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| 1 | History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer显示文摘Helicobacter pylori(H.pylori)infection underlies gastric ulcer disease,gastric cancer and duodenal ulcer disease.The disease expression reflects the pattern and extent of gastritis/gastric atrophy(i.e.,duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis).Gastric and duodenal ulcers and gastric cancer have been known for thousands of years.Ulcers are generally non-fatal and until the 20th century were difficult to diagnose.However,the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present.It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century.Here,we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern,as it proved to be when it could be examined directly in the late 19th century.The environment before the 20th century favored acquisition of H.pylori infection and atrophic gastritis(e.g.,poor sanitation and standards of living,seasonal diets poor in fresh fruits and vegetables,especially in winter,vitamin deficiencies,and frequent febrile infections in childhood).The latter part of the 19th century saw improvements in standards of living,sanitation,and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent.In the early 20th century physician’s believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for'surgical disease'or for'Sippy'diets.We show that while H.pylori remained common and virulent in Europe and the United States,environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H.pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H.pylori-related diseases. | David Y Graham | 2014 | World Journal of Gastroenterology2014，20，18： | 52 |
| 2 | Immunotherapy in gastric cancer显示文摘Gastric cancer is the second most common of cancerrelated deaths worldwide.In the majority of cases gastric cancer is advanced at diagnosis and although medical and surgical treatments have improved,survival rates remain poor.Cancer immunotherapy has emerged as a powerful and promising clinical approach for treatment of cancer and has shown major success in breast cancer,prostate cancer and melanoma.Here,we provide an overview of concepts of modern cancer immunotherapy including the theory,current approaches,remaining hurdles to be overcome,and the future prospect of cancer immunotherapy in the treatment of gastric cancer.Adaptive cell therapies,cancer vaccines,gene therapies,monoclonal antibody therapies have all been used with some initial successes in gastric cancer.However,to date the results in gastric cancer have been disappointing as current approaches often do not stimulate immunity efficiently allowing tumors continue to grow despite the presence of a measurable immune response.Here,we discuss the identification of targets for immunotherapy and the role of biomarkers in prospectively identifying appropriate subjects or immunotherapy.We also discuss the molecular mechanisms by which tumor cells escape host immunosurveillance and produce an immunosuppressive tumor microenvironment.We show how advances have provided tools for overcoming the mechanisms of immunosuppression including the use of monoclonal antibodies to block negative regulators normally expressed on the surface of T cells which limit activation and proliferation of cytotoxic T cells.Immunotherapy has greatly improved and is becoming an important factor in such fields as medical care and welfare for human being.Progress has been rapid ensuring that the future of immunotherapy for gastric cancer is bright. | Satoko Matsueda David Y Graham | 2014 | World Journal of Gastroenterology2014，20，7： | 19 |
