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| 1 | Advances in immuno-oncology biomarkers for gastroesophageal cancer:programmed death ligand 1,microsatellite instability,and beyond显示文摘Blockade of the programmed death ligand 1(PD-L1) and programmed cell death 1(PD-1) receptor axis represents an effective form of cancer immunotherapy. Preclinical evidence initially suggested that gastric and gastroesophageal junction(GEJ) cancers are potentially immunotherapy-sensitive tumors. Early phase clinical trials have demonstrated promising antitumor activity with PD-1/PD-L1 blockade in advanced or metastatic gastric/GEJ cancer. Microsatellite instability(MSI) and PD-L1 expression have been shown to predict higher response to PD-1 inhibitors as highlighted by the recent approvals of pembrolizumab in treatmentrefractory solid tumors with MSI status and the thirdline or greater treatment of PD-L1 positive advanced gastric/GEJ cancers. However, predictive and prognostic biomarkers remain an ongoing need. In this review, we detail the preclinical evidence and early tissue biomarker analyses illustrating potential predictive biomarkers to PD-1/PD-L1 blockade in gastric/GEJ cancer. We also review the clinical development of PD-1/PD-L1 inhibitors in gastric/GEJ cancer and highlight several areas in need of future investigation in order to optimize the efficacy of PD-1/PD-L1 blockade in gastric/GEJ cancer. | Emily M Lin Jun Gong Samuel J Klempner Joseph Chao | 2018 | World Journal of Gastroenterology2018，24，25： | 10 |
| 2 | 大气二氧化氮与每日总死亡率、心血管和呼吸系统疾病死亡率的短期关联:398个城市的多中心分析显示文摘目的:采用统一的分析方案,评估全球多个国家/地区的二氧化氮(NO_(2))与总死亡率、心血管和呼吸系统疾病死亡率之间的短期关联。研究设计:采用两阶段的时间序列分析方法、过度离散的广义线性模型和多水平meta分析。研究地点:22个低到高收入国家/地区的398个城市。主要结局指标:1973—2018年逐日总死亡人数(6280万人)、心血管疾病死亡人数(1970万人)和呼吸系统疾病死亡人数(550万人)。结果:平均而言,NO_(2)浓度在滞后1天(前1天)每增加10μg/m^(3),会导致总死亡率、心血管和呼吸系统疾病死亡率分别增加0.46%(95%可信区间0.36%~0.57%)、0.37%(0.22%~0.51%)、0.47%(0.21%~0.72%)。在对共污染物(PM_(10)、PM_(2.5)、臭氧、二氧化硫和一氧化碳)进行调整后,这些关联仍然很稳定。所有3种死因的暴露-反应曲线几乎是线性的,没有明显的阈值。在398个城市中,可归因于高过假定零水平的NO_(2)浓度造成的死亡比例为1.23%(95%可信区间0.96%~1.51%)。结论:这项多中心研究提供了关于NO_(2)短期暴露与总死亡率、心血管和呼吸系统死亡风险之间的独立和线性关联的关键证据,说明通过加强NO_(2)的控制和监管限制标准,可获得人群水平的健康收益。 | 孟夏 刘聪(校) 陈仁杰 郑湃(译) 阚海东(校) Francesco Sera Ana Vicedo-Cabrera Ai Milojevic Maria Guo Yuming Tong Shilu Micheline de Sousa Zanotti Stagliorio Coelh Paulo Hilario Nascimento Saldiva Eric Lavigne Patricia Matus Correa Nicolas Valdes Ortega Samuel Osorio Garcia Jan Kysely Ales Urban Hans Orru Marek Maasikmets Jouni J K Jaakkola Niilo Ryti Veronika Huber Alexandra Schneider Klea Katsouyanni Antonis Analitis Masahiro Hashizume Yasushi Honda Chris Fook Sheng Ng Baltazar Nunes João Paulo Teixeira Iulian Horia Holobaca Simona Fratianni Ho Kim Aurelio Tobias Carmeníniguez Bertil Forsberg ChristoferÅström Martina S Ragettli Yue-Liang Leon Guo Shih-Chun Pan Shanshan Li Michelle L Bell Antonella Zanobetti Joel Schwartz Tangchun Wu Antonio Gasparrini | 2021 | 英国医学杂志中文版2021，24，8： | 7 |
| 3 | Gastroenterologist perceptions of faecal microbiota transplantation显示文摘AIM: To explore gastroenterologist perceptions towards and experience with faecal microbiota transplantation(FMT).METHODS: A questionnaire survey consisting of 17 questions was created to assess gastroenterologists' attitude towards and experience with FMT. This was anonymously distributed in hard copy format amongst attendees at gastroenterology meetings in Australia between October 2013 and April 2014. Basic descriptive statistical analyses were performed.RESULTS: Fifty-two clinicians participated. Twenty one percent had previously referred patients for FMT,8% more than once. Ninety percent would refer patients with Clostridium difficile infection(CDI) for FMT if easily available,37% for ulcerative colitis,13% for Crohn's disease