Comparing the effectiveness of behavioral activation in group vs. self-help format for reducing depression, repetitive thoughts, and enhancing performance of patients with major depressive disorder: a randomized clinical trial.

BACKGROUND: Behavioral activation has gained increasing attention as an effective treatment for depression. However, the effectiveness of Behavioral Activation Group Therapy (BAGT) in controlled conditions compared to its self-help programs requires more investigation. The present study aimed to compare their effectiveness on depressive symptoms, repetitive negative thinking (RNT), and performance in patients with major depressive disorder (MDD). METHODS: In this randomized clinical trial, 40 patients diagnosed with Major Depressive Disorder (MDD) were recruited based on a structured clinical interview for DSM-5 (SCID-5). Participants were allocated to BAGT (n = 20) and self-help behavioral activation (SBA; n = 20) groups. BAGT received ten weekly sessions (90 min), while the SBA group followed the same protocol as the self-help intervention. Participants were evaluated at pre-treatment, post-treatment, and the 2-month follow-up using the Beck Depression Inventory-II (BDI-II), repetitive thinking questionnaire (RTQ-31), and work and social adjustment scale (WSAS). RESULTS: The results of a Mixed ANOVA analysis revealed that participants who underwent BAGT showed significant improvement in depression, rumination, work, and social functioning post-treatment and at the 2-month follow-up. However, the SBA group did not show significant changes in any outcome. The study also found that, based on clinical significance, 68% of the BAGT participants were responsive to treatment, and 31% achieved a high final performance status at the 2-month follow-up. DISCUSSION: BAGT was more effective than SBA in MDD patients. Participants' engagement with self-help treatment is discussed. TRIAL REGISTRATION: The present trial has been registered in the Iranian Registry of Clinical Trials Center (IRCT ID: IRCT20181128041782N1|| http://www.irct.ir/ ) (Registration Date: 04/03/2019).

Suppressor of Cytokine Signaling Proteins 3 and 5 Potentially Delineate Polarization of Th cells in Chronic Rhinosinusitis.

Background: Chronic rhinosinusitis (CRS) is an inflammatory condition classified into chronic rhinosinusitis with nasal polyps (CRSwNP) and chronic rhinosinusitis without nasal polyps (CRSsNP). Th cells manage inflammatory cells in CRS. Suppressor of Cytokine Signaling (SOCS) proteins regulate Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway in Th cells by polarizing toward Th1, Th2, and Th17 cells. This study evaluated the levels of SOCS1,3,5 in CRS patients to find associations with Th cells. Methods: In this cross-sectional study, 20 CRSwNP patients, 12 CRSsNP patients, and 12 controls participated. The infiltration of CD4+ T cells was determined using immunohistochemistry. The expression of specific transcription factors and SOCS proteins was assessed using real-time PCR. Cytokine levels were evaluated using ELISA. SOCS protein levels were investigated using western blot analysis. Results: The expression of SOCS3 increased in the CRSwNP group compared to CRSsNP and control groups (p <0.001). SOCS3 protein levels increased in the CRSwNP group compared to CRSsNP (p <0.05) and control (p <0.001) groups. Although there was a significant difference in SOCS5 expression between CRSsNP and control groups, SOCS5 protein levels were significantly different between CRSsNP and control (p <0.001) and CRSwNP (p <0.05) groups. Conclusions: Targeted therapies may be suggested for CRS by modulating SOCS3 and SOCS5 proteins that are responsible for polarization of Th cells toward Th2 or Th1 cells, respectively. JAK-STAT pathway targeting, which encompasses numerous cells, can be limited to SOCS proteins to more effectively orchestrate Th cell differentiation.

The role of noncoding RNAs in metabolic reprogramming of cancer cells.

Metabolic reprogramming is a well-known feature of cancer that allows malignant cells to alter metabolic reactions and nutrient uptake, thereby promoting tumor growth and spread. It has been discovered that noncoding RNAs (ncRNAs), including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA), have a role in a variety of biological functions, control physiologic and developmental processes, and even influence disease. They have been recognized in numerous cancer types as tumor suppressors and oncogenic agents. The role of ncRNAs in the metabolic reprogramming of cancer cells has recently been noticed. We examine this subject, with an emphasis on the metabolism of glucose, lipids, and amino acids, and highlight the therapeutic use of targeting ncRNAs in cancer treatment.

The Serum Levels of IL-36 in Patients with Coronary Artery Disease and Their Correlation with the Serum Levels of IL-32, IL-6, TNF-α, and Oxidative Stress.

