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1.
Chinese Journal of Pathophysiology ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-521498

ABSTRACT

AIM: To investigate the expression of neurok inin-2 receptor (NK-2R) in normal pancreas and chronic pancreatitis (CP) tissues. The relation of expres sion of NK-2R with pain in CP was also evaluated. METHODS: CP tis sues were ob tained from 18 men and 7 women undergoing pancreatic head resection as a result of CP. Normal human pancreatic tissues were obtained from 20 patients (11 males/ 9 females). Real-time quantitative reverse transcription polymerase chain reacti on was used to determine the mRNA expression of NK-2R, Western blot analysis was used to determine its protein expression level, and immunohistochemistry was us ed to localize expression site of NK-2R protein. NK-2R mRNA level and pain were also analysed whether correlation exists. RESULTS: NK-2R mRNA and p rotein level were enhanced expressed in CP tissue samples compared with normal pancreas. Ove rexpression of NK-2R was related to the intensity ( r=0 59, P

2.
Chinese Journal of Pathophysiology ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-521196

ABSTRACT

AIM: To study the expression and the role of neurokinin-1 receptor(NK-1R) and neurokinin-2 receptor (NK-2R) in distal ileum during acute necrotizing pancreatitis(ANP).METHODS: 130 adult Sprague-Dawley rats were divided into 2 groups: the rats in ANP group( n=80 ) were induced by the retrograde intraductal infusion of 5% sodium taurocholate. The rats in sham operation control group ( n=50 ) received laparotomy only. Reverse transcription polymerase chain reaction (RT-PCR) was used to determine the mRNA expression of NK-1R and NK-2R, Western blot was used to investigate expression level of NK-1R.RESULTS: NK-1R and NK-2R mRNA levels were enhanced in the distal ileum of ANP rats compared with controls. Western blot revealed stronger NK-1R immunoreactivity exited in intestinal mucosa in ANP rats. The overexpression of NK-1R was associated with mucosal pathological score( r=0.77,P

3.
Chinese Journal of General Surgery ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-673913

ABSTRACT

Objective To investigate the expression of neurokinin 3 receptor (NK 3R) in normal pancreas and pancreatic cancer, and to study the localization of this receptor in pancreatic cancer Methods The expression of NK 3R mRNA was investigated using reverse transcription polymerase chain reaction (RT PCR) in normal pancreas and pancreatic cancer tissues The protein level of NK 3R was investigated by Western blot Immunohistochemistry was used to localize expression site of NK 3R Results NK 3R mRNA was overexpressed in pancreatic cancer tissue when compared with normal pancreas NK 3R protein was 1 1?0 5 in normal pancreas and 14 6?3 6 in pancreatic cancer, P

4.
Chinese Journal of General Surgery ; (12)1997.
Article in Chinese | WPRIM | ID: wpr-520887

ABSTRACT

Objective To investigate the role of substance P (SP) and its neurokinin-1 receptor (NK-1R) in the pathophysiologic process of Crohn′s disease. Methods In 23 surgical patients of Crohn′s disease and 24 healthy controls, reverse transcription polymerase chain reaction (RT-PCR) was used to determine the mRNA expression of NK-1R, Western blot analysis was used to determine NK-1R protein expression levels, and immunohistochemistry was used to localize expression of NK-1R. Results Compared with normal gut NK-1R mRNA and NK-1R protein in Crohn′s disease were overexpressed. In Crohn′s disease moderate to strong intestinal NK-1R immunoreactivity was found in the lamina propria mononuclear cells, lymphoid follicles, and the surface and crypt epithelium, lymphoid follicles, submucosal vessels, smooth muscle and myoenteric plexus neurones. Conclusions In cases of Crohn′s disease, overexpression of NK-1R may disturb neuropeptides loop balance, and may be involved in the pathophysiological change in this disease.

5.
Chinese Journal of General Surgery ; (12)1993.
Article in Chinese | WPRIM | ID: wpr-520231

ABSTRACT

Objective To investigate the mechanism by which pancreatic cancer cells(PCC) acquire drug resistance against 5-FU and gemcitabine. Methods The cytotoxic effects of 5-FU and gemcitabine on PCC ( Panc-1, Mia-Paca-2 andCapan-1) were assessed by using Sulforhodamine B and the expression of anti-apoptotic genes of the Bcl-x L and mcl-1 were analyzed by RNase protection assay and Western blot. Results5-FU and gemcitabine effect cytotoxicity towards PCC. After repeated treatment with 5-FU, the IC 50 values in Capan-1 cells increased by 2.1 fold (P

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