Tokushima University / Educator and Researcher Directory --- Kawaguchi, Tomoyuki

Field of Study

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Academic Paper (Judged Full Paper):

1.	Masahiro Sogabe, Toshiya Okahisa, Miwako Kagawa, Takanori Kashihara, shota Fujimoto, Tomoyuki Kawaguchi, reiko yokoyama, Kaizo Kagemoto, Hironori Tanaka, Yoshifumi Kida, Tetsu Tomonari, Yutaka Kawano, Yasushi Sato, Masahiko Nakasono and Tetsuji Takayama : Impact of alcohol consumption on metabolic dysfunction-associated fatty liver disease development and remission: A longitudinal cohort study., Eur J Clin Invest, Vol.Online ahead of print., 2024. (Link to Publication Site) ● Publication site (DOI): 10.1111/eci.14221. (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38634705 ● Search Scopus @ Elsevier (PMID): 38634705 ● Search Scopus @ Elsevier (DOI): 10.1111/eci.14221. (DOI: 10.1111/eci.14221., PubMed: 38634705)
2.	Ryo Shinomiya, Yasushi Sato, Takanori Yoshimoto, Tomoyuki Kawaguchi, Akihiro Hirao, Koichi Okamoto, Yutaka Kawano, Masahiro Sogabe, Hiroshi Miyamoto and Tetsuji Takayama : A case of treatmentresistant advanced gastric cancer with FGFR2gene alteration successfully treated with pemigatinib., International Cancer Conference Journal, Vol.in press, 2024. (Link to Publication Site) ● Publication site (DOI): 10.1007/s13691-024-00669-3 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1007/s13691-024-00669-3 (DOI: 10.1007/s13691-024-00669-3)
3.	Koichi Okamoto, Tomoyuki Kawaguchi, Kaizo Kagemoto, Yoshifumi Kida, Yasuhiro Mitsui, Yasushi Sato and Tetsuji Takayama : "Tip-in underwater endoscopic mucosal resection" without submucosal injection for superficial nonampullary duodenal adenomas., Endoscopy, Vol.55, No.S1, E965-E966, 2023. (Keyword) Humans / Endoscopic Mucosal Resection / Duodenal Neoplasms / Duodenum / Injections (Tokushima University Institutional Repository) ● Metadata: 118931 (Link to Publication Site) ● Publication site (DOI): 10.1055/a-2134-9080 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37604451 ● Summary page in Scopus @ Elsevier: 2-s2.0-85168452995 (Tokushima University Institutional Repository: 118931, DOI: 10.1055/a-2134-9080, PubMed: 37604451, Elsevier: Scopus)
4.	Yasushi Sato, Koichi Okamoto, Yutaka Kawano, Akinari kasai, Tomoyuki Kawaguchi, Tamotsu Sagawa, Masahiro Sogabe, Hiroshi Miyamoto and Tetsuji Takayama : Novel Biomarkers of Gastric Cancer: Current Research and Future Perspectives., Journal of Clinical Medicine, Vol.12, 4646, 2023. (Link to Publication Site) ● Publication site (DOI): 10.3390/jcm12144646 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85166316472 (DOI: 10.3390/jcm12144646, Elsevier: Scopus)
5.	Yoshifumi Kida, Toshiya Okahisa, Yasushi Sato, Masahiro Bando, Shota Fujimoto, ma beibei, Tadahiko Nakagawa, Tomoyuki Kawaguchi, Fumika Nakamura, Koichi Okamoto, Hiroshi Miyamoto, Masahiro Sogabe, Koichi Tsuneyama and Tetsuji Takayama : Urokinase-type plasminogen activator blockade ameliorates experimental colitis in mice., Scientific Reports, Vol.13, No.1, 2899, 2023. (Summary) Although several angiogenesis-related factors are reportedly involved in the pathogenesis of ulcerative colitis (UC), the mechanisms by which they contribute to disease are unclear. We first examined the expression of angiogenesis-related factors in inflamed colorectal tissue of UC patients using antibody array, and identified the 5 factors with highest expression, which included matrix metalloproteinase-8, urokinase-type plasminogen activator (uPA), angiostatin/plasminogen, hepatocyte growth factor and endoglin. Subsequent real-time PCR experiments using additional colorectal tissues revealed that uPA mRNA levels were significantly higher in inflamed tissues than in non-inflamed tissues, and significantly correlated with the severity of UC. Mirror section immunohistochemistry revealed that uPA was expressed in the neutrophils of inflamed colorectal tissues. We administered dextran sulfate sodium (DSS) in drinking water to uPA knockout (uPA) mice, and found that the disease activity index in uPA mice was marginally lower and the histological score in uPA mice was significantly lower than those in wild-type mice, suggesting the importance of uPA in colitis. When an uPA-selective inhibitor, UK122, was administered to DSS-treated C57BL6J mice, the disease activity index and histological score in those mice were significantly lower compared with control mice. Multiple cytokine/chemokine assay using colorectal tissues from uPA and UK122-treated mice revealed significantly lowered level of RANTES. In conclusion, uPA was highly expressed in neutrophils of the inflamed mucosa of UC patients, and the expression level correlated with the severity of UC. Genetic uPA deletion or pharmacological uPA blockade significantly ameliorated colitis in mice, concomitant with downregulation of RANTES. (Keyword) Animals / Mice / Urokinase-Type Plasminogen Activator / Colitis / Colitis, Ulcerative / Serine Proteases / Colorectal Neoplasms (Tokushima University Institutional Repository) ● Metadata: 118522 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-023-29824-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36806262 ● Search Scopus @ Elsevier (PMID): 36806262 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-023-29824-1 (Tokushima University Institutional Repository: 118522, DOI: 10.1038/s41598-023-29824-1, PubMed: 36806262)
