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| 1 | Relaxin prevents the development of severe acute pancreatitis显示文摘瞄准:为了调查尖锐胰腺炎(AP ) 的严厉,被联系到白血球激活,煽动性的起来规定和联系到 ischemia-reperfusion 损害的微循环混乱的紧张。支持 inflammatory 调停人的 Microvascular 完整和抑制在 AP 的进化是关键因素的。松弛激素是被归因的像胰岛素的荷尔蒙经由氮的氧化物小径的 vasorelaxant 性质当作为糖皮质激素受体收缩筋表现时。方法:AP 被 bilio 胰腺的 duct-outlet-exclusion closed-duodenal-loops 模型导致。有松弛激素的处理在不同时间点被做。由由 mifepristone 的阻塞被考虑的 L 名字和糖皮质激素受体(GR ) 的氮的氧化物 synthase 抑制。AP 严厉被生物化学、组织病理学说的分析估计。结果:有松弛激素的处理减少了浆液淀粉酶,脂肪分解酵素, C 反应的蛋白质, IL-6, IL-10, hsp72, LDH 和 8-isoprostane 象一样胰腺并且肺 myeloperoxidase。腺泡和脂肪坏死,出血和 neutrophil 渗透也被减少。当 caspases 2-3-8 和 9 项活动被增加时, ATP 弄空和 ADP/ATP 比率被减少。L 名字和 mifepristone 减少了松弛激素的效率。结论:松弛激素结果在当保存微发行量并且在坏死上赞成 apoptosis 时,联合 GR 收缩筋的性质的 AP 的处理有益。 | Laura Iris Cosen-Binker Marcelo Gustavo Binker Rodica Cosen Gustavo Negri Osvaldo Tiscornia | 2006 | World Journal of Gastroenterology2006，12，10： | 10 |
| 2 | Acute pancreatitis:The stress factor显示文摘Acute pancreatitis is an inflammatory disorder of the pancreas that may cause life-threatening complications.Etiologies of pancreatitis vary,with gallstones accounting for the majority of all cases,followed by alcohol.Other causes of pancreatitis include trauma,ischemia,mechanical obstruction,infections,autoimmune,hereditary,and drugs.The main events occurring in the pancreatic acinar cell that initiate and propagate acute pancreatitis include inhibition of secretion,intracellular activation of proteases,and generation of inflammatory mediators.Small cytokines known as chemokines are released from damaged pancreatic cells and attract inflammatory cells,whose systemic action ultimately determined the severity of the disease.Indeed,severe forms of pancreatitis may result in systemic inflammatory response syndrome and multiorgan dysfunction syndrome,characterized by a progressive physiologic failure of several interdependent organ systems.Stress occurs when homeostasis is threatened,and stressors can include physical or mental forces,or combinations of both.Depending on the timing and duration,stress can result in beneficial or harmful consequences.While it is well established that a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis,the worsening effects of chronic stress on the exocrine pancreas have received relatively little attention.This review will focus on the influence of both prior acute-short-term and chronic stress in acute pancreatitis. | Marcelo G Binker Laura I Cosen-Binker | 2014 | World Journal of Gastroenterology2014，20，19： | 10 |
| 3 | Chronic stress sensitizes rats to pancreatitis induced by cerulein:Role of TNF-α显示文摘AIM:To investigate chronic stress as a susceptibility factor for developing pancreatitis,as well as tumor necrosis factor-α (TNF-α) as a putative sensitizer.METHODS:Rat pancreatic acini were used to analyze the influence of TNF-α on submaximal (50 pmol/L) cholecystokinin (CCK) stimulation.Chronic restraint (4 h every day for 21 d) was used to evaluate the effects of submaximal (0.2 μg/kg per hour) cerulein stimulation on chronically stressed rats.RESULTS:In vitro exposure of pancreatic acini toTNF-α disorganized the actin cytoskeleton.This was further increased by TNF-α/CCK treatment,which additionally reduced amylase secretion,and increased trypsin and nuclear factor-κB activities in a protein-kinase-C δ and ε-dependent manner.TNF-α/CCK also enhanced caspases' activity and lactate dehydrogenase release,induced ATP loss,and augmented the ADP/ATP ratio.In vivo,rats under chronic restraint exhibited elevated serum and pancreatic TNF-α levels.Serum,pancreatic,and lung inflammatory parameters,as well as caspases' activity in pancreatic and lung tissue,were substantially enhanced in stressed/cerulein-treated rats,which also experienced tissues' ATP loss and greater ADP/ATP ratios.Histological examination revealed that stressed/cerulein-treated animals developed abundant pancreatic and lung edema,hemorrhage and leukocyte infiltrate,and pancreatic necrosis.Pancreatitis severity was greatly decreased by treating animals with an anti-TNF-αantibody,which diminished all inflammatory parameters,histopathological scores,and apoptotic/necrotic markers in stressed/cerulein-treated rats.CONCLUSION:In rats,chronic stress increases susceptibility for developing pancreatitis,which involves TNF-α sensitization of pancreatic acinar cells to undergo injury by physiological cerulein stimulation. | Marcelo G Binker Andres A Binker-Cosen Daniel Richards Herbert Y Gaisano Rodica H de Cosen Laura I Cosen-Binker | 2010 | World Journal of Gastroenterology2010，16，44： | 7 |
