Many common pathological features have been observed for both autism spectrum disorders (ASDs) and obsessive-compulsive disorder (OCD). However, no systematic analysis of the common gene markers associated with both ASD and OCD has been conducted so far. Here, two batches of large-scale literature-based disease–gene relation data (updated in 2017 and 2019, respectively) and gene expression data were integrated to study the possible association between OCD and ASD at the genetic level. Genes linked to OCD and ASD present significant overlap (P-value <2.64e-39). A genetic network of over 20 genes was constructed, through which OCD and ASD may exert influence on each other. The 2017-based analysis suggested six potential common risk genes for OCD and ASD (CDH2, ADCY8, APOE, TSPO, TOR1A, and OLIG2), and the 2019-based study identified two more genes (DISP1 and SETD1A). Notably, the gene APOE identified by the 2017-based analysis has been implicated to have an association with ASD in a recent study (2018) with DNA methylation analysis. Our results support the possible complex genetic associations between OCD and ASD. Genes linked to one disease are worth further investigation as potential risk factors for the other.

To evaluate the electrophysiological changes in patients with acute tetrodotoxin (TTX) poisoning from ingestion of globefish (Tetraodontidae) patients exposed to TTX were compared with age-matched controls. The cohort of TTX-poisoning cases was clinically subdivided into mild, moderate, or severe cases. The motor nerve conduction velocity (MCV), sensory nerve conduction velocity (SCV), F-wave, H-reflex, and somatosensory-evoked potentials (SEP) of the median, ulnar, and common peroneal nerve (CPN) were determined using established techniques. Four of the 64 (6.3%) TTX-poisoning cases died and were omitted from the final analysis. The MCV and SCV of the median, ulnar, and CPN nerves in all the TTX-poisoning cases were significantly slower than the healthy controls. Severe cases of TTX poisoning had more significant reduction in nerve function. Thus, electroneurophysiological analysis could be used to determine the extent, course, and range of nerve system damage in patients with acute TTX poisoning.

Background: Schizophrenia risk genes are widely investigated, but a systemic analysis of miRNAs contributing to schizophrenia is lacking.Methods: Schizophrenia-associated genetic loci profiles were derived from a genomewide association study (GWAS) from the Schizophrenia Working Group of the Psychiatric Genomics Consortium (PGC) dataset. Experimentally confirmed relationships between miRNAs and their target genes were retrieved from a miRTarBase. A competitive gene set association analysis for miRNA-target regulations was conducted by the Multi-marker Analysis of GenoMic Annotation (MAGMA) and further validated by literature-based functional pathway analysis using Pathway Studio. The association between the targets of three miRNAs and schizophrenia was further validated using a GWAS of antipsychotic treatment responses.Results: Three novel schizophrenia-risk miRNAs, namely, miR-208b-3p, miR-208a-3p, and miR-494-5p, and their targetomes converged on calcium voltage-gated channel subunit alpha1 C (CACNA1C) and B-cell lymphoma 2 (BCL2), and these are well-known contributors to schizophrenia. Both miR-208a-3p and miR-208b-3p reduced the expression of the RNA-binding protein Quaking (QKI), whose suppression commonly contributes to demyelination of the neurons and to ischemia/reperfusion injury. On the other hand, both QKI and hsa-miR-494-5p were involved in gliomagenesis. Conclusion:Presented results point at an orchestrating role of miRNAs in the pathophysiology of schizophrenia. The sharing of regulatory networks between schizophrenia and other pathologies may explain higher cardiovascular mortality and lower odds of glioma previously reported in psychiatric patients.