6.	Yasushi Sato, Yasuyuki Okada, Yasuteru Fujino, Tomoyuki Kawaguchi, Yoshifumi Kida, Yasuhiro Mitsui, Hironori Tanaka, Tetsu Tomonari, Shinji Kitamura, Koichi Okamoto, Yutaka Kawano, Hiroshi Miyamoto, Masahiro Sogabe and Tetsuji Takayama : Clinical Outcomes of Comprehensive Genomic Profiling Tests for Gastrointestinal Cancers: Experience from Tokushima University Hospital., The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 154-159, 2023. (Summary) In Japan, cancer genome profiling (CGP) for cancer patients without standard treatment has been covered by public insurance since June 2019. This study analyzed data of 122 patients with gastrointestinal tumors who underwent CGP to clarify cancer genome medicine's current status and possible problems at the Tokushima University Hospital. The major types of cancer included pancreatic (n=30), colorectal (n=25), biliary tract (n=15), gastric (n=11), and hepatocellular carcinoma (n=8). CGP tests included F1CDx in 70 patients (57%), F1LCDx in 36 (30%), TSO500 in 14 (11%), and NCC Oncopanel in 2 (2%). Actionable gene alterations were identified in 72 patients (59%), but only 5 patients (4%) were treated for pancreatic (n=1), colorectal (n=3), and small bowel cancers (n=1). The main reasons for not receiving genotype-matched therapy included the lack of appropriate drugs or clinical trials that matched the actionable gene alterations (n=40) and the inability to participate in clinical trials (n=10). There is still not a sufficient number of patients receiving genotype-matched treatment for gastrointestinal cancers. To promote cancer genome medicine in regional areas, attempts to improve access to genotype-matched therapies are required, as well as to promote the development of new molecular-targeted drugs and clinical trials for these drugs. J. Med. Invest. 70 : 154-159, February, 2023. (Keyword) Humans / Gastrointestinal Neoplasms / Neoplasms / Colorectal Neoplasms / Genomics / Hospitals / Japan (Tokushima University Institutional Repository) ● Metadata: 118346 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.70.154 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164713 ● Search Scopus @ Elsevier (PMID): 37164713 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.154 (Tokushima University Institutional Repository: 118346, DOI: 10.2152/jmi.70.154, PubMed: 37164713)
7.	Megumi Yamasaki, Yasushi Sato, Koichi Okamoto, Akira Fukuya, Tomoyuki Kawaguchi, Kazuyoshi Noda, Kaizo Kagemoto, Yasuhiro Mitsui, Hiroshi Miyamoto and Tetsuji Takayama : Two cases of anal squamous cell carcinoma achieving complete response after docetaxel + cisplatin + S1 (DCS) induction chemotherapy followed by chemoradiation., Clinical Journal of Gastroenterology, Vol.16, No.2, 180-186, 2022. (Summary) Anal squamous cell carcinoma (ASCC) is an uncommon tumor. However, its incidence is increasing worldwide. Surgical resection of locally advanced cases requires permanent anal prosthesis. Thus, chemoradiotherapy (CRT) is preferred as the first-line treatment; however, high local recurrence rate remains an issue. Here, we describe two cases of locally advanced ASCC treated with docetaxel + cisplatin + S-1 (DCS) followed by CRT with S-1 that showed complete response. The two patients, aged 69 and 65 years, were diagnosed with ASCC (cStage IIIB) at our hospital. Due to extensive lymph node metastases, the patients were treated with triple induction chemotherapy (DCS) followed by CRT with S-1. Positron emission tomography/computed tomography performed six months after starting the treatment showed disappearance of tumors, indicating a complete response. The patients continued to receive S-1 for one year and achieved relapse-free long-term survival since the completion of treatment. Therefore, induction chemotherapy with DCS, prior to CRT with S-1 may benefit patients with locally advanced ASCC. (Link to Publication Site) ● Publication site (DOI): 10.1007/s12328-022-01736-z (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36409453 ● Search Scopus @ Elsevier (PMID): 36409453 ● Search Scopus @ Elsevier (DOI): 10.1007/s12328-022-01736-z (DOI: 10.1007/s12328-022-01736-z, PubMed: 36409453)
8.	Masahiro Sogabe, Toshiya Okahisa, Takeshi Kurihara, Miwako Kagawa, Hiroyuki Ueda, Tomoyuki Kawaguchi, Akira Fukuya, Kaizoh Kagemoto, Hironori Tanaka, Yoshifumi Kida, Tetsu Tomonari, Tatsuya Taniguchi, Koichi Okamoto, Hiroshi Miyamoto, Yasushi Sato, Masahiko Nakasono and Tetsuji Takayama : Comparison of the role of alcohol consumption and qualitative abdominal fat on NAFLD and MAFLD in males and females., Scientific Reports, Vol.12, No.1, 16048, 2022. (Summary) The clinical difference between nonalcoholic fatty liver disease (NAFLD) and metabolic-associated fatty liver disease (MAFLD) between the two sexes is unclear. This study aimed to determine the influences of alcohol consumption and qualitative abdominal fat between male and female patients with NAFLD and MAFLD. This cross-sectional study examined 11,766 participants who underwent health check-ups comparing lifestyle habits, biochemical features, and noninvasive liver fibrosis scores, between non-MAFLD and MAFLD groups. Furthermore, differences in alcohol consumption and qualitative abdominal fat were examined between male and female patients with NAFLD and MAFLD. The prevalence of metabolic dysregulation, ratio of visceral fat area to subcutaneous fat area, and noninvasive liver fibrosis scores were significantly higher in male patients with MAFLD than in those with NAFLD (p < 0.05), but these were not significantly different in female patients. Among male patients with an alcohol consumption of > 70 g/week, several noninvasive liver fibrosis scores were significantly higher in the MAFLD group than in the NAFLD group (all p < 0.05). The influences of alcohol consumption and qualitative abdominal fat on NAFLD and MAFLD were different between sexes. The development of liver fibrosis should be considered in male patients with MAFLD who exceed mild drinking. (Keyword) Alcohol Drinking / Cross-Sectional Studies / Female / Humans / Intra-Abdominal Fat / Liver Cirrhosis / Male / Non-alcoholic Fatty Liver Disease (Tokushima University Institutional Repository) ● Metadata: 117853 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-022-20124-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36163355 ● Search Scopus @ Elsevier (PMID): 36163355 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-022-20124-8 (Tokushima University Institutional Repository: 117853, DOI: 10.1038/s41598-022-20124-8, PubMed: 36163355)
