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Background: The association of changes in oxidative and proinflammatory states with vascular function after diet and exercise intervention among obese children has not been previously explored. Methods: In this 6-week diet and exercise intervention study in 35 obese children, age 12 to 18 years, we evaluated the relationship between changes in anthropometric indices, measures of insulin resistance, C-reactive protein (CRP), oxidized LDL (ox-LDL), and oxidative stress markers with changes in carotid intima-media thickness (C-IMT) and flow mediated dilation (FMD) of the brachial artery. Results: At the end of the study, body mass index (BMI), waist circumference, and percentage body fat were decreased (P <0.05), but participants remained overweight (BMI ≥ 95th percentile). Although FMD improved (P <0.05), the improvement in C-IMT did not reach statistical significance. The changes in BMI, waist circumference, fat mass, ox-LDL, malondialdehyde (MDA), CRP, insulin, and homeostasis model assessment for insulin resistance (HOMA-IR) had an inverse correlation with the changes in mean FMD after adjustment for age and sex, with the highest correlations documented for ox-LDL, CRP, and WC. The age- and sex-adjusted changes in ox-LDL, waist circumference, CRP, MDA, and body fat mass had the highest correlations with changes in C-IMT. Conclusions: Our findings suggest that a common inflammatory stress condition associated with childhood obesity, notably with abdominal fat deposition, may play a role in the development of the earliest stages of proatherosclerotic inflammatory processes and subsequent vascular dysfunction. These changes might be partially reversible by short-term diet and exercise intervention, even if patients do not reach ideal body weight.

BackgroundBreast cancer (BC) is considered to be one of the most important causes of death worldwide, and it affects the Iranian female population a decade earlier than female in other parts of the world. Human telomerase reverse transcriptase (hTERT) is a main subunit of the telomerase complex. MNS16A is located downstream of the hTERT gene and is recognized as the regulator of hTERT promoter activity. The aim of the present study was to access the possible impact of hTERT variants on BC risk in an Iranian population in southeast Iran.MethodsA total of 491 subjects including 266 BC patients and 225 healthy women participated in the study. Polymerase chain reaction (PCR) was used to genotype the MNS16A variable number of tandem repeats and 177 bp ins/del polymorphisms in the hTERT gene. PCR-RFLP and ARMS-PCR were used to genotype hTERT rs2736098 and 2735940, respectively. The association between genotypes and BC was assessed by computing the odds ratio (OR) and 95% confidence intervals (95% CI) from logistic regression analyses. A p-value of <0.05 was considered statistically significant.ResultsThe MNS16A genotype frequency distribution in BC patients was: LL, 43.2%; LS, 51.1%; and SS, 5.7%, and in controls: LL, 29.5%; LS, 68.3%; and SS, 2.2%. The LS genotype decreased the risk of BC compared with LL (OR = 0.51, 95% CI = 0.35-0.75, p < 0.001). The hTERT 177 bp ins/del polymorphism was not polymorphic in our population. All subjects had the ins/ins genotype. Our findings indicate that the MNS16A genotype and hTERT rs2736098 variant were associated with BC risk in the study. We also showed that the rs2736098 A/G polymorphism increased the risk of BC (OR = 1.80, 95% CI = 1.12-2.88, p = 0.017, AG vs AA; OR = 1.80, 95% CI = 1.06-3.06, p = 0.033, GG vs AA; OR = 1.87, 95% CI = 1.19-2.94, p = 0.006, AG + GG vs AA). No significant association was found between the rs2735940 C/T variant and BC.ConclusionOur findings indicate that the MNS16A genotype and the hTERT rs2736098 variant influence the risk of BC in an Iranian population in southeast Iran.

The association studies between miR-34b/c rs4938723 polymorphism and cancer risk showed conflicting results. This study aimed to assess the impact of rs4938723 polymorphism on prostate cancer risk. This case-control study was done on 151 prostate cancer (PCa) patients and 152 benign prostate hyperplasia to examine whether rs4938723 polymorphism in the promoter of pri-miR-34b/c was linked to the carcinogenesis of PCa in a sample of Iranian population. Genotyping of Pri-miR-34 b/c rs4938723 polymorphism was performed by using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. The results showed that rs4938723 variant significantly increased the risk of PCa in codominant (OR = 1.92, 95% CI = 1.15 - 3.18, p= 0.012, TC vs TT), dominant (OR = 1.99, 95% CI = 1.23 - 3.24, p= 0.005, TC + CC vs TT), and allelic (OR = 1.79, 95% CI = 1.20 - 2.68, p= 0.005, C vs T) inheritance model. Our findings propose that Pri-miR-34 b/c rs4938723 variant may be a risk factor for the development of PCa in a sample of Iranian population. Larger sample sizes with different ethnicities are required to validate our findings.

ABSTRACT. The protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene, which encodes an intracellular lymphoid-specific phosphatase, is considered an important regulator of T-cell activation. We investigated a possible association between the PTPN22 C1858T (R620W) polymorphism and pulmonary tuberculosis in an Iranian population. Single nucleotide polymorphisms of PTPN22 C1858T (rs2476601) were genotyped in 172 pulmonary tuberculosis cases and 204 normal subjects from Zaheden, Iran. Frequencies of genotypes CC, CT and TT of the PTPN22 C1858T polymorphism were 98.3, 1.7 and 0% in the pulmonary tuberculosis patients, and 96.1, 3.9 and 0% in the control group, respectively (P = 0.239). The frequency of the minor (T) allele was 0.8% in pulmonary tuberculosis patients and 2.0% in controls. Significant differences were not observed in genotype or allele frequencies of PTPN22 C1858T in the comparison between pulmonary tuberculosis patients and healthy subjects in our Iranian population sample.