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| 1 | 华南地区中生代Cu-(Mo)-W-Sn矿床成矿作用与洋岭/转换断层俯冲显示文摘华南地区是我国重要的金属矿产资源产地,除了发育大量的钨锡钼铋和稀土等金属矿产外,还有铜金矿床分布。本文通过对华南地区29个典型Cu-Mo-W-Sn矿床的时空分布及其与之有关的花岗质岩体的侵位年龄分析,探讨了与不同成矿类型有关的花岗质岩石的地球化学特征。本文认为华南地区10个典型的与Cu有关的矿床主要发生在180~170Ma、160~150Ma以及105~90Ma三个时期,而10个钨矿床主要集中于170~130Ma;4个W-Sn矿床集中于170~130Ma和120~110Ma;而5个Sn矿床则发育于170~150Ma、130~110Ma以及100~90Ma三个时期。Cu矿床主要与同熔型花岗岩有关,而Mo、W-Sn既与同熔型花岗岩有关,又与改造型花岗岩有关。在岩石地球化学上,与Cu-(Mo)-W-Sn成矿作用有关的花岗质岩石也表现出不同的地球化学特点,如,从Cu-(Mo)矿床到W-Sn矿床SiO2含量有逐渐增大、氧化性逐渐降低、还原性逐渐增加以及分异演化程度有逐渐增高的趋势。与Cu-(Mo)-Au矿床有关的花岗质岩石具有较低的SiO2(60.3%~68.1%),氧化性较高(Fe2O3/FeO=0.31~1.81),分异演化程度较低(Rb/Sr=0.05~3.3)的特点;与Cu-(Pb)-(Zn)矿床有关的花岗质岩石具有相对较高的SiO2(73.3%~75.2%),氧化性稍高(Fe2O3/FeO=0.68~1.74),分异程度稍低(Rb/Sr=10.8~57.8)的特点;而与Mo矿床有关的花岗质岩石具有较宽的SiO2(67.3%~76.2%)变化范围,氧化性稍低(Fe2O3/FeO=0.68~1.74),分异演化程度稍低(Rb/Sr=0.6~9.29);与W矿有关的花岗质岩石的SiO2含量为69.9%~80.1%,还原性稍低(Fe2O3/FeO=0.19~0.76),分异演化程度稍高(Rb/Sr=21.9~61.7);与W-Sn矿床有关的SiO2为74.8%~78.7%,还原性较低(Fe2O3/FeO=0.08~0.59),分异程度较高(Rb/Sr=10.8~139);与Sn矿床有关的花岗质岩石的SiO2为64.8%~76.9%,还原性高(Fe2O3/FeO=0.01~0.58),分异演化程度高(Rb/Sr=1~530)。在结合华南地区花岗岩类岩石的分布特征以及盆岭构造的特点,本文提出华南地区Cu-Mo-W-Sn矿床的成矿作用是不同时期大洋板块或者洋岭多阶段俯冲结果的新成因模型,即早侏罗世休眠的Farallon-Izanagi洋岭俯冲导致早—中侏罗世Cu成矿作用;中—晚侏罗世活动的Farallon-Izanagi洋岭和转换断层俯冲是中晚侏罗世Cu-(Mo)-(W)成矿作用以及多阶段W-Sn成矿作用的触发动力,而白垩纪Izanagi大洋板块俯冲则是白垩纪斑岩型Cu-W-Sn成矿作用的诱因。该模型的提出较好地解释了华南中生代大规模岩石圈拆沉—减薄—伸展的机制及其大规模成矿作用的动力。 | 李晓峰 Watanabe Yasushi 华仁民 毛景文 | 2008 | 地质学报2008，82，5： | 78 |
| 2 | Biomarkers for the early diagnosis of hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) is the fifth most common cancer and the second leading cause of cancer-related deaths worldwide. Although the prognosis of patients with HCC is generally poor, the5-year survival rate is > 70% if patients are diagnosed at an early stage. However, early diagnosis of HCC is complicated by the coexistence of inflammation and cirrhosis. Thus, novel biomarkers for the early diagnosis of HCC are required. Currently, the diagnosis of HCC without pathological correlation is achieved by analyzing serum α.fetoprotein levels combined with imaging techniques. Advances in genomics and proteomics platforms and biomarker assay techniques over the last decade have resulted in the identification of numerous novel biomarkers and have improved the diagnosis of HCC. The most promising biomarkers,such as glypican-3, osteopontin, Golgi protein-73 and nucleic acids including microRNAs, are most likely to become clinically validated in the near future. These biomarkers are not only useful for early diagnosis of HCC, but also provide insight into the mechanisms driving oncogenesis. In addition, such molecular insight creates the basis for the development of potentially more effective treatment strategies. In this article,we provide an overview of the biomarkers that are currently used for the early diagnosis of HCC. | Nobuhiro Tsuchiya Yu Sawada Itaru Endo Keigo Saito Yasushi Uemura Tetsuya Nakatsura | 2015 | World Journal of Gastroenterology2015，21，37： | 72 |
| 3 | 江西永平铜矿花岗质岩石的岩石结构、地球化学特征及其成矿意义显示文摘江西永平铜矿位于华南怀玉山—北武夷山铜铅锌多金属成矿带内,是赣东北地区除了德兴铜矿外的另一个大型铜矿基地。该矿区存在两种类型的花岗质岩石,一种是花岗岩;另一种是英安斑岩。英安斑岩具有典型斑状结构和石英眼结构,而花岗岩则具有单向固结结构。在化学成分上,两者属于高钾的钙碱性系列岩石,英安斑岩贫硅、富Al、Fe、Mg、Ca,以及具有较大的Na_2O/K_2O(0.02~0.64)等特点;而花岗岩富硅、贫Al、Ca,以及富碱和具有较小的Na_2O/K_2O(0.02~0.03)等特点。两种类型的岩石具有一致的REE配分曲线。它们均富集大离子亲石元素(Ba、Rb、K),亏损高场强元素(Th、Nd、Ta、Ti)以及元素Sr和P,显示了与俯冲作用有关的岩浆作用。在结构和化学成分上,花岗岩则类似于美国Climax斑岩钼(铜)矿成矿斑岩的性质(如具有单向固结结构、较高的分异指数、富Si、贫Al、Ca、富Na_2O+K_2O以及K_2O>Na_2O)。与英安斑岩有关的蚀变作用主要有夕卡岩化、黑云母化、白云母化、绿泥石化和萤石化,而与花岗岩有关的蚀变作用主要是白云母化和萤石化;相应地,与英安斑岩有关的成矿作用主要为铜,而与花岗岩有关的成矿作用则主要为钼。2件辉钼矿样品的Re-Os年龄分别为156.7±2.8Ma和155.7±3.6Ma,表明与花岗岩有关的钼成矿作用发生在156Ma左右。本文认为,永平铜钼矿的成矿地球动力学背景应是由挤压向伸展的转换环境。 | 李晓峰 Yasushi Watanabe 屈文俊 | 2007 | 岩石学报2007，23，10： | 42 |