| 4 | Rac1 inhibition decreases the severity of pancreatitis and pancreatitis-associated lung injury in mice显示文摘 | BINKER M G BINKER COSEN A A GAISANO H Y | 2008 | Exp Physiol2008，93，10： | 1 |
| 5 | In- hibition of Racl decreases the severity of pancreati- tis and pancreatitis-associated lung injury in mice 显示文摘 | Binker MG Binker-Cosen AA Gaisano HY | 2008 | Exp Physiol2008，93，10： | 1 |
| 6 | Influence of stress in acute pancreatitis and correlation with stress - induced gastric ulcer 显示文摘 | Cosen - Binker LI Binker MG Negri G | 2004 | Pancreatology2004，4，16： | 1 |
| 7 | Inhibi-tion of Rac 1 decreases the severity of pancreatitis and pan- creatitis associated lung injury in mice 显示文摘 | Binker MG Binker-Cosen AA Gaisano HY | 2008 | Exp Physiol2008，93，： | 1 |
| 8 | Microvascular free flap reconstruction in pediatrec lower extremity trauma:a 10-year review显示文摘 | Binker B Valerio IL Stewart DH | 2005 | Plast Reconstr Surg2005，115，6： | 1 |
| 9 | Experimental model of acute pancreatitis in Wistar rat: glucocorticoid treatment profile显示文摘 | Cosen-Binker LI Binker MG Negri G | 2003 | Dig Dis and Sci2003，48，8： | 1 |
| 10 | TGF-β in- creases invasiveness of SWl990 cells through Racl/ROS/ NF-k B/IL-6/MMP-2显示文摘 | Binker MG Binker-Cosen AA Gaisano HY | 2011 | Biochem Biophys Res Commun2011，405，1： | 1 |
| 11 | VAMP8 is the v-SNARE that mediates basolateral exocytosis in a mouse model of alcoholic pancreatitis显示文摘 | Cosen-Binker Laura I Binker Marcelo G Wang Cheng-Chun Hong Wanjin Gaisano Herbert Y | 2008 | Journal of Clinical Investigation2008，，： | 1 |
| 12 | EGF promotes invasion by PANC-1 cells through Rac1/ROS-dependent secretion and activation of MMP-2显示文摘 | Marcelo G. Binker Andres A. Binker-Cosen Daniel Richards Brenda Oliver Laura I. Cosen-Binker | 2008 | Biochemical and Biophysical Research Communications2008，，2： | 1 |
| 13 | Hypoxia–reoxygenation increase invasiveness of PANC-1 cells through Rac1/MMP-2显示文摘 | Marcelo G. Binker Andres A. Binker-Cosen Daniel Richards Herbert Y. Gaisano Rodica H. de Cosen Laura I. Cosen-Binker | 2010 | Biochemical and Biophysical Research Communications2010，，3： | 1 |
| 14 | Alcohol redirects CCK- mediated apical exocytosis to the acinar basolateral membrane in alcoholic pancreatitis显示文摘 | Lam PP Cosen Binker LI Lugea A | 2007 | Traffic2007，8，5： | 1 |
| 15 | Influenceof nitric oxide-donating nonsteroidal anti-inflammatorydrugs on the evolution of acute pancreatitis显示文摘 | Cosen-Binker LI Binker MG Cosen R | 2006 | Shoe2006，25，2： | 1 |
| 16 | Hypoxia-reox-ygenation increase invasiveness of PANC-I cells through Racl/ MMP-2显示文摘 | Binker MG Binker-Cosen AA Richards D | 2010 | Biochem Biophys Res Commun2010，393，3： | 1 |
| 17 | Hypoxia- reoxygenation increase invasiveness of PANC-1 ceils through Racl/MMP-2显示文摘 | Binker MG Binker-Cosen AA Richards D | 2010 | Biochem Biophys Res Commun2010，393，3： | 1 |
| 18 | Structural revision and synthesis of altechromone A 显示文摘 | Konigs P Binker B Waldvogel S R | 2010 | J Nat Prod2010，73，： | 1 |
| 19 | Inhibition of Rac1 decreases the severity of pancreatitis and pancreatitis-associated lung injury in mice显示文摘 | Binker M G Binker-Cosen A A Gaisano H Y | 2008 | Exp Physiol2008，93，10： | 1 |
| 20 | Influence of nitric oxide-donating nonsteroidal anti-inflammatory drugs on the evolution of acute pancreatitis显示文摘 | Cosen-Binker LI Binker MG Cosen R | 2006 | Shock2006，25，2： | 1 |
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