Details of a Researcher - TAKADA Kouichi

Papers - TAKADA Kouichi

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Apoptosis supercedes necrosis in mitochondrial DNA-depleted Jurkat cells by cleavage of receptor-interacting protein and inhibition of lysosomal cathepsin.

Sato T, Machida T, Takahashi S, Murase K, Kawano Y, Hayashi T, Iyama S, Takada K, Kuribayashi K, Sato Y, Kobune M, Takimoto R, Matsunaga T, Kato J, Niitsu Y

Journal of immunology (Baltimore, Md. : 1950) ( 1 ) 181 ( 1 ) 197 - 207 2008.07 [Refereed]

PubMed

Case report of a focal nodular hyperplasia-like nodule present in cirrhotic liver

Sho Takahashi, Koji Miyanishi, Kohichi Takada, Yutaka Kawano, Tamotsu Sagawa, Yasushi Sato, Rishu Takimoto, Tetsuji Takayama, Junji Kato, Mutsuko Omatsu, Tadashi Hasegawa, Masamichi Kojiro, Yoshiro Niitsu

HEPATOLOGY RESEARCH ( BLACKWELL PUBLISHING ) 38 ( 5 ) 521 - 528 2008.05 [Refereed]

An 81-year-old female was referred to Sapporo Medical University Hospital because of a nodular lesion 20 mm in diameter found in the liver S8 during follow-up for type C liver cirrhosis. Abdominal ultrasonography showed a capsule-like structure, and contrast computed tomography revealed hypervascularity at the early phase and inner pooling of the contrast medium with ring enhancement at the late phase. Magnetic resonance T2-weighted imaging (T2WI) demonstrated a hyperintensity nodule with further hyperintensity signals in some parts of the nodule, and the signal pattern differed from that of typical fibrosis. SPIO-magnetic resonance imaging showed partial hypointensity signals by T2WI, which indicated the presence of Kupffer cells. Angiography did not show a spoke-wheel pattern. The results by imaging modalities indicated that the nodule was atypical for hepatocellular carcinoma (HCC) and focal nodular hyperplasia (FNH), and liver nodule biopsy was performed for histological diagnosis. Compared with the background liver, the nodule revealed high cellular density, cellular dysplasia at the periphery, a pseudo-crypt structure and irregular hepatic cord arrangement in some parts of the nodule. Among them, there was immature fibrous tissue containing arterioles with muscular hypertrophy. There has been no report of well-differentiated HCC with a central scar, and this case was presumed to be an FNH-like nodule with dysplasia physically associated with cirrhotic tissue.

DOI PubMed

A phase I trial of arterial infusion chemotherapy with gemcitabine and 5-fluorouracil for unresectable advanced pancreatic cancer after vascular supply distribution via superselective embolization

Koji Miyanishi, Hirotoshi Ishiwatari, Tsuyoshi Hayashi, Minoru Takahashi, Yutaka Kawano, Kohichi Takada, Hideyuki Ihara, Toshinori Okuda, Kunihiro Takanashi, Sho Takahashi, Yasushi Sato, Takuya Matsunaga, Hisato Homma, Junji Kato, Yoshiro Niitsu

JAPANESE JOURNAL OF CLINICAL ONCOLOGY ( OXFORD UNIV PRESS ) 38 ( 4 ) 268 - 274 2008.04 [Refereed]

