Updated on 2025/04/10

Information

 

写真a

 
IMOTO KOJI
 
Organization
Kyushu University Hospital Department of Hepatology and Pancreatology Assistant Professor
Title
Assistant Professor
External link

Research Areas

  • Life Science / Gastroenterology

Research Interests・Research Keywords

  • Research theme: 急性肝不全

    Keyword: 急性肝不全

    Research period: 2024

  • Research theme: 代謝機能障害関連脂肪肝炎

    Keyword: 代謝機能障害関連脂肪肝炎

    Research period: 2024

  • Research theme: フォンタン関連肝疾患

    Keyword: フォンタン関連肝疾患

    Research period: 2024

  • Research theme: 肝臓

    Keyword: 肝臓

    Research period: 2024

  • Research theme: 非アルコール性脂肪肝炎

    Keyword: 非アルコール性脂肪肝炎

    Research period: 2024

Papers

  • Stratifying and predicting progression to acute liver failure during the early phase of acute liver injury

    Raiki Yoshimura, Masatake Tanaka, Miho Kurokawa, Naotoshi Nakamura, Takeshi Goya, Koji Imoto, Motoyuki Kohjima, Katsuhito Fujiu, Shingo Iwami, Yoshihiro Ogawa

    PNAS Nexus   4 ( 2 )   pgaf004   2025.2   eISSN:2752-6542

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    Abstract

    Acute liver failure (ALF) is a serious disease that progresses from acute liver injury (ALI) and that often leads to multiorgan failure and ultimately death. Currently, effective treatment strategies for ALF, aside from transplantation, remain elusive, partly because ALI is highly heterogeneous. Furthermore, clinicians lack a quantitative indicator that they can use to predict which patients hospitalized with ALI will progress to ALF and the need for liver transplantation. In our study, we retrospectively analyzed data from 319 patients admitted to the hospital with ALI. By applying a machine-learning approach and by using the SHapley Additive exPlanations (SHAP) algorithm to analyze time-course blood test data, we identified prothrombin time activity percentage (PT%) as a biomarker reflecting individual ALI status. Unlike previous studies predicting the need for liver transplantation in patients with ALF, our study focused on PT% dynamics. Use of this variable allowed us to stratify the patients with highly heterogeneous ALI into six groups with distinct clinical courses and prognoses, i.e. self-limited, intensive care–responsive, or intensive care–refractory patterns. Notably, these groups were well predicted by clinical data collected at the time of admission. Additionally, utilizing mathematical modeling and machine learning, we assessed the predictability of individual PT% dynamics during the early phase of ALI. Our findings may allow for optimizing medical resource allocation and early introduction of tailored individualized treatment, which may result in improving ALF prognosis.

    DOI: 10.1093/pnasnexus/pgaf004

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  • Microcirculatory disturbance in acute liver injury is triggered by IFNγ-CD40 axis. International journal

    Miho Kurokawa, Takeshi Goya, Motoyuki Kohjima, Masatake Tanaka, Sadahiro Iwabuchi, Shigeyuki Shichino, Satoshi Ueha, Tomonobu Hioki, Tomomi Aoyagi, Motoi Takahashi, Koji Imoto, Shigeki Tashiro, Hideo Suzuki, Masaki Kato, Shinichi Hashimoto, Hideo Matsuda, Kouji Matsushima, Yoshihiro Ogawa

    Journal of inflammation (London, England)   21 ( 1 )   23 - 23   2024.6   ISSN:1476-9255

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Journal of Inflammation (United Kingdom)  

    BACKGROUND: Acute liver failure (ALF) is a life-threatening disorder that progresses from self-limiting acute liver injury (ALI). Microcirculatory disturbance characterized by sinusoidal hypercoagulation and subsequent massive hypoxic hepatocyte damage have been proposed to be the mechanism by which ALI deteriorates to ALF; however, the precise molecular pathway of the sinusoidal hypercoagulation remains unknown. Here, we analyzed ALI patients and mice models to uncover the pathogenesis of ALI with microcirculatory disturbance. METHODS: We conducted a single-center retrospective study for ALI and blood samples and liver tissues were analyzed to evaluate the microcirculatory disturbance in ALI patients (n = 120). Single-cell RNA sequencing analysis (scRNA-seq) was applied to the liver from the concanavalin A (Con A)‑induced mouse model of ALI. Interferon-gamma (IFNγ) and tumor necrosis factor-alpha knockout mice, and primary human liver sinusoidal endothelial cells (LSECs) were used to assess the mechanism of microcirculatory disturbance. RESULTS: The serum IFNγ concentrations were significantly higher in ALI patients with microcirculatory disturbance than in patients without microcirculatory disturbance, and the IFNγ was upregulated in the Con A mouse model which presented microcirculatory disturbance. Hepatic IFNγ expression was increased as early as 1 hour after Con A treatment prior to sinusoidal hypercoagulation and hypoxic liver damage. scRNA-seq revealed that IFNγ was upregulated in innate lymphoid cells and stimulated hepatic vascular endothelial cells at the early stage of liver injury. In IFNγ knockout mice treated with Con A, the sinusoidal hypercoagulation and liver damage were remarkably attenuated, concomitant with the complete inhibition of CD40 and tissue factor (TF) upregulation in vascular endothelial cells. By ligand-receptor analysis, CD40-CD40 ligand interaction was identified in vascular endothelial cells. In human LSECs, IFNγ upregulated CD40 expression and TF was further induced by increased CD40-CD40 ligand interaction. Consistent with these findings, hepatic CD40 expression was significantly elevated in human ALI patients with microcirculatory disturbance. CONCLUSION: We identified the critical role of the IFNγ-CD40 axis as the molecular mechanism of microcirculatory disturbance in ALI. This finding may provide novel insights into the pathogenesis of ALI and potentially contribute to the emergence of new therapeutic strategies for ALI patients.

