Dong-Fang Wang

Vitamin D and Graves' disease: a meta-analysis update.

The association between vitamin D levels and Graves’ disease is not well studied. This update review aims to further analyze the relationship in order to provide an actual view of estimating the risk. We searched for the publications on vitamin D and Graves’ disease in English or Chinese on PubMed, EMBASE, Chinese National Knowledge Infrastructure, China Biology Medical and Wanfang databases. The standardized mean difference (SMD) and 95% confidence interval (CI) were calculated for the vitamin D levels. Pooled odds ratio (OR) and 95% CI were calculated for vitamin D deficiency. We also performed sensitivity analysis and meta-regression. Combining effect sizes from 26 studies for Graves’ disease as an outcome found a pooled effect of SMD = −0.77 (95% CI: −1.12, −0.42; p < 0.001) favoring the low vitamin D level by the random effect analysis. The meta-regression found assay method had the definite influence on heterogeneity (p = 0.048). The patients with Graves’ disease were more likely to be deficient in vitamin D compared to the controls (OR = 2.24, 95% CI: 1.31, 3.81) with a high heterogeneity (I2 = 84.1%, p < 0.001). We further confirmed that low vitamin D status may increase the risk of Graves’ disease.

Human Adenovirus 36 Infection Increased the Risk of Obesity: A Meta-Analysis Update

AbstractHuman adenovirus 36 (HAdV-36), as the key pathogen, was supposed and discussed to be associated with obesity. We searched the references on the association between HAdV-36 infection and obesity with the different epidemiological methods, to explore the relationship with a larger sample size by meta-analysis and compare the differences of epidemiological methods and population subsets by the subgroup analyses.We conducted literature search on the association between HAdV-36 infections and obesity in English or Chinese published up to July 1, 2015. The primary outcome was the HAdV-36 infection rate in the obese and lean groups; the secondary outcomes were the BMI level and BMI z-score in the HAdV-36 positive and negative groups. The pooled odds ratio (OR) was calculated for the primary outcome; the standardized mean differences (SMDs) were calculated for the secondary and third outcomes. Prediction interval (PI) was graphically presented in the forest plot of the random effect meta-analyses. Metaregression analysis and subgroup analysis were performed.Finally 24 references with 10,191 study subjects were included in the meta-analysis. The obesity subjects were more likely to be infected with HAdV-36 compared to the lean controls (OR = 2.00; 95%CI: 1.46, 2.74; PI: 0.59, 6.76; P < 0.001) with a high heterogeneity (I2 = 80.1%; P < 0.001) estimated by the random effect model. Subgroup analysis demonstrated that the pooled OR of HAdV-36 infection for obesity were 1.77 (95%CI: 1.19, 2.63; PI: 0.44, 7.03; P = 0.005) and 2.26 (95%CI: 1.67, 3.07; PI: 1.45, 3.54; P < 0.001) in the adults and children, respectively. Compared to the HAdV-36 negative subjects, the SMD of BMI was 0.28 (95% CI: 0.08, 0.47; PI: −0.53, 1.08; P = 0.006) in the HAdV-36 positive subjects with a high heterogeneity (I2 = 86.5%; P < 0.001). The BMI z-score in the children with HAdV-36 infection was higher than those without HAdV-36 infection (SMD = 0.19; 95%CI: −0.31, 0.70; PI: −2.10, 2.49), which had no significantly statistical difference (P = 0.453).HAdV-36 infection increased the risk of obesity. HAdV-36 also increased the risk of weight gain in adults, which was not observed in children.

Meta-Analyses of Manganese Superoxide Dismutase Activity, Gene Ala-9Val Polymorphism, and the Risk of Schizophrenia.