Background: We previously reported that arterial infusion chemotherapy improved the response rate and survival of the patients with pancreatic cancer at advanced stages in an open trial. We conducted a Phase I trial of arterial infusion chemotherapy with gemcitabine and 5-fluorouracil for advanced pancreatic cancer after vascular supply distribution via super-selective embolization. Methods: Patients were treated after arterial embolization for hemodynamic change to restrict the blood flow into the pancreas (mainly to the great pancreatic artery and the caudal pancreatic artery). Arterial infusion chemotherapy consisted of gemcitabine in doses that were increased from 600 to 1000 mg/m(2) in subsequent cohorts on Day 1 plus continuous infusion of 5-fluorouracil 300 mg/m(2)/day on Days 1-5 every 2 weeks. Result: Twelve patients were enrolled. The maximum tolerated dose of gemcitabine was determined to be Level 3 (1000 mg/m(2)). Only very mild hematological and non-hematological toxicities were noted. The overall response rate was 33.3%. The median survival time was 22.7 (95% CI; 9.5-24.5) months and the 1- and 2-year overall survival rates were 83.3 and 25.0%, respectively. Conclusion: Arterial infusion chemotherapy using 1000 mg/m(2) gemcitabine on Day 1 and 300 mg/m(2)/day 5-fluorouracil on Days 1-5 every 2 weeks warrants a Phase II study.

DOI PubMed

非アルコール性脂肪性肝疾患の病態と治療非アルコール性脂肪性肝炎における肝内鉄過剰蓄積機序の解析

高田弘一, 加藤淳二, 河野豊, 高橋祥, 小船雅義, 瀧本理修, 宮西浩嗣, 佐藤康史, 佐藤勉, 高山哲治, 新津洋司郎

肝臓 ( (一社)日本肝臓学会 ) 49 ( Suppl.1 ) A32 - A32 2008.04 [Refereed]

Adenoviral vector-mediated transfer of the Indian hedgehog gene modulates lymphomyelopoiesis in vivo

Masayoshi Kobune, Junii Kato, Yutaka Kawano, Katsunori Sasaki, Hiroaki Uchida, Kohichi Takada, Sho Takahashi, Rishu Takimoto, Yoshiro Niitsu

STEM CELLS ( WILEY ) 26 ( 2 ) 534 - 542 2008.02 [Refereed]

Indian hedgehog (Ihh) plays an essential role in angiogenesis, hematogenesis, and epiphysis formation during embryogenesis. In the present study, we injected an adenoviral vector (Adv) carrying the mock-control (Adv-control) or Ihh (Adv-Ihh) gene into severe combined immunodeficiency (SCID) or BALB/c mice to evaluate the effects of Ihh on the regulation of postnatal hematopoiesis in vivo. After the i.v. injection of Adv-Ihh, the expression of vector-derived Ihh mRNA was detected in the liver. Four weeks after administration of Adv-Ihh to SCID mice, we observed an increase in the number of c-Kit+ cells and clonogenic cells per 10(5) mononuclear cells in the bone marrow compared with Advcontrol-administered mice. Moreover, after administration of Adv-Ihh to BALB/c mice, the number of splenic B220+IgM(low)-CD23(int)CD2(int) B lymphocytes and CD4+ T lymphocytes was strongly increased. Furthermore, the number of thymic double-negative (DN)2, DN3, CD8+ immature single-positive, and CD4+/CD8- cells was significantly elevated relative to the number in mice that received the control Adv vector. Our results suggest that enhanced signaling by Ihh can modulate the proliferation and differentiation of splenic B lymphocytes and thymic T lymphocytes during bone marrow hematopoiesis in vivo. Thus, modulation of the hedgehog signaling pathway may provide a therapeutic strategy to stimulate lymphomyelopoiesis in vivo.

DOI PubMed

腫瘍内出血により急速に増大した悪性黒色腫肝転移の1例

高田弘一, 高山哲治, 河野豊, 高橋祥, 高橋究, 山口正人, 早坂享子, 林毅, 石渡裕俊, 宮西浩嗣, 加藤淳二, 名取博, 山下利春, 新津洋司郎

超音波医学 ( (公社)日本超音波医学会 ) 35 ( 1 ) 73 - 73 2008.01 [Refereed]

胆管過誤腫と胆管細胞腺腫を内在した胆管細胞癌の1例

高橋祥, 高田弘一, 宮西浩嗣, 河野豊, 石渡裕俊, 林毅, 加藤淳二, 新津洋司郎, 水口徹, 尾松睦子, 長谷川匡

肝臓 ( (一社)日本肝臓学会 ) 48 ( Suppl3 ) A577 - A577 2007.11 [Refereed]

