Pilot study of genome-wide DNA methylation and gene expression for treatment response to escitalopram in panic disorder.

BACKGROUND: Antidepressants, particularly selective serotonin reuptake inhibitors, are currently considered the first-line treatment for panic disorder (PD). However, little is known about the relationship between the biomarkers that may predict better treatment. AIM: To compare genome-wide methylation and gene expression patterns between responsive and non-responsive patients with PD after 4 wk of escitalopram treatment. METHODS: Thirty patients with PD were enrolled in this study (responders = 13; non-responders = 17). All patients were assessed using the PD Severity Scale-Chinese version before and after treatment. The Illumina Infinium MethylationEPIC (850k) BeadChip for genome-wide methylation screening and mRNA sequencing was used in all patients with PD. RESULTS: A total of 701 differentially methylated positions (DMPs) were found between responders and non-responders (|Δß| ≥ 0.06, q < 0.05), and the hyper- and hypomethylated CpG sites were 511 (72.9%) and 190 (27.1%), respectively. Relative to non-responders, there were 59 differential transcripts, of which 20 were downregulated and 39 were upregulated (q < 0.05). However, no differentially expressed genes were identified by mRNA sequencing after correcting for multiple testing (|log2(FC)| > 1, q > 0.05). CONCLUSION: This preliminary study showed that DMPs might be associated with the treatment response to escitalopram in PD; however, these DMPs need to be verified in large samples.

Glutamate decarboxylase 1 gene polymorphisms are associated with respiratory symptoms in panic disorder.

BACKGROUND: Genetic factors play an important role in the pathogenesis of panic disorder (PD). However, the effect of genetic variants on PD remains controversial. AIM: To evaluate the associations between glutamate decarboxylase 1 (GAD1) gene polymorphisms and PD risk and assess the effect of GAD1 gene polymorphisms on the severity of clinical symptoms in PD. METHODS: We recruited 230 PD patients and 224 healthy controls in this study. All participants were assessed for anxiety and panic symptom severity using the Hamilton Anxiety Rating Scale (HAM-A) and Panic Disorder Severity Scale (PDSS). GAD1 gene polymorphisms (rs1978340 and rs3749034) were genotyped and assessed for allele frequencies. RESULTS: There were no significant differences between cases and controls in the genotype distributions or allele frequencies of GAD1 (rs1978340 and rs3749034). In addition, the effect of GAD1 (rs1978340 and rs3749034) on PD severity was not significant. However, regarding respiratory symptoms, patients with the GAD1 rs1978340 A/A genotype had significantly higher scores than those with the A/G or G/G genotype. CONCLUSION: Here, we showed that the A/A genotype of GAD1 rs1978340 was associated with increased severity of respiratory symptoms in patients with PD.

Identification and characterization of noncoding RNAs-associated competing endogenous RNA networks in major depressive disorder.

BACKGROUND: Major depressive disorder (MDD) is a common and serious mental illness. Many novel genes in MDD have been characterized by high-throughput methods such as microarrays or sequencing. Recently, noncoding RNAs (ncRNAs) were suggested to be involved in the complicated environmental-genetic regulatory network of MDD occurrence; however, the interplay among RNA species, including protein-coding RNAs and ncRNAs, in MDD remains unclear. AIM: To investigate the RNA expression datasets downloaded from a public database and construct a network based on differentially expressed long noncoding RNA (lncRNAs), microRNAs (miRNAs), and mRNAs between MDD and controls. METHODS: Gene expression data were searched in NCBI Gene Expression Omnibus using the search term "major depressive disorder." Six array datasets from humans were related to the search term: GSE19738, GSE32280, GSE38206, GSE52790, GSE76826, and GSE81152. These datasets were processed for initial assessment and subjected to quality control and differential expression analysis. Differentially expressed lncRNAs, miRNAs, and mRNAs were determined, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed, and protein-protein interaction network was generated. The results were analyzed for their association with MDD. RESULTS: After analysis, 3 miRNAs, 12 lncRNAs, and 33 mRNAs were identified in the competing endogenous RNA network. Two of these miRNAs were earlier shown to be involved in psychiatric disorders, and differentially expressed mRNAs were found to be highly enriched in pathways related to neurogenesis and neuroplasticity as per Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. The expression of hub gene fatty acid 2-hydroxylase was enriched, and the encoded protein was found to be involved in myelin formation, indicating that neurological development and signal transduction are involved in MDD pathogenesis. CONCLUSION: The present study presents candidate ncRNAs involved in the neurogenesis and neuroplasticity pathways related to MDD.

Experimental study on pollutant movement in surf zone.

The experiments on pollutant movement in surf zone were conducted on the two gentle beaches (with slope of 1:100 and 1:40, respectively), for diverse wave cases. The movement contours and direction of pollutants, under the action of regular and random waves with diverse wave amplitudes, were provided and studied in this paper. It was shown that, due to complicated hydrodynamics in surf zone, the pollutant movement state is quite complicated and different from that in pure current zone.