|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Epithelial restitution and wound healing in inflammatory bowel disease显示文摘Inflammatory bowel disease is characterized by a chronic inflammation of the intestinal mucosa. The mucosal epithelium of the alimentary tract constitutes a key element of the mucosal barrier to a broad spectrum of deleterious substances present within the intestinal lumen including bacterial microorganisms, various dietary factors, gastrointestinal secretory products and drugs. In addition, this mucosal barrier can be disturbed in the course of various intestinal disorders including inflammatory bowel diseases. Fortunately, the integrity of the gastrointestinal surface epithelium is rapidly reestablished even after extensive destruction. Rapid resealing of the epithelial barrier following injuries is accomplished by a process termed epithelial restitution, followed by more delayed mechanisms of epithelial wound healing including increased epithelial cell proliferation and epithelial cell differentiation. Restitution of the intestinal surface epithelium is modulated by a range of highly divergent factors among them a broad spectrum of structurally distinct regulatory peptides, variously described as growth factors or cytokines. Several regulatory peptide factors act from the basolateral site of the epithelial surface and enhance epithelial cell restitution through TGF-β-dependent pathways. In contrast, members of the trefoil factor family (TFF peptides) appear to stimulate epithelial restitution in conjunction with mucin glycoproteins through a TGF-β-independent mechanism from the apical site of the intestinal epithelium. In addition, a number of other peptide molecules like extracellular matrix factors and blood clotting factors and also non- peptide molecules including phospholipids, short-chain fatty acids (SCFA), adenine nucleotides, trace elements and pharmacological agents modulate intestinal epithelial repair mechanisms. Repeated damage and injury of the intestinal surface are key features of various intestinaldisorders including inflammatory bowel diseases and require constant repair of the epithelium. Enhancement of intestinal repair mechanisms by regulatory peptides or other modulatory factors may provide future approaches for the treatment of diseases that are characterized by injuries of the epithelial surface. | Andreas Sturm Axel U Dignass | 2008 | World Journal of Gastroenterology2008，14，3： | 24 |
| 2 | Sporadic versus hereditary gastrinomas of the duodenum and pancreas: Distinct clinico-pathological and epidemiological features显示文摘Gastrinomas are defined as gastrin secreting tumors that are associated with Zollinger-Ellison syndrome (ZES). ZES is characterized by elevated fasting gastrin serum levels, positive secretin stimulation test and clinical symptoms such as recurrent peptic ulcer disease, gastroesophageal re?ux disease and occasional diarrhea. Genetically, nonhereditary (sporadic) gastrinomas are distinguished from hereditary gastrinomas, which are associated with multiple endocrine neoplasia type 1 (MEN1) syndrome. In general, duodenal gastrinomas are small and solitary if they are sporadic and multiple as well as hereditary. The sporadic gastrinomas occur in the duodenum or in the pancreas while the hereditary gastrinomas almost all occur in the duodenum. Our series of 77 sporadic duodenal neuroendocrine tumors (NETs) includes 18 patients (23.4%) with gastrinomas and ZES. Of 535 sporadic NETs in the pancreas collected from the NET archives of the departments of pathology in Zürich, Switzerland, and Kiel, Germany, 24 patients (4.5%) suffered from sporadic pancreatic gastrinomas and ZES. These NETs have to be distinguished fromtumors with immunohistochemical positivity for gastrin but without evidence of ZES. An additional 19 patients suffered from MEN1 and ZES. These patients showed exclusively duodenal gastrinomas, but not pancreatic gastrinomas. The prognosis of sporadic and MEN1- associated duodenal gastrinomas is better than that of pancreatic gastrinomas, since they progress slowly to liver metastasis. In summary, sporadic and MEN1- associated gastrinomas in the duodenum and pancreas show different clinico-pathological and genetic features. The incidence of sporadic duodenal gastrin-producing tumors is increasing, possibly due to optimized diagnostic procedures. In contrast, pancreatic MEN1- associated gastrinomas seem to be extremely rare. A considerable subset of tumors with immunohistochemical expression of gastrin but without evidence of ZES should be designated as functionally inactive NETs expressing gastrin, but not as gastrinomas. | Martin Anlauf Nele Garbrecht Tobias Henopp Anja Schmitt Regina Schlenger Andreas Raffel Markus Krausch Oliver Gimm Claus F Eisenberger Wolfram T Knoefel Henning Dralle Paul Komminoth Philipp U Heitz Aurel Perren Günter Klppel | 2006 | World Journal of Gastroenterology2006，12，34： | 7 |
| 3 | Abnormal High-Density Lipoprotein Induces Endothelial Dysfunction via Activation of Toll-Like Receptor-2显示文摘 | Thimoteus Speer Lucia Rohrer Przemyslaw Blyszczuk Rukshana Shroff Kira Kuschnerus Nicolle Kr?nkel Gabriela Kania Stephen Zewinger Alexander Akhmedov Yi Shi Tina Martin Damir Perisa Stephan Winnik Maja F. Müller Urban Sester Gabriel Wernicke Andreas Jung U | 2013 | Immunity2013，，： | 2 |
