Association of tumor necrosis factor-alpha gene promoter polymorphism and its mRNA expression level in coronary artery disease

Background: umor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine that may play an important role in inflammatory diseases like coronary artery disease (CAD). As a result of controversy on the impact of polymorphisms in the promoter region of TNF-α gene on transcription, this case control study was designed to evaluate the effects of TNF-α -308G > A (rs1800629) and TNF-α − 238G > A (rs361525) on mRNA expression level and risk of CAD. Methods: Overall, 379 patients with CAD and 461 healthy controls participated in this study. Subjects were matched in terms of age, sex and ethnic origin. Genotyping was performed using single specific primer-polymerase chain reaction (SSP-PCR) and TNF-α mRNA expression analysis was carried out by quantitative real time PCR. Results: A/A and A/G genotypes in TNF-α (−308G > A) gene were significantly more frequent among patients than controls. The TNF-α (−238G > A) did not differ between CAD patients and controls (the TNF-α (−238G > A) genotypes and allele frequency showed no significant differences). Combination of AA TNF-α (−308) /GG TNF-α (−238) and AG TNF-α (−308) /AG TNF-α (−238) genotypes demonstrated higher frequencies in patients than in controls (P A polymorphism with TNF-α expression level and pathogenesis of CAD in the studied population, The TNF-α (−308G > A) gene polymorphism was associated with its expression and development of CAD. © 201

Association study of G+2044A (R130Q) polymorphism in IL-13 gene with risk of developing Multiple Sclerosis in Iranian population

Background: Multiple Sclerosis (MS) is an autoimmune and progressive neurodegeneration disease of the central nervous system (CNS) that diagnosed by inflammation and demyelination of neurons. MS is a multifactorial disease that occurs due to interactions between environment and genetic factors. IL-13 is a cytokine and one of the candidate genes for MS that its expression reduces in MS patients. Material and methods: In this study, 174 unrelated MS patients and 283 healthy individuals were examined. We assessed G+2044A (R130Q) polymorphism in exon 4, a single nucleotide polymorphism (SNP), in the coding region of the IL-13 gene. Genotyping of G+2044A polymorphism was performed using sequence-specific primer-polymerase chain reaction (SSP-PCR). Results: No significant association was found between Genotypes and allele frequency in patients and healthy individuals (P > 0.05). Comparison of the frequency of MS cases and healthy individuals based on ethnicity, a significant association was observed between Turkmen patients and MS with a protective role P < 0.05, OR = 0.01, CI (0.004�0.04) Moreover no significant association was seen between the inheritance models for the G+2044A SNP, but there is a significant association between gender and susceptibility to MS (P = 0.01). Conclusion: According to our results, there is no significant difference in Genotype and allele frequency of G+2044A polymorphism among MS patients and healthy individuals. But a significant association was observed between Turkmen patients and MS with a protective role. © 201

Frequency-dependent electrophysiological properties of concealed slow pathway of isolated rabbit atrioventricular node preparation after fast pathway ablation in a functional model

Introduction: Intranodal pathways of atrioventricular (AV) node play a vital role in the delay of conduction time in response to various atrial inputs. The present study was aimed to determine the frequency-dependent electrophysiological properties of concealed slow pathway according to a functional model of isolated rabbit atrioventricular node preparation after fast pathway ablation. Methods: Experiments were carried out in rabbit isolated heart AV-nodal preparations (N=8) by superfused/perfused mode. Extracellular recording was carried out from transitional cells of posterior and anterior extension of AV-node and upper part of atrium and its bundle. Unipolar silver electrode (100 μm) and direct voltage (100-110 V) was applied to create AV-nodal fast pathway ablation. Results: Minimum conduction time (AHmin) was significantly increased after fast pathway ablation (p<0.05). Fast pathway ablation had no significant impact on fatigue phenomenon but significantly reduced facilitation value (p<0.05). Rate-dependency properties of concealed slow pathway were explained according to functional nodal model. Conclusion: The mathematical functional model accurately simulated frequency-dependent electrophysiological properties of concealed slow pathway after fast pathway ablation, but some modifications are necessary for accurate prediction of nodal behavior in various cycle lengths and in arrhythmia. Concealed slow pathway may be considered as a potential electrophysiological substrate of fatigue and facilitation phenomenon