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Schistosomiasis is a public health problem in many countries. Its prevalence is increasing annually; the current infection rate is one in 30 individuals. The WHO reported that at least 206.4 million people all over the world required preventive treatments for schistosomiasis in 2016. Chronic schistosomiasis, hepatitis B virus (HBV) and hepatitis C virus (HCV) co-infection are common in countries where schistosomiasis is endemic. The effects of the hepatotropic virus co-infection may modify the Th2-dominated granulomatous phase of schistosomal infection. These viruses induce a strong-specific T cell response, with infiltration of large numbers of specific interferon-γ-producing CD8+ cells into the liver. The outcome of liver diseases depends on the underlying causes, host immune response and concomitant infections. Co-infection of schistosomiasis with HBV/HCV infection causes advanced liver disease and worsens the outcome, especially with higher viral load titers, which increase the mortality rate through an increased incidence of liver cirrhosis and hepatocellular carcinoma. The exposure risk for HBV in patients with HCV and schistosomiasis was two and half times greater than that in CHC patients without schistosomiasis. Finally, chronic schistosomiasis and HBV/HCV co-infection have serious effects on liver pathology. Co-infection accelerates the progression of liver disease and leads to advanced liver diseases and liver failure. [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by T-cell immune-dysregulation and loss of tolerance to self-antigens. CTLA-4 and PTPN-22 are involved in the inhibition of T-lymphocytes activation. IL-37 is an anti-inflammatory cytokine that suppresses innate immunity. The relative expression of CTLA-4 , IL-37 and PTPN-22 were evaluated as negative regulators of immune response in SLE patients, lupus nephritis (LN) and disease activity. Real-Time PCR was performed to determine relative CTLA-4 , IL-37 , and PTPN-22 mRNA expressions in fifty-eight SLE patients, who were divided into two groups: 29 SLE patients without nephritis and 29 patients with LN, versus fifty controls. There was a significantly high-expression of CTLA-4 and IL-37 genes in SLE patients compared to controls (p = 0.005; 0.018 respectively). There was no difference in relative PTPN-22 mRNA expression between the SLE patients and controls. Relative CTLA-4 mRNA expression decreased in LN patients (p = 0.044), however, relative IL-37 mRNA over-expressed in LN patients (p = 0.001) compared to those without LN. There was a significant over-expression of relative IL-37 and PTPN-22 mRNA in active SLE patients. But, there was a non-significant difference in CTLA-4 expression with disease activity. Regression analysis revealed patients with relative IL-37 mRNA over-expression had two times more to develop lupus nephritis (OR = 1.906, 95% CI = 1.218–2.983, p = 0.005). Relative IL-37mRNA expression was elevated in SLE patients and associated with renal involvement and disease activity. It could be considered as a new promising predicting tool for LN. Relative PTPN-22 mRNA expression was correlated with disease activity only in SLE patients. [ABSTRACT FROM AUTHOR]

Background: Plasmid-mediated quinolone resistance genes (PMQR) are mainly associated with clinical isolates of Enterobacteriaceae and complicate treatment of infections caused by these isolates worldwide. Extended-spectrum-beta-lactamase (ESBL)-producing bacteria are resistant to common antibiotics and also through many mechanisms, ESBL could be disabling other types of antibiotics. This study aimed to assess the prevalence of quinolone resistance and ESBL among Enterobacteriaceae strains and investigated the presence of qnrA and qnrB genes in these strains which were isolated from urinary tract infections in Ismailia, Egypt. Ninety-four Enterobacteriaceae isolates were collected from cases of UTIs admitted to the intensive care unit, Suez-Canal University Hospitals, between October 2017 and January 2018. Antibacterial susceptibility was determined by the disk diffusion method. A polymerase chain reaction assay was used to detect qnrA and qnrB resistance genes in quinolone- and fluoroquinolone-resistant and ESBL strains. Also, ciprofloxacin MIC was determined by the agar dilution method. Results: Resistance rates were 59.6%, 54.3%, 53.2%, 53.2%, and 53.2% to NA, LEV, NOR, CIP, and FX, respectively. Of 56 NA-resistant isolates, 7 (12.5%) and 6 (10.7%) were positive for qnrA and qnrB, respectively, with only one isolate co-harboring both genes. ESBL-producing bacteria was 66.2% of isolates. The MICs for ciprofloxacin ranged from 32–256 μg/ml in ciprofloxacin-resistant isolates. Conclusion: Our study shows high resistance rates of Enterobacteriaceae to quinolones and ESBL in our hospital which necessitate appropriate use of these antibiotics to reserve their application for therapy. The prevalence of quinolone-resistant and ESBL-producing Enterobacteriaceae was approximately 60% and 70% respectively. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a chronic, progressive, inflammatory, autoimmune disease that could be disabling throughout its course. It affects people in their most reproductive years with relatively high morbidity and mortality. Long non-coding RNAs became one of the epigenetic mechanisms to prove a link to RA pathogenesis and development, including H19 and MALAT1 genes. These two genes' expressions had proved to increase in multiple diseases, attracting attention to their polymorphisms and their possible risk role. Assess the association between H19 SNP (rs2251375) and MALAT1 SNP (rs3200401) and the susceptibility of RA and its disease activity. In this pilot study, 200 hundred subjects (100 RA patients and 100 healthy controls) were investigated for a possible link between the polymorphisms H19 SNP (rs2251375) and MALAT1 SNP (3200401) and RA susceptibility and disease activity. RA-related investigations and clinical assessment were done. Real-time PCR genotyping of both SNPs was done using TaqMan® MGB probes. There was no association between the SNPs and risk of developing RA. However, both SNPs had a significant association with high disease activity. H19 SNP (rs2251375) heterozygous genotype CA had an association with elevated levels of ESR (p = 0.04) and higher DAS28-ESR score (p = 0.03). MALAT1 (rs3200401) C allele had an association with elevated ESR (p = 0.001), DAS28-ESR (p = 0.03), and DAS28-CRP (p = 0.007), while CC genotype had an association with DAS28-CRP (p = 0.015). Linkage disequilibrium and haplotyping of the alleles of both SNPs were analyzed as both genes are present on chromosome 11, but no significant association was found between any of the combinations of the alleles (p > 0.05), denoting that (rs2251375) and (rs3200401) are not in linkage disequilibrium. There is no association between H19 SNP (rs2251375) and MALAT1 SNP (rs3200401) and the susceptibility of RA. However, there is an association between H19 SNP (rs2251375) genotype CA and MALAT1 SNP (rs3200401) genotype CC with RA high disease activity. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is an inflammatory autoimmune disease that destroys joint cartilage and causes disability. Synovial inflammation, with angiogenesis, is an early event in the progression of the disease. Angiopoietin 2 (ANGPT2) is a cytokine with both inflammatory and angiogenic effects. Many genes can influence RA susceptibility and disease activity. The aim is to assess the relationship between ANGPT2 gene polymorphism (rs3020221) and RA. The study was a case-control study that included 212 RA patients and 238 age-and gender-matched healthy volunteers. RA disease activity was assessed using the Disease Activity Score 28 index. Erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor, and antibody to cyclic citrullinated peptide were measured. ANGPT2 rs3020221 C > T SNP genotyping was done using real-time polymerase chain reaction (PCR). The TT genotype was more frequently represented in RA patients than in healthy controls (18.9% and 7.1%, respectively, p < 0.001) and increased the chance of developing RA four-fold, as compared to other genotypes (OR = 4.00, 95% CI = 2.09–7.63) (p < 0.001). The CT genotype was associated with elevated levels of the inflammatory markers ESR and CRP in RA patients (p = 0.012 and 0.037, respectively) as well as the DAS28 ESR Score (p < 0.001). The presence of the T allele either under the dominant model (for genotypes CT and TT) or the recessive model (for the genotype TT) predicts RA disease. Assessment of ANGPT2 gene polymorphism is useful to predict the patients with susceptibility to RA. The presence of T allele increased the risk of developing RA disease by two folds. [ABSTRACT FROM AUTHOR]