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| 1 | A complete sequence and comparative analysis of a SARS-associated virus(Isolate BJ01)显示文摘The genome sequence of the Severe Acute Respiratory Syndrome (SARS)-associated virus provides essential information for the identification of pathogen(s), exploration of etiology and evolution, interpretation of transmission and pathogenesis, development of diagnostics, prevention by future vaccination, and treatment by developing new drugs. We report the complete genome sequence and comparative analysis of an isolate (BJ01) of the coronavirus that has been recognized as a pathogen for SARS. The genome is 29725 nt in size and has 11 ORFs (Open Reading Frames). It is composed of a stable region encoding an RNA-dependent RNA polymerase (composed of 2 ORFs) and a variable region representing 4 CDSs (coding sequences) for viral structural genes (the S, E, M, N proteins) and 5 PUPs (putative uncharacterized proteins). Its gene order is identical to that of other known coronaviruses. The sequence alignment with all known RNA viruses places this virus as a member in the family of Coronaviridae. Thirty putative substitutions have been identified by comparative analysis of the 5 SARS- associated virus genome sequences in GenBank. Fifteen of them lead to possible amino acid changes (non-synonymous mutations) in the proteins. Three amino acid changes, with predicted alteration of physical and chemical features, have been detected in the S protein that is postulated to beinvolved in the immunoreactions between the virus and its host. Two amino acid changes have been detected in the Mprotein, which could be related to viral envelope formation. Phylogenetic analysis suggests the possibility of non-human origin of the SARS-associated viruses but provides noevidence that they are man-made. Further efforts should focus on identifying the etiology of the SARS-associated virus and ruling out conclusively the existence of otherpossible SARS-related pathogen(s). | QIN E'de ZHU Qingyu YU Man FAN Baochang CHANG Guohui SI Bingyin YANG Bao PENG Wenming JIANG Tao LIU Bohua DENG Yongqiang LIU Hong ZHANG Yu WANG Cui LI Yuquan GAN Yonghua LI Xiaoyu L Fushuang TAN Gang CAO Wuchun, YANG Ruifu Institute of Microbiology and Epidemiology, Chinese Academy of Military Medical Sciences, Beijing 100071, China WANG Jian, LI Wei, XU Zuyuan, LI Yan, WU Qingfa, LIN Wei, CHEN Weijun, TANG Lin, DENG Yajun, HAN Yujun, LI Changfeng, LEI Meng, LI Guoqing, LI Wenjie, L Hong, SHI Jianping, TONG Zongzhong, ZHANG Feng, LI Songgang, LIU Bin, LIU Siqi, DONG Wei, WANG Jun, Gane K-S Wong, YU Jun & YANG Huanming* Beijing Genomics Institute, Chinese Academy of Sciences, Beijing 101300 National Center for Genome Information, Beijing 101300, China | 2003 | Chinese Science Bulletin2003，48，10： | 121 |
| 2 | Interplay between inflammation,immune system and neuronal pathways:Effect on gastrointestinal motility显示文摘Sepsis is a systemic inflammatory response representing the leading cause of death in critically ill patients,mostly due to multiple organ failure.The gastrointestinal tract plays a pivotal role in the pathogenesis of sepsisinduced multiple organ failure through intestinal barrier dysfunction,bacterial translocation and ileus.In this review we address the role of the gastrointestinal tract,the mediators,cell types and transduction pathways involved,based on experimental data obtained from models of inflammation-induced ileus and (preliminary) clinical data.The complex interplay within the gastrointestinal wall between mast cells,residential macrophages and glial cells on the one hand,and neurons and smooth muscle cells on the other hand,involves intracellular signaling pathways,Toll-like receptors and a plethora of neuroactive substances such as nitric oxide,prostaglandins,cytokines,chemokines,growth factors,tryptases and hormones.Multidirectional signaling between the different components in the gastrointestinal wall,the spinal cord and central nervous system impacts inflammation and its consequences.We propose that novel therapeutic strategies should target inflammation on the one hand and gastrointestinal motility,gas-trointestinal sensitivity and even pain signaling on the other hand,for instance by impeding afferent neuronal signaling,by activation of the vagal anti-inflammatory pathway or by the use of pharmacological agents such as ghrelin and ghrelin agonists or drugs interfering with the endocannabinoid system. | Benedicte Y De Winter Joris G De Man | 2010 | World Journal of Gastroenterology2010，16，44： | 23 |
