---

Background: Gestational diabetes mellitus (GDM) is defined as glucose intolerance with first dignosis during pregnancy. There is some evidence indicating that chemerin play a role in the development of GDM. In this study, for the first time, a possible association of rs17173608 polymorphism in the chemerin gene with the risk of GDM in Arak population was investigated.

Materials and Methods: In this case-control study, 120 GDM and 150 pregnant women with normal glucose tolerance were selected. GDM was confirmed by oral glucose tolerance according to the new IADPSG criteria. Genomic DNA was extracted from EDTA treated whole blood. The polymorphism of chemerin gene was determined using tetra-amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR).

Results: The genotype frequencies of  TT, GT and GG at rs17173608 were respectively 81.7%, 17.5% and 0.8% in the GDM group and 73.3%, 25.3% and 1.3% in the control group. There were no statistical differences in genotype frequencies between case group and the control group. Also, allele frequencies in the GDM group  (T 90.4% , G 9.6%), did not differ significantly from the control group ( T 96% ,G 14%). No association was found between genotype frequencies and FBS, 1h, 2 h and BMI.

Conclusion: The present study show that the rs17173608 polymorphism in the chemerin gene is not associated with the development of glucose intolerance and GDM in the studied population.

---

Background: A small percent of patients with colorectal cancer (CRC) respond to 5-Fluorouracil (5-FU), as a first line of chemotherapy. In this study in, in order to design a new chemotherapy protocol, the effect of 5-FU and acriflavine (ACF) cotreatment on mortality rate of CRC cell lines was investigated.

Materials and Methods: Cytotoxicity of 5-FU and ACF against CRC cell lines (LS174T, SW480 and HCT116) was detected using MTT assay. Cells were treated with different concentrations of 5-FU (0.5-64 µM) or ACF (0.07-5 µM) for 72 hours and then cell viability and drugs IC50 was calculated. To assess the effect of ACF on anticancer activity of 5-FU, cells were cotreated with different concentrations of 5-FU and IC30 concentration of ACF.

Results: ACF and 5-FU suppress the viability of CRC cell lines in dose-dependent manner. 5-FU and ACF have most cytotoxic effect on LS174T and the lowest cytotoxic effect on SW480 cells. Cotreatment of ACF with 5-FU could not significantly change the sensitivity of cells against 5-FU (p>0.05).

Conclusion: In this study, the fatal and cytotoxic effect of ACF on three CRC cell lines was shown. However, cotreatment of ACF with 5-FU could not improve the anticancer activity of 5-FU.

---

Abstract

Background: Human exposure to air pollution is associated with an increased risk of diseases such as heart failure, asthma and cancer. It has been suggested that oxidative stress is involved in air pollution-induced disorders. Recently, γ-glutamyltransferase (GGT) is known as a marker of oxidative stress. This study was aimed to evaluate the effect of exposure to outdoor air pollution on enzyme activity of GGT and also usage of GGT serum level as a marker for studying of harmful effects of air pollution in the resident with high air pollution level.

Materials and Methods: In this analytical cross-sectional study, 110 healthy adult men, never-smoking, who worked in an area with high air pollution and 90 men who worked in an area with low air pollution, as control group, were enrolled. All subjects were in the age range of 25-45 years with minimum work history of three years. The GGT activity in the serum samples was determined using a spectrophotometric method.

Results: Our results showed that the serum levels of GGT in the subjects in the areas with high air pollution (33.92 ± 1.61 U/L) did not differ significantly with those of control region (33.62 ± 1.74 U/L).

Conclusion: Overall, this study did not support the hypothesis that GGT enzyme could be considered as an oxidative stress marker following exposure to outdoor air pollution. Further studies with a larger sample sizes and also trials in other areas are required to confirm these results.

---

Coronavirus disease-19 (COVID-19) is a new member of the coronavirus family causing acute respiratory infection. Patients with COVID-19 have a higher risk of developing oxidative stress during this infection. Moreover, the virus induces ROS production that activates cellular pathways for viral replication. 
Nuclear factor erythroid 2-related factor (Nrf2) is a crucial transcription factor in cellular antioxidant defense by mediating Virus-induced oxidative stress and ROS production. This article suggests that an Nrf2 activator may be beneficial in preventing oxidative stress development in COVID-19 patients. Coronaviruses are a significant group of viruses that cause different illnesses in humans and animals. These illnesses can range from the common cold to more severe diseases such as SARS (Severe acute respiratory syndrome), Middle East Respiratory Syndrome (MERS), and COVID-19. COVID-19 is a new viral disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 
The main symptoms of COVID-19-infected patients are fever, dry cough, fatigue, and sometimes respiratory problems such as shortness of breath, sore throat, and infection [1]. 

---

Introduction: Oculocutaneous Albinism is a hereditary disease with an autosomal recessive pattern. The incidence of this disease is about 1 in every 17 thousand births. Most of the affected people in Iran are the result of consanguineous marriages. White hair, fair skin, and reduction of iris pigments are the main manifestations of this disease. Also, exposure to sunlight increases the susceptibility of these patients to skin cancer. This study aimed to investigate the genetic cause of a person with Oculocutaneous Albinism by whole exome sequencing.
Methods: A 6cc peripheral blood sample was obtained from a child with oculocutaneous Albinism with an autosomal recessive inheritance pattern. DNA extraction and whole exome sequencing were performed. After analyzing the exome sequencing data, the pathogenic mutation was identified. Then, the Sanger sequencing method was used to confirm and segregate.
Results: The affected case showed homozygous pathogenic mutation (NM_000372.5): c.286dupA p.(Met96AsnfsTer73) in exon 1 of the TYR gene. Oculocutaneous albinism IA was determined according to the mutated gene. Also, the parents of the affected person were heterozygous for the mutation.
Conclusions: The mutation causing oculocutaneous albinism was identified in the affected person using the high-efficiency whole exome sequencing method and then confirming the mutation through Sanger sequencing. Considering the parents' consanguineous marriage of the parents, this finding can be used for preventive measures in the future.