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| 1 | Insulin resistance and chronic liver disease显示文摘Increased insulin resistance is frequently associated with chronic liver disease and is a pathophysiological feature of hepatogenous diabetes.Distinctive factors including hepatic parenchymal cell damage,portalsystemic shunting and hepatitis C virus are responsible for the development of hepatogenous insulin resistance/diabetes.Although it remains unclear whether insulin secretion from pancreatic beta cells is impaired as it is in type 2 diabetes,retinopathic and cardiovascular risk is low and major causes of death in cirrhotic patients with diabetes are liver failure,hepatocellular carcinoma and gastrointestinal hemorrhage.Hemoglobin A1c is an inaccurate marker for the assessment and management of hepatogenous diabetes.Moreover,exogenous insulin or sulfonylureas may be harmful because these agents may promote hepatocarcinogenesis.Thus,pathogenesis,cause of death,assessment and therapeutic strategy for hepatogenous insulin resistance/diabetes differ from those for lifestyle-related type 2 diabetes.In this article,we review features of insulin resistance in relationship to chronic liver disease.We also discuss the impact of anti-diabetic agents on interferon treatment and hepatocarcinogenesis. | Takumi Kawaguchi Eitaro Taniguchi Minoru Itou Masahiro Sakata Shuji Sumie Michio Sata | 2011 | World Journal of Hepatology2011，3，5： | 25 |
| 2 | Dipeptidyl peptidase-4: A key player in chronic liver disease显示文摘Dipeptidyl peptidase-4 (DPP-4) is a membrane-associated peptidase, also known as CD26. DPP-4 has widespread organ distribution throughout the body and exerts pleiotropic effects via its peptidase activity. A representative target peptide is glucagon-like peptide-1, and inactivation of glucagon-like peptide-1 results in the development of glucose intolerance/diabetes mellitus and hepatic steatosis. In addition to its peptidase activity, DPP-4 is known to be associated with immune stimulation, binding to and degradation of extracellular matrix, resistance to anti-cancer agents, and lipid accumulation. The liver expresses DPP-4 to a high degree, and recent accumulating data suggest that DPP-4 is involved in the development of various chronic liver diseases such as hepatitis C virus infection, non-alcoholic fatty liver disease, and hepatocellular carcinoma. Furthermore, DPP-4 occurs in hepatic stem cells and plays a crucial role in hepatic regeneration. In this review, we described the tissue distribution and various biological effects of DPP-4. Then, we discussed the impact of DPP-4 in chronic liver disease and the possible therapeutic effects of a DPP-4 inhibitor. | Minoru Itou Takumi Kawaguchi Eitaro Taniguchi Michio Sata | 2013 | World Journal of Gastroenterology2013，19，15： | 22 |
| 3 | Association of glypican-3 expression with growth signaling molecules in hepatocellular carcinoma显示文摘AIM:To clarify the association of glypican-3(GPC3)expression with Wnt and other growth signaling molecules in hepatocellular carcinoma(HCC). METHODS:Expression of GPC3,Wnt,matrix metalloproteinases(MMPs),sulfatase(SULF)1,SULF2,and other growth signaling molecules was analyzed in HCC cell lines and tissue samples by real-time reverse transcriptionpolymerase chain reaction,immunoblotting,and/or immunostaining.Expression of various genes in GPC3 siRNA-transfected HCC cells was analyzed. RESULTS:GPC3 was overexpressed in most HCCs at mRNA and protein levels and its serum levels weresignificantly higher in patients with HCC than in non- HCC subjects(P<0.05).Altered expressions of various MMPs and growth signaling molecules,some of which were correlated with GPC3 expression,were observed in HCCs.Down-regulation of GPC3 expression by siRNA in GPC3-overexpressing HCC cell lines resulted in a significant decrease in expressions of MMP2,MMP14,fibroblast growth factor receptor 1,insulin-like growth factor 1 receptor.GPC3 expression was significantly correlated with nuclear/cytoplasmic localization ofβ-catenin. CONCLUSION:These results suggest that GPC3,in conjunction with MMPs and growth signaling molecules, might play an important role in the progression of HCC. | Noriyuki Akutsu Hiroyuki Yamamoto Shigeru Sasaki Hiroaki Taniguchi Yoshiaki Arimura Kohzoh Imai Yasuhisa Shinomura | 2010 | World Journal of Gastroenterology2010，16，28： | 20 |
