Search

Your search keyword '"Kyo, S"' showing total 960 results
Start Over Author "Kyo, S"
960 results on '"Kyo, S"'

4. Allogeneic amniotic membrane-derived mesenchymal stromal cell transplantation in a porcine model of chronic myocardial ischemia

Author

Kimura M, Toyoda M, Gojo S, Itakura Y, Kami D, Miyoshi S, Kyo S, Ono M, and Umezawa A

Subjects
Amniotic membrane, Mesenchymal stromal cell, Allogeneic cell transplantation, Chronic myocardial ischemia, Porcine model, Medicine, Medicine (General), R5-920
Abstract

Introduction. Amniotic membrane contains a multipotential stem cell population and is expected to possess the machinery to regulate immunological reactions. We investigated the safety and efficacy of allogeneic amniotic membrane-derived mesenchymal stromal cell (AMSC) transplantation in a porcine model of chronic myocardial ischemia as a preclinical trial. Methods. Porcine AMSCs were isolated from amniotic membranes obtained by cesarean section just before delivery and were cultured to increase their numbers before transplantation. Chronic myocardial ischemia was induced by implantation of an ameroid constrictor around the left circumflex coronary artery. Four weeks after ischemia induction, nine swine were assigned to undergo either allogeneic AMSC transplantation or normal saline injection. Functional analysis was performed by echocardiography, and histological examinations were carried out by immunohistochemistry 4 weeks after AMSC transplantation. Results. Echocardiography demonstrated that left ventricular ejection fraction was significantly improved and left ventricular dilatation was well attenuated 4 weeks after AMSC transplantation. Histological assessment showed a significant reduction in percentage of fibrosis in the AMSC transplantation group. Injected allogeneic green fluorescent protein (GFP)-expressing AMSCs were identified in the immunocompetent host heart without the use of any immunosuppressants 4 weeks after transplantation. Immunohistochemistry revealed that GFP colocalized with cardiac troponin T and cardiac troponin I. Conclusions. We have demonstrated that allogeneic AMSC transplantation produced histological and functional improvement in the impaired myocardium in a porcine model of chronic myocardial ischemia. The transplanted allogeneic AMSCs survived without the use of any immunosuppressants and gained cardiac phenotype through either their transdifferentiation or cell fusion.

Published
2012

36. Acute biological mitral valve thrombosis after the left atrial venting in a patient with a venoarterial extracorporeal membrane oxygenator.

Author

Lee, Kyo S., Jung, Yochun, Jeong, In S., Song, Sang Y., Na, Kook J., and Oh, Sang G.

Subjects
*MITRAL valve, *LEFT heart atrium, *PROSTHETIC heart valves, *OXYGENATORS, *THROMBOSIS
Abstract

Background: Left atrial venting through atrial septotomy in patients with decreased left ventricular (LV) contractility after venoarterial extracorporeal membrane oxygenation (VA‐ECMO) is a simple and effective method for treating LV decompression. Materials & Methods: We report a case of prosthetic mitral valve thrombosis after left atrial venting in a patient with VA‐ECMO. Results: In patients undergoing mitral valve replacement, left atrial venting reduces the flow through the mitral valve and forms a prosthetic thrombosis. Discussion: Therefore, excessive left atrial venting should be avoided. Other venting methods that can maintain the flow through the mitral valve should be considered after mitral valve replacement. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

47. Outcomes of Jarvik 2000 LVAD as a Bridge to Heart Transplantation: Data from the Japanese Registry for Mechanically Assisted Circulatory Support (J-MACS)

Author

Kohno, H., primary, Matsumiya, G., additional, Sawa, Y., additional, Ono, M., additional, Saiki, Y., additional, Shiose, A., additional, Yamazaki, K., additional, Matsui, Y., additional, Niinami, H., additional, Matsuda, H., additional, Kitamura, S., additional, Nakatani, T., additional, and Kyo, S., additional

Published
2017
Full Text
View/download PDF

48. Prognostic role and implications of mutation status of tumor suppressor gene ARID1A in cancer: A systematic review and meta-analysis

Author

Luchini, C. Veronese, N. Solmi, M. Cho, H. Kim, J.-H. Chou, A. Gill, A.J. Faraj, S.F. Chaux, A. Netto, G.J. Nakayama, K. Kyo, S. Lee, S.Y. Kim, D.-W. Yousef, G.M. Scorilas, A. Nelson, G.S. Köbel, M. Kalloger, S.E. Schaeffer, D.F. Yan, H.-B. Liu, F. Yokoyama, Y. Zhang, X. Pang, D. Lichner, Z. Sergi, G. Manzato, E. Capelli, P. Wood, L.D. Scarpa, A. Correll, C.U.

Abstract

Loss of the tumor suppressor gene AT-rich interactive domain-containing protein 1A (ARID1A) has been demonstrated in several cancers, but its prognostic role is unknown. We aimed to investigate the risk associated with loss of ARID1A (ARID1A-) for all-cause mortality, cancer-specific mortality and recurrence of disease in subjects with cancer. PubMed and SCOPUS search from database inception until 01/31/2015 without language restriction was conducted, contacting authors for unpublished data. Eligible were prospective studies reporting data on prognostic parameters in subjects with cancer, comparing participants with presence of ARID1A (ARID1A+) vs. ARID1A-, assessed either via immunohistochemistry (loss of expression) or with genetic testing (presence of mutation). Data were summarized using risk ratios (RR) for number of deaths/recurrences and hazard ratios (HR) for time-dependent risk related to ARID1A- adjusted for potential confounders. Of 136 hits, 25 studies with 5,651 participants (28 cohorts; ARID1A-: n = 1,701; ARID1A+: n = 3,950), with a mean follow-up period of 4.7 ± 1.8 years, were meta-analyzed. Compared to ARID1A+, ARID1A- significantly increased cancer-specific mortality (studies = 3; RR = 1.55, 95% confidence interval (CI) = 1.19-2.00, I2 = 31%). Using HRs adjusted for potential confounders, ARID1A- was associated with a greater risk of cancer-specific mortality (studies = 2; HR = 2.55, 95%CI = 1.19-5.45, I2 = 19%) and cancer recurrence (studies = 10; HR = 1.93, 95%CI = 1.22-3.05, I2 = 76%). On the basis of these results, we have demonstrated that loss of ARID1A shortened time to cancer-specific mortality, and to recurrence of cancer when adjusting for potential confounders. For its role, this gene should be considered as an important potential target for personalized medicine in cancer treatment.

Published
2015

Catalog

Books, media, physical & digital resources
See catalog results