Gaming disorder has become a global concern and it could have a variety of health and social consequences. The trauma model has been applied to the understanding of different types of addictions as behavioral addictions can sometimes be conceptualized as self-soothing strategies to avoid trauma-related stressors or triggers. However, much less is known about the relationship between trauma exposure and gaming disorder.

To inform prevention and intervention strategies and to facilitate further research, we conducted the first scoping review to explore and summarize the literature on the relationship between trauma and gaming disorder.

A systematic search was conducted on the Web of Science, Scopus and ProQuest. We looked for original studies published in English that included a measure of trauma exposure and a measure of gaming disorder symptoms, as well as quantitative data regarding the relationship between trauma exposure and gaming disorder.

The initial search generated 412 articles, of which 15 met the inclusion criteria. All of them were cross-sectional studies, recruiting participants from both clinical and non-clinical populations. Twelve of them (80%) reported significant correlations between trauma exposure and the severity of gaming disorder symptoms (r = 0.18 to 0.46, p < 0.010). Several potential mediators, including depressive symptoms and dissociative experiences, have been identified. One study found that parental monitoring moderated the relationship between trauma and gaming disorder symptoms. No studies reported the prevalence of trauma or trauma-related symptoms among people with gaming disorder.

There is some evidence supporting the association between trauma and gaming disorder, at small to medium effect sizes. Future studies should investigate the mediators and moderators underlying the relationship between trauma and gaming disorder. The longitudinal relationship between trauma exposure and the development of gaming disorder should be clarified. A trauma-informed approach may be a helpful strategy to alleviate gaming disorder symptoms.

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Associations between childhood trauma (CT), social support (SS), brain functions and major depressive disorder (MDD) is unknown.

This study aimed to investigate whether brain functions mediated associations between CT, SS, and MDD.

164 MDD and 98 healthy controls (HC) were recruited and measured by HAMD-24 and HAMA. Some completed CT questionnaire (CTQ) and social support rating scale (SSRS). We examined amplitude of low-frequency fluctuation (ALFF) between the two groups and correlations between HAMD-24, HAMA and ALFF in MDD. Then, the peak voxels of the ALFF changed regions were used as seeds to analyze whole-brain functional connectivity (FC). Next, correlations between FC and clinical variables of MDD were performed. Last, mediation analysis was used to further determine whether ALFF or FC could mediate the associations between CT, SS, and different clinical variables in MDD patients.

Compared to HC, MDD showed decreased ALFF in right posterior cingulate (PCC_R), left postcentral gyrus, right precentral gyrus, and left thalamus (THA_L), but increased ALFF in right medial frontal gyrus, left subgenual anterior cingulate, and left middle occipital gyrus as well as decreased FC in bilateral PCC and THA_R. HAMD-24 had negative correlation with ALFF of THA_L, while positive with sexual abuse (SA) score in MDD. Mediation analysis revealed that FC of PCC_R mediated association between SA and baseline HAMD-24, and itself or together with SS mediated association between CT and onset age of MDD.

CT may influence the depression severity and onset age of MDD by moderating FC of PCC_R only or together with SS.

Major depressive disorder (MDD) is a severe, disabling condition with unknown etiology. Misdiagnosis is common when clinical symptomology criteria are used solely. Considerable evidence suggests that the upregulation of inflammatory factors and cortisol, and a decrease in neurotrophic factors, are involved in the pathogenesis of MDD.

This study explored the application of platforms composed of these serum proteins in the objective diagnosis of MDD.

Serum samples from all participants including 30 MDD patients and 30 well-matched healthy controls were collected at enrollment, eight serum proteins selected initially according to previous studies were analyzed with ELISA. A logistic regression model with these proteins was built to construct the diagnostic platform for the MDD and the receiver operating characteristic (ROC) curve was used to analyze the diagnostic potential of the model.