| 4 | Transcriptional silencing of Dickkopf gene family by CpG island hypermethylation in human gastrointestinal cancer显示文摘AIM: To clarify alterations of Dickkopfs (Dkks) and Kremen2 (Krm2) in gastrointestinal cancer. METHODS: We investigated the expression profiles and epigenetic alterations of Dkks and Krm2 genes in gastrointestinal cancer using RT-PCR, tissue microarray analysis, and methylation specific PCR (MSP). Cancer cells were treated with the demethylating agent and/or histone deacetylase inhibitor. WST-8 assays and in vitro invasion assays after treatment with specific siRNA for those genes were performed. RESULTS: Dkks and Krm2 expression levels were reduced in a certain subset of the gastrointestinal cancer cell lines and cancer tissues. This was correlated with promoter hypermethylation. There were significant correlations between Dkks over-expression levels and beta-catenin over-expression in colorectal cancer. In colorectal cancers with beta-catenin over-expression, Dkk-1 expression levels were significantly lower in those with lymph node metastases than in those without. Down-regulation of Dkks expression by siRNA resulted in a significant increase in cancer cell growth and invasiveness in vitro.CONCLUSION: Down-regulation of the Dkks associated to promoter hypermethylation appears to be frequently involved in gastrointestinal tumorigenesis. | Tadateru Maehata Hiroaki Taniguchi Hiroyuki Yamamoto Katsuhiko Nosho Yasushi Adachi Nobuki Miyamoto Chie Miyamoto Noriyuki Akutsu Satoshi Yamaoka Fumio Itoh | 2008 | World Journal of Gastroenterology2008，14，17： | 19 |
| 5 | Long-term outcome of percutaneous ethanol injection therapy for minimum-sized hepatocellular carcinoma显示文摘AIM: To evaluate long-term follow-up of minimum-sized hepatocellular carcinoma (HCC) treated with percutaneous ethanol injection (PEI). METHODS: PEI was applied to 42 lesions in 31 patients (23 male and eight female) with HCC < 15 mm in diameter, over the past 15 years. RESULTS: Overall survival rate was 74.1% at 3 years, 49.9% at 5 years, 27.2% at 7 years and 14.5% at 10 years. These results are superior to, or at least the same as those for hepatic resection and radiofrequency ablation. Survival was affected only by liver function, but not by sex, age, etiology of Hepatitis B virus or Hepatitis C virus, α-fetoprotein levels, arterial and portal blood flow, histological characteristics, and tumor multiplicity or size. Patients in Child-Pugh class A and B had 5-, 7- and 10-years survival rates of 76.0%, 42.2% and 15.8%, and 17.1%, 8.6% and 0%, respectively (P = 0.025). CONCLUSION: Treatment with PEI is best indicated for patients with HCC < 15 mm in Child-Pugh class A. | Miyuki Taniguchi Soo Ryang Kim Susumu Imoto Hirotsugu Ikawa Kenji Ando Keiji Mita Shuichi Fuki Noriko Sasase Toshiyuki Matsuoka Masatoshi Kudo Yoshitake Hayashi | 2008 | World Journal of Gastroenterology2008，14，13： | 16 |
| 6 | Interrelationship between microsatellite instability and microRNA in gastrointestinal cancer显示文摘There is an increasing understanding of the roles that microsatellite instability (MSI) plays in Lynch syndrome (by mutations) and sporadic (by mainly epigenetic changes) gastrointestinal (GI) and other cancers. Deficient DNA mismatch repair (MMR) results in the strong mutator phenotype known as MSI, which is the hallmark of cancers arising within Lynch syndrome. MSI is characterized by length alterations within simple repeated sequences called microsatellites. Lynch syndrome occurs primarily because of germline mutations in one of the MMR genes, mainly MLH1 or MSH2 , less frequently MSH6 , and rarely PMS2 . MSI is also observed in about 15% of sporadic colorectal, gastric, and endometrial cancers and in lower frequencies in a minority of other cancers where it is often associated with the hypermethylation of the MLH1 