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64篇 您的检索式:作者名="Wound"
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1Rapid mitogen-activated protein kinase by basic fibroblast growth factor in rat intestine after ischemia/reperfusion injury显示文摘AIM: Previous studies showed that exogenous basic fibroblast growth factor (bFGF or FGF-2) could improve physiological dysfunction after intestinal ischemia/reperfusion (I/R) injury. However, the mechanisms of this protective effect of bFGF are still unclear. The present study was to detect the effect of bFGF on the activities of mitogen-activated protein kinase (MAPK) signaling pathway in rat intestine after I/R injury, and to investigate the protective mechanisms of bFGF on intestinal ischemiain jury.METHODS: Rat intestinal I/R injury was produced by clamping the superior mesenteric artery (SMA) for 45 minutes and followed by reperfusion for 48 hours. Seventy-eight Wistar rats were used and divided randomly into sham-operated group (A), normal saline control group (B),bFGF antibody pre-treated group (C), and bFGF treated group (D). In group A, SMA was separated without occlusion. In groups B, C and D, SMA was separated and occluded for 45 minutes, then, released for reperfusion for 48 hours. After the animals were sacrificed, blood and tissue samples were taken from the intestine 45 minutes after ischemia in group A and 2, 6, 24, and 48 hours after reperfusion in the other groups. Phosphorylated forms of p42/p44 MAPK, p38 MAPK and stress activated protein kinase/C-Jun N-terminal kinase (SAPK/JNK) were measured by immunohistochemistry. Plasma levels of D-lactate were examined and histological changes were observed under the light microscope.RESULTS: Intestinal I/R injury induced the expression of p42/p44 MAPK, p38 MAPK, and SAPK/JNK pathways and exogenous bFGF stimulated the early activation of p42/p44 MAPK and p38 MAPK pathways. The expression of phosphorylated forms of p42/p44 MAPK was primarily localized in the nuclei of crypt cells and in the cytoplasm and nuclei of villus cells. The positive expression of p38 MAPK was localized mainly in the nuclei of crypt cells, very few in villus cells. The activities of p42/p44 MAPK and p38 MAPK peaked 6 hours after reperfusion in groups B and C,while SAPK/JNK peaked 24 hours after reperfusion. The activities of p42/p44 MAPK and p38 MAPK peaked 2 hours after reperfusion in group D and those of SAPK/JNK were not changed in group B. D-lactate levels and HE staining showed that the intestinal barrier was damaged severely 6 hours after reperfusion, however, histological structures were much improved 48 hours after reperfusion in group D than in the other groups.CONCLUSION: The results indicate that intestinal I/R injury stimulates the activities of MAPK pathways, and that p42/p44 MAPK and p38MAPK activities are necessary for the protective effect of exogenous bFGF on intestinal I/R injury.The protective effect of bFGF on intestinal dysfunction may be mediated by the early activation of p42/p44 MAPK and p38 MAPK signaling pathways.Xiao-Bing Fu Yin-Hui Yang Tong-Zhu Sun Wei Chen Jun-You Li Zhi-Yong Sheng Wound Healing and Cell Biology Laboratory,Burns Institute,304 Hospital,Trauma Center of Postgraduate Medical College,Beijing 100037,China 2003World Journal of Gastroenterology2003,9,6:11
2Activation of phosphorylating-p38 mitogen-activated protein kinase and its relationship with localization of intestinal stem cells in rats after ischemia-reperfusion injury显示文摘AIM: To investigate the expression of phosphorylating p38mitogen-activated protein kinase (MAPK) in rat small intestine after ischemia-reperfusion (I/R) insult and its relationship with the localization of intestinal stem cells.METHODS: Forty-eight Wistar rats were divided randomly into three groups, namely intestinal ischemia-reperfusion group (R), intestinal ischemia group (Ⅰ) and sham-operated control group (C). In group I, the animals were killed 45minutes after superior mesenteric artery (SMA) occlusion,while in group R the rats sustained SMA occlusion for 45 minutes and reperfusion for 2, 6, 12 or 24 hours respectively. In shamoperated control group, SMA was separated, but