AIM: To compare the therapeutic effects of proton pump inhibitors vs H2 receptor antagonists for upper gastrointestinal bleeding in patients after successful endoscopy.METHODS: We searched the Cochrane library, MEDLIN...AIM: To compare the therapeutic effects of proton pump inhibitors vs H2 receptor antagonists for upper gastrointestinal bleeding in patients after successful endoscopy.METHODS: We searched the Cochrane library, MEDLINE, EMBASE and Pub Med for randomized controlled trials until July 2014 for this study. The risk of bias was evaluated by the Cochrane Collaboration's tool and all of the studies had acceptable quality. The main outcomes included mortality, re-bleeding, received surgery rate, blood transfusion units and hospital stay time. These outcomes were estimated using odds ratios(OR) and mean difference with 95% confidence interval(CI). Rev Man 5.3.3 software and Stata 12.0 software were used for data analyses. RESULTS: Ten randomized controlled trials involving 1283 patients were included in this review; 678 subjects were in the proton pump inhibitors(PPI) group and the remaining 605 subjects were in the H2 receptor antagonists(H2RA) group. The meta-analysis results revealed that after successful endoscopic therapy, compared with H2 RA, PPI therapy had statistically significantly decreased the recurrent bleeding rate(OR = 0.36; 95%CI: 0.25-0.51) and receiving surgery rate(OR = 0.29; 95%CI: 0.09-0.96). There were no statistically significant differences in mortality(OR = 0.46; 95%CI: 0.17-1.23). However, significant heterogeneity was present in both the numbers of patients requiring blood transfusion after treatment [weighted mean difference(WMD),-0.70 unit; 95%CI:-1.64- 0.25] and the time that patients remained hospitalized [WMD,-0.77 d; 95%CI:-1.87- 0.34]. The Begg's test(P = 0.283) and Egger's test(P = 0.339) demonstrated that there was no publication bias in our meta-analysis.CONCLUSION: In patients with upper gastrointestinal bleeding after successful endoscopic therapy, compared with H2 RA, PPI may be a more effective therapy.展开更多
Ten cases of gastrointestinal adenocarcinomas were histochemically investigated fortheir lectin receptors by avidin—biotin-peroxidase complex(ABC)method.Results showed thatgastric adenocarcinomas expressed more types...Ten cases of gastrointestinal adenocarcinomas were histochemically investigated fortheir lectin receptors by avidin—biotin-peroxidase complex(ABC)method.Results showed thatgastric adenocarcinomas expressed more types of lectin receptors than large boweladenocarcinomas.Positive rates of Glc/Man-and GlcNAc-specific lectin receptors in these tu-mors were kigher than those of Gal/GalNAc-and Fuc-specific lectin receptors.From the stom-ach to rectum,the spectrum of the lectin receptors in pericarcinomatous tissues graduallychanged from the gastric type to the rectal type.The expression of lectin receptors ingustrointestinal adenocarcinomas was obviously different Jrom that in their correspondingpericarcinomatous tissues.The increase and decrease of lectin receptor expression,theappearance and disappearance of some types of lectin receptors as well as the change of thereceptor distribution are indirectly regulated by cellular genome.展开更多
BACKGROUND For lung adenocarcinoma with epidermal growth factor receptor(EGFR)gene mutation,small molecule tyrosine kinase inhibitors are more effective.Some patients could not obtain enough histological specimens for...BACKGROUND For lung adenocarcinoma with epidermal growth factor receptor(EGFR)gene mutation,small molecule tyrosine kinase inhibitors are more effective.Some patients could not obtain enough histological specimens for EGFR gene mutation detection.Specific imaging features can predict EGFR mutation status to a certain extent.AIM To assess the associations of EGFR mutations with high-resolution computerized tomography(HRCT)features in ground-glass nodular lung adenocarcinoma.METHODS This study retrospectively assessed patients with ground-glass nodular lung adenocarcinoma diagnosed between January 2011 and March 2017.EGFR gene mutations in exons 18-21 were detected.The patients were classified into mutant EGFR and wild-type groups,and general data and HRCT image characteristics were assessed.RESULTS Among 98 patients,31(31.6%)and 67(68.4%)had mutated and wild-type EGFR in exons 18-21,respectively.Gender,age,smoking history,location of lesions,morphology,edges,borders,pleural indentations,and associations of nodules with bronchus and blood vessels were comparable in both groups(all P>0.05).Patients with mutant EGFR had larger nodules than those with the wild-type(17.19±6.79 and 14.37±6.30 mm,respectively;P=0.047).Meanwhile,the vacuole/honeycomb sign was more frequent in the mutant EGFR group(P=0.011).The logistic regression prediction model included the combination of nodule size and vacuole/honeycomb sign(OR=1.120,95%CI:1.023-1.227,P=0.014)revealed a sensitivity of 83.9%,a specificity of 52.2%and an AUC of 0.698(95%CI:0.589-0.806;P=0.002).CONCLUSION Nodule size and vacuole/honeycomb features could independently predict EGFR mutation status in ground-glass nodular lung adenocarcinoma.展开更多
