukutani Tomiko Motegi Hiroshi Hayakawa Takashi Tamura Shigeo Nagafuchi Yutaka Nakahori Yasuo Nakagome 《Journal of human genetics》1992,37(2):157-162
Summary Results of DNA study on two patients of gonadal dysgenesis with a 45,X/46,X,Ynf (non-fluorescent Y chromosome) karyotype are described. In one patient who developed gonadoblastoma, all 12 loci on the non-fluorescent part of Yq were detected. Another patient did not have gonadoblastoma at 20 years, and only the proximal 6 loci out of 12 were detected. 相似文献
52.
Akagi M Inui K Nakajima S Shima M Nishigaki T Muramatsu T Kokubu C Tsukamoto H Sakai N Okada S 《Journal of human genetics》2000,45(1):60-62
Fanconi-Bickel syndrome (FBS), or glycogen storage disease type XI, is a rare autosomal recessive disorder characterized
by hepatorenal glycogen accumulation, Fanconi nephropathy, and impaired utilization of glucose and galactose. Recently, this
disease was elucidated to link mutations in the glucose transporter 2 (GLUT2) gene. Only three mutations in three FBS families have been reported. Therefore, it is important to elucidate mutations in
the GLUT2 gene in FBS by answering the question of whether the syndrome is a single gene disease. In this report, we describe two patients
in two unrelated families clinically diagnosed with FBS. No mutation in the entire protein coding region of the GLUT2 gene was detected in patient 1, which suggested that no mutation existed in the GLUT 2 gene, or that some mutations had affected the expression of the GLUT 2 gene. In patient 2, a novel homozygous nonsense mutation (W420X, Trp at codon 420 to stop codon) was detected. These results
support the correlation between GLTU2 gene mutation and FBS syndrome. However, many patients must be analyzed to determine whether other genes are involved in
FBS.
Received: July 16, 1999 / Accepted: September 3, 1999 相似文献
53.
Shigeo Takebayashi Akinori Kamio Isamu Kubota Seiya Tauba 《Pathology international》1972,22(4):697-721
In various arterial lesions including atherosclerotic lesions, the main morphological change involves smooth muscle cells. The potential sensitivity is different among the arterial smooth muscle cells, venous smooth muscle cells and smooth muscle cells of other organs. The modified smooth muscle cells characterized by the increase of rough endoplasmic reticula are considered to express their latent ability to synthesize collagen fibers, elastic fibers and other ground substances.
The foam cells noted in atherosclerosis and fatty streak consist of lipid accumulated smooth muscle cells and hematogenous macrophages. Lipid metabolism and synthesis in the latter differ from those in the former. The ratio of the two kinds of foam cells in atheroma or fatty streak varies by the stage of the lesion.
It is possible to suppose that there exists a factor which would selectively attack the media smooth muscle cells of small arteries or arterioles. This is observed electron microscopically as focal cytoplasmic necrosis (cytoplasmolysis) of smooth muscle cells and plays an important role in the histogenesis of fibrinoid necrosis.
In case of experimental periarteritis nodosa the early stage begins with cytoplasmolysis of smooth muscle cells and marked increase of rough endoplasmic reticula in adjacent smooth muscle cells. 相似文献
The foam cells noted in atherosclerosis and fatty streak consist of lipid accumulated smooth muscle cells and hematogenous macrophages. Lipid metabolism and synthesis in the latter differ from those in the former. The ratio of the two kinds of foam cells in atheroma or fatty streak varies by the stage of the lesion.
It is possible to suppose that there exists a factor which would selectively attack the media smooth muscle cells of small arteries or arterioles. This is observed electron microscopically as focal cytoplasmic necrosis (cytoplasmolysis) of smooth muscle cells and plays an important role in the histogenesis of fibrinoid necrosis.
In case of experimental periarteritis nodosa the early stage begins with cytoplasmolysis of smooth muscle cells and marked increase of rough endoplasmic reticula in adjacent smooth muscle cells. 相似文献
54.
Shigeo Aizawa Masafumi Suzuki Yasushi Kikuchi Takashi Nikaido Kenji Matsumoto 《Pathology international》1987,37(7):947-954
Seven metastasizing small renal cell carcinomas smaller than 30 mm in the greatest diameter were clinicopathologically studied for a better understanding of their characteristic features as compared to those of small tumors without metastases. Grayish-white infiltrating tumors in gross appearance and alveolar or solid microscopic structure consisting of granular or spindle cells and of atypical nuclei were suggestive of having metastases. Two tumors which had positive reactions to the lower nephron markers such as SB A, PNA, and/or DBA were considered to be of lower nephron origin and displayed poor prognosis. ACTA PATHOL. JPN. 37: 947–954, 1987. 相似文献
55.
Frequent importation of enterovirus 71 from surrounding countries into the local community of Yamagata, Japan, between 1998 and 2003 下载免费PDF全文
Mizuta K Abiko C Murata T Matsuzaki Y Itagaki T Sanjoh K Sakamoto M Hongo S Murayama S Hayasaka K 《Journal of clinical microbiology》2005,43(12):6171-6175
Phylogenetic analysis of 45 enterovirus 71 (EV71) isolates for 6 years in Yamagata, Japan, clarified that the annual outbreak of hand-foot-and-mouth disease was due to four genetically distinct subgenogroups, including a novel "B5." Our results suggest that the importation of EV71 from surrounding countries has had a major epidemiological impact on the local community used in our study. 相似文献
56.