    DOI: 10.1186/s12950-024-00387-w

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  • Acute kidney injury is an unfavorable prognostic factor in acute liver failure and is associated with tumor necrosis factor-alpha. International journal

    Koji Imoto, Masatake Tanaka, Takeshi Goya, Yuki Azuma, Tomonobu Hioki, Tomomi Aoyagi, Motoi Takahashi, Miho Kurokawa, Masaki Kato, Motoyuki Kohjima, Yoshihiro Ogawa

    Medicine   102 ( 45 )   e35931   2023.11   ISSN:0025-7974 eISSN:1536-5964

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Medicine (United States)  

    Acute kidney injury (AKI) is a common complication of acute liver failure (ALF); but its pathogenesis is unknown. ALF was divided into 2 subgroups; ALF with hepatic coma, which corresponds to ALF in the US and Europe, and ALF without hepatic coma. AKI has been shown to worsen the prognosis of ALF patients with hepatic coma; however, its prognostic significance in ALF without hepatic coma remains unknown. A single-center retrospective study of 174 patients with ALF was performed. AKI was defined according to KDIGO criteria. AKI developed in 29 (66.0%) of 44 ALF patients with hepatic coma and 27 (38.5%) of 130 ALF patients without hepatic coma. Systemic inflammatory response syndrome (SIRS) was found to be significantly associated with AKI incidence in ALF patients (P < .001). Tumor necrosis factor-alpha (TNF-α) was found to be significantly associated with the presence and severity of AKI (P = .0039 and P = .0140, respectively). On multivariate analysis, TNF-α was an independent risk factor linked with AKI (P = .0103). Even in the absence of hepatic coma, the transplant-free survival rate of ALF was significantly associated with the presence and severity of AKI. Even when hepatic coma is absent, AKI complicated in ALF is strongly associated with TNF-α and worsens the transplant-free survival rate. Before the onset of hepatic coma, plasma exchange, or extracorporeal blood purification to remove inflammatory cytokines should be considered in ALF patients.

    DOI: 10.1097/MD.0000000000035931

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  • Clinicopathologic Features of Adult-onset Still's Disease Complicated by Severe Liver Injury.

    Miho Kurokawa, Tomonobu Hioki, Tomomi Aoyagi, Motoi Takahashi, Koji Imoto, Takeshi Goya, Masatake Tanaka, Motoyuki Kohjima, Yoshihiro Ogawa

    Internal medicine (Tokyo, Japan)   2023.6

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    Adult-onset Still's disease (AOSD) is a systemic inflammatory disorder. Severe liver injury has rarely been reported, although liver enzyme elevation is a common complication of AOSD. We herein report four cases of relapsed AOSD with severe liver disorder by tapering or terminating corticosteroids. Liver specimens revealed robust infiltration of inflammatory cells throughout the lobule, especially cluster of differentiation (CD) 8-positive cells. Relapsed AOSD was refractory to corticosteroid reintroduction and required immunosuppressants. Severe liver injury with AOSD is pathologically characterized by extensive lobular infiltration of CD8-positive cells, and we should consider additive immunosuppressive agents on corticosteroids for treatment.

    DOI: 10.2169/internalmedicine.2043-23

  • Transcatheter arterial steroid injection therapy improves the prognosis of patients with acute liver failure. International journal

    Akifumi Kuwano, Tasuku Okui, Motoyuki Kohjima, Miho Kurokawa, Takeshi Goya, Masatake Tanaka, Tomomi Aoyagi, Motoi Takahashi, Koji Imoto, Shigeki Tashiro, Hideo Suzuki, Nobuhiro Fujita, Yasuhiro Ushijima, Kousei Ishigami, Shoji Tokunaga, Masaki Kato, Yoshihiro Ogawa

    Medicine   102 ( 10 )   e33090   2023.3

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    Acute liver failure (ALF) is a disorder defined by coagulopathy and encephalopathy with a poor prognosis. No effective therapies have been established except for liver transplantation. We previously reported a subgroup of patients with acute liver injury who developed microcirculatory disturbance. We also established and reported transcatheter arterial steroid injection therapy (TASIT) as a new treatment of ALF. Here, we analyze the effectiveness of TASIT in a larger cohort and evaluate the impact on ALF patients with or without microcirculatory disturbance. We conducted a single-center retrospective study to evaluate the effectiveness of TASIT in patients with ALF admitted at Kyushu University Hospital between January 2005 and March 2018. TASIT is performed by injecting methylprednisolone via the proper hepatic artery for 3 days. One hundred ninety-4 patients with ALF were enrolled and analyzed in this study. Of the 87 patients given TASIT, 71 (81.6&#37;) recovered without any complications and 16 (18.4&#37;) died or underwent liver transplantation. Of the 107 patients not administered TASIT, 77 (72.0&#37;) recovered and 30 (28.0&#37;) progressed to irreversible liver failure. In the high-lactate dehydrogenase subgroup, 52 (86.7&#37;) of the 60 patients with TASIT recovered, and the survival rate was significantly higher than that in patients who did not receive TASIT. Multivariate regression analysis revealed that the TASIT procedure was one of the significant prognostic factors in the high-lactate dehydrogenase subgroup and was significantly associated with prothrombin activity percentage improvement. TASIT is an effective treatment for patients with ALF, especially in those with microcirculatory disturbance.