腫瘍内出血により血小板減少を来たした悪性黒色腫多発肝転移にDSM併用CDDP動注化学療法が有効であった1例

高田弘一, 加藤淳二, 河野豊, 高橋祥, 林毅, 石渡裕俊, 宮西浩嗣, 山下利春, 新津洋司郎

肝臓 ( (一社)日本肝臓学会 ) 48 ( Suppl3 ) A632 - A632 2007.11 [Refereed]

全身MRIが診断に有用であった肝細胞癌坐骨転移の症例

河野豊, 宮西浩嗣, 高田弘一, 高橋祥, 加藤淳二, 新津洋司郎

肝臓 ( (一社)日本肝臓学会 ) 48 ( Suppl3 ) A612 - A612 2007.11 [Refereed]

Long-term phlebotomy with low-iron diet therapy lowers risk of development of hepatocellular carcinoma from chronic hepatitis C

Junji Kato, Koji Miyanishi, Masayoshi Kobune, Tokiko Nakamura, Kohichi Takada, Rishu Takimoto, Yutaka Kawano, Sho Takahashi, Minoru Takahashi, Yasushi Sato, Tetsuji Takayama, Yoshiro Niitsu

JOURNAL OF GASTROENTEROLOGY ( SPRINGER TOKYO ) 42 ( 10 ) 830 - 836 2007.10 [Refereed]

Background. We have previously demonstrated that in patients with chronic hepatitis C (CHC), iron depletion improves serum alanine aminotransferase (ALT) levels as well as hepatic oxidative DNA damage. However, it has not been determined whether continuation of iron depletion therapy for CHC favorably influences its progression to hepatocellular carcinoma (HCC). Methods. We conducted a cohort study on biopsy-proven CHC patients with moderate or severe liver fibrosis who failed to respond to previous interferon (IFN) therapy or had conditions for which IFN is contradicted. Patients were divided into two groups: subjects in group A (n = 35) underwent weekly phlebotomy (200 g) until they reached a state of mild iron deficiency, followed by monthly maintenance phlebotomy for 44-144 months (median, 107 months), and they were advised to consume a low-iron diet (5-7 mg iron/day); group B (n = 40) comprised CHC patients who declined to receive iron depletion therapy. Results. In group A, during the maintenance phase, serum ALT levels decreased to less than 60 IU/l in all patients and normalized (< 40 IU/l) in 24 patients (69%), whereas in group B no spontaneous decrease in serum ALT occurred. Hepatocarcinogenesis rates in groups A and B were 5.7% and 17.5% at the end of the fifth year, and 8.6% and 39% in the tenth year, respectively. Multivariate analysis revealed that iron depletion therapy significantly lowered the risk of HCC (odds ratio, 0.57) compared with that of untreated patients (P = 0.0337). Conclusions. Long-term iron depletion for CHC patients is a promising modality for lowering the risk of progression to HCC.

DOI PubMed

[Reactivation of hepatitis B virus due to rituximab plus CHOP after preemptive lamivudine administration in a patient with diffuse large B-cell lymphoma].

Kaoru Ono, Satoshi Iyama, Takuya Matsunaga, Tsutomu Sato, Yasushi Sato, Toshinori Okuda, Kohichi Takada, Yutaka Kawano, Tsuyoshi Hayashi, Koji Miyanishi, Tamotsu Sagawa, Masayoshi Kobune, Rishu Takimoto, Junji Kato, Yoshiro Niitsu

Gan to kagaku ryoho. Cancer & chemotherapy ( 9 ) 34 ( 9 ) 1509 - 12 2007.09 [Refereed] [Domestic journal]

A 59-year-old woman received eight cycles of R-CHOP for diffuse large B-cell lymphoma from July, 2004. Pretreatment HBV serological tests were positive, however, the transaminases were within normal limits, and she remained asymptomatic. Lamivudine (LAM) was administered orally from the start of R-CHOP. HBV-DNA levels gradually decreased and were not detected until December, 2004. LAM was administered until 3 months after the end of chemotherapy, with the entire treatment lasting less than 1 year. Two months after the cessation of treatment, she was re-admitted for general malaise. A liver function test revealed severe abnormalities, and HBVDNA levels were increased. Clinically, she was experiencing acute hepatitis due to HBV reactivation. She was then treated with LAM and interferon-beta immediately. Her HBV-DNA levels soon decreased, and liver function improved.

