Peroxymonosulfate activation by walnut shell activated carbon supported nano zero-valent iron for the degradation of tetracycline: Performance, degradation pathway and mechanism.

In this study, activated carbon (WS-AC) was prepared from walnut shell. Nano-zero-valent iron (nZVI) was loaded on walnut shell activated carbon by liquid phase reduction method and used as catalyst (WS-AC/nZVI) to activate peroxymonosulfate (PMS) to efficiently degrade tetracycline (TC) in solution. The composite material with a mass ratio of WS-AC to nZVI of 1:1 has the highest catalytic performance for activating PMS to degrade TC. The results showed that under the conditions of TC concentration of 100 ppm, PMS dosage of 0.2 mM and WS-AC/nZVI dosage of 0.1 g/L, the removal efficiency of TC could reach 81%. Based on quenching experiments and electron spin resonance (EPR), it was verified that •OH, SO4•- and 1O2 bound on the catalyst surface were the main reactive oxygen species during the reaction. The intermediate products of TC were identified by liquid chromatography-mass spectrometry (HPLC-MS) and DFT calculation, and the possible degradation pathway of TC was proposed. The catalyst still maintained high removal efficiency of TC after four cycles of experiments, and the minimal iron loss on the surface of the catalyst indicated that it had good stability. The efficient and stable WS-AC/nZVI activated PMS showed great potential in the degradation of antibiotics.

Genome-wide identification and analysis of the eQTL lncRNAs in multiple sclerosis based on RNA-seq data.

The pathogenesis of multiple sclerosis (MS) is significantly regulated by long noncoding RNAs (lncRNAs), the expression of which is substantially influenced by a number of MS-associated risk single nucleotide polymorphisms (SNPs). It is thus hypothesized that the dysregulation of lncRNA induced by genomic variants may be one of the key molecular mechanisms for the pathology of MS. However, due to the lack of sufficient data on lncRNA expression and SNP genotypes of the same MS patients, such molecular mechanisms underlying the pathology of MS remain elusive. In this study, a bioinformatics strategy was applied to obtain lncRNA expression and SNP genotype data simultaneously from 142 samples (51 MS patients and 91 controls) based on RNA-seq data, and an expression quantitative trait loci (eQTL) analysis was conducted. In total, 2383 differentially expressed lncRNAs were identified as specifically expressing in brain-related tissues, and 517 of them were affected by SNPs. Then, the functional characterization, secondary structure changes and tissue and disease specificity of the cis-eQTL SNPs and lncRNA were assessed. The cis-eQTL SNPs were substantially and specifically enriched in neurological disease and intergenic region, and the secondary structure was altered in 17.6% of all lncRNAs in MS. Finally, the weighted gene coexpression network and gene set enrichment analyses were used to investigate how the influence of SNPs on lncRNAs contributed to the pathogenesis of MS. As a result, the regulation of lncRNAs by SNPs was found to mainly influence the antigen processing/presentation and mitogen-activated protein kinases (MAPK) signaling pathway in MS. These results revealed the effectiveness of the strategy proposed in this study and give insight into the mechanism (SNP-mediated modulation of lncRNAs) underlying the pathology of MS.

The roles of immune system and autoimmunity in pulmonary arterial hypertension: A review.

Pulmonary arterial hypertension (PAH) is a chronic disease characterized by increased pulmonary artery pressure which if left untreated, can lead to poor quality of life and ultimately death. It is a group of conditions and includes idiopathic PAH, familial/hereditary PAH and associated PAH. The condition has been studied for many years and its association with the immune system and in particular autoimmunity has been investigated. The mechanisms for the pathobiology of PAH are unclear although research has highlighted the role of adaptive and innate immune systems in its development. Diagnostics and therapeutic approaches range from cytokine treatments to the use of immunomodulating drugs, although there is still scope for improvements in the field. This article discusses the mechanisms linked to PAH, its association with other conditions and recent therapeutic interventions.

Effective recycling of Co and Sr from Co/Sr-bearing wastewater via an integrated Fe coagulation and hematite precipitation approach.

