Due to the drastic surge of COVID-19 patients, many countries are considering or already graduating health professional students early to aid professional resources. We aimed to assess outbreak-related psychological distress and symptoms of acute stress reaction (ASR) in health professional students and to characterize individuals with potential need for interventions.

We conducted a prospective cohort study of 1442 health professional students at Sichuan University, China. At baseline (October 2019), participants were assessed for childhood adversity, stressful life events, internet addiction, and family functioning. Using multivariable logistic regression, we examined associations of the above exposures with subsequent psychological distress and ASR in response to the outbreak.

Three hundred and eighty-four (26.63%) participants demonstrated clinically significant psychological distress, while 160 (11.10%) met the criterion for a probable ASR. Individuals who scored high on both childhood adversity and stressful life event experiences during the past year were at increased risks of both distress (ORs 2.00–2.66) and probable ASR (ORs 2.23–3.10), respectively. Moreover, internet addiction was associated with elevated risks of distress (OR 2.05, 95% CI 1.60–2.64) and probable ASR (OR 2.15, 95% CI 1.50–3.10). By contrast, good family functioning was associated with decreased risks of distress (OR 0.43, 95% CI 0.33–0.55) and probable ASR (OR 0.48, 95% CI 0.33–0.69). All associations were independent of baseline psychological distress.

Our findings suggest that COVID-19 related psychological distress and high symptoms burden of ASR are common among health professional students. Extended family and professional support should be considered for vulnerable individuals during these unprecedented times.

To investigate the executive function and learning ability of the patients with first-episode schizophrenia, and its relationship with the patients’ clinical symptoms.

50 schizophrenia patients and 50 healthy controls were tested by the Tower of London (TOL). All the subjects received two phases of the test of TOL continuously, with a break of 1 minute. And Positive and Negative Symptom Scale (PANSS) was used to assess the clinical symptoms of the patients.

Compared with the control group, the number of reply during the 1st phase (x1) and the 2nd phase (x2)of the patients group, was lower (P<0.01); the reaction time during the 1st phase (t1) and the 2nd phase (t2) was longer (P<0.01); while the rate of correct answer during the 1st phase (p1) and the 2nd phase (p2) do not differ. For the control group, x2 was higher than x1 (P<0.01), and t2 was shorter than t1 (P<0.01). However, for the schizophrenia group, there were no difference between x1 and x2, t1 and t2. The value of x1, p1, x2 of the patients were correlated negatively with the PANSS negative subscale score (P< 0.05), and t1 and t2 were correlated positively with the the negative subscale score (P< 0.01). The performance of the TOL did not correlated with the PANSS positive subscale score and general psychopathology subscale score.

The executive function and learning ability of the schizophrenics are impaired and the impairment of the cognitive function is significantly correlated with the negative symptoms of schizophrenia patients.

Several genome-wide linkage scans have reported that chromosome 22q11-13 might contain susceptibility loci for both schizophrenia and mood disorder.

We genotyped 44 Chinese Han family trios with mixed family history of schizophrenia and mood disorder with 11 DNA microsatellite markers on chromosome 22q11-13. These markers spanned 56.55 cM on 22q11-13 with mean intervals of 5.66 cM and average heterozygosity 0.71.The transmission disequilibrium test (TDT) was used to search for susceptibility loci to schizophrenia and mood disorder.

Including all family trios regardless of proband diagnosis, we found six markers associated with susceptibility to psychotic disorders., including D22S420 (χ2=4.76, df=1, P=0.029)%3001D22S277 (χ2=5.44, df=1, P=0.020)%3001D22s315 (allele 5, χ2=7.00, df=1, P=0.008; allele 7, χ2=-4.83, df=1, P=0.028; allele 11, χ2=4.00, df=1, P=0.046)%3001D22S274 (allele 7, χ2=-5.40, df=1, P=0.020; allele 10, χ2=6.23 df=1, P=0.013)%3001D22S1160 (χ2=-4, df=1, P=0.046) and D22S1161 (χ2=5.14, df=1, P=0.023). When grouped separately into schizophrenia and mood disorder according to proband diagnosis, four markers D22S420(χ2=7.36, df=1, P=0.007) %3001D22S315 (allele 5, χ2=4., df=1, P=0.046; allele 7, χ2=-8.89, df=1, P=0.003)%3001D22S1161(χ2=6.23, df=1, P=0.013) and D22S280 (χ2=4, df=1, P=0.046) were significantly associated with schizophrenia, but were not significantly associated with mood disorder, D22S274(allele 7, χ2=5., df=1, P=0.025; allele 10, χ2=6, df=1, P=0.014) were significantly associated with mood disorder only, and D22S277(χ2=4, df=1, P=0.046) was associated with both schizophrenia and mood disorder.

These results indicate that chromosome 22q11-13 contains the susceptibility loci to schizophrenia and mood disorder, and that overlapping regions may be shared by these disorders.

Cognitive dysfunction was thought to be one of the core features of schizophrenia. And the executive function of the patients was paid more attention by more and more researchers and clinicians.

To investigate the executive function and the learning ability of the patients with first-episode schizophrenia, and their relationships with psychiatric symptoms.

