Objective To investigate the prevalence and risk factors of non?suicidal self injury among middle school students. Methods Data were collected from 2 140 middle school students with the mean age of 13.92 by stratified sampling method. All students were evaluated with Beck Depression Scale (BDI),Barratt Im?pulsiveness Scale ( BIS ) , Adolescent Self?Rating Life Events Check List ( ASLEC ) , Adolescents Health related Risk Behaviors Inventory ( AHRBI ) , Chinese version of Family Adaptability and Cohesion Evaluation Scales ( FACES II?CV) ,and self?made investigate questionnaire. Results The prevalence of non?suicidal self injury a?mong local middle school students was 23.2%,total 495 adolescents were endorsed non?suicidal self injury,and 49.7% were girls.The results of in multivariable logistic regression showed the main risk factors for non?suicidal self injury among adolescents were being female,depressive symptoms,impulsiveness,negative life events and health re?lated risk behaviors. Conclusion Non?suicidal self injury is high among Chinese adolescent in the city of Dujian?gyan,and it is necessary to take effective interventions.

Objective:To investigate the relationship between TP53 gene mutation and overall survival (OS) time of myelodysplastic syndrome (MDS).Methods:Databases, including PubMed, Cochrane Library and Embase were searched for relevant studies published up to 20 October, 2019. The corresponding hazard ratio ( HR) and their 95% confidence interval ( CI) for OS from multivariate Cox proportional hazard models were extracted. The combined HR with their 95% CI was calculated by using fixed or random effect models. Meta-analysis was performed by using Revman 5.3 software. Results:A total of 1 033 patients from 6 studies were enrolled. Meta-analysis results showed that OS time in TP53 gene mutation group was shorter than that in wild type group for patients with MDS ( HR = 2.16, 95% CI 1.52-3.07, P < 0.01). The prognostic risk for post-transplantation patients with MDS ( HR = 2.69, 95% CI 1.63-4.43, P < 0.01) was lower compared with that for patients treated by azacitidine( HR = 2.89, 95% CI 1.37-6.08, P = 0.005). Conclusion:TP53 gene mutation is a risk factor affecting OS of MDS patients.

Objective To investigate the expression of connective tissue growth factor (CTGF) and heat shock protein 47 (HSP47) in peritoneum fibrosis rats,and the mechanism of 1,25-dihydroxyvitamin D3 [1,25-(OH)2-VitD3] in inhibiting the peritoneum fibrosis.Methods Adult male Sprague-Dawley rats were randomly divided into 3 groups:control group (n=8),model group (n=8) and 1,25-dihydroxyvitamin D3 group (VitD3,n=8).The model of peritoneum fibrosis rats were induced by daily intraperitoneally injection of 15％ chlorhexidine gluconate (CHX) 0.2 ml/d with 0.1％ glucose for 4 weeks.Rats in VitD3 group were also treated with 1,25-(OH)2-VitD3 [i.p.6 ng· (100 g) 1 · d-1].Peritoneal transport function,renal function,peritoneum thickness and serum level of 25hydroxyvitamin D3 were detected.In vitro,primary cultured peritoneal mesothelial cells were divided into control group,high glucose group (HG,2.5％),CTGF siRNA intervention group (CTGF siRNA+HG),VitD3 intervention group (VitD3+HG) and combined intervention group (CTGF siRNA+VitD3+HG).Real-time PCR,Western blotting and immunofluorescence were applied to measure the expression of CTGF and HSP47,also ELISA was used to detect the protein level of FN in peritoneum and peritoneal mesothelial cells.Results Compared with control group,the peritoneal ultrafiltration in peritoneum fibrosis rats were significantly decreased (P ＜ 0.05),the absorbance level of peritoneal fibrosis,peritoneum thickness,the rate of dialysate urea nitrogen and blood urea nitrogen (DUN/BUN) and the expressions of CTGF and HSP47 were increased (all P＜0.05).After application of 1,25-dihydroxyvitamin D3,peritoneal fibrosis lesion was significantly improved,the peritoneum thickness,the expressions of CTGF and HSP47 were decreased (all P ＜ 0.05).In vitro,2.5％ high glucose induced-peritoneal mesothelial cells were respectively treated by CTGF siRNA,1,25-(OH)2-VitD3 and combined interventions,the expression of FN,CTGF and HSP47 was significantly lower than that in high glucose group (all P ＜ 0.05).Conclusions The expression of CTGF and HSP47 is significantly increased in peritoneal fibrosis rats.1,25-(OH)2-VitD3 may ameliorate the progression of peritoneal fibrosis via reducing the expression of CTGF,decreasing the expression of HSP47 and FN.