    DOI: 10.1097/MD.0000000000033090

  • Elevated Pancreatic Enzymes Associated with Acute Liver Injury Were Mediated by Tumor Necrosis Factor-Alpha Signaling

    Takeshi Goya, Miho Kurokawa, Tomonobu Hioki, Tomomi Aoyagi, Motoi Takahashi, Koji Imoto, Shigeki Tashiro, Hideo Suzuki, Masatake Tanaka, Masaki Kato, Motoyuki Kohjima, Yoshihiro Ogawa

    HEPATITIS MONTHLY   22 ( 1 )   2022.12

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    Background: Acute liver failure (ALF) is caused by massive hepatocyte death and accompanied by severe coagulation disorder and encephalopathy. It often leads to multiple organ failure and subsequently death. However, the association between ALF and other organ failure remains unclear.Objectives: Here, we evaluated patients with acute liver injury (ALI) and elevated pancreatic enzymes to demonstrate the association between ALI and pancreatic disorder.Methods: We conducted a single-center retrospective study to analyze patients with ALI. Between 2012 and 2017, 163 patients with ALI were treated in our hospital. We stratified patients based on whether serum amylase and lipase were elevated above 1.5 times the upper limit of normal. We compared the baseline characteristics, severity, prognosis, and serum cytokine levels between the two groups.Results: Of the 163 patients, 75 (54.0&#37;) presented elevated pancreatic enzymes above 1.5 times the upper limit of normal. Computed tomography imaging findings associated with pancreatitis were observed in 29 patients (17.8&#37;). The elevation of pancreatic enzymes was associated with ALI severity. High level of serum tumor necrosis factor-alpha (TNF-alpha) was associated with the elevation of pancreatic enzymes (elevation group Vs. no elevation group: 134.0 +/- 177.2 pg/mL Vs. 89.4 +/- 159.8 pg/mL).Conclusions: The elevation of pancreatic enzymes was often accompanied by ALI and associated with ALI severity. TNF-alpha signaling was involved in the elevation of pancreatic enzymes. It is possible that the pancreatic disorder reflected ALI severity, consequently correlated with mortality, and did not directly aggravate ALI pathogenesis. These findings provide novel insights into the pathogenesis of ALF.

    DOI: 10.5812/hepatmon-128106

  • The Efficacy of Tofogliflozin on Metabolic Dysfunction-Associated Fatty Liver Disease

    Takeshi Goya, Koji Imoto, Shigeki Tashiro, Tomomi Aoyagi, Motoi Takahashi, Miho Kurokawa, Hideo Suzuki, Masatake Tanaka, Masaki Kato, Motoyuki Kohjima, Yoshihiro Ogawa

    GASTROENTEROLOGY INSIGHTS   13 ( 1 )   20 - 26   2022.3

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    The increasing number of patients with fatty liver disease is a major health problem. Fatty liver disease with metabolic dysfunction has been recognized as nonalcoholic fatty liver disease (NAFLD). Although there is no standard therapy for NAFLD, previous reports support the effect of sodium-glucose cotransporter 2 (SGLT2) inhibitors on NAFLD. Recently, fatty liver disease with metabolic dysfunction was proposed to be defined as a novel concept, "metabolic associated fatty liver disease (MAFLD)", and it was proposed that new criteria for MAFLD diagnosis be established. To clarify the effect of SGLT2 inhibitors on MAFLD, we analyzed the efficacy of tofogliflozin in patients with MAFLD. We conducted a single-center, retrospective study to evaluate the efficacy of tofogliflozin in patients with MAFLD treated at Kyushu University Hospital between 2017 and 2019. Tofogliflozin was used to treat 18 patients with MAFLD. To determine the efficacy of tofogliflozin, we evaluated glucose metabolism, insulin resistance, liver injury, hepatic steatosis, and body composition three and six months after drug initiation. Although our study was a preliminary study because of some limitations (e.g., retrospective, observational, single-arm study, small sample size), we show that tofogliflozin could improve liver injury in patients with MAFLD by improving glucose metabolism and insulin resistance without causing muscle loss.

    DOI: 10.3390/gastroent13010003

  • Corticosteroid suppresses urea-cycle-related gene expressions in ornithine transcarbamylase deficiency. Reviewed International journal

    Koji Imoto, Masatake Tanaka, Takeshi Goya, Tomomi Aoyagi, Motoi Takahashi, Miho Kurokawa, Shigeki Tashiro, Masaki Kato, Motoyuki Kohjima, Yoshihiro Ogawa

    BMC gastroenterology   22 ( 1 )   144 - 144   2022.3

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    BACKGROUND: Ornithine transcarbamylase deficiency (OTCD) is most common among urea cycle disorders (UCDs), defined by defects in enzymes associated with ureagenesis. Corticosteroid administration to UCD patients, including OTCD patients, is suggested to be avoided, as it may induce life-threatening hyperammonemia. The mechanism has been considered nitrogen overload due to the catabolic effect of corticosteroids; however, the pathophysiological process is unclear. METHODS: To elucidate the mechanism of hyperammonemia induced by corticosteroid administration in OTCD patients, we analyzed a mouse model by administering corticosteroids to OTCspf-ash mice deficient in the OTC gene. Dexamethasone (DEX; 20 mg/kg) was administered to the OTCspf-ash and wild-type (WT) mice at 0 and 24 h, and the serum ammonia concentrations, the levels of the hepatic metabolites, and the gene expressions related with ammonia metabolism in the livers and muscles were analyzed. RESULTS: The ammonia levels in Otcspf-ash mice that were administered DEX tended to increase at 24 h and increased significantly at 48 h. The metabolomic analysis showed that the levels of citrulline, arginine, and ornithine did not differ significantly between Otcspf-ash mice that were administered DEX and normal saline; however, the level of aspartate was increased drastically in Otcspf-ash mice owing to DEX administration (P < 0.01). Among the enzymes associated with the urea cycle, mRNA expressions of carbamoyl-phosphate synthase 1, ornithine transcarbamylase, arginosuccinate synthase 1, and arginosuccinate lyase in the livers were significantly downregulated by DEX administration in both the Otcspf-ash and WT mice (P < 0.01). Among the enzymes associated with catabolism, mRNA expression of Muscle RING-finger protein-1 in the muscles was significantly upregulated in the muscles of WT mice by DEX administration (P < 0.05). CONCLUSIONS: We elucidated that corticosteroid administration induced hyperammonemia in Otcspf-ash mice by not only muscle catabolism but also suppressing urea-cycle-related gene expressions. Since the urea cycle intermediate amino acids, such as arginine, might not be effective because of the suppressed expression of urea-cycle-related genes by corticosteroid administration, we should consider an early intervention by renal replacement therapy in cases of UCD patients induced by corticosteroids to avoid brain injuries or fatal outcomes.