Among the eight selected proteins, three (TNF-alpha, IL-6 and IL-1beta) were removed because the measurements in more than 1/3 participants were below the detectable limits of ELISA kits. Forward logistic stepwise regression analysis screened out three serum proteins including BDNF, cortisol and IFN-gamma to build the model. The regression equation was Z = 1/[1 + e−(1.438+0.005(BDNF)-0.049(cortisol)-0.007(IFN-gamma))], and the diagnostic efficacy of thees three proteins-combined achieved an area under the ROC curve of 0.884 with sensitivity of 86.7% and specificity of 83.3%.

The results of this study provided a more reliable method to diagnose MDD, and the combination of serum BDNF, cortisol and IFN-gamma may provide an objective diagnostic platform for MDD.

Increasing evidence supports that 5HTTLPR polymorphism of the serotonin transporter gene(5HTTLPR) might associate to bipolar disorder and affective temperaments as measured by TEMPS-A. But the results are discrepant, furthermore, there are no data from Chinese population.

The present study was designed to investigate association between 5HTTLPR and bipolar disorder and affective temperaments of patients with bipolar disorder in the specific Chinese population and add new evidence to the field.

There hundred and five patients with bipolar disorder and 272 normal controls were included in the present case-control study⌧Temperament Evaluation of Memphis, Pisa, Paris and San Diego -autoquestionnaire version (TEMPS-A) in Chinese was used to assess affective temperament. Chi-square test, T test, Nonparametric test and ANOVA were employed to explore association between 5HTTLPR polymorphism and bipolar disorder and affective temperament of patients with bipolar disorder.

5-HTTLPR L/S polymorphism was associated with bipolar disorder in female (genotype χ2 = 6.769⌧P = 0.034⌧allele χ2 = 6.028⌧P = 0.014) and the S allele was associated with anxious temperament (t = 8.248⌧P = 0.005) in patients with bipolar disorder. the LA allele of 5-HTTLPR rs25531 A/G polymorphism was associated with hyperthymic temperament in patients with bipolar disorder (Z = −2.205⌧P = 0.027).

5-HTTLPR might have an effect on the prevalence of bipolar disorder in female and regulate affective temperaments of patients with bipolar disorder in some degree in Chinese population.

rs10761482 in ANK3 gene showed a significant association with schizophrenia in a genome-wide association study (GWAS). Another marker rs10994336 in ANK3 with the risk of bipolar disorder (BD) which might have more genetic overlap with schizophrenia, had been reported in two meta-analyses of GWAS. In this study, we investigated the association between ANK3 polymorphisms and the susceptibility of schizophrenia in Chinese Han population.

Population-based (schizophrenia patients = 516 and controls = 400) and family based (trios of early onset schizophrenia= 81) study was performed through genotyping the most promising makers rs10761482, rs10994336, and two missenses rs3808942 and rs3808943 near promoter of ANK3. Particularly, we conducted an association analysis for the combined case-control and family samples.

Our population-based study replicated the association between rs10761482 (P = 0.0268 with C allele) and schizophrenia, and detected a novel association with rs10994336 (P = 4.0 × 10−4 with T allele). Haplotype analysis revealed the higher frequencies of C-T, and T-C (rs10761482–10994336) in the cases than controls (P = 0.0032 and P = 0.0012, respectively). In the family study, the C allele of rs10761482 (P = 0.0940) and T allele of rs10994336 (P = 0.0832) were slightly over-transmitted, and T-C was significantly associated with schizophrenia (P = 0.0304). The results from the combined samples analysis were consistent with independent analysis. rs10761482, rs10994336, C-T, and T-C were significantly associated with schizophrenia (P = 3.3 × 10−6∼3.9 × 10−5), whilst rs3808942 and rs3808943 did not reach normal significance.

Our data strongly support ANK3 gene is a schizophrenia susceptibility gene, and also provide further evidence for the shared susceptibility loci between schizophrenia and BD.

rs10761482 in ANK3 gene showed a significant association with schizophrenia in a genome-wide association study (GWAS). Another marker rs10994336 in ANK3 with the risk of bipolar disorder (BD) which might have more genetic overlap with schizophrenia, had been reported in two meta-analyses of GWAS.

