Objective: To 1) assess IL-6 levels in the serum of patients with rheumatoid arthritis (RA). 2) study IL-6 promoter -174 G>C "single nucleotide polymorphism (SNP)" as an imminent factor for the disease development. 3) find any relation between the level of serum IL-6 cytokine and other parameters such as age, gender, clinical severity of diseases and "disease activity scores (DAS28)". Materials & methods:This research was carried out through a case -control approach at "Ibn -Senna Teaching Hospital" in Mosul city between November 2020 and July 2021. It included 61 RA patients diagnosed according to "ACR / EULAR 2010 criteria" and 50 healthy individuals. IL-6 serum levels were ascertained by ELISA and genotyping of IL-6 promoter was accomplished by "sequence-specific primerpolymerase chain reaction (SSP-PCR)". Results: Mean IL-6 level in RA (69.42 ng /l ± 62.99) was elevated in comparison to healthy people (14.66 ng /l ± 23.58), P < 0.001. No age or gender effects on IL-6 concentration were noted. The ideal cut-off of IL-6 for discrimination of RA with best discriminative utility compared to healthy controls was 22.80 ng/l. At this value the IL-6 sensitivity was 91.8%, specificity 82.0% and accuracy rate 73.80%. G/G genotype was the most pervasive genotype in both RA patients and controls (70.5% in RA and 64% in healthy controls). However, it did not seem to be a risk factor for RA development compared to G/C or C/C genotypes "(OR = 1.3438, 95% CI=0.605-2.984,P=0.469)". The mean IL-6 level in patients with GG genotype was (73.70 ng / l ± 71.09) compared to (58.37 ng /l ± 37.86) in patients with GC genotype. There was no significant difference in the IL-6 level between patients with GG and patients with GC genotypes (P = 0.2375). Although higher IL-6 mean concentration was reported in severe RA, however, no significant difference was found between patients with mild, moderate and severe RA respectively. No correlation of serum levels of IL-6 with genetic promoter polymorphism, clinical severity of diseases or DAS 28 score were reported. Conclusion:The concentration of serum IL-6 was elevated in RA in regard to healthy controls which confirmed its pivotal role in RA pathogenesis. Our data did not support the role of IL-6 promoter -174 G> C polymorphism as a risk factor for RA, nor seem to play a major role in the increase of IL-6 level among our patients with RA.
Most approaches to combat antibiotic resistant bacteria concentrate on discovering new antibiotics or modifying existing ones. However, one of the most promising alternatives is the use of bacteriophages. This study was focused on the isolation of bacteriophages that are specific to some of commonly human pathogens namely E. coli, Streptococcus pyogenes, Staphylococcus aureus, Proteus mirabilis, Pseudomonas aeruginosa, Salmonella spp. and Klebsiella pneumoniae. These bacteriophages were isolated from sewages that were collected from four different locations in Kirkuk City. Apart from S. pyogenes, bacteriophages specific to all tested bacteria were successfully isolated and tested for their effectiveness by spot test. The most effective bacteriophages that were isolated from sewages and sewage water of Al-Jumhori Hospital compared to other sites. It is concluded that the sewage water of hospitals represents a perfect environment for these bacteriophages.
The contribution of anti-inflammatory cytokines to rheumatoid arthritis (RA) is not fully comprehended. In the current research we assessed the serum concentration of interleukin (IL)-37 anti-inflammatory cytokine in RA, studied its association to disease activity score 28 (DAS28) and investigated single nucleotide polymorphism (rs2723176) of IL-37 gene as a threat for RA development. The case-control study included 60 RA patients and 30 normal control individuals. Serum IL-37 was assessed by ELISA and genotyped by “sequence-specific primer-polymerase chain reaction (SSP-PCR)”. The mean IL-37 was elevated in RA patients (69.42 ng /l ± 62.99) compared to control individuals (14.66 ng /l ± 23.58, p < 0.001). IL-37 tended to increase with age where highest levels were noted in patients more than 60 years (p = 0.037). No Gender influence was found on IL-37 level (p>0.05). At best cut-off value of 31.5 ng/ l, IL-37 had a sensitivity of 73.3% and specificity of 83.3%. No correlation of IL-37 with DAS 28 score was observed (r=0.1497, p=0.2535). For IL-37 (rs2723176) gene polymorphism, C/C genotype was prevailing in both RA (90%) and normal controls (93.3%) compared to A/C or A/A. Also, no variation was found between patents and controls in regard to C/C genotype (OR = 0.643, 95% CI (0.122-3.39, p=0.603). The mean IL-37 concentration in RA patients with C/C genotype (59.70± 67.92) was not different from AC genotype (80.54± 94.18, p=0.4748). We concluded that serum IL-37 had the implication as a diagnostic marker in RA. However, it did not correlate with clinical severity of the disease. Meanwhile, IL-37 (rs2723176) gene polymorphism did not seem to be as a risk factor for RA, nor contributed to the increase of IL-37 level among patients.
Background: Tumor necrosis factoralpha (TNF-α) has been proposed to play an important role in the etiopathology of congenital heart diseases (CHD) worldwide. However, no previous study about the role of TNF-α in the pathogenesis of CHDs in Mosul city / Iraq has been reported . Objectives: 1) To evaluate the serum levels of TNF-α cytokine in cyanotic and a cyanotic congenital heart diseases (CHDs and to compare the results with control healthy children in Mosul city 2) To find any association between the level of this pro-inflammatory marker and other demographic parameters such as age and gender 3) To test the diagnostic validity of this cytokine for the diagnosis of CHD at different cut-off values.
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