INTRODUCTION: Atherosclerosis is a chronic inflammatory process maintained during all stages of the disease by several proinflammatory mediators, such as cytokines and chemokines. Interleukin (IL)-36 cytokines are proinflammatory and have an essential role in innate and adaptive immunity, but the role of IL-36 has not been determined in coronary artery disease (CAD). This study aimed to measure the serum levels of IL-36 in patients with CAD and their association with the serum levels of tumor necrosis factor (TNF)-α, IL-6, and IL-32 and also investigate their correlation with the serum levels of malondialdehyde (MDA) and ferric reducing antioxidant power (FRAP). METHODS: A total of 168 subjects (84 CAD and 84 control subjects) were examined in this research. The total serum levels of IL-36 were measured using the enzyme-linked immunosorbent assay (ELISA). Also, some oxidative stress parameters were evaluated by FRAP and MDA assays in the serum. RESULTS: The serum levels of IL-36 and MDA were significantly higher, and FRAP was significantly lower in the CAD group compared to the controls. Furthermore, the serum levels of IL-36, MDA, and FRAP significantly correlated with the CAD group's cardiac arterial stenosis. Also, the serum levels of IL-36 had a positive and significant correlation with the serum levels of TNF-α, IL-6, IL-32, and biochemical parameters in the CAD group. CONCLUSION: Higher serum levels of IL-36 and its association with the serum levels of TNF-α, IL-32, and IL-6 may play a key role in the pathogenesis of CAD, leading to an increased risk of clogged arteries and oxidative stress.

In Vitro Study: Synthesis and Evaluation of Fe3O4/CQD Magnetic/Fluorescent Nanocomposites for Targeted Drug Delivery, MRI, and Cancer Cell Labeling Applications.

In the present study, first, Fe3O4 nanoparticles were functionalized using glutaric acid and then composited with CQDs. Doxorubicin (DOX) drug was loaded to evaluate the performance of the nanocomposite for targeted drug delivery applications. The XRD pattern confirmed the presence of characteristic peaks of CQDs and Fe3O4. In the FTIR spectrum, the presence of carboxyl functional groups on Fe3O4/CQDs was observed; DOX (positive charge) is loaded onto Fe3O4/CQDs (negative charge) by electrostatic absorption. FESEM and AFM images showed that the particle sizes of Fe3O4 and CQDs were 23-75 and 1-3 nm, respectively. The hysteresis curves showed superparamagnetic properties for Fe3O4 and Fe3O4/CQDs (57.3 and 8.4 emu/g). The Fe3O4 hysteresis curve showed superparamagnetic properties (Ms and Mr: 57.3 emu/g and 1.46 emu/g. The loading efficiency and capacity for Fe3O4/CQDs were 93.90% and 37.2 mg DOX/g MNP, respectively. DOX release from Fe3O4/CQDs in PBS showed pH-dependent release behavior where after 70 h at pH 5 and 7.4, about 50 and 21% of DOX were released. Fluorescence images of Fe3O4/CQD-treated cells showed that Fe3O4/CQDs are capable of labeling MCF-7 and HFF cells. Also, T2-weighted MRI scans of Fe3O4/CQDs in water exhibited high r2 relaxivity (86.56 mM-1 S-1). MTT assay showed that DOX-loaded Fe3O4/CQDs are highly biocompatible in contact with HFF cells (viability = 95%), but they kill MCF-7 cancer cells (viability = 45%). Therefore, the synthesized nanocomposite can be used in MRI, targeted drug delivery, and cell labeling.

Expression levels of miR-27a, miR-329, ABCA1, and ABCG1 genes in peripheral blood mononuclear cells and their correlation with serum levels of oxidative stress and hs-CRP in the patients with coronary artery disease.