| 3 | Operative link for gastritis assessment vs operative link on intestinal metaplasia assessment显示文摘AIM:To compare the reliability of gastritis staging sys-tems in ranking gastritis-associated cancer risk in a large series of consecutive patients.METHODS:Gastric mucosal atrophy is the precancer-ous condition in which intestinal-type gastric cancer(GC)most frequently develops.The operative link for gas-tritis assessment(OLGA)staging system ranks the GC risk according to both the topography and the severity of gastric atrophy(as assessed histologically on the ba-sis of the Sydney protocol for gastric mucosal biopsy).Both cross-sectional and long-term follow-up trials have consistently associated OLGA stages Ⅲ-Ⅳ with a higher risk of GC.A recently-proposed modification of the OLGA staging system(OLGIM)basically incorporates the OLGA frame,but replaces the atrophy score with an assessment of intestinal metaplasia(IM)alone.A series of 4552 consecutive biopsy sets(2007-2009)was re-trieved and reassessed according to both the OLGA and the OLGIM staging systems.A set of at least 5 biopsy samples was available for all the cases considered.RESULTS:In 4460 of 4552 cases(98.0%),both the high-risk stages(Ⅲ + Ⅳ)and the low-risk stages(0 +Ⅰ + Ⅱ)were assessed applying the OLGA and OL-GIM criteria.Among the 243 OLGA high-risk stages,14(5.8%)were down-staged to a low risk using OLGIM.The 67(1.5%)incidentally-found neoplastic lesions(intraepithelial or invasive)were consistently associated with high-risk stages,as assessed by both OLGA and OLGIM(P < 0.001 for both).Two of 34 intestinal-type GCs coexisting with a high-risk OLGA stage(stage Ⅲ)were associated with a low-risk OLGIM stage(stage Ⅱ).CONCLUSION:Gastritis staging systems(both OLGA and OLGIM)convey prognostically important informa-tion on the gastritis-associated cancer risk.Because of its clinical impact,the stage of gastritis should be included as a conclusive message in the gastritis histol-ogy report.Since it focuses on IM alone,OLGIM staging is less sensitive than OLGA staging in the identif ication of patients at high risk of gastric cancer. | Massimo Rugge Matteo Fassan Marco Pizzi Fabio Farinati Giacomo Carlo Sturniolo Mario Plebani David Y Graham | 2011 | World Journal of Gastroenterology2011，17，41： | 19 |
| 4 | Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency in the 21^(st) century显示文摘Restitution of normal fat absorption in exocrine pancreatic insufficiency remains an elusive goal. Although many patients achieve satisfactory clinical results with enzyme therapy, few experience normalization of fat absorption, and many, if not most, will require individualized therapy. Increasing the quantity of lipase administered rarely eliminates steatorrhea but increases the cost of therapy. Enteric coated enzyme microbead formulations tend to separate from nutrients in the stomach precluding coordinated emptying of enzymes and nutrients. Unprotected enzymes mix well and empty with nutrients but are inactivated at pH 4 or below. We describe approaches for improving the results of enzyme therapy including changing to, or adding, a different product, adding non-enteric coated enzymes,(e.g., giving unprotected enzymes at the start of the mealand acid-protected formulations later), use of antisecretory drugs and/or antacids, and changing the timing of enzyme administration. Because considerable lipid is emptied in the first postprandial hour, it is prudent to start therapy with enteric coated microbead prior to the meal so that some enzymes are available during that first hour. Patients with hyperacidity may benefit from adjuvant antisecretory therapy to reduce the duodenal acid load and possibly also sodium bicarbonate to prevent duodenal acidity. Comparative studies of clinical effectiveness of different formulations as well as the characteristics of dispersion, emptying, and dissolution of enteric-coated microspheres of different diameter and density are needed; many such studies have been completed but not yet made public. We discuss the history of pancreatic enzyme therapy and describe current use of modern preparations, approaches to overcoming unsatisfactory clinical responses, as well as studies needed to be able to provide reliably effective therapy. | Tony Trang Johanna Chan David Y Graham | 2014 | World Journal of Gastroenterology2014，20，33： | 17 |
