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| 1 | Diagnosis of alcoholic liver disease显示文摘Alcohol is a hepatotoxin that is commonly consumed worldwide and is associated with a spectrum of liver injury including simple steatosis or fatty liver, alcoholic hepatitis, fibrosis, and cirrhosis. Alcoholic liver disease(ALD) is a general term used to refer to this spectrum of alcohol-related liver injuries. Excessive or harmful alcohol use is ranked as one of the top five risk factors for death and disability globally and results in 2.5 million deaths and 69.4 million annual disability adjusted life years. All patients who present with clinical features of hepatitis or chronic liver disease or who have elevated serum elevated transaminase levels should be screened for an alcohol use disorder. The diagnosis of ALD can generally be made based on history, clinical and laboratory findings. However, the diagnosis of ALD can be clinically challenging as there is no single diagnostic test that confirms the diagnosis and patients may not be forthcoming about their degree of alcohol consumption. In addition, clinical findings may be absent or minimal in early ALD characterized by hepatic steatosis. Typical laboratory findings in ALD include transaminase levels with aspartate aminotransferase greater than alanine aminotransferase as well as increased mean cor-puscular volume, gamma-glutamyltranspeptidase, and IgA to IgG ratio. In unclear cases, the diagnosis can be supported by imaging and liver biopsy. The histological features of ALD can ultimately define the diagnosis according to the typical presence and distribution of hepatic steatosis, inflammation, and Mallory-Denk bodies. Because of the potential reversible nature of ALD with sobriety, regular screening of the general population and early diagnosis are essential. | Cara Torruellas Samuel W French Valentina Medici | 2014 | World Journal of Gastroenterology2014，20，33： | 26 |
| 2 | Alcohol,nutrition and liver cancer:Role of Toll-like receptor signaling显示文摘This article reviews the evidence that ties the development of hepatocellular carcinoma (HCC) to the natural immune pro-inflammatory response to chronic liver disease, with a focus on the role of Toll-like receptor (TLR) signaling as the mechanism of liver stem cell/progenitor transformation to HCC. Two exemplary models of this phenomenon are reviewed in detail. One model applies chronic ethanol/lipopolysaccharide feeding to the activated TLR4 signaling pathway. The other applies chronic feeding of a carcinogenic drug, in which TLR2 and 4 signaling pathways are activated. In the drug-induced model, two major methyl donors, S-adenosylmethionine and betaine, prevent the upregulation of the TLR signaling pathways and abrogate the stem cell/progenitor proliferation response when fed with the carcinogenic drug. This observation supports a nutritional approach to liver cancer prevention and treatment. The observation that upregulation of the TLR signaling pathways leads to liver tumor formation gives evidence to the popular concept that the chronic pro-inflammatory response is an important mechanism of liver oncogenesis. It provides a nutritional approach, which could prevent HCC from developing in many chronic liver diseases. | Samuel W French Joan Oliva Barbara A French Fawzia Bardag-Gorce | 2010 | World Journal of Gastroenterology2010，16，11： | 11 |
| 3 | 改良DBL法测定稻米中的赖氨酸含量显示文摘 | 王红梅 刘巧泉 Joyce W C Ma Samuel S M Sun | 2002 | 扬州大学学报(农业与生命科学版)2002，23，4： | 5 |
| 4 | Chaperones in hepatitis C virus infection显示文摘The hepatitis C virus(HCV) infects approximately 3% of the world population or more than 185 million people worldwide. Each year, an estimated 350000-500000 deaths occur worldwide due to HCV-associated diseases including cirrhosis and hepatocellular carcinoma. HCV is the most common indication for liver transplantation in patients with cirrhosis worldwide. HCV is an enveloped RNA virus classified in the genus Hepacivirus in the Flaviviridae family. The HCV viral life cycle in a cell can be divided into six phases:(1) binding and internalization;(2) cytoplasmic release and uncoating;(3) viral polyprotein translation and processing;(4) RNA genome replication;(5) encapsidation(packaging) and assembly; and(6) virus morphogenesis(maturation) and secretion. Many host factors are involved in the HCV life cycle. Chaperones are an important group of host cytoprotective molecules that coordinate numerous cellular processes including protein folding, multimeric protein assembly, protein trafficking, and protein degradation. All phases of the viral life cycle require chaperone activity and the interaction of viral proteins with chaperones. This review will present our current knowledge and understanding of the role of chaperones in the HCV life cycle. Analysis of chaperones in HCV infection will provide further insights into viral/host interactions and potential therapeutic targets for both HCV and other viruses. | Ronik Khachatoorian Samuel W French | 2016 | World Journal of Hepatology2016，8，1： | 5 |
| 5 | Season of the year influences infection rates following total hip arthroplasty显示文摘AIM To research the influence of season of the year on periprosthetic joint infections.METHODS We conducted a retrospective review of the entire Medicare files from 2005 to 2014. Seasons were classified as spring, summer, fall or winter. Regional variations were accounted for by dividing patients into four geographic regions as per the United States Census Bureau(Northeast, Midwest, West and South). Acute postoperative infection and deep periprosthetic infections within 90 d after surgery were tracked. RESULTS In all regions, winter had the highest incidence of periprosthetic infections(mean 0.98%, SD 0.1%) and was significantly higher than other seasons in the Midwest, South and West(P < 0.05 for all) but not the Northeast(P = 0.358). Acute postoperative infection rates were more frequent in the summer and were significantly affected by season of the year in the West.CONCLUSION Season of the year is a risk factor for periprosthetic joint infection following total hip arthroplasty(THA). Understanding the influence of season on outcomes following THA is essential when risk-stratifying patients to optimize outcomes and reduce episode of care costs. | Samuel Rosas Alvin C Ong Leonard T Buller Karim G Sabeh Tsun yee Law Martin W Roche Victor H Hernandez | 2017 | World Journal of Orthopedics2017，8，12： | 4 |
