Whilst methods exist to indirectly measure the effects of increased flow or gastro-oesophageal refluxing, they cannot quantitatively measure the amount of acid travelling back up into the oesophagus during reflux, nor...Whilst methods exist to indirectly measure the effects of increased flow or gastro-oesophageal refluxing, they cannot quantitatively measure the amount of acid travelling back up into the oesophagus during reflux, nor can they indicate the flow rate through the oesophagogastric junction (OGJ). Since OGJ dysfunction affects flow it seems most appropriate to describe the geometry of the OGJ and its effect on the flow. A device known as the functional lumen imaging probe (FLIP) has been shown to reliably measure the geometry of and pressure changes in the OGJ. FLIP cannot directly measure flow but the data gathered from the probe can be used to model flow through the junction by using computational flow dynamics (CFD). CFD uses a set of equations known as the Navier-Stokes equations to predict flow patterns and is a technique widely used in engineering. These equations are complex and require appropriate assumptions to provide simplifications before useful data can be obtained. With the assumption that the cross-sectional areas obtained via FLIP are circular, the radii of these circles can be obtained. A cubic interpolation scheme can then be applied to give a high-resolution geometry for the OGJ. In the case of modelling a reflux scenario, it can be seen that at the narrowest section a jet of fluid squirts into the oesophagus at a higher velocity than the fluid surrounding it. This jet has a maximum velocity of almost 2 ms-1 that occurs where the OGJ is at its narrowest. This simple prediction of acid ‘squirting’ into the oesophagusillustrates how the use of numerical methods can be used to develop a better understanding of the OGJ. This initial work using CFD shows some considerable promise for the future.展开更多
AIM: To investigate the difference of gene expression profiles between Barrett's esophagus and reflux esophagitis induced by gastroduodenoesophageal reflux in rats.METHODS: Eight-week-old Sprague-Dawley rats were ...AIM: To investigate the difference of gene expression profiles between Barrett's esophagus and reflux esophagitis induced by gastroduodenoesophageal reflux in rats.METHODS: Eight-week-old Sprague-Dawley rats were treated esophagoduodenostomy to produce gastroduodenoesophageal reflux, and another group received sham operation as control. Esophageal epithelial tissues were dissected and frozen in liquid nitrogen immediately for pathology 40 wk after surgery. The expression profiles of 4 096 genes in reflux esophagitis and Barrett's esophagus tissues were compared with normal esophageal epithelium by cDNA microarray.RESULTS: Four hundred and forty-eight genes in Barrett'sesophagus were more than three times different from those in normal esophageal epithelium, including 312 up regulated and 136 down-regulated genes. Two hundred and thirty-twogenes in RE were more than three times different from those in normal esophageal epithelium, 90up-regulated and 142 down-regulated genes. Compared to reflux esophagitis, there were 214 up-regulated and 142 down-regulated genes in Barrett's esophagus. CONCLUSION: Esophageal epithelium exposed excessively to harmful ingredients of duodenal and gastric reflux can develop esophagitis and Barrett's esophagus gradually.The gene expression level is different between reflux esophagitis and Barrett's esophagus and the differentially expressed genes might be related to the occurrence and development of Barrett's esophagus and the promotion or progression in adenocarcinoma.展开更多
AIM: To study the different gene expression profiles in rats with Barrett's esophagus (BE) and esophageal adenocarcinoma (EA) induced by gastro-duodenoesophageal reflux.METHODS: Esophagoduodenostomy was performed ...AIM: To study the different gene expression profiles in rats with Barrett's esophagus (BE) and esophageal adenocarcinoma (EA) induced by gastro-duodenoesophageal reflux.METHODS: Esophagoduodenostomy was performed in 8-wk old Sprague-Dawley rats to induce gastro-duodenoesophageal reflux, and a group of rats that received sham operation served as control. Esophageal epithelial pathological tissues were dissected and frozen in liquid nitrogen immediately. The expression profiles of 4 096genes in EA and BE tissues were compared to normal esophagus epithelium in normal control (NC) by cDNA microarray.RESULTS: Four hundred and forty-eight genes in BE were more than three times different from those in NC, including 312 upregulated and 136 downregulated genes. Three hundred and seventy-seven genes in EA were more than three times different from those in NC, including 255upregulated and 142 downregulated genes. Compared to BE, there were 122 upregulated and 156 downregulated genes in EA. In the present study, the interested genes were those involved in carcinogenesis. Among them, the upregulated genes included cathepsin C, aminopeptidase M, arachidonic acid epoxygenase, tryptophan-2,3-dioxygenase, ubiquitin-conjugating enzyme, cyclic GMP-stimulated phosphodiesterase, tissue inhibitor of metalloproteinase-1, betaine-homocysteine methyltransferase, lysozyme, complement 4b binding protein,complement 9 protein, insulin-like growth factor binding protein, UDP-glucuronosyltransferase, tissue inhibitor of metalloproteinase-3, aldolase B, retinoid X receptor gamma, carboxylesterase and testicular cell adhesion molecule 1. The downregulated genes included glutathione synthetase, lecithin-cholesterol acyltransferase, p55CDC,heart fatty acid binding protein, cell adhesion regulator and endothelial cell selectin ligand.CONCLUSION: Esophageal epithelium exposed excessively to harmful ingredients of duodenal and gastric reflux may develop into BE and even EA gradually. The gene expression level is different between EA and BE, and may be related to the occurrence and progression of EA.展开更多
