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Your search keyword '"Tagaya, Masafumi"' showing total 118 results
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118 results on '"Tagaya, Masafumi"'

9. Carotid Intima-Media Thickness and Risk of Cardiovascular Events in High-Risk Patients

Author

Kitagawa, Kazuo, Hougaku, Hidetaka, Yamagami, Hiroshi, Hashimoto, Hiroyuki, Itoh, Taiji, Shimizu, Yoshiomi, Takahashi, Daisuke, Murata, Shinji, Seike, Yujiro, Kondo, Kimito, Hoshi, Taku, Furukado, Shigetaka, Abe, Yuko, Yagita, Yoshiki, Sakaguchi, Manabu, Tagaya, Masafumi, Etani, Hideki, Fukunaga, Ryuzo, Nagai, Yoji, Matsumoto, Masayasu, and Hori, Masatsugu

Published
2007

10. Delayed neuronal death in ischemic hippocampus involves stimulation of protein tyrosine phosphorylation

Author

Toshiho, Ohtsuki, Matsumoto, Masayasu, Kitagawa, Kazuo, Mabuchi, Takuma, Mandai, Kenji, Matsushita, Kohji, Kuwabara, Keisuke, Tagaya, Masafumi, Ogawa, Satoshi, Ueda, Hirokazu, Kamada, Takenobu, and Yanagihara, Takehiko

Subjects
Cerebral ischemia -- Physiological aspects, Protein tyrosine kinase -- Physiological aspects, Cell death -- Physiological aspects, Neurons -- Physiological aspects, Phosphorylation -- Physiological aspects, Cellular signal transduction -- Physiological aspects, Biological sciences
Abstract

Tyrosine kinase acts as a messenger of neuronal cell death during the selective degeneration of hippocampal pyramid cells in transient forebrain ischemia models. Protein tyrosine phosphorylation of pp42 was detected after the nonlethal and lethal ischemia of the hippocampus and cerebral cortex. The ischemic hippocampal CA1 neurons also exhibited increased expression of phosphotyrosyl proteins indicating the anti-microtubule-associated protein kinase activity of pp42.

Published
1996

21. Editorial Comment

Author

Tagaya, Masafumi and del Zoppo, Gregory J.

Published
1995

24. Abstract T P145: Physiological Parameters and Radiological Findings of Cerebral Small Vessel Disease

Author

Doijiri, Ryosuke, primary, Saito, Kozue, additional, Motoyama, Rie, additional, Tsutsumi, Yukiko, additional, Uchiyama, Shinichiro, additional, Matsumoto, Masayasu, additional, Fujishiro, Kentaro, additional, Tadokoro, Yasuhiro, additional, Kitagawa, Kazuo, additional, Takekawa, Hidehiro, additional, Yamamura, Osamu, additional, Tagaya, Masafumi, additional, and Nagatsuka, Kazuyuki, additional

Published
2014
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38. A new gerbil model of hindbrain ischemia by extracranial occlusion of the bilateral vertebral arteries

Author

Hata, Ryuji, primary, Matsumoto, Masayasu, additional, Kitagawa, Kazuo, additional, Matsuyama, Tomohiro, additional, Ohtsuki, Toshiho, additional, Tagaya, Masafumi, additional, Handa, Nobuo, additional, Niinobe, Michio, additional, Mikoshiba, Katsuhiko, additional, Nishimura, Tsunehiko, additional, Yanagihara, Takehiko, additional, and Kamada, Takenobu, additional

Published
1994
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45. ‘Ischemic tolerance’ phenomenon found in the brain

Author

Kitagawa, Kazuo, primary, Matsumoto, Masayasu, additional, Tagaya, Masafumi, additional, Hata, Ryuji, additional, Ueda, Hirokazu, additional, Niinobe, Michio, additional, Handa, Nobuo, additional, Fukunaga, Ryuzo, additional, Kimura, Kazufumi, additional, Mikoshiba, Katsuhiko, additional, and Kamada, Takenobu, additional

Published
1990
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46. A validation study on the reproducibility of transcranial doppler velocimetry

Author

Maeda, Hiroaki, primary, Etani, Hideki, additional, Handa, Nobuo, additional, Tagaya, Masafumi, additional, Oku, Naohiko, additional, Kim, Bong-Ha, additional, Naka, Masashi, additional, Kinoshita, Naokazu, additional, Nukada, Tadaatsu, additional, Fukunaga, Ryuzo, additional, Isaka, Yoshinari, additional, Matsumoto, Masayasu, additional, Kimura, Kazufumi, additional, and Kamada, Takenobu, additional

Published
1990
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47. Characterisation of [[sup 123]I]iomazenil distribution in a rat model of focal cerebral ischaemia in relation to histopathological findings.