9.	Hironori Wada, Yasushi Sato, Shota Fujimoto, Koichi Okamoto, Masahiro Bando, Tomoyuki Kawaguchi, Hiroshi Miyamoto, Naoki Muguruma, Katsuhisa Horimoto, Yui Matsuzawa, Michihiro Mutoh and Tetsuji Takayama : Resveratrol inhibits development of colorectal adenoma via suppression of LEF1; comprehensive analysis with connectivity map., Cancer Science, Vol.113, No.12, 4374-4384, 2022. (Summary) Although many chemopreventive studies on colorectal tumors have been reported, no effective and safe preventive agent is currently available. We searched for candidate preventive compounds against colorectal tumor comprehensively from United States Food and Drug Administration (FDA)-approved compounds by using connectivity map (CMAP) analysis coupled with in vitro screening with colorectal adenoma (CRA) patient-derived organoids (PDOs). We generated CRA-specific gene signatures based on the DNA microarray analysis of CRA and normal epithelial specimens, applied them to CMAP analysis with 1309 FDA-approved compounds, and identified 121 candidate compounds that should cancel the gene signatures. We narrowed them down to 15 compounds, and evaluated their inhibitory effects on the growth of CRA-PDOs in vitro. We finally identified resveratrol, one of the polyphenolic phytochemicals, as a compound showing the strongest inhibitory effect on the growth of CRA-PDOs compared with normal epithelial PDOs. When resveratrol was administered to Apc mice at 15 or 30 mg/kg, the number of polyps (adenomas) was significantly reduced in both groups compared with control mice. Similarly, the number of polyps (adenomas) was significantly reduced in azoxymethane-injected rats treated with 10 or 100 mg/resveratrol compared with control rats. Microarray analysis of adenomas from resveratrol-treated rats revealed the highest change (downregulation) in expression of LEF1, a key molecule in the Wnt signaling pathway. Treatment with resveratrol significantly downregulated the Wnt-target gene (MYC) in CRA-PDOs. Our data demonstrated that resveratrol can be the most effective compound for chemoprevention of colorectal tumors, the efficacy of which is mediated through suppression of LEF1 expression in the Wnt signaling pathway. (Keyword) Mice / Rats / Animals / Resveratrol / Adenoma / Colorectal Neoplasms / Wnt Signaling Pathway / Chemoprevention / Lymphoid Enhancer-Binding Factor 1 (Tokushima University Institutional Repository) ● Metadata: 117988 (Link to Publication Site) ● Publication site (DOI): 10.1111/cas.15576 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36082704 ● Search Scopus @ Elsevier (PMID): 36082704 ● Search Scopus @ Elsevier (DOI): 10.1111/cas.15576 (Tokushima University Institutional Repository: 117988, DOI: 10.1111/cas.15576, PubMed: 36082704)
10.	Beibei Ma, Hiroyuki Ueda, Koichi Okamoto, Masahiro Bando, Shota Fujimoto, Yasuyuki Okada, Tomoyuki Kawaguchi, Hironori Wada, Hiroshi Miyamoto, Mitsuo Shimada, Yasushi Sato and Tetsuji Takayama : TIMP1 promotes cell proliferation and invasion capability of right-sided colon cancers via the FAK/Akt signaling pathway., Cancer Science, Vol.113, No.12, 4244-4257, 2022. (Summary) Although right-sided colorectal cancer (CRC) shows a worse prognosis than left-sided CRC, the underlying mechanism remains unclear. We established patient-derived organoids (PDOs) from left- and right-sided CRCs and directly compared cell proliferation and invasion capability between them. We then analyzed the expression of numerous genes in signal transduction pathways to clarify the mechanism of the differential prognosis. Cell proliferation activity and invasion capability in right-sided cancer PDOs were significantly higher than in left-sided cancer PDOs and normal PDOs, as revealed by Cell Titer Glo and transwell assays, respectively. We then used quantitative RT-PCR to compare 184 genes in 30 pathways among right-sided and left-sided cancer and normal PDOs and found that the TIMP1 mRNA level was highest in right-sided PDOs. TIMP1 protein levels were upregulated in right-sided PDOs compared with normal PDOs but was downregulated in left-sided PDOs. TIMP1 knockdown with shRNA significantly decreased cell proliferation activity and invasion capability in right-sided PDOs but not in left-sided PDOs. Moreover, TIMP1 knockdown significantly decreased pFAK and pAkt expression levels in right-sided PDOs but not in left-sided PDOs. A database analysis of The Cancer Genome Atlas revealed that TIMP1 expression in right-sided CRCs was significantly higher than in left-sided CRCs. Kaplan-Meier survival analysis showed significantly shorter overall survival in high-TIMP1 patients versus low-TIMP1 patients with right-sided CRCs but not left-sided CRCs. Our data suggest that TIMP1 is overexpressed in right-sided CRCs and promotes cell proliferation and invasion capability through the TIMP1/FAK/Akt pathway, leading to a poor prognosis. The TIMP1/FAK/Akt pathway can be a target for therapeutic agents in right-sided CRCs. (Keyword) Humans / Prognosis / Signal Transduction / Colorectal Neoplasms / Colonic Neoplasms / Cell Proliferation / Tissue Inhibitor of Metalloproteinase-1 (Tokushima University Institutional Repository) ● Metadata: 117615 (Link to Publication Site) ● Publication site (DOI): 10.1111/cas.15567 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36073574 ● Search Scopus @ Elsevier (PMID): 36073574 ● Search Scopus @ Elsevier (DOI): 10.1111/cas.15567 (Tokushima University Institutional Repository: 117615, DOI: 10.1111/cas.15567, PubMed: 36073574)