| 4 | Association of Fusobacterium nucleatum with immunity andmolecular alterations in colorectal cancer显示文摘The human intestinal microbiome plays a major role in human health and diseases, including colorectal cancer. Colorectal carcinogenesis represents a heterogeneous process with a differing set of somatic molecular alterations, influenced by diet, environmental and microbial exposures, and host immunity. Fusobacterium species are part of the human oral and intestinal microbiota. Metagenomic analyses have shown an enrichment of Fusobacterium nucleatum(F. nucleatum) in colorectal carcinoma tissue. Using 511 colorectal carcinomas from Japanese patients, we assessed the presence of F. nucleatum. Our results showed that the frequency of F. nucleatum positivity in the Japanese colorectal cancer was 8.6%(44/511), which was lower than that in United States cohort studies(13%). Similar to the United States studies, F. nucleatum positivityin Japanese colorectal cancers was significantly associated with microsatellite instability(MSI)-high status. Regarding the immune response in colorectal cancer, high levels of infiltrating T-cell subsets(i.e., CD3+, CD8+, CD45RO+, and FOXP3+ cells) have been associated with better patient prognosis. There is also evidence to indicate that molecular features of colorectal cancer, especially MSI, influence T-cell-mediated adaptive immunity. Concerning the association between the gut microbiome and immunity, F. nucleatum has been shown to expand myeloid-derived immune cells, which inhibit T-cell proliferation and induce T-cell apoptosis in colorectal cancer. This finding indicates that F. nucleatum possesses immunosuppressive activities by inhibiting human T-cell responses. Certain micro RNAs are induced during the macrophage inflammatory response and have the ability to regulate host-cell responses to pathogens. Micro RNA-21 increases the levels of IL-10 and prostaglandin E2, which suppress antitumor T-cell-mediated adaptive immunity through the inhibition of the antigen-presenting capacities of dendritic cells and T-cell proliferation in colorectal cancer cells. Thus, emerging evidence may provide insights for strategies to target microbiota, immune cells and tumor molecular alterations for colorectal cancer prevention and treatment. Further investigation is needed to clarify the association of Fusobacterium with T-cells and micro RNA expressions in colorectal cancer. | Katsuhiko Nosho Yasutaka Sukawa Yasushi Adachi Miki Ito Kei Mitsuhashi Hiroyoshi Kurihara Shinichi Kanno Itaru Yamamoto Keisuke Ishigami Hisayoshi Igarashi Reo Maruyama Kohzoh Imai Hiroyuki Yamamoto Yasuhisa Shinomura | 2016 | World Journal of Gastroenterology2016，22，2： | 44 |
| 5 | 铟矿床研究现状及其展望显示文摘铟是一种稀有金属,它在高科技产业中的应用价值越来越受到人们的普遍关注。由于供求矛盾突出,其消费价格水平不断上涨。目前,世界矿业界在铟业投入的技术和资金支持不断增加,以寻求满足日益增长的经济发展的需求。但相对来说,与铟有关的地质工作程度较低,新探明的储量远远跟不上其消费的增长水平,因此,有必要加大地质投入,探求新的资源量,保障世界经济可持续发展的要求。文章在总结前人研究成果的基础上,综述了世界上铟矿床的分布及其地质构造背景,以及铟矿物学、矿床成因和成矿机制等方面的最新研究成果。文章指出,为了寻找潜在的铟资源,必须加强铟的基础地质研究工作,在对铟的成因矿物学、成矿机制及其成矿环境进行深入系统研究的基础上,建立铟矿床的成矿模型和找矿勘查模型。 | 李晓峰 Watanabe Yasushi 毛景文 | 2007 | 矿床地质2007，26，4： | 39 |
