|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Challenges in diagnosing mesenteric ischemia显示文摘Early identification of acute mesenteric ischemia (AMI) is challenging. The wide variability in clinical presentation challenges providers to make an early accurate diagnosis. Despite major diagnostic and treatment advances over the past decades, mortality remains high. Arterial embolus and superior mesenteric artery thrombosis are common causes of AMI. Non-occlusive causes are less common, but vasculitis may be important, especially in younger people. Because of the unclear clinical presentation and non-specific laboratory findings, low clinical suspicion may lead to loss of valuable time. During this diagnostic delay, progression of ischemia to transmural bowel infarction with peritonitis and septicemia may further worsen patient outcomes. Several diagnostic modalities are used to assess possible AMI. Multi-detector row computed tomographic angiography is the current gold standard. Although computed tomographic angiography leads to an accurate diagnosis in many cases, early detection is a persistent problem. Because early diagnosis is vital to commence treatment, new diagnostic strategies are needed. A non-invasive simple biochemical test would be ideal to increase clinical suspicion of AMI and would improve patient selection for radiographic evaluation. Thus, AMI could be diagnosed earlier with follow-up computed tomographic angiography or high spatial magnetic resonance imaging. Experimental in vitro and in vivo studies show promise for alpha glutathione S transferase and intestinal fatty acid binding protein as markers for AMI. Future research must confirm the clinical utility of these biochemical markers in the diagnosis of mesenteric ischemia. | Teun C van den Heijkant Bart AC Aerts Joep A Teijink Wim A Buurman Misha DP Luyer | 2013 | World Journal of Gastroenterology2013，19，9： | 31 |
| 2 | Non-invasive assessment of barrier integrity and function of the human gut显示文摘Over the past decades evidence has been accumulating that intestinal barrier integrity loss plays a key role in the development and perpetuation of a variety of disease states including inflammatory bowel disease and celiac disease,and is a key player in the onset of sepsis and multiple organ failure in situations of intestinal hypoperfusion,including trauma and major surgery.Insight into gut barrier integrity and function loss is important to improve our knowledge on disease etiology and pathophysiology and contributes to early detection and/or secondary prevention of disease.A variety of tests have been developed to assess intestinal epithelial cell damage,intestinal tight junction status and consequences of intestinal barrier integrity loss,i.e.increased intestinal permeability.This review discusses currently available methods for evaluating loss of human intestinal barrier integrity and function. | Joep Grootjans Geertje Thuijls Froukje Verdam Joep PM Derikx Kaatje Lenaerts Wim A Buurman | 2010 | World Journal of Gastrointestinal Surgery2010，2，3： | 18 |
| 3 | Life and death at the mucosal-luminal interface: New perspectives on human intestinal ischemia-reperfusion显示文摘Intestinal ischemia is a frequently observed phenomenon. Morbidity and mortality rates are extraordinarily high and did not improve over the past decades. This is in part attributable to limited knowledge on the pathophysiology of intestinal ischemia-reperfusion(IR) in man, the paucity in preventive and/or therapeutic options and the lack of early diagnostic markers for intestinal ischemia. To improve our knowledge and solve clinically important questions regarding intestinal IR, we developed a human experimental intestinal IR model. With this model, we were able to gain insight into the mechanisms that allow the human gut to withstand short periods of IR without the development of severe inflammatory responses. The purpose of this review is to overview the most relevant recent advances in our understanding of the pathophysiology of human intestinal IR, as well as the(potential) future clinical implications. | Joep Grootjans Kaatje Lenaerts Wim A Buurman Cornelis HC Dejong Joep PM Derikx | 2016 | World Journal of Gastroenterology2016，22，9： | 11 |