and 6% for irritable bowel syndrome. Six percent would not refer any indication,including recurrent CDI. Eighty-six percent would enroll patients in FMT clinical trials. Thirty-seven percent considered the optimal mode of FMT administration transcolonoscopic,17% nasoduodenal,13% enema and 8% oral capsule. The greatest concerns regarding FMT were: 42% lack of evidence,12% infection risk,10% non infectious adverse effects/lack of safety data,10% aesthetic,10% lack of efficacy,4% disease exacerbation,and 2% inappropriate use; 6% had no concerns. Seventy seven percent believed there is a lack of accessibility while 52% had an interest in learning how to provide FMT. Only 6% offered FMT at their institution.CONCLUSION: Despite general enthusiasm,most gastroenterologists have limited experience with,or access to,FMT. The greatest concerns were lack of supportive evidence and safety issues. However a significant proportion would refer indications other than CDI for FMT despite insufficient evidence. These data provide guidance on where education and training are required. | Sudarshan Paramsothy Alissa J Walsh Thomas Borody Douglas Samuel Johan van den Bogaerde Rupert WL Leong Susan Connor Watson Ng Hazel M Mitchell Nadeem O Kaakoush Michael A Kamm | 2015 | World Journal of Gastroenterology2015，21，38： | 5 |
| 4 | Computational fluid dynamics simulation on the longwall gob breathing显示文摘In longwall mines, atmospheric pressure fluctuations can disturb the pressure balance between the gob and the ventilated working area, resulting in a phenomenon known as ‘‘gob breathing'. Gob breathing triggers gas flows across the gob and the working areas and may result in a condition where an oxygen deficient mixture or a methane accumulation in the gob flows into the face area. Computational Fluid Dynamics(CFDs) modeling was carried out to analyze this phenomenon and its impact on the development of an explosive mixture in a bleeder-ventilated panel scheme. Simulation results indicate that the outgassing and ingassing across the gob and the formation of Explosive Gas Zones(EGZs) are directly affected by atmospheric pressure changes. In the location where methane zones interface with mine air, EGZ fringes may form along the face and in the bleeder entries. These findings help assess the methane ignition and explosion risks associated with fluctuating atmospheric pressures. | Samuel A.Lolon Jürgen F.Brune Gregory E.Bogin Jr. John W.Grubb Saqib A.Saki Aditya Juganda | 2017 | International Journal of Mining Science and Technology2017，27，2： | 5 |
| 5 | Effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase III study: 5-year analysis of the EORTC-NCIC trial显示文摘 | Roger Stupp Monika E Hegi Warren P Mason Martin J van den Bent Martin JB Taphoorn Robert C Janzer Samuel K Ludwin Anouk Allgeier Barbara Fisher Karl Belanger Peter Hau Alba A Brandes Johanna Gijtenbeek Christine Marosi Charles J Vecht Karima Mokhtari Piet | 2009 | Lancet Oncology2009，，5： | 4 |
| 6 | Failure of P-selectin blockade alone to protect the liver from ischemia-reperfusion injury in the isolated blood-perfused rat liver显示文摘AIM:To determine if blockade of P-selectin in the isolated blood-perfused cold ex vivo rat liver model protects the liver from ischemia-reperfusion injury. METHODS:The effect of P-selectin blockade was assessed by employing an isolated blood-perfused cold ex vivo rat liver with or without P-selectin antibody treatment before and after 6 h of cold storage in University of Wisconsin solution. RESULTS:In our isolated blood-perfused rat liver model,pre-treatment with P-selectin antibody failed to protect the liver from ischemia-reperfusion injury,as judged by the elevated aspartate aminotransferase activity. In addition,P-selectin