| 3 | Future prospectives for the management of chronic hepatitis B显示文摘Chronic hepatitis B virus infection affects about 400 million people around the globe and causes approximately one million deaths a year. Since the discovery of interferon-α as a therapeutic option the treatment of hepatitis B has evolved fast and management has become increasingly complicated. The amount of viral replication reflected in the viral load (HBV-DNA) plays an important role in the development of cirrhosis and hepatocellular carcinoma. The current treatment modalities for chronic hepatitis B are immunomodulatory (interferons) and antiviral suppressants (nucleoside and nucleotide analogues) all with their own advantages and limitations. An overview of the treatment efficacy for both immunomodulatory as antiviral compounds is provided in order to provide the clinician insight into the factors influencing treatment outcome. With nucleoside or nucleotide analogues suppression of viral replication by 5-7 log10 is feasible, but not all patients respond to therapy. Known factors influencing treatment outcome are viral load, ALT levels and compliance. Many other factors which might influence treatment are scarcely investigated. Identifying the factors associated with response might result in stopping rules, so treatment could be adapted in an early stage to provide adequate treatment and avoid the development of resistance. The efficacy of compounds for the treatment of mutant virus and the cross- resistance is largely unknown. However, genotypic and phenotypic testing as well as small clinical trials provided some data on efficacy in this population. Discontinuation of nucleoside or nucleotide analogues frequently results in viral relapse; however, some patients have a sustained response. Data on the risk factors for relapse are necessary in order to determine when treatment can be discontinued safely. In conclusion: chronic hepatitis B has become a treatable disease; however, much research is needed to tailor therapy to an individual patient, to predict the sustainability of response and determine thebest treatment for those failing treatment. | WF Leemans HLA Janssen RA de Man | 2007 | World Journal of Gastroenterology2007，13，18： | 14 |
| 4 | Covalently closed-circular hepatitis B virus DNA reduction with entecavir or lamivudine显示文摘AIM: To investigate the reduction in hepatitis B virus(HBV) covalently closed-circular DNA(ccc DNA) with entecavir(ETV) or lamivudine(LAM). METHODS: This analysis included patients who had participated in the randomized Phase Ⅲ study ETV-022 comparing ETV vs LAM in nucleos(t)ide-naive, HBe Agpositive patients. Patients received ETV(0.5 mg daily) or LAM(100 mg daily) for a minimum of 52 wk. Patients were eligible to participate in this sub-study if they had paired biopsies at baseline and week 48 with evaluable measurements for hepatic HBV ccc DNA and total hepatic HBV DNA. The main objective was to compare changes in hepatic HBV ccc DNA and total hepatic HBV DNA at week 48 of ETV or LAM treatment, which was a secondary endpoint of study ETV-022. Additional post hoc analyses included linear regression analyses to assess associations of baseline levels and on-treatment changes of ccc DNA with other baseline factors [sex,age, serum HBV DNA, alanine aminotransferase(ALT), Knodell necroinflammatory score, Ishak fibrosis score, total hepatic HBV DNA, and HBV genotype], or ontreatment factors(changes from baseline at week 48 in serum HBV DNA, ALT, Knodell