    DOI: 10.1186/s12876-022-02213-0

  • The Combination of Nucleotide Analog Therapy and Steroid Pulse Therapy for Acute HBV Infection Effectively Promotes HBV Clearance

    Takeshi Goya, Tomoyuki Kurashige, Miho Kurokawa, Masatake Tanaka, Tomomi Aoyagi, Motoi Takahashi, Koji Imoto, Shigeki Tashiro, Hideo Suzuki, Masaki Kato, Motoyuki Kohjima, Yoshihiro Ogawa

    GASTROENTEROLOGY INSIGHTS   13 ( 1 )   1 - 8   2022.3

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    Acute hepatitis B virus (HBV) infection occasionally progresses to acute liver failure, often with poor prognosis. The appropriate pharmacological approach is yet to be established. Although nucleotide analogs (NA) and corticosteroids are candidates for the treatment of acute HBV infection, their therapeutic effects, especially their effect on HBV clearance, remain unclear. To clarify effects on the HBV clearance of combination therapy of NA and steroid pulse therapy (SPT) for acute HBV infection, we first analyze the effectiveness of this therapy in patients with HBV infection compared with NA monotherapy (NAM). Of the 57 consecutive patients with acute hepatitis B infection from May 2007 to December 2018, we have included 25 patients for this study, whom we followed up until HBV clearance. According to the administration of NA and SPT, we divided patients into two groups (NAM group and NA + SPT group) and compared their results. Of the 25 patients, 10 received NAM, whereas 15 received NA + SPT. There were no appreciable adverse effects related to SPT. The time required for the clearance of HBsAg (76 (43-116) days vs. 26 (14-51) days, p = 0.0418) and HBV-DNA (NAM group vs. NA + SPT group: 180 (83.5-220) vs. 69 (43-136) days, p = 0.0420) was significantly shorter in the NA + SPT group than in the NAM group. The hazard ratio of NA + SPT for the clearance of HBsAg and HBV-DNA were 0.45 (0.19-1.09) and 0.35 (0.14-0.89), respectively. In conclusion, we showed that NA + SPT promoted HBV elimination. These findings support the use of the NA + SPT combination for acute HBV infection without the concern of persistent HBV infection.

    DOI: 10.3390/gastroent13010001

  • Pirfenidone attenuates acetaminophen-induced liver injury via suppressing c-Jun N-terminal kinase phosphorylation. International journal

    Shigeki Tashiro, Masatake Tanaka, Takeshi Goya, Tomomi Aoyagi, Miho Kurokawa, Koji Imoto, Akifumi Kuwano, Motoi Takahashi, Hideo Suzuki, Motoyuki Kohjima, Masaki Kato, Yoshihiro Ogawa

    Toxicology and applied pharmacology   434   115817 - 115817   2022.1

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    Acetaminophen (APAP)-induced liver injury is the most frequent cause of acute liver failure in Western countries. Pirfenidone (PFD), an orally bioavailable pyridone derivative, is clinically used for idiopathic pulmonary fibrosis treatment and has antifibrotic, anti-inflammatory, and antioxidant effects. Here we examined the PFD effect on APAP-induced liver injury. In a murine model, APAP caused serum alanine aminotransferase elevation attenuated by PFD treatment. We performed terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) and vital propidium iodide (PI) stainings simultaneously. APAP induced TUNEL-positive/PI-negative necrosis around the central vein and subsequent TUNEL-negative/PI-positive oncotic necrosis with hemorrhage and caused the upregulation of hypercoagulation- and hypoxia-associated gene expressions. PFD treatment suppressed these findings. Western blotting revealed PFD suppressed APAP-induced c-Jun N-terminal kinase (JNK) phosphorylation despite no effect on JNK phosphatase expressions. In conclusion, simultaneous TUNEL and vital PI staining is useful for discriminating APAP-induced necrosis from typical oncotic necrosis. Our results indicated that PFD attenuated APAP-induced liver injury by suppressing TUNEL-positive necrosis by directly blocking JNK phosphorylation. PFD is promising as a new option to prevent APAP-induced liver injury.