antibody treatment did not significantly reduced hepatic polymorphonuclear leukocyte accumulation after 120 min of perfusion. Histological evaluation of liver sections obtained at 120 min of perfusion showed significant oncotic necrosis in liver sections of both ischemic control and P-selectin antibody-treated groups. However,total bile production after 120 min of perfusion was signifi cantly greater in P-selectin antibody-treated livers,compared to control livers. No signifi cant difference in P-selectin and ICAM-1 mRNAs and proteins,GSH,GSSG,and nuclear NF-κB was found between control and P-selectin antibody-treated livers. CONCLUSION:In conclusion,we have shown that blockade of P-selectin alone failed to reduced polymorphonuclear leukocyte accumulation in the liver and protect hepatocytes from ischemia-reperfusion injury in the isolated blood-perfused cold-ex vivo rat liver model. | Samuel Wyllie Neal R Barshes Saul J Karpen John A Goss | 2008 | World Journal of Gastroenterology2008，14，44： | 4 |
| 7 | Electrocardiographic markers of cardiac resynchronization therapy response:delayed time to intrinsicoid deflection onset in lateral leads显示文摘Cardiac resynchronization therapy(CRT)has emerged as an important intervention for patients with heart failure(HF)with reduced ejection fraction and delayed ventricular activation.In these patients,CRT has demonstrated to improve quality of life,promote reverse left ventricular(LV)remodeling,reduce HF hospitalizations,and extend survival.However,despite advancements in our understanding of CRT,a significant number of patients do not respond to this therapy.Several invasive and non-invasive parameters have been assessed to predict response to CRT,but the electrocardiogram(ECG)has remained as the prevailing screening method albeit with limitations.Ideally,an accurate,simple,and reproducible ECG marker or set of markers would dramatically overcome the current limitations.We describe the clinical utility of an old ECG parameter that can estimate ventricular activation delay:the onset to intrinsicoid deflection(ID).Based on the concept of direct measurement of ventricular activation time(intrinsic deflection onset),time to ID onset measures on the surface ECG the time that the electrical activation time takes to reach the area subtended by the corresponding surface ECG lead.Based on this principle,the time to ID on the lateral leads can estimate the delay activation to the lateral LV wall and can be used as a predictor for CRT response,particularly in patients with non-specific intraventricular conduction delay or in patients with left bundle branch block and QRS<150 ms.The aim of this review is to present the current evidence and potential use of this ECG parameter to estimate LV activation and predict CRT response. | Rubén KA Tapia-Orihuela S Michael Gharacholou Samuel J Asirvatham Freddy Del-Carpio Munoz | 2022 | Journal of Geriatric Cardiology2022，19，1： | 3 |
| 8 | Immune checkpoint inhibitor-mediated colitis in gastrointestinal malignancies and inflammatory bowel disease显示文摘Immune checkpoint inhibitors(ICI)have markedly changed the landscape of cancer therapy.By re-invigorating the immune system against tumors,ICI provide novel therapeutic options for a broad variety of malignancies,including many gastrointestinal(GI)cancers.However,these therapies can also induce autoimmune-like side effects in healthy tissue across the body.One of the most common of these side effects is ICI-mediated colitis and diarrhea(IMC).Here,we review the incidence and risk of IMC in ICI therapy,with a focus on what is known regarding IMC in patients with GI malignancies.We also discuss data available on the use of ICI and risk of IMC in patients with pre-existing inflammatory bowel disease,as these patients may have increased risk of IMC due to their underlying intestinal pathology. | Alexa R Weingarden Samuel J S Rubin John Gubatan | 2021 | World Journal of Gastrointestinal Oncology2021，13，8： | 3 |