Gastrointestinal stromal tumors(GISTs) are the most common soft tissue sarcoma of the gastrointestinal tract,resulting from an activating mutation of stem cell factor receptor(KIT),and an activating mutation of the ho...Gastrointestinal stromal tumors(GISTs) are the most common soft tissue sarcoma of the gastrointestinal tract,resulting from an activating mutation of stem cell factor receptor(KIT),and an activating mutation of the homologous platelet-derived growth factor receptor alpha(PDGFRA) kinase.Most GISTs(90%-95%) are KIT-positive.About 5% of GISTs are truly negative for KIT expression.GISTs have been documented to resistant conventional chemotherapeutics.Due to the KIT activation that occurs in the majority of the cases,KIT inhibition is the primary treatment approach in the adjuvant treatment of metastatic GISTs.Imatinib mesylate is an oral agent that is a selective protein tyrosine kinase inhibitor of the KIT protein tyrosine kinase,and it has demonstrated clinical benefit and objective tumor responses in most GIST patients in phase Ⅱ and Ⅲ trials.The presence and the type of KIT or PDGFRA mutation are predictive of response to imatinib therapy in patients with advanced and metastatic disease.Molecular analysis in phaseⅠ-Ⅱ trials revealed significant differences in objective response,progression-free survival,and overall survival between GISTs with different kinase mutations.The aim of this letter is to touch on the need for exon mutation analysis for adjuvant treatment with imatinib in GIST patients.展开更多
Sendur et al pointed out the attention on the importance of mutational analysis for adjuvant treatment of gastrointestinal stromal tumor (GIST) in an article published in World Journal of Gastroenterology . In particu...Sendur et al pointed out the attention on the importance of mutational analysis for adjuvant treatment of gastrointestinal stromal tumor (GIST) in an article published in World Journal of Gastroenterology . In particular, they suggested that the optimal dose and duration of adjuvant therapy could be defined by the mutational status of the primary disease. This comment would underline the importance of centralised laboratories, given the increasingly important role of molecular analysis in the work-flow of all GIST, and the need of retrospective analyses for subgroups population stratified for the mutational status from the available studies in the adjuvant setting, in order to define the role of mutational analysis in choosing the optimal dose and duration of adjuvant therapy.展开更多
Mazur and Clark introduced the term ＂gastrointestinal stromal tumor＂ （GIST）. These tumors are thought to originate from mesenchymal stem cells that differentiate toward the interstitial cells of Cajal. Activation ...Mazur and Clark introduced the term ＂gastrointestinal stromal tumor＂ （GIST）. These tumors are thought to originate from mesenchymal stem cells that differentiate toward the interstitial cells of Cajal. Activation of c-kit or platelet-derived growth factor receptor alpha （PDGFRA） gene mutation has been shown to be a major force in GIST pathogenesis leading to down-stream phosphorylation of substrate proteins and subsequently activation of networks of signal transduction pathways that regulate cell proliferation,survival, apoptosis, motility and other important cell functions. Immunohistochemically, a great majority of GISTs show strong, diffuse c-kit expression. The diagnosis of GIST is currently based on morphologic features and immunohistochemical demonstration of c-kit （CD117）. However, in some cases c-kit immunoreactivity is weak or undetectable.展开更多
A review is presented on the theories concerning the cause of pyloric stenosis with emphasis on the primary position of inherited hyperacidity in pathogenesis. Existing theories are critically analysed and the hyperac...A review is presented on the theories concerning the cause of pyloric stenosis with emphasis on the primary position of inherited hyperacidity in pathogenesis. Existing theories are critically analysed and the hyperacidity theory is precisely defined in the light of recent physiological insights into the gastrointestinal hormone motilin. The progressive fixed fasting hypergastrinaemia within the first few weeks of life will, in the baby who inherits acid secretion at the top of the normal range, produce hyperacidity of sufficient severity to trigger the process of acid-induced work hypertrophy of the pylorus. The potential contribution of motilin is discussed. The baby who inherits a normal gastric acidity will not reach acid levels severe enough to trigger sphincter hypertrophy despite the early gastrin stimulus. The potential threat will cease when gastrin naturally declines with age and the pyloric canal becomes wider. Genetic factors clearly must also be involved and these are separately discussed.展开更多