| 6 | Magnifying colonoscopy as a non-biopsy technique for differential diagnosis of non-neoplastic and neoplastic lesions显示文摘瞄准:为了澄清与放大结肠镜检查观察的粘膜地窟模式是否对可行,把非肿瘤的息肉与肿瘤的息肉区分开来。方法:从通过 2000 年 3 月的 1999 年 6 月,有 210 损害的 180 个连续病人与放大结肠镜诊断了(CF-200Z,天堂光有限公司,东京,日本) 被注册。有 0.2% 靛青洋红染料的放大和多彩石印版内视镜检查法为粘膜地窟观察被用于每损害。损害出现打字我和 II 地窟模式被活体检视组织学地认为非肿瘤、检验,而损害证明到 V 地窟模式的类型 III 被移开内视镜的联盟者或通过手术。内视镜的诊断和 histologic 诊断的关联然后被调查。结果:在内视镜检查法, 24 损害证明我或 II 坑模式,和 186 损害显示出的一种类型打 III 到 V 坑模式。与 histologic 检查, 26 损害作为非肿瘤的息肉被诊断,并且 184 损害作为肿瘤的息肉被诊断。全面诊断精确性是 99.1%(208/210 ) 。敏感和特性是 92.3%(24/26 ) 并且 99.8%(184/186 ) 分别地。结论:放大结肠镜检查能作为一种非活体检视技术被使用区分肿瘤、非肿瘤的息肉。 | Shigeharu Kato Kuang I Fu Yasushi Sano Takahiro Fujii Yutaka Saito Takahisa Matsuda Ikuro Koba Shigeaki Yoshida Takahiro Fujimori | 2006 | World Journal of Gastroenterology2006，12，9： | 31 |
| 7 | Shear wave velocity is a useful marker for managing nonalcoholic steatohepatitis显示文摘AIM:To investigate whether a noninvasive measurement of tissue strain has a potential usefulness for management of nonalcoholic steatohepatitis(NASH).METHODS:In total 26 patients,23 NASHs and 3 normal controls were enrolled in this study.NASH was staged based on Brunt criterion.At a region of interest(ROI),a shear wave was evoked by implementing an acoustic radiation force impulse(ARFI),and the propagation velocity was quantif ied.RESULTS:Shear wave velocity(SWV) could be reproducibly quantified at all ROIs in all subjects except for 4 NASH cases,in which a reliable SWV value was not calculated at several ROIs.An average SWV of 1.34 ± 0.26 m/s in fibrous stage 0-1 was significantly slower than 2.20 ± 0.74 m/s and 2.90 ± 1.01 m/s in stages 3 and 4,respectively,but was not significantly different from 1.79 ± 0.78 m/s in stage 2.When a cutoff value was set at 1.47 m/s,receiver operating characteristic analysis showed significance to dissociate stages 3 and 4 from stage 0-1(P=0.0092) with sensitivity,specificity and area under curve of 100%,75% and 94.2%,respectively.In addition,the correlation between SWV and hyaluronic acid was significant(P<0.0001),while a tendency toward negative correlation was observed with serum albumin(P=0.053).CONCLUSION:The clinical implementation of ARFI provides noninvasive repeated evaluations of liver stiffness at an arbitrary position,which has the potential to shed new light on NASH management. | Akihiko Osaki Tomoyuki Kubota Takeshi Suda Masato Igarashi Keisuke Nagasaki Atsunori Tsuchiya Masahiko Yano Yasushi Tamura Masaaki Takamura Hirokazu Kawai Satoshi Yamagiwa Toru Kikuchi Minoru Nomoto Yutaka Aoyagi | 2010 | World Journal of Gastroenterology2010，16，23： | 30 |
| 8 | Clinical features of gastroduodenal injury associated with long-term low-dose aspirin therapy显示文摘Low-dose aspirin(LDA) is clinically used for the prevention of cardiovascular and cerebrovascular events with the advent of an aging society.On the other hand,a very low dose of aspirin(10 mg daily) decreases the gastric mucosal prostaglandin levels and causes significant gastric mucosal damage.The incidence of LDAinduced gastrointestinal mucosal injury and bleeding has increased.It has been noticed that the incidence of LDA-induced gastrointestinal hemorrhage has increased more than that of non-aspirin non-steroidal anti-inflammatory drug(NSAID)-induced lesions.The pathogenesis related to inhibition of cyclooxygenase(COX)-1 includes reduced mucosal flow,reduced mucus and bicarbonate secretion,and impaired platelet aggregation.The pathogenesis related to inhibition of COX-2 involves reduced angiogenesis and increased leukocyte adherence.The pathogenic mechanisms related to direct epithelial damage are acid back diffusion and impaired platelet aggregation.The factors associated with an increased risk of upper gastrointestinal(GI) complications in subjects taking LDA are aspirin dose,history