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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2009.03.025 Byline: Kazuo Shimamura (a), Toru Kuratani (a), Goro Matsumiya (a), Yukitoshi Shirakawa (a), Mugiho Takeuchi (a), Hiroshi Takano (b), Yoshiki Sawa (a) Abbreviations: 3DCT, 3-dimensional computed tomography; BCA, brachiocephalic artery; DHCA, deep hypothermic circulatory arrest; LCCA, left common carotid artery; LSA, left subclavian artery; RCP, retrograde cerebral perfusion; TEVAR, thoracic endovascular aortic repair Abstract: We advanced the open stent-grafting technique with a branched endoprosthesis, which reconstructs simultaneously the cervical branches and descending aorta within an acceptably short interval of deep hypothermic circulatory arrest. In this study, we evaluated the efficacy of this new technique and assessed the early and midterm results. Author Affiliation: (a) Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan (b) Department of Cardiovascular Surgery, Osaka General Medical Center, Osaka, Japan Article History: Received 2 May 2008; Revised 18 November 2008; Accepted 15 March 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2007.02.030 Byline: Koichi Toda (a), Kazuhiro Taniguchi (a), Hiroki Hata (a), Yasuhiro Shudo (a), Hajime Matsue (b), Satoru Kuki (c), Yoshiki Sawa (b) Abbreviations: CT, computed tomography; LET, long elephant trunk; TAR, total arch replacement Abstract: The purpose of this study was to investigate the medium-term results of arch aneurysms repaired by total arch replacement with a long elephant trunk and to evaluate whether this technique requires a subsequent distal anastomosis at the descending aorta when complete aneurysmal thrombosis is achieved around a long elephant trunk. Author Affiliation: (a) Department of Cardiovascular Surgery, Japan Labor Health and Welfare Organization Osaka Rosai Hospital, Sakai, Japan (b) Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Suita, Japan (c) Department of Cardiovascular Surgery, Takarazuka Municipal Hospital, Takarazuka, Japan. Article History: Received 21 November 2006; Revised 20 February 2007; Accepted 23 February 2007

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2005.06.041 Byline: Takashi Yamauchi (a), Yoshiki Sawa (a), Masahiro Sakurai (b), Takano Hiroshi (b), Goro Matsumiya (b), Koji Abe (c), Hikaru Matsuda (a) Abbreviations: BDNF, brain-derived neurotrophic factor; ERK, extracellular signal-regulated kinase; MEK, mitogen-activated protein kinase/ERK kinase; p-ERK, phosphorylated extracellular signal-regulated kinase Abstract: The mechanism of spinal cord injury is believed to be related to the vulnerability of spinal motor neuron cells to ischemia. The aim of this study was to investigate whether ONO-5046, a specific inhibitor of neutrophil elastase that can attenuate tissue or organ injury in various pathologic conditions, could protect against ischemic spinal cord damage. Author Affiliation: (a) Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan (b) Department of Cardiovascular Surgery, National Hospital Organization Sendai Medical Center, Sendai, Japan (c) Department of Neurology, Okayama University Graduate School of Medicine, Okayama, Japan Article History: Received 26 December 2004; Revised 20 April 2005; Accepted 20 June 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2005.05.016 Byline: Goro Matsumiya, Osamu Monta, Norihide Fukushima, Yoshiki Sawa, Toshihiro Funatsu, Kouichi Toda, Hikaru Matsuda Abstract: We sought to elucidate the incidence and timing of myocardial recovery in patients with idiopathic dilated cardiomyopathy during prolonged support with a left ventricular assist system and to characterize the factors influencing this phenomenon. Author Affiliation: Division of Cardiovascular Surgery, Department of Surgery, Osaka University Graduate School of Medicine, Osaka, Japan. Article History: Received 25 December 2004; Revised 28 April 2005; Accepted 2 May 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2004.02.045 Byline: Yukitoshi Shirakawa (a), Yoshiki Sawa (a), Yoshiaki Takewa (b), Eisuke Tatsumi (b), Yasufumi Kaneda (c), Yoshiyuki Taenaka (b), Hikaru Matsuda (a) Abstract: Although a left ventricular assist device is often used to provide circulatory support until transplantation in severe heart failure, the mortality of long-term use of left ventricular assist devices remains high. We have shown that hepatocyte growth factor causes angiogenesis, antifibrosis, and antiapoptosis in the myocardium. Therefore, gene therapy with hepatocyte growth factor-complementary DNA plasmids may enhance the chance of 'bridge to recovery.' In this study, we performed gene therapy with hepatocyte growth factor in the impaired goat heart with a left ventricular assist device. Author Affiliation: (a) Department of Surgery, E1, Division of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan (b) Department of Artificial Organs, National Cardiovascular Center Research Institute, Osaka, Japan (c) Department of Gene Therapy Science, Osaka University Graduate School of Medicine, Osaka, Japan Article History: Received 16 October 2003; Revised 15 February 2004; Accepted 26 February 2004

