Correlation analysis and gender differences of cognitive function based on mini-mental state examination (MMSE) and suicidal tendency in patients with schizophrenia.

BACKGROUND: The aim of this study was to investigate the correlation and gender differences between cognition and suicidal tendency in patients with schizophrenia. METHODS: A total of 554 patients with schizophrenia were recruited. The Mini-Mental State Examination (MMSE), Positive and Negative Syndrome Scale (PANSS), Interpersonal Reactivity Index (IRI), Toronto Alexithymia Scale (TAS), and Insomnia Severity Index (ISI) were used to assess clinical symptoms. RESULTS: In male patients, MMSE score and the incidence of suicidal tendency were correlated (P = 0.04, OR = 1.06, 95%CI: 1.00-1.12). Among patients with cognitive dysfunction, IRI score (P = 0.01, OR = 1.04, 95%CI: 1.01-1.06), and types of antipsychotic drugs (P < 0.01, OR = 3.97, 95%CI: 1.76-8.97) in male patients were associated risk factors for suicidal ideation. Among patients without cognitive dysfunction, PANSS positive subscale score (P = 0.03, OR = 1.06, 95%CI: 1.01-1.11), and PANSS general psychopathology score (P = 0.02, OR = 1.05, 95%CI: 1.01-1.08) were associated risk factors for suicidal ideation in male patients and PANSS positive subscale score (P < 0.01, OR = 1.15, 95%CI: 1.05-1.26) were associated risk factors for suicidal ideation in female patients. CONCLUSIONS: There were significant gender differences in the correlation between cognitive functioning and suicidal ideation in patients with schizophrenia. Cognitive function may play an important mediating role in other factors on suicide.

Gender differences in prevalence and clinical risk factors of suicide attempts in young adults with first-episode drug-naive major depressive disorder.

BACKGROUND: Suicide rates in adolescents with major depressive disorder (MDD) change with age and gender. Early adulthood is an important transitional stage between late adolescence and adulthood, in which an individual's mind gradually matures. However, there are fewer studies on prevalence and variables linked to the suicide attempts of young adults with MDD. AIMS: To explore gender differences in the prevalence and risk factors associated with suicide attempts in young adults with first-episode drug-naive MDD. METHOD: The Hamilton Rating Scale for Depression (HRSD), Hamilton Rating Scale for Anxiety (HRSA) and Positive Subscale of the Positive and Negative Syndrome Scale (PANSS) were used to assess depression, anxiety and psychotic symptoms respectively and various biochemical indicators were assessed. RESULTS: Among 293 young adults with first-episode drug-naive MDD, the prevalence of suicide attempts was 15.45% (19/123) for males and 14.12% (24/170) for females. Males with suicide attempts had higher levels of thyroid-stimulating hormone (TSH) and higher PANSS Positive Subscale scores, whereas females with suicide attempts had higher TSH, serum total cholesterol, fasting blood glucose and diastolic blood pressure levels and higher scores on the HRSD, HRSA, PANSS Positive Subscale (all Bonferroni corrected P < 0.05). In males, PANSS Positive Subscale score (B = 0.17, P = 0.03, OR = 1.19, 95% CI 1.02-1.38) was a risk factor for suicide attempts. CONCLUSIONS: There were significant gender differences in the risk factors for suicide attempts in young adults with first-episode drug-naive MDD.

The effect of cognitive impairment based on Mini-Mental State Examination (MMSE) on suicidal tendency in patients with schizophrenia: A large cross-sectional study.