11.	Fumika Nakamura, Yasushi Sato, Koichi Okamoto, Yasuteru Fujino, Yasuhiro Mitsui, kaizo kagemoto, Tomoyuki Kawaguchi, Hiroshi Miyamoto, Naoki Muguruma, Tomoko Sonoda, Koichi Tsuneyama and Tetsuji Takayama : Colorectal carcinoma occurring via the adenoma-carcinoma pathway in patients with serrated polyposis syndrome., Journal of Gastroenterology, Vol.57, No.4, 286-299, 2022. (Summary) Although serrated polyposis syndrome (SPS) is associated with an increased colorectal cancer (CRC) risk, the carcinogenic mechanisms remain unknown. We investigated clinicopathological characteristics and genetic abnormalities in colorectal polyps and CRC to elucidate carcinogenic mechanisms in SPS. We retrospectively analyzed clinicopathological features of colorectal polyps in 44 SPS patients, and examined mutations of genes including APC, RAS, BRAF, and TP53, and microsatellite instability (MSI) in CRC tissues. Of the 44 patients, 25 (56%) fulfilled WHO criterion 1, 11 (25%) fulfilled criterion 2, and 8 (18%) fulfilled both. A total of 956 polyps were observed; 642 (67%) hyperplastic polyps (HP), 204 (21%) sessile serrated lesions (SSL), 10 (1%) traditional serrated adenoma (TSA), and 100 (11%) adenomas. The median numbers of polyps (/patient) were 10.5 (IQR 2.75-23) HPs, 4.0 (2.0-6.0) SSLs, 0 (0-0) TSA, and 1 (0-3.3) adenoma. SSL and HP located preferentially in the proximal and distal colon, respectively. Twenty-two CRCs were found in 18 patients. Based on the histological coexistence of SSL/TSA, BRAF mutation and MSI, 5 CRCs (26%) were classified as serrated-neoplasia pathway. Conversely, based on the coexistence of adenoma, APC/RAS and TP53 mutations, 11 CRCs (58%) were classified as adenoma-carcinoma pathway. The remaining three were unclassifiable. Most CRCs through adenoma-carcinoma pathway were located in the left-side colorectum and patients bearing those met criterion 2, characterized by many HP and advanced adenomas. Adenoma was a significant risk factor for CRC. Our results suggest that more than half of the CRCs, particularly those in the left-side colorectum, developed through the adenoma-carcinoma pathway in SPS patients. Adenoma was a risk factor for CRCs, suggesting its importance in colorectal carcinogenesis. (Keyword) Adenoma / Carcinoma / Colonic Polyps / Colorectal Neoplasms / Humans / Intestinal Polyposis / Microsatellite Instability / Mutation / Proto-Oncogene Proteins B-raf / Retrospective Studies (Tokushima University Institutional Repository) ● Metadata: 117614 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00535-022-01858-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35194694 ● Search Scopus @ Elsevier (PMID): 35194694 ● Search Scopus @ Elsevier (DOI): 10.1007/s00535-022-01858-8 (Tokushima University Institutional Repository: 117614, DOI: 10.1007/s00535-022-01858-8, PubMed: 35194694)
12.	Noriaki Murayama, Koichi Okamoto, Tadahiko Nakagawa, Jinsei Miyoshi, Kensei Nishida, Tomoyuki Kawaguchi, kaizo kagemoto, Shinji Kitamura, Beibei Ma, Hiroshi Miyamoto, Naoki Muguruma, Mitsuyasu Yano, Koichi Tsuneyama, Takahiro Fujimori, Yasushi Sato and Tetsuji Takayama : miR-144-3p/miR-451a promotes lymphovascular invasion through repression of PTEN/p19 in rectal neuroendocrine tumors., Journal of Gastroenterology and Hepatology, Vol.37, No.5, 919-927, 2022. (Summary) Although rectal neuroendocrine tumor (NET-G1) have potential metastatic capability, even among small tumors, no predictive biomarker for invasion and metastasis has been reported. We analyzed microRNA (miRNA) expression profiles in rectal NET-G1 tissues with and without lymphovascular invasion (LVI). Moreover, we then investigated their target genes to clarify the mechanism of invasion/metastasis in NET-G1. miRNA array analysis was performed using seven rectal NET-G1 tissues with LVI and seven without LVI. miRNA expression was confirmed by quantitative real-time PCR. A NET cell line H727 was transfected with miRNA mimic or target gene small interfering RNA, and migration and invasion assays were performed. The expression levels of miR-144-3p and miR-451a were significantly higher in NET-G1 with LVI versus without LVI, as determined by miRNA array analysis and RT-qPCR. A significant correlation was observed between miR-144-3p and miR-451a expression levels, strongly suggesting miR144/451 cluster overexpression in NET-G1 with LVI. Bioinformatic analysis of target genes revealed that miR-144-3p and miR-451a directly interact with PTEN and p19 mRNA, respectively. Immunohistochemistry revealed significantly lower expression of PTEN and p19 in NET-G1 tissues with LVI than in those without LVI. The miR-144-3p and miR-451a mimic significantly increased cell migration/invasion capability, respectively. Knockdown of PTEN and p19 induced significant augmentation of cell invasion and migration capability, respectively. Our data suggest that overexpression of miR-144/miR-451 cluster promotes LVI via repression of PTEN and p19 in rectal NET-G1 cells. miR-144/451 cluster may be a novel biomarker for predicting invasion/metastasis in rectal NET-G1. (Keyword) Biomarkers / Cell Line, Tumor / Cell Movement / Cell Proliferation / Gene Expression Regulation, Neoplastic / Humans / MicroRNAs / Neuroendocrine Tumors / PTEN Phosphohydrolase / Rectal Neoplasms (Tokushima University Institutional Repository) ● Metadata: 117699 (Link to Publication Site) ● Publication site (DOI): 10.1111/jgh.15833 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35332577 ● Search Scopus @ Elsevier (PMID): 35332577 ● Search Scopus @ Elsevier (DOI): 10.1111/jgh.15833 (Tokushima University Institutional Repository: 117699, DOI: 10.1111/jgh.15833, PubMed: 35332577)