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2005.02.024 Byline: Imran A. Memon, Yoshiki Sawa, Shigeru Miyagawa, Satoshi Taketani, Hikaru Matsuda Abstract: Cellular cardiomyoplasty with isolated skeletal myoblasts and bone marrow mononuclear cells is an encouraging therapeutic strategy for heart failure. We investigated the achievements accomplished with combined cell therapy of skeletal myoblast and bone marrow mononuclear cell transplantation to the ischemic canine myocardium. Author Affiliation: Osaka University Graduate School of Medicine, Department of Surgery E1, Division of Cardiovascular Surgery, Osaka, Japan Article History: Received 17 August 2004; Revised 4 January 2005; Accepted 4 February 2005 Article Note: (footnote) Supported by the 1st Department of Surgery, Osaka University.

Byline: Youichi Kawahira, Yoshiki Sawa, Motonobu Nishimura, Satoru Sakakida, Hideki Ueda, Yasufumi Kaneda, Hikaru Matsuda Abstract: Background: Beta-adrenergic receptor system has a major role in cardiac contraction. If the receptor can be increased by gene transfection by means of intracoronary infusion of beta 2-adrenergic receptor to the hearts in which the receptor is down-regulated, this maneuver may improve the cardiac function and may be applied as one therapeutic approach during cardiopulmonary bypass or percutaneous cardiopulmonary support. Methods and results: The beta 2-adrenergic receptor complementary DNA was transfected in vivo to the normal rat heart by intracoronary infusion by means of a hemagglutinating virus of Japan liposome method, and the transfected heart was transplanted into the abdomen of another rat. Four days after transfection, the sarcolemma of the cardiomyocytes was well labeled by immunohistochemical labeling. Expression of beta-adrenergic receptor in the heart was approximately 4 times greater than that in control hearts (134 [+ or -] 42 vs 33 [+ or -] 4 fmol/mg protein) according to a ligand binding assay. The cardiac response of the transfected heart to isoproterenol was shown to be enhanced in a Langendorff perfusion system: after isoproterenol, developed pressure and maximal derivative of the left ventricle were greater than in the control heart (200 [+ or -] 12 vs 174 [+ or -] 6 mm Hg and 4110 [+ or -] 130 vs 3491 [+ or -] 255 mm Hg/sec), and the minimal derivative of the left ventricle was markedly smaller (-3040 [+ or -] 267 vs -2528 [+ or -] 131 mm Hg/sec). Conclusions: These results indicate that expression of beta 2-adrenergic receptor was approximately 4 times greater than in normal rat hearts by gene transfection using a hemagglutinating virus of Japan liposome method, and the transfected hearts demonstrated marked enhancements in cardiac response to beta-agonist, suggesting that transfer of this gene by intracoronary infusion has potential as a novel approach to enhance cardiac function. (J Thorac Cardiovasc Surg 1999;118:446-51) Article History: Received 3 December 1998; Revised 7 January 1999; Revised 9 March 1999; Accepted 29 April 1999 Article Note: (footnote) [star] From the First Department of Surgerya and Institute of Molecular Biology,b Osaka University Medical School, Osaka, Japan., [star][star] Address for reprints: Yoshiki Sawa, MD, Department of Surgery, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka, 565 Japan (E-mail: ykawahir@hsp.ncvc.go.jp )., a 0022-5223/99 $8.00 + 0 12/1/99730