Objective: To explore susceptibility genes for autism spectrum disorders (ASD). Methods: Whole-exome sequencing was carried out for 60 family trios affected with sporadic ASD. Genetic variants discovered in over 10% of the patients were selected for genotype-phenotype correlation and pathway enrichment analysis using Phenolyzer software and metascape database. Combining gene-phenotypic scores, pathway-related genes associated with neural and neurite triggering were screened for the candidates. Results: A total of 170 common variants were found to be associated with the ASD phenotype. Among these, there was only one high-confidence gene [SHANK2 (0.8146)] and four medium-confidence genes [ERBB2 (0.1322), LAMC3 (0.1117), PPFIA4 (0.1059), DISC1 (0.1002)]. Twenty-pathways and four biological processes were found to be statistically significant by pathway enrichment analysis, which included neuron projection morphogenesis (GO: 0048812), regulation of neuroblast proliferation (GO: 1902692), modulation of excitatory postsynaptic potential (GO: 0098815), and dendrite morphogenesis (GO: 0048813). Twenty-one genes were found to be closely associated with neurological and neurite triggering, among which only SHANK2, ERBB2, and DISC1 had above-medium confidence correlation scores with the ASD phenotypes. Conclusion Abnormal neuron projection morphogenesis (GO: 0048812) may be closely related to the occurrence of ASD. SHANK2, ERBB2, and DISC1 are susceptibility genes for ASD.

Liver-qi stagnation and spleen deficiency syndrome can be seen in a variety of clinical diseases,such as chronic hepatitis,liver cirrhosis,chronic gastritis,peptic ulcer,irritable bowel syndrome (IBS),p.sychosis and so on.Disease characteristics determine the symptom characteristic and criterion of syndrome differentiation and treatment.Therefore,different diseases with liver-qistagnation and spleen deficiency syndrome have different clinical manifestation and diagnostic criteria.This paper summarized the modern biological basis of liver-qistagnation and spleen deficiency syndrome from the nervous system,endocrine system,digestive system,circulatory system,immune system and metabolic system,in order to provide reference for researches on modern biology basis of liver-qistagnation and spleen deficiency syndrome.

OBJECTIVE: To analyze the pathogenic variants of the KIF1A gene and its corresponding protein structure in an autism spectrum disorder (ASD) family trio carrying harmful missense variants in the KIF1A gene. METHODS: The peripheral blood DNA of the patient and his parents was extracted and sequenced using whole exome sequencing (WES) technology and verified by Sanger sequencing. Bioinformatics software SIFT, PolyPhen-2, Mutation Taster, and CADD software were used to analyze the harmfulness and conservation of variants. The Human Brain Transcriptome (HBT) database was used to analyze the expression of the KIF1A gene in the brain. PredictProtein and SWISS-MODEL were further used to predict the secondary structure and tertiary structure of KIF1A wild-type protein and variant protein. PyMOL V2.4 was utilized to investigate the change of hydrogen bond connection after protein variant. RESULTS: The WES sequencing revealed a missense variant c.664A>C (p.Asn222His) in the child's KIF1A gene, and this variant was a de novo variant. The harmfulness prediction results suggest that this variant is harmful. By analyzing expression level of KIF1A gene in the brain. It is found that KIF1A gene widely expressed in various brain regions during embryonic development. By analyzing the variant protein structure, the missense variant of KIF1A will cause many changes in the secondary structure of protein, such as alpha-helix, beta-strand, and protein binding domain. The connection of hydrogen bond and spatial structure will also change, thereby changing the original biological function. CONCLUSION The KIF1A gene may be a risk gene for ASD.
Autism Spectrum Disorder/genetics* ; Child ; Female ; Humans ; Kinesin/genetics* ; Mutation ; Mutation, Missense ; Pregnancy ; Protein Domains ; Whole Exome Sequencing

Cardiac senescence can change the structure and function of the heart and increase the risk of cardiovascular disease.Cardiac senescence is not only closely related to telomere damage, oxidative stress, mitochondrial dysfunction and autophagy, but also is regulated by non-coding RNA.Therefore, this article will give an overview of cardiac senescence and relative pathogenetic mechanisms, in order to provide new ideas for preventing and treating cardiac senescence and for achieving healthy and longevity.