Faculty Profiles - NAKAO Atsunori

Papers - NAKAO Atsunori

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Nitrite protects rat lung grafts from ischemia/reperfusion injury via nitric oxide Reviewed

Ryujiro Sugimoto, Atsunori Nakao, Junichi Kohmoto, Yinna Wang, Mark T. Gladwin, Timothy R. Billiar, Kenneth R. McCurry

AMERICAN JOURNAL OF TRANSPLANTATION 8 498 - 498 2008.5

Hydrogen inhalation ameliorates cold ischemia/reperfusion injury of rat cardiac grafts Reviewed

Atsunori Nakao, David J. Kaczorowski, Ryujiro Sugimoto, Yinna Wang, Timothy R. Billiar, Kenneth R. McCurry

AMERICAN JOURNAL OF TRANSPLANTATION 8 501 - 501 2008.5

Application of heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury. Reviewed

Atsunori Nakao, David J Kaczorowski, Ryujiro Sugimoto, Timothy R Billiar, Kenneth R McCurry

Journal of clinical biochemistry and nutrition 42 ( 2 ) 78 - 88 2008.3

Language：English Publishing type：Research paper (scientific journal) Publisher：JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION

Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.

DOI： 10.3164/jcbn.2008013

Web of Science

PubMed

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Reduction of cerebral infarction in rats by biliverdin associated with amelioration of oxidative stress Reviewed International journal

Kentaro Deguchi, Takeshi Hayashi, Shoko Nagotani, Yoshihide Sehara, Han Zhe Zhang, Atsushi Tsuchiya, Yasuyuki Ohta, Koji Tomiyama, Nobutoshi Morimoto, Masahiro Miyazaki, Nam ho Huh, Atsunori Nakao, Tatsushi Kamiya, Koji Abe

Brain Research 1188 ( 1 ) 1 - 8 2008.1

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER

Biliverdin (BV), one of the byproducts of heme catalysis through heme oxygenase (HO) system, is a scavenger of reactive oxygen species (ROS). We hypothesized that BV treatment could protect rat brain cells from oxidative injuries via its anti-oxidant efficacies. Cerebral infarction was induced by transient middle cerebral artery occlusion (tMCAO) for 90 min, followed by reperfusion. BV or vehicle was administered intraperitoneally immediately after reperfusion. The size of the cerebral infarction 2 days after tMCAO was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) stain. Superoxide generation 4 h after tMCAO was determined by detection of oxidized hydroethidine. In addition, the oxidative impairment of neurons were immunohistochemically assessed by stain for lipid peroxidation with 4-hydroxy-2-nonenal (4-HNE) and damaged DNA with 8-hydroxy-2′-deoxyguanosine (8-OHdG). BV treatment significantly reduced infarct volume of the cerebral cortices associated with less superoxide production and decreased oxidative injuries of brain cells. The present study demonstrated that treatment with BV ameliorated the oxidative injuries on neurons and decreased brain infarct size in rat tMCAO model. © 2007 Elsevier B.V. All rights reserved.

DOI： 10.1016/j.brainres.2007.07.104

Toll-like receptor 4 mediates the early inflammatory response after cold ischemia/reperfusion. Reviewed International journal

David J Kaczorowski, Atsunori Nakao, Kevin P Mollen, Raghuveer Vallabhaneni, Ryujiro Sugimoto, Junichi Kohmoto, Kimimasa Tobita, Brian S Zuckerbraun, Kenneth R McCurry, Noriko Murase, Timothy R Billiar