gene. miRNAs are small noncoding RNAs that regulate gene expression at the posttranscriptional level and are critical in many biological processes and cellular pathways. There is accumulating evidence to support the notion that the interrelationship between MSI and miRNA plays a key role in the pathogenesis of GI cancer. As a possible new mechanism underlying MSI, overexpression of miR-155 has been shown to downregulate expression of MLH1, MSH2, and MSH6. Thus, a subset of MSI-positive (MSI+) cancers without known MMR defects may result from miR-155 overexpression. Target genes of frameshift mutation for MSI are involved in various cellular functions, such as DNA repair, cell signaling, and apoptosis. A novel class of target genes that included not only epigenetic modifier genes, such as HDAC2 , but also miRNA processing machinery genes, including TARBP2 and XPO5 , were found to be mutated in MSI+ GI cancers. Thus, a subset of MSI+ colorectal cancers (CRCs) has been proposed to exhibit a mutated miRNA machinery phenotype. Genetic, epigenetic, and transcriptomic differences exist between MSI+ and MSI cancers. Molecular signatures of miRNA expression apparently have the potential to distinguish between MSI+ and MSI CRCs. In this review, we summarize recent advances in the MSI pathogenesis of GI cancer, with the focus on its relationship with miRNA as well as on the potential to use MSI and related alterations as biomarkers and novel therapeutic targets. | Hiroyuki Yamamoto Yasushi Adachi Hiroaki Taniguchi Hiroaki Kunimoto Katsuhiko Nosho Hiromu Suzuki Yasuhisa Shinomura | 2012 | World Journal of Gastroenterology2012，18，22： | 14 |
| 7 | Treatment of over 20 mm gastric cancer by endoscopic submucosal dissection using an insulation-tipped diathermic knife显示文摘AIM: To evaluate the effectiveness of endoscopic submucosal dissection using an insulation-tipped diathermic knife (IT-ESD) for the treatment of patients with over 20 mm early gastric cancer (EGC). METHODS: A total of 112 patients with over 10 mm EGC were treated with IT-ESD at Sumitomo Besshi Hospital and Shikoku Cancer Center in the 5 year period from January 2002 to December 2006, including 40 patients with over 20 mm EGC. We compared patient backgrounds, the one-piece resection rate, complete resection (CR) rate, operation time, bleeding rate, perforation rate between patients with over 20 mm EGC [over 20 mm group (21-40 mm)] and the remaining patients (under 20 mm group). RESULTS: We found no significant difference in the rate of underlying cardiopulmonary disease (over 20 mm group vs under 20 mm group, 5.0% vs 5.6%), one- piece resection rate (95% vs 96%), CR rate (85% vs 89%), operation time (72.3 min vs 66.5 min), bleeding rate (5% vs 4.2%), and perforation rate (0% vs 1.4%) between the 2 groups. Three patients in each group had submucosal invasion and two in each groups underwent additional surgery. CONCLUSION: There was no significant difference in the outcome resulting from IT-ESD between the 2 groups. Our study proves that IT-ESD is a feasible treatment for patients with over 20 mm mucosal gastric cancer although the long-term outcome should be evaluated in the future. | Shoji Hirasaki Hiromitsu Kanzaki Minoru Matsubara Kohei Fujita Fusao Ikeda Hideaki Taniguchi Eiichiro Yumoto Seiyuu Suzuki | 2007 | World Journal of Gastroenterology2007，13，29： | 13 |
| 8 | An updated review of gastric cancer in the next-generation sequencing era:Insights from bench to bedside and vice versa显示文摘Gastric cancer(GC)is one of the most common malignancies and remains the second leading cause of cancer-related death worldwide.There is an increasing understanding of the roles that genetic and epigenetic alterations play in GCs.Recent studies using nextgeneration sequencing(NGS)have revealed a number of potential cancer-driving genes in GC.Whole-exome sequencing of GC has identified recurrent somatic mutations in the chromatin remodeling gene ARID1A and alterations in the cell adhesion gene FAT4,a member of the cadherin gene family.Mutations in chromatin remodeling genes(ARID1A,MLL3 and MLL)have been found