without occlusion. The activity of plasma diamine oxidase (DAO)was determined. Intestinal tissue samples were also taken for histological analysis and immunohistochemical analysis of MAPK p38 detection and intestinal stem cell localization.RESULTS: The changes in histological structure and plasma DAO levels indicated that the intestinal barrier was damaged after intestinal I/R injury. In group C and I, each crypt contained 5-6 p38 MAPK positive cells, which were mainly located in the lower region of the crypts. This was consistent with the distribution of intestinal stem cells. The presence of positive cells in crypts increased with the time of reperfusion and reached its peak at 12 hours after reperfusion (35.6%).CONCLUSION: After intestinal T/R injury, the expression of phosphorylating-p38 MAPK in small intestine increased with the duration of reperfusion, and its distribution coincided with that of intestinal stem cells and their daughter cells,indicating that phosphorylating-p38 might be a possible marker of intestinal stem cells.Xiao-Bing Fu Feng Xing Yin-Hui Yang Tong-Zhu Sun Bao-Chen Guo Wound Healing and Cell Biology Laboratory,Institute of Burns,304 Hospital,Trauma Center of Postgraduate Medical College,Beijing 100037,China 2003World Journal of Gastroenterology2003,9,9:10
3Detrimental effects of beta-blockers in COPD: a concern for nonselective beta-blockers显示文摘van der WOUND HJ ZAAGSMA J POSTMAS DS et td 2005Chest2005,127,3:1
4Vacuum2assisted complex wound closure with elas-tic vessel loop augmentation 显示文摘Wound Care 2003a novel technique2003,12,6:1
5Prevalence and incidenee:a Toolkit for clinicians monitoring prevalence and incidence of pressured ulcers 显示文摘Wound Ostomy and Continence Nurses Society 2004Professional Practice Manual2004,,:1
6Vacuum-assisted complex wound closure with elastic vessel loop augmentation 显示文摘Wound Care 2003A novel technique2003,12,6:1
7Vacuum-assisted complex wound closure with elastic vessel loop augmentation显示文摘Wound Care 2003Novel Technique2003,12,6:1
8Wound, ostomy and continence nrses society position statement on avoidable versus unavoidable pressure ulcer显示文摘Wound Ostomy and Continence Nurses Society 2009Journal of Wound Ostomy&Continence Nursing2009,36,4:1
9What are we giving our patients显示文摘Southern EP Huo MH Mehta JR et aL Unwashed wound drainage blood 1995Clin Orthop Relat Res1995,320,:1
10Continence nurses society position statement on avoida-ble versus unavoidable pressure ulcers显示文摘Wound O 0,,04:1
11Prevalence and incidence: a toolkit for clinicians:monitoring prevalence and incidence of pressure ulcers显示文摘Wound Ostomy and-Continence Nurses Society 2004Professional Practice Manual2004,,:1
12Vacuum-assisted complex wound closure with elasticvesselloop augmentation显示文摘Wound Care 2003A Novel Technique2003,12,6:1
13Vacuum2assisted complex wound closurewith elastic vessel loop augmentation显示文摘Wound Care 2003A Novel Tech-nique2003,12,:1
14显示文摘Huang Z Pereira C Toliver-Kinsky T Effect of transforming growth factor-beta neutralization on survival and bacterial clearance in a murine model of Pseudomonas aeruginosa burn wound infection 2006J Burn Care Res2006,27,5:1
15Vacuum - assisted complex wound closure with elas- tic vessel loop augmentation 显示文摘Wound Care 2003A Novel Technique2003,12,6:1
16local anaesthetic agents for laparoscopic cholecystectomy 显示文摘LOIZIDES S GURUSAMY Wound infiltration with K S NAGENDRAN M 2014Cochrane Database Syst Rev2014,12,00:1
17Vacuum 2 assisted complex wound closure with elastic vessel loop augmentation显示文摘WOUND CARE 2003a novel technique2003,12,6:1
18Prevalence and Incidence : A Toolkit for Clinicians 显示文摘Wound Ostomy Continence Nurses Society (WOCN) 2004New Jersey: WOCN2004,,:1
19ASCRS and WOCN joint position Statement on the value of preoperative stoma marking for patients undergoing fecal ostomy surgery显示文摘American Society of Colon and Rectal Surgeons Committee Members Wound Ostomy Continence Nurses Society Committee Members 2007J Wound Ostomy Continence Nurs2007,34,6:1
20Local structure of amorphous Zr3Fe显示文摘VINCZE I VANDER WOUNDE F SCOTT M G 1981Solid State Communications1981,37,:1
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