Transplantation 84 ( 10 ) 1279 - 87 2007.11

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

BACKGROUND: Ischemia/reperfusion (I/R) injury leads to graft dysfunction and may contribute to alloimmune responses posttransplantation. The molecular mechanisms of cold I/R injury are only partially characterized but may involve toll-like receptor (TLR)-4 activation by endogenous ligands. We tested the hypothesis that TLR4 mediates the early inflammatory response in the setting of cold I/R in a murine cardiac transplant model. METHODS: Syngeneic heart transplants were performed in mutant mice deficient in TLR4 signaling (C3H/HeJ) and wild-type mice (C3H/HeOuJ). Transplants were also performed between the strains (mutant hearts into wild-type recipients and the converse). Donor hearts were subjected to 2 hr of cold ischemia. The grafts were retrieved at 3 and 24 hr after reperfusion. Serum samples were collected for cytokine analysis. Reverse-transcription polymerase chain reaction and histologic analysis were used to assess intra-graft inflammation. RESULTS: After transplant, serum tumor necrosis factor (TNF), interleukin (IL)-6, JE/monocyte chemotractant protein (MCP)-1, IL-1beta, and troponin I levels, as well as intragraft TNF, IL-1beta, IL-6, early growth response (EGR)-1, intercellular adhesion molecule (ICAM)-1, and inducible nitric oxide synthase (iNOS) mRNA levels, were significantly lower in the mutant-->mutant group compared to the wild-type-->wild-type group (P< or =0.05). Intermediate levels of serum IL-6, JE/MCP-1, as well as intragraft TNF, IL-1beta, IL-6, and ICAM-1 mRNA were observed after transplants in the mutant-->wild-type and wild-type-->mutant groups. Immunohistochemistry revealed less myocardial nuclear factor-kappaB nuclear translocation at and less neutrophil infiltration in the mutant-->mutant group compared to the wild-type-->wild-type group. CONCLUSIONS: These findings demonstrate that TLR4 signaling is central to both the systemic and intragraft inflammatory responses that occur after cold I/R in the setting of organ transplantation and that TLR4 signaling on both donor and recipient cells contributes to this response.

DOI： 10.1097/01.tp.0000287597.87571.17

Web of Science

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Carbon monoxide differentially inhibits TLR signaling pathways by regulating ROS-induced trafficking of TLRs to lipid rafts. International journal

Kiichi Nakahira, Hong Pyo Kim, Xue Hui Geng, Atsunori Nakao, Xue Wang, Noriko Murase, Peter F Drain, Xiaomei Wang, Madhu Sasidhar, Elizabeth G Nabel, Toru Takahashi, Nicholas W Lukacs, Stefan W Ryter, Kiyoshi Morita, Augustine M K Choi

The Journal of experimental medicine 203 ( 10 ) 2377 - 89 2006.10

Language：English Publishing type：Research paper (scientific journal)

Carbon monoxide (CO), a byproduct of heme catabolism by heme oxygenase (HO), confers potent antiinflammatory effects. Here we demonstrate that CO derived from HO-1 inhibited Toll-like receptor (TLR) 2, 4, 5, and 9 signaling, but not TLR3-dependent signaling, in macrophages. Ligand-mediated receptor trafficking to lipid rafts represents an early event in signal initiation of immune cells. Trafficking of TLR4 to lipid rafts in response to LPS was reactive oxygen species (ROS) dependent because it was inhibited by diphenylene iodonium, an inhibitor of NADPH oxidase, and in gp91(phox)-deficient macrophages. CO selectively inhibited ligand-induced recruitment of TLR4 to lipid rafts, which was also associated with the inhibition of ligand-induced ROS production in macrophages. TLR3 did not translocate to lipid rafts by polyinosine-polycytidylic acid (poly(I:C)). CO had no effect on poly(I:C)-induced ROS production and TLR3 signaling. The inhibitory effect of CO on TLR-induced cytokine production was abolished in gp91(phox)-deficient macrophages, also indicating a role for NADPH oxidase. CO attenuated LPS-induced NADPH oxidase activity in vitro, potentially by binding to gp91(phox). Thus, CO negatively controlled TLR signaling pathways by inhibiting translocation of TLR to lipid rafts through suppression of NADPH oxidase-dependent ROS generation.

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Heart allograft protection with low-dose carbon monoxide inhalation: effects on inflammatory mediators and alloreactive T-cell responses. Reviewed International journal

Atsunori Nakao, Hideyoshi Toyokawa, Masanori Abe, Tetsuma Kiyomoto, Kiichi Nakahira, Augustine M K Choi, Michael A Nalesnik, Angus W Thomson, Noriko Murase

Transplantation 81 ( 2 ) 220 - 30 2006.1

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Carbon monoxide (CO), a byproduct of heme catalysis, has lately received considerable attention as a regulatory molecule in cellular and biological processes. CO has been shown to provide potent protection against a variety of tissue injuries. We hypothesized in this study that low concentration CO would be beneficial for organ allografts, which frequently undergo several types of injury such as ischemia/reperfusion, alloimmune reaction, and inflammation METHODS: The efficacy of low-dose CO was examined in a fully allogeneic LEW to BN rat heterotopic heart transplantation (HHTx) model. Recipients were kept in air or exposed to low-dose CO (20 ppm) for 14, 28, or 100 days after HHTx under short-course tacrolimus RESULTS: CO treatment (d0-28, 0-100) was remarkably effective in prolonging heart allograft survival to a median of >100 from 45 days in the air-control group, with significant reductions of arteritis, fibrosis, and cellular infiltration, including macrophages and T cells. CO inhibited intragraft upregulation of Th1 type cytokines (IL-2, IFNgamma), proinflammatory mediators (IL-1beta, TNFalpha, IL-6, COX-2), and adhesion molecule. Shorter CO exposure in early (0-13d) and late (14-28d) posttransplant periods also prolonged graft survival, with a significant inhibition of inflammatory mediators CONCLUSIONS: These results show that low dose CO inhalation protects heart allografts and can considerably prolong their survival. CO appears to function via multiple mechanisms, including direct inhibition of Th1 type cytokine production and regulation of inflammatory responses.