in 47%of GCs.Whole-genome sequencing and whole-transcriptome sequencing analyses have also discovered novel alterations in GC.Recent studies of cancer epigenetics have revealed widespread alterations in genes involved in the epigenetic machinery,such as DNA methylation,histone modifications,nucleosome positioning,noncoding RNAs and microRNAs.Recent advances in molecular research on GC have resulted in the introduction of new diagnostic and therapeutic strategies into clinical settings.The antihuman epidermal growth receptor 2(HER2)antibody trastuzumab has led to an era of personalized therapy in GC.In addition,ramucirumab,a monoclonal antibody targeting vascular endothelial growth factor receptor(VEGFR)-2,is the first biological treatment that showed survival benefits as a single-agent therapy in patients with advanced GC who progressed after firstline chemotherapy.Using NGS to systematically identify gene alterations in GC is a promising approach with remarkable potential for investigating the pathogenesis of GC and identifying novel therapeutic targets,as well as useful biomarkers.In this review,we will summarize the recent advances in the understanding of the molecular pathogenesis of GC,focusing on the potential use of these genetic and epigenetic alterations as diagnostic biomarkers and novel therapeutic targets. | Hiroyuki Yamamoto Yoshiyuki Watanabe Tadateru Maehata Ryo Morita Yoshihito Yoshida Ritsuko Oikawa Shinya Ishigooka Shun-ichiro Ozawa Yasumasa Matsuo Kosuke Hosoya Masaki Yamashita Hiroaki Taniguchi Katsuhiko Nosho Hiromu Suzuki Hiroshi Yasuda Yasuhisa Shinomura Fumio Itoh | 2014 | World Journal of Gastroenterology2014，20，14： | 12 |
| 9 | Hepatic schwannoma:Imaging findings on CT,MRI and contrast-enhanced ultrasonography显示文摘A primary benign schwannoma of the liver is extremely rare and is difficult to preoperatively discriminate from a malignant tumor.We compared the imaging and pathological findings,and examined the possibility of preoperatively diagnosing a benign liver schwannoma.A 72-year-old woman was admitted to our hospital because of a 4.6-cm mass in the liver.A malignant tumor was suspected,and a right hepatectomy was performed.After this,the diagnosis of a primary benign schwannoma of the liver was made through pathological examination.Contrast-enhanced ultrasonography(CEUS) with Sonazoid showed minute blood flows into the septum and solid areas of the tumor in the vascular phase;most likely due to increased arterial flow associated with infiltration of chronic inflammatory cells.In the postvascular phase,CEUS showed contrast defect of cystic areas and delayed enhancement of solid areas;most likely due to aggregation of siderophores.Because discriminating between a benign and malignant schwannoma of the liver is difficult,surgery is generally recommended.However,the two key findings from CEUS may be useful in discriminating ancient schwannoma by recognizing the hemorrhage involved in the secondary degeneration and aggregation of siderophores. | Yu Ota Kazunobu Aso Kenji Watanabe Takahiro Einama Koji Imai Hidenori Karasaki Ryuji Sudo Yosui Tamaki Mituyoshi Okada Yosihiko Tokusashi Toru Kono Naoyuki Miyokawa Masakazu Haneda Masahiko Taniguchi Hiroyuki Furukawa | 2012 | World Journal of Gastroenterology2012，18，35： | 11 |
| 10 | Hepatic clearance measured with ^(99m)Tc-GSA single-photon emission computed tomography to estimate liver fibrosis显示文摘AIM: To evaluate the clinical utility of hepatic clearance(HC) measured with technetium-99m-diethylenetriaminepenta-acetic acid-galactosyl human serum albumin(99mTc-GSA) single-photon emission computed tomography(SPECT) to estimate the degree of liver fibrosis.METHODS:Seventy-eight consecutive patients who underwent initial hepatectomy due to hepatocellular carcinoma were enrolled in this study.Indocyanine green clearance(ICG R15),quantitative indices estimated by 99mTc-GSA[the receptor index(LHL15 and HH15)and HC via SPECT analysis],and conventional liver function tests were performed before hepatectomy.Correlations among the quantitative indices for liver functional reserve,conventional