BACKGROUND: The effect of cognitive function on suicidal tendency in patients with schizophrenia is still inconclusive. This study aimed to explore the effect of cognitive impairment on suicidal tendency in schizophrenia patients and the risk factors of suicidal tendency in schizophrenia patients with cognitive impairment. METHODS: A total of 988 subjects were recruited for this study and finally 517 patients were included in the statistical analysis. Sociodemographic information was collected for each subject. Mini-Mental State Examination (MMSE) was used to assess patients' cognitive functioning. In addition, the Positive and Negative Syndrome Scale (PANSS) positive subscale, Insomnia Severity Index (ISI), and Beck Scale for Suicide Ideation (BSI) were used to assess psychotic symptoms, severity of insomnia, and intensity of suicidal ideation, respectively. RESULTS: Schizophrenia patients with cognitive dysfunction were significantly less likely to develop suicidal tendencies than those without cognitive dysfunction (P < 0.05, OR = 0.58, 95%CI: 0.39-0.81). In patients with cognitive impairment, those with suicidal tendency had substantially higher scores on BSI, ISI, EC, PD, IRI, F1, and PANSS positive subscale, and took more types of antipsychotic drugs than those without suicidal tendency (all P < 0.05), and the results of binary logistic regression analysis showed that, PANSS positive subscale score (B = 0.06, p = 0.04, OR = 1.07, 95%CI: 1.00-1.13) was a risk factor for suicidal tendencies. CONCLUSIONS: Our findings suggest that schizophrenia patients with cognitive dysfunction are significantly less likely to develop suicidal tendencies. Moreover, positive symptom is a risk factor for suicidal tendencies in schizophrenia patients with cognitive dysfunction.

Altered levels of cytokine, T- and B-lymphocytes, and PD-1 expression rates in drug-naïve schizophrenia patients with acute phase.

Many studies have investigated the changes of immune cells and proinflammatory cytokines in patients with acute schizophrenia, but few studies have investigated the functional phenotypes of immune cells and the expression rate of programmed cell death protein 1 (PD-1)/ programmed cell death-Ligand 1 (PD-L1). The aim of this study was to investigate the extent of immune cells activation, PD-1/PD-L1 expressions, and altered cytokine levels in drug-naïve schizophrenia patients with acute-phase. 23 drug-naïve schizophrenia patients in acute-phase and 23 healthy individuals were enrolled in this study as experimental and control groups, separately. Socio-demographic information including gender, age, duration of illness, and smoking status was collected for each subject. Beckman DXFLEX triple laser thirteen-color flow cytometer and self-contained software CytoFLEX flow cytometric analysis software were used to detect the expressions of PD-1/PD-L1 on CD4+/CD8+ T lymphocytes, B lymphocytes, monocytes and NK cells. BD Bioscience was used to examine the levels of cytokines including interferon (IFN)-γ, tumor necrosis factor (TNF)-α, Interleukin (IL)-2, IL-4, IL-6, and IL-10. Drug-naïve schizophrenia patients in acute-phase had higher levels of peripheral blood CD4+ T lymphocytes and B lymphocytes, higher PD-1 expression in B lymphocytes, and lower levels of CD8+ T lymphocytes. In addition, IL-6 levels of peripheral blood were higher in schizophrenia patients (all P < 0.05). Significant immune stress was present in schizophrenia patients with acute-phase.

Prevalence and correlates of dyslipidemia in first-episode and drug-naïve major depressive disorder patients with comorbid abnormal glucose metabolism: Sex differences.

Background: Lipid metabolism is associated with glucose metabolism, but whether there are variations between sexes in risk factors and prevalence of abnormal lipid metabolism in major depressive disorder (MDD) patients with glucose metabolism abnormalities remains ambiguous. In the present study, the frequency and risk factors of dyslipidemia in first-episode and drug-naïve (FEDN) MDD patients with dysglycemia were examined according to sex. Methods: One thousand seven hundred and eighteen FEDN MDD patients were recruited and their demographic data, clinical data, various biochemical indicators and scale assessment scores including 17-item Hamilton Rating Scale for Depression (HAMD-17), 14-item Hamilton Anxiety Rating Scale (HAMA-14), and positive subscale of the Positive and Negative Syndrome Scale (PANSS) were collected. Results: The prevalence of abnormal lipid metabolism in both male and female MDD patients with abnormal glucose metabolism was higher than that in patients without abnormal glucose metabolism. Among male MDD patients with abnormal glucose metabolism, TC was positively correlated with HAMD score, TSH and TgAb levels, but negatively correlated with PANSS positive subscale scores. LDL-C was positively correlated with TSH and BMI, but negatively correlated with PANSS positive subscale scores. HDL-C was negatively correlated with TSH levels. Among females, TC was positively correlated with HAMD score, TSH, and BMI, but negatively correlated with PANSS positive subscale score. LDL-C was positively correlated with HADM score and negatively correlated with FT3 level. HDL-C was negatively correlated with TSH and BMI levels. Conclusion: There are sex differences in the correlated factors of lipid markers in MDD patients with impaired glucose.

