|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | 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 |
| 2 | 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 |
| 3 | 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 |
| 4 | 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 |
| 5 | 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 |
| 6 | 早发急性心肌梗死的长期结局和风险评估:10年随访研究显示文摘早发急性心肌梗死(acute myocardial infarction,AMI)是一种罕见的疾病,发病率和死亡率很高。该文在再灌注治疗广泛应用的大环境下,纳入前瞻性研究人群进行早发AMI的预后研究。方法:这项前瞻性多中心研究中连续纳入102例AMI存活者(≤40岁),临床预后通过奥地利死亡登记处和维也纳集中患者管理系统进行查询。 | 刘莉 叶鹏 Winter MP Blessberger H Alimohammadi A Pavo N Huber K Wojta J Lang IM Wiesbauer F Goliasch G | 2017 | 中华高血压杂志2017，25，4： | 5 |
| 7 | A rat model of bone cancer pain显示文摘 | S.J Medhurst K Walker M Bowes B.L Kidd M Glatt M Muller M Hattenberger J Vaxelaire T O’Reilly G Wotherspoon J Winter J Green L Urban | 2002 | Pain2002，，： | 2 |
| 8 | Man-made antibodies显示文摘 | Milstein C | 1991 | Nature1991，349，6307： | 1 |
| 9 | A Baseline Model of Industry Evolution显示文摘 | KANIOVSKI Y M DOSI G | 2003 | J Evol Econ2003，13，12： | 1 |
| 10 | The immunogenicity of chimeric antibodies显示文摘 | Bruggemann M Winter G | 1989 | J Exp Med1989，170，： | 1 |
| 11 | Man-made antibody 显示文摘 | Winter G Milstein C | 1991 | Nature1991，349，6307： | 1 |
| 12 | Making antibodies by phage display technology 显示文摘 | Winter G Griffiths AD Hawkins RE | 1994 | Annu Rev Immunol1994，12，： | 1 |
| 13 | Recombinant spider silk particles for controlled delivery of protein drugs 显示文摘 | HOFER M WINTER G MYSCHIK J | 2012 | Bio- materials2012，33，5： | 1 |
| 14 | Cyclic and acyclic sulfites: new solvents and electrolyte additives for lithium ion batteries with graphitic anodic显示文摘 | WRODNIGG G H BESENHARD J O WINTER M | 2001 | Journal of Power Sources2001，9798，： | 1 |
| 15 | Humanized antibodies显示文摘 | Winter G Harris WJ | 1993 | Trends Pharmacol Sci1993，14，5： | 1 |
| 16 | 'Diabodies':small bivalent and bispecific antibody fragments显示文摘 | Prospero T Winter G | 1993 | Proc Natl Acad Sci USA1993，90，14： | 1 |
| 17 | The Satisficing Principle in Capability Learning 显示文摘 | Winter S G | 2000 | Strategic Management Journal2000，，21： | 1 |
| 18 | Replieation as strategy显示文摘 | WINTER S G SZULANSKI G | 2001 | Organization Science2001，12，6： | 1 |
| 19 | Driven-right-leg circuit design显示文摘 | WINTER B B WEBSTER J G | | 0，，01： | 1 |
| 20 | Assessing Forest Naturalness显示文摘 | Mcroberts R E Winter S Chirici G | 2012 | Forest Science2012，58，3： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员