| 5 | What is artificial meat and what does it mean for the future of the meat industry?显示文摘The meat industry cannot respond to increases in demand by ever increasing resource use. The industry must find solutions to issues regarding animal welfare, health and sustainability and will have to do so in the face of competition from emerging non-traditional meat and protein products in an increasingly complex regulatory environment. These novel meat and protein products, otherwise known as ‘artificial meat' are utilising ground breaking technologies designed to meet the issues facing the conventional meat industry. These artificial meats, in vitro or cultured meat and meat from genetically modified organisms have no real capacity to compete with conventional meat production in the present environment. However, meat replacements manufactured from plant proteins and mycoproteins are currently the biggest competitors and are gaining a small percentage of the market. Manufactured meats may push conventional meat into the premium end of the market, and supply the bulk, cheap end of the market if conventional meat products become more expensive and the palatability and versatility of manufactured meats improve. In time the technology for other artificial meats such as meat from genetic modified organisms or cultured meat may become sufficiently developed for these products to enter the market with no complexity of the competition between meat products. Conventional meat producers can assimilate agroecology ecology concepts in order to develop sustainable animal production systems. The conventional meat industry can also benefit from assimilating biotechnologies such as cloning and genetic modification technologies, using the technology to adapt to the changing environment and respond to the increasing competition from artificial meats. Although it will depend at least partly on the evolution of conventional meat production, the future of artificial meat produced from stem cells appears uncertain at this time. | Sarah P F Bonny Graham E Gardner David W Pethick Jean-Franois Hocquette | 2015 | Journal of Integrative Agriculture2015，14，2： | 15 |
| 6 | Regulation of AMP-activated protein kinase by natural and synthetic activators显示文摘The AMP-activated protein kinase(AMPK)is a sensor of cellular energy status that is almost universally expressed in eukaryotic cells.While it appears to have evolved in single-celled eukaryotes to regulate energy balance in a cell-autonomous manner,during the evolution of multicellular animals its role has become adapted so that it also regulates energy balance at the whole body level,by responding to hormones that act primarily on the hypothalamus.AMPK monitors energy balance at the cellular level by sensing the ratios of AMP/ATP and ADP/ATP,and recent structural analyses of the AMPK heterotrimer that have provided insight into the complex mechanisms for these effects will be discussed.Given the central importance of energy balance in diseases that are major causes of morbidity or death in humans,such as type 2 diabetes,cancer and inflammatory disorders,there has been a major drive to develop pharmacological activators of AMPK.Many such activators have been described,and the various mechanisms by which these activate AMPK will be discussed.A particularly large class of AMPK activators are natural products of plants derived from traditional herbal medicines.While the mechanism by which most of these activate AMPK has not yet been addressed,I will argue that many of them may be defensive compounds produced by plants to deter infection by pathogens or grazing by insects or herbivores,and that many of them will turn out to be inhibitors of mitochondrial function. | David Grahame Hardie | 2016 | Acta Pharmaceutica Sinica B2016，6，1： | 11 |
