Background: Cardiovascular diseases (CVDs) are recognized as one of the leading causes of death worldwide. Studies have shown the impact of genetic predisposition and dietary factors on developing these diseases. Dietary patterns and genetic factors such as polymorphisms related to the level of adiponectin may also interact with each other and produce variances in the effects of these factors on different individuals. The purpose of this study is to investigate the interactions between food intake patterns and polymorphisms on ADIPOQ and ARL15 genes in relation to cardiometabolic risk factors. Methods: This cross‑, sectional study is conducted on 380 adults (20 to 70 years old) living in Yazd, Iran. Individuals were selected from the participants in Yazd Health Study (YaHS) and its sub‑, study called Taghziyeh Mardom‑, e Yazd (TAMYZ) after reviewing the inclusion and exclusion criteria. YaHS is a population‑, based cohort study which has been conducted on 9962 adults living in Yazd since 2014. In the present study, rotated principle component analysis (PCA) with Varimax rotation is used to identify the major dietary patterns. The polymerase chain reaction‑, restricted fragment length polymorphism (PCR‑, RFLP) method is used in order to identify rs1501299 and rs6450176 variants (on ADIPOQ and ARL15 genes, respectively). General linear models (GLM) as well as regression models are used to investigate the interactions between the studied genotypes and the extracted dietary patterns. Conclusions: The results of this study can help to personalize dietary recommendations for the prevention of CVDs according to the genetic predisposition of individuals.

Obesity is a multifactorial disorder that has increased dramatically in recent years in developing countries. The disproportion of energy uptake and expenditure, which is the result of several factors such as diet, behavior, environment, as well as metabolic and genetic factors, could eventually lead to this disease. Mutations in genes that regulate appetite and metabolism could affect various aspects of obesity. Adiponectin protein, the product of the ADIPOQ gene, is an essential adipokine for controlling energy homeostasis and fat storage and is secreted in white adipose tissues. It is an insulin-sensitive hormone whose blood concentration declines in obesity. In this study, we examined the association of rs2241766 +45 T>G polymorphism of the ADIPOQ gene with obesity and blood levels of High-Density Lipoprotein (HDL), Low-Density Lipoprotein (LDL), Triglyceride (TG), and total cholesterol in the population of Borujen City. In this case-control study, blood samples were collected from people referred to Tamin Ejtemaee Laboratory of Borujen who suffered from obesity problems. Triglyceride, total cholesterol, LDL, and HDL levels were analyzed in the patient's blood using the alpha6 auto-analyzer. In the next step, total DNA was extracted from the blood samples and subjected to Restriction Fragment Length Polymorphism (RFLP) methods to investigate the rs2241766 polymorphism of the ADIPOQ gene. According to the results of this study, there is no significant correlation between any alleles and genotypes of this polymorphism with obesity (Chi-square p-value was 0.82 and 0.85 respectively for alleles and genotypes, odds-ratio 1.155, 95% CI= 0.32-4.14). There is no significant correlation between the blood lipid characteristics of the patients and the genotypes of the studied polymorphism. According to our results, it seems that the alleles and genotypes of the ADIPOQ gene rs2241766 do not affect the etiology of obesity in our samples.

Background: Prostaglandin-endoperoxide synthase 2, recognized as cyclooxygenase 2 (COX-2), is an important enzyme contributing to the generation of proinflammatory prostaglandins. It can play a role in increased tumor angiogenesis, apoptosis inhibition, metastasis, and invasion of tumors. Single nucleotide polymorphisms (SNPs) of the COX-2 promoter may associate with the cancer predisposition. In the present work, we aimed to explore whether SNPs of COX-2 gene affect both the risk of development and grade of bladder cancer.Method: This case-control study was performed and the genetic polymorphisms of six COX-2 SNPs including, intron 1 (rs2745557), intron 5 (rs16825748), intron 6 (rs2066826), T+8473C (rs5275), G-765 (rs20417), and A-1195G (rs68946) were genotyped in 80 healthy controls and 80 bladder cancer patients using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). To select independent prognostic factors, the univariate and multivariate analyses were implemented.Results: Univariate logistic regression model indicated a significant association between COX-2 765G>C heterozygous GC genotype and greater risk of bladder cancer (OR: 2.07; 95% CI: 1.03 - 4.15; P = 0.04). However, the multivariate logistic regression analysis showed no associations between COX-2 variants and bladder cancer development.Conclusion: We concluded that COX-2 polymorphisms do not contribute to the genetic susceptibility to urothelial bladder cancer in an Iranian population. However, the only genotype in which the frequency of alleles significantly differed between the two groups of high-grade tumors and low-grade tumors was COX-2 8473T> C (rs5275). Moreover, our findings showed that both smoking and family history of cancer play a role in susceptibility to bladder cancer.

Milk protein genetic polymorphisms are associated with economically important traits in dairy cattle. The objective of this study is to genotype a single nucleotide polymorphism (SNP) responsible for the amino acid changes in the beta-lactoglobulin (β-Lg) variants A and B on 85 unrelated DNA representing Algerian cattle populations: Chelifienne (28), Cheurfa (31) and Guelmoise (26). The method used is the PCR-RFLP (Polymerase Chain Reaction-Restriction Fragment Length Polymorphism). Genetic polymorphism was detected by digestion of PCR products amplified of exon II of β-Lg gene by with the endonuclease HaeIII enzyme. The results revealed that the amplified product was observed as 247 bp. Restriction digestion with HaeIII revealed three genotypes: AA, AB and BB. The genotypic frequencies of AA, AB and BB genotypes were 0.08, 0.41, 0.50; 0.08, 0.41, 0.50 and 0.01, 0.19, 0.56 in Chelifienne, Cheurfa and Guelmoise and respectively. Frequency of AA genotype was absent in Guelmoise population. Frequencies of A and B alleles were 0.29 and 0.71 in both Chelifienne and Cheurfa and 0.25 and 0.75 Guelmoise population. These results further confirm that Bos torus cattle are predominantly of β-Lactoglobulin B type. The Chi-square test at p-value < 0.05 results revealed that the Chelifienne and Cheurfa populations were in Hardy-Weinberg equilibrium and the results are not significant for the Guelmoise. This genetic information could be useful to estimate the effect of polymorphism on different milk production of Algerian bovine populations.

Burkholderia mallei is the main cause of glanders as a dangerous contagious zoonosis disease that is mostly observed in single-hoofed animals, especially horses. Modern molecular techniques have been recently employed to improve epidemiology for identifying and searching for strains of this bacterium at different times and locations. Due to the unknown number of circulating strains and lack of preventive methods, glanders is still observed in the form of epidemics. The present study aimed to evaluate six field isolates plus two laboratory strains of Borkolderia mallei and Burkholderia pseudomallei using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. All the isolates and strains were microbially cultured in the glycerol nutrient and glycerol agar media. The individually grown colonies of the bacterium were used in the biochemical tests. The DNA of isolates was extracted by boiling, and the PCR-RFLP test was conducted on their genome. Finally, the bacterium was injected into guinea pigs to induce the Straus reaction. The biochemical assays (or bioassays) confirmed the isolates as Burkholderia mallei. The PCR-RFLP assay demonstrated a product for Burkholderia mallei with a length of 650 bp. Nevertheless, 250 and 400 bp were produced for Burkholderia pseudomallei. The swollen scrotum pointed to the occurrence of the Straus reaction. The PCR-RFLP is a proper differential diagnosis technique for B. mallei; moreover, it is a suitable method for differentiating between Burkholderia mallei and Burkholderia pseudomallei. This technique can detect Burkholderia mallei in a short time with high precision and sensitivity.

Background: The aim of this study was to investigate the association between thyroid cancer and 16C/A single nucleotide polymorphism (SNP) in C-C motif chemokine 22 (CCL22) as well as 1014C/T SNP in C-C chemokine receptor type 4 (CCR4).Method: In this case-control study, polymerase chain reaction restriction-fragment length polymorphism (PCR-RFLP) was performed for 113 thyroid cancer patients and 112 age-sex matched healthy controls to investigate the genotype distribution.Results: At position 16C/A in CCL22, 95 patients (84.3%) were found to have CC genotype, while 17 individuals (14.8%) inherited CA genotype and 1 (0.9%) had AA genotype. In the control group, 92 volunteers (82.1%) inherited CC genotype, 18 individuals (16.1%) had CA genotype, and 2 (1.8%) had AA genotype. The frequency of CC, CT, and TT genotypes of 1014C/T SNP in CCR4 gene was 60 (53.1%), 43 (38.1%), and 10 (8.8%) in the patients, and 57 (53.3%), 43 (40.2%), and 7 (6.5%) in the control group, respectively. There were no statistically significant differences between the patients and controls in terms of 16C/A polymorphism in CCL22 (P = 0.816) and 1014C/T SNP in CCR4 1014C/T gene position (P = 0.801). Nevertheless, the study of their association indicated that inheriting the CC genotype of CCR4 was significantly associated with higher stages (stages 3 and 4) in thyroid cancer.Conclusion: 1014C/T genetic variation in CCR4 and 16C/A polymorphism in CCL22 were not found to have a role in genetic susceptibility to thyroid cancer. Inheriting CC genotype at 1014 locus in CCR4 may; however, affect cancer progression in patients with thyroid cancer.

Background: Genetic polymorphisms are predictors of the immune response and susceptibility to certain infectious diseases, including pulmonary tuberculosis (TB). We evaluated the association of monocyte chemoattractant protein-1 (MCP1) (-2581 A/G) and interferon-gamma (IFNγ) (+874 T/A) polymorphisms with susceptibility to pulmonary TB in an Iranian population. Methods: A total of 124 patients with pulmonary tuberculosis and 244 healthy subjects (121 related normal controls and 123 unrelated subjects) were included. The MCP1 polymorphic region (-2518 A/G) was genotyped by PCR-RFLP, while ARMS-PCR was used to amplify and detect IFNγ (+874 T/A). SNPStats and SPSS v. 20 were used for the statistical analysis of the data. Results: The comparison of MCP1 (-2518 A/G) alleles and genotypes in TB patients and healthy subjects showed no significant association in all the constructed heredity models. No association was observed between TB patients and normal subjects in all the constructed inheritance models for IFNγ (+874 T/A) alleles and genotypes. Conclusion: Due to the lack of association between MCP1 (-2518 A/G) and IFNγ (874 T/A) polymorphisms and susceptibility to PT in our study and the conflicting results of some previous studies, further clinical and molecular research is needed to clarify the role of the studied polymorphisms in the pathogenesis of tuberculosis.