| 9 | p53-mediated transcriptional regulation and activation of the actin cytoskeleton regulatory RhoC to LIMK2 signaling pathway promotes cell survival显示文摘响应 DNA 损坏的房间命运的中央仲裁人是 p53,它调整涉及房间周期拘捕,幸存和 apoptosis 的基因的表示。尽管 DNA 损坏开始的许多回答被描绘了,肌动朊细胞骨架管理者的角色大部分是未知的。我们现在显示出那 RhoC 和秘鲁利玛机场之代号 kinase (LIMK2 ) 2 是 genotoxic 代理人导致的直接 p53 目标基因。尽管 RhoC 和 LIMK2 在肌动朊细胞骨架规定有生长得很好的角色,我们的结果显示 LIMK2 的激活也有支持幸存的功能追随者 DNA 损坏。由调停 siRNA 的击倒或选择的药理学封锁的 LIMK 抑制敏化房间到无线电 -- 或化疗,以便当与 LIMK 抑制结合了时,当单身地管理了时,是尚不致命的治疗导致了房间死亡。我们的调查结果建议把 LIMK 禁止者与 genotoxic 治疗相结合能比单个代理人的管理更有效,并且加亮在肌动朊细胞骨架管理者和 DNA 之间的一个新奇连接导致损坏的房间幸存机制。 | Daniel R Croft Diane Crighton Michael S Samuel Filipe C Lourenco June Munro Jenifer Wood Karim Bensaad Karen H Vousden Owen J Sansom Kevin M Ryan Michael F Olson | 2011 | Cell Research2011，21，4： | 3 |
| 10 | Staining for p53 and Ki-67 increases the sensitivity of EUS-FNA to detect pancreatic malignancy显示文摘AIM:To investigate whether tumor marker staining can improve the sensitivity of endoscopic ultrasound-guided fine needle aspiration(EUS-FNA)to diagnose pancreatic malignancy. METHODS:Patients who underwent EUS-FNA were retrospectively identified.Each EUS-FNA specimen was evaluated by routine cytology and stained for tumor markers p53,Ki-67,carcinoembryonic antigen(CEA) and CA19-9.Sensitivity,specificity,positive and negative predictive values(PPV and NPV),and positive and negative likelihood ratios(PLR and NLR)were calculated in order to evaluate the performance of each test to detect malignancy. RESULTS:Sixty-one specimens had complete sets of stains,yielding 49 and 12 specimens from pancreatic adenocarcinomas and benign pancreatic lesions due to pancreatitis,respectively.Cytology alone had sensitivity and specificity of 41%and 100%to detect malignancy, respectively.In 46%of the specimens,routine cytology alone was deemed indeterminate.The addition of either p53 or Ki-67 increased the sensitivity to 51%and 53%,respectively,with perfect specificity,PPV and PLR (100%,100%and infinite).Both stains in combination increased the sensitivity to 57%.While additional staining with CEA and CA19-9 further increased the sensitivity to 86%,the specificity,PPV and PLR were significantly reduced(at minimum 42%,84%and 1,respectively).Markers in all combinations performed poorly as a negative test(NPV 26%to 47%,and NLR 0.27 and 0.70).CONCLUSION:Immunohistochemical staining for p53 and Ki-67 can improve the sensitivity of EUS-FNA to diagnose pancreatic adenocarcinoma. | Alexander W Jahng Sonya Reicher David Chung Donna Varela Rahul Chhablani Anil Dev Binh Pham Jose Nieto Rose J Venegas Samuel W French Bruce E Stabile Viktor E Eysselein | 2010 | World Journal of Gastrointestinal Endoscopy2010，2，11： | 3 |
| 11 | Antimicrobial peptides and the gut microbiome in inflammatory bowel disease显示文摘Antimicrobial peptides(AMP)are highly diverse and dynamic molecules that are expressed by specific intestinal epithelial cells,Paneth cells,as well as immune cells in the gastrointestinal(GI)tract.They play critical roles in maintaining tolerance to gut microbiota and protecting against enteric infections.Given that disruptions in tolerance to commensal microbiota and loss of barrier function play major roles in the pathogenesis of inflammatory bowel disease(IBD)and converge on the function of AMP,the significance of AMP as potential biomarkers and novel therapeutic targets in IBD have been increasingly recognized in recent years.In this frontier article,we discuss the function and mechanisms of AMP in the GI tract,examine the interaction of AMP with the gut microbiome,explore the role of AMP in the pathogenesis of IBD,and review translational applications of AMP in patients with IBD. | John Gubatan Derek R Holman Christopher J Puntasecca Danielle Polevoi Samuel JS Rubin Stephan Rogalla | 2021 | World Journal of Gastroenterology2021，27，43： | 3 |