liver function tests,andthe degree of liver fibrosis were evaluated.RESULTS:The degree of liver fibrosis was correlated with ICG R15,HH15,LHL15,and HC.HC showed the best correlation with conventional liver function tests.According to multivariate analysis,HC and LHL15 were significant independent predictors of severe fibrosis.HC was the most valuable index for predicting severe fibrosis.CONCLUSION:HC measured with 99mTc-GSA SPECT is a reliable index for assessing liver fibrosis before hepatectomy. | Masahiko Taniguchi Atsutaka Okizaki Kenji Watanabe Koji Imai Koichiro Uchida Takahiro Einama Noriyuki Shuke Naoyuki Miyokawa Hiroyuki Furukawa | 2014 | World Journal of Gastroenterology2014，20，44： | 11 |
| 11 | Overexpression of the receptor tyrosine kinase EphA4 in human gastric cancers显示文摘AIM: To clarify the expression and role of Ephrin receptor A4 (EphA4) in gastric cancer in relation to clinicopathological characteristics and the expression of fibroblast growth factor receptor 1 (FGFR1) and ephrin ligands. METHODS: Eleven gastric carcinoma cell lines, 24 paired surgical fresh specimens of gastric adenocarcinoma and adjacent nontumor tissue, 74 conventional formalin-fixed, paraffin-embedded tumor specimens, and 55 specimens spotted on tissue microarray (TMA) were analyzed. Reverse transcription-PCR (RT-PCR), real-time RT-PCR, immunohistochemistry, and cell growth assays were performed. RESULTS: Overexpression of EphA4 mRNA expres-sion was observed in 8 (73%) of 11 gastric cancer cell lines and 10 (42%) of 24 gastric cancer tissues. Over-expression of EphA4, analyzed by immunohistochemistry, was observed in 62 (48%) of 129 gastric cancer tissues. EphA4 overexpression, at the protein level, was significantly associated with depth of invasion and recurrence. EphA4 overexpression was also correlated with FGFR1 overexpression. Patients with EphA4-positive cancer had significantly shorter overall survival periods than did those with EphA4-negative cancer (P = 0.0008). The mRNAs for ephrin ligands were coexpressed in various combinations in gastric cancer cell lines and cancer tissues. Downregulation of EphA4 expression by siRNA in EphA4-overexpressing gastric cancer cell lines resulted in a significant decrease in cell growth. CONCLUSION: Our results suggest that overexpres-sion of EphA4 plays a role in gastric cancer. | Mariko Oki Hiroyuki Yamamoto Hiroaki Taniguchi Yasushi Adachi Kohzoh Imai Yasuhisa Shinomura | 2008 | World Journal of Gastroenterology2008，14，37： | 11 |
| 12 | Effects of ghrelin on interdigestive contractions of the rat gastrointestinal tract显示文摘Ghrelin causes interdigestive contractions of the stom- ach in rats. However, it remains unknown whether ghrelin causes interdigestive contractions in the small intestine. Four strain gauge transducers were implanted on the antrum, duodenum, proximal and distal jejunum. After an overnight fast, gastrointestinal (GI) contrac- tions were recorded in freely moving conscious rats. Spontaneous phase Ⅲ-like contractions were observed at every 13-16 min in rat GI tract. The fasted motor patterns were replaced by the fed motor pattern immediately after food intake. Two minutes after f inishing the spontaneous phase Ⅲ-like contractions in the antrum, acyl ghrelin (0.8, 2.4 and 8.0 μg/kg per min) was con- tinuously infused for 30 min. Three-f ive minutes after the starting ghrelin infusion, augmented phase Ⅲ-like contractions were observed at the antrum, duodenum, and jejunum. Ghrelin infusion (0.8, 2.4 and 8.0 μg/kg per min) signif icantly increased motility index of phase Ⅲ-like contractions at the antrum and jejunum in a dose dependent manner, compared to that of saline in- jection. Thus, it is likely that exogenously administered ghrelin causes phase Ⅲ-like contraction at the antrum, which migrates to the duodenum and jejunum. The possible role of 5-HT, in addition to ghrelin, in mediating intestinal migrating motor complex (MMC), is discussed. | Hiroshi Taniguchi Hajime Ariga Kirk Ludwig Toku Takahashi | 2008 | World Journal of Gastroenterology2008，14，41： | 10 |
