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Articles by Yuji Taketani
Total Records ( 3 ) for Yuji Taketani
  Kei Kawana , Junko Matsumoto , Shiho Miura , Li Shen , Yukiko Kawana , Takeshi Nagamatsu , Toshiharu Yasugi , Tomoyuki Fujii , Tomoyuki Fujii , Alison J. Quayle , Yuji Taketani and Danny J. Schust
  Mucosal epithelia of the human lower reproductive tract (vagina, cervix, and penile urethra) are exposed to sexually transmitted microbes, including Chlamydia trachomatis. The in vivo susceptibility of each tissue type to infection with C. trachomatis is quite distinct. CD1d is expressed on the surface of antigen-presenting cells, including mucosal epithelial cells, and interacts specifically with invariant NKT cells. Invariant NKT cells play a role in both innate and adaptive immune responses to microbes. Here we assessed CD1d expression in normal reproductive tissues by using immunohistochemistry. Immortalized epithelial cell lines from the human lower reproductive tract (vagina, endocervix, and penile urethra) were examined for CD1d expression and for ligand-induced cytokine production induced by CD1d cross-linking. CD1d expression in normal tissue was strong in the vagina but weak in the endocervix and penile urethra. Gamma interferon exposure induced CD1d transcription in all of the cell types studied, with the strongest induction in vaginal cells. Flow cytometry revealed cell surface expression of CD1d in vaginal and penile urethral epithelial cells but not in endocervical cells. Ligation of surface-expressed CD1d by monoclonal antibody cross-linking promoted interleukin-12 (IL-12) and IL-15, but not IL-10, production in vaginal and penile urethral cells. No induction was demonstrated in endocervical cells. CD1d-mediated cytokine production in penile urethral cells was abrogated by C. trachomatis infection. Basal deficiency in CD1d-mediated immune responsiveness may result in susceptibility to sexually transmitted agents. Decreased CD1d-mediated signaling may help C. trachomatis evade detection by innate immune cells.
  Daichi Maeda , Yutaka Takazawa , Satoshi Ota , Yuko Takeuchi , Akira Seta , Shunsuke Nakagawa , Tetsu Yano , Yuji Taketani and Masashi Fukayama
  Primary adenocarcinoma of the fallopian tube is an uncommon female genital tract tumor. In situ or minimally invasive tubal cancer often poses a diagnostic challenge because of the absence of specific clinical and radiological findings. Here, we report a rare case of bilateral microscopic fallopian tube cancer that initially presented with malignant findings in an endometrial cytologic smear. The patient was a 57-year-old postmenopausal woman. An endometrial smear performed during a routine checkup revealed clusters of malignant cells. During the clinical diagnosis of endometrial cancer, she underwent bilateral salpingo-oophorectomy, total hysterectomy, and partial omentectomy. Histologically, no carcinoma was found in the uterus or ovaries. In toto sectioning of the fallopian tubes and their fimbriated ends revealed minute foci of serous adenocarcinoma in the left tubal mucosa and right fimbria. In situ adenocarcinoma components were present in both lesions. Microinvasive carcinoma was observed in the right fimbria. Although there was no macroscopic dissemination in the peritoneum at the time of surgery, positive intraoperative peritoneal cytology suggests that the patient was at risk of developing peritoneal serous carcinoma if not treated. Clinicians and pathologists should consider the possibility of early tubal cancer when there is no clinically detectable pelvic mass, and malignant cells appear in endometrial cytology specimens.
  Madoka Kouzu-Fujita , Yoshihiro Mezaki , Shun Sawatsubashi , Takahiro Matsumoto , Ikuko Yamaoka , Tetsu Yano , Yuji Taketani , Hirochika Kitagawa and Shigeaki Kato
  Estrogen exerts its diverse effects through two subtypes of estrogen receptors (ER), ERα and ERβ. Each subtype has its own distinct function and expression pattern in its target tissues. Little, however, is known about the transcriptional regulatory mechanism of ERβ in the major ERβ-expressing tissues. Using biochemical methods, we identified and described a novel ERβ coactivator. This protein, designated GIOT-4, was biochemically purified from 293F cells. It coactivated ERβ in ovarian granulosa cells. GIOT-4 expression was induced by stimulation with follicle-stimulating hormone (FSH). GIOT-4 recruited an SWI/SNF-type complex in a ligand-independent manner to ERβ as an ER subtype-specific physical bridging factor and induced subsequent histone modifications in the ERβ target gene promoters in a human ovarian granulosa cell line (KGN). Indeed, two ERβ-specific target genes were upregulated by FSH at a specific stage of a normal ovulatory cycle in intact mice. These findings imply the presence of a novel regulatory convergence between the gonadotropin signaling cascade and ERβ-mediated transcription in the ovary.
 
 
 
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