AIM:To investigate the association between central serous chorioretinopathy(CSC)and Helicobacter pylori(Hp)by summarizing all available evidence.METHODS:The Scopus,Embase,EBSCO,PubMed,Web of Science,and Cochrane Libra...AIM:To investigate the association between central serous chorioretinopathy(CSC)and Helicobacter pylori(Hp)by summarizing all available evidence.METHODS:The Scopus,Embase,EBSCO,PubMed,Web of Science,and Cochrane Library databases for all relevant studies published from inception to October 2022 were searched,and manually searched for relevant reference lists as a supplement.Studies investigating the association between CSC and Hp infection were included.Finally,8 case-control studies were included in the Meta-analysis after study selection.RESULTS:The results showed no significant correlation between Hp infection and CSC[odds ratio(OR)1.89,95%confidential interval(CI)0.58–6.15,I2=96%,P=0.29].After subgroup analysis based on the degree of development of the study(developing/developed countries),it was found that the results of the two subgroups were the same as the whole,and no significant difference between the two subgroups existed.Meta-regression showed that the effect of sample size on heterogeneity among studies was more prominent(P<0.01,adjusted R^(2)=89.72%),which can explain 89.72%of the sources of heterogeneity.CONCLUSION:This Meta-analysis reveals no significant correlation between Hp infection and CSC,which still warrants further well-designed extensive sample studies to reach a more reliable conclusion and promote a better understanding of the treatment of CSC.展开更多
BACKGROUND The increased stroke risk associated with atrial fibrillation(AF)burden exceeding 5 min is a matter of debate.In addition,the potential linear or nonlinear relationship between AF burden and stroke risk has...BACKGROUND The increased stroke risk associated with atrial fibrillation(AF)burden exceeding 5 min is a matter of debate.In addition,the potential linear or nonlinear relationship between AF burden and stroke risk has been largely unexplored.AIM To determine the association between AF burden>5 min and the increased risk of stroke and explore the potential dose-response relationship between these two factors.METHODS Sixteen studies from six databases with 53141 subjects(mean age 65 years)were included.Fifteen studies were observational studies,and one was a randomized controlled trial study.The potential nonlinear dose-response association was characterized using a restricted cubic splines regression model.AF burden for each 1 h and 2 h was associated with an increased risk of stroke.Trial sequential analysis with a random-effect model was used to evaluate the robustness of the evidence from the included 16 studies.RESULTS AF burden>5 min was associated with an increased risk of clinical AF[adjusted risk ratio(RR)=4.18,95%confidence interval(CI):2.26-7.74].However,no association was found with an increased risk of all-cause mortality(adjusted RR=1.55,95%CI:0.87-2.75).Patients with AF burden>5 min had an increased risk of stroke(adjusted RR=2.49,95%CI:1.79-3.47).Moreover,a dose-response analysis showed that the increased stroke risk was paralleled by an increase in AF burden at a rate of 2.0%per hour(Pnonlinear=0.656,RR=1.02,95%CI:1.01-1.03).Trial sequential analysis provided robust evidence of the association between AF burden>5 min and an increased risk of stroke.CONCLUSION AF burden was a significant risk factor for clinical AF and future stroke.A significant linear association was documented between increased AF burden and risk of future stroke.展开更多
Background and Aims:RAS protein activator like 2(RASAL2)is a newly discovered metabolic regulator involved in energy homeostasis and adipogenesis.However,whether RASAL2 is involved in hepatic lipid metabolism remains ...Background and Aims:RAS protein activator like 2(RASAL2)is a newly discovered metabolic regulator involved in energy homeostasis and adipogenesis.However,whether RASAL2 is involved in hepatic lipid metabolism remains undetermined.This study explored the function of RASAL2 and elucidated its potential mechanisms in nonalcoholic fatty liver disease(NAFLD).Methods:NAFLD models were established either by feeding mice a high-fat diet or by incubation of hepatocytes with 1 mM free fatty acids(oleic acid:palmitic acid=2:1).Pathological changes were observed by hematoxylin and eosin staining.Lipid accumulation was assessed by Oil Red O staining,BODIPY493/503 staining,and triglyceride quantification.The in vivo secretion rate of very lowdensity lipoprotein was determined by intravenous injection of tyloxapol.Gene regulation was analyzed by chromatin immunoprecipitation assays and hydroxymethylated DNA immunoprecipitation combined with real-time polymerase chain reaction.Results:RASAL2 deficiency ameliorated hepatic steatosis both in vivo and in vitro.Mechanistically,RASAL2 deficiency upregulated hepatic TET1 expression by activating the AKT signaling pathway and thereby promoted MTTP expression by DNA hydroxymethylation,leading to increased production and secretion of very low-density lipoprotein,which is the major carrier of triglycerides exported from the liver to distal tissues.Conclusions:Our study reports the first evidence that RASAL2 deficiency ameliorates hepatic steatosis by regulating lipid metabolism through the AKT/TET1/MTTP axis.These findings will help understand the pathogenesis of NAFLD and highlight the potency of RASAL2 as a new molecular target for NAFLD.展开更多
基金Supported by 1.3.5 Project for Disciplines of Excellence,West China Hospital,Sichuan University(No.ZYJC21025)。
文摘AIM:To investigate the association between central serous chorioretinopathy(CSC)and Helicobacter pylori(Hp)by summarizing all available evidence.METHODS:The Scopus,Embase,EBSCO,PubMed,Web of Science,and Cochrane Library databases for all relevant studies published from inception to October 2022 were searched,and manually searched for relevant reference lists as a supplement.Studies investigating the association between CSC and Hp infection were included.Finally,8 case-control studies were included in the Meta-analysis after study selection.RESULTS:The results showed no significant correlation between Hp infection and CSC[odds ratio(OR)1.89,95%confidential interval(CI)0.58–6.15,I2=96%,P=0.29].After subgroup analysis based on the degree of development of the study(developing/developed countries),it was found that the results of the two subgroups were the same as the whole,and no significant difference between the two subgroups existed.Meta-regression showed that the effect of sample size on heterogeneity among studies was more prominent(P<0.01,adjusted R^(2)=89.72%),which can explain 89.72%of the sources of heterogeneity.CONCLUSION:This Meta-analysis reveals no significant correlation between Hp infection and CSC,which still warrants further well-designed extensive sample studies to reach a more reliable conclusion and promote a better understanding of the treatment of CSC.