In this study, we investigated the association between ANK3 polymorphisms and the susceptibility of schizophrenia in Chinese Han population.

Population-based (schizophrenia patients = 516 and controls = 400) and family based (trios of early onset schizophrenia= 81) study was performed through genotyping the most promising makers rs10761482, rs10994336, and two missenses rs3808942 and rs3808943 near promoter of ANK3. Particularly, we conducted an association analysis for the combined case-control and family samples.

Our population-based study replicated the association between rs10761482 (P = 0.0268 with C allele) and schizophrenia, and detected a novel association with rs10994336 (P = 4.0 × 10−4 with T allele). Haplotype analysis revealed the higher frequencies of C-T, and T-C (rs10761482–10994336) in the cases than controls (P = 0.0032 and P = 0.0012, respectively). In the family study, the C allele of rs10761482 (P = 0.0940) and T allele of rs10994336 (P = 0.0832) were slightly over-transmitted, and T-C was significantly associated with schizophrenia (P = 0.0304). The results from the combined samples analysis were consistent with independent analysis. rs10761482, rs10994336, C-T, and T-C were significantly associated with schizophrenia (P = 3.3 × 10−6∼3.9 × 10−5), whilst rs3808942 and rs3808943 did not reach normal significance.

Our data strongly support ANK3 gene is a schizophrenia susceptibility gene, and also provide further evidence for the shared susceptibility loci between schizophrenia and BD.

Bioinformatic investigations indicate that has-mir-206 (microRNA-206, miRNA-206) could regulate BDNF protein synthesis by interfering with BDNF mRNA translation, which is disrupted in bipolar disorder (BPD).

This study is to investigate whether miRNA-206 gene variants were associated with BPD susceptibility in a Han Chinese population.

342 patients who met DSM-IV criteria for bipolar disorder type I (BPD-I) or type II (BPD-II) and 386 matched health controls were enrolled into this study. the miRNA-206 gene and +/-500bp were selected for gene sequencing. for the case-control genetic comparisons, differences in the genotype and allele distributions between patients and controls were examined using Pearson's χ2 test.

Gene sequencing showed that there are two polymorphisms rs16882131(C/T) and rs62408583 (A/C) located at the upstream of miRNA-206 gene, which are complete linkage disequilibrium. the association analysis showed that there was no significant difference for genotype frequencies (χ2 = 2.075, df = 2, P = 0.354) or for allele frequencies (χ2 = 0.041, df = 1, P = 0.839) between BPD patients and controls. Similarly, no significant difference was found between BPD-I patients and controls (genotype χ2 = 1.411, df = 2, P = 0.494; allele χ2 = 0.380, df = 1, P = 0.538). However, there was significant difference between BPD-II patients and controls (genotype χ2 = 7.933, df = 2, P = 0.019; allele χ2 = 5.403, df = 1, P = 0.020).

Our findings do not support that BPD susceptibility was associated with miRNA-206 gene polymorphisms in the studied Han Chinese population. the association between miRNA-206 gene polymorphisms and bipolar disorder type II is needed to be carefully interpreted. Further studies are necessary to elucidate the involvement miRNA-206 in the pathophysiology of BPD.

The present study compared the expression profile and made the classification with the leukocytes by using whole-genome cRNA microarrays among patients with SSD, major depressive disorder (MDD) and healthy controls.

Gene expression profiling was conducted in peripheral blood leucocytes from drug-free first-episode subjects with SSD, MDD, and matched controls (8 subjects in each group) using global mRNA expression arrays. Support vector machines (SVMs) were utilized for training and testing on candidate signature expression profiles from signature selection step.

