Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by Y Mori
Total Records ( 5 ) for Y Mori
  R Inoue , L. J Jensen , Z Jian , J Shi , L Hai , A. I Lurie , F. H Henriksen , M Salomonsson , H Morita , Y Kawarabayashi , M Mori , Y Mori and Y. Ito
 

TRPC6 is a non–voltage-gated Ca2+ entry/depolarization channel associated with vascular tone regulation and remodeling. Expressed TRPC6 channel responds to both neurohormonal and mechanical stimuli, the mechanism for which remains controversial. In this study, we examined the possible interactions of receptor and mechanical stimulations in activating this channel using the patch clamp technique. In HEK293 cells expressing TRPC6, application of mechanical stimuli (hypotonicity, shear, 2,4,6-trinitrophenol) caused, albeit not effective by themselves, a prominent potentiation of cationic currents (ITRPC6) induced by a muscarinic receptor agonist carbachol. This effect was insensitive to a tarantula toxin GsMTx-4 (5 µmol/L). A similar extent of mechanical potentiation was observed after activation of ITRPC6 by GTPS or a diacylglycerol analog 1-oleoyl-2-acetyl-sn-glycerol (OAG). Single TRPC6 channel activity evoked by carbachol was also enhanced by a negative pressure added in the patch pipette. Mechanical potentiation of carbachol- or OAG-induced ITRPC6 was abolished by small interfering RNA knockdown of cytosolic phospholipase A2 or pharmacological inhibition of -hydroxylation of arachidonic acid into 20-HETE (20-hydroxyeicosatetraenoic acid). Conversely, direct application of 20-HETE enhanced both OAG-induced macroscopic and single channel TRPC6 currents. Essentially the same results were obtained for TRPC6-like cation channel in A7r5 myocytes, where its activation by noradrenaline or Arg8 vasopressin was greatly enhanced by mechanical stimuli via 20-HETE production. Furthermore, myogenic response of pressurized mesenteric artery was significantly enhanced by weak receptor stimulation dependently on 20-HETE production. These results collectively suggest that simultaneous operation of receptor and mechanical stimulations may synergistically amplify transmembrane Ca2+ mobilization through TRPC6 activation, thereby enhancing the vascular tone via phospholipase C/diacylglycerol and phospholipase A2/-hydroxylase/20-HETE pathways.

  Y Mori , T Kodaka , T Kato , E. M Kanagawa and O. Kanagawa
 

IFN- signaling-deficient non-obese diabetic (NOD) mice develop diabetes with similar kinetics to those of wild-type NOD mice. However, the immunization of IFN- signaling-deficient NOD mice with CFA failed to induce long-term protection, whereas wild-type NOD mice receiving CFA remained diabetes-free. CFA also failed to protect IFN- receptor-deficient (IFN-R–/–) NOD mice from the autoimmune rejection of transplanted islets, as it does in diabetic NOD mice, and from disease transfer by spleen cells from diabetic NOD mice. These data clearly show that the pro-inflammatory cytokine IFN- is necessary for the CFA-mediated protection of NOD mice from diabetes. There is no difference in the Th1/Th17 balance between IFN-R–/– NOD and wild-type NOD mice. There is also no difference in the total numbers and percentages of regulatory T (Treg) cells in the lymph node CD4+ T-cell populations between IFN-R–/– NOD and wild-type NOD mice. However, pathogenic T cells lacking IFN-R are resistant to the suppressive effect of Treg cells, both in vivo and in vitro. Therefore, it is likely that CFA-mediated protection against diabetes development depends on a change in the balance between Treg cells and pathogenic T cells, and IFN- signaling seems to control the susceptibility of pathogenic T cells to the inhibitory activity of Treg cells.

  K Okoshi , S Nagayama , M Furu , Y Mori , A Yoshizawa , J Toguchida and Y. Sakai
 

A 54-year-old man was referred to our hospital because of a huge, unresectable rectal cancer occupying his entire pelvic space with a solitary liver metastasis. He had undergone a laparotomy for surgical resection, but ended up with a sigmoid colostomy due to possible invasion into the urinary bladder and pelvic wall. At the completion of seven cycles of FOLFOX regimen, radiographic examination revealed remarkable reduction of the primary rectal tumor and regional lymph nodes, and also a complete response (CR) of the liver metastasis. The tumor was extirpated without any macroscopic residues by a low anterior resection of the rectum, along with a partial resection of the urinary bladder and seminal vesicles. Since pathological and immunohistochemical examinations showed no viable cancer cells in any parts of the resected specimens, the lesion was regarded as a pathologically CR. Analysis for single-nucleotide polymorphisms in the genes involved in nucleotide excision repair, excision repair cross-complementing group 1 and xeroderma pigmentosum group D, showed a genotypic pattern sensitive to oxaliplatin. To our knowledge, this is a rare case of an initially unresectable primary rectal cancer, which was down-staged to a pathologically CR by FOLFOX chemotherapy instead of chemoradiotherapy.

  Y Okuchi , S Nagayama , Y Mori , J Kawamura , S Matsumoto , T Nishimura , A Yoshizawa and Y. Sakai
 

We present a case of pseudo-meigs’ syndrome caused by a metastatic ovarian tumor of rectal cancer origin, and examine the possible involvement of vascular endothelial growth factor (VEGF) in the pathogenesis of refractory fluid retention. A 42-year-old woman with advanced rectal cancer underwent a laparoscopic anterior resection of the rectum. During systemic chemotherapy treatment, she complained of severe abdominal distension 16 months following the operation. We failed to improve massive ascites by diuretics and repeated abdominocenteses. Without any definite evidence of carcinomatous peritonitis, we chose to extirpate an enlarged ovarian tumor on the presumptive diagnosis of pseudo-meigs’ syndrome. Ascites disappeared promptly after resecting the ovarian tumors and the subject resumed systemic chemotherapy. Preoperative high levels of serum VEGF were normalized promptly after the operation. Levels of VEGF expression in metastatic ovarian tumors were as weak as in the primary tumor upon immunohistochemical staining. In contrast, increased VEGF expression was evident in epithelial cells of oviducts. For patients with massive and refractory ascites, we need to keep in mind the disease entity of pseudo-meigs’ syndrome, since surgical intervention possibly improves conditions. Furthermore, the hypersecretion of VEGF from oviducts may play a role in the pathogenesis of clinical manifestations of pseudo-meigs’ syndrome.

  M Omatsu Kanbe , T Yamamoto , Y Mori and H. Matsuura
 

The present study was designed to examine the postnatal developmental changes of atypically shaped cardiomyocytes (ACMs) prepared from the heart of newborn [postnatal day 1 (day-1)] through aged (12-month-old) mice. ACMs were identified as a novel type of self-beating cardiomyocyte with a peculiar morphology in mouse cardiac ventricles. The cell length of ACMs significantly increased during the first three postnatal months and further increased over the following 9 months. In contrast, the population of ACMs was significantly decreased within the first 5 weeks and reached a plateau in the adult stage. ACMs obtained from newborn and adult mice exhibited similar spontaneous action potentials. The expression of the fetal cardiac gene products atrial natriuretic peptide and voltage-gated T-type Ca2+ channel CaV3.2 was confirmed by immunostaining in ACMs obtained from both newborn and aged mice. These observations provide evidence that ACMs that exhibit spontaneous beating survive the long-term postnatal development of cardiac ventricles while preserving the expression of fetal cardiac genes. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials. (J Histochem Cytochem 58:543–551, 2010)

 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility