Background: Coronary artery disease (CAD) is a multifactorial disease that may be caused by the interaction between environmental and genetic risk factors. Glutathione S-transferases (GSTs) are known to participate in detoxification and metabolism of a wide range of xenobiotic compounds and oxidative stress products. Considering the interaction between environmental and genetic factors in CAD, we investigated the genetic polymorphisms of GSTM1, GSTT1, and GSTP1 in the Iranian population. Patients and Methods: Two hundred and forty-four CAD cases and 281 healthy controls were studied. The genotype of GSTM1, GSTT1, and GSTP1 genes was determined by multiplex polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) techniques. Multivariable logistic regression analysis was used to calculate the odds ratios (ORs) and 95% confidence intervals (CI). Multifactor dimensionality reduction (MDR) analysis was also carried out to analyze the gene-gene and gene-environment interaction.Results: The genotype and allele distribution of the three variations were not significantly different between CAD patients and controls (p > 0.05). The subgroup analysis revealed no significant gene-gene interactions or gene-gene combination effects linked to CAD susceptibility. However, MDR analysis selected the GSTM, GSTT pairwise and three genes combination models associated with the susceptibility to CAD. In addition, its result revealed that smoking in combination with GSTM1 (two-way) and GSTT, GSTP (three-way) genes might increase the risk of CAD. Furthermore, a significant interaction between GSTT1-null polymorphism and dyslipidemia was found in multivariable logistic regression analyses in the gene-environmental interactions on CAD risk. Conclusion: Our results suggest that the GSTM1, GSTT1 and GSTP1 genetic variations are not directly associated with the susceptibility to CAD in Iranian patients. Due to MDR results, there might be a non-linear association between interactions of two or three genes and smoking with CAD. There is also an association between CAD risk factors and GST variations, which requires supplementary confirmation with larger sample sizes.

Background:Asthenozoospermia is one of the etiologies for male factor infertility. It was shown that any abnormality in protamines genes, reduction of protamines transcript and protamines deficiency may play a key role in asthenozoospermia.Objective:The aim of the current study was the evaluation of protamine-1 and 2 genes (PRM1 and PRM2) polymorphisms in asthenozoospermic men.Materials and Methods: In this case-control study, the samples were corresponded to asthenozoospermic specimens of infertile men. The normozoospermic samples were considered as the control group. DNA sequence amplification was performed using four PRM1 and PRM2 primers, designed from 5' to 3' flank regions. The human PRM1 and PRM2 gene sequences were screened in search of potential mutations in highly prevalent polymorphism regions in asthenozoospermia versus normozoospermia.Results: Totally, nine highly prevalent polymorphism regions between the forward and reverse primers were screened. Three of them corresponded to PRM1 and six to PRM2. The most prevalent polymorphism regions in PRM1 were related to 102G>T (rs35576928), 49C>T (rs140477029) and 139C>A (rs737008). In the PRM2, 6 highly prevalent polymorphisms regions were screened, including 248C>T (rs779337774), 401G>A (rs545828790), 288C>T (rs115686767), 288G>C (rs201933708), 373C>A (rs2070923), and 298G>C (rs1646022). The allele frequencies of three upper mentioned single nucleotide polymorphisms in asthenozoospermic men including 373C>A, 298G>C and 139C>A was higher than the control group.Conclusion:Our findings indicated that the frequency of some altered genotypes in asthenozospermia was slightly higher than control group. We proposed more extensive studies to be sure that; these genotypes can precisely be related to diagnosis of asthenozoospermia, as the molecular markers.

Background and Objectives: Antimicrobial resistance (AMR) is an increasing threat for efficient treatment of infections. Determining the epidemiology of healthcare-associated infections and causative agents in various hospital wards helps appropriate selection of antimicrobial agents. Materials and Methods: This retrospective study was performed by analyzing antibiograms from March 2017 to March 2018 among patients admitted to the different wards of Imam Khomeini Hospital Complex in Tehran, Iran. Results: Among 2440 hospital acquired infections, 59.3% were Gram-negative bacilli: E. coli (n = 469, 22.2%), K. pneumoniae (n = 457, 21.7%), Acinetobacter spp. (n = 282, 13.4%), P. aeruginosa (n = 139, 6.6%) and important Gram-positive bacteria were Enterococcus spp. (n = 216, 10.2%), S. aureus (n = 148, 7%), S. epidermidis (n = 118, 5.6). Generally, there was a high antimicrobial resistance in bacterial isolates in this study. Methicillin resistant Staphylococcus aureus (MRSA) was 56.3 % and MRSE 62.9 %. Vancomycin resistant enterococci (VRE) was 60.7%. K. pneumoniae- ESBL was 79.6% and its resistance to carbapenem was 38.4%. E. coli-ESBL was 42% and its resistance to carbapenems was 2.3%. P. aeruginosa resistance to ceftazidime was 74.4%, to fluroquinolones 63.3%, to aminoglycosides 64.8%, to piperacillin tazobactam 47.6% and to carbapenems 62.1%. Acinetobacter baumannii resistance to ceftazidime was 98.7%, to fluroquinolones 97%, to aminoglycosides 95.9%, to ampicillin sulbactam 84%, to carbapenems 96.4% and to colistin 4%. Conclusion: The study revealed an alarming rate of resistance to the commonly used antimicrobial agents used in treating HAIs. Also the relationship between AMR and some risk factors and thus taking steps towards controlling them have been shown.