AbstractSchizophrenia is a complex and disabling psychiatric disorder, and tardive dyskinesia (TD) is a severe adverse drug effect occurring in 20% to 40% of schizophrenic patients chronically treated with typical neuroleptics. Previous studies suggested that the manganese superoxide dismutase (MnSOD) activity was associated with the development of schizophrenia. Ala-9Val polymorphism, a functional polymorphism of MnSOD gene, has been reported to be related to the risk of schizophrenia and TD. However, these studies did not lead to consistent results. We performed meta-analyses aiming to assess the association between MnSOD activity and schizophrenia, as well as the association of MnSOD Ala-9Val polymorphism with schizophrenia and TD in schizophrenic patients.We search for the literature on MnSOD and schizophrenia in English or Chinese published up to May 1, 2015 on PubMed, EMBASE, the Cochrane Databases, Chinese National Knowledge Infrastructure, China Biology Medical and Wanfang databases. Two investigators independently reviewed retrieved literature and evaluated eligibility. Discrepancy was resolved by consensus with a third reviewer. Data were pooled using fixed-effect or random-effect models. The standardized mean difference (SMD) and 95% confidence interval (CI) were calculated for the MnSOD activity. Pooled odds ratio (OR) and 95% CI were calculated for Ala-9Val genotype and allele frequencies.There were 6, 6, and 10 studies entering 3 parts of meta-analyses, respectively. The MnSOD activity of patients was significantly lower than that of controls (SMD = −0.94; 95% CI: −1.76, −0.12; P = 0.025). No significant associations of Ala-9Val genotypes (OR = 1.14; 95% CI: 0.97, 1.33; P = 0.109) and alleles (OR = 1.06; 95% CI: 0.94, 1.20; P = 0.361) with the risk of schizophrenia were observed. We also did not reveal significant associations of the genotypes (OR = 0.82; 95% CI: 0.66, 1.02; P = 0.075) and alleles (OR = 0.90; 95% CI: 0.76, 1.06; P = 0.215) with the risk of TD in schizophrenia.The decreased MnSOD activity may be associated with the risk of chronic schizophrenia in Chinese population, while MnSOD Ala-9Val polymorphism may not play a significant role in the development of schizophrenia and TD. Longitudinal studies with larger sample sizes and different ethnicities are needed to confirm the association of the MnSOD Ala-9Val variants with schizophrenia and TD.

Serum metabolic profiling using small molecular water-soluble metabolites in individuals with schizophrenia: A longitudinal study using a pre-post-treatment design: Metabolic profiling for schizophrenia

We sought to compare alterations in serum bioenergetic markers within a well‐characterized sample of adults with schizophrenia at baseline and after 8 weeks of pharmacological treatment with the hypothesis that treatment would be associated with significant changes in bioenergetic markers given the role of bioenergetic dysfunction in schizophrenia.

A comparative study of the typical toxic metals in serum by patients of schizophrenia and healthy controls in China

Toxic metals are ubiquitous environmental pollutants, and their potential risks associated with the development of schizophrenia remain a subject of debate. In this study, we investigated the associations between six typical toxic metals (mercury, lead, chromium, silver, antimony, and uranium) in serum with the risk of schizophrenia using a case-control study design. In total, 109 patients with schizophrenia (cases) and 106 normal subjects (controls) from Shandong Province, China were recruited. Fasting blood samples were collected from all participants, as well as serum samples from the cases before and after medical treatment. The six metals were analyzed by inductively coupled plasma mass spectrometry. Only three metals (antimony, silver and uranium) had acceptable detection rates of >80%. The concentrations of antimony and uranium were significantly higher in the cases than in the controls, while no significant difference for silver. Moreover, the serum concentrations of antimony and uranium were significantly lower after medical treatment. Clear dose-response relationships between serum metal concentrations and the risk of schizophrenia were observed, even after adjusting for potential covariates. This suggests that higher levels of antimony and uranium may be one of the factors associated with an elevated risk of schizophrenia.

Association on DISC1 SNPs with schizophrenia risk: A meta-analysis

Schizophrenia is a major psychiatric disorder with complex genetic, environmental, and psychological etiologies. Although DISC1 gene has been shown as a risk factor for schizophrenia in some reports, there is a lack of a consensus. We therefore performed separate meta-analyses aiming to assess the associations between DISC1 SNPs and schizophrenia risk. We found that SNP rs821597 is significantly associated with schizophrenia risk in terms of both allelic and genotypic distribution, while SNP rs821616 is associated with schizophrenia in terms of genotypic distribution, especially in cases above 40 years old.