13.	Akihiro Hirao, Yasushi Sato, Hironori Tanaka, Kensei Nishida, Tetsu Tomonari, Misato Hirata, Masahiro Bando, Yoshifumi Kida, Takahiro Tanaka, Tomoyuki Kawaguchi, Hironori Wada, Tatsuya Taniguchi, Koichi Okamoto, Hiroshi Miyamoto, Naoki Muguruma, Toshihito Tanahashi and Tetsuji Takayama : MiR-125b-5p is Involved in Sorafenib Resistance through Ataxin-1-Mediated Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma., Cancers, Vol.13, No.19, 4917, 2021. (Summary) The mechanism of resistance to sorafenib in hepatocellular carcinoma (HCC) remains unclear. We analyzed miRNA expression profiles in sorafenib-resistant HCC cell lines (PLC/PRF5-R1/R2) and parental cell lines (PLC/PRF5) to identify the miRNAs responsible for resistance. Drug sensitivity, migration/invasion capabilities, and epithelial-mesenchymal transition (EMT) properties were analyzed by biochemical methods. The clinical relevance of the target genes to survival in HCC patients were assessed using a public database. Four miRNAs were significantly upregulated in PLC/PRF5-R1/-R2 compared with PLC/PRF5. Among them, miR-125b-5p mimic-transfected PLC/PRF5 cells (PLC/PRF5-miR125b) and showed a significantly higher IC50 for sorafenib compared with controls, while the other miRNA mimics did not. PLC/PRF5-miR125b showed lower E-cadherin and higher Snail and vimentin expression-findings similar to those for PLC/PRF5-R2-which suggests the induction of EMT in those cells. PLC/PRF5-miR125b exhibited significantly higher migration and invasion capabilities and induced sorafenib resistance in an in vivo mouse model. Bioinformatic analysis revealed ataxin-1 as a target gene of miR-125b-5p. PLC/PRF5 cells transfected with ataxin-1 siRNA showed a significantly higher IC50, higher migration/invasion capability, higher cancer stem cell population, and an EMT phenotype. Median overall survival in the low-ataxin-1 patient group was significantly shorter than in the high-ataxin-1 group. In conclusion, miR-125b-5p suppressed ataxin-1 and consequently induced Snail-mediated EMT and stemness, leading to a poor prognosis in HCC patients. (Tokushima University Institutional Repository) ● Metadata: 116647 (Link to Publication Site) ● Publication site (DOI): 10.3390/cancers13194917 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34638401 ● Search Scopus @ Elsevier (PMID): 34638401 ● Search Scopus @ Elsevier (DOI): 10.3390/cancers13194917 (Tokushima University Institutional Repository: 116647, DOI: 10.3390/cancers13194917, PubMed: 34638401)
14.	Shinji Kitamura, Naoki Muguruma, Koichi Okamoto, Kaizo Kagemoto, Yoshifumi Kida, Yasuhiro Mitsui, Hiroyuki Ueda, Tomoyuki Kawaguchi, Hiroshi Miyamoto, Yasushi Sato, Rika Aoki, Joji Shunto, Yoshimi Bando and Tetsuji Takayama : Clinicopathological characteristics of early gastric cancer associated with autoimmune gastritis., JGH Open, Vol.5, No.10, 1210-1215, 2021. (Tokushima University Institutional Repository) ● Metadata: 116931 (Link to Publication Site) ● Publication site (DOI): 10.1002/jgh3.12656 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34622010 ● Summary page in Scopus @ Elsevier: 2-s2.0-85114915216 (Tokushima University Institutional Repository: 116931, DOI: 10.1002/jgh3.12656, PubMed: 34622010, Elsevier: Scopus)
15.	Sayo Takahashi, Koichi Okamoto, Toshihito Tanahashi, Shota Fujimoto, Tadahiko Nakagawa, Masahiro Bando, beibei ma, Tomoyuki Kawaguchi, Yasuteru Fujino, Yasuhiro Mitsui, Shinji Kitamura, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma, Yoshimi Bando, Toshiro Sato, Takahiro Fujimori and Tetsuji Takayama : S100P expression via DNA hypomethylation promotes cell growth in the sessile serrated adenoma/polyp-cancer sequence., Digestion, Vol.102, No.5, 789-802, 2021. (Summary) Sessile serrated adenomas/polyps (SSA/Ps) are a putative precursor lesion of colon cancer. Although the relevance of DNA hypermethylation in the SSA/P-cancer sequence is well documented, the role of DNA hypomethylation is unknown. We investigated the biological relevance of DNA hypomethylation in the SSA/P-cancer sequence by using 3-dimensional organoids of SSA/P. We first analyzed hypomethylated genes using datasets from our previous DNA methylation array analysis on 7 SSA/P and 2 cancer in SSA/P specimens. Expression levels of hypomethylated genes in SSA/P specimens were determined by RT-PCR and immunohistochemistry. We established 3-dimensional SSA/P organoids and performed knockdown experiments using a lentiviral shRNA vector. DNA hypomethylation at CpG sites of the gene was quantitated by MassARRAY analysis. The mean number of hypomethylated genes in SSA/P and cancer in SSA/P was 41.6 ± 27.5 and 214 ± 19.8, respectively, showing a stepwise increment in hypomethylation during the SSA/P-cancer sequence. S100P, S100α2, PKP3, and MUC2 were most commonly hypomethylated in SSA/P specimens. The mRNA and protein expression levels of S100P, S100α2, and MUC2 were significantly elevated in SSA/P compared with normal colon tissues, as revealed by RT-PCR and immunohistochemistry, respectively. Among these, mRNA and protein levels were highest for S100P. Knockdown of the S100P gene using a lentiviral shRNA vector in 3-dimensional SSA/P organoids inhibited cell growth by >50% (p < 0.01). The mean diameter of SSA/P organoids with S100P gene knockdown was significantly smaller compared with control organoids. MassARRAY analysis of DNA hypomethylation in the S100P gene revealed significant hypomethylation at specific CpG sites in intron 1, exon 1, and the 5'-flanking promoter region. These results suggest that DNA hypomethylation, including S100P hypomethylation, is supposedly associated with the SSA/P-cancer sequence. S100P overexpression via DNA hypomethylation plays an important role in promoting cell growth in the SSA/P-cancer sequence. (Tokushima University Institutional Repository) ● Metadata: 115966 (Link to Publication Site) ● Publication site (DOI): 10.1159/000512575 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33395688 ● Summary page in Scopus @ Elsevier: 2-s2.0-85099095900 (Tokushima University Institutional Repository: 115966, DOI: 10.1159/000512575, PubMed: 33395688, Elsevier: Scopus)