基金Supported by National Natural Science Funds of China,No.81102784/H2803the key project in scientific research from ministry of education,No.212032Liaoning Innovative Research Team in University,No.LT2013022
文摘AIM: To compare the therapeutic effects of proton pump inhibitors vs H2 receptor antagonists for upper gastrointestinal bleeding in patients after successful endoscopy.METHODS: We searched the Cochrane library, MEDLINE, EMBASE and Pub Med for randomized controlled trials until July 2014 for this study. The risk of bias was evaluated by the Cochrane Collaboration's tool and all of the studies had acceptable quality. The main outcomes included mortality, re-bleeding, received surgery rate, blood transfusion units and hospital stay time. These outcomes were estimated using odds ratios(OR) and mean difference with 95% confidence interval(CI). Rev Man 5.3.3 software and Stata 12.0 software were used for data analyses. RESULTS: Ten randomized controlled trials involving 1283 patients were included in this review; 678 subjects were in the proton pump inhibitors(PPI) group and the remaining 605 subjects were in the H2 receptor antagonists(H2RA) group. The meta-analysis results revealed that after successful endoscopic therapy, compared with H2 RA, PPI therapy had statistically significantly decreased the recurrent bleeding rate(OR = 0.36; 95%CI: 0.25-0.51) and receiving surgery rate(OR = 0.29; 95%CI: 0.09-0.96). There were no statistically significant differences in mortality(OR = 0.46; 95%CI: 0.17-1.23). However, significant heterogeneity was present in both the numbers of patients requiring blood transfusion after treatment [weighted mean difference(WMD),-0.70 unit; 95%CI:-1.64- 0.25] and the time that patients remained hospitalized [WMD,-0.77 d; 95%CI:-1.87- 0.34]. The Begg's test(P = 0.283) and Egger's test(P = 0.339) demonstrated that there was no publication bias in our meta-analysis.CONCLUSION: In patients with upper gastrointestinal bleeding after successful endoscopic therapy, compared with H2 RA, PPI may be a more effective therapy.
文摘Ten cases of gastrointestinal adenocarcinomas were histochemically investigated fortheir lectin receptors by avidin—biotin-peroxidase complex(ABC)method.Results showed thatgastric adenocarcinomas expressed more types of lectin receptors than large boweladenocarcinomas.Positive rates of Glc/Man-and GlcNAc-specific lectin receptors in these tu-mors were kigher than those of Gal/GalNAc-and Fuc-specific lectin receptors.From the stom-ach to rectum,the spectrum of the lectin receptors in pericarcinomatous tissues graduallychanged from the gastric type to the rectal type.The expression of lectin receptors ingustrointestinal adenocarcinomas was obviously different Jrom that in their correspondingpericarcinomatous tissues.The increase and decrease of lectin receptor expression,theappearance and disappearance of some types of lectin receptors as well as the change of thereceptor distribution are indirectly regulated by cellular genome.
基金by the Zhejiang Province Traditional Chinese Medicine Science and Technology Plan-Zhejiang Province Traditional Chinese Medicine Project for Traditional Chinese Medicine Scientific Research(2020)(Class B),No.2020ZB117。
文摘BACKGROUND For lung adenocarcinoma with epidermal growth factor receptor(EGFR)gene mutation,small molecule tyrosine kinase inhibitors are more effective.Some patients could not obtain enough histological specimens for EGFR gene mutation detection.Specific imaging features can predict EGFR mutation status to a certain extent.AIM To assess the associations of EGFR mutations with high-resolution computerized tomography(HRCT)features in ground-glass nodular lung adenocarcinoma.METHODS This study retrospectively assessed patients with ground-glass nodular lung adenocarcinoma diagnosed between January 2011 and March 2017.EGFR gene mutations in exons 18-21 were detected.The patients were classified into mutant EGFR and wild-type groups,and general data and HRCT image characteristics were assessed.RESULTS Among 98 patients,31(31.6%)and 67(68.4%)had mutated and wild-type EGFR in exons 18-21,respectively.Gender,age,smoking history,location of lesions,morphology,edges,borders,pleural indentations,and associations of nodules with bronchus and blood vessels were comparable in both groups(all P>0.05).Patients with mutant EGFR had larger nodules than those with the wild-type(17.19±6.79 and 14.37±6.30 mm,respectively;P=0.047).Meanwhile,the vacuole/honeycomb sign was more frequent in the mutant EGFR group(P=0.011).The logistic regression prediction model included the combination of nodule size and vacuole/honeycomb sign(OR=1.120,95%CI:1.023-1.227,P=0.014)revealed a sensitivity of 83.9%,a specificity of 52.2%and an AUC of 0.698(95%CI:0.589-0.806;P=0.002).CONCLUSION Nodule size and vacuole/honeycomb features could independently predict EGFR mutation status in ground-glass nodular lung adenocarcinoma.