| 4 | Controlling postoperative ileus by vagal activation显示文摘Postoperative ileus is a frequently occurring surgical complication, leading to increased morbidity and hospital stay. Abdominal surgical interventions are known to result in a protracted cessation of bowel movement. Activation of inhibitory neural pathways by nociceptive stimuli leads to an inhibition of propulsive activity, which resolves shortly after closure of the abdomen. The subsequent formation of an inflammatory infiltrate in the muscular layers of the intestine results in a more prolonged phase of ileus. Over the last decade, clinical strategies focusing on reduction of surgical stress and promoting postoperative recovery have improved the course of postoperative ileus. Additionally, recent experimental evidence implicated antiinflammatory interventions, such as vagal stimulation, as potential targets to treat postoperative ileus and reduce the period of intestinal hypomotility. Activation of nicotinic receptors on inflammatory cells by vagal input attenuates inflammation and promotes gastrointestinal motility in experimental models of ileus. A novel physiologicalintervention to activate this neuroimmune pathway is enteral administration of lipid-rich nutrition. Perioperative administration of lipid-rich nutrition reduced manipulation-induced local inflammation of the intestine and accelerated recovery of bowel movement. The application of safe and easy to use antiinflammatory interventions, together with the current multimodal approach, could reduce postoperative ileus to an absolute minimum and shorten hospital stay. | Tim Lubbers Wim Buurman Misha Luyer | 2010 | World Journal of Gastroenterology2010，16，14： | 10 |
| 5 | Non-invasive markers of gut wall integrity in health and disease显示文摘The intestinal mucosa is responsible for the absorption of nutrients from the lumen and for the separation of the potentially toxic luminal content(external environment) from the host(internal environment).Disruption of this delicate balance at the mucosal interface is the basis for numerous(intestinal) diseases.Experimental animal studies have shown that gut wall integrity loss is involved in the development of various inflammatory syndromes,including post-operative or post-traumatic systemic inflammatory response syndrome,sepsis,and multiple organ failure.Assessment of gut wall integrity in clinical practice is still a challenge,as it is difficult to evaluate the condition of the gut non-invasively with currently available diagnostic tools.Moreover,non-invasive,rapid diagnostic means to assess intestinal condition are needed to evaluate the effects of treatment of intestinal disorders.This review provides a survey of non-invasive tests and newly identified markers that can be used to assess gut wall integrity. | Joep PM Derikx Misha DP Luyer Erik Heineman Wim A Buurman | 2010 | World Journal of Gastroenterology2010，16，42： | 9 |
| 6 | Human small intestine is capable of restoring barrier function after short ischemic periods显示文摘AIM To assess intestinal barrier function during human intestinal ischemia and reperfusion(IR).METHODS In a human experimental model,6 cm of jejunum was selectively exposed to 30 min of ischemia(I) followed by 30 and 120 min of reperfusion(R). A sham procedure was also performed. Blood and tissue was sampled at all-time points. Functional barrier function was assessed using dual-sugar absorption tests with lactulose(L) and rhamnose(R). Plasma concentrations of citrulline,an amino acid described as marker for enterocyte function were measured as marker of metabolic enterocytes restoration. Damage to the epithelial lining was assessed by immunohistochemistry for tight junctions( TJs),by plasma marker for enterocytes damage(I-FABP) and analyzed by electron microscopy(EM) using lanthanum nitrate as an electrondense marker.RESULTS Plasma L/R ratio's were significantly increased after 30 min of ischemia(30 I) followed by 30 min of reperfusion(30 R) compared to control(0.75 ± 0.10 vs 0.20 ± 0.09,P < 0.05). At 120 min of reperfusion(120 R),ratio's normalized(0.17 ± 0.06) and were not significantly different from control. Plasma levels of I-FABP correlated with plasma L/R ratios measured at the same time points(correlation: 0.467,P < 0.01). TJs staining shows distortion of staining at 30 I. An intact lining of TJs was again observed at 30 I120 R. Electron microscopy analysis revealed disrupted TJs after 30 I with paracellular leakage of lanthanum nitrate,which restored after 30 I120 R. Furthermore,citrulline concentrations closely paralleled the histological perturbations during intestinal IR.CONCLUSION This study directly correlates histological data with intestinal permeability tests,revealing that the human gut has the ability of to withstand short episodes of ischemia,with morphological and functional recovery of the intestinal barrier within 120 min of reperfusion. | Dirk HSM Schellekens Inca HR Hundscheid Claire AJI Leenarts Joep Grootjans Kaatje Lenaerts Wim A Buurman Cornelis HC Dejong Joep PM Derikx | 2017 | World Journal of Gastroenterology2017，23，48： | 4 |