necroinflammatory score, Ishak fibrosis score, total hepatic HBV DNA, and HBe Ag loss at week 48).RESULTS: Overall, 305 patients(ETV = 159; LAM = 146) of ETV-022 had paired baseline and week 48 liver biopsies with evaluable measurements for hepatic HBV ccc DNA and total hepatic HBV DNA, and were included in this analysis. Baseline demographics and disease characteristics were comparable between the two arms. After 48 wk, ETV resulted in significantly greater reductions in hepatic HBV ccc DNA [-0.9 log10 copies/human genome equivalent(HGEq) vs-0.7 log10 copies/HGEq; P = 0.0033] and total hepatic DNA levels(-2.1 log10 copies/HGEq vs-1.6 log10 copies/HGEq; P < 0.0001) than LAM. Virologic, biochemical, and histologic response rates at week 48 were also greater with ETV than with LAM. Baseline HBV ccc DNA levels were positively associated with baseline levels of serum HBV DNA and total hepatic HBV DNA, and negatively associated with HBV genotype F. On-treatment changes in HBV ccc DNA levels were negatively associated with baseline levels of serum HBV DNA and baseline ALT, and were positively associated with on-treatment changes in the levels of serum HBV DNA, total hepatic HBV DNA levels, and ALT, change in Knodell necroinflammatory score, and HBe Ag loss.CONCLUSION: Forty-eight weeks of ETV resulted in greater reductions in ccc DNA and total hepatic HBV DNA than LAM, but long-term therapy may be needed for ccc DNA elimination. | Scott Bowden Stephen Locarnini Ting-Tsung Chang You-Chen Chao Kwang-Hyub Han Robert G Gish Robert A de Man Miao Yu Cyril Llamoso Hong Tang | 2015 | World Journal of Gastroenterology2015，21，15： | 11 |
| 5 | Schistosoma mansoni proteins attenuate gastrointestinal motility disturbances during experimental colitis in mice显示文摘AIM:To investigate the therapeutic effect of Schistosoma mansoni(S.mansoni) soluble worm proteins on gastrointestinal motility disturbances during experimental colitis in mice. METHODS:Colitis was induced by intrarectal injection of trinitrobenzene sulphate(TNBS) and 6 h later,mice were treated ip with S.mansoni proteins.Experiments were performed 5 d after TNBS injection.Inflammationwas quantified using validated inflammation parameters. Gastric emptying and geometric center were measured to assess in vivo gastrointestinal motility.Peristaltic activity of distal colonic segments was studied in vitro using a modified Trendelenburg set-up.Cytokine profiles of T-lymphocytes isolated from the colon were determined by real time reverse transcriptase-polymerase chain reaction. RESULTS:Intracolonic injection of TNBS caused severe colitis.Treatment with S.mansoni proteins significantly ameliorated colonic inflammation after 5 d.TNBS did not affect gastric emptying but significantly decreased the geometric center and impaired colonic peristaltic activity 5 d after the induction of colitis.Treatment with S.mansoni proteins ameliorated these in vivo and in vitro motility disturbances.In addition,TNBS injection caused a downregulation of effector T cell cytokines after 5 d,whereas a S.mansoni protein effect was no longer observed at this time point. CONCLUSION:Treatment with S.mansoni proteins attenuated intestinal inflammation and ameliorated motility disturbances during murine experimental colitis. | Nathalie E Ruyssers Benedicte Y De Winter Joris G De Man Natacha D Ruyssers Ann J Van Gils Alex Loukas Mark S Pearson Joel V Weinstock Paul A Pelckmans Tom G Moreels | 2010 | World Journal of Gastroenterology2010，16，6： | 11 |
