AIM:To investigate whether peripheral corticotropin releasing hormone (CRH), which is up-regulated in intestinal inflammation, mediates the post-inflammatory visceral hypersensitivity in a rat model of colitis. METHOD...AIM:To investigate whether peripheral corticotropin releasing hormone (CRH), which is up-regulated in intestinal inflammation, mediates the post-inflammatory visceral hypersensitivity in a rat model of colitis. METHODS:We measured mucosal myeloperoxidase (MPO) activity as a marker of inflammation, plasma CRH level, and abdominal withdrawal reflex (AWR) to colorectal distension as a visceral nociceptive response at 2, 7 and 14 d after the induction of colitis with 4% acetic acid. RESULTS:Colonic inflammation, quantified by MPO activity, significantly increased on d 2 and subsided thereafter, which indicated a resolution of inflammation within 7 d. On the contrary, plasma CRH level and AWR score were increased on d 2, remained high on d 7, and returned to control level on d 14. Intraperitoneal injection of a CRH antagonist, astressin (30 μg/kg), significantly attenuated the post-inflammatory visceral hypersensitivity on d 7. Furthermore, intraperitoneal administration of CRH (3 and 10 μg/kg) mimicked the post-inflammatory visceral hypersensitivity in naive rats. CONCLUSION:These results suggest that increased peripheral CRH mediates the enhanced visceral nociception in rats recovered from experimental colitis.展开更多
AIM: To investigate the effects of gastrin and cholecystokinin (CCK) and their specific antagonists on the growth of pancreatic and biliary tract cancer cell lines. METHODS: Five pancreatic and 6 biliary cancer cell l...AIM: To investigate the effects of gastrin and cholecystokinin (CCK) and their specific antagonists on the growth of pancreatic and biliary tract cancer cell lines. METHODS: Five pancreatic and 6 biliary cancer cell lines with 2 conrtol cells were used in this study. Cell proliferation study was done using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) test and direct cell count method. Reverse transcription-polymerase chain reaction (RT-PCR) and slot blot hybridization were performed to examine and quantify the expression of hormonal receptors in these cell lines. RESULTS: SNU-308 showed a growth stimulating effect by gastrin-17, as did SNU-478 by both gastrin-17 and CCK-8. The trophic effect of these two hormones was completely blocked by specific antagonists (L-365, 260 for gastrin and L-364, 718 for CCK). Other cell lines did not respond to gastrin or CCK. In RT-PCR, the presence of CCK-A receptor and CCK-B/gastrin receptor mRNA was detected in all biliary and pancreatic cancer cell lines. In slot blot hybridization, compared to the cell lines which did not respond to hormones, those that responded to hormones showed high expression of receptor mRNA. CONCLUSION: Gastrin and CCK exert a trophic action on some of the biliary tract cancers.展开更多
Objective： To evaluate the local risk factors of traumatic brain injury （TBI） patients developing gastrointestinal （GI） bleeding during the early hospitalization in neurosurgery intensive care unit （NICU）. Met...Objective： To evaluate the local risk factors of traumatic brain injury （TBI） patients developing gastrointestinal （GI） bleeding during the early hospitalization in neurosurgery intensive care unit （NICU）. Method： From September 2005 to February 2006, 41 patients admitted to NICU and 13 healthy volunteers were involved in our study. Blood samples at 24 hours, 2-3 days and 5-7 days were obtained from each patient via arterial line at 8 a.m. to measure the concentrations of serum adrenocorticotropic hormone （ACTH）, total cortisol and gastrin. The collected serum was immersed in an ice bath and tested by the Immulite 1000 systems. Data were analyzed by SPSS 11.5. Results： Within 24 hours following TBI, the concentrations of total cortisol, ACTH and gastrin increased proportionally to the severity of injury, especially significant in the experimental group （P〈0.05）. The concentrations of ACTH and gastrin were higher in the GI bleeding positive group than in the GI bleeding negative group, （F=1.413, P=0.253） for ACTH and （F=9.371, P=0.006） for gastrin. GI bleeding had a positive correlation with gastrin concentration （r=0. 312, P〈0.05） and a negative correlation with serum hemoglobin （Hb） （r=-0.420, P〈0.01）. The clinical incidence of GI bleeding was 24.39% （10/41） in the experimental group. Within 24 hours, GI bleeding had a strong correlation with gastrin concentration （OR=26.643, P〈0.05） and hematocrit （Hct） （OR=5.385, P〈0.05）. High ACTH concentration （〉100 pg/ml） increased the frequency of GI bleeding. For patients with severe TBI and treated with routine antacids, the incidence of GI bleeding was 40.91% （9/22） and the mortality rate was 20%（2/10）. Conclusions： Low Glasgow coma scale scores, low Hb, high concentrations of gastrin and ACTH （〉 100 pg/ml） are risk factors and can be predictive values for post-traumatic GI bleeding. Severe TBI patients have high risks of GI bleeding with high mortality.展开更多