| 12 | Prolonged feeding with guanidinoacetate, a methyl group consumer, exacerbates ethanol-induced liver injury显示文摘AIM To investigate the hypothesis that exposure to guanidinoacetate(GAA, a potent methyl-group consumer) either alone or combined with ethanol intake for a prolonged period of time would cause more advanced liver pathology thus identifying methylation defects as the initiator and stimulator for progressive liver damage.METHODS Adult male Wistar rats were fed the control or ethanolLieber De Carli diet in the absence or presence of GAA supplementation. At the end of 6 wk of the feeding regimen, various biochemical and histological analyses were conducted. RESULTS Contrary to our expectations, we observed that GAA treatment alone resulted in a histologically normal liver without evidence of hepatosteatosis despite persistence of some abnormal biochemical parameters. This protection could result from the generation of creatine from the ingested GAA. Ethanol treatment for 6 wk exhibited changes in liver methionine metabolism and persistence of histological and biochemical defects as reported before. Further, when the rats were fed the GAA-supplemented ethanol diet, similar histological and biochemical changes as observed after 2 wk of combined treatment, including inflammation, macroand micro-vesicular steatosis and a marked decrease in the methylation index were noted. In addition, rats on the combined treatment exhibited increased liver toxicity and even early fibrotic changes in a subset of animals in this group. The worsening liver pathology could be related to the profound reduction in the hepatic methylation index, an increased accumulation of GAA and the inability of creatine generated to exert its hepato-protective effects in the setting of ethanol.CONCLUSION To conclude, prolonged exposure to a methyl consumer superimposed on chronic ethanol consumption causes persistent and pronounced liver damage. | Natalia A Osna Dan Feng Murali Ganesan Priya F Maillacheruvu David J Orlicky Samuel W French Dean J Tuma Kusum K Kharbanda | 2016 | World Journal of Gastroenterology2016，22，38： | 2 |
| 13 | Role of anti-stromal polypharmacy in increasing survival after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma显示文摘AIM: To investigate the survival impact of common pharmaceuticals, which target stromal interactions, following a pancreaticoduodenectomy for pancreatic ductal adenocarcinoma. METHODS: Data was collected retrospectively for 164 patients who underwent a pancreaticoduodenectomy for pancreatic ductal adenocarcinoma(PDAC). Survival analysis was performed on patients receiving the following medications: angiotensin-converting enzyme inhibitors(ACEI)/angiotensin Ⅱ receptor blockers(ARB), calcium channel blockers(CCB), aspirin, and statins. Statistical analysis included Kaplan-meier survival estimates and cox multivariate regression; the latter of which allowed for any differences in a range of prognostic indicators between groups. Medications showing a significant survival benefit were investigated in combination with other medications to evaluate synergistic effects.RESULTS: No survival benefit was observed with respect to ACEI/ARB(n = 41), aspirin or statins on individual drug analysis(n = 39). However, the entire CCB group(n = 26) showed a significant survival benefit on multivariate cox regression; hazard ratio(HR) of 0.475(CI = 0.250-0.902, P = 0.023). Further