| 13 | Impact of lymph node micrometastasis in hilar bile duct carcinoma patients显示文摘瞄准:组织化学地在门胆汁管癌(HBDC ) 并且到检验微转移和 VEGF-C 表示到免疫评估结果的临床的意义。方法:从有节点否定的 HBDC 的 25 个病人的 361 个地区性的淋巴节点的一个总数是对 cytokeratins 与抗体染色的免疫 8 和 18 (凸轮 5.2 ) ,并且免疫 VEGF-C 的组织化学的染色在 34 个主要 resected 肿瘤被执行。结果:淋巴节点微转移在 6 被检测(24%) 25 个病人并且 10 (2.8%) 361 个淋巴节点。没有,有微转移的病人比那些显示出显著地更差的幸存率(P = 0.025 ) 。VEGF-C 表示是积极的在里面(50%) 17 与淋巴节点转移 34 HBDC,并且显著地相关(P = 0.042 ) 并且显微镜的静脉的侵略(P = 0.035 ) 。结论:免疫组织化学地检测了微转移影响的淋巴节点,这被建议 HBDC 的结果。VEGF-C 表示高度在 HBDC 与淋巴节点转移被相关并且可能因此是一个有用预言者。 | Kentaro Taniguchi Taku Iida Tomohide Hori Shintaro Yagi Hiroshi Imai Taizo Shiraishi Shinji Uemoto | 2006 | World Journal of Gastroenterology2006，12，16： | 9 |
| 14 | Quantitative evaluation of long-term liver repopulation and the reconstitution of bile ductules after hepatocellular transplantation显示文摘AIM: The treatment of liver disease is severely limited by a shortage of donor livers. In trying to address this growing problem, hepatocellular transplantation (HTx) has received much attention as an alternative to whole organ transplant.However, the expansion of transplanted cells is at low level,and the reconstitution of functional liver tissue is limited by this cellular property. We set up an animal model to better understand cell dose effect and the kinetics of liver repopulation following HTx.METHODS: Dipeptidyl peptidase Ⅳ (DPPIV)-deficient rats treated with retrorsine and subjected to partial hepatectomy were infused with DPPIV-positive hepatocytes. Rats were injected with varying numbers of donor hepatocytes down to 100 cells low, and liver repopulation was examined at different time points up to 20 mo long. Repopulation was assessed by computer-aided quantitative detection.RESULTS: Transplanted hepatocytes underwent multiple rounds of proliferation and stably repopulated the injured livers after 20 mo and at all cell doses. Transplanted cells divided 14 times within the 3-mo time period following infusion, and the liver repopulation reached a plateau between 3 and 20 mo. Approximately 90% replacement occurred. Donor-derived cells also reconstituted the bile ductules of the recipients.CONCLUSION: The ability of transplanted hepatocytes to fully reconstitute injured livers strongly supports further investigation into the clinical potential of HTx. Additionally,the observation that transplanted hepatocytes also form components of the biliary system suggests that these cells may have bi-potential property of the stem cells. | Yun-Wen Zheng Nobuhiro Ohkohchi Hideki Taniguchi | 2005 | World Journal of Gastroenterology2005，11，39： | 9 |
| 15 | Dehiscence following successful endoscopic closure of gastric perforation during endoscopic submucosal dissection显示文摘Gastric perforation is one of the most serious complications that can occur during endoscopic submucosal dissection(ESD).In terms of the treatment of such perforations,we previously reported that perforations immediately observed and successfully closed with endoclips during endoscopic resection could be managed conservatively.We now report the first case in our medical facility of a gastric perforation during ESD that was ineffectively treated conservatively even after successful endoscopic closure.In December 2006,we performed ESD on a recurrent early gastric cancer in an 81-year-old man with a medical history of laparotomy for cholelithiasis.A perforation occurred during ESD that was immediately observed and successfully closed with endoclips so that ESD could be continued resulting in an en-bloc resection.Intensive conservative management was conducted following ESD,however,an endoscopic examination five days after ESD revealed dehiscence of the perforation requiring an emergency laparotomy. | Masau Sekiguchi Haruhisa Suzuki Ichiro Oda Shigetaka Yoshinaga Satoru Nonaka Makoto Saka Hitoshi Katai Hirokazu Taniguchi Ryoji Kushima Yutaka Saito | 2012 | World Journal of Gastroenterology2012，18，31： | 7 |