文摘Gastrointestinal stromal tumors(GISTs) are the most common soft tissue sarcoma of the gastrointestinal tract,resulting from an activating mutation of stem cell factor receptor(KIT),and an activating mutation of the homologous platelet-derived growth factor receptor alpha(PDGFRA) kinase.Most GISTs(90%-95%) are KIT-positive.About 5% of GISTs are truly negative for KIT expression.GISTs have been documented to resistant conventional chemotherapeutics.Due to the KIT activation that occurs in the majority of the cases,KIT inhibition is the primary treatment approach in the adjuvant treatment of metastatic GISTs.Imatinib mesylate is an oral agent that is a selective protein tyrosine kinase inhibitor of the KIT protein tyrosine kinase,and it has demonstrated clinical benefit and objective tumor responses in most GIST patients in phase Ⅱ and Ⅲ trials.The presence and the type of KIT or PDGFRA mutation are predictive of response to imatinib therapy in patients with advanced and metastatic disease.Molecular analysis in phaseⅠ-Ⅱ trials revealed significant differences in objective response,progression-free survival,and overall survival between GISTs with different kinase mutations.The aim of this letter is to touch on the need for exon mutation analysis for adjuvant treatment with imatinib in GIST patients.
文摘Sendur et al pointed out the attention on the importance of mutational analysis for adjuvant treatment of gastrointestinal stromal tumor (GIST) in an article published in World Journal of Gastroenterology . In particular, they suggested that the optimal dose and duration of adjuvant therapy could be defined by the mutational status of the primary disease. This comment would underline the importance of centralised laboratories, given the increasingly important role of molecular analysis in the work-flow of all GIST, and the need of retrospective analyses for subgroups population stratified for the mutational status from the available studies in the adjuvant setting, in order to define the role of mutational analysis in choosing the optimal dose and duration of adjuvant therapy.
文摘Mazur and Clark introduced the term ＂gastrointestinal stromal tumor＂ （GIST）. These tumors are thought to originate from mesenchymal stem cells that differentiate toward the interstitial cells of Cajal. Activation of c-kit or platelet-derived growth factor receptor alpha （PDGFRA） gene mutation has been shown to be a major force in GIST pathogenesis leading to down-stream phosphorylation of substrate proteins and subsequently activation of networks of signal transduction pathways that regulate cell proliferation,survival, apoptosis, motility and other important cell functions. Immunohistochemically, a great majority of GISTs show strong, diffuse c-kit expression. The diagnosis of GIST is currently based on morphologic features and immunohistochemical demonstration of c-kit （CD117）. However, in some cases c-kit immunoreactivity is weak or undetectable.
文摘A review is presented on the theories concerning the cause of pyloric stenosis with emphasis on the primary position of inherited hyperacidity in pathogenesis. Existing theories are critically analysed and the hyperacidity theory is precisely defined in the light of recent physiological insights into the gastrointestinal hormone motilin. The progressive fixed fasting hypergastrinaemia within the first few weeks of life will, in the baby who inherits acid secretion at the top of the normal range, produce hyperacidity of sufficient severity to trigger the process of acid-induced work hypertrophy of the pylorus. The potential contribution of motilin is discussed. The baby who inherits a normal gastric acidity will not reach acid levels severe enough to trigger sphincter hypertrophy despite the early gastrin stimulus. The potential threat will cease when gastrin naturally declines with age and the pyloric canal becomes wider. Genetic factors clearly must also be involved and these are separately discussed.
