RESUMO
Objective:To estimate the prevalence and trend of autism spectrum disorders (ASD) in children aged 0-6 years in China.Methods:Systematic literature searches were conducted in PubMed,Web of Science,Scopus,China National Knowledge Infrastructure (CNKI),Chinese Biomedical Literature Database (CBM),Wanfang and Weipu Database (VIP),and the literatures published before February 25,2017 were selected according to the same criteria.Prevalence Data of three periods were abstracted,then pooled using random effect model.Subgroup analysis was done across data resource,age group,screening criteria,diagnostic criteria,and literature quality.Results:In the study,9 ASD studies and 20 autism (also known as autistic disorder,AD) studies were eligible for review.The pooled prevalence of AD in children aged 0-6 years in 2006-2010 and 2011-2015 was 1.74 ‰ (95％ CI:1.12‰o-2.69‰) and 1.80‰ (95％ CI:1.33‰-2.43‰),and there was no significant difference between the two groups (P =0.898),but they were higher than 0.94‰ (95％ CI:0.67‰-1.33‰) in 1996-2005 (P =0.031;P =0.005) significantly.The pooled prevalence of ASD in children aged 0-6 years was 3.52 ‰ (95％ CI:1.48‰-8.34‰) and 3.48‰ (95％ CI:1.77‰-6.84‰) in 2006-2010 and 2011-2015,respectively,and the difference between the two periods was not significant (P =0.983).There was no significant difference between the pooled prevalence in the three periods among the boys,and girls' too.The pooled prevalence of ASD in children aged 0-6 years was 3.51‰(95％ CI:2.15‰-5.74‰) and AD was 1.77‰ (95％ CI:1.40‰-2.24‰) in 2006-2015,with prevalence ratios of boys to girls 2.59:1 and 3.63:1,respectively.The pooled prevalence of AD was lower in 0-6 years children than in other age groups and higher in high-quality studies than in low-quality studies,which was the same as ASD.Data resource,screening and diagnostic criteria were not significantly related with the pooled prevalence of AD and ASD.Conclusion:The prevalence of ASD and AD in children aged 0-6 years in China from 2006 to 2015 was stable,and there was not enough evidence to prove that it was higher than before 2005.National survey and monitoring of early childhood autism should to be conducted.
RESUMO
Purpose To explore the β-catenin role in the process of invasion and metastasis of esophageal cancer.Methods Transfection-effective β-catenin gene segments of siRNA interference in human esophageal Eca-109 cells was used to downregulate β-catenin expression:CCK-8 multiplication experiment was carried out to observe the esophageal cancer cell proliferation.Transwell chambers experiment was used to observe its invasion,migration ability.Western blot was used to detect the expression of WISP2 and TCF4,E-cadherin protein.Results CCK-8 multiplication experiment showed that in the interference group (the efficient transfection of β-catenin down-regulation group by siRNA) cell proliferation ability significantly decreased as compared with the blank control group (the untreated group)and the negative control group (the transfection group meaningless fragments) (P ＜ 0.05),and there was no statistical significance between the blank and negative control groups (P ＞0.05).The invasion and migration ability of the interference group was lower than that in the blank control group and the negative control group (P ＜ 0.05) by the transwell chambers experiment.Western blot showed that the protein lever of WISP2 and E-cadherin in interference group was higher than those in the blank control group and the negative control group (P ＜ 0.05).TCF4 protein expression in the interference group was lower than that of the blank control group and the negative control group (P ＜ 0.05).Conclusions After the β-catenin expression is down-regulated,Wnt signaling pathway-related factors are significantly changed.It can be speculated that the silencing of β-catenin in Wnt signaling pathway may hinder the esophageal cancer cell proliferation by up-regulating E-cadherin expression to obstruct epithelial mesenchymal transition (EMT) and to inhibit tumor cell proliferation.Invasion and metastasis of the tumor are also inhibited by reducing TCF4 expression and promoting WISP2 downstream target genes expression.Therefore,β-catenin gene is expected to be a target for the treatment of esophageal cancer.
RESUMO
AIM:To study the protective effect of heat shock factor1(HSF1) on the mice with lipopolysaccha-ride (LPS)-induced acute lung injury(ALI),and to screen the relevant differentially-expressed genes. METHODS:ALI mouse model was established by LPS intracheal instillation. The macroscopic and pathological changes of the lung tissue were observed,and the concentrations of total protein,TNF-α, IL-β, IL-6 and VEGF in the bronchoalveolar lavage fluid (BALF) were analyzed. Differentially-expressed genes in the lung tissues of HSF1 +/ +mice and HSF1 -/- mice with ALI induced by LPS were screened by gene chips. The key gene was verified by real-time qPCR. RESULTS:The macroscopic and pathological changes of the lung injury in HSF1 -/- +LPS mice were more serious than those in HSF1 +/ ++LPS mice.The concentrations of total protein,VEGF,TNF-α,IL-1β and IL-6 in the BALF of HSF1 -/- +LPS mice were significantly higher than those of HSF1 +/ ++LPS mice(P<0.05). Compared with the HSF1 +/ +mice,a total of 918 differentially-ex-pressed genes were indentified in the HSF1 -/- mice, among which the expression levels of 65 genes had obvious diffe-rence,with 28 genes up-regulated,including Atg7,ccr1,cxcr2,Tbl1xr1,Mmp9,Pparg,Plcb2,Arrb2,Cntn1,Col4a6, etc, and 37 genes down-regulated,including Fgfr1,Fgfr2,Map4k4,Ddx58,Tfg,Stat3,Smad4,Lamc1,Sdc3,etc. The results of real-time qPCR showed that the mRNA level of CXCR2 in HSF1 -/- + LPS mice was significantly higher than that in HSF1 +/ ++ LPS mice,which was consistent with the results of gene chips. CONCLUSION:HSF1 has protective effect on the mice with LPS-induced ALI. CXCR2 may be involved in the protective effect of HSF1 on this process.