Atherosclerosis is a chronic inflammatory disease with high mortality worldwide. The reverse cholesterol transport pathway in macrophage plays an important role in the pathogenesis of coronary artery disease (CAD) and is strongly controlled by regulatory factors. The microRNAs can promote or prevent the formation of atherosclerotic lesions by post-transcriptional regulation of vital genes in this pathway. Therefore, this study was conducted to investigate the relationship between the expression levels of miR-27a, miR-329, ABCA1, and ABCG1 genes and serum levels of hs-CRP, ox-LDL, and indices of oxidative stress in the patients with established CAD and controls. A total of 84 subjects (42 patients with CAD and 42 controls) were included in this study. Expression levels of miR-27a-3p, miR-329-3p, ABCA1, and ABCG1 genes in the peripheral blood mononuclear cells (PBMCs) and serum concentration of hs-CRP and ox-LDL were measured by real time-PCR and ELISA, respectively. Also, oxidative stress parameters in the serum were evaluated by ferric-reducing antioxidant power (FRAP) and malondialdehyde (MDA) assays. ABCA1 and ABCG1 gene expression in PBMC and serum concentration of FRAP were significantly lower in the CAD group compared to the control group. Expression levels of miR-27a and miR-329 and serum levels of hs-CRP, ox-LDL, and MDA were significantly higher in the CAD group compared to the control group. Serum levels of hs-CRP, ox-LDL, and expression level of miR-27a have inversely related to ABCA1 and ABCG1 gene expression in all the subjects. An increase in the expression levels of miR-27a and miR-329 may lead to the progression of atherosclerosis plaque by downregulating the expression of ABCA1 and ABCG1 genes.

The impacts of C1q/TNF-related protein-15 and adiponectin on Interleukin-6 and tumor necrosis factor-α in primary macrophages of patients with coronary artery diseases.

Atherosclerosis is a progressive inflammatory disease characterized by the accumulation of lipids in the arterial wall. Inflammation plays a key role in the pathogenesis of atherosclerosis and some previous studies have shown the role of adipokines during the inflammatory process of atherosclerosis. Therefore, the present study aimed to evaluate the impacts of adiponectin and CTRP15 on inflammatory cytokines secretions from THP1 and primary macrophages. METHODS: THP1 monocytes were differentiated to macrophages and primary monocytes were then isolated from patients with coronary artery disease and controls who were differentiated to macrophages. Macrophages were treated with LPS, LPS+adiponectin, and LPS+CTRP15. RESULTS: Adiponectin and CTRP15 have reduced IL-6 and TNF-α secretions from LPS-induced THP1 macrophages, and the CTRP15 indicated a more potent anti-inflammatory property compared to adiponectin. In addition, adiponectin reduced cytokines' expressions and secretions in primary macrophages of both patient and control groups. However, CTRP15 has only reduced cytokines' expressions and secretions in controls and it was not able to ameliorate inflammation in macrophages of CAD patients. CONCLUSION: The results of the present study indicate anti-inflammatory impact of adiponectin and CTRP15, while this property was stronger for CTRP15. In addition, it seems likely that anti-inflammatory CTRP15's impact on macrophages in the CAD patients was weaker than macrophages from the controls.

Klotho, FOXO1 and cytokines associations in patients with coronary artery disease.

INTRODUCTION: Atherosclerosis is one of the main reasons for adult mortality in advanced populations and countries with high stress levels. Klotho family are single-pass trans-membrane proteins that involve in the genesis and progression of various diseases, including acardiovascular disease, apoptosis and stress oxidative imbalance. Present study, investigates the pattern of changes in Klotho and FOXO1 gene expressions and levels in atherosclerosis. METHODS: Present case control study consisted of 79 patients with atherosclerosis and 78 healthy controls. PBMC (peripheral mono-nuclear blood cells) expression levels of Klotho and FOXO1 were assayed, using qPCR method. Serum concentration of Klotho and FOXO1 were measured by ELISA method. RESULTS: A significant reduction was found in PBMC genes expression levels of Klotho (P < 0.01) of patients as comparison with controls. PBMC Gene expression of FOXO1 in patients was increased significantly (P < 0.01) when compared with controls. Pearson analysis showed a positive correlation between PBMC Klotho gene expression and Klotho levels of patients (P < 0.01). The correlation between serum concentrations of Klotho and FOXO1 of patients was also positive significantly (P < 0.01). AUC of ROC for gene expression and serum concentration of Klotho in patients were 0.701 and 0.737 respectively. CONCLUSION: Investigating the PBMC gene expression and serum concentration of Klotho in patients with atherosclerosis is suggested could be a convenient novel biomarker for predicting, prognosis, monitoring the disease progression and designing a suitable drug for patients with atherosclerosis.

Serum levels of IL-32 in patients with coronary artery disease and its relationship with the serum levels of IL-6 and TNF-α.