of ulcer or upper GI bleeding,age > 70 years,concomitant use of non-aspirin NSAIDs including COX-2-selective NSAIDs,and Helicobacter pylori(H.pylori) infection.Moreover,no significant differences have been found between ulcer and non-ulcer groups in the frequency and severity of symptoms such as nausea,acid regurgitation,heartburn,and bloating.It has been shown that the ratios of ulcers located in the body,fundus and cardia are significantly higher in bleeding patients than the ratio of gastroduodenal ulcers in patients taking LDA.Proton pump inhibitors reduce the risk of developing gastric and duodenal ulcers.In contrast to NSAIDinduced gastrointestinal ulcers,a well-tolerated histamine H2-receptor antagonist is reportedly effective in prevention of LDA-induced gastrointestinal ulcers.The eradication of H.pylori is equivalent to treatment with omeprazole in preventing recurrent bleeding.Continuous aspirin therapy for patients with gastrointestinal bleeding may increase the risk of recurrent bleeding but potentially reduces the mortality rates,as stopping aspirin therapy is associated with higher mortality rates.It is very important to prevent LDA-induced gastroduodenal ulcer complications including bleeding,and every effort should be exercised to prevent the bleeding complications. | Junichi Iwamoto Yoshifumi Saito Akira Honda Yasushi Matsuzaki | 2013 | World Journal of Gastroenterology2013，19，11： | 29 |
| 9 | Effectiveness of probiotic therapy for the prevention of relapse in patients with inactive ulcerative colitis显示文摘AIM: to evaluate the effectiveness of probiotic therapy for suppressing relapse in patients with inactive ulcerative colitis(UC).METHODS: Bio-Three tablets, each containing 2 mg of lactomin(Streptococcus faecalis T-110), 10 mg of Clostridium butyricum TO-A, and 10 mg of Bacillus mesentericus TO-A, were used as probiotic therapy.Sixty outpatients with UC in remission were randomly assigned to receive 9 Bio-Three tablets/day(BioThree group) or 9 placebo tablets/day(placebo group)for 12 mo in addition to their ongoing medications.Clinical symptoms were evaluated monthly or on the exacerbation of symptoms or need for additional medication. Fecal samples were collected to analyze bacterial DNA at baseline and 3-mo intervals. Terminal restriction fragment length polymorphism and cluster analyses were done to examine bacterial components of the fecal microflora.RESULTS: Forty-six patients, 23 in each group,completed the study, and 14 were excluded. The relapse rates in the Bio-Three and placebo groups were respectively 0.0% vs 17.4% at 3 mo(P = 0.036), 8.7%vs 26.1% at 6 mo(P = 0.119), and 21.7% vs 34.8%(P = 0.326) at 9 mo. At 12 mo, the remission rate was 69.5% in the Bio-Three group and 56.6% in the placebo group(P = 0.248). On cluster analysis of fecal flora, 7 patients belonged to cluster Ⅰ, 32 to cluster Ⅱ,and 7 to cluster Ⅲ.CONCLUSION: Probiotics may be effective formaintaining clinical remission in patients with quiescent UC, especially those who belong to cluster Ⅰ on fecal bacterial analysis. | Yasushi Yoshimatsu Akihiro Yamada Ryuichi Furukawa Koji Sono Aisaku Osamura Kentaro Nakamura Hiroshi Aoki Yukiko Tsuda Nobuo Hosoe Nobuo Takada Yasuo Suzuki | 2015 | World Journal of Gastroenterology2015，21，19： | 21 |
