Association of Plasminogen Activator Inhibitor-1 Gene Polymorphism with Inflammatory Bowel Disease in Iranian Azeri Turkish Patients

Background/Aim:

Previous studies have shown the association of some genetic factors, such as Plasminogen activator inhibitor type-1 (PAI-1) 4G/5G polymorphism, with the development of inflammatory bowel disease (IBD). We aimed to study this polymorphism as a risk factor in IBD patients in this cohort.

Patients and Methods:

One hundred and fifteen IBD patients and 95 healthy controls were selected from Iranian Azeri Turks and -6754G/5G polymorphism of PAI-1 gene was tested by polymerase chain reaction using allele-specific primers confirmed by sequencing.

Results:

There was no significant difference of PAI-1 polymorphism between IBD patients and the control group (P > 0.05). Furthermore, these data showed no significant difference between Crohn''s disease and ulcerative colitis patients. However, 4G/4G homozygotes have reduced probability to progression of loss of appetite, whereas 5G/5G genotypes have increased risk for development of chronic diarrhea without blood, nausea, and loss of appetite.

Conclusions:

Although our study showed no significant association of PAI-1 polymorphism between patients and control group, the carriers of 4G/4G genotype and 4G allele had reduced risk for the progression of IBD features in this cohort.     

Increased Radioresistance to Lethal Doses of Gamma Rays in Mice and Rats after Exposure to Microwave Radiation Emitted by a GSM Mobile Phone Simulator

The aim of this study was to investigate the effect of pre-irradiation with microwaves on the induction of radioadaptive response. In the 1^st phase of the study, 110 male mice were divided into 8 groups. The animals in these groups were exposed/sham-exposed to microwave, low dose rate gamma or both for 5 days. On day six, the animals were exposed to a lethal dose (LD). In the 2^nd phase, 30 male rats were divided into 2 groups of 15 animals. The 1^st group received microwave exposure. The 2^nd group (controls) received the same LD but there was no treatment before the LD. On day 5, all animals were whole-body irradiated with the LD. Statistically significant differences between the survival rate of the mice only exposed to lethal dose of gamma radiation before irradiation with a lethal dose of gamma radiation with those of the animals pre-exposed to either microwave (p=0.02), low dose rate gamma (p=0.001) or both of these physical adapting doses (p=0.003) were observed. Likewise, a statistically significant difference between survival rates of the rats in control and test groups was observed. Altogether, these experiments showed that exposure to microwave radiation may induce a significant survival adaptive response.     

Integrated Cr and S poisoning of a La0.6Sr0.4Co0.2Fe0.8O3−δ (LSCF) cathode for solid oxide fuel cells

Strontium segregation in a La_0.6Sr_0.4Co_0.2Fe_0.8O_3−δ (LSCF) electrode reacts with Cr and S in a solid oxide fuel cell (SOFC), which can cause cell performance deterioration. Integrated Cr and S poisoning for LSCF cathodes of SOFC was studied at 800 °C of 200 mA cm⁻² (cathodic) for 20 h. After polarization in Cr and S at 800 °C for 20 h, polarization and ohmic resistances for LSCF were 2.4 Ω cm² and 3.4 Ω cm², which were larger than those for LSCF electrodes after Cr deposition only and S deposition only, respectively. The results illustrated that Cr and S deposition occurred on the surface of LSCF, which could form SrCrO₄ and SrSO₄. Compared to Cr deposition only and S deposition only, integrated Cr and S deposition was unsystematic, and the degradation phenomenon of Cr and S poisoning was more severe. The integrated Cr and S deposition of the LSCF electrodes was induced via interactions among CrO, SO₂ and segregated SrO from LSCF.

Strontium segregation in a La_0.6Sr_0.4Co_0.2Fe_0.8O_3−δ (LSCF) electrode reacts with Cr and S in a solid oxide fuel cell (SOFC), which can cause cell performance deterioration.     

Renin-angiotensin system polymorphisms and renal graft function in renal transplant recipients

OBJECTIVE: To analyze the role of 3 polymorphisms of the renin-angiotensin system (RAS) in renal transplant recipients (RTRs) and correlate them with graft function. METHODS: The present study was performed in the Drug Applied Research Center, Tabriz Medical University, Tabriz, Iran from September 2003 to December 2005 on 108 RTRs (66 males and 42 females, with a mean age of 37.34 +/- 4.97 years) with stable allograft function (creatinine < or =2.2 mg/dl). Following the DNA extraction from the blood leukocytes, the genotypes of the angiotensin converting enzyme (ACE I/D), angiotensinogen (ANG M235T), and angiotensin II type 1 receptor (ATR1 A1166C) were determined by polymerase chain reaction. The magnitude of clearance of creatinine (ClCr) in the setting of each of the above RAS polymorphisms was determined. The ClCr was measured by modification of diet in renal disease formula. Values were expressed as mean +/- SD; p< or =0.05 was considered to indicate statistical significance. RESULTS: There was no association of each genotype of the RAS alone with ClCr, serum urea, cyclosporine through level and the degree of urinary protein excretion rate. However, patients with the DD genotype of angiotensin converting enzyme + CC genotype of angiotensin II type I receptor polymorphisms had lower ClCr (p=0.05) and a higher urinary protein excretion rate (p=0.03). Other combination genotypes of RAS had no effect on allograft function. Interestingly, the percent of hypertensive patients in the C allele (70%) was more than the A allele (30%) of ATR1 polymorphism (p=0.04). CONCLUSION: Although none of the single gene polymorphisms of the RAS affected renal allograft function, combinations of these genotypes were associated with the outcome of allograft function.     

TNF-α gene polymorphisms in Iranian Azeri Turkish patients with Behcet’s Disease

Genetic factors that predispose individuals to Behcet’s disease (BD) are considered to play an important role in the development of the disease. The serum level of tumor necrosis factor (TNF) is elevated in patients with BD, and a dramatic response to anti-TNF-α antibody treatment further supports the role of TNF in BD. We investigated the distribution of TNF-α promoter −1031T/C and −308G/A polymorphisms in 53 BD patients of Iranian Azeri Turks and 79 matched healthy controls, via the PCR–RFLP technique. The frequency of the TNF-α −1031C allele was significantly higher in Behcet’s patients than in healthy controls (p < 0.0001, OR = 3.08; 95% CI = 1.73–5.47), whereas the frequency of the TNF-α −308A allele was similar in the two compared groups. The frequency of CG haplotype was significantly higher (p < 0.0001, OR = 3.42; 95% CI = 1.89–6.18), and that of the TA haplotype was significantly lower in BD patients than in healthy controls. These results suggest that TNF-α is a susceptibility gene for BD in patients from Iranian Azeri Turk ethnic group.