PubMed

【NASH 最新の知見】NASHの成因と病態 NASHにおける鉄代謝異常

高田弘一, 加藤淳二, 河野豊, 新津洋司郎

臨床消化器内科 ( (株)日本メディカルセンター ) 22 ( 11 ) 1467 - 1472 2007.09 [Refereed]

NASH(非アルコール性脂肪性肝炎)の発症・進展には酸化ストレスの関与が示唆されている.この酸化ストレス増加の原因の一つとして,肝への鉄過剰蓄積が関与している可能性が示唆されている.本稿では,最近わかってきたNASHにおける鉄代謝異常に関して概説した.NASHにおいては肝臓に鉄が過剰に蓄積し,血清フェリチン値やトランスフェリン飽和度が上昇していることから,鉄がNASHの病態を修飾していると考えられる.また,肝内鉄過剰の原因として消化管からの鉄吸収が亢進していることが推測された.その機序は,十二指腸粘膜でのDMTI,DcytbおよびHephaestinの発現が上昇していることによると考えられた.NASHに対する除鉄療法(瀉血+低鉄栄養療法)は,血清ALT値およびIV型コラーゲン値を改善させ,かつ組織学的改善も得られ,有効な治療である.(著者抄録)

非アルコール性脂肪性肝炎における鉄代謝異常の分子機構解析

高田弘一, 加藤淳二, 河野豊, 高橋祥, 小船雅義, 瀧本理修, 宮西浩嗣, 新津洋司郎

アルコールと医学生物学 ( (株)響文社 ) 27 160 - 163 2007.09 [Refereed]

非アルコール性脂肪性肝炎(NASH)患者の消化管からの鉄吸収動態を評価するとともに、十二指腸における鉄吸収関連分子および肝由来の鉄代謝調節ホルモンであるHepcidin mRNA発現量を測定し、肝に鉄が蓄積する機序について解析した。肝生検を施行し、組織学的に診断したNASH患者13例を対象とした。鉄代謝の評価指標として血清鉄、%トランスフェリン飽和度、血清フェリチン濃度を測定した。NASH患者は鉄過剰状態にあると考えられた。NASH患者ではクエン酸第一鉄100mgを経口摂取後、健常人に比較して有意に上昇した。鉄吸収試験の結果から、NASH患者では消化管からの鉄吸収が亢進していることが明らかとなった。コントロール群に比較してNASH患者ではHepcidin mRNA発現量が有意に上昇した。

[A case of resection of synchronous multiple liver metastases from colorectal cancer after hepatic infusion chemotherapy and systemic chemotherapy].

Tamotsu Sagawa, Yasushi Sato, Tetsuji Takayama, Masahiro Hirakawa, Seiichiro Abe, Satoshi Iyama, Koji Miyanishi, Yutaka Kawano, Kohichi Takada, Tokiko Nakamura, Junji Kato, Yoshiro Niitsu

Gan to kagaku ryoho. Cancer & chemotherapy ( 9 ) 34 ( 9 ) 1481 - 4 2007.09 [Refereed] [Domestic journal]

A 70-year-old man was admitted for tranverse colon cancer with multiple liver metastases. Hepatic arterial infusion chemotherapy and systemic chemotherapy (FOLFOX 4) were conducted postoperatively. Thirteen months after the first surgery, liver metastases became resectable and hepatectomy was performed. Though multiple liver metastases were unresectable at the time of the first examination, hepatectomy was possible followed by hepatic arterial infusion chemotherapy and systemic chemotherapy.