DOI： 10.1097/01.tp.0000188637.80695.7f

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Multiple hepatic adenomas caused by long-term administration of androgenic steroids for aplastic anemia in association with familial adenomatous polyposis

NAKAO Atsunori, SAKAGAMI Kenichi, NAKATA Yusei, KOMAZAWA Katsutaka, AMIMOTO Tatsuya, NAKASHIMA Koichiro, ISOZAKI Hiroshi, TAKAKURA Norihisa, TANAKA Noriaki

J Gastroenterol 35 ( 7 ) 557 - 562 2000.7

Generalized Peritonitis Due to Spontaneously Perforated Pyometra Presenting as Pneumoperitoneum : Report of a Case

NAKAO ATSUNORI, MIMURA HISASHI, FUJISAWA KENJI, EZAWA KAZUHIKO, OKAMOTO TAKAHIRO, IWAGAKI HIROMI, ISOZAKI HIROSHI, TAKAKURA NORIHISA, TANAKA NORIAKI

Surg Today 30 ( 5 ) 454 - 457 2000.5

Gastric Perforation Caused by a Bulimic Attack in an Anorexia Nervosa Patient : Report of a Case

NAKAO ATSUNORI, ISOZAKI HIROSHI, IWAGAKI HIROMI, KANAGAWA TAIICHIRO, TAKAKURA NORIHISA, TANAKA NORIAKI

Surg Today 30 ( 5 ) 435 - 437 2000.5

Gallbladder torsion : case report and review of 245 cases reported in the Japanese literature

NAKAO A

J Hepatobiliary Pancreat Surg 6 418 - 421 1999.12

Portal venous gas associated with splenic abscess secondary to colon cancer

NAKAO A

Anticancer Res 19 5641 - 5644 1999.12

Dermoid Cyst of the Spleen: Report of a Case

NAKAO Atsunori, SAITO Shinya, YAMANO Taketoshi, TAKAKURA Norihisa, ISOZAKI Hiroshi, NOTOHARA Kenji, TANAKA Noriaki

Surg Today 29 ( 7 ) 660 - 662 1999.7

Gastric carcinoma with predominant choriocarcinomatous component

NAKAO Atsunori, SAKAGAMI Kenichi, UDA Masashi, MITSUOKA Shintaro, YAMASHITA Naoto, ITO Hisao

3 ( 6 ) 403 - 405 1998.12

Benign Fibrous Mesothelioma Successfully Treated by Thoracoscope-Assisted Surgery : Report of a Case

NAKAO ATSUNORI, SAKAGAMI KENICHI, UDA MASASHI, MITSUOKA SHINTARO, ITO HISAO

Surg Today 28 ( 10 ) 1087 - 1090 1998.10

所属リンパ節にサルコイド反応がみられた胆管癌の1症例

中尾篤典

胆と膵 17 963 - 966 1996.12

Use of the Bobbin Threader^<【○!R】> for Cranioplasty

NAKAO Atsunori, HIROHATA Taizo, OBAYASHI Naohiko

Japanese journal of neurosurgery 5 ( 6 ) 470 - 471 1996.11

Authorship：Lead author Language：Japanese Publishing type：Research paper (scientific journal) Publisher：The Japanese Congress of Neurological Surgeons

During cranioplasty, surgeons secure the cranial flap with thread or thin wire sutures by inserting them through holes made in the skull. we have devised a new insertion method using the Bobbin Threader^[○!R] . The major advantages of this technique are ease in suturing, shortened closure time, and minimal risk of dural injury.

CiNii Article

CiNii Books

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粘膜内癌を伴った巨大な直腸villous tumorの1例??10cm以上の大腸villous tumor本邦報告15例の検討

中尾篤典

広島医学 49 970 - 972 1996.7

抗血小板療法中に起きた大腿神経麻痺を伴う腸腰筋血腫の1例

中尾篤典

外科診療 6 745 - 747 1996.6

肝癌術後の肺転移に対し, Epirubicinの少量頻回投与が有効であった2症例

中尾篤典

癌と化学療法 22 1831 - 1834 1995.10

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