Murata K Inami M Hasegawa A Kubo S Kimura M Yamashita M Hosokawa H Nagao T Suzuki K Hashimoto K Shinkai H Koseki H Taniguchi M Ziegler SF Nakayama T 《International immunology》2003,15(8):987-992
CD69, known as an early activation marker antigen on T and B cells, is also expressed on platelets and activated neutrophils, suggesting certain roles in inflammatory diseases. In order to address the role of CD69 in the pathogenesis of arthritis, we established CD69-null mice. CD69-null mice displayed a markedly attenuated arthritic inflammatory response when injected with anti-type II collagen antibodies. Cell transfer experiments with neutrophils, but not T cells or spleen cells, from wild-type mice into CD69-null mice restored the induction of arthritis. These results indicate a critical role for CD69 in neutrophil function in arthritis induction during the effector phase. Thus, CD69 would be a possible therapeutic target for arthritis in human patients. 相似文献
57.
Atsuo Murata Hitoshi Toda Ken -Ichi Uda Hirohito Hayashida Takeshi Kato Hidewaki Nakagawa Shigekazu Yokoyama Hideaki Morishita Toru Yamakawa Jiro Hirose Takesada Mori Nariaki Matsuura 《Inflammation》1994,18(4):337-347
Severe inflammatory responses after major surgeries, trauma, and infection develop multiple organ dysfunction. In the mechanisms of the pathogenesis of these responses, activated neutrophils are thought to be important in terms of their ability to produce various kinds of proteinases, which can degrade various proteins constructing human tissues. Among their proteinases, neutrophil elastase is the strongest serine proteinase secreted from activated neutrophils. Thus, we examined in this study the inhibitory effect and therapeutic efficacy of newly produced recombinant human Kunitz-type proteinase inhibitor (R-020), which coded the second domain of human urinary trypsin inhibitor. R-020 was effective in significantly improving the survival rate after induction of the rat lethal peritonitis model (cecal ligation and punctureinduced septic shock model). We suggest that various serine proteinases are implicated in the pathogenesis of neutrophil-related multiple organ failure and that recombinant human Kunitz-type proteinase inhibitor might be effective in the treatment of these kinds of organ dysfunction. 相似文献
58.
Alexander M Wolf Sadamitsu Asoh Ikuroh Ohsawa Shigeo Ohta 《Nippon Ika Daigaku zasshi》2008,75(2):66-67
Redox-sensitive green fluorescent protein (roGFP) is a fluorescent protein in which two cysteines are placed adjacently in the barrel structure. Disulfide formation (oxidation) increases the absorption at short wavelengths (410 nm) at the expense of absorption at longer wavelengths (490 nm). The fluorescence ratio indicates reduction/oxidation, i.e., the redox potential at specific cellular locations. 相似文献
59.
Takashi Kojima Toshinobu Yamamoto Mengdong Lan Masaki Murata Ken-ichi Takano Mitsuru Go Shingo Ichimiya Hideki Chiba Norimasa Sawada 《Medical Electron Microscopy》2004,37(2):101-113
The signal transduction pathways and activation of the MAP kinase or PI3 kinase signaling cascade regulate a variety of cellular processes, including proliferation and differentiation in hepatocytes. To elucidate the mechanisms of signal transmission required for the regulation of gap and tight junctions during DNA synthesis in rat hepatocytes, we determined changes of expression and function of gap and tight junctions of cells grown in primary culture, using inhibitors of signaling pathways for MAP kinase (PD98059) and PI3 kinase (LY294002). During the stimulation of DNA synthesis induced by epidermal growth factor (EGF), immunoreactivity and mRNAs of gap junction protein Cx32 and of tight junction protein claudin-1 markedly decreased with reduction of gap junctional intercellular communication (GJIC) and the fence function of tight junctions. In Western blots, whole-cell lysate of claudin-1 protein decreased and phosphorylated Cx32 protein in the insoluble fraction of Triton X-100 increased during the stimulation of DNA synthesis. During reinhibition of DNA synthesis, the changes of Cx32 and claudin-1 returned to control levels, as did both functions. In treatment with the inhibitors before DNA synthesis, PD98059 inhibited the changes of expression and function of Cx32, but not claudin-1, without inhibition of cell growth, whereas LY294002 completely inhibited cell growth. These findings indicate that the PI3 kinase pathway rather than the MAP kinase pathway plays an important role for EGF-induced proliferation of rat hepatocytes, and that changes of Cx32 in hepatocytes during the stimulation of DNA synthesis may be in part controlled through MAP kinase. Furthermore, Cx32, but not claudin-1, protein may be a target of activated MAP kinase in hepatocytes. 相似文献
60.
The critical role of ocular-infiltrating macrophages in the development of choroidal neovascularization 总被引:9,自引:0,他引:9
Tsutsumi C Sonoda KH Egashira K Qiao H Hisatomi T Nakao S Ishibashi M Charo IF Sakamoto T Murata T Ishibashi T 《Journal of leukocyte biology》2003,74(1):25-32
Choroidal neovascularization (CNV) is directly related to visual loss in some eye diseases, such as age-related macular degeneration. Although several human histological studies have suggested the participation of macrophages in CNV formation, the precise mechanisms are still not fully understood. In this study, we elucidated the role of ocular-infiltrating macrophages in experimental CNV using CCR2 knockout (KO) mice, wild-type mice, and C57BL/6 (B6) mice. CCR2 is the receptor of monocyte chemoattractant protein-1, and the number of infiltrating macrophage and the area of CNV were significantly reduced in CCR2 KO mice. Enriched ocular-infiltrating macrophages from B6 mice actually showed angiogenic ability in a dorsal air sac assay. Moreover, their expression of class II, CD40, B7-1 and B7-2 molecules, and the mRNA for potential angiogenic factors, such as vascular endothelial growth factor, basic fibroblast growth factor, and tumor necrosis factor alpha, was also observed. Collectively, we conclude that ocular-infiltrating macrophages play an important role in CNV generation. 相似文献