PubMed

当科におけるPSE施行症例の検討

高橋祥, 宮西浩嗣, 河野豊, 高田弘一, 庵原秀之, 石渡裕俊, 林毅, 加藤淳二, 新津洋司郎

日本消化器病学会雑誌 ( (一財)日本消化器病学会 ) 104 ( 臨増大会 ) A689 - A689 2007.09 [Refereed]

肝動注療法および全身化学療法にて切除可能となった大腸癌肝転移の1例

佐川保, 佐藤康史, 高山哲治, 平川昌宏, 阿部清一郎, 井山諭, 宮西浩嗣, 河野豊, 高田弘一, 中村とき子, 加藤淳二, 新津洋司郎

癌と化学療法 ( (株)癌と化学療法社 ) 34 ( 9 ) 1481 - 1484 2007.09 [Refereed]

症例は70歳、男性。横行結腸癌、多発性肝転移と診断した。原発巣による狭窄症状があったことより、横行結腸切除術を施行。肝転移に対しては肝動注、全身化学療法FOLFOX4を施行した。肝転移は縮小し単発となったので13ヵ月後に手術可能となり、肝切除術を施行した。肝動注、全身化学療法により切除可能となった横行結腸癌、多発性肝転移症例を経験したので報告する。(著者抄録)

[A case of intraductal papillary mucinous neoplasm with internal pancreatic fistula causing left ureteral obstruction].

Sho Takahashi, Hisato Homma, Takehide Akiyama, Shinichi Mesawa, Kenichiro Hirata, Katsuhisa Kogawa, Kunihiro Takanashi, Hirotoshi Ishiwatari, Yutaka Kawano, Tsuyoshi Hayashi, Kohichi Takada, Koji Miyanishi, Junji Kato, Yoshiro Niitsu

Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology ( 8 ) 104 ( 8 ) 1236 - 44 2007.08 [Refereed] [Domestic journal]

A 75-year-old man had been admitted to another hospital because of left abdominal pain, and was given a diagnosis of left hydronephrosis and acute pancreatitis. After a JJ stent insertion and medication, he was transferred to our hospital for further examinations. US and EUS revealed a chronic pancreatitis-like pattern and multicystic lesion in the pancreas head and body. At that time enhanced CT findings showed an extrapancreatic low density area to be inflammatory change, extending from the pancreas body to the left crus of the diaphragm and posteriorly the spreading from the left crus of the diaphragm via the left urinary duct into the left iliopsoas muscle, in which MRI revealed partial high intensity. ERCP and MRCP showed focal irregular narrowing of the pancreatic duct of unknown cause, and we decided that an internal pancreatic fistula due to pancreatitis had induced left ureteral obstruction, caused by a protein plug or alcohol. Follow-up 6 months later showed that extrapancreatic spreading of the low density area had markedly regressed without any change in the ureteral obstruction.

DOI PubMed

Wnt3/RhoA/ROCK signaling pathway is involved in adhesion-mediated drug resistance of multiple myeloma in an autocrine mechanism

Masayoshi Kobune, Hiroki Chiba, Junji Kato, Kazunori Kato, Kiminori Nakamura, Yutaka Kawano, Kohichi Takada, Rishu Takimoto, Tetsuji Takayama, Hirofumi Hamada, Yoshiro Niitsu

MOLECULAR CANCER THERAPEUTICS ( AMER ASSOC CANCER RESEARCH ) 6 ( 6 ) 1774 - 1784 2007.06 [Refereed]