We identified SSD and MDD gene signatures from blood-based gene expression profile and build a SSD- MDD disorder model with higher predictive power. Firstly, we identified 63 differentially expressed SSD signatures in contrast to control (P <= 5.0E-4) and 30 differentially expressed MDD signatures in contrast to control, respectively. Then, 123 gene signatures were identified with significantly differential expression level between SSD and MDD. Secondly, in order to conduct priority selection for biomarkers for SSD and MDD together, we selected top gene signatures from each group of pair-wise comparison results, and merged the signatures together to generate better profiles used for clearly classify SSD and MDD sets in the same time. In details, we tried different combination of signatures from the three pair-wise compartmental results and finally determined 48 gene expression signatures with 100% accuracy.

Blood cell-derived RNA may have significant value for performing diagnostic functions and identifying disease biomarkers in SSD and MDD. These 48 gene model could classify SSD, MDD, and healthy controls.

To study the relationship between insulin-like growth factor 1 receptor (IGF1R)and subsyndromal symptomatic depression (SSD).

In this case-control study, real-time quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) with TaqMan MGB was used to analyzing the differences of IGF1R gene mRNA expression in peripheral leukocytes between subsyndromal symptomatic depression group(n = 47) and healthy controls(n = 52). At the same time Hamilton Depression Rating Scale -17(HAMD17) were assessed.

IGF1R gene mRNA expression was 0.21 ± 0.11 in SSD group, 0.56 ± 0.37 in healthy group, and there was significant difference between both groups on IGF1R expression(z = 39.54, P < 0.001). the expression levels of IGF1R in SSD patients was not correlated with Hamilton score(r = −0.292, p = 0.275).

This study suggested that the decreased expression of IGF1R were related with the pathophysiology of SSD.

Epigenetic changes may play a role in the etiology of psychotic diseases. It has been demonstrated that olig2 is implicated in schizophrenia (SCZ) and bipolar disorder (BPD). the aim of this study was to investigate the methylation status of a promoter region of the olig2 gene in BPD and SCZ patients.

Our study included 41 BPD and 45 SCZ (DSM-IV criteria) as well as 53 control subjects. DNA was extracted from blood leukocytes and bisulfited sequence analysis was used to determine the DNA methylation status of a typical CpGs island within the promoter region of olig2.

We found the methylated cytosines occurred mainly in two clusters. Olig2 gene promoter was hyper-methylated(∼30%) in DNA derived from the blood leukocytes in SCZ and BD compared to the controls subjects(P = 0.01 and P = 0.03, respectively). There was no statistically significant difference in frequency of site-specific cytosine methylation modification of Olig2 gene between SCZ patients and BD patients(P = 0.21).

We observed increased DNA methylation in the promoter region of the olig2 gene of SCZ and BPD. This could explain the reported decrease of the gene expression. the current study supports the growing interest of DNA methylation in psychopathology.

Suicide-related behaviours are common in schizophrenia and are significantly associated with premature death. The objective of this meta-analysis study was to estimate the pooled prevalence of suicide-related behaviours in schizophrenia patients in China.

The relevant literature was searched systematically via the relevant electronic databases (PubMed, Embase, PsycINFO, Chinese National Knowledge Infrastructure, Wanfang Databases and Chinese Biological Medical Literature Database) from their inception until 14 September 2016. Only original studies that reported the prevalence of suicide-related behaviours including suicidal ideation (SI), suicide plan, suicide attempt (SA) and completed suicide were selected.

Nineteen articles met the inclusion criteria and were analysed. The pooled lifetime prevalence of SI and SA were 25.8% (95% CI 14.7–41.1%) and 14.6% (95% CI 9.1–22.8%), respectively. The 1-month prevalence of SI was 22.0% (95% CI 18.2–26.4%). Subgroup analyses of lifetime SI and SA showed that gender, sample size, survey year, study location and source of patients have no significant mediating effects on the results.

Suicide-related behaviours are common in Chinese schizophrenia patients. Due to the high mortality risk, regular screening and effective suicide prevention programmes are warranted.