Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease with a complex pathogenesis. Neuropsychiatric systemic lupus erythematosus (NPSLE) is a serious complication of SLE that involves the nervous system and produces neurological or psychiatric symptoms. After decades of research, it is now believed that the diverse clinical manifestations of NPSLE are associated with intricate mechanisms, and that genetic factors, blood-brain barrier dysfunction, vascular lesions, multiple autoimmune antibodies, cytokines, and neuronal cell death may all contribute to the development of NPSLE. The complexity and diversity of NPSLE manifestations and the clinical overlap with other related neurological or psychiatric disorders make its accurate diagnosis difficult and time-consuming. Therefore, in this review, we describe the known pathogenesis and potential causative factors of NPSLE and briefly outline its treatment that may help in the diagnosis and treatment of NPSLE.

Background:Methotrexate (MTX) is widely used and considered a first-line disease modifying antirheumatic drug (DMARD) for the treatment of rheumatoid arthritis (RA). However, 10% to 30% of patients discontinue therapy within a year of starting the treatment, usually because of undesirable side effects. Many of the relevant genes have been investigated to estimate the association between gene polymorphisms and MTX toxicity in RA patients, although inconsistent results have been reported.Methods:We searched EMBASE and PubMed in February 2016 for polymorphisms and pharmacogenomics study of the toxicity of MTX monotherapy in RA patients. The meta-analysis was stratified by whether genetic variants associated with MTX toxicity.Results:A total of 42 publications that included 28 genes with 88 gene SNPs associated with the transporters, enzymes, and metabolites of MTX or the progression of RA were included in the SR, and 31 studies were included in 7 meta-analyses. The meta-analysis showed a significant association between the toxicity of MTX and the RFC-1 80G > A (rs1051266) polymorphism in the European RA patients.Conclusion:RFC-1 80G > A (rs1051266) polymorphism was associated with MTX toxicity, and larger and more stringent study designs may provide more accurate results for the effect of these SNPs on the MTX toxicity.

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Given the importance of wood in many industrial applications, much research has focused on wood formation, especially lignin biosynthesis. However, the mechanisms governing the regulation of lignin biosynthesis in the rubber tree (Hevea brasiliensis) remain to be elucidated. Here, we gained insight into the mechanisms of rubber tree lignin biosynthesis using reaction wood (wood with abnormal tissue structure induced by gravity or artificial mechanical treatment) as an experimental model. We performed transcriptome analysis of rubber tree mature xylem from tension wood (TW), opposite wood (OW), and normal wood (NW) using RNA sequencing (RNA-seq). A total of 214, 1,280, and 32 differentially expressed genes (DEGs) were identified in TW vs. NW, OW vs. NW, and TW vs. OW, respectively. GO and KEGG enrichment analysis of DEGs from different comparison groups showed that zeatin biosynthesis, plant hormone signal transduction, phenylpropanoid biosynthesis, and plant–pathogen interaction pathways may play important roles in reaction wood formation. Sixteen transcripts involved in phenylpropanoid biosynthesis and 129 transcripts encoding transcription factors (TFs) were used to construct a TF–gene regulatory network for rubber tree lignin biosynthesis. Among them, MYB, C2H2, and NAC TFs could regulate all the DEGs involved in phenylpropanoid biosynthesis. Overall, this study identified candidate genes and TFs likely involved in phenylpropanoid biosynthesis and provides novel insights into the mechanisms regulating rubber tree lignin biosynthesis.