Comparison of GAP, R-GAP, and new trauma score (NTS) systems in predicting mortality of traffic accidents that injure hospitals at Mashhad University of medical sciences.

Background: There are several trauma scoring systems with varying levels of accuracy and reliability that have been developed to predict and classify mortality in trauma patients in the hospital admission. Considering the importance of the country's emergency organization and the World Health Organization in the category of traffic accidents, we used this information in the study. The objective of this study is to evaluate and compare the predictive power of three scoring systems (R-GAP, GAP, and NTS) on traffic accident injuries.

Demethylation of CDKN2A in systemic lupus erythematosus and rheumatoid arthritis: a blood biomarker for diagnosis and assessment of disease activity.

Introduction/objectives: Considering the phenotypic and serological heterogeneity of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), significant challenges may intervene with the precise diagnosis. In this regard, numerous studies have shown that changes in DNA methylation levels can be used to distinguish between healthy individuals and those with SLE and RA, as well as to predict disease activity and prognosis.

Methods: In the current study, we evaluated quantitative methylation level of CDKN2A promoter in peripheral blood mononuclear cells (PBMCs) of SLE and RA patients, and healthy controls by methylation-quantification of endonuclease-resistant DNA (MethyQESD), a bisulfite conversion-independent method.

Significant hypomethylation of gene promoter in patients with systemic lupus erythematosus.

Objective: Scholars are exploring novel diagnostic and prognostic biomarkers with higher sensitivity and specificity for systemic lupus erythematosus (SLE). In this regard, DNA methylation alterations have aroused attention. The association between the dysfunction of and genes and SLE has been previously demonstrated.

Identification of gene signature in RNA-Seq hepatocellular carcinoma data by Pareto-optimal cluster algorithm.

Aim: This study aimed to detect gene signatures in RNA-sequencing (RNA-seq) data using Pareto-optimal cluster size identification.

Background: RNA-seq has emerged as an important technology for transcriptome profiling in recent years. Gene expression signatures involving tens of genes have been proven to be predictive of disease type and patient response to treatment.

A functional microRNA binding site variant in IL-23R gene in systemic lupus erythematosus and rheumatoid arthritis: is there any correlation?

Background: IL-23 receptor (IL-23R) dysregulation has been shown to have critical roles in pathogenesis of different autoimmune diseases including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) via suppression of regulatory T cells (Tregs) as well as differentiation, expansion, and survival of T helper 17 (Th17) cells, followed by upregulation of interleukin 17 (IL-17). Here, we assessed the association of a functional microRNAs (miRNAs)-related single nucleotide polymorphism (miR-SNPs: rs10889677) in IL-23R, which was correlated with its overexpression and increased risk for SLE and RA in the Iranian population.

Methods: Genotype and allele distribution of rs10889677 variant were investigated in 105 RA patients, 100 SLE cases and 105 healthy controls via polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP) method.

Assessment of the association between TNIP1 polymorphism with clinical features and risk of systemic lupus erythematosus.

Objective: Over the past decades, has been identified as a strong risk locus in multiple genome-wide association studies (GWAS), spanning multiple populations and various autoimmune diseases. is a polyubiquitin-binding protein that works as a physiological inhibitor of NF-κB and maintains immune homeostasis. Some studies have confirmed that is downregulated in autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).

Association of rs3135500 and rs3135499 Polymorphisms in the MicroRNA-binding Site of Nucleotide-binding Oligomerization Domain 2 (NOD2) Gene with Susceptibility to Rheumatoid Arthritis.

The nucleotide-binding oligomerization domain 2 (NOD2) is the key regulator of inflammatory responses and has been involved in the pathogenesis of rheumatoid arthritis (RA). Laboratory and in silico evaluations have demonstrated that some polymorphisms in 3'UTR of NOD2 gene could influence the secondary structure of this region and similarly thermodynamic features of hybridization site and finally deregulate the expression of NOD2. In the current study, for the first time, we evaluated the possible association between single nucleotide polymorphisms (SNPs) rs3135500 and rs3135499 in the NOD2 gene with RA risk in the Iranian population.