| 6 | Surveillance for hepatocellular carcinoma in chronic liver disease:Evidence and controversies显示文摘Primary liver cancer is the sixth most common cancer in the world and the third cause of cancer-related death.Hepatocellular carcinoma(HCC)represents more than90%of primary liver cancers and generally occurs in patients with underlying chronic liver disease such as viral hepatitis,hemochromatosis,primary biliary cirrhosis and non-alcoholic steatohepatitis.Especially cirrhotic patients are at risk of HCC and regular surveillance could enable early detection and therapy,with potentially improved outcome.We here summarize existing evidence for surveillance including ultrasound,other radiological modalities and various serum biomarkers,and current international guideline recommendations for surveillance.Ultrasound andα-fetoprotein(alone or in combination)are most frequently used for surveillance,but their sensitivities and specificities are still far from perfect,and evidence for surveillance remains weak and controversial.Various other potential surveillance tools have been tested,including serum markers as des-carboxyprothrombin,lectin-boundα-fetoprotein,and(most recently)circulating TIE2-expressing monocytes,and radiological investigations such as computed tomographyscan or magnetic resonance imaging-scan.Although early results appear promising,these tools have generally been tested in diagnostic rather than surveillance setting,and in most cases,no detailed information is available on their cost-effectiveness.For the near future,it remains important to define those patients with highest risk of HCC and most benefit from surveillance,and to restrict surveillance to these categories. | Suzanne van Meer Robert A de Man Peter D Siersema Karel J van Erpecum | 2013 | World Journal of Gastroenterology2013，19，40： | 10 |
| 7 | Neuroanatomy of lower gastrointestinal pain disorders显示文摘Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal,immune and endocrine signaling pathways within the intestines,the peripheral and the central nervous system.In this article we review how the sensory nerve information from the healthy and the hypersensitive bowel is encoded and conveyed to the brain.The gut milieu is continuously monitored by intrinsic enteric afferents,and an extrinsic nervous network comprising vagal,pelvic and splanchnic afferents.The extrinsic afferents convey gut stimuli to second order neurons within the superficial spinal cord layers.These neurons cross the white commissure and ascend in the anterolateral quadrant and in the ipsilateral dorsal column of the dorsal horn to higher brain centers,mostly subserving regulatory functions.Within the supraspinal regions and the brainstem,pathways descend to modulate the sensory input.Because of this multiple level control,only a small proportion of gut signals actually reaches the level of consciousness to induce sensation or pain.In inflammatory bowel disease(IBD)and irritable bowel syndrome(IBS)patients,however,long-term neuroplastic changes have occurred in the brain-gut axis which results in chronic abdominal pain.This sensitization may be driven on the one hand by peripheral mechanisms within the intestinal wall which encompasses an interplay between immunocytes,enterochromaffin cells,resident macrophages,neurons and smooth muscles.On the other hand,neuronal synaptic changes along with increased neurotransmitter release in the spinal cord and brain leads to a state of central wind-up.Also life factors such as but not limited to inflammation and stress contribute to hypersensitivity.All together,the degree to which each of these mechanisms contribute to hypersensitivity in IBD and IBS might be diseaseand even patient-dependent.Mapping of sensitization throughout animal and human studies may significantly improve our understanding of sensitization in IBD and IBS.On the long run,this knowledge can be put forward in potential therapeutic targets for abdominal pain in these conditions. | Wim Vermeulen Joris G De Man Paul A Pelckmans Benedicte Y De Winter | 2014 | World Journal of Gastroenterology2014，20，4： | 7 |