16.	Tomoyuki Kawaguchi, Koichi Okamoto, Shota Fujimoto, Masahiro Bando, Hironori Wada, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma, Katsuhisa Horiimoito and Tetsuji Takayama : Lansoprazole Inhibits the Development of Sessile Serrated Lesions by Inducing G1 Arrest via Skp2/p27 Signaling Pathway., Journal of Gastroenterology, Vol.59, No.1, 11-23, 2021. (Summary) Although the serrated-neoplasia pathway reportedly accounts for 15-30% of colorectal cancer (CRC), no studies on chemoprevention of sessile serrated lesions (SSLs) have been reported. We searched for effective compounds comprehensively from a large series of compounds by employing Connectivity Map (CMAP) analysis of SSL-specific gene expression profiles coupled with in vitro screening using SSL patient-derived organoids (PDOs), and validated their efficacy using a xenograft mouse model of SSL. We generated SSL-specific gene signatures based on DNA microarray data, and applied them to CMAP analysis with 1309 FDA-approved compounds to select candidate compounds. We evaluated their inhibitory effects on SSL-PDOs using a cell viability assay. SSL-PDOs were orthotopically transplanted into NOG mice for in vivo evaluation. The signal transduction pathway was evaluated by gene expression profile and protein expression analysis. We identified 221 compounds by employing CMAP analysis of SSL-specific signatures, which should cancel the gene signatures, and narrowed them down to 17 compounds. Cell viability assay using SSL-PDOs identified lansoprazole as having the lowest IC50 value (47 µM) among 17 compounds. When SSL-PDO was orthotopically transplanted into murine intestinal tract, the tumor grew gradually. Administration of lansoprazole to mice inhibited the growth of SSL xenograft whereas the tumor in control mice treated with vehicle alone grew gradually over time. The Ki67 index in xenograft lesions from the lansoprazole group was significantly lower compared with the control group. Cell cycle analysis of SSL-PDOs treated with lansoprazole exhibited a significant increase in G1 phase cell population. Microarray and protein analysis revealed that lansoprazole downregulated Skp2 expression and upregulated p27 expression in SSL-PDOs. Our data strongly suggest that lansoprazole is the most effective chemopreventive agent against SSL, and that lansoprazole induces G1 cell cycle arrest by downregulating Skp2 and upregulating p27 in SSL cells. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00535-023-02052-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37989907 ● Search Scopus @ Elsevier (PMID): 37989907 ● Search Scopus @ Elsevier (DOI): 10.1007/s00535-023-02052-0 (DOI: 10.1007/s00535-023-02052-0, PubMed: 37989907)

Review, Commentary:

1.	Yasushi Sato, Koichi Okamoto, Tomoyuki Kawaguchi, Fumika Nakamura, Hiroshi Miyamoto and Tetsuji Takayama : Treatment Response Predictors of Neoadjuvant Therapy for Locally Advanced Gastric Cancer: Current Status and Future Perspectives., Biomedicines, Vol.10, No.7, 1614, Jul. 2022. (Summary) Neoadjuvant chemotherapy (NAC) for locally advanced gastric cancer (LAGC) has been recognized as an effective therapeutic option because it is expected to improve the curative resection rate by reducing the tumor size and preventing recurrence of micrometastases. However, for patients resistant to NAC, not only will operation timing be delayed, but they will also suffer from side effects. Thus, it is crucial to develop a comprehensive strategy and select patients sensitive to NAC. However, the therapeutic effect of NAC is unpredictable due to tumor heterogeneity and a lack of predictive biomarkers for guiding the choice of optimal preoperative treatment in clinical practice. This article summarizes the related research progress on predictive biomarkers of NAC for gastric cancer. Among the many investigated biomarkers, metabolic enzymes for cytotoxic agents, nucleotide excision repair, and microsatellite instability, have shown promising results and should be assessed in prospective clinical trials. Noninvasive liquid biopsy detection, including miRNA and exosome detection, is also a promising strategy. (Tokushima University Institutional Repository) ● Metadata: 117415 (Link to Publication Site) ● Publication site (DOI): 10.3390/biomedicines10071614 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35884916 ● Search Scopus @ Elsevier (PMID): 35884916 ● Search Scopus @ Elsevier (DOI): 10.3390/biomedicines10071614 (Tokushima University Institutional Repository: 117415, DOI: 10.3390/biomedicines10071614, PubMed: 35884916)

Proceeding of International Conference:

1.	Yoshifumi Kida, Toshiya Okahisa, Yasushi Sato, Masahiro Bando, shota fujimoto, Tadahiko Nakagawa, Tomoyuki Kawaguchi, Fumika Nakamura, Koichi Okamoto, Hiroshi Miyamoto, Masahiro Sogabe, Koichi Tsuneyama and Tetsuji Takayama : Thepapeutic strategy of Ulcerative Colitis targeting Urokinase-type Plasminogen Activator., DDW2023, May 2023.
2.	Tomoyuki Kawaguchi, Koichi Okamoto, shota fujimoto, Masahiro Bando, hironori wada, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : Lansoprazole as an effective chemopreventive agent for serrated-neoplasia pathway; A comprehensive analysis using connectivity map., DDW2023, May 2023.