analysis revealed that this was influenced by a group of patients who were taking aspirin in combination with CCB; median survival was significantly higher in the CCB + aspirin group(n = 15) compared with the group taking neither drug(n = 98); 1414 d vs 601 d(P = 0.029, logrank test). Multivariate cox regression revealed neither aspirin nor CCB had a statistically significant impact on survival when given alone, however in combination the survival benefit was significant; HR = 0.332(CI = 0.126-0.870, P = 0.025). None of the other medications showed a survival benefit in any combination.CONCLUSION: Aspirin + CCB in combination appears to increase survival in patients with PDAC, highlighting the potential clinical use of combination therapy to target stromal interactions in pancreatic cancer. | Samuel J Tingle John A Moir Steven A White | 2015 | World Journal of Gastrointestinal Pathophysiology2015，6，4： | 2 |
| 14 | Safety and efficacy of protease inhibitors to treat hepatitis C after liver transplantation: A multicenter experience显示文摘 | Audrey Coilly Bruno Roche Jér?me Dumortier Vincent Leroy Danielle Botta-Fridlund Sylvie Radenne Georges-Philippe Pageaux Si-Nafaa Si-Ahmed Olivier Guillaud Teresa Maria Antonini Stéphanie Ha?m-Boukobza Anne-Marie Roque-Afonso Didier Samuel Jean-Charles Du | 2014 | Journal of Hepatology2014，，1： | 2 |
| 15 | Sepsis stimulates nonlysosomal,energy-dependent proteolysis and increases ubiquitin mRNA levels in rat skeletal muscle显示文摘 | Tiao G Fagan J M Samuels N | 1994 | J Clin Invest1994，94，： | 2 |
| 16 | Human cord blood-derived cells can differentiate into hepatocytes in the mouse liver with no evidence of cellular fusion显示文摘 | Philip N Newsome Ingolfur Johannessen Shelagh Boyle Evangelos Dalakas Karen A Mcaulay Kay Samuel Frances Rae Lesley Forrester Marc L Turner Peter C Hayes David J Harrison Wendy A Bickmore John N Plevris | 2003 | Gastroenterology2003，，7： | 2 |
| 17 | Biomarker-guided sequential targeted therapies to overcome therapy resistance in rapidly evolving highly aggressive mammary tumors显示文摘组合指向的治疗在由堵住治疗癌症是更有效的绕过机制或导致的合成致命性。然而,他们的临床的申请被抵抗和毒性妨碍。遇见这重要挑战,我们用 ErbB2-overexpressing/PTEN-low 开发了并且测试各种各样的指向的治疗的指导 biomarker 的顺序的应用程序的一个新奇概念,高度好攻击的乳癌作为我们的模型。惊人地,从遗传上设计的鼠标与 intratumoral 异质从病人和乳房的肿瘤在两 PTEN-low/trastuzumab-resistant 乳癌支撑了 ErbB2 和下游的小径驱动器 trastuzumab 抵抗的激活。尽管 lapatinib 开始禁止了 trastuzumab 抵抗的鼠标肿瘤,肿瘤由激活表明由量的蛋白质数组出现的网络的 PI3K/mTOR 绕过抑制。有趣地,小径也是的 mTOR 的激活在 neoadjuvant 观察了表明 lapatinib 抵抗的对待 lapatinib 的病人。Trastuzumab + lapatinib 抵抗被一个 PI3K/mTOR 双 kinase 禁止者(BEZ235 ) 的顺序的申请有效地没有重要毒性克服。然而,我们的 p-RTK 数组分析证明 BEZ235 治疗在遗传上设计的老鼠肿瘤导致了增加的 ErbB2 表示和 phosphorylation,导致 BEZ235 抵抗并且在 3-D,然而并非 2-D,文化。机械学地,我们作为 BEZ235 抵抗的新奇机制识别了 ErbB2 蛋白质稳定和激活,它被随后的治疗与 lapatinib + BEZ235 联合颠倒。显著地, biomarker 指导的指向的治疗的这个顺序的应用程序在很快发展加倍的抵抗的肿瘤改变忍受极其好攻击的肿瘤的鼠标的寿命。使用的这条根本上新奇的途径有效地在一个顺序的顺序罐头指向了治疗目标和改编在在治疗期间发展抵抗的癌症的发信号的网络。 | Ozgur Sahin Qingfei Wang Samuel W Brady Kenneth Ellis Hai Wang Chia-Chi Chang Qingling Zhang Preety Priya Rui Zhu Stephen T Wong Melissa D Landis William J Muller Francisco J Esteva Jenny Chang Dihua Yu | 2014 | Cell Research2014，24，5： | 2 |
| 18 | Cloning and sequencing of a Shiga - like toxin type II variant from Esche- richia coli strain responsible for edema disease of swine 显示文摘 | WEINSTEIN D L JACKSON M P SAMUEL J E | 1988 | Bacteri- ol1988，170，9： | 1 |
| 19 | Binding of shiga toxin 2e to porcine erythrocytes in vivo and in vitro 显示文摘 | Matise I Cornick N A Samuel J E | 2003 | Infect Immun2003，71，： | 1 |
| 20 | Polycyclic aromatic hydrocarbons in sediments and soils from oil exploration areas of the Niger Delta, Nigeria显示文摘 | SAMUEL S O S WANG J Z SONIBARE O O | 2010 | Journal of hazardous materials2010，174，1： | 1 |
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