| 16 | ARID1A expression in gastric adenocarcinoma:Clinicopathological significance and correlation with DNA mismatch repair status显示文摘AIM:To analyze the mismatch repair(MMR)status and the ARID1A expression as well as their clinicopathological significance in gastric adenocarcinomas.METHODS:We examined the expressions of MMR proteins and ARID1A by immunohistochemistry in consecutive 489 primary gastric adenocarcinomas.The results were further correlated with clinicopathological variables.RESULTS:The loss of any MMR protein expression,indicative of MMR deficiency,was observed in 38cases(7.8%)and was significantly associated with an older age(68.6±9.2 vs 60.4±11.7,P<0.001),a female sex(55.3%vs 31.3%,P=0.004),an antral location(44.7%vs 25.7%,P=0.021),and a differentiated histology(57.9%vs 39.7%,P=0.023).Abnormal ARID1A expression,including reduced or loss of ARID1A expression,was observed in 109 cases(22.3%)and was significantly correlated with lymphatic invasion(80.7%vs 69.5%,P=0.022)and lymph node metastasis(83.5%vs 73.7%,P=0.042).The tumors with abnormal ARID1A expression more frequently indicated MMR deficiency(47.4%vs 20.2%,P<0.001).A multivariate analysis identified abnormal ARID1A expression as an independent poor prognostic factor(HR=1.36,95%CI:1.01-1.84;P=0.040).CONCLUSION:Our observations suggest that the AIRD1A inactivation is associated with lymphatic invasion,lymph node metastasis,poor prognosis,and MMR deficiency in gastric adenocarcinomas. | Ryo Inada Shigeki Sekine Hirokazu Taniguchi Hitoshi Tsuda Hitoshi Katai Toshiyoshi Fujiwara Ryoji Kushima | 2015 | World Journal of Gastroenterology2015，21，7： | 7 |
| 17 | 白细胞素2/白细胞介素2受体系统的新进展显示文摘本文综述了白细胞介素2受体(IL-2R)的三种组成成份的分布、作用、基因组成,尤其是IL-2与IL-2R相互作用而介导的信号传递途径与可能的机制,从而提出IL-2R链成分可能与其他非细胞因子受体分子发生联系而产生新的信号复合体这一大胆而诱人的新观点. | Tatatsugu Taniguchi yasuhiro Minami 李翠玲 | 1993 | 国外医学(免疫学分册)1993，16，6： | 6 |
| 18 | BMP-induced Atoh8 attenuates osteoclastogenesis by suppressing Runx2 transcriptional activity and reducing the Rankl/Opg expression ratio in osteoblasts显示文摘Adult bone structural integrity is maintained by remodeling via the coupling of osteoclastic bone resorption and osteoblastic bone formation.Osteocytes or osteoblasts express receptor activator of nuclear factor k-B ligand(Rankl)or osteoprotegerin(Opg)to promote or inhibit osteoclastogenesis,respectively.Bone morphogenetic protein(BMP)is a potent bone inducer,but its major role in adult bone is to induce osteocytes to upregulate sclerostin(Sost)and increase the Rankl/Opg expression ratio,resulting in promotion of osteoclastogenesis.However,the precise effect of BMP-target gene(s)in osteoblasts on the Rankl/Opg expression ratio remains unclear.In the present study,we identified atonal homolog 8(Atoh8),which is directly upregulated by the BMPSmadl axis in osteoblasts.In vivo,Atoh8 was detected in osteoblasts but not osteocytes in adult mice.Although global Atoh8-knockout mice showed only a mild phenotype in the neonate skeleton,the bone volume was decreased and osteoclasts were increased in the adult phase.Atoh8-null marrow stroma cells were more potent than wild-type cells in inducing osteoclastogenesis in marrow cells.Atoh8 loss in osteoblasts increased Runx2 expression and the Rankl/Opg expression ratio,while Runx2 knockdown normalized the Rankl/Opg expression ratio.Moreover,Atoh8 formed a protein complex with Runx2 to inhibit Runx2 transcriptional activity and decrease the Rankl/Opg expression ratio.These results suggest that bone remodeling is regulated elaborately by BMP signaling;while BMP primarily promotes bone resorption,it simultaneously induces Atoh8 to inhibit Runx2 and reduce the Rankl/Opg expression ratio in osteoblasts,suppressing osteoclastogenesis and preventing excessive BMP-mediated bone resorption. | Yuhei Yahiro Shingo Maeda Masato Morikawa Daizo Koinuma Go Jokoji Toshiro ljuin Setsuro Komiya Ryoichiro Kageyama Kohei Miyazono Noboru Taniguchi | 2020 | Bone Research2020，8，3： | 6 |