| 8 | Visceral hypersensitivity in inflammatory bowel diseases and irritable bowel syndrome: The role of proteases显示文摘Proteases, enzymes catalyzing the hydrolysis of peptide bonds, are present at high concentrations in the gastrointestinal tract. Besides their well-known role in the digestive process, they also function as signaling molecules through the activation of protease-activated receptors(PARs). Based on their chemical mechanism for catalysis, proteases can be classified into several classes: serine, cysteine, aspartic, metallo- and threonine proteases represent the mammalian protease families. In particular, the class of serine proteases will play a significant role in this review. In the last decades, proteases have been suggested to play a key role in the pathogenesis of visceral hypersensitivity, which is a major factor contributing to abdominal pain in patients with inflammatory bowel diseases and/or irritable bowel syndrome. So far, only a few preclinical animal studies have investigated the effect of protease inhibitors specifically on visceral sensitivity while their effect on inflammation is described in more detail. In our accompanying review we describe their effect on gastrointestinal permeability. On account of their promising results in the field of visceral hypersensitivity, further research is warranted. The aim of this review is to give an overview on the concept of visceral hypersensitivity as well as on the physiological and pathophysiological functions of proteases herein. | Hannah Ceuleers Hanne Van Spaendonk Nikita Hanning Jelena Heirbaut Anne-Marie Lambeir Jurgen Joossens Koen Augustyns Joris G De Man Ingrid De Meester Benedicte Y De Winter | 2016 | World Journal of Gastroenterology2016，22，47： | 7 |
| 9 | Regulation of intestinal permeability: The role of proteases显示文摘The gastrointestinal barrier is-with approximately 400 m^2-the human body's largest surface separating the external environment from the internal milieu. This barrier serves a dual function: permitting the absorption of nutrients, water and electrolytes on the one hand, while limiting host contact with noxious luminal antigens on the other hand. To maintain this selective barrier, junction protein complexes seal the intercellular space between adjacent epithelial cells and regulate the paracellular transport. Increased intestinal permeability is associated with and suggested as a player in the pathophysiology of various gastrointestinal and extraintestinal diseases such as inflammatory bowel disease, celiac disease and type 1 diabetes. The gastrointestinal tract is exposed to high levels of endogenous and exogenous proteases, both in the lumen and in the mucosa. There is increasing evidence to suggest that a dysregulation of the protease/antiprotease balance in the gut contributes to epithelial damage and increased permeability. Excessive proteolysis leads to direct cleavage of intercellular junction proteins, or to opening of the junction proteins via activation of protease activated receptors. In addition, proteases regulate the activity and availability of cytokines and growth factors, which are also known modulators of intestinal permeability. This review aims at outlining the mechanisms by which proteases alter the intestinal permeability. More knowledge on the role of proteases in mucosal homeostasis and gastrointestinal barrier function will definitely contribute to the identification of new therapeutic targets for permeability-related diseases. | Hanne Van Spaendonk Hannah Ceuleers Leonie Witters Eveline Patteet Jurgen Joossens Koen Augustyns Anne-Marie Lambeir Ingrid De Meester Joris G De Man Benedicte Y De Winter | 2017 | World Journal of Gastroenterology2017，23，12： | 6 |
| 10 | Management and outcome of hepatocellular adenoma with massive bleeding at presentation显示文摘AIM To evaluate outcome of acute management and risk of rebleeding in patients with massive hemorrhage due to hepatocellular adenoma(HCA). METHODS This retrospective cohort study included all consecutive patients who presented to our hospital with massive hemorrhage(grade Ⅱ or Ⅲ) due to ruptured HCA and were admitted for observation and/or intervention between 1999-2016. The diagnosis of HCA was based on radiological findings from contrastenhanced magnetic resonance imaging(MRI) or pathological findings from biopsy or resection of the HCA. Hemorrhage was diagnosed based on findings from computed tomography or MRI. Medical records were reviewed for demographic features, clinical