Author

Kaji, Tomohito, Kuge, Yuji, Yokota, Chiaki, Tagaya, Masafumi, Inoue, Hiroyasu, Shiga, Tohru, Minematsu, Kazuo, and Tamaki, Nagara

Subjects
NUCLEAR medicine, RADIOACTIVE tracers, MEDICAL radiology, IODINE, CEREBRAL ischemia, DNA
Abstract

Iodine-123 labelled iomazenil ([[sup 123]I]IMZ) has been reported to be a useful marker of neuronal viability. The brain distribution of [[sup 123]I]IMZ, however, has not been correlated with the pathophysiological response in detail after an ischaemic insult. To characterise [[sup 123]I]IMZ as a marker of neuronal viability, we compared its brain distribution with cyclooxygenase-2 (COX-2) expression, DNA fragmentation and cellular integrity. [[sup 123]I]IMZ and [[sup 125]I]IMP were injected into rats with focal cerebral ischaemia for the purpose of dual-tracer autoradiography. COX-2 and microtubule-associated protein-2 (MAP-2, a marker of cellular integrity) were immunostained. In situ DNA polymerase-I-dependent dUTP incorporation into damaged DNA was used as an indicator of DNA fragmentation. Lesion to normal ratios (LNRs) for [[sup 123]I]IMP and [[sup 125]I]IMZ were calculated. [[sup 123]I]IMZ accumulation was preserved in several regions with impaired [[sup 123]I]IMP accumulation. COX-2 expression was occasionally observed, whereas neither DNA fragmentation nor MAP-2 denaturation was detected in these regions. DNA fragmentation and impaired MAP-2 immunostaining were observed only in the regions with reduced LNRs for both tracers. The LNR for [[sup 123]I]IMZ was significantly lower in regions with impaired MAP-2 immunostaining (0.120±0.152, P<0.0001), in regions positive for dUTP incorporation (0.488±0.166, P<0.0001) and in regions positive for COX-2 expression (0.626±0.186, P<0.001) than in histologically normal regions (0.784±0.213). Thus, neuronal DNA is still intact and cellular integrity is maintained in the ischaemic regions with preserved [[sup 123]I]IMZ accumulation. The impairment of [[sup 123]I]IMZ accumulation precedes DNA fragmentation and denaturation of cellular integrity. These results provide the molecular basis of [[sup 123]I]IMZ distribution. [ABSTRACT FROM AUTHOR]

Published
2004
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49. Activated Microvessels Express Vascular Endothelial Growth Factor and Integrin αvβ3During Focal Cerebral Ischemia

Author

Abumiya, Takeo, Lucero, Jacinta, Heo, Ji Hoe, Tagaya, Masafumi, Koziol, James A., Copeland, Brian R., and del Zoppo, Gregory J.

Abstract

Both vascular endothelial growth factor (VEGF) and integrin αvβ3play roles in angiogenesis. In noncerebral vascular systems, VEGF can induce endothelial integrin αvβ3expression. However, it is unknown whether VEGF, like integrin αvβ3, appears in the initial response of microvessels to focal brain ischemia. Their coordinate expression in microvessels of the basal ganglia after middle cerebral artery occlusion (MCAO) in the nonhuman primate model was examined quantitatively. Cells incorporating deoxyuridine triphosphate (dUTP+) by the polymerase I reaction at 1 hour (n = 3), 2 hours (n = 3), and 7 days (n = 4) after MCAO defined the ischemic core (Ic) and peripheral regions. Both VEGF and integrin αvβ3were expressed by activated noncapillary (7.5- to 30.0-μm diameter) microvessels in the Ic region at 1 and 2 hours after MCAO. At 7 days after MCAO, the number of VEGF+, integrin αvβ3+, or proliferating cell nuclear antigen-positive microvessels had decreased within the Ic region. The expressions of VEGF, integrin αvβ3, and proliferating cell nuclear antigen were highly correlated on the same microvessels using hierarchical log-linear statistical models. Also, VEGF and subunit αvmessenger ribonucleic acids were coexpressed on selected microvessels. Here, noncapillary microvessels are activated specifically early during a focal cerebral ischemic insult and rapidly express VEGF and integrin αvβ3together.

Published
1999
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50. Trends and Future Developments in the Pharmacological Treatment of Acute Ischaemic Stroke

Author

Zoppo, Gregory, Wagner, Simone, and Tagaya, Masafumi

Abstract

Stroke stands as the third leading cause of death. It makes great demands on patients, who must not only survive the complications of the acute stages, but must cope then with the great physical and economic costs of long-term disabilities. Therefore, there is urgent need to establish generally useful regimens for the acute treatment of ischaemic stroke. Three treatment approaches are based upon pathophysiologic concepts derived from experimental work with focal cerebral ischaemia. These include pharmacologic strategies for arterial recanalisation, inhibition of inflammatory processes and neural protection. Focal cerebral ischaemia secondary to occlusion of a brain-supplying artery initiates neuronal and microvascular events, and the simultaneous processes of inflammation which further injure tissue. The use of plasminogen activators to mediate thrombus and lysis in the acute setting has been shown to be clinically beneficial. Further work with arterial reperfusion strategies is under way. Early clinical studies with polymorphonuclear leukocyte-dependent endothelial adhesion receptor antagonists are being completed, but a strategy has yet to emerge. A large effort examining the potential efficacy of agents which may stabilise or protect neurons from ischaemic injury has shown promise in experimental models, and has been translated into clinical trials. Experimental work, and limited clinical experience, have indicated that: (a) the time window for intervention is important in limiting ischaemic and inflammatory injury, and for reducing the risk of haemorrhagic transformation; (b) putative neuroprotective strategies may potentially elongate the time interval for treatment; and (c) limitations from the adverse effects of plasminogen activators and of agents which beneficially affect neuronal dysfunction during ischaemia must yet be overcome. This review surveys pharmacological approaches currently undergoing evaluation which provide the goal of establishing effective strategies for the treatment of patients with acute cerebral ischaemia.

Published
1997
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