Objective: To explore the latent profiles of psychological help seeking intentions among adolescents in Wuhan, and to investigate their association with non suicidal self injury (NSSI), in order to provide a theoretical basis for constructing an early intervention system for adolescents NSSI. Methods: From October to December 2022, a convenient sampling method was used to select 3 975 students from grades 7 to 12 in Wuhan. A self administered questionnaire assessed psychological help seeking intentions, followed by a post survey interview using the Ottawa Self injury Inventory to evaluate NSSI behaviors. Latent profile analysis(LPA) was used to explore the potential categories of help seeking intentions in adolescents. Multinomial Logistic regression was used to analyze factors associated with the latent profiles of help seeking intentions and multiple Logistic regression was used to analyze the association between latent profiles of help seeking intentions and NSSI. Results: Based on latent profile analysis, four latent profiles of help seeking intentions in adolescents were identified, namely overall low, moderate, and high help seeking group, as well as family/friendfocused help seeking group, accouting for 14.1%, 20.9%, 43.1% and 21.8%, respectively. Multinomial Logistic regression analysis showed that compared to senior high school students, junior high school students were more willing to seek help from family and friends ( OR =1.56); compared to males, females were more likely to exhibit moderate help seeking intentions( OR =1.37); students with extroverted or balanced personalities were more likely to exhibit high level help seeking intentions( OR =1.50, 1.49); students with average or good family economic status, better parental relationships, and adequate mental health knowledge were more likely to exhibit moderate and high level help seeking intentions( OR =1.59, 2.02; 1.80, 2.64; 1.44, 1.55; 1.34, 1.58) (all P <0.05). Students with moderate or severe family dysfunction were less likely to seek help from family and friends or to exhibit moderate and high level help seeking intentions( OR =0.51, 0.60, 0.25; 0.22, 0.27, 0.06, all P <0.01). Students whose parents exhibited stigma towards mental illness were less likely to show high level help seeking intentions( OR= 0.78 , P <0.05). Multivariable Logistic regression analysis results indicated that compared to the overall low help seeking intentions group, reduced risk of NSSI was observed among students in the overall moderate and overall high groups, as well as in the family/friend focused help seeking group( OR =0.73, 0.60, 0.70, all P <0.05). Conclusions Active psychological help seeking intentions can reduce NSSI behaviors in adolescents. Interventions should focus on improving family support environment to enhance adolescents intentions to seek psychological help.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

Objective:To improve recognition of the clinical phenotype and genotype of achondroplasia(ACH).Methods:The clinical data and genetic test results of 2 children with ACH were analyzed retrospectively, and the related literature was reviewed.Results:Case 1 was a 1-year-old girl whose mother was short in stature.She was admitted to the hospital due to knee reflexes of both lower limbs for more than 9 months.Physical examination showed that her head circumference was 45 cm and she had short stature, short limbs, low muscle tension of both lower limbs, the developmental quotient was 65 scores.Bilateral ilium and hip joint lesions by X-ray were considered as ACH.According to the submitted gene results, FGFR3 gene c. 1138G >A (p.Gly380Arg) of the girl showed the heterozygous variation, and that gene of her mother showed the heterozygous variation.Case 2 was a 10-month-old girl, who was admitted to the hospital due to limb weakness for over 5 months.Physical examination showed head circumference of 46 cm, short stature, short limbs, reduced muscle tension of limbs, grade 4 muscle strength of limbs, and the developmental quotient was 41 scores.X-ray showed that both lower limbs were in accordance with ACH.The gene results suggested the heterozygous variation of FGFR3 gene c. 1138G >A (p.Gly380Arg) in the girl(a novel mutation), and a wild-type gene in her parents. Conclusions:The clinical features of achondroplasia are diverse.The bone changes and nerve development also need to be recognized and discriminated.

A great number of studies have demonstrated functional abnormalities in children with attention-deficit/hyperactivity disorder (ADHD), although conflicting results have also been reported. And few studies analyzed homotopic functional connectivity between hemispheres. In this study, resting-state functional magnetic resonance imaging (MRI) data were recorded from 45 medication-naïve ADHD children and 26 healthy controls. The regional homogeneity (ReHo), degree centrality (DC) and voxel-mirrored homotopic connectivity (VMHC) values were compared between the two groups to depict the intrinsic brain activities. We found that ADHD children exhibited significantly lower ReHo and DC values in the right middle frontal gyrus and the two values correlated with each other; moreover, lower VMHC values were found in the bilateral occipital lobes of ADHD children, which was negatively related with anxiety scores of Conners' Parent Rating Scale (CPRS-R) and positively related with completed categories of Wisconsin Card Sorting Test (WCST). Our results might suggest that less spontaneous neuronal activities of the right middle frontal gyrus and the bilateral occipital lobes in ADHD children.

Objective The aim of present study was to detect methylation rate of CpG unit of brain derived neurotrophic factor (BDNF) promoter and to study the epigenetic mechanism of autism spectrum disorders (ASD).Methods Total of 12 ASD patients and 12 healthy controls were recruited.The methylation rate of CpG unit in BDNF promoter Ⅰ and Ⅳ were detected using Sequenom MassArray method.The methylation model,correlationship,evolutionary relationship of CpG units in BDNF promoter Ⅰ and Ⅳ were detected and compared between ASD patients and healthy controls.Results The methylation rate was identified in 17 and 8 CpG units in BDNF promoter][and BDNF promoter Ⅳ.A close correlation distance was detected in BDNF promoter Ⅰ CpG units 4,7,10,35,and BDNF promoter Ⅳ CpG units 11.12,14.BDNF promoter][CpG units 4,7,10,35,and BDNF promoter Ⅳ CpG units 11.12,14 could be clustered.ASD patients had a significant lower methylation rate in BDNF promoter Ⅰ CpG unit 5.6 and Ⅳ CpG units 3 and 15 compare with healthy controls (P＜0.05).Conclusions The DNA methylation rate in BDNF pronoter Ⅰ CpG unit 5.6 and Ⅳ CpG units 3 and 15 may be used as potential biomarkers of ASD.