| 7 | 英国胃肠病学会关于胃癌风险患者的诊断和管理指南显示文摘胃癌预后较差,部分原因在于诊断较晚。胃癌的危险因素包括幽门螺杆菌(H.pylori,HP)感染和胃癌家族史,尤其是遗传性弥漫性胃癌和恶性贫血。胃癌发展的阶段包括慢性胃炎、胃黏膜萎缩(GA)、胃黏膜肠化生(GIM)和异型增生。胃癌早期发现和提高生存率的关键是在内镜检查前以非侵入性方式识别高危人群。然而,尽管生物标志物可能有助于检测慢性萎缩性胃炎,但尚无足够的证据支持其用于人群筛查。高质量内镜检查是胃癌早期发现的重要组成部分,图像增强内镜结合组织病理学活检是GA和GIM最佳的诊断方法,并能准确进行风险分层。按照悉尼标准从胃窦、角切迹、小弯和大弯进行活检,既能明确诊断,也能对胃癌进行风险分层。理想状态应当是在高质量内镜检查中对GA或GIM区域活检。英国属于低危地区,可根据需要接受常规诊断性胃镜检查,但没有足够证据支持筛查,对于广泛GA或GIM的患者,每3年检查内镜。对于胃异型增生和早期癌,只要满足标准,内镜下黏膜切除术或内镜黏膜下剥离术的治疗有效,成功率高,复发率低。 | Matthew Banks David Graham Marnix Jansen TakujiGotoda Sergio Coda Massimiliano di Pietro NoriyaUedo Pradeep Bhandari D Mark Pritchard Ernst J Kuipers Manuel Rodriguez-Justo Marco R Novelli KrishRagunath Neil Shepherd Mario Dinis-Ribeiro 乌雅罕(译) 张冬雪(译) 牛占岳(校) 刘鑫(校) 丁士刚(译/校) | 2020 | 中华胃肠内镜电子杂志2020，7，2： | 10 |
| 8 | Autoimmune gastritis:Pathologist's viewpoint显示文摘Western countries are seeing a constant decline in the incidence of Helicobacter pylori-associated gastritis, coupled with a rising epidemiological and clinical impact of autoimmune gastritis. This latter gastropathy is due to autoimmune aggression targeting parietal cells through a complex interaction of auto-antibodies against the parietal cell proton pump and intrinsic factor, and sensitized T cells. Given the specific target of this aggression, autoimmune gastritis is typically restricted to the gastric corpus-fundus mucosa. In advanced cases, the oxyntic epithelia are replaced by atrophic(and metaplastic) mucosa, creating the phenotypic background in which both gastric neuroendocrine tumors and(intestinal-type) adenocarcinomas may develop. Despite improvements in our understanding of the phenotypic changes or cascades occurring in this autoimmune setting, no reliable biomarkers are available for identifying patients at higher risk of developing a gastric neoplasm. The standardization of autoimmune gastritis histology reports and classifications in diagnostic practice is a prerequisite for implementing definitive secondary prevention strategies based on multidisciplinary diagnostic approaches integratingendoscopy, serology, histology and molecular profiling. | Irene Coati Matteo Fassan Fabio Farinati David Y Graham Robert M Genta Massimo Rugge | 2015 | World Journal of Gastroenterology2015，21，42： | 8 |
| 9 | Hybrid therapy for Helicobacter pylori infection:A systemic review and meta-analysis显示文摘AIM: To compare the effectiveness of hybrid therapy with other recommended regimens using metaanalysis.METHODS: Bibliographical searches for randomized trials comparing hybrid and other therapies were performed in Pubmed, the Cochrane Library and relevant congresses up to February 2015 using the following keywords(all fields and/or me SH):('Helicobacter pylori ' or 'H. pylori') and('hybrid therapy' or 'sequential-concomitant therapy'). metaanalyses were performed with Cochrane Review manager 5.1. The random effect model proposed by Der Simonian and Laird and the mantel-Haenszel method were used to estimate the pooled relative risk and 95%CI of the efficacy outcomes between hybrid therapy and other eradication therapies. RESULTS: Eight studies(2516 subjects) met entry criteria. The antimicrobial resistance in the study groups ranged from 6.9% to 23.5%. The mean cure rates of hybrid therapy by intention-to-treat(ITT) and perprotocol analyses were 88.5%(n = 1207; range: 80.0% to 97.4%) and 93.3%(n = 1109; range: 85.7% to99.1%), respectively. meta-analysis showed there was no significant difference in ITT eradication rate between hybrid and sequential therapy(relative risk: 1.01; 95%CI: 0.92-1.11). Subgroup analysis revealed hybrid therapy was more effective than sequential therapy in the non-Italian populations(95%CI: 1.01-1.18) and was only less effective in one, Italian population(95%CI: 0.83-0.98). There was no significant difference in eradication rate between hybrid therapy and concomitant therapy(95%CI: 0.93-1.02). No head-tohead comparisons of hybrid therapy and standard triple therapy or bismuth quadruple therapy were found. However, a multicenter, randomized trial showed that reverse hybrid therapy was superior to standard triple therapy(95.5% vs 88.6% ITT; P = 0.011).CONCLUSION: Hybrid therapy appears to be an effective, safe, and well-tolerated treatment for H. pylori infection in the era of increasing antibiotic resistance. | Ping-I Hsu Pei-Chin Lin David Y Graham | 2015 | World Journal of Gastroenterology2015，21，45： | 8 |