Unbiased lipidomic profiling reveals metabolomic changes during the onset and antipsychotics treatment of schizophrenia disease

IntroductionSchizophrenia (SCH) is one of the most common psychiatric disorders, which involves impairments in motivation and cognition. The pathological mechanisms underlying SCH are still unknown, and no effective therapies can prevent or treat perfectly the cognitive impairments and deficit symptoms caused by SCH.ObjectivesWe aimed to find the lipid expression change in plasma that underlie SCH onset and antipsychotics treatment.MethodsWe performed a data independent acquisition-based untargeted lipidomic approach on a quadrupole-time of flight liquid chromatography coupled to mass spectrometry platform. The plasma lipidomic profiles of SCH patients (n = 20) pre- and post-antipsychotics treatment were acquired as well as healthy controls (n = 29). Grouped or paired t-test were used to analyze the data.ResultsOver 1000 features were detected by our lipidomic analysis, of which 445 lipids belonging to 17 lipid species were reliably identified by tandem mass spectrometry. After statistical analysis, 47 lipids belonging to 9 lipid species were found to be dysregulated between naive SCH patients and healthy controls, and 50 lipids belonging to 9 lipid species were found to be dysregulated after antipsychotics treatment. These findings include several new SCH-relevant lipid species such as sphingomyelin, acylcarnitine and ceramide. Four types of lipid expression regulative patterns can be concluded from the above mentioned findings, revealing information about mechanism, side-effect and potential target of antipsychotics.ConclusionsThe work presented here have revealed several new lipid species which are significantly dysregulated in SCH disease development or antipsychotics treatment. These lipids provide new evidence for the pathological studies of SCH and new antipsychotics development, or can be considered as potentially candidate biomarkers for further validation.

Alterations of eicosanoids and related mediators in patients with schizophrenia

Schizophrenia (SCZ) is a multifactorial psychiatric disorder. Currently, its molecular pathogenesis remains largely unknown, and no reliable test for diagnosis and therapy monitoring is available. Polyunsaturated fatty acids (PUFAs) and their derived eicosanoid signaling abnormalities are relevant to the pathophysiology of schizophrenia. However, comprehensive analysis of eicosanoids and related mediators for schizophrenia is very rare. In this study, we applied a targeted liquid chromatography-mass spectrometry based method to monitor 158 PUFAs, eicosanoids and related mediators from enzyme-dependent or independent pathways, in the serum samples of 109 healthy controls, and 115 schizophrenia patients at baseline and after an 8-week period of antipsychotic therapy. Twenty-three metabolites were identified to be significantly altered in SCZ patients at baseline compared to healthy controls, especially arachidonic acid (AA) derived eicosanoids. These disturbances may be related to altered immunological reactions and neurotransmitter signaling. After 8-week antipsychotic treatment, there were 22 metabolites, especially AA and linoleic acid derived eicosanoids, significantly altered in posttreatment patients. Some metabolites, such as several AA derived prostaglandins, thromboxanes, and di-hydroxy-eicosatrienoic acids were reversed toward normal levels after treatment. Based on univariate analysis and orthogonal partial least-squares discriminant analysis, anandamide, oleoylethanolamine, and AA were selected as a panel of potential biomarkers for differentiating baseline SCZ patients from controls, which showed a high sensitivity (0.907), good specificity (0.843) and excellent area under the receiver operating characteristic curve (0.940). This study provided a new perspective to understand the pathophysiological mechanism and identify potential biomarkers of SCZ.

Characterizing amino-acid biosignatures amongst individuals with schizophrenia: a case–control study

Amino acids and derivatives participate in the biosynthesis and downstream effects of numerous neurotransmitters. Variations in specific amino acids have been implicated in the pathophysiology of schizophrenia. Herein, we sought to compare levels of amino acids and derivatives between subjects with schizophrenia and healthy controls (HC). Two hundred and eight subjects with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria (DSM-IV)-defined schizophrenia and 175 age- and sex-matched HC were enrolled. The levels of twenty-five amino acids and seven related derivatives were measured in plasma samples using hydrophilic interaction liquid chromatography (HILIC) liquid chromatography–tandem mass spectrometry (LC–MS). After controlling for age, sex and body mass index (BMI), four amino acids and derivatives (i.e., cysteine, GABA, glutamine and sarcosine) were observed to be higher in the schizophrenia group when compared with HC; seven amino acids and derivatives were lower in the schizophrenia group (i.e., arginine, l-ornithine, threonine, taurine, tryptophan, methylcysteine, and kynurenine). Statistically significant differences in plasma amino-acid profiles between subjects with first-episode vs. recurrent schizophrenia for aspartate and glutamine were also demonstrated using generalized linear models controlling for age, sex, and BMI. The differences in amino acids and derivatives among individuals with schizophrenia when compared to HC may represent underlying pathophysiology, including but not limited to dysfunctional proteinogenic processes, alterations in excitatory and inhibitory neurotransmission, changes in ammonia metabolism and the urea cycle. Taken together, amino-acid profiling may provide a novel stratification approach among individuals with schizophrenia.