Fifty cases of first-episode schizophrenia patients and fifty age- and gender-matched healthy controls were tested by a computerized version of Tower of London (TOL) test. The scores of the Positive and Negative Syndrome Scale(PANSS) in the group of schizophrenia patients were over 60.

The numbers of the correct answer [x1 :(14.62 ± 4.12), x2: (14.80 ± 4.70)] during the first session and the second session of the TOL test of the patients group were significantly lower than that of the control group [x1: (17.48 ± 3.79), x2:(18.68 ± 3.19)], and the reaction times [t1: (9.27 ± 4.37) seconds, t2: (9.51 ± 5.58) seconds] of the two sessions of TOL were longer than the control group [t1: (7.28 ± 2.04) seconds, t2: (6.67 ± 1.51) seconds], P < 0.01. For the control group, x2 was significantly greater than x1, and t2 shorter than t1 (P < 0.01), while for the patients group, there was no difference between the performances of the first session and the second session. The scores of TOL in the schizophrenia patients were correlated with the negative symptom score of PANSS (P < 0.05) and were not correlated with the scores of other subscales of PANSS (P > 0.05).

The executive function and the learning ability of schizophrenia are impaired and the cognitive dysfunction is correlated with negative symptoms.

Menopausal syndrome has been reported to be a worldwide women's mental health problem. Aborigines in rural areas have poorer access to mental health services. Thus, it is important to evaluate such symptoms of female aborigines with different menopausal statuses and their association with depression.

The aim of the study is to evaluate the association between physiological menopausal symptoms and depression during different menopausal period among female Taiwanese aborigines.

A total of 672 Taiwanese aboriginal women, aged 40–60, were recruited in the interviewing study and classified as pre-, peri-, and postmenopausal according to menstrual bleeding patterns in the previous 12 months. Then, the postmenopausal symptoms, depression, self-perceived health, family support, and associated demographic variables were assessed by questionnaire based on the results of interviewing by research assistants.

The results revealed that perimenopausal statuses were associated with depression and women with a perimenopausal status had a higher prevalence of depression than those with a premenopausal status. A higher score on physiological postmenopausal symptoms was found to be significantly associated with depression. Furthermore, somatic symptoms were associated with depression for pre-, peri-, and postmenopausal statuses. Moreover, sexual dysfunction and vasomotor symptoms were associated with depression only in the premenopausal status and postmenopausal status, respectively.

Depression should be routinely evaluated for female Taiwanese aborigines consulting with physicians for menopause symptoms, especially for somatic symptoms. Furthermore, attention should be provided to premenopausal women with sexual dysfunction and postmenopausal women with vasomotor symptoms for depression.

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.

To explore the difference in the clinical features between bipolar disorder and unipolar depression from the clinical phenomenology.

Two hundred bipolar patients with their current depressive episode and five hundred and sixty three recurrent depression were involved in the study. Clinical features of these two groups were compared and stepwise Logistic regression was used to identify the relationship between clinical features and bipolar disorder.

Clinical features of depressive episode which was different between two groups and were associated with bipolar disorder were as follows: age at onset of bipolar was earlier than that of unipolar depression; Bipolar patients whose age at onset before 25 years were more than unipolar depression; Sexual appetites which was one of atypical depressive symptoms were more common in bipolar depression than in unipolar depression; with psychiatric symptoms, psychomotor retardation, mood instability and duration of every depressive episode < 3 months, were more common in bipolar depression group than in unipolar depression group; Cognitive impairment factor, one of factors of HAMD-17 score, was significantly higher in bipolar depression group than in unipolar depression group. The odd ratio were 1.54, 1.50, 3.25, 1.99, 1.89, 1.48, 1.63, 1.63, and 1.42 separately.

The founding suggested that unipolar depression and bipolar depression might be distinct disorder, and age at onset, age at onset < 25, sexual appetites, psychiatric symptoms, psychomotor retardation, mood instability and duration of every depressive episode < 3 months might be potential to be the predictors of bipolar disorder.

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.

Recently, a triple-network model suggested the abnormal interactions between the executive-control network (ECN), default-mode network (DMN) and salience network (SN) are important characteristics of addiction, in which the SN plays a critical role in allocating attentional resources toward the ECN and DMN. Although increasing studies have reported dysfunctions in these brain networks in Internet gaming disorder (IGD), interactions between these networks, particularly in the context of the triple-network model, have not been investigated in IGD. Thus, we aimed to assess alterations in the inter-network interactions of these large-scale networks in IGD, and to associate the alterations with IGD-related behaviors.

DMN, ECN and SN were identified using group-level independent component analysis (gICA) in 39 individuals with IGD and 34 age and gender matched healthy controls (HCs). Then alterations in the SN-ECN and SN-DMN connectivity, as well as in the modulation of ECN versus DMN by SN, using a resource allocation index (RAI) developed and validated previously in nicotine addiction, were assessed. Further, associations between these altered network coupling and clinical assessments were also examined.

Compared with HCs, IGD had significantly increased SN-DMN connectivity and decreased RAI in right hemisphere (rRAI), and the rRAI in IGD was negatively associated with their scores of craving.

These findings suggest that the deficient modulation of ECN versus DMN by SN might provide a mechanistic framework to better understand the neural basis of IGD and might provide novel evidence for the triple-network model in IGD.