    DOI: 10.1016/j.taap.2021.115817

  • Upregulated expression of hypoxia reactive genes in peripheral blood mononuclear cells from chronic liver disease patients. International journal

    Akifumi Kuwano, Masatake Tanaka, Hideo Suzuki, Miho Kurokawa, Koji Imoto, Shigeki Tashiro, Takeshi Goya, Motoyuki Kohjima, Masaki Kato, Yoshihiro Ogawa

    Biochemistry and biophysics reports   27   101068 - 101068   2021.9

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    Liver fibrosis induces intrahepatic microcirculation disorder and hypoxic stress. Hypoxic stress has the potential for an increase in the possibility of more liver fibrosis and carcinogenesis. Liver biopsy is a standard method that evaluates of intrahepatic hypoxia, however, is invasive and has a risk of bleeding as a complication. Here, we investigated the hypoxia reactive gene expressions in peripheral blood mononuclear cells (PBMC) from chronic liver disease patients to evaluate intrahepatic hypoxia in a non-invasive manner. The subjects enrolled for this study were composed of 20 healthy volunteers (HV) and 48 patients with chronic liver disease (CLD). CLD patients contained 24 patients with chronic hepatitis(CH)and 24 patients with liver cirrhosis (LC). PBMC were isolated from heparinized peripheral blood samples. We measured the transcriptional expression of hypoxia reactive genes and inflammatory cytokines by quantitative RT-PCR. mRNA expression of adrenomedullin (AM), vascular endothelial growth factor A (VEGFA) superoxide dismutase (SOD), glutathione peroxidase (GPx) (p < 0.05), Interleukin-6 (IL-6), transforming growth factor-beta (TGF-β) and heme oxygenase-1 (HO-1) in CLD group were significantly higher than HV. AM mRNA expression is correlated with serum lactate dehydrogenase (LDH), serum albumin (Alb), IL6, and SOD mRNA expression. The hypoxia reactive gene expression in PBMCs from CLD patients was more upregulated than HV. Especially, angiogenic genes were notably upregulated and correlated with liver fibrosis. Here, we suggest that mRNA expression of AM in PBMCs could be the biomarker of intrahepatic hypoxia.

    DOI: 10.1016/j.bbrep.2021.101068

  • Microcirculatory disturbance in acute liver injury. International journal

    Akifumi Kuwano, Miho Kurokawa, Motoyuki Kohjima, Koji Imoto, Shigeki Tashiro, Hideo Suzuki, Masatake Tanaka, Seiji Okada, Masaki Kato, Yoshihiro Ogawa

    Experimental and therapeutic medicine   21 ( 6 )   596 - 596   2021.6

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    Microcirculatory disturbance is thought to be involved in the pathogenesis of acute liver injury (ALI). The current study examined the pathophysiologic role of hepatic microcirculatory disturbance in patients with ALI and in mouse models of ALI. Using serum aminotransferase (ALT)/lactate dehydrogenase (LDH) ratio as a hypoxic marker, 279 patients with ALI were classified into the low ALT/LDH ratio (ALT/LDH ≤1.5) and high ALT/LDH ratio group (ALT/LDH >1.5). In the low ALT/LDH ratio group, serum ALT, LDH, fibrinogen degradation products and prothrombin time-international normalized ratio were increased relative to the high ALT/LDH ratio group. Histologically, hepatic expression of tissue factor (TF) and hypoxia-related proteins was enhanced in the low ALT/LDH ratio group, and this was accompanied by sinusoidal fibrin deposition. Sinusoidal hypercoagulation and intrahepatic hypoxia was also analyzed in two different mouse models of ALI; Concanavalin A (ConA) mice and Galactosamine/tumor necrosis factor (TNF)-α (G/T) mice. Serum ALT/LDH ratio in ConA mice was significantly lower compared with G/T mice. Pimonidazole staining revealed the upregulation of hypoxia-related proteins in ConA mice. Recombinant human soluble thrombomodulin improved liver damage in ConA mice in association with reduced sinusoidal hypercoagulation and intrahepatic hypoxia. The present study provides evidence that serum ALT/LDH ratio aids in the identification of patients with ALI and intrahepatic hypoxia as a result of microcirculatory disturbance. The results facilitate the improved understanding of the pathogenesis of ALI, thereby offering a novel therapeutic strategy against ALI, which arises from sinusoidal hypercoagulation.

    DOI: 10.3892/etm.2021.10028

  • Hypoxic hepatitis with marked elevation of serum ferritin probably due to activation of intrahepatic macrophages: Another form of hypoxic hepatitis hitherto not reported?

    M. Tanaka, T. Goya, H. Suzuki, M. Takahashi, K. Imoto, M. Kurokawa, S. Tashiro, A. Kuwano, S. Okada, M. Kato, Motoyuki Kohjima, K. Kotoh, Y. Ogawa

    Acta Gastro-Enterologica Belgica   84 ( 2 )   317 - 320   2021.4

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    Background and study aims: Hypoxic hepatitis (HH) is an acute liver injury that develops in patients with underlying diseases, such as heart failure, respiratory failure, septic/toxic shock. However, some patients do not have underlying diseases or episodes which are known to result in HH. Here, we analyzed the clinical characteristics of this particular patient group (called ‘unknown HH’ hereafter) to understand its pathogenesis. Patients and methods: Between October 2010 and January 2016, 157 consecutive patients with acute liver injury were admitted to our hospital. Among these patients, 15 patients were categorized as unknown HH. Medical histories and blood test results of unknown HH were analyzed. Results: Among 15 patients of unknown HH, 11 were habitual drinkers and all experienced one of digestive symptoms which might result in mild hypovolemia such as vomiting, diarrhea, appetite loss, and epigastralgia. All patients of unknown HH presented marked elevation of serum ferritin concentration paralleled with aspartate transaminase (AST), alanine transaminase (ALT), and lactate dehydrogenase (LDH) concentrations. The serum levels of ferritin, ALT, LDH, and prothrombin time-international normalized ratio (PT-INR) were rapidly decreased during hospitalization and all 15 patients of unknown HH recovered without any complication. Conclusions: We found the particular group of HH with marked elevation of serum ferritin probably due to intrahepatic macrophage activation. Anti-inflammatory treatments might be effective for this group of hypoxic hepatitis.

