Background: Preeclampsia (PE) is a serious problem of pregnancy and its etiology is still unknown. The inheritance of preeclampsia is one of the theories regarding to the etiology of preeclampsia. Methylenetetrahydrofolatereductase (MTHFR) is a key enzyme in folate metabolism and the C677T polymorphism of the MTHFR gene is associated with decrease MTHFR activity, and therefore cause higher blood levels of homocysteine and leads to vascular disease that can be the reason of preeclampsia. The aim of this study was to evaluate the relationship between MTHFR gene C677T polymorphism with PE development in south-west of Iran.

Materials and Methods: This case-control study was performed in 129 preeclamptic pregnant women and 125 control individuals.The C677T polymorphism of the MTHFR gene was determined by PCR-RFLP method.

Results: The CC, CT and TT genotypes frequency of C677T polymorphism of MTHFR gene were 57.4, 38.8 and 3.9 percent in preeclamptic women and 53.6, 40 and 6.4 percent in control group. They were not significantly different (p=0.614). However, the frequency of TT genotype was higher in control group (p=0.36). There was not any significant difference in T allele distribution between preeclamptic women (23.3%) and control group (26.4%).

Conclusion: Our results showed that there was not any correlation between the C677T polymorphism and PE but the TT genotype of C677T polymorphism seems to be a protective factor for preeclampsia.

Background: Hypertrophic cardiomyopathy (HCM) is a various collection of heart diseases with autosomal dominant inheritance affecting 0.2% of the global population. HCM is also the most common cause of sudden cardiac death in individuals younger than 35 years old. Approximately, 40% of affected cases are associated with MYBPC3 gene. The aim of this study is to investigate the possible presence of mutation in 15 and 18 exons of MYBPC3 gene in patients with HCM in Chaharmahal Va Bakhtiyari province.

Materials and Methods: In this experimental study, 30 HCM patients were selected. DNA was extracted using standard phenol-chloroform method. Certain exons were amplified by PCR method. And then, SSCP and HA methods were run.

Results: Significant differences were observed between the positive control samples and other samples. However, there were no difference in studied exons or shift in the bands.

Conclusion: Mutations in the exons of MYBPC3 gene may cause the HCM disease, and change in other exons may be the causative agent in this geographical region and change in this studied exons may not have contributed to the HCM disease. However, it is necessary to study more patients for getting a better conclusion.