Adhesion of myeloma cells to bone marrow stromal cells is now considered to play a critical role in chemoresistance. However, little is known about the molecular mechanism governing cell adhesion-mediated drug resistance (CAM-DR) of myeloma cells. In this study, we focused our interests on the implication of the Wnt signal in CAM-DR. We first screened the expression of Wnt family in myeloma cell lines and found that Wnt3 was overexpressed in all the myeloma cells examined. KMS-5 and ARH77, which highly expressed Wnt3 protein, tightly adhered to human bone marrow stromal cells, and accumulation of (3-catenin and GTP-bounded RhoA was observed in these myeloma cell lines. Conversely, RPM18226 and MM1S, which modestly expressed Wnt3 protein, rather weakly adhered to human bone marrow stromal. We then examined the relevance of Wnt3 expression to adhesive property to stromal cells and to CAM-DR of myeloma cells. KMS-5 and ARH-77 exhibited apparent CAM-DR against doxorubicin. This CAM-DR was significantly reduced by anti-integrin (it antibody, antiintegrin as antibody and a Wnt-receptor competitor, secreted Frizzled-related protein-1, and Rho kinase inhibitor Y27632, but not by the specific inhibitor of canonical signaling (Dickkopf-1), indicating that Wnt-mediated CAMDR that is dependent on integrin alpha(6)/beta(1) (VLA-6)-mediated attachment to stromal cells is induced by the Wnt/RhoA/Rho kinase pathway signal. This CAM-DR was also significantly reduced by Wnt3 small interfering RNA transfer to KMS-5. These results indicate that Wnt3 contributes to VLA-6-mediated CAM-DR via the Wnt/RhoA/ROCK pathway of myeloma cells in an autocrine manner. Thus, the Wnt3 signaling pathway could be a promising molecular target to overcome CAM-DR of myeloma cells.

DOI PubMed

Iron/IRP-1-dependent regulation of mRNA expression for transferrin receptor, DMT1 and ferritin during human erythroid differentiation

Junji Kato, Masayoshi Kobune, Shunichi Ohkubo, Koshi Fujikawa, Maki Tanaka, Rishu Takimoto, Kohichi Takada, Daisuke Takahari, Yutaka Kawano, Yutaka Kohgo, Yoshiro Niitsu

EXPERIMENTAL HEMATOLOGY ( ELSEVIER SCIENCE INC ) 35 ( 6 ) 879 - 887 2007.06 [Refereed]

Objective. We investigated iron regulatory protein (IRP)-dependent expression of transferrin receptor (TfR), divalent metal transpoter-1 (DMT1) and ferritin during erythroid differentiation system using an in vitro three-phase liquid culture. Method. Peripheral blood hematopoietic progenitor cells were cultured with interleukin-3 and stem cell factor (SCF) for 7 days (first phase), subsequently with SCF, erythropoietin (EPO) and insulin-like growth factor-I (IGF-I) for 5 days (second phase), and finally with EPO and IGF-I for 3 days (third phase). Cells were subjected to colony assay, flow-cytometric analysis, mRNA assessment, electrophoretic mobility shift assay (EMSA), immunoblotting, and immunoprecipitation. Results. In the second/third phases, erythroid cells serially differentiated. Expression of TfR and DMT1 mRNA, which have iron-responsive elements (IREs) at 3'-UTR, reached a maximum on second phase, and thereafter decreased, while expression of ferritin mRNA, which has an IRE at the 5'-UTR, decreased reciprocally on second phase. IRP in the cytosol after precipitation of polysome decreased on second phase, suggesting that IRP bound to IREs of these mRNAs in the polysome. When cells were incubated with (FeCl3)-Fe-59, Fe-59-bound IRP-1 immunoprecipitated with anti-IRP-1 antibodies was detected on first phase and third phase, but was not detected on second phase. Conclusion. These results suggest that IRP-1/IRE interactions, which are supposedly induced after sensing a decrease of the intracellular non-Heme iron levels, play a crucial role on the posttranscriptional regulation of TfR, DMT1, and ferritin mRNAs during differentiation of normal human erythropoietic cells. (c) 2007 International Society for Experimental Hematology. Published by Elsevier Inc.

DOI PubMed

C型慢性肝炎および非アルコール性脂肪性肝炎における鉄吸収関連分子の解析

高田弘一, 加藤淳二, 河野豊, 高橋祥, 小船雅義, 瀧本理修, 宮西浩嗣, 新津洋司郎

肝臓 ( (一社)日本肝臓学会 ) 48 ( Suppl.1 ) A31 - A31 2007.04 [Refereed]

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Papers - TAKADA Kouichi