Flocculant overdose has been considered an inefficient technique for precipitating heavy metals from wastewater at low levels due to the high yield of hazardous waste sludge that should be treated properly before it can be disposed of safely in landfills. This problem was effectively solved in this study via a novel method that recycles sludge separately into high-purity hematite and heavy metal-bearing products. The wastewater, which contained 10.3 mg/L of Co and 4.8 mg/L of Sr, was coagulated by adding ferric salt to generate Co/Sr-bearing sludge. The sludge was dissolved in HNO3, followed by hydrothermal treatment with the addition of organic matter (e.g. methanol or isopropanol). Without the addition of organic matter, only 56.5% of total Fe was removed as irregular hematite particles, whilst Co/Sr remained unchanged in the acid. Over 99.5% of total Fe was eliminated as hematite nanoparticles with 97.7% Fe2O3 content, but more than 98% Co/Sr remained in the acid when methanol with a molar ratio (Mmethanol/MFe) of 5 was added. Nearly 100% Co was precipitated by adjusting the pH of the acid to 8 to generate Co hydroxide with 83.9% purity. Meanwhile, the residual Sr was further precipitated by adding Na2CO3 to generate SrCO3 with 96.8% purity. Isopropanol achieved total Fe removal similar to that of methanol. The optimal molar ratio (MIsopropanol/MFe) was 1, which corresponded to the removal of 98.7% total Fe. Methanol and isopropanol can react with NO3- in acid to reduce NO2- concentration and improve acid pH, promoting hydrolysis followed by the crystallisation of ferric Fe with hematite as the final product. This paper is the first report on an environment-friendly method for enriching Co/Sr without generating any waste.

Meta-analysis of association between TCF7L2 polymorphism rs7903146 and type 2 diabetes mellitus.

BACKGROUND: Large scale association studies have found a significant association between type 2 diabetes mellitus (T2DM) and transcription factor 7-like 2 (TCF7L2) polymorphism rs7903146. However, the quality of data varies greatly, as the studies report inconsistent results in different populations. Hence, we perform this meta-analysis to give a more convincing result. METHODS: The articles, published from January 1st, 2000 to April 1st, 2017, were identified by searching in PubMed and Google Scholar. A total of 56628 participants (34232 cases and 22396 controls) were included in the meta-analysis. A total of 28 studies were divided into 4 subgroups: Caucasian (10 studies), East Asian (5 studies), South Asian (5 studies) and Others (8 studies). All the data analyses were analyzed by the R package meta. RESULTS: The significant association was observed by using the dominant model (OR = 1.41, CI = 1.36 - 1.47, p < 0.0001), recessive model (OR = 1.58, CI = 1.48 - 1.69, p < 0.0001), additive model(CT vs CC) (OR = 1.34, CI = 1.28-1.39, p < 0.0001), additive model(TT vs CC) (OR = 1.81, CI = 1.69-1.94, p < 0.0001)and allele model (OR = 1.35, CI = 1.31-1.39, p < 0.0001). CONCLUSION: The meta-analysis suggested that rs7903146 was significantly associated with T2DM in Caucasian, East Asian, South Asian and other ethnicities.

LncRNA2Target: a database for differentially expressed genes after lncRNA knockdown or overexpression.

Long non-coding RNAs (lncRNAs) have emerged as critical regulators of genes at epigenetic, transcriptional and post-transcriptional levels, yet what genes are regulated by a specific lncRNA remains to be characterized. To assess the effects of the lncRNA on gene expression, an increasing number of researchers profiled the genome-wide or individual gene expression level change after knocking down or overexpressing the lncRNA. Herein, we describe a curated database named LncRNA2Target, which stores lncRNA-to-target genes and is publicly accessible at http://www.lncrna2target.org. A gene was considered as a target of a lncRNA if it is differentially expressed after the lncRNA knockdown or overexpression. LncRNA2Target provides a web interface through which its users can search for the targets of a particular lncRNA or for the lncRNAs that target a particular gene. Both search types are performed either by browsing a provided catalog of lncRNA names or by inserting lncRNA/target gene IDs/names in a search box.

Association Between COVID-19 and Neurological Diseases: Evidence from Large-Scale Mendelian Randomization Analysis and Single-Cell RNA Sequencing Analysis.