| 10 | Sequential and Concomitant Therapy With Four Drugs Is Equally Effective for Eradication of H pylori Infection显示文摘 | Deng–Chyang Wu Ping–I. Hsu Jeng–Yih Wu Antone R. Opekun Chao–Hung Kuo I.–Chen Wu Sophie S.W. Wang Angela Chen Wen–Chun Hung David Y. Graham | 2010 | Clinical Gastroenterology and Hepatology2010，，1： | 7 |
| 11 | All-silicon carrier accumulation modulator based on a lateral metal-oxide-semiconductor capacitor显示文摘In silicon photonics, the carrier depletion scheme has been the most commonly used mechanism for demonstrating high-speed electro-optic modulation. However, in terms of phase modulation efficiency, carrieraccumulation-based devices potentially offer almost an order of magnitude improvement over those based on carrier depletion. Previously reported accumulation modulator designs only considered vertical metal-oxidesemiconductor(MOS) capacitors, which imposes serious restrictions on the design flexibility and integratability with other photonic components. In this work, for the first time to our knowledge, we report experimental demonstration of an all-silicon accumulation phase modulator based on a lateral MOS capacitor. Using a Mach–Zehnder interferometer modulator with a 500-μm-long phase shifter, we demonstrate high-speed modulation up to 25 Gbit∕s with a modulation efficiency(V_πL_π) of 1.53 V·cm. | KAPIL DEBNATH DAVID J.THOMSON WEIWEI ZHANG ALI Z.KHOKHAR CALLUM LITTLEJOHNS JAMES BYERS LORENZO MASTRONARDI MUHAMMAD K.HUSAIN KOUTA IBUKURO FREOERIC Y.GARDES GRAHAM T,REED SHINICHI SAITO | 2018 | Photonics Research2018，6，5： | 6 |
| 12 | Rational Helicobacter pylori therapy: evidence based medicine rather than medicine based evidence显示文摘 | David Y. Graham Yi-Chia Lee Ming-Shiang Wu | 2013 | Clinical Gastroenterology and Hepatology2013，，： | 6 |
| 13 | Diversity and production in an Afromontane Forest显示文摘Background:This contribution evaluates the effect of forest structure and tree species diversity on plot productivity and individual tree growth in the unique Knysna forests in Southern Africa using mapped tree data from an observational study that has been re-measured over a period of 40 years.Methods:The effects of tree species diversity and forest structure on tree growth and forest production are evaluated on three levels of resolution:a) the forest community(canopy,sub-canopy species),b) the subplots(number of trees per ha,skewness of the diameter distribution,diameter coefficient of variation) and c) the immediate neighborhood of selected reference trees('Mingling','Dominance',Aggregation' and 'Size Variation').Results:An analysis of the community level identified two distinct clusters,one including dominant/canopy species with the highest growth rates and a greater variation of growth,and another cluster which includes the remaining subcanopy species which have a smaller maximum size and lower rates of growth.The area-based structure variables on plot level have a highly significant effect on total basal area growth.However,the effects of forest density and species richness on productivity were not straight forward.Maximum basal area production of about 0.75 m^2/ha/year is achieved at medium levels of richness(around 20 species per ha) and medium levels of density(around 30 m^2/ha basal area) using percentile regression estimates.The relative 'Dominance' of a selected reference tree had a highly significant effect on individual tree growth on all investigated species.Other neighbourhood structure variables were only occasionally significant or not significant at all.Conclusion:This contribution presents a new theoretical framework for analysing natural forests that includes community,plot and neighborhood variables of forest structure and diversity,and a first specific analysis of the structure and dynamics of the Knysna Afromontane Forest,based on a unique set of longterm observations.The species-area(SAR) model developed in this study,represents a new general approach that can be used to derive a common standard of tree species diversity for different plot sizes,the species richness per hectare. | Klaus v.Gadow GongQiao Zhang Graham Durrheim David Drew Armin Seydack | 2016 | Forest Ecosystems2016，3，4： | 5 |