| 19 | EFFECT OF INTERPHASE LIFT FORCE ON THE FLUID FLOW IN AN AIR-STIRRED CYLINDRICAL VESSEL显示文摘In the present paper, based on the two-phase model (Eulerian model), the two dimensional fluid flow liz air-stirred water systems is simulated, and the effect of interphase lift force on the fluid flow is specially discussed. In the Eulerian two-phase model, gas and liquid phase are considered to be two different continuous fluids interacting with each other through the finite inter-phase areas. The exchange between the phases is represented by source terms in conversation equations. Turbulence is assumed to be a property of the liquid phase, k - ε model is used to describe the behavior of the liquid phase. The dispersion of phases due to turbulence is represented by introducing a diffusion term in mass consecrvation equation. The contribution of bubble movement to the turbulent energy and its dissipation rate is taken into accounted by adding extra volumetric source terms to the equations of turbulent enemy and its dissipation rate. The comparison between the mathematical simulation and experiment data indicates that the interphase lift force has a big effect on the flow behavior, and considering both drug force and lift force as interphase forces is important to accurately simulate the gas-water two-phase fluid flow in air-stirred systems. The interphase lift force makes bubbles move away from the centerline, the gas concentration is decreased near the centerline, and increased near the wall. The lift force is smaller than drug force at the same place, especially far away from the centerline. | L.F. Zhang K.K. Cai Y. Qu and Y.S. Shen Postdoctoral Fellow of Japan Science Promotion Society Taniguchi Lab., Department of Metallurgy, Graduate School of Engineering, Tohoku University, Sendai980-8579, Japan School of Metallurgy, University of Scien | 2000 | Acta Metallurgica Sinica(English Letters)2000，13，4： | 6 |
| 20 | A novel animal model for in vivo study of liver cancer metastasis显示文摘AIM:To establish an animal model with human hepatocyte-repopulated liver for the study of liver cancer metastasis.METHODS:Cell transplantation into mouse livers was conducted using alpha-fetoprotein(AFP)-producing hu-man gastric cancer cells(h-GCCs) and h-hepatocytes as donor cells in a transgenic mouse line expressing urokinase-type plasminogen activator(uPA) driven by the albumin enhancer/promoter crossed with a severe combined immunodeficient(SCID) mouse line(uPA/SCID mice).Host mice were divided into two groups(A and B).Group A mice were transplanted with h-GCCs alone,and group B mice were transplanted with h-GCCs and h-hepatocytes together.The replacement index(RI),which is the ratio of transplanted h-GCCs and h-hepatocytes that occupy the examined area of a histological section,was estimated by measuring h-AFP and h-albumin concentrations in sera,respectively,as well as by immunohistochemical analyses of h-AFP and human cytokeratin 18 in histological sections.RESULTS:The h-GCCs successfully engrafted,repopulated,and colonized the livers of mice in group A(RI = 22.0% ± 2.6%).These mice had moderately differentiated adenocarcinomatous lesions with disrupted glandular structures,which is a characteristics feature of gastric cancers.The serum h-AFP level reached 211.0 ± 142.2 g/mL(range,7.1-324.2 g/mL).In group B mice,the h-GCCs and h-hepatocytes independently engrafted,repopulated the host liver,and developed colonies(RI = 12.0% ± 6.8% and 66.0% ± 12.3%,respectively).h-GCC colonies also showed typical adenocarcinomatous glandular structures around the h-hepatocyte-colonies.These mice survived for the full 56 day-study and did not exhibit any metastasis of h-GCCs in the extrahepatic regions during the observational period.The mice with an h-hepatocyte-repopulated liver possessed metastasized h-GCCs and therefore could be a useful humanized liver animal model for studying liver cancer metastasis in vivo.CONCLUSION:A novel animal model of human liver cancer metastasis was established using the uPA/SCID mouse line.This model could be useful for in vivo testing of anti-cancer drugs and for studying the mechanisms of human liver cancer metastasis. | Shinsuke Fujiwara Hikaru Fujioka Chise Tateno Ken Taniguchi Masahiro Ito Hiroshi Ohishi Rie Utoh Hiromi Ishibashi Takashi Kanematsu Katsutoshi Yoshizato | 2012 | World Journal of Gastroenterology2012，18，29： | 6 |
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