    DOI: 10.51821/84.2.317

  • Recombinant human soluble thrombomodulin ameliorates acetaminophen-induced liver toxicity in mice. International journal

    Akifumi Kuwano, Motoyuki Kohjima, Hideo Suzuki, Akihiro Yamasaki, Tomoko Ohashi, Koji Imoto, Miho Kurokawa, Yusuke Morita, Masaki Kato, Yoshihiro Ogawa

    Experimental and therapeutic medicine   18 ( 2 )   1323 - 1330   2019.8

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    Recombinant human soluble thrombomodulin alpha (rhTM) has been developed as an anticoagulant with anti-inflammatory activity. Notably, acetaminophen (APAP) -induced liver disease (AILI) is caused by direct metabolite-induced hepatotoxicity as well as hepatic hyper-coagulation. To evaluate the utility of anticoagulant for the treatment of AILI, rhTM was administered in a mouse AILI model and liver damage was analyzed. AILI was induced in 8-week-old mice by intraperitoneal injection of APAP. rhTM (20 mg/kg) or placebo was injected at the same time as APAP administration. Serum alanine aminotransferase, fibrin degradation products and high-mobility group box 1 levels were significantly decreased in the rhTM-treated group compared with the control group. Furthermore, rhTM reduced the necrotic area and fibrin deposition in liver sections. rhTM suppressed the mRNA expression of heme oxygenase-1, plasminogen activator inhibitor type-1, tissue factors, and inflammatory cytokines compared with the control group. rhTM did not change the hepatic GSH content at 2 h after APAP injection, but restored them at 4 h after the insult. rhTM ameliorated liver damage in mice with AILI, probably via the improvement in liver perfusion induced by it's anticoagulant acitivity, which can lead to the suppression of secondary liver damage.

    DOI: 10.3892/etm.2019.7665

  • Successful endoscopic treatment of hepatoduodenal fistula formed during sorafenib treatment for hepatocellular carcinoma with duodenal invasion Reviewed

    Koji Imoto, Motoyuki Kohjima, Tomoyuki Kurashige, Taiji Mutsuki, Shigeki Tashiro, Hideo Suzuki, Akifumi Kuwano, Masaki Kato, Yoshihiro Ogawa

    Acta Hepatologica Japonica   60 ( 3 )   91 - 98   2019.3

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    DOI: 10.2957/kanzo.60.91

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  • 組織線維化と線維症 NASHと肝線維化

    合谷 孟, 井本 効志, 田中 正剛, 小川 佳宏

    炎症と免疫   33 ( 1 )   58 - 62   2024.12   ISSN:0918-8371

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    Language:Japanese   Publisher:(株)先端医学社  

    肥満人口の増加に伴って代謝機能障害関連脂肪性肝炎(metabolic dysfunction-associated steatohepatitis:MASH)による肝硬変は増加傾向である.肝脂肪化の発症にはインスリン抵抗性に代表される全身複数臓器の代謝異常が関与し,慢性的な肝細胞障害の持続は線維芽細胞の活性化を惹起して組織の線維化が進行する.このプロセスにはマクロファージをはじめとする種々の免疫細胞が関与しており,病態特異的なマクロファージの亜集団が病態形成に寄与することが判明している.本稿ではMASHにおける肝線維化の機序について概説する.(著者抄録)

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    肝臓   65 ( Suppl.1 )   A432 - A432   2024.4   ISSN:0451-4203 eISSN:1881-3593

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  • 【微小環境から読み解く肝癌】MASLD関連肝細胞癌の微小環境

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    肝胆膵   88 ( 4 )   467 - 471   2024.4   ISSN:0389-4991

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    肝臓   2023.4

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    肝臓   2023.4

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    肝臓   2023.4

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    肝臓   2023.4

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    肝臓   2023.3

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    肝臓   2023.2

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    肝臓   2023.2

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    日本成人先天性心疾患学会雑誌   2023.1

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    日本消化器病学会九州支部例会・日本消化器内視鏡学会九州支部例会プログラム・抄録集   2022.12

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    肝臓   2022.4

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  • APAP肝障害マウスモデルにおけるPirfenidoneによる肝障害抑制効果の検討

    田代 茂樹, 東 夕喜, 大野 あかり, 青柳 知美, 高橋 基, 黒川 美穂, 井本 効志, 合谷 孟, 田中 正剛, 国府島 庸之, 小川 佳宏

    肝臓   2022.4

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  • NASH関連肝癌モデルマウスを用いた抗PD-1抗体の肝癌に対する効果についての検討

    高橋 基, 国府島 庸之, 東 夕喜, 大野 あかり, 青柳 知美, 井本 効志, 黒川 美穂, 田代 茂樹, 合谷 孟, 田中 正剛, 小川 佳宏

    肝臓   2022.4

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  • OTC欠損モデルマウスにおけるアンモニア代謝動態の検討

    井本 効志, 東 夕喜, 大野 あかり, 青柳 知美, 高橋 基, 黒川 美穂, 田代 茂樹, 合谷 孟, 田中 正剛, 国府島 庸之, 小川 佳宏

    肝臓   2022.4

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  • 急性肝不全モデルマウスにおけるExtracellular trapsの関与についての検討

    高橋 基, 田中 正剛, 東 夕喜, 大野 あかり, 青柳 知美, 井本 効志, 黒川 美穂, 田代 茂樹, 合谷 孟, 国府島 庸之, 小川 佳宏

    肝臓   2022.4

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  • 急性肝障害時の類洞血流障害発症におけるIFNγの関与

    黒川 美穂, 高橋 基, 井本 効志, 田代 茂樹, 青柳 知美, 大野 あかり, 東 夕喜, 合谷 孟, 田中 正剛, 国府島 庸之, 小川 佳宏

    肝臓   2022.4

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  • 好酸球増多症による肝障害を発症した一例

    伊地知 嵩治, 日置 智惟, 川元 美緒, 高橋 基, 井本 効志, 黒川 美穂, 田代 茂樹, 鈴木 秀生, 合谷 孟, 田中 正剛, 国府島 庸之, 小川 佳宏