基金Supported by National Natural Science Foundation of China,No.81673259Natural Science Foundation of Jiangsu Province,China,No.BK20161435.
文摘BACKGROUND The increased stroke risk associated with atrial fibrillation(AF)burden exceeding 5 min is a matter of debate.In addition,the potential linear or nonlinear relationship between AF burden and stroke risk has been largely unexplored.AIM To determine the association between AF burden>5 min and the increased risk of stroke and explore the potential dose-response relationship between these two factors.METHODS Sixteen studies from six databases with 53141 subjects(mean age 65 years)were included.Fifteen studies were observational studies,and one was a randomized controlled trial study.The potential nonlinear dose-response association was characterized using a restricted cubic splines regression model.AF burden for each 1 h and 2 h was associated with an increased risk of stroke.Trial sequential analysis with a random-effect model was used to evaluate the robustness of the evidence from the included 16 studies.RESULTS AF burden>5 min was associated with an increased risk of clinical AF[adjusted risk ratio(RR)=4.18,95%confidence interval(CI):2.26-7.74].However,no association was found with an increased risk of all-cause mortality(adjusted RR=1.55,95%CI:0.87-2.75).Patients with AF burden>5 min had an increased risk of stroke(adjusted RR=2.49,95%CI:1.79-3.47).Moreover,a dose-response analysis showed that the increased stroke risk was paralleled by an increase in AF burden at a rate of 2.0%per hour(Pnonlinear=0.656,RR=1.02,95%CI:1.01-1.03).Trial sequential analysis provided robust evidence of the association between AF burden>5 min and an increased risk of stroke.CONCLUSION AF burden was a significant risk factor for clinical AF and future stroke.A significant linear association was documented between increased AF burden and risk of future stroke.
基金supported by National Natural Science Foundation of China (grant number 82070591)Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program (grant number 2017BT01S131)Postdoctoral Science Foundation of China (grant number 2018M641919).
文摘Background and Aims:RAS protein activator like 2(RASAL2)is a newly discovered metabolic regulator involved in energy homeostasis and adipogenesis.However,whether RASAL2 is involved in hepatic lipid metabolism remains undetermined.This study explored the function of RASAL2 and elucidated its potential mechanisms in nonalcoholic fatty liver disease(NAFLD).Methods:NAFLD models were established either by feeding mice a high-fat diet or by incubation of hepatocytes with 1 mM free fatty acids(oleic acid:palmitic acid=2:1).Pathological changes were observed by hematoxylin and eosin staining.Lipid accumulation was assessed by Oil Red O staining,BODIPY493/503 staining,and triglyceride quantification.The in vivo secretion rate of very lowdensity lipoprotein was determined by intravenous injection of tyloxapol.Gene regulation was analyzed by chromatin immunoprecipitation assays and hydroxymethylated DNA immunoprecipitation combined with real-time polymerase chain reaction.Results:RASAL2 deficiency ameliorated hepatic steatosis both in vivo and in vitro.Mechanistically,RASAL2 deficiency upregulated hepatic TET1 expression by activating the AKT signaling pathway and thereby promoted MTTP expression by DNA hydroxymethylation,leading to increased production and secretion of very low-density lipoprotein,which is the major carrier of triglycerides exported from the liver to distal tissues.Conclusions:Our study reports the first evidence that RASAL2 deficiency ameliorates hepatic steatosis by regulating lipid metabolism through the AKT/TET1/MTTP axis.These findings will help understand the pathogenesis of NAFLD and highlight the potency of RASAL2 as a new molecular target for NAFLD.