presentation, tumor features, initial and subsequent management, short-and long-term complications and patient and lesion follow-up. RESULTS All patients were female(n = 23). Treatment in the acute phase consisted of embolization(n = 9, 39.1%), conservative therapy(n = 13, 56.5%), andother intervention(n = 1, 4.3%). Median hemoglobin level decreased significantly more on days 0-3 in the intervention group than in the patients initially treated conservatively(0.9 mmol/L vs 2.4 mmol/L respectively, P = 0.006). In total, 4 patients suffered severe shortterm complications, which included hypovolemic shock, acute liver failure and abscess formation. After a median follow-up of 36 mo, tumor regression in nonsurgically treated patients occurred with a median reduction of 76 mm down to 25 mm. Four patients underwent secondary(elective) treatment(i.e., tumor resection) to address HCA size of > 5 cm and/or desire for future pregnancy. One case of rebleeding was documented(4.3%). None of the patients experienced long-term complication(mean follow-up time: 36 mo). CONCLUSION With a 4.3% risk of rebleeding, secondary(elective) treatment of HCA after massive hemorrhage may only be considered in patients with persistent HCA > 5 cm. | Anne J Klompenhouwer Robert A de Man Maarten GJ Thomeer Jan NM Ijzermans | 2017 | World Journal of Gastroenterology2017，23，25： | 5 |
| 11 | Three-Year Efficacy and Safety of Tenofovir Disoproxil Fumarate Treatment for Chronic Hepatitis B显示文摘 | E. Jenny Heathcote Patrick Marcellin Maria Buti Edward Gane Robert A. De Man Zahary Krastev George Germanidis Samuel S. Lee Robert Flisiak Kelly Kaita Michael Manns Iskren Kotzev Konstantin Tchernev Peter Buggisch Frank Weilert Oya Ovunc Kurdas Mitchell L | 2011 | Gastroenterology2011，，1： | 5 |
| 12 | Pegylated interferon alfa-2b alone or in combination with lamivudine for HBeAg-positive chronic hepatitis B: a randomised trial显示文摘 | Harry LA Janssen Monika van Zonneveld Hakan Senturk Stefan Zeuzem Ulus S Akarca Yilmaz Cakaloglu Christopher Simon Thomas MK So Guido Gerken Robert A de Man Hubert GM Niesters Pieter Zondervan Bettina Hansen Solko W Schalm | 2005 | The Lancet . 2005 (9454)2005，，： | 2 |
| 13 | Increased incidence of early de novo cancer in liver graft recipients treated with cyclosporine: An association with C显示文摘 | Angela S. W. Tjon Jerome Sint Nicolaas Jaap Kwekkeboom Robert A. de Man Geert Kazemier Hugo W. Tilanus Bettina E. Hansen Luc J. W. van der Laan Thanyalak Tha‐In Herold J. Metselaar | 2010 | Liver Transpl2010，，7： | 2 |
| 14 | A prospective study on elective umbilical hernia repair in patients with liver cirrhosis and ascites显示文摘 | Hasan H. Eker G.H. van Ramshorst B. de Goede H.W. Tilanus H.J. Metselaar R.A. de Man J.F. Lange G. Kazemier | 2011 | Surgery2011，，3： | 2 |
| 15 | Analysis of intrahepatic HBV-specific cytotoxic T-cells during and after acute HBV infection in humans显示文摘 | Dave Sprengers Renate G. van der Molen Johannes G. Kusters Robert A. De Man Hubert G.M. Niesters Solko W. Schalm Harry L.A. Janssen | 2006 | Journal of Hepatology2006，，2： | 2 |
| 16 | A comparison of entecavir and lamivudine for HBeAg-positive chronic hepatitis B显示文摘 | CHANG T T GISH R G DE MAN R | 2006 | N Engl J Med2006，354，： | 1 |
| 17 | Isoflurane pretreatment inhibits cytokine-induced cell death in rat smooth muscle cells and human endothelial cells显示文摘 | De Klaver MJM Manning L Palmer LA | 2002 | Anesthesiology2002，97，1： | 1 |
| 18 | Development of a quan titative real-time detection assay for hepatitis B virus DNA and comparison with two commercial assay s显示文摘 | Pas sd Fries E De Man R A | 2000 | Clin Microbiol2000，39，8： | 1 |
| 19 | A control strategy for a robot with one articulate leg hopping on irregular terrain 显示文摘 | Vermeulen J Lefebor D De Man H | 2000 | Professional Engineering Publishing2000，，10： | 1 |
| 20 | Exacerbation of chronic hepatitis B infection after delivery显示文摘 | Ter Borg MJ Leemans WF De Man RA | 2008 | Journal of Viral Hepatitis2008，15，1： | 1 |
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