| 10 | Molecular Cloning and Functional Characterization of Porcine MyD88 Essential for TLR Signaling显示文摘We isolated cDNA encoding porcine MyD88 (poMyD88) from Peyer's patches (Pps) of GALT. The complete open reading frame (ORF) of poMyD88 contains 879 bp encoding a deduced 293 aa residues. The amino acid sequence of poMyD88 was characterized by N-terminal death,intermediate and C-terminal Toll/IL-1 receptor (TIR) domains. The putative poMyD88 protein shares a higher level of homology with its human (87.2% amino acid identity) than with its mouse (77.4% amino acid identity) counterpart. Overexpression of poMyD88 participated in the further enhanced activation of NF-κB in human embryonic kidney (HEK) 293 cells expressing porcine TLR2 and porcine TLR4/MD-2,but not porcine RP105/MD-1 after stimulation with the corresponding ligands. The expression levels of MyD88 were highest in the spleen and mesenteric lymph nodes (MLNs),and lower in digestive tissues of newborn swine. In adult swine,the expression levels in the digestive tissues were lower than those in MLNs and the spleen. These results suggest that an MyD88-dependent signaling pathway is present in newborn as well as in adult swine and that it is involved in the innate immune system of these animals. | Masanori Tohno Tomoyuki Shimazu Hisashi Aso Yasushi Kawai Tadao Saito Haruki Kitazawa | 2007 | Cellular & Molecular Immunology2007，4，5： | 20 |
| 11 | Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial显示文摘 | Yung-Jue Bang Eric Van Cutsem Andrea Feyereislova Hyun C Chung Lin Shen Akira Sawaki Florian Lordick Atsushi Ohtsu Yasushi Omuro Taroh Satoh Giuseppe Aprile Evgeny Kulikov Julie Hill Michaela Lehle Josef Rüschoff Yoon-Koo Kang | 2010 | The Lancet2010，，9742： | 20 |
| 12 | 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 |
| 13 | Alterations in the human epidermal growth factor receptor 2-phosphatidylinositol 3-kinase-v-Akt pathway in gastric cancer显示文摘AIM:To investigate human epidermal growth factor receptor 2(HER2)-phosphatidylinositol 3-kinase(PI3K)-vAkt murine thymoma viral oncogene homolog signaling pathway.METHODS:We analyzed 231 formalin-fixed,paraffinembedded gastric cancer tissue specimens from Japanese patients who had undergone surgical treatment.The patients' age,sex,tumor location,depth of invasion,pathological type,lymph node metastasis,and pathological stage were determined by a review of the medical records.Expression of HER2 was analyzed by immunohistochemistry(IHC) using the HercepTest TM kit.Standard criteria for HER2 positivity(0,1+,2+,and 3+) were used.Tumors that scored 3+ were considered HER2-positive.Expression of phospho Akt(pAkt) was also analyzed by IHC.Tumors were considered pAkt-positive when the percentage of positive tumor cells was 10% or more.PI3K,catalytic,alpha polypeptide(PIK3CA) mutations in exons 1,9 and 20 were analyzed by pyrosequencing.Epstein-Barr virus(EBV) infection was analyzed by in situ hybridization targeting EBV-encoded small RNA(EBER) with an EBER-RNA probe.Microsatellite instability(MSI) was analyzed by polymerase chain reaction using the mononucleotide markers BAT25 and BAT26.RESULTS:HER2 expression levels of 0,1+,2+ and 3+ were found in 167(72%),32(14%),12(5%) and 20(8.7%) samples,respectively.HER2 overexpression(IHC 3+) significantly correlated with intestinal histological type(15/20 vs 98 /205,P = 0.05).PIK3CA mutations were present in 20 cases(8.7%) and significantly correlated with MSI(10/20 vs 9/211,P < 0.01).The mutation frequency was high(21%) in T4 cancers and very low(6%) in T2 cancers.Mutations in exons 1,9 and 20 were detected in 5(2%),9(4%) and 7(3%) cases,respectively.Two new types of PIK3CA mutation,R88Q and R108H,were found in exon1.All PIK3CA mutations were heterozygous missense singlebase substitutions,the most common being