| 4 | TheModi- fled Cramer-Rao Bound and Its Application to Synchro- nization Problems 显示文摘 | D'Andrea A N D Mengali U Reggiannini R | 1994 | Communications IEEE Transac- tions on1994，42，234： | 1 |
| 5 | Feedforward joint phase and timing estimation with OQPSK modulation 显示文摘 | D'Amico A A D'Andrea A N and Mengali U | 1999 | IEEE Transactions on Vehicular Technology1999，48，3： | 1 |
| 6 | Blomass burning aerosol emissions from vegetation fires:Particle number and mass emission factors and size distnibutions显示文摘 | Janh 11 S Andreae M O P schl U | | 0，，03： | 1 |
| 7 | The impact of antimicrobial drug consumption and alcohol-based hand rub use on the emergence and spread of extended-spectrum beta-lactamase-producing strains:a time-series analysis显示文摘 | Kaier K Frank U Andreas H | | 0，，03： | 1 |
| 8 | Channel Estimation for Ultra-Wideband Communications显示文摘 | Lottici V Andrea A Mengali U | 2002 | IEEE Journal on Selected Areas in Communications2002，20，9： | 1 |
| 9 | Systemic risk in Europe an sovereign debt markets: a CoVaR-copula approach 显示文摘 | JUAN C R ANDREA U | 2015 | Journal of International Money and Finance2015，，51： | 1 |
| 10 | Symbol timing estimation with CPM modulation显示文摘 | D′Andrea A N Mengali U Morelli M | 1996 | IEEE Trans Commun1996，44，10： | 1 |
| 11 | Cellulose-degrading potentials and phylogenetic classification of carboxymethyl-cellulose decomposing bacteria isolated from Soil 显示文摘 | Stephan W Andreas U | 2002 | Systematic and Applied Microbiology2002，25，4： | 1 |
| 12 | Channel estimation for ultra-wideband communications显示文摘 | LOTTICI V D'ANDREA A MENGALI U | 2002 | IEEE Journal on Selected Areas in Communications2002，20，9： | 1 |
| 13 | Obstructive sleep apnea and coronary artery disease显示文摘 | L(U)THJE L ANDREAS S | 2008 | Sleep Med Rev2008，12，： | 1 |
| 14 | Review Chromatography of tea constituents显示文摘 | Andreas F Susanne K Engelhardt U H | 1992 | J of Chromatography1992，624，： | 1 |
| 15 | Channel estimation for ultrawideband communications显示文摘 | Lottici V Andrea A D Mengali U | 2002 | IEEE J Select Areal Commun2002，20，9： | 1 |
| 16 | Channel estimation for ultra wideband communications显示文摘 | LOTTICI V ANDREA A D MENGALI U | 2002 | IEEE J Select Areas Commun2002，20，9： | 1 |
| 17 | Oxidation kinetics of selected taste and odor compounds during ozonation of drinking water显示文摘 | ANDREAS P VON G U | 2007 | Environ Sci Techno12007，41，2： | 1 |
| 18 | The modified Cramer-Rao bound and its applications to sync-hronization problems显示文摘 | Aldo N Andrea D Mengali U and Reggiannini R | 1994 | IEEE Transactions on Communications1994，42，2： | 1 |
| 19 | The Modified Cramer-Rao Bound and its Application to Synchronization Problems 显示文摘 | D' Andrea A N Mengali U Reggiannini R | 1994 | IEEE Transactions on Communications1994，42，234： | 1 |
| 20 | Porcine model characterizing various parameters assessing the outcome after acetaminophen intoxication induced acute liver failure显示文摘AIM To investigate the changes of hemodynamic and laboratory parameters during the course of acute liver failure following acetaminophen overdose.METHODS Eight pigs underwent a midline laparotomy following jejunal catheter placement for further acetaminophen intoxication and positioning of a portal vein Doppler flow-probe. Acute liver failure was realized by intrajejunal acetaminophen administration in six animals, two animals were sham operated. All animals were invasively monitored and received standardized intensive care support throughout the study. Portal blood flow, hemodynamic and ventilation parameters were continuously recorded. Laboratory parameters were analysed every eight hours. Liver biopsies were sampled every 24 h following intoxication and upon autopsy.RESULTS Acute liver failure (ALF) occurred after 28 ± 5 h resulted in multiple organ failure and death despite maximal support after further 21 ± 1 h (study end). Portal blood flow (baseline 1100 ± 156 m L/min) increased to a maximum flow of 1873 ± 175 m L/min at manifestation of ALF, which was significantly elevated(P < 0.01). Immediately after peaking, portal flow declined rapidly to 283 ± 135 m L/min at study end. Thrombocyte values (baseline 307 × 103/μL± 34 × 103/μL) of intoxicated animals declined slowly to values of 145 × 103/μL± 46 × 103/μL when liver failure occurred. Subsequent appearance of severe thrombocytopenia in liver failure resulted in values of 11 × 103/μL± 3 × 103/μL preceding fatality within few hours which was significant(P > 0.01).CONCLUSION Declining portal blood flow and subsequent severe thrombocytopenia after acetaminophen intoxication precede fatality in a porcine acute liver failure model. | Karolin Thiel Wilfried Klingert Kathrin Klingert Matthias H Morgalla Martin U Schuhmann Pamela Leckie Yalda Sharifi Nathan A Davies Rajiv Jalan Andreas Peter Christian Grasshoff Alfred Konigsrainer Martin Schenk Christian Thiel | 2017 | World Journal of Gastroenterology2017，23，9： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员