The coronary artery disease (CAD) is a chronic inflammatory disease caused by atherosclerosis, in which arteries become clogged due to plaque formation, fat accumulation, and various sorts of immune cells. IL-32 is a proinflammatory cytokine, which enhances inflammation through inducing the secretion of different inflammatory cytokines. The main objective of the current study was to assess the serum levels of IL-32 in subjects with obstructive CAD and its relationship with the serum levels of IL-6 and TNF-α. This study was performed on 42 subjects with obstructive CAD and 42 subjects with non-obstructive CAD. The serum levels of TNF-α, IL-6, and IL-32 were measured using the enzyme-linked immunosorbent assay (ELISA). The serum levels of TNF-α, IL-6, and IL-32 were 3.2, 3.48, and 2.7 times higher in obstructive CAD compared to non-obstructive CAD, respectively. Moreover, the serum levels of TNF-α and IL-32 in obstructive CAD with cardiac arterial stenosis in one major vessel were significantly higher than the levels in obstructive CAD with cardiac arterial stenosis in more than one major vessel. ROC curve analysis revealed that the serum levels of TNF-α, IL-6, and IL-32 were good predictors of obstructive CAD. Moreover, multiple logistic regression analyses suggested that the serum levels of TNF-α, IL-6, IL-32, LDL, and ox-LDL were independently related to the presence of obstructive CAD, while serum levels of HDL were not. TNF-α, IL-32, and IL-6 showed an increase in obstructive CAD, and the serum levels of these cytokines showed a satisfactory ability for predicting obstructive CAD.

Increased the circulating levels of malondialdehyde in patients with obstructive sleep apnea: a systematic review and meta-analysis.

PURPOSE: Obstructive sleep apnea (OSA) is a prevalent sleep disorder associated with increased risk of cardiovascular disease. Several studies have demonstrated elevated oxidative stress in patients with OSA. This oxidative stress is a direct inducer of lipid peroxidation. Malondialdehyde (MDA), a robust marker of lipid peroxidation, has been evaluated in patients with OSA but results have been inconsistent. The present systematic review and meta-analysis was performed to quantify the circulating levels of MDA in patients with OSA compared to controls. METHODS: Search was performed in data bases of PubMed, Scopus, EMBASE, Web of Science, and Cochrane library, to find out those studies that measured MDA in patients with OSA compared to controls. RESULTS: The search produced 563 records and after removing duplicates, 383 records remained. Screening by title and abstract and the evaluation of the full text resulted in the selection of 14 articles, which were included in the meta-analysis. Pooled analysis demonstrated higher levels of MDA in the patients compared to the controls (SMD (95% CI): 1.18 (0.68, 1.68), p < 0.0001). CONCLUSION: The results of this meta-analysis demonstrated considerable elevation of MDA in patients with OSA compared to controls. The meta-analysis also indicated a positive association of MDA levels with the degree of severity of OSA. These results suggest a state of increased lipid peroxidation in patients with OSA.

Interleukin-22 and intestinal homeostasis: Protective or destructive?

Interleukin (IL)-22 is a member of IL-10 family cytokines with various immunologic functions. As its name implies, IL-22 is known to be secreted mainly by Th22 cells, a recently discovered lineage of CD4+ T cells. Also, Th17, Th1, natural killer cells, γδT cells, and innate immune cells along with some nonlymphoid cells have been confirmed as secondary cellular sources of IL-22. Different cell types such as bronchial and intestinal epithelial cells, keratinocytes, hepatocytes, dermal fibroblasts, and tubular epithelial cells are affected by IL-22. Both pathologic and protective roles have been attributed to IL-22 in maintaining gut homeostasis and inflammation. According to the latest fast-growing investigations, IL-22 is significantly involved in various pathologies including allergic diseases, infection, autoimmunity, and cancer development. Regulating gut immune responses, barrier integrity, and inflammation is dependent on a diverse complex of cytokines and mediators which are secreted by mucosal immune cells. Several investigations have been designed to recognize the role of IL-22 in gastrointestinal immunity. This article tries to discuss the latest knowledge on this issue and clarify the potential of IL-22 to be used in the future therapeutic approaches of intestinal disorders including inflammatory bowel diseases and colon cancer.

Serum levels of C1q/TNF-related protein-3 in inflammatory bowel disease patients and its inverse association with inflammatory cytokines and insulin resistance.