H1047R(6/20,30%) in exon20.Eighteen cancers(8%) were EBV-positive and this positivity significantly correlated with a diffuse histological type(13/18 vs 93/198,P = 0.04).There were 7 cases of lymphoepithelioma-like carcinomas(LELC) and 6 of those cases were EBV-positive(percent/EBV:6/18,33%;percent/all LELC:6/7,86%).pAkt expression was positive in 119(53%) cases but showed no correlation with clinicopathological characteristics.pAkt expression was significantly correlated with HER2 overexpression(16/20 vs 103/211,P < 0.01) but not with PIK3CA mutations(12/20 vs 107/211,P = 0.37) or EBV infection(8/18 vs 103/211,P = 0.69).The frequency of pAkt expression was higher in cancers with exon20 mutations(100%) than in those with exon1(40%) or exon9(56%) mutations.One case showed both HER2 overexpression and EBV infection and 3 cases showed both PIK3CA mutations and EBV infection.However,no cases showed both PIK3CA mutations and HER2 overexpression.One EBVpositive cancer with PIK3CA mutation(H1047R) was MSI-positive.Three of these 4 cases were positive for pAkt expression.In survival analysis,pAkt expression significantly correlated with a poor prognosis(hazard ratio 1.75;95%CI:1.12-2.80,P = 0.02).CONCLUSION:HER2 expression,PIK3CA mutations and EBV infection in gastric cancer were characterized.pAkt expression significantly correlates with HER2 expression and with a poor prognosis. | Yasutaka Sukawa Hiroyuki Yamamoto Katsuhiko Nosho Hiroaki Kunimoto Hiromu Suzuki Yasushi Adachi Mayumi Nakazawa Takayuki Nobuoka Mariko Kawayama Masashi Mikami Takashi Matsuno Tadashi Hasegawa Koichi Hirata Kohzoh Imai Yasuhisa Shinomura | 2012 | World Journal of Gastroenterology2012，18，45： | 19 |
| 14 | Potentiality of immunotherapy against hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC),the predominant form of primary liver cancer,is the fifth most common cancer worldwide and the second leading cause of cancer-related death. Despite the high incidence,treatment options remain limited for advanced HCC,and as a result prognosis continues to be poor. Current therapeutic options,surgery,chemotherapy and radiotherapy,have only modest efficacy. New treatment modalities to prolong survival and to minimize the risk of adverse response are desperately needed for patients with advanced HCC. Tumor immunotherapy is a promising,novel treatment strategy that may lead to improvements in both treatment-associated toxicity and outcome. The strategies have developed in part through genomic studies that have yielded candidate target molecules and in part through basic biology studies that have defined the pathways and cell types regulating immune response. Here,we summarize the various types of HCC immunotherapy and argue that the newfound field of HCC immunotherapy might provide critical advantages in the effort to improve prognosis of patients with advanced HCC. Already several immunotherapies,such as tumor-associated antigen therapy,immune checkpoint inhibitors and cell transfer immunotherapy,have demonstrated safety and feasibility in HCC patients. Unfortunately,immunotherapy currently has low efficacy in advanced stage HCC patients; overcoming this chal lenge will place immunotherapy at the forefront of HCC treatment,possibly in the near future. | Nobuhiro Tsuchiya Yu Sawada Itaru Endo Yasushi Uemura Tetsuya Nakatsura | 2015 | World Journal of Gastroenterology2015，21，36： | 19 |