Prevalence and clinical correlates of abnormal lipid metabolism in first-episode and drug-naïve patients with major depressive disorder with abnormal glucose metabolism.

Comorbid glucose metabolism abnormalities are very common in patients with major depressive disorder (MDD), and glucose metabolism and lipid metabolism are closely related. However, there are few researches on the incidence and related factors of lipid metabolism abnormalities among MDD patients with comorbid glucose metabolism abnormalities. A cross-sectional study involving 1718 first-episode and drug-naïve (FEDN) MDD patients was conducted. The 17-item Hamilton Depression Scale (HAMD-17), Hamilton Anxiety Rating Scale (HAMA) and Positive and Negative Syndrome Scale (PANSS) positive subscale were utilized to evaluate depressive, anxiety and psychotic symptom, respectively. Serum thyroid function-related parameters, glucose- and lipid-metabolism parameters were measured. The prevalence of abnormal lipid metabolism was significantly higher in FEDN MDD patients with abnormal glucose metabolism than in those without abnormal glucose metabolism (P < 0.001). In MDD patients with abnormal glucose metabolism, TSH, FT3 and body mass index (BMI) levels were significantly higher in the abnormal lipid metabolism subgroup than in the non-abnormal lipid metabolism subgroup. Binary logistic regression analysis showed that TSH, FT3 and BMI were the influencing factors of abnormal lipid metabolism in MDD patients with abnormal glucose metabolism (all P < 0.05). MDD patients with abnormal glucose metabolism have a high prevalence of abnormal lipid metabolism. Moreover, abnormal glucose metabolism was an independent risk factor for abnormal lipid metabolism in patients with MDD. In addition, thyroid hormone function and BMI may contribute to the co-occurrence of abnormal lipid metabolism in MDD patients with abnormal glucose metabolism.

Prevalence and clinical correlates of thyroid dysfunction in first-episode and drug-naïve major depressive disorder patients with metabolic syndrome.

BACKGROUND: Few studies have investigated the relative factors of thyroid dysfunction in major depressive disorder (MDD) patients with Metabolic syndrome (MetS). This study aimed to explore the prevalence and related factors associated with thyroid dysfunction in drug-naïve (FEDN) MDD patients with MetS. METHODS: 1718 FEDN MDD patients were recruited and their demographic data, clinical data were collected. Various biochemical indicators including fasting blood glucose (FBG), blood lipids and thyroid hormones were measured. The 17-item Hamilton Rating Scale for Depression (HAMD-17), 14-item Hamilton Anxiety Rating Scale (HAMA-14) and positive subscale of the Positive and Negative Syndrome Scale (PANSS) were used to assess clinical symptoms. RESULTS: Among FEDN MDD patients, MetS was an independent risk factor for TSH abnormality (P < 0.001, Adjusted OR = 3.77, 95%CI: 2.82-5.05). In patients with MetS, those with TSH abnormality had significantly longer duration of illness, higher HAMD, HAMA, and PANSS positive subscale scores, higher levels of TC, LDL-C, blood glucose, pressure, lower levels of HDL-C, and a higher probability of suicide attempt (all P < 0.01). CONCLUSIONS: MetS is significantly associated with thyroid dysfunction in patients with FEDN MDD. Related factors for thyroid dysfunction include a number of clinical indicators and psychiatric symptoms.

Identification of immune-related and autophagy-related genes for the prediction of survival in bladder cancer.