Byline: Yoshiki Sawa, Hajime Ichikawa, Koji Kagisaki, Toshihiro Ohata, Hikaru Matsuda Abstract: Background: Reperfusion injury in the myocardium has recently been considered to be a type of inflammation, and close attention has been paid to the possible involvement of neutrophils, complement, and cytokines in the onset of this injury. Recently, it has been reported that serum levels of interleukin-6 are elevated significantly after myocardial infarction. The major site of interleukin-6 production and its exact roles are still unknown. In this study, we hypothesized that myocytes may produce interleukin-6 during hypoxia and this may play a role in neutrophil-mediated reperfusion injury. Methods and results: In the clinical study, 20 patients who underwent coronary artery bypass grafting were divided into 2 groups: group F, in which patients were treated with a serine protease inhibitor (FUT-175, 2 mg/kg per hour) during cardiopulmonary bypass, and group C (untreated patients). In group C, myocardial interleukin-6 production, as determined by the difference between the interleukin-6 level in the cardiopulmonary bypass circuit and its level in coronary venous blood, increased significantly after reperfusion (12 [+ or -] 4 pg/mL) as compared with that before aortic crossclamping (2 [+ or -] 2 pg/mL). In group F, the increase in the interleukin-6 level was suppressed significantly (before aortic crossclamping, 3 [+ or -] 2 pg/mL; after reperfusion, 4 [+ or -] 3 pg/mL). The interleukin-6 production differed significantly between group C and group F. In the in vitro experimental study, the supernatant from myocytes exposed to 2 hours of hypoxia (group 2H) showed significantly higher levels of interleukin-6 (455 [+ or -] 260 pg/mL) than that from normoxic myocytes (group N) (47 [+ or -] 15 pg/mL). This interleukin-6 production was suppressed by the addition of FUT-175 (123 [+ or -] 24 pg/mL). The interleukin-6 production by endothelial cells of coronary vessels did not differ between group 2H (283 [+ or -] 151 pg/mL) and group N (151 [+ or -] 86 pg/mL). In a coincubation system with a monolayer of endothelial cells on collagen membrane and myocytes under collagen membrane in a modified Boyden chamber, 2 hours of coincubation showed a significantly higher percent of neutrophil transendothelial migration (group 2H vs N, 78% [+ or -] 13% vs 26% [+ or -] 11%), value of chemiluminescence (22 [+ or -] 8 vs 5 [+ or -] 2 x 10.sup.3 counts/3 minutes), and percent of irreversibly damaged myocytes (48% [+ or -] 17% vs 12% [+ or -] 8%) than normoxic coincubation. In contrast, anti-interleukin-6 monoclonal antibody significantly attenuated neutrophil transendothelial migration (42% [+ or -] 19%) and irreversible damage of myocytes (26% [+ or -] 15%) in 2 hours of coincubation. Conclusions: Interleukin-6 is produced from myocardium during ischemia and reperfusion in patients undergoing coronary bypass grafting. This interleukin-6 may be derived from hypoxic myocytes and play a role in neutrophil-mediated reperfusion injury in myocardium. (J Thorac Cardiovasc Surg 1998;116:511-7) Article History: Received 29 December 1998; Revised 23 February 1998; Revised 30 April 1998; Accepted 13 May 1998 Article Note: (footnote) [star] From the First Department of Surgery, Osaka University Medical School, Osaka, Japan.