| 15 | Comparison of DWI and PET/CT in evaluation of lymph node metastasis in uterine cancer显示文摘AIM: To investigate diffusion-weighted imaging (DWI) and positron emission tomography and computed tomography (PET/CT) with Ⅳ contrast for the preoperative evaluation of pelvic lymph node (LN) metastasis in uterine cancer. METHODS: Twenty-five patients with endometrial or cervical cancer who underwent both DWI and PET/CT before pelvic lymphadenectomy were included in this study. For area specific analysis, LNs were divided into eight regions: both common iliac, external iliac, internal iliac areas, and obturator areas. The classification for malignancy on DWI was a focally abnormal signal intensity in a location that corresponded to the LN chains on the T1WI and T2WI. The criterion for malignancy on PET/CT images was increased tracer uptake by the LN.RESULTS: A total of 36 pathologically positive LN areas were found in 9 patients. With DWI, the sensitivity, specificity, positive predictive value, negative predictive value and accuracy for detecting metastatic LNs on an LN area-by-area analysis were 83.3%, 51.2%, 27.3%, 93.3% and 57.0%, respectively, while the corresponding values for PET/CT were 38.9%, 96.3%, 70.0%, 87.8% and 86.0%. Differences in sensitivity, specificity and accuracy were significant (P < 0.0005). CONCLUSION: DWI showed higher sensitivity and lower specificity than PET/CT. Neither DWI nor PET/CT were sufficiently accurate to replace lymphadenectomy. | Kazuhiro Kitajima Erena Yamasaki Yasushi Kaji Koji Murakami Kazuro Sugimura | 2012 | World Journal of Radiology2012，4，5： | 16 |
| 16 | ACE and ACE2 in kidney disease显示文摘Renin angiotensin system(RAS) activation has a significant influence on renal disease progression. The classical angiotensin-converting enzyme(ACE)-angiotensin Ⅱ(Ang Ⅱ)-Ang Ⅱ type 1(AT1) axis is considered to control the effects of RAS activation on renal disease.However, since its discovery in 2000 ACE2 has also been demonstrated to have a significant impact on the RAS.The synthesis and catabolism of Ang Ⅱ are regulated via a complex series of interactions, which involve ACE and ACE2. In the kidneys, ACE2 is expressed in the proxima tubules and less strongly in the glomeruli. The synthesisof inactive Ang 1-9 from Ang Ⅰ and the catabolism of Ang Ⅱ to produce Ang 1-7 are the main functions of ACE2. Ang 1-7 reduces vasoconstriction, water retention, salt intake, cell proliferation, and reactive oxygen stress, and also has a renoprotective effect. Thus, in the nonclassical RAS the ACE2-Ang 1-7-Mas axis counteracts the ACE-Ang Ⅱ-AT1 axis. This review examines recent human and animal studies about renal ACE and ACE2. | Sonoo Mizuiri Yasushi Ohashi | 2015 | World Journal of Nephrology2015，4，1： | 15 |
| 17 | A candidate targeting molecule of insulin-like growth factor-Ⅰ receptor for gastrointestinal cancers显示文摘Advances in molecular research in cancer have brought new therapeutic strategies into clinical usage.One new group of targets is tyrosine kinase receptors,which can be treated by several strategies,including small molecule tyrosine kinase inhibitors(TKIs) and monoclonal antibodies(mAbs).Aberrant activation of growth factors/receptors and their signal pathways are required for malignant transformation and progression in gastrointestinal(GI) carcinomas.The concept of targeting specif ic carcinogenic receptors has been validated by successful clinical application of many new drugs.Type I insulin-like growth factor(IGF) receptor(IGF-IR) signaling potently stimulates tumor progression and cellular differentiation,and is a promising new molecular target in human malignancies.In this review,we focus on this promising