文摘AIM:To investigate whether peripheral corticotropin releasing hormone (CRH), which is up-regulated in intestinal inflammation, mediates the post-inflammatory visceral hypersensitivity in a rat model of colitis. METHODS:We measured mucosal myeloperoxidase (MPO) activity as a marker of inflammation, plasma CRH level, and abdominal withdrawal reflex (AWR) to colorectal distension as a visceral nociceptive response at 2, 7 and 14 d after the induction of colitis with 4% acetic acid. RESULTS:Colonic inflammation, quantified by MPO activity, significantly increased on d 2 and subsided thereafter, which indicated a resolution of inflammation within 7 d. On the contrary, plasma CRH level and AWR score were increased on d 2, remained high on d 7, and returned to control level on d 14. Intraperitoneal injection of a CRH antagonist, astressin (30 μg/kg), significantly attenuated the post-inflammatory visceral hypersensitivity on d 7. Furthermore, intraperitoneal administration of CRH (3 and 10 μg/kg) mimicked the post-inflammatory visceral hypersensitivity in naive rats. CONCLUSION:These results suggest that increased peripheral CRH mediates the enhanced visceral nociception in rats recovered from experimental colitis.
基金Supported by a grant from Seoul National University Research Fund (03-99-080 and 082)
文摘AIM: To investigate the effects of gastrin and cholecystokinin (CCK) and their specific antagonists on the growth of pancreatic and biliary tract cancer cell lines. METHODS: Five pancreatic and 6 biliary cancer cell lines with 2 conrtol cells were used in this study. Cell proliferation study was done using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) test and direct cell count method. Reverse transcription-polymerase chain reaction (RT-PCR) and slot blot hybridization were performed to examine and quantify the expression of hormonal receptors in these cell lines. RESULTS: SNU-308 showed a growth stimulating effect by gastrin-17, as did SNU-478 by both gastrin-17 and CCK-8. The trophic effect of these two hormones was completely blocked by specific antagonists (L-365, 260 for gastrin and L-364, 718 for CCK). Other cell lines did not respond to gastrin or CCK. In RT-PCR, the presence of CCK-A receptor and CCK-B/gastrin receptor mRNA was detected in all biliary and pancreatic cancer cell lines. In slot blot hybridization, compared to the cell lines which did not respond to hormones, those that responded to hormones showed high expression of receptor mRNA. CONCLUSION: Gastrin and CCK exert a trophic action on some of the biliary tract cancers.
文摘Objective： To evaluate the local risk factors of traumatic brain injury （TBI） patients developing gastrointestinal （GI） bleeding during the early hospitalization in neurosurgery intensive care unit （NICU）. Method： From September 2005 to February 2006, 41 patients admitted to NICU and 13 healthy volunteers were involved in our study. Blood samples at 24 hours, 2-3 days and 5-7 days were obtained from each patient via arterial line at 8 a.m. to measure the concentrations of serum adrenocorticotropic hormone （ACTH）, total cortisol and gastrin. The collected serum was immersed in an ice bath and tested by the Immulite 1000 systems. Data were analyzed by SPSS 11.5. Results： Within 24 hours following TBI, the concentrations of total cortisol, ACTH and gastrin increased proportionally to the severity of injury, especially significant in the experimental group （P〈0.05）. The concentrations of ACTH and gastrin were higher in the GI bleeding positive group than in the GI bleeding negative group, （F=1.413, P=0.253） for ACTH and （F=9.371, P=0.006） for gastrin. GI bleeding had a positive correlation with gastrin concentration （r=0. 312, P〈0.05） and a negative correlation with serum hemoglobin （Hb） （r=-0.420, P〈0.01）. The clinical incidence of GI bleeding was 24.39% （10/41） in the experimental group. Within 24 hours, GI bleeding had a strong correlation with gastrin concentration （OR=26.643, P〈0.05） and hematocrit （Hct） （OR=5.385, P〈0.05）. High ACTH concentration （〉100 pg/ml） increased the frequency of GI bleeding. For patients with severe TBI and treated with routine antacids, the incidence of GI bleeding was 40.91% （9/22） and the mortality rate was 20%（2/10）. Conclusions： Low Glasgow coma scale scores, low Hb, high concentrations of gastrin and ACTH （〉 100 pg/ml） are risk factors and can be predictive values for post-traumatic GI bleeding. Severe TBI patients have high risks of GI bleeding with high mortality.