Byline: Yoshiki Sawa, Keishi Kadoba, Ken Suzuki, Hong-Zhi Bai, Yasufumi Kaneda, Ryota Shirakura, Hikaru Matsuda Abstract: Objective: To confirm gene transfer techniques especially into the whole heart, we tried out a gene transfer method involving liposome with the viral envelope hemagglutinating virus of Japan liposome as an alternative to existing techniques such as cationic lipofection or other viral vectors. Method: For this study, hemagglutinating virus of Japan liposome (H group) or cationic liposome(L group) was used to compare the efficacy of gene transfection of oligonucleotide labeled with fluorescein isothiocyanate and cDNA of [beta]-galactosidase and human manganese-superoxide dismutase. Fluorescein-labeled oligonucleotide, cDNA of [beta]-galactosidase, or manganese-superoxide dismutase was complexed with liposomes, DNA-binding nuclear protein, and the viral protein coat of hemagglutinating virus of Japan. After donor rat hearts arrested by cardioplegia had been harvested, the coronary artery during cardioplegic arrest was infused via an aortic cannula with the liposome-gene complex. Next, the hearts were transplanted into the abdomen of recipient rats of the same strain, and all recipients were put to death after 3 days of transfection. Results: Fluorescein isothiocyanate was detected in the nuclei of more than 70% of the myocytes (75% [+ or -] 14%, n = 5) in the H group compared with fewer than 10% in the L group (7% [+ or -] 5%, n = 5). The intensity of fluorescein isothiocyanate was significantly higher in the H group (979 [+ or -] 112 FI) than in the L group (116 [+ or -] 68 FI). [beta]-Galactosidase was expressed in the cytosol of more than 50% of the myocytes in the H group (61% [+ or -] 7%, n = 5) compared with none in the L group (0%, n = 5). After 3 days of gene transfection, and when exposed to ischemia (30 minutes, 37[degrees] C) and reperfusion (30 minutes, 37[degrees] C) with Langendorff apparatus, the hearts transfected with manganese-superoxide dismutase (S group, n = 5) showed a significantly higher percentage of recovery of left ventricular end-diastolic pressure (S vs C, 86% [+ or -] 3% vs 54% [+ or -] 12%) and coronary flow (98% [+ or -] 2% vs 66% [+ or -] 12%) than did the control hearts (C group, n = 5). Western blotting analysis showed an apparent increased expression of manganese-superoxide dismutase in the hearts transfected with manganese-superoxide dismutase compared with the control hearts. These results clearly demonstrated that the donor hearts were transfected with fluorescein-labeled oligonucleotide and the [beta]-galactosidase gene as a result of coronary infusion of the hemagglutinating virus of Japan liposome during cardioplegic arrest at the time of harvest. Furthermore, the hearts transfected with manganese-superoxide dismutase showed significant improvement in tolerance against ischemia-reperfusion injury. Conclusion: We believe that this method represents a novel in vivo gene transfer technique for the heart and thus may provide a new tool for research and therapy of heart transplantation. (J Thorac Cardiovasc Surg 1997;113:512-9) Article History: Received 6 May 1996; Revised 12 June 1996; Revised 11 October 1996; Accepted 21 October 1996 Article Note: (footnote) [star] From the First Department of Surgery,a Department of Institute for Molecular and Cellular Biology,b and Department of Organ Transplantation,c Osaka University Medical School, Suita, Osaka 565, Japan., [star][star] Read at the Seventy-sixth Annual Meeting of The American Association for Thoracic Surgery, San Diego, Calif., April 28-May 1, 1996., a Address for reprints: Hikaru Matsuda MD, First Department of Surgery, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565, Japan., aa 0022-5223/97 $5.00 + 0 12/6/78770

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2005.02.008 Byline: Masamichi Ono, Norihide Fukushima, Hajime Ichikawa, Toru Ishizaka, Yoshiki Sawa, Hikaru Matsuda Author Affiliation: Division of Cardiovascular Surgery, Department of Surgery, Osaka University Graduate School of Medicine, Osaka, Japan. Article History: Received 26 January 2005; Accepted 10 February 2005

Byline: Nobuaki Hirata, Shin Takiuchi, Syouhei Maeda, Shigeaki Ohtake, Yoshiki Sawa, Hikaru Matsuda Abstract: J Thorac Cardiovasc Surg 1999;117:1215-7 Author Affiliation: First Department of Surgery, Osaka University Medical School, Osaka, Japan Article History: Received 12 January 1999; Accepted 20 January 1999 Article Note: (footnote) [star] Address for reprints: Nobuaki Hirata, MD, First Department of Surgery, Osaka University Medical School, 2-2, Yamadaoka, Suita, Osaka 565-0871, Japan., [star][star] 12/54/97381

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2008.02.005 Byline: Koji Takeda (a), Goro Matsumiya (a), Hajime Matsue (a), Seiki Hamada (b), Tomoyuki Fujita (a), Yoshiki Sawa (a) Author Affiliation: (a) Division of Cardiovascular Surgery, Department of Surgery, Osaka University Graduate School of Medicine, Osaka, Japan (b) Department of Radiology, Osaka University Graduate School of Medicine, Osaka, Japan Article History: Received 26 November 2007; Accepted 2 February 2008

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2006.02.044 Byline: Koji Takeda, Goro Matsumiya, Hiroshi Takano, Masahiro Koh, Keiji Iwata, Yoshiki Sawa Author Affiliation: Division of Cardiovascular Surgery, Department of Surgery, Osaka University Graduate School of Medicine, Osaka, Japan Article History: Received 10 February 2006; Accepted 22 February 2006

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2004.11.003 Byline: Goro Matsumiya, Yuji Miyamoto, Osamu Monta, Hiroshi Takano, Yoshiki Sawa, Hikaru Matsuda Author Affiliation: Division of Cardiovascular Surgery, Department of Surgery, Osaka University Gradu ate School of Medicine, Osaka,Japan. Article History: Received 7 September 2004; Revised 1 November 2004; Accepted 3 November 2004