| 14 | Metachronous gastric cancer after successful Helicobacter pylori eradication显示文摘The high incidence of gastric cancer in Japan initially resulted in establishment of a country-wide gastric cancer screening program to detect early and treatable cancers. In 2013 countrywide Helicobacter pylori(H. pylori) eradication was approved coupled with endoscopy to assess for the presence of chronic gastritis. Current data support the notion that cure of the infection in those with non-atrophic gastritis will prevent development of gastric cancer. However, while progression to more severe damage is halted in those who have already developed, atrophic gastritis/gastric atrophy remain at risk for subsequent development of gastric cancer. That risk is directly related to the extent and severity of atrophic gastritis. Methods to stratify cancer risk include those based on endoscopic assessment of the atrophic border, histologic grading, and non-invasive methods based on serologic testing of pepsinogen levels. Continued surveillance is required because those with atrophic gastritis/gastric atrophy retain considerable gastric cancer risk even after H. pylori eradication. Those who have already experienced a resectable early gastric cancer are among those at highest risk as metachronous lesions are frequent even after H. pylorieradication. We review the role of H. pylori and effect of H. pylori eradication indicating the incidence and the predictive factors on development of metachronous cancer after endoscopic therapy of early gastric cancer. Studies to refine risk markers to stratify for risk, surveillance methods, intervals, and duration after successful H. pylori eradication, and whether adjuvant therapy would change risk are needed. | Akiko Shiotani Ken Haruma David Y Graham | 2014 | World Journal of Gastroenterology2014，20，33： | 5 |
| 15 | Clinical Performance of an Automated Stool DNA Assay for Detection of Colorectal Neoplasia显示文摘 | Graham P. Lidgard Michael J. Domanico Janelle J. Bruinsma James Light Zubin D. Gagrat Rebecca L. Oldham-Haltom Keith D. Fourrier Hatim Allawi Tracy C. Yab Julie A. Simonson Mary Devens Russell I. Heigh David A. Ahlquist Barry M. Berger | 2013 | Clinical Gastroenterology and Hepatology2013，，： | 5 |
| 16 | The Stool DNA Test Is More Accurate Than the Plasma Septin 9 Test in Detecting Colorectal Neoplasia显示文摘 | David A. Ahlquist William R. Taylor Douglas W. Mahoney Hongzhi Zou Michael Domanico Stephen N. Thibodeau Lisa A. Boardman Barry M. Berger Graham P. Lidgard | 2012 | Clinical Gastroenterology and Hepatology2012，，3： | 4 |
| 17 | Helicobacter pylori Infection – A Boon or a Bane: Lessons from Studies in a Low‐Prevalence Population显示文摘 | Yeong Yeh Lee Sundramoorthy Mahendra Raj David Y. Graham | 2013 | Helicobacter2013，，5： | 4 |
| 18 | Incubation Phase of Acute Hepatitis B in Man: Dynamic of Cellular Immune Mechanisms显示文摘 | George J.M. Webster Stephanie Reignat Mala K. Maini Simon A. Whalley Graham S. Ogg Abigail King David Brown Peter L. Amlot Roger Williams Diego Vergani Geoffrey M. Dusheiko Antonio Bertoletti | 2000 | Hepatology2000，，5： | 4 |
| 19 | Regulation of proprietary traditional Chinese medicines in Australia显示文摘This review article describes the regulation of proprietary Chinese medicines for the Australian market, which may permit many medicines used in Traditional Chinese Medicine to have a simplified process of market access provided that certain criteria for acceptable public safety are met. | David T. Graham | 2017 | Chinese Journal of Natural Medicines2017，15，1： | 4 |
| 20 | 治疗 幽门螺杆菌根治后应用质子泵抑制剂可能增加胃癌发病风险显示文摘背景 幽门螺杆菌感染是胃癌发生最常见的诱因。幽门螺杆菌根治是否能降低或消除胃癌发病风险取决于根治时的风险。对于有黏膜损害和胃酸过少者,幽门螺杆菌根治可恢复泌酸。幽门螺杆菌根治后应用质子泵抑制剂(PPI)可极度减少胃酸分泌。然而,幽门螺杆菌根治后应用PPI对于胃癌发生风险的影响仍不清楚。 | Mimi Chang Tan David Y Graham 霍永丰(译) | 2018 | 英国医学杂志中文版2018，21，11： | 3 |
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