Objective To investigate the clinical significance and changes of neuron-specific enolase (NSE) and S100 protein in blood serum in patients with enterovirus 71 infection.Methods A total of 176 children with enterovirus 71 infection admitted from March 1,2012 through October 31,2012 were enrolled for a prospective and control study.According to diagnostic criteria of the enterovirus 71 (EV71) infection instituted by expert consensus for treatment of severe patients sets in 2011,the patients were divided into three groups:mild group (n =62),severe group (n =65) and critically care group (n =49),and another 30 healthy children served as control group.The demographics of patients including age and sex were comparable between control group and the sick children groups.Four milliliter of peripheral blood were taken from ill children on the first day before treatment and on the first,second,third day after treatment.The blood samples of healthy children were taken on the first day after physical examination.At the same time,the clinical data of blood routine,blood biochemistry,myocardial enzymes and C-reactive protein during the first 24 hours were collected.Immunohistochemical technique was used to study the change of NSE and S100 levels in serum.Data were expressed in mean ± standard deviation ((x) ± s) and were statistically analyzed by using SPSS 13.0 statistical software.Comparisons were carried out among different groups with one way analysis of variance (ANOVA) and between groups were performed with the Student t test.Changes were considered as statistically significant if P values was less than 0.05.Results ①Compared with mild group and control group,the levels of NSE and S100 protein were significantly higher in severe group and critically care group (P ＜0.05).②The serum levels of NSE and S100 protein in severe group were higher than in those in mild group with better outcomes (P ＜ 0.05).Conclusion The serum levels of NSE and S100 protein as biomarkers can be used to evaluate the severity of EV71 infection,and can also be used to determine the efficacy of treatment.

BACKGROUND: Methamphetamine (MA) has neurotoxic effects to central nervous system. However, as the 5-hydroxytryplamine reuptake enhancer, it is uncertain that if there are protective effects of tianeptine to the damages of 5-hydroxytryp-taminergic neurons caused by MA.OBJECTIVE: To investigate the neurotoxicity of MA and the neuroprotective effects of tianeptine as well as the acting mechanism.DESIGN: Randomized case control study based on animals.SETTING: Animal research room and pathology research room of a university.MATERIALS: The experiment was completed in the Experimental Animal Centre of Sichuan University and Molecular Pathology Laboratory of West China Hospital during June to August 2003. Totally 25 male Wistar rats were injected MA through abdominal cavity to build model. Methamphetamine was provided by National Institute for the Control of Pharmaceutical and Biological Products(NICPBP) while tianeptine was given by French Servier Company (Batch No. OE3086). The TUNEL testing kit was purchased from Boehringer Mannheim Company.INTERVENTIONS: There were one control group and four experimental groups(A, B, C, D). A group was used intraperitoneal injection of MA while B, C, D, groups were administered tianeptine 7 days, 4 days before and the same day of MA administration. Normal saline with same volume was injected into rats of control group. HE stain and silver stain were conducted after experiment to observe the morphologic changes of neurons. And TUNEL method was used to detect apoptotic cells.MAIN OUTCOME MEASURES: The HE stain and silver stain of brain tissue sections and counts of TUNEL positive neurons.RESULTS: MA could damage the axon and dendrite of neurons and the absorbance of silver positive cell was(50.74 ± 1.86) . It could also induce cell apoptosis while the apoptotic cell count every high power field was 29.26 ±4. 14. There were less apoptotic cells in the group with 7 days usage of tianeptine with the cell count of( 18.90 ± 1.60) per high power field.CONCLUSION: MA can cause neurotoxicity by inducing cell apoptosis.And giving tianeptine in advance can protect neurons.

Objective: A double-blind and double-simulated study was used to evaluate the effects of cognitive functioning in schizophrenics receiving different antipsychotic medications. Method: Forty Patients with schizophrenia were randomly divided into quetiapine group (n=20) and chlorpromazine group (n=20). Neuropsychologiacal tests were done before treatment and in the fourth and sixth week after therapy, which included knowledge, arithmetic, digital sign, digital span, game of puzzle, logical memory visual reproduction,STROOP test, verbal fluency, score and plan time of tower of Hanoi and WCST. Twelve healthy individuals were tested in same time to study the learning effects. Double-blind and a double-simulated means was adopted in this study. Results: Marked improvement was found in patients after quetiapine treatment. While chlorpromazine do not appear to favorably affect on cognitive functioning in schizophrenics. Scores of improvement on some neuropsychological assessment of quetiapine group were higher than that of chlorpromazine group, especially in attention and executive function(P

Objective: To investigate the effect of heroin on executive function in heroin addicts Methods: Executive function of thi rty-six heroin addicts and thirty-six normal controls was assessed with a batter y of neuropsychological evaluation instruments in Chengdu city of China The to ols include of block design test, Stroop test (C, CW), Wisconsin card sorting te st (WCST-M)Results: There were significance difference between the two groups, heroin addicts had lower score of Block design and more time spent, number of errors in Stroop test (C、CW) Further more, the addicts had more total error, perseverative err o rs and lower number of categories in WCST than control group (P