BACKGROUND: Bladder cancer has the characteristics of high morbidity and mortality, and the prevalence of bladder cancer has been increasing in recent years. Immune and autophagy related genes play important roles in cancer, but there are few studies on their effects on the prognosis of bladder cancer patients. METHODS: Using gene expression data from the TCGA-BLCA database, we clustered bladder cancer samples into 6 immune-related and autophagy-related molecular subtypes with different prognostic outcomes based on 2208 immune-related and autophagy-related genes. Six subtypes were divided into two groups which had significantly different prognosis. Differential expression analysis was used to explore genes closely related to the progression of bladder cancer. Then we used Cox stepwise regression to define a combination of gene expression levels and immune infiltration indexes to construct the risk model. Finally, we built a Nomogram which consist of risk score and several other prognosis-related clinical indicators. RESULTS: The risk model suggested that high expression of C5AR2, CSF3R, FBXW10, FCAR, GHR, OLR1, PGLYRP3, RASGRP4, S100A12 was associated with poor prognosis, while high expression level of CD96, IL10, MEFV pointed to a better prognosis. Validation by internal and external dataset suggested that our risk model had a high ability to discriminate between the outcomes of patients with bladder cancer. The immunohistochemical results basically confirmed our results. The C-Index value and Calibration curves verified the robustness of Nomogram. CONCLUSIONS: Our study constructed a model that included a risk score for patients with bladder cancer, which provided a lot of helps to predict the prognosis of patients with bladder cancer.

Aberrantly expressed HORMAD1 disrupts nuclear localization of MCM8-MCM9 complex and compromises DNA mismatch repair in cancer cells.

HORMAD1 is a meiosis-specific protein that promotes synapsis and recombination of homologous chromosomes in meiotic prophase. Originally identified as a cancer/testis antigen, HORMAD1 is also aberrantly expressed in several cancers. However, the functions of HORMAD1 in cancer cells are still not clear. Here, we show that HORMAD1 is aberrantly expressed in a wide variety of cancers and compromises DNA mismatch repair in cancer cells. Mechanistically, HORMAD1 interacts with MCM8-MCM9 complex and prevents its efficient nuclear localization. As a consequence, HORMAD1-expressing cancer cells have reduced MLH1 chromatin binding and DNA mismatch repair defects. Consistently, HORMAD1 expression is associated with increased mutation load and genomic instability in many cancers. Taken together, our study provides mechanistic insights into HORMAD1's functions in cancer cells, which can potentially be exploited for targeted therapy of HORMAD1-expressing cancers.

Mechanisms of glucose-induced expression of pancreatic-derived factor in pancreatic beta-cells.

Pancreatic-derived factor (PANDER) is a cytokine-like peptide highly expressed in pancreatic beta-cells. PANDER was reported to promote apoptosis of pancreatic beta-cells and secrete in response to glucose. Here we explored the effects of glucose on PANDER expression, and the underlying mechanisms in murine pancreatic beta-cell line MIN6 and primary islets. Our results showed that glucose up-regulated PANDER mRNA and protein levels in a time- and dose-dependent manner in MIN6 cells and pancreatic islets. In cells expressing cAMP response element-binding protein (CREB) dominant-negative construct, glucose failed to induce PANDER gene expression and promoter activation. Treatment of the cells with calcium chelator [EGTA, 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl)ester (BAPTA/AM)], the voltage-dependent Ca(2+) channel inhibitor (nifedipine), the protein kinase A (PKA) inhibitor (H89), the protein kinase C (PKC) inhibitor (Go6976), or the MAPK kinase 1/2 inhibitor (PD98059), all significantly inhibited glucose-induced PANDER gene expression and promoter activation. Further studies showed that glucose induced CREB phosphorylation through Ca(2+)-PKA-ERK1/2 and Ca(2+)-PKC pathways. Thus, the Ca(2+)-PKA-ERK1/2-CREB and Ca(2+)-PKC-CREB signaling pathways are involved in glucose-induced PANDER gene expression. Wortmannin (phosphatidylinositol 3-kinase inhibitor), ammonium pyrrolidinedithiocarbamate (nuclear factor-kappaB inhibitor and nonspecific antioxidant), and N-acetylcysteine (antioxidant) were also found to inhibit glucose-induced PANDER promoter activation and gene expression. Because there is no nuclear factor-kappaB binding site in the promoter region of PANDER gene, these results suggest that phosphatidylinositol 3-kinase and reactive oxygen species be involved in glucose-induced PANDER gene expression. In conclusion, glucose induces PANDER gene expression in pancreatic beta-cells through multiple signaling pathways. Because PANDER is expressed by pancreatic beta-cells and in response to glucose in a similar way to those of insulin, PANDER may be involved in glucose homeostasis.