Observational studies have suggested that SARS-CoV-2 infection increases the risk of neurological diseases, but it remains unclear whether the association is causal. The present study aims to evaluate the causal relationships between SARS-CoV-2 infections and neurological diseases and analyzes the potential routes of SARS-CoV-2 entry at the cellular level. We performed Mendelian randomization (MR) analysis with CAUSE method to investigate causal relationship of SARS-CoV-2 infections with neurological diseases. Then, we conducted single-cell RNA sequencing (scRNA-seq) analysis to obtain evidence of potential neuroinvasion routes by measuring SARS-CoV-2 receptor expression in specific cell subtypes. Fast gene set enrichment analysis (fGSEA) was further performed to assess the pathogenesis of related diseases. The results showed that the COVID-19 is causally associated with manic (delta_elpd, - 0.1300, Z-score: - 2.4; P = 0.0082) and epilepsy (delta_elpd: - 2.20, Z-score: - 1.80; P = 0.038). However, no significant effects were observed for COVID-19 on other traits. Moreover, there are 23 cell subtypes identified through the scRNA-seq transcriptomics data of epilepsy, and SARS-CoV-2 receptor TTYH2 was found to be specifically expressed in oligodendrocyte and astrocyte cell subtypes. Furthermore, fGSEA analysis showed that the cell subtypes with receptor-specific expression was related to methylation of lysine 27 on histone H3 (H3K27ME3), neuronal system, aging brain, neurogenesis, and neuron projection. In summary, this study shows causal links between SARS-CoV-2 infections and neurological disorders such as epilepsy and manic, supported by MR and scRNA-seq analysis. These results should be considered in further studies and public health measures on COVID-19 and neurological diseases.

Transcriptome comparative analysis of amygdala-hippocampus in depression: A rat model induced by chronic unpredictable mild stress (CUMS).

BACKGROUND: Depression is a common and complex mental disease, and its pathogenesis involves several brain regions. Abnormalities in the amygdala-hippocampal neural circuits have been shown to be involved in depression. However, the underlying molecular mechanisms remain unclear. METHODS: A rat model was used to determine the transcriptome changes in the amygdala-hippocampal neural network under chronic unpredictable mild stress (CUMS). Depression-related modules in this neural network were identified using weighted gene co-expression network analysis (WGCNA). Difference and enrichment analyses were used to determine differential gene expression in the two brain regions. RESULTS: The modules in the amygdala and hippocampus associated with depression-like behavior contained 363 and 225 genes, respectively. Forty-two differentially expressed genes were identified in the amygdala candidate module and 37 in the hippocampus. Enrichment analysis showed that candidate genes in the amygdala were associated with neuronal myelination and candidate genes in the hippocampus were associated with synaptic transmission. Finally, based on module hub gene statistics, differential gene expression, and protein-protein interaction networks, 11 central genes were found in the amygdala candidate module, and one central gene was found in the hippocampal module. LIMITATIONS: Our study was based on a rat CUMS model. Further evidence is needed to prove that our results are applicable to patients with depression. CONCLUSION: This study identified critical modules and central genes involved in the amygdala-hippocampal circuit in the context of depression, and may provide further understanding of the pathogenesis of depression and help identify potential targets for antidepressant therapy.

Genome-Wide Analysis for the Regulation of Gene Alternative Splicing by DNA Methylation Level in Glioma and its Prognostic Implications.

Glioma is a primary high malignant intracranial tumor with poorly understood molecular mechanisms. Previous studies found that both DNA methylation modification and gene alternative splicing (AS) play a key role in tumorigenesis of glioma, and there is an obvious regulatory relationship between them. However, to date, no comprehensive study has been performed to analyze the influence of DNA methylation level on gene AS in glioma on a genome-wide scale. Here, we performed this study by integrating DNA methylation, gene expression, AS, disease risk methylation at position, and clinical data from 537 low-grade glioma (LGG) and glioblastoma (GBM) individuals. We first conducted a differential analysis of AS events and DNA methylation positions between LGG and GBM subjects, respectively. Then, we evaluated the influence of differential methylation positions on differential AS events. Further, Fisher's exact test was used to verify our findings and identify potential key genes in glioma. Finally, we performed a series of analyses to investigate influence of these genes on the clinical prognosis of glioma. In total, we identified 130 glioma-related genes whose AS significantly affected by DNA methylation level. Eleven of them play an important role in glioma prognosis. In short, these results will help to better understand the pathogenesis of glioma.