Background: Immunological and inflammatory mechanisms play an important role in schizophrenia. The neutrophil-to-lymphocyte ratio (NLR) is a value obtained by dividing the absolute number of neutrophils by the absolute lymphocyte count and represents a biomarker of systemic inflammatory response. There are studies investigating NLR association with psychopathology. However, the relationship has been only studied in small numbers of patients with schizophrenia, which leads to conflicting results and makes the meta-analytic data difficult to interpret. The aim of this study is to perform large-scale cross-sectional analysis on the potential correlation between NLR and disease severity in schizophrenic patients with or without medication. Methods: This cross-sectional retrospective study was conducted in Nanjing Medical University Affiliated Brain Hospital. We identified inpatients with schizophrenia between July 12, 2018 and March 27, 2019 and collected data of NLR, the Clinical Global Impression Severity scale (CGI-S) score and the Brief Psychiatric Rating Scale (BPRS) score. Results: The records of 1,144 identified patients (10.8% drug-free patients) were analyzed. We found that NLR was significantly decreased in schizophrenic patients after antipsychotic administration and there was the discrepant correlation between NLR and psychiatric symptoms in patients with or without antipsychotic medication. The results of multivariate logistic regressions showed that NLR was positively associated with the severity of disease (i.e., the CGI-S score and the BPRS total score) in drug-free patients, and it was negatively associated with the BPRS negative symptoms (i.e., the BPRS negative symptoms score) in drug-therapy patients. Conclusion: The study is the first to confirm the hypothesis that NLR is independently associated with severe psychopathology in schizophrenia and is changed by antipsychotic administration.

Background: Parkinson’s disease (PD) is a common neurodegenerative disease affecting the movement of elderly patients. Environmental exposures are the risk factors for PD; however, gut environmental risk factors for PD are critically understudied. The proof-of-concept study is to identify gut metabolites in feces, as environmental exposure risk factors, that are associated with PD and potentially increase the risk for PD by using leverage of known toxicology results.Materials and methods: We collected the data regarding the gut metabolites whose levels were significantly changed in the feces of patients with PD from the original clinical studies after searching the following databases: EBM Reviews, PubMed, Embase, MEDLINE, and Elsevier ClinicalKey. We further searched each candidate metabolite-interacting PD gene set by using the public Comparative Toxicogenomics Database (CTD), identified and validated gut metabolites associated with PD, and determined gut metabolites affecting specific biological functions and cellular pathways involved in PD by using PANTHER tools.Results: Sixteen metabolites were identified and divided into the following main categories according to their structures and biological functions: alcohols (ethanol), amino acids (leucine, phenylalanine, pyroglutamic acid, glutamate, and tyrosine), short-chain fatty acids (propionate and butyrate), unsaturated fatty acids (linoleic acid and oleic acid), energy metabolism (lactate, pyruvate, and fumarate), vitamins (nicotinic acid and pantothenic acid), and choline metabolism (choline). Finally, a total of three identified metabolites, including butyrate, tyrosine, and phenylalanine, were validated that were associated with PD.Conclusion: Our findings identified the gut metabolites that were highly enriched for PD genes and potentially increase the risk of developing PD. The identification of gut metabolite exposures can provide biomarkers for disease identification, facilitate an understanding of the relationship between gut metabolite exposures and response, and present an opportunity for PD prevention and therapies.

Excessive iodine intake has been associated with increased risk of thyroid cancer (TC) in many studies, but the results have not been consistent. Since it was common knowledge that urinary iodine (UI) is considered a sensitive marker of current iodine intake, we conducted a meta-analysis to clarify the association between high UI and TC. We adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement, and the Cochrane Collaboration. Between-group meta-analyses were performed to compare UI between TC patients and the healthy/euthyroid subjects in local residents and benign thyroid nodules (BTN) patients. Then, between-group meta-analyses to compare the incidence rate of iodine excess were also conducted. The 22 case-control studies included in the meta-analyses represented 15,476 participants. It is the first time to clarify that UI was increased in PTC patients, but was not altered by regional population iodine intake status. Compared with BTN patients, PTC patients exhibited both higher UIC and higher odds ratio of iodine excess only in adequate iodine intake status subgroup; UIC, not the odds ratio of iodine excess, was higher in patients with PTC than those with BTN in above requirements iodine intake subgroup. A novel insight is offered that high UI in PTC patients was less influenced by regional population iodine intake status. It is indicted that high iodine intake is not a risk factor for PTC and high urinary iodine is just a specific characteristic of the disease.

Objectives: The policy of the standardized workload has been implemented among primary and secondary schoolteachers in Shanxi Province. The aim of this cross-sectional cohort study is to assess teacher stress among primary and secondary schoolteachers in Datong, a city of Shanxi Province and...