| 6 | Epigenetics of proteasome inhibition in the liver of rats fed ethanol chronically显示文摘AIM:To examine the effects of ethanol-induced proteasome inhibition,and the effects of proteasome inhibition in the regulation of epigenetic mechanisms. METHODS:Rats were fed ethanol for 1 mo using the Tsukamoto-French model and were compared to rats given the proteasome inhibitor PS-341(Bortezomib, Velcade?)by intraperitoneal injection.Microarray analysis and real time PCR were performed and proteasome activity assays and Western blot analysis were performed using isolated nuclei. RESULTS:Chronic ethanol feeding caused a significant inhibition of the ubiquitin proteasome pathway in the nucleus,which led to changes in the turnover of transcriptional factors,histone-modifying enzymes, and,therefore,affected epigenetic mechanisms. Chronic ethanol feeding was related to an increase in histone acetylation,and it is hypothesized that the proteasome proteolytic activity regulated histone modifications by controlling the stability of histone modifying enzymes,and,therefore,regulated the chromatin structure,allowing easy access to chromatin by RNA polymerase,and,thus,proper gene expression.Proteasome inhibition by PS-341 increased histone acetylation similar to chronic ethanol feeding. In addition,proteasome inhibition caused dramatic changes in hepatic remethylation reactions as there was a significant decrease in the enzymes responsible for the regeneration of S-adenosylmethionine,and, in particular,a significant decrease in the betaine- homocysteine methyltransferase enzyme.This suggested that hypomethylation was associated with proteasome inhibition,as indicated by the decrease in histone methylation. CONCLUSION:The role of proteasome inhibition in regulating epigenetic mechanisms,and its link to liver injury in alcoholic liver disease,is thus a promising approach to study liver injury due to chronic ethanol consumption. | Joan Oliva Jennifer Dedes Samuel W French Fawzia Bardag-Gorce | 2009 | World Journal of Gastroenterology2009，15，6： | 4 |
| 7 | Langerhans cell histiocytosis masquerading as acute appendicitis: Case report and review显示文摘Langerhans cell histiocytosis(LCH) is a rare syndrome characterized by unifocal,multifocal unisystem,or disseminated/multi-system disease that commonly involves the bone,skin,lymph nodes,pituitary,or sometimes lung(almost exclusively in smokers) causing a variety of symptoms from rashes and bone lesions to diabetes insipidus or pulmonary infiltrates.We present a previously unreported case of gastrointestinal LCH as well as a novel characteristic lesion affecting the colon of a young woman who presented with signs and symptoms mimicking acute on chronic appendicitis.Immunohistochemical analysis of appendectomy specimen and nodular specimens on colonoscopy demonstrated S-100,CD1a,and langerin reactivity.The patient underwent systemic chemotherapy with cytarabine and demonstrated excellent response to therapy. | Mohammad M Karimzada Michele N Matthews Samuel W French Daniel De Ugarte Dennis Y Kim | 2017 | World Journal of Gastrointestinal Endoscopy2017，9，3： | 3 |
| 8 | 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 |
| 9 | 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 |
| 10 | 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 |
| 11 | Chromism and luminescence in regioregular poly(3-dodecylthiophene)显示文摘 | Rumbles G Samuel I D W Magnani L | 1996 | Synthetic Metals1996，76，： | 1 |
| 12 | Evalutation of cytokine gene expression in porcine spleen cells, peripheral blood mononuclear cells, and alveolar macrophages by competitive RT-PCR显示文摘 | In-Soo C Ellen W C Samuel K M | 2002 | FEMS Immunol Med Microbiol2002，34，： | 1 |
| 13 | Observation of a non-constant mean curvature interface in an ABC tribloek copolymer显示文摘 | Samuel P Gido Dwight W Schwark Edwin L Thomas | 1993 | Macromolecules1993，26，： | 1 |
| 14 | Effect of solution heat treatment and additives on the microstructure of Al-Si automotive alloys显示文摘 | MOUSTAFA M A SAMUEL F H DOTY H W | 2004 | Materials Science Forum2004，，1： | 1 |
| 15 | Femtosecond transient absorption measurements in poly(arylenevinylene)s 显示文摘 | Samuel D W Raksi F Bradley D D C | 1993 | Synthetic Metals1993，，55： | 1 |
| 16 | Investment efficiency:a comprehensive ROI显示文摘 | McDowell Samuel W | 2001 | Industrial Management2001，43，1： | 1 |
| 17 | Fascioloides magna in white tailed deer ( Odocoileus virginianus ) : observations on thepairing tendency显示文摘 | Foreyt W J Samuel W M Todd A C | 1977 | J Parasitol1977，63，： | 1 |
| 18 | Iron intermetallie phases in the A1 comer of the A1-Si-Fe system显示文摘 | KHALIFA W SAMUEL F H GRUZLESKI J E | 2003 | Metallurgical and Materials Transactions A2003，34，13： | 1 |
| 19 | A photoactivatable push-pull fluorophore for single-molecule imaging in live cells显示文摘 | Lord S J Conley N R Lee H L D Samuel R Liu N Twieg R J Moerner W E | | 0，，29： | 1 |
| 20 | An overview of the femtocell concept显示文摘 | Claussen H Ho L T W Samuel L G | 2008 | Bell Labs Technical Journal2008，13，1： | 1 |
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