3.	Tetsuji Takayama, Yoshifumi Kida, Toshiya Okahisa, Yasushi Sato, Masahiro Bando, shota Fujimoto, Tomoyuki Kawaguchi, Fumika Nakamura, Koichi Okamoto, Hiroshi Miyamoto, Koichi Tsuneyama and Masahiro Sogabe : The relevance of urokinase-type plasminogen activator in pathogenesis of ulcerative colitis., WCOG2022 (World Congress of Gastroenterology), Dubai, Dec. 2022.
4.	Toshiya Okahisa, Masahiro Sogabe, Ryosuke Ogata, Takatoshi Komatsu, Yoshiaki Ohnishi, Hiroyuki Ueda, Tomoyuki Kawaguchi, Akira Fukuya, Yoshifumi Kida, Tetsu Tomonari, Hiroshi Miyamoto and Tetsuji Takayama : Concentration Ratio Self-regulation Function of Ascites Filtration and Concentration Equipment for Cell-free and Concentrated Ascites Reinfusion Therapy, ASAIO 67th Annual Conference, Chicago, Jun. 2022.
5.	Hiroyuki Ueda, Yasuhiro Mitsui, Makoto Takishita, Mitsuyasu Yano, Masanori Takehara, Akira Fukuya, Tomoyuki Kawaguchi, Kazuyoshi Noda, Shinji Kitamura, Koichi Okamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : Clinicopathologial Analysis of Six Families with Gastric Adenocarcinoma and Proximal Polyposis of the stomach (GAPPS)., DDW2020, May 2020.
6.	Naoki Muguruma, Daisaku Fujimot, Tomoyuki Kawaguchi, Kaizoh Kagemoto, Satoshi Teramae, Yoshifumi Kida, Hironori Wada, Fumika Nakamura, Yasuteru Fujino, Shinji Kitamura, Koichi Okamoto, Hiroshi Miyamoto, Toshihito Tanahashi, Hiroshi Miyamoto, Yasushi Sato and Tetsuji Takayama : Linked Color Imaging Improves Detection Rate of Sessile Serrated Adenoma/Polyp in the Colon: A Prospective Randomized Controlled Trial., UEG Week 2019, Barcelona, Oct. 2019.

Proceeding of Domestic Conference:

1.	Tomoyuki Kawaguchi, Koichi Okamoto, shota fujimoto, Hiroyuki Ueda, Masahiro Sogabe, Yasushi Sato and Tetsuji Takayama : Stage I食道癌に対するESD後追加CRTの治療成績に関する検討., 第20回日本消化管学会総会学術集会, Feb. 2024.
2.	Koichi Okamoto, Motoko Sei, shota fujimoto, ta mitsuhashi, takanori yoshimoto, Tomoyuki Kawaguchi, Kaizo Kagemoto, Yoshifumi Kida, Yasuhiro Mitsui, Fumika Nakamura, Yasushi Sato and Tetsuji Takayama : Serrated polyposis syndromeの右側及び左側大腸病変の臨床病理学的および分子生物学的解析, 第10回消化管ポリポーシス研究会, Jan. 2024.
3.	Reiko Yokoyama, Yasushi Sato, Fumika Nakamura, Tomoyuki Kawaguchi, Kaizo Kagemoto, Yoshifumi Kida, Yasuhiro Mitsui, Yasuteru Fujino, Koichi Okamoto, Yutaka Kawano, Hiroshi Miyamoto and Tetsuji Takayama : 直腸悪性黒色腫に対する免疫チェックポイント阻害剤の効果予測因子としての irAE の意義., 第 61 回日本癌治療学会学術集会, Oct. 2023.
4.	Tomoyuki Kawaguchi, Koichi Okamoto, shota fujimoto, Hiroyuki Ueda, hironori wada, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : Connectivity Mapによる大腸癌予防薬の網羅的解析とSessile serrated lesionのオルガノイドを用いた抑制効果の検討., がん予防学術大会2023金沢, Sep. 2023.
5.	Sayaka Ogimoto, Koichi Okamoto, Akira Takahashi, shota Fujimoto, Takanori Yoshimoto, Takeshi Mitsuhashi, Tomoyuki Kawaguchi, Kaizo Kagemoto, Yoshifumi Kida, Yasuhiro Mitsui, Fumika Nakamura, Yasushi Sato and Tetsuji Takayama : 内視鏡による積極的大腸ポリープ摘除術を施行しているリンチ症候群の一例., 第5回がんゲノム医療時代におけるLynch症候群研究会学術集会, Aug. 2023.
6.	Tomoyuki Kawaguchi, Koichi Okamoto, shota fujimoto, Hiroyuki Ueda, hironori wada, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : 前癌病変Sessile serrated lesionのオルガノイドを用いたLansoprazoleの抑制効果およびその機序の検討., 第40回サイトプロテクション研究会, Mar. 2023.
7.	Tomoyuki Kawaguchi, Koichi Okamoto, Hironori Wada, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : 前癌病変 Sessile serrated lesion のオルガノイドを用いた Lansoprazole の抑制効果およびその機序の検討., 第19回日本消化管学会総会学術集会, Feb. 2023.
8.	Hiroyuki Ueda, Tomoyuki Kawaguchi, Hironori Wada, Fumika Nakamura, Shinji Kitamura, Koichi Okamoto, Yasushi Sato and Tetsuji Takayama : 右側大腸癌における TIMP1 の予後不良因子としての意義:右側及び左側大腸癌を比較して., 第19回日本消化管学会総会学術集会, Feb. 2023.
9.	Koichi Okamoto, Fumika Nakamura, 八木麻衣, 岡田明子, 藤井祥平, Takanori Yoshimoto, 横山怜子, Tomoyuki Kawaguchi, Kaizo Kagemoto, Yoshifumi Kida, Yasuhiro Mitsui, Yasushi Sato and Tetsuji Takayama : Serrated polyposis syndrome に合併した大腸腺腫の臨床病理学的特徴., 第98回大腸癌研究会学術集会, Jan. 2023.