    日本消化器病学会九州支部例会・日本消化器内視鏡学会九州支部例会プログラム・抄録集   2021.6

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  • 非アルコール性脂肪性肝疾患の組織学的特徴に関連した臨床病態及び遺伝子発現変化の検討

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    肝臓   2021.4

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  • IFNγは急性肝障害の類洞血流障害に関与する

    黒川 美穂, 桑野 哲史, 日置 智惟, 川元 美緒, 高橋 基, 井本 効志, 田代 茂樹, 鈴木 秀生, 合谷 孟, 田中 正剛, 加藤 正樹, 国府島 庸之, 小川 佳宏

    肝臓   2021.4

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  • 肝生検で診断した免疫チェックポイント阻害剤による肝障害の臨床的特徴

    日置 智惟, 川元 美緒, 高橋 基, 井本 効志, 黒川 美穂, 鈴木 秀生, 田代 茂樹, 合谷 孟, 田中 正剛, 加藤 正樹, 国府島 庸之, 小川 佳宏

    肝臓   2021.4

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  • 肝細胞癌における糖・脂質代謝関連遺伝子発現の変化 高分化型肝細胞癌における脂肪蓄積のメカニズム

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    肝臓   2021.4

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  • 肝細胞癌患者におけるlenvatinib血中濃度と奏功率および有害事象の関連

    高橋 基, 日置 智惟, 川元 美緒, 井本 効志, 黒川 美穂, 田代 茂樹, 鈴木 秀生, 秦 晃二郎, 合谷 孟, 田中 正剛, 加藤 正樹, 国府島 庸之, 小川 佳宏

    肝臓   2021.4

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  • 急性肝障害に伴う膵酵素上昇

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    肝臓   2021.2

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  • MC4R欠損マウスを用いた閉経後女性におけるNASH発症メカニズムの解析

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    日本消化器病学会雑誌   2020.7

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  • APAP肝障害マウスモデルにおけるPirfenidoneによる肝障害抑制効果の検討

    田代 茂樹, 豊田 優貴, 大角 真央, 日置 智惟, 倉重 智之, 井本 効志, 黒川 美穂, 鈴木 秀生, 桑野 哲史, 田中 正剛, 國府島 庸之, 加藤 正樹, 小川 佳宏

    日本消化器病学会雑誌   2020.7

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  • 膵機能低下に伴う肝脂肪化症例の臨床的特徴と遺伝子発現変化

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    肝臓   2020.4

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  • MC4R欠損マウスを用いた閉経後女性におけるNASH発症メカニズムの解析

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    肝臓   2020.4

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  • NAFLDにおける組織学的肝内微小構造形成に関わる臨床的特徴と遺伝子発現変化

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    肝臓   2020.4

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  • 免疫チェックポイント阻害剤による肝障害の臨床的特徴

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    肝臓   2020.4

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  • 好中球リンパ球比を用いた非アルコール性脂肪性肝疾患(NAFLD)患者における発癌高リスク群の囲い込み

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    肝臓   2020.4

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  • 急性肝障害における超音波造影剤による血行動態評価の有用性

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    肝臓   2020.4

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  • 肝細胞癌との鑑別が困難であったFallot四徴症修復術後に発症した肝原発悪性リンパ腫の一例

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    日本消化器病学会九州支部例会・日本消化器内視鏡学会九州支部例会プログラム・抄録集   2019.5

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  • 閉経後女性における脂肪肝発症メカニズムの解析とその臨床的特徴の検討

    鈴木 秀生, 国府島 庸之, 倉重 智之, 正月 泰士, 井本 効志, 田代 茂樹, 桑野 哲史, 田中 正剛, 加藤 正樹, 小川 佳宏

    肝臓   2019.4

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  • APAP肝障害マウスモデルにおけるPirfenidoneによる肝障害抑制効果の検討

    田代 茂樹, 加藤 正樹, 倉重 智之, 正月 泰士, 井本 効志, 鈴木 秀生, 桑野 哲史, 田中 正剛, 国府島 庸之, 小川 佳宏

    肝臓   2019.4

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  • NAFLDにおけるSteatosis、Inflammation、Ballooning、Mallory-Denk body、Fibrosisの各因子と関連する臨床的特徴と遺伝子発現変化

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    肝臓   2019.4

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  • 分子標的薬と免疫チェックポイント阻害薬による肝障害(症例報告も可) 当院における免疫チェックポイント阻害剤での肝障害の臨床的特徴

    井本 効志, 国府島 庸之, 加藤 正樹

    肝臓   2019.4

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  • 当院におけるFib-4 index上昇患者の臨床的特徴についての検討

    倉重 智之, 加藤 正樹, 正月 泰士, 井本 効志, 田代 茂樹, 鈴木 秀生, 桑野 哲史, 田中 正剛, 国府島 庸之, 小川 佳宏

    肝臓   2019.4

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  • 急性肝障害における類洞内皮細胞障害と類洞内過凝固の関与の検討

    正月 泰士, 加藤 正樹, 倉重 智之, 井本 効志, 田代 茂樹, 鈴木 秀生, 桑野 哲史, 田中 正剛, 国府島 庸之, 小川 佳宏

    肝臓   2019.4

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  • 急性肝障害に合併する腎障害の臨床的特徴

    井本 効志, 倉重 智之, 正月 泰士, 田代 茂樹, 鈴木 秀生, 桑野 哲史, 田中 正剛, 加藤 正樹, 国府島 庸之, 小川 佳宏

    肝臓   2019.4

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  • 急性肝障害に対する肝類洞血流障害に注目した治療戦略

