Search Results - (Author, Cooperation:N. Yamanaka)
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1N. Yamanaka, S. Hashimoto, T. Kaneko, and H. Ohki (JLQCD Collaboration)
American Physical Society (APS)
Published 2018Staff ViewPublication Date: 2018-09-26Publisher: American Physical Society (APS)Print ISSN: 0556-2821Electronic ISSN: 1089-4918Topics: PhysicsKeywords: Lattice field theories, lattice QCDPublished by: -
2N. Yamanaka ; N. M. Romero ; F. A. Martin ; K. F. Rewitz ; M. Sun ; M. B. O'Connor ; P. Leopold
American Association for the Advancement of Science (AAAS)
Published 2013Staff ViewPublication Date: 2013-09-07Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Darkness ; Drosophila Proteins/agonists/genetics ; Drosophila melanogaster/*growth & development ; Enzyme Activation ; *Escape Reaction ; Insect Hormones/genetics/*physiology ; Larva/growth & development ; *Light ; *Light Signal Transduction ; Neurons/*physiology ; Neurosecretory Systems/*physiology ; RNA Interference ; Receptor Protein-Tyrosine Kinases/agonists/geneticsPublished by: -
3Tatsuguchi, A. ; Sakamoto, C. ; Fukuda, Y. ; Wada, K. ; Akamatsu, T. ; Tsukui, T. ; Miyake, K. ; Futagami, S. ; Kishida, T. ; Yamanaka, N. ; Kobayashi, M.
Oxford, UK : Blackwell Science Ltd
Published 2000Staff ViewISSN: 1365-2036Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background: Increasing evidence suggests that mesothelial cells contribute to the control of inflammation in the peritoneal cavity by secreting prostaglandins. A study has shown that cyclo-oxygenase (COX)-2 knockout mice die partly as a result of peritonitis. Aim: To investigate the expression and location of COX in peritonitis associated with peptic ulcer perforation. Methods: Gastric and duodenal tissues were collected intraoperatively from nine and four patients, respectively, and immunohistochemical staining for COX-1 and COX-2 was performed. Results: Histologically, all patients had severe peritonitis around the perforation sites, into which many inflammatory cells and fibroblasts had infiltrated, and reactive mesothelial cells exhibited hyperplastic change. The COX-1 protein was not detected, whereas COX-2 was abundant in reactive mesothelial cells near the perforation site and disappeared away from the site. Macrophages and fibroblasts around the perforation site also revealed immunostaining for COX-2. Conclusions: Our results showed that COX-2 protein is induced in mesothelial cells, as well as in macrophages and fibroblasts, in inflamed peritoneal tissues associated with peptic ulcer perforation, suggesting involvement of COX-2 in tissue repair.Type of Medium: Electronic ResourceURL: -
4Koizumi, K. ; Kano-Tanaka, K. ; Shimizu, S. ; Nishida, K. ; Yamanaka, N. ; Ota, K.
Amsterdam : ElsevierStaff ViewISSN: 0005-2760Keywords: (Rat thymocy te plasma membrane) ; Lipid composition ; Sphingomyelin deficiencySource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyMedicinePhysicsType of Medium: Electronic ResourceURL: -
5Staff View
ISSN: 0005-2736Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyMedicinePhysicsType of Medium: Electronic ResourceURL: -
6Koizumi, K. ; Shimizu, S. ; Koizumi, K.T. ; Nishida, K. ; Sato, C. ; Ota, K. ; Yamanaka, N.
Amsterdam : ElsevierStaff ViewISSN: 0005-2736Keywords: (Mouse lymphoid cell) ; Lipid composition ; Malignancy ; Membrane fluidity ; Plasma membraneSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyMedicinePhysicsType of Medium: Electronic ResourceURL: -
7Staff View
ISSN: 0003-9861Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
8Oda, O. ; Maeda, K. ; Yamaga, H. ; Kanamono, Y. ; Iwata, H. ; Miura, T. ; Yoshida, M. ; Miyata, S. ; Ohta, K. ; Yamanaka, N.
Amsterdam : ElsevierStaff ViewISSN: 0009-8981Keywords: Plasma protein ; Rheumatoid arthritis ; Two-dimensional electrophoresisSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: MedicineType of Medium: Electronic ResourceURL: -
9Staff View
ISSN: 0009-8981Keywords: Bacterial metabolite ; Infusion ; Lactyl lactateSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: MedicineType of Medium: Electronic ResourceURL: -
10Staff View
ISSN: 0014-5793Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
11Shiraishi, S. ; Sakamoto, N. ; Maeda, K. ; Ohki, T. ; Hosoi, M. ; Ohta, K. ; Yamanaka, N.
Amsterdam : ElsevierStaff ViewISSN: 0378-4347Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: Chemistry and PharmacologyType of Medium: Electronic ResourceURL: -
12Ohki, T. ; Saito, A. ; Yamanaka, N. ; Ohta, K. ; Sakakibara, J. ; Niwa, T. ; Maeda, K.
Amsterdam : ElsevierStaff ViewISSN: 0378-4347Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: Chemistry and PharmacologyType of Medium: Electronic ResourceURL: -
13Maeda, K. ; Shiraishi, S. ; Sakamoto, N. ; Ohki, T. ; Hosoi, M. ; Ohta, K. ; Yamanaka, N.