10.	Kaizo Kagemoto, Fumika Nakamura, Koichi Okamoto, Takanori Yoshimoto, Tomoyuki Kawaguchi, 横山怜子, Yoshifumi Kida, Yasuhiro Mitsui, Shinji Kitamura, Hiroshi Miyamoto, Yasushi Sato and Tetsuji Takayama : 鋸歯状ポリポーシス症候群における大腸腫瘍の病理像と発癌機序についての解析., 第60回癌治療学会学術集会, Oct. 2022.
11.	Fumika Nakamura, Koichi Okamoto, kaizo kagemoto, 平田圭市郎, takanori yoshimoto, 横山怜子, Tomoyuki Kawaguchi, Yoshifumi Kida, Yasuhiro Mitsui, Kumiko Tanaka, Shinji Kitamura, Yasushi Sato and Tetsuji Takayama : Serrated polyposis syndromeにおける発癌リスクとその予防., 第29回日本がん予防学会総会, Jul. 2022.
12.	Tomoyuki Kawaguchi, Koichi Okamoto and Tetsuji Takayama : Sessile serrated lesionのオルガノイド培養を用いた大腸癌予防薬の開発∼Connectivity Mapを用いた網羅的な解析∼, 第108回日本消化器病学会総会, Apr. 2022.
13.	Tomoyuki Kawaguchi, Koichi Okamoto, Masahiro Bando, hiroyuki ueda, 和田浩典, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : 前癌病変Sessile serrated lesionのオルガノイドを用いた大腸癌予防薬の開発∼Connectivity Mapを用いた網羅的な分析∼, 第18回日本消化管学会学術集会, Feb. 2022.
14.	Noriaki Murayama, Koichi Okamoto, Jinsei Miyoshi, Tomoyuki Kawaguchi, Shinji Kitamura, beibei ma, Hiroshi Miyamoto, Naoki Muguruma, Yasushi Sato and Tetsuji Takayama : miR-144-3p/miR-451aは，PTEN/p19を介して直腸カルチノイド(NET-G1)の浸潤に関与する., 第59回日本癌治療学会学術集会, Oct. 2021.
15.	Beibei Ma, Hiroyuki Ueda, Naoki Muguruma, Koichi Okamoto, Tomoyuki Kawaguchi, Akira Fukuya, Yoshifumi Kida, Yasuyuki Okada, Tatsuya Taniguchi, Yasushi Sato and Tetsuji Takayama : Activation of EGFR signaling pathway in the left-side colorectal cancerLeft-side vs. right-side cancer organoids., 第80回日本癌学会学術総会, Sep. 2021.
16.	Tomoyuki Kawaguchi, Naoki Muguruma and Tetsuji Takayama : 内視鏡生検組織を用いたSessile serrated lesion(SSL)のオルガノイド培養とSSL動物モデルの樹立., 第101回日本消化器内視鏡学会総会, May 2021.
17.	上田浩之, Yasuhiro Mitsui, 滝下誠, 矢野充保, 福家慧, Tomoyuki Kawaguchi, Yoshifumi Kida, Shinji Kitamura, Koichi Okamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : Clinicopathological analysis of six families with Gastric Adenocarcinoma and Proximal Polyposis of the Stomach(GAPPS)., 第18回日本臨床腫瘍学会学術集会, Feb. 2021.
18.	多田理香, 竹内彩郁薫, 山田青季, 井形直紀, Masaki Oono, Masami Shishibori, Masao Fuketa, Kenji Terada, Yoshifumi Kida, Tomoyuki Kawaguchi, Yasuhiro Mitsui, Tatsunao Sueuchi, Naoki Muguruma, Tetsuji Takayama, Masahiro Sogabe and Toshiya Okahisa : 睡眠中の腸蠕動音の解析に適した腸音図システムの試作開発., 第58回日本人工臓器学会大会, Nov. 2020.
19.	Tomoyuki Kawaguchi, shota Fujimoto, Masahiro Bando, 上田浩之, 和田浩典, Koichi Okamoto, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : Connectivity Map とsessile serrated lesion オルガノイドを用いた網羅的な大腸癌予防薬の検索., がん予防学術大会2020米子, Sep. 2020.
20.	Takanori Kashihara, Yoshihiko Miyamoto, Shota Fujimoto, 和田浩典, Tomoyuki Kawaguchi, Yoshifumi Kida, Fumika Nakamura, Kumiko Tanaka, Shinji Kitamura, Koichi Okamoto, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : 大腸腫瘍に発現するepidermal growth factor receptor in colorectal tumors., 第16回日本消化管学会総会学術集会, Feb. 2020.
21.	Tomoyuki Kawaguchi, Masanori Takehara, Kaizoh Kagemoto, Satoshi Teramae, Fumika Nakamura, Takahiro Tanaka, Shinji Kitamura, Koichi Okamoto, Hiroshi Miyamoto, Yasushi Sato, Naoki Muguruma and Tetsuji Takayama : 胸腺を含む5臓器にわたって10個の同時性多発重複癌を呈したLynch症候群の一例 ., 第57回日本癌治療学会学術集会, Oct. 2019.
22.	Masanori Takehara, Yasushi Sato, Tomoyuki Kawaguchi, Kazuyoshi Noda, Akira Fukuya, Shinji Kitamura, Koichi Okamoto, Hiroshi Miyamoto, Naoki Muguruma and Tetsuji Takayama : 癌関連脂肪細胞は膵癌のSAA1発現を誘導し，転移・浸潤を促進する., 第57回日本癌治療学会学術集会, Oct. 2019.
23.	taro mizutani, ju nishioka, naoki igata, kazuhide iwasa, tetsuya honda, Tomoyuki Kawaguchi, Yasuhiro Mitsui, Jinsei Miyoshi, Tatsunao Sueuchi, Koichi Okamoto, Hiroshi Miyamoto, Naoki Muguruma, Tetsuji Takayama, Masahiro Sogabe and Toshiya Okahisa : 携帯型小型腸音図システムの試作による腸蠕動音測定時間の最適化., 第56回日本人工臓器学会大会, Nov. 2018.

Designated Assistant Professor : Kawaguchi, Tomoyuki

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