    桑野 哲史, 国府島 庸之, 倉重 智之, 正月 泰士, 井本 効志, 田代 茂樹, 鈴木 秀生, 田中 正剛, 加藤 正樹, 小川 佳宏

    肝臓   2019.4

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  • 肝細胞癌十二指腸浸潤に対するソラフェニブ治療後に生じた肝十二指腸瘻を内視鏡的に閉鎖しえた一例

    井本 効志, 国府島 庸之, 倉重 智之, 正月 泰士, 田代 茂樹, 鈴木 秀生, 桑野 哲史, 加藤 正樹, 小川 佳宏

    肝臓   2019.3

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    症例は79歳女性。肝細胞癌術後およびC型肝硬変SVR後で当院通院中であった。2017年10月黒色便を主訴に受診し、精査の結果肝細胞癌の再発とその十二指腸浸潤部からの腫瘍出血と診断された。浸潤部からの出血は自然止血した。動脈塞栓術や外科的治療の適応は乏しいと判断され、ソラフェニブ400mg/dayを開始した。2018年1月に腹部CTおよび上部消化管内視鏡検査では、再発癌部は縮小し十二指腸浸潤部には肝十二指腸瘻が出現していた。瘻孔閉鎖のためポリグリコール酸シートとフィブリン糊による内視鏡的瘻孔閉鎖処置を行い、さらに瘻孔周囲をアルゴンプラズマ凝固にて焼灼した。瘻孔は縮小傾向を示しソラフェニブ治療を継続したところ、同年5月には瘻孔は閉鎖した。十二指腸浸潤を伴う肝細胞癌の縮小とともに生じた肝十二指腸瘻を、内視鏡的に閉鎖しえた症例を経験したので報告する。(著者抄録)

  • 当院での免疫チェックポイント阻害剤による肝障害の臨床的特徴

    井本 効志, 国府島 庸之, 加藤 正樹

    日本消化器病学会雑誌   2018.10

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  • 肥満合併症としての肝疾患-NASHと肝細胞癌をどう捉えるか- NASH病態進展・肝細胞癌発症における代謝異常

    国府島 庸之, 鈴木 秀生, 黒川 美穂, 井本 効志, 倉重 智之, 正月 泰士, 田代 茂樹, 桑野 哲史, 大橋 朋子, 加藤 正樹, 小川 佳宏

    肥満研究   2018.9

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  • 当院での免疫チェックポイント阻害剤による肝障害の臨床的特徴

    井本 効志, 国府島 庸之, 加藤 正樹

    肝臓   2018.9

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  • 腹部超音波を用いた急性肝障害症例における門脈血流と肝硬度の経時的変化の検討

    森田 祐輔, 井本 効志, 黒川 美穂, 鈴木 秀生, 桑野 哲史, 国府島 庸之, 山崎 晃裕, 大橋 朋子, 加藤 正樹, 小川 佳宏

    肝臓   2018.4

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  • NAFLD患者における肥満と体組成の関与

    黒川 美穂, 森田 祐輔, 井本 効志, 鈴木 秀生, 桑野 哲史, 国府島 庸之, 加藤 正樹, 小川 佳宏

    肝臓   2018.4

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  • 急性発症型自己免疫性肝炎の臨床的特徴の検討

    井本 効志, 国府島 庸之, 加藤 正樹

    肝臓   2018.4

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  • 急性肝障害における類洞血流障害の関与

    桑野 哲史, 井本 効志, 黒川 美穂, 森田 祐輔, 鈴木 秀生, 國府島 庸之, 加藤 正樹, 小川 佳宏

    肝臓   2018.4

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  • 高度肝障害を伴った急性発症still病4例の検討

    黒川 美穂, 井本 効志, 森田 祐輔, 鈴木 秀生, 桑野 哲史, 国府島 庸之, 加藤 正樹, 小川 佳宏

    肝臓   2017.11

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  • 急性発症型自己免疫性肝炎の臨床的特徴

    井本 効志, 黒川 美穂, 森田 祐輔, 鈴木 秀生, 桑野 哲史, 國府島 庸之, 加藤 正樹, 小川 佳宏

    肝臓   2017.11

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  • 内臓脂肪蓄積と異所性脂肪/臓器連関 NAFLD病態進展における体組成・体脂肪分布の関与

    国府島 庸之, 黒川 美穂, 井上 千絵子, 森田 祐輔, 井本 効志, 鈴木 秀生, 桑野 哲史, 山崎 晃裕, 大橋 朋子, 牧 俊允, 木村 真一郎, 前田 泰孝, 園田 紀之, 加藤 正樹, 小川 佳宏

    肥満研究   2017.9

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  • B型肝細胞癌術後経過中に認められた異時性肝内胆管癌の1例

    井本 効志, 高見 裕子, 立石 昌樹, 龍 知記, 和田 幸之, 才津 秀樹

    肝臓   2011.11

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Professional Memberships

Research Projects

  • 急性肝障害における肝再生機構の多様性の解明

    Grant number:24K18977  2024.4 - 2027.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

    井本 効志

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    Grant type:Scientific research funding

    肝細胞の多方向性を示す形質転換の詳細を明らかにするために、① 各細胞集団のキャラクタライズ、② 阻害実験による各細胞集団の肝再生への寄与の確認、③ 異なる肝障害での再生機構の確認、④ 臨床検体を用いた各細胞集団、シグナルパスウェイの確認を行い、同定できた肝再生機構から治療標的となる候補分子を推定して、⑤ 急性肝不全の新規治療開発を目指す。

    CiNii Research

  • フォンタン関連肝疾患における肝線維化の病態解明

    Grant number:23K19591  2023 - 2024

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Research Activity start-up

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    Authorship:Principal investigator  Grant type:Scientific research funding