| 7 | hsa-mir-183 is frequently methylated and related to poor survival in human hepatocellular carcinoma显示文摘AIM To screen clinically relevant micro RNAs (mi RNAs) silenced by DNA methylation in human hepatocellular carcinoma(HCC).METHODS Knockdown of DNA methyltransferases (DNMTs) using si RNAs and mi RNA profiling in HCC cell lines were performed to identify DNA hypermethylation-mediated mi RNA downregulation. Confirmation using individual quantitative real-time PCR (qR T-PCR) assays was thenperformed followed by DNA methylation quantification at the promoter of the mi RNA genes. Quantification of DNA methylation and mi RNA expression was then performed in primary HCC tumor samples and related with clinicopathological variables.RESULTS mi RNA profiling after DNMT knockdown in HCC cell lines revealed upregulation of mi R-23, mi R-25 and mi R-183. After q RT-PCR confirmation and Cp G island methylation quantification of these miR NAs in cell lines, further analysis in primary HCC specimens showed that hsa-mi R-183 is hypermethylated in 30% of HCC (n = 40). Expression of mature miR-183 showed an inverse correlation with DNA methylation levels. In HCC cells, DNMT knockdown and 5-aza-2'-deoxycytidine treatment reduced methylation and stimulated expression of mi R-183. In HCC patients, hypermethylation at hsami R-183 promoter significantly correlates with poor survival (log-rank test P = 0.03). DNA methylation analysis in healthy liver, benign liver tumors (hepatocellular adenoma and focal nodular hyperplasia) and their corresponding adjacent tissues showed absence of hypermethylation supporting the notion that aberrant methylation at hsa-miR-183 is specific for the malignant transformation of hepatocytes.CONCLUSION Our data indicate that hypermethylation of hsa-miR-183 is a frequent event in HCC and potentially useful as a novel surrogate diagnostic and prognostic marker. | Sumadi Lukman Anwar Till Krech Britta Hasemeier Elisa Schipper Nora Schweitzer Arndt Vogel Hans Kreipe Reena Buurman Britta Skawran Ulrich Lehmann | 2017 | World Journal of Gastroenterology2017，23，9： | 3 |
| 8 | INTESTINAL CYTOSKELETON DEGRADATION PRECEDES TIGHT JUNCTION LOSS FOLLOWING HEMORRHAGIC SHOCK显示文摘 | Geertje Thuijls Jacco-Juri de Haan Joep P. M. Derikx Isabelle Daissormont M’hamed Hadfoune Erik Heineman Wim A. Buurman | 2009 | SHOCK2009，，2： | 2 |
| 9 | A Pilot Study on the Noninvasive Evaluation of Intestinal Damage in Celiac Disease Using I-FABP and L-FABP显示文摘 | Joep P. M. Derikx Anita C. E. Vreugdenhil Anita M. Van den Neucker Joep Grootjans Annemarie A. van Bijnen Jan G. M. C. Damoiseaux L. W. Ernest van Heurn Erik Heineman Wim A. Buurman | 2009 | Journal of Clinical Gastroenterology2009，，8： | 2 |
| 10 | Convergence and amplification of toll-like receptor (TLR) and receptor for advanced glycation end products (RAGE) signaling pathways via high mobility group B1 (HMGB1)显示文摘 | Judy R. Beijnum Wim A. Buurman Arjan W. Griffioen | 2008 | Angiogenesis2008，，1： | 2 |
| 11 | 8000 yr of black carbon accumulation in a colluvial soil from NW Spain 显示文摘 | Kaal J Martinez-Cortizas A Buurman P | 2008 | Quaternary Research2008，69，1： | 1 |
| 12 | In situ preservation of kidneys from donors after cardiac death:results and complications显示文摘 | Snoeijs MG Dekkers AJ Buurman WA | 2007 | Ann Surg2007，246，5： | 1 |
| 13 | Comprehensive geriatric assessment, multifactorial interventions and nurse - led care coordination to prevent functional decline in community - dwelling older persons : protocol of a cluster randomized trial 显示文摘 | Suijker JJ Buurman BM ter Riet G | 2012 | BMC Health Serv Res2012，，12： | 1 |
| 14 | Low molecular weight heparin attenuates multiple organ failure in a murine model of disseminated intravascular coagulation 显示文摘 | Slofstra SH van't Veer C Buurman WA | 2005 | Crit Care Med2005，33，6： | 1 |
| 15 | In vivo expression of Toll-like receptor 2 and 4 by renal epithelial cells:IFN-γ and TNF-γ mediated up-regulation during inflammation显示文摘 | Wolfs TG Buurman WA van Schadewijk A | 2002 | J Immunol2002，168，3： | 1 |
| 16 | Evi-dence for a relation between metabolic derangements and in- creased levels of inflammatory mediators in a subgroup of pa- tients with chronic obstructive pulmonary disease显示文摘 | Schols AM Buurman WA Staal van den Brekel A | 1996 | Thorax1996，51，8： | 1 |
| 17 | Low concentrations of ethanol induce apoptosis in human intestinal cells显示文摘 | ASAI K BUURMAN W A REUTELINGSPERGER C P | 2003 | Scand J Gastroenterol2003，38，11： | 1 |
| 18 | Liver manipulation causes hepatoeyte injury and precedes systemic inflammation in patients undergoing liver resection显示文摘 | Van-de-poll MC Derikx JP Buurman WA | 2007 | World J Surg2007，31，： | 1 |
| 19 | INTESTINAL CYTOSKELETON DEGRADATION PRECEDES TIGHT JUNCTION LOSS FOLLOWING HEMORRHAGIC SHOCK显示文摘 | Geertje Thuijls Jacco-Juri de Haan Joep P. M. Derikx Isabelle Daissormont M’hamed Hadfoune Erik Heineman Wim A. Buurman | 2009 | SHOCK2009，，2： | 1 |
| 20 | Evidence for auto/paracrine actions of vitamin D in bone: lalpha-hydrox- ylase expression and activity in human bone cells显示文摘 | Van Driel ML Koedam M Buurman C J | 2006 | FASEB J2006，20，20： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员