Amsterdam : ElsevierStaff ViewISSN: 0378-4347Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: Chemistry and PharmacologyType of Medium: Electronic ResourceURL: -
14Staff View
ISSN: 0003-9861Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
15Staff View
ISSN: 0375-9601Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: PhysicsType of Medium: Electronic ResourceURL: -
16Staff View
ISSN: 1437-773XKeywords: Key words Cerebral blood flow ; Blood–brain barrier ; Repeated brief cerebral ischemia ; Hippocampal CA1 ; UltrastructureSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Neuronal damage and changes in cerebral blood flow (CBF) and the permeability of the blood–brain barrier (BBB) following repeated brief periods of ischemia were studied in Mongolian gerbils. The cerebral ischemia was produced by three repeated occlusions of bilateral common carotid arteries for 3 min at 1-h intervals. CBF and permeability of the BBB were examined with tracers (China ink and silver nitrate) at 1, 3, and 7 days post ischemia using light and electron microscopy. Three days after the reperfusion, significant extravasation of tracers, consequential reduction of CBF, extensive neuronal destruction, and intravascular platelet aggregation were observed. Such vascular changes in the CA1 region were more severe than those in the frontal cortex. These findings strongly support the view that microcirculatory disturbance may be a mechanism responsible for delayed neuronal death in the CA1 region of the hippocampus.Type of Medium: Electronic ResourceURL: -
17Staff View
ISSN: 1432-2307Keywords: Acute tubular necrosis ; Tubular dilatation ; Basement membrane ; Epithelial hyperplasia ; Repair processSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract To elucidate the mechanisms of renal tubular dilatation in acute tubular necrosis (ATN), morphological findings after 60 min ischaemia were studied in rats. The characteristics of the tubular basement membrane (BM) were also examined. A morphometric analysis of cell proliferation, epithelial cellularity and the circumference of damaged tubules was performed. The ischaemic injury resulted in widespread necrosis of renal tubules at day 1, and the BM of damaged tubules appeared thin. The intensity of the immunohistochemical staining for BM components decreased. The epithelial cell proliferation was particularly active in the early phase. Dilatation of the damaged tubules began at day 2, and the degree of dilatation increased up to day 6. Regenerative epithelial hyperplasia occurred and abnormalities of tubular BM were seen. Epithelial hyperplasia and dilatation of damaged tubules was most prominent at day 6 and the tubular BM was thickened by newly produced BM components. Tubular obstruction was not seen and tubules returned to normal size by day 28. Epithelial hyperplasia and abnormalities of tubular BM disappeared progressively. Regenerative tubular epithelial hyperplasia and abnormalities of tubular BM may play an important role in pathogenesis of tubular dilatation in ATN, and tubular dilatation is not due to tubular obstruction.Type of Medium: Electronic ResourceURL: -
18Staff View
ISSN: 1432-2307Keywords: Glomerular endothelial cells ; Mesangial proliferative glomerulonephritis ; Habu-snake venom ; Tissue repair ; Endothelial regenerationSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract In this study, the kinetics of glomerular endothelial cells during the repair process following glomerular injury was investigated in a model of mesangial proliferative glomerulonephritis induced by Habu-snake venom (HSV) in rats. Intravenous injection of HSV led to a cystic ballooning type lesion at day 1. Subsequently a marked segmental proliferative lesion was observed in the cystic areas at day 5. Thereafter cellularity decreased and reconstruction of the glomerular tuft was gradually observed with time. The histological structure of the glomeruli had almost returned to normal 21 days following HSV injection. After prominent depletion at day 1, the number of endothelial cells increased rapidly and reached a plateau at day 7, not significantly different from that of the control group. Morphologically endothelial cell elongation from the vascular pole into the cystic lesion was seen together with premature capillary formation in the proliferative lesion. Accompanying the reduction of mesangial expansion, the endothelial cells gradually formed definite capillary lumens. We conclude that the mesangial proliferative glomerulonephritis induced by HSV recovers to its original structural state and that the migration and proliferation of endothelial cells with accompanying capillary formation are essential for the repair process, in addition to mesangial cell proliferation.Type of Medium: Electronic ResourceURL: -
19Goto, M. ; Yoshida, H. ; Honda, A. ; Kumazawa, T. ; Ohbayashi, T. ; Inagaki, J. ; Yamanaka, N. ; Ota, K.
Springer
Published 1993Staff ViewISSN: 1432-1041Keywords: Adriamycin ; Haemodialysis ; adriamycinol ; pharmacokinetics ; moment analysisSource: Springer Online Journal Archives 1860-2000Topics: Chemistry and PharmacologyMedicineType of Medium: Electronic ResourceURL: -
20Staff View
ISSN: 1573-6865Source: Springer Online Journal Archives 1860-2000Topics: BiologyMedicineNotes: Abstract In order to optimize collagen antigen unmasking in paraffin-embedded tissue sections, the effects of various fixatives and duration of fixation in relation to enzyme pretreatment and microwave irradiation for collagen antigen unmasking were studied. A streptavidin--biotin-- peroxidase complex method was used for the immunolocalization of type III and IV collagen antigens. Fixatives and fixation time had significant adverse effects on the immunoreactivity of the antigens. Enzyme pretreatment was found to be superior to microwave irradiation for collagen antigen unmasking. Fixation with paraformaldehyde required shorter enzyme pretreatment and yielded a more enhanced reaction than treatment with formalin and Bouin's fluid. The optimum conditions for type III and IV collagen unmasking were found to be fixation with 4% paraformaldehyde in 0.01 m phosphate-buffered saline, pH 7.4, for up to 3 weeks followed by enzyme pretreatment with 1 mg ml−1 pepsin in 0.01 n hydrochloric acid, pH 2.0, for 30 min (human tissues) or 60 min (rat tissues) at 37°C. It is concluded that collagen antigen unmasking by enzyme pretreatment in tissue sections fixed for a long period of time can be successful if appropriate enzyme(s) and incubation time(s) are employed with regard to the antigen under study and fixative and fixation time used for tissue preparationType of Medium: Electronic ResourceURL: