Autism is a neurodevelopmental disorder that is recognized by stereotypic and repetitive behaviors after 2 years of old. Dysregulation of the immune system, especially inflammation which is mostly regulated by IL-6, imposes a deficit in CNS development. Along with this crucial biomarker, researchers have proposed BCL-2, micro RNA-23a-3p (miR-23a-3p), miR-181b-5p as other probable biomarkers involved in inflammation and apoptosis. selleck chemical The aim of the study was to evaluate the alteration in the expression of these biomarkers in a group of autism spectrum disorder (ASD) children. Peripheral blood mononuclear cells (PBMCs) were obtained from 37 autistic patients. After RNA extraction with precipitation method, the Syber green qReal-time Polymerase Chain Reaction (PCR) was performed in order to evaluate the possible alteration in the expression of IL-6, BCL-2, miR-181b-5p, and miR-23a-3p. The results were compared with healthy controls. IL-6 was significantly upregulated in ASD patients (p=0.003). On the other hand, miR-23a was upregulated and BCL-2 downregulated in ASD patients but the changes were not significant. In initial evaluations, expression changes of miR-181b-5p were not statistically significant. However, when Patients were divided into two groups of upregulated and downregulated, re-evaluation showed that both up- (p=0.005) and down-regulation (p=0.004) (i.e. changes regardless of the direction) of miR-181b were significant in autistic children. IL-6 and miR-181b-5p can have proper diagnostic values and are reliable biomarkers with high sensitivity and specificity. On the other hand, PBMC can be utilized for such studies and also evaluation of patients’ condition instead of brain tissue as it is less accessible.Thyroid autoimmunity, being recognized by the presence of auto-antibodies against thyroid peroxidase (TPO) and thyroglobulin, has known to be associated with increased risk of recurrent spontaneous abortion (RSA), even in euthyroid subjects. There was no robust evidence regarding T cell deviations in anti-TPO positive RSA patients. The aim of this study was to investigate if the numbers of different CD4+T  subsets were different in women who experienced RSA and have an anti-TPO antibody from those without autoantibody and normal fertile women or not. In this study, peripheral blood samples were obtained from three groups of women (age 20-35 years) including RSA anti-TPO positive (n=17), RSA anti-TPO negative (n=27), and fertile (n=29) groups. The frequency of T helper (Th) 1, Th2, Th17, and regulatory T cells (Tregs) and also, the proportions of Th1/Th2 and Th17/Treg were measured by flow cytometry and compared between groups in different menstrual phases. The findings indicated elevated levels of Th1 in anti-TPO+ RSA in comparison with those without anti-TPO (p-value 0.004), exclusively in the luteal phase. Other T cell subsets were different only between RSA and control groups. Also, the Th1/Th2 and Th17/Treg ratios were increased in both RSA groups compared to fertile women. The only subset of CD4+ T cell different between RSA groups (i.e. with and without anti-TPO) was Th1 cells. Other CD4+ T cells’ deviations including Th2, Th17, and Treg cells could be related to the presence of abortion, regardless of the underlying thyroid autoimmunity state.Slow coronary flow (SCF) is a coronary artery disorder. Several inflammatory mediators have been reported to be associated with vascular homeostasis and endothelial dysfunction. The aim of this study was to investigate the association between cytokines and miRNAs in patients with SCF compared to the controls. In this regard, blood samples were acquired from 45 SCF patients and 45 age- and sex-matched healthy control subjects. Serum and peripheral blood mononuclear cells (PBMCs) were separated. Expression levels of miRNAs and cytokines in PBMCs were measured by real-time PCR. As a final point, serum levels of cytokines were quantified by ELISA. Expression levels of miR-1, miR-133, miR-208a, miR-206, miR-17, miR-29, miR-223, miR-326, and miR-155 as considerable indicators of inflammatory function significantly increased in SCF patients while the expression levels of miR-15a, miR-21, miR-25, miR-126, miR-17, miR-16 and miR-18a as considerable indicators of anti-inflammatory function significantly decreased in patients with SCF compared to the control group. Additionally, serum IL-1β, IL-8, and TNF-α concentrations were significantly higher in the SCF group than controls. However, no significant differences were observed in IL-10 production in SCF patients compared to the controls. This study provided the potential role of miRNAs as biomarkers for SCF diagnosis as well as suitable markers for monitoring coronary artery disease (CAD) development in these patients. More investigations are still necessary to unravel the detailed essential mechanisms of circulating miRNA levels in patients with heart failure and SCF.Cigarette smoking and opium use are risk factors for coronary artery disease (CAD). It has been known that scavenger receptors such as CD36 and CD68 play critical roles in the pathogenesis of CAD. CD9, as a member of the tetraspanin, has been shown to interact with scavenger receptors. The aim of this study was to investigate the effects of these risk factors on expression levels of CD9, CD36, and CD68 on the THP-1 cell line. The THP-1 cell line treated with cigarette smoke extract (CSE( and opium, both individually and combinatory, in 24 h incubation. The protein and mRNA levels of CD9, CD36, and CD68 were evaluated by flow cytometry and quantitative reverse transcription-Polymerase Chain Reaction (qRT-PCR) techniques, respectively. CD36 and CD68 mRNA and protein expression levels were significantly increased in the cells treated with cigarette smoke extract compared to the control (p less then 0.001 in mRNA expression levels and p=0.016 and p=0.012 in protein expression levels, respectively). The CSE increased the level of CD9 protein expression compared to the control group (p=0.041) on the human macrophage cell line THP-1. No significant differences were observed in the CD9, CD36, and CD68 gene expression and at the protein levels between opium-treated THP-1 cells and controls. In conclusion, cigarettes by increasing the levels of CD36, CD68, and CD9 can be a risk factor in the development of many inflammatory diseases, including cardiovascular diseases, chronic obstructive pulmonary disease (COPD) and lung carcinoma.