基金Supported by a Science Foundation Ireland through the ETS Walton Visiting Professor Programme a grant from the Higher Education Authority in Ireland
文摘Whilst methods exist to indirectly measure the effects of increased flow or gastro-oesophageal refluxing, they cannot quantitatively measure the amount of acid travelling back up into the oesophagus during reflux, nor can they indicate the flow rate through the oesophagogastric junction (OGJ). Since OGJ dysfunction affects flow it seems most appropriate to describe the geometry of the OGJ and its effect on the flow. A device known as the functional lumen imaging probe (FLIP) has been shown to reliably measure the geometry of and pressure changes in the OGJ. FLIP cannot directly measure flow but the data gathered from the probe can be used to model flow through the junction by using computational flow dynamics (CFD). CFD uses a set of equations known as the Navier-Stokes equations to predict flow patterns and is a technique widely used in engineering. These equations are complex and require appropriate assumptions to provide simplifications before useful data can be obtained. With the assumption that the cross-sectional areas obtained via FLIP are circular, the radii of these circles can be obtained. A cubic interpolation scheme can then be applied to give a high-resolution geometry for the OGJ. In the case of modelling a reflux scenario, it can be seen that at the narrowest section a jet of fluid squirts into the oesophagus at a higher velocity than the fluid surrounding it. This jet has a maximum velocity of almost 2 ms-1 that occurs where the OGJ is at its narrowest. This simple prediction of acid ‘squirting’ into the oesophagusillustrates how the use of numerical methods can be used to develop a better understanding of the OGJ. This initial work using CFD shows some considerable promise for the future.
基金Supported by Ministry of Health Clinical Subject Key Project, No. 20012130
文摘AIM: To investigate the difference of gene expression profiles between Barrett's esophagus and reflux esophagitis induced by gastroduodenoesophageal reflux in rats.METHODS: Eight-week-old Sprague-Dawley rats were treated esophagoduodenostomy to produce gastroduodenoesophageal reflux, and another group received sham operation as control. Esophageal epithelial tissues were dissected and frozen in liquid nitrogen immediately for pathology 40 wk after surgery. The expression profiles of 4 096 genes in reflux esophagitis and Barrett's esophagus tissues were compared with normal esophageal epithelium by cDNA microarray.RESULTS: Four hundred and forty-eight genes in Barrett'sesophagus were more than three times different from those in normal esophageal epithelium, including 312 up regulated and 136 down-regulated genes. Two hundred and thirty-twogenes in RE were more than three times different from those in normal esophageal epithelium, 90up-regulated and 142 down-regulated genes. Compared to reflux esophagitis, there were 214 up-regulated and 142 down-regulated genes in Barrett's esophagus. CONCLUSION: Esophageal epithelium exposed excessively to harmful ingredients of duodenal and gastric reflux can develop esophagitis and Barrett's esophagus gradually.The gene expression level is different between reflux esophagitis and Barrett's esophagus and the differentially expressed genes might be related to the occurrence and development of Barrett's esophagus and the promotion or progression in adenocarcinoma.
基金Supported by the Major Program of Clinical Medicine of Ministry of Public Health, No. 20012130
文摘AIM: To study the different gene expression profiles in rats with Barrett's esophagus (BE) and esophageal adenocarcinoma (EA) induced by gastro-duodenoesophageal reflux.METHODS: Esophagoduodenostomy was performed in 8-wk old Sprague-Dawley rats to induce gastro-duodenoesophageal reflux, and a group of rats that received sham operation served as control. Esophageal epithelial pathological tissues were dissected and frozen in liquid nitrogen immediately. The expression profiles of 4 096genes in EA and BE tissues were compared to normal esophagus epithelium in normal control (NC) by cDNA microarray.RESULTS: Four hundred and forty-eight genes in BE were more than three times different from those in NC, including 312 upregulated and 136 downregulated genes. Three hundred and seventy-seven genes in EA were more than three times different from those in NC, including 255upregulated and 142 downregulated genes. Compared to BE, there were 122 upregulated and 156 downregulated genes in EA. In the present study, the interested genes were those involved in carcinogenesis. Among them, the upregulated genes included cathepsin C, aminopeptidase M, arachidonic acid epoxygenase, tryptophan-2,3-dioxygenase, ubiquitin-conjugating enzyme, cyclic GMP-stimulated phosphodiesterase, tissue inhibitor of metalloproteinase-1, betaine-homocysteine methyltransferase, lysozyme, complement 4b binding protein,complement 9 protein, insulin-like growth factor binding protein, UDP-glucuronosyltransferase, tissue inhibitor of metalloproteinase-3, aldolase B, retinoid X receptor gamma, carboxylesterase and testicular cell adhesion molecule 1. The downregulated genes included glutathione synthetase, lecithin-cholesterol acyltransferase, p55CDC,heart fatty acid binding protein, cell adhesion regulator and endothelial cell selectin ligand.CONCLUSION: Esophageal epithelium exposed excessively to harmful ingredients of duodenal and gastric reflux may develop into BE and even EA gradually. The gene expression level is different between EA and BE, and may be related to the occurrence and progression of EA.