therapeutic target,IGF-IR.The IGF/IGF-IR axis is an important modifier of tumor cell proliferation,survival,growth,and treatment sensitivity in many malignant diseases,including human GI cancers.Preclinical studies demonstrated that downregulation of IGF-IR signals reversed the neoplastic phenotype and sensitized cells to anticancer treatments.These results were mainly obtained through our strategy of adenoviruses expressing dominant negative IGF-IR(IGF-IR/dn) against gastrointestinal cancers,including esophagus,stomach,colon,and pancreas.We also summarize a variety of strategies to interrupt the IGFs/IGF-IR axis and their preclinical experiences.Several mAbs and TKIs targeting IGF-IR have entered clinical trials,and early results have suggested that these agents have generally acceptable safety profiles as single agents.We summarize the advantages and disadvantages of each strategy and discuss the merits/demerits of dual targeting of IGF-IR and other growth factor receptors,including Her2 and the insulin receptor,as well as other alternatives and possible drug combinations.Thus,IGF-IR might be a candidate for a molecular therapeutic target in human GI carcinomas. | Yasushi Adachi Hiroyuki Yamamoto Hirokazu Ohashi Takao Endo David P Carbone Kohzoh Imai Yasuhisa Shinomura | 2010 | World Journal of Gastroenterology2010，16，46： | 14 |
| 18 | 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 |
| 19 | Endoscopic hemostasis techniques for upper gastrointestinal hemorrhage: A review显示文摘Upper gastrointestinal hemorrhage (UGIH) is an urgent disease that is often encountered in daily medical practice. Endoscopic hemostasis is currently indispensable for the treatment of UGIH. Initially, when UGIH is suspected, a cause of UGIH is presumed from the medical interview and physical findings. After ample primary treatment, urgent endoscopy is performed. Many methods of endoscopic hemostasis are in wide use, including hemoclip, injection and thermo-coagulation methods. Although UGIH develops from a wide variety of diseases, such as esophageal varices and gastric and duodenal ulcer, hemostasis is almost always possible. Identification of the causative diseases, primary treatment and characteristic features of endoscopic hemostasis are needed to allow appropriate treatment. | Hajime Anjiki Terumi Kamisawa Masaki Sanaka Taro Ishii Yasushi Kuyama | 2010 | World Journal of Gastrointestinal Endoscopy2010，2，2： | 13 |
| 20 | Serrated polyps of the colon and rectum:Remove or not?显示文摘In recent years,the serrated neoplasia pathway where serrated polyps arise as a colorectal cancer has gained considerable attention as a new carcinogenic pathway.Colorectal serrated polyps are histopathologically classified into hyperplastic polyps(HPs),sessile serrated lesions,and traditional serrated adenomas;in the serrated neoplasia pathway,the latter two are considered to be premalignant.In western countries,all colorectal polyps,including serrated polyps,apart from diminutive rectosigmoid HPs are removed.However,in Asian countries,the treatment strategy for colorectal serrated polyps has remained unestablished.Therefore,in this review,we described the clinicopathological features of colorectal serrated polyps and proposed to remove HPs and sessile serrated lesions≥6 mm in size,and traditional serrated adenomas of any size. | Wataru Sano Daizen Hirata Akira Teramoto Mineo Iwatate Santa Hattori Mikio Fujita Yasushi Sano | 2020 | World Journal of Gastroenterology2020，26，19： | 12 |
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