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Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), led to a pandemic in March 2020. During a viral infection, it has been reported that epigenetic changes occur for both sides: Infected cells elicit an antiviral environmental response, which induces and initiates certain pathways for proper response to the virus, while the virus silences the expression of vital genes in the anti-viral host cell. In this study, we aimed to examine the methylation level of the MX1 gene promoter in different stages in COVID-19 patients compared to the control group.In total, 470 COVID-19 patients with a positive polymerase chain reaction (PCR) test (235 women and 235 men) were recruited into the study as the test group. Patients were divided based on the World Health Organization (WHO) classification into three groups: moderate, severe, and critical. Moreover, 100 healthy individuals (50 women and 50 men) were selected as the control group. Peripheral white blood cells were collected and PCR was performed using two types of primers designed for methylated and unmethylated states of the MX1 gene. The PCR products were then loaded on agarose gel and the band intensities were calculated by ImageJ software.The results showed a decrease in the methylation of the MX1 gene promoter in moderate and severe groups and an increase in the MX1 gene promoter methylation in the critical group. In addition, the level of methylation was higher in men than in women.Increased methylation of the MX1 gene in the critical group may indicate the role of SARS-CoV-2 in reducing the expression levels of this antiviral gene and thus promoting virus replication and disease progression.

Graphical abstract, Introduction Hyper-inflammatory reactions play a crucial role in the pathogenesis of the severe forms of COVID-19. However, clarification of the molecular basis of the inflammatory-related factors needs more consideration. The aim was to evaluate the gene expression of two fundamental molecules contributing to the induction of inflammatory like CCR2 and DPP9 in cells from peripheral blood samples from patients with various patterns of COVID-19. Methods Peripheral blood samples were collected from 470 patients (235 male and 235 female) with RT-qPCR-confirmed COVID-19 test exhibiting moderate, severe, and critical symptoms based on WHO criteria. 100 healthy subjects (50 male and 50 female) were also enrolled in the study as a control group. The gene expression of DPP-9 and CCR-2 was assessed in the blood samples using real-time PCR method. Results The COVID-19 patients in severe stage expressed higher levels of CCR2 and DPP9 compared with healthy controls. In male and female patients, the levels of CCR2 and DDP9 expression significantly differed between moderate, severe, and critical patterns (p

Recruitment of leukocytes is one of the earliest events in the pathogenesis of ischemic heart disease (IHD) and chemokines play an important role in the migration of these cells into the inflammation sites. The aim of this study was to evaluate the CXCL10, CCL20 and CCL22 levels and the single nucleotide polymorphisms (SNPs) rs4508917, rs6749704 and rs4359426 in chemokine genes in patients with IHD to clarify any association. A total of 300 patients with IHD as having acute myocardial infarction (AMI; n=100), stable angina (SA; n=100) or unstable angina (UA; n=100) and 100 healthy subjects as a control group were enrolled to study. Serum samples from all participants were tested for the CXCL10, CCL20 and CCL22 levels by using ELISA. The SNPs were determined by polymerase chain reaction-restriction length polymorphism (PCR-RFLP) method. The mean serum concentrations of CXCL10, CCL20 and CCL22 in AMI patients (395.97±21.20Pg/mL, 108.38±10.31Pg/mL and 1852.58±205.77Pg/mL), SA patients (405.48±27.36Pg/mL, 90.20±7.69Pg/mL and 2322.04±231.23Pg/mL) and UA patients (396.69±22.79Pg/mL, 141.87±18.10Pg/mL and 2754.89±211.70Pg/mL) were significantly higher than in the healthy group (179.38±8.85Pg/mL, 51.92±4.62Pg/mL and 451.82±23.76Pg/mL, respectively; P

OBJECTIVE Much attention has recently been focused on the underlying role of circulating inflammatory biomarkers such as high-sensitivity C-reactive protein for predicting cardiovascular disease progression. We therefore set out to assess the relationship between the value of high-sensitivity C-reactive protein and (i) coronary artery disease severity, and (ii) left ventricular end diastolic pressure. DESIGN A cross-sectional study. SETTING The Shafa hospital in Kerman, Iran. PATIENTS A total of 107 consecutive patients referred for coronary angiography from January 2008 to January 2009 were prospectively studied. INTERVENTION AND MAIN OUTCOME MEASURES All patients underwent coronary angiography. They all had undergone left ventricular end diastolic pressure measurement, involving a 6-Fr pigtail catheter and a properly zeroed fluid-filled pressure transducer. For each patient, the level of high-sensitivity C-reactive protein was also determined using enzyme-linked immunosorbent assay kits. RESULTS The high-sensitivity C-reactive protein levels could strongly predict increased left ventricular end diastolic pressure (standardised beta=1.010; P=0.008), with other patient variables being confounders, but there was no significant association between these levels and Gensini scores. Multiple linear regression analysis showed that among the study parameters, systolic hypertension (standardised beta=1.611; P=0.047) and a family history of coronary artery disease (standardised beta=1.911; P=0.005) were the main predictors of high Gensini scores in study patients. CONCLUSION High-sensitivity C-reactive protein level is a clinical parameter that could predict left ventricular end diastolic pressure and left ventricular dysfunction, but was not associated with the severity of coronary artery disease.

Complete blood count (CBC) is one of the most common and conventional blood test that physicians usually request. However the results of this test are affected by different factors such as, the temperature and duration of incubation, therefore the aim of this survey was to evaluate the effect of temperature and time of incubation on CBC, red blood cells (RBC) indices and white blood cells (WBC) differential count.In a cross-sectional study, blood samples were taken from 30 healthy medical students of Rafsanjan University (15 males and 15 females). The samples divided into three parts; CBC were done on the samples up to 48 hours incubation at temperature of 25, 30, and 370 C at the time of sampling, and after 2, 8, 24 and 48 hours. Data were statistically analyzed and the following results were obtained.RBC count, hematocrit, MCH, percent of monocytes and eosinophils were constant in different temperatures, WBC count, MCHC, hemoglobin, platelets count, the percent of lymphocytes and neutrophils were constant up to 24 hours and then tend to increase with increasing temperature except lymphocytes percent that tend to decrease. MCV decreased with increasing temperature up to 8 hours and then significantly increased (from 83.89 to 87.50 fmol/l, p0.001). WBC, hematocrit, MCV, platelets count, and neutrophils' percent tend to increase by the time of incubation, but RBC count, MCHC, lymphocytes' percent decreased. Hemoglobin, MCH, and the percent of monocytes and eosinophils were constant.The finding of this survey showed that some of CBC parameters can be changed with the incubation, therefore it is better to do the CBC test after blood taking as soon as possible.