Ulcerative colitis (UC) and Crohn's disease (CD) are two major forms of inflammatory bowel disease (IBD), which is an inflammatory disease. Studies have shown that adipose tissue and inflammation play important roles in the pathogenesis of IBD. C1q/TNF-related protein-3 (CTRP3) is a newly discovered adipokine playing a substantial role during inflammatory process, and for the first time in the present study, serum levels of this adipokine were measured in the UC and CD patients. This case-control study included 70 control, 50 UC, and 50 CD patients who were diagnosed by standard criteria. Serum levels of adiponectin, IL-6, TNF-α, TGF-ß, and CTRP3 were evaluated using ELISA kits. Serum levels of IL-6, TNF-α, and TGF-ß elevated in the UC and CD patients compared with the controls while adiponectin and CTRP3 diminished in the patient's groups compared with the control. Furthermore, decrease in CTRP3 serum levels was associated with the risk of UC and CD diseases. Moreover, CTRP3 indicated negative correlation with BMI, FBS, insulin, homeostasis model assessment of insulin resistance, IL-6, TNF-α, and TGF-ß and also a positive correlation with adiponectin in both the UC and CD patients. For the first time, the present study demonstrated lower levels of CTRP3 in the UC and CD patients. Decreased serum levels of CTRP3 and its inverse relationship with inflammatory cytokines and TGF-ß levels suggested a possible role for CTRP3 in the pathogenesis of UC and CD diseases.

Serum levels of IL-32 in patients with type 2 diabetes mellitus and its relationship with TNF-α and IL-6.

Type 2 diabetes mellitus (T2DM) is an important public health worldwide. The main underlying mechanism of T2DM is insulin resistance which is associated with chronic inflammation. Interleukin-32 (IL-32) is a pro-inflammatory cytokine which has been implicated in pro-inflammatory responses of several human diseases. Previous studies have reported higher levels of IL-32 in inflammatory disease and obesity. The present study aimed to evaluate the serum concentrations of IL-32 in patients with T2DM and its association with cardio-metabolic parameters. This study was undertaken on 93 patients with TDM and 74 healthy controls. T2DM was diagnosed based on ADA criteria. Serum levels of IL-32, adiponectin, TNF-α, and IL-6 were measured by ELISA technique. Our findings revealed independent elevated levels of IL-32 in T2DM group (1061 (841.9-1601) pg/mL) compared to the control (630.4 (331.1-830.9) pg/mL). Furthermore, it was associated with increased risk of T2DM incidence. IL-32 indicated a positive correlation with body mass index, fasting blood glucose, TNF-α, and IL-6 in patients with T2DM. Furthermore, linear regression showed independent association between IL-32 and IL-6 plus TNF-α in patients' group. The results of the present study revealed higher levels of IL-32 in T2DM patients which have been associated with inflammatory markers. These results suggest the possible role of IL-32 in chronic inflammation in patients with T2DM.

Circulating levels of oxidized low-density lipoprotein in patients with obstructive sleep apnea: a systematic review and meta-analysis.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with an increased risk of developing atherosclerotic cardiovascular disease (ASCVD). Patients with OSA have increased levels of oxidative stress and several studies have shown higher levels of oxidative stress markers. Oxidized-LDL (Ox-LDL) is an important risk factor for ASCVD and a number of studies have measured its levels in patients with OSA, though results from these studies are conflicting. This meta-analysis aimed to reassess circulating levels of Ox-LDL in patients with OSA in comparison with controls. METHODS: Studies evaluating Ox-LDL levels in patients with OSA and controls were explored in databases of PubMed, EMBASE, Scopus, and Web of Science. Two authors independently performed the search from January 1990 to February 2019. Two authors independently screened the studies according to title, abstract, and full text. In addition, the Newcastle-Ottawa Quality Assessment Scale was utilized to evaluate the quality of the studies. The impact of OSA on Ox-LDL levels was determined using the random effects model. RESULTS: Of 195 articles retrieved, 98 were duplicates, 49 were excluded by title, 20 excluded by abstract, and 22 by full texts. Six eligible studies were included in the meta-analysis. Pooled analysis demonstrated that Ox-LDL increased in patients with OSA compared with controls. In addition, subgroup analysis revealed that studies matching age or BMI between OSA patients and controls showed no significant difference between patients with OSA and healthy controls, while unmatched studies had higher levels of Ox-LDL in patients with OSA in comparison with controls. CONCLUSION: This study demonstrated higher circulating concentrations of Ox-LDL in patients with OSA. However, no significant difference was found in studies in which patients and controls were matched for age and BMI, suggesting the involvement of these two confounding factors as a cause for elevated concentrations of circulating Ox-LDL in patients with OSA.

Update of spectrum c.35delG and c.-23+1G>A mutations on the GJB2 gene in individuals with autosomal recessive nonsyndromic hearing loss.

Hearing loss (HL) is the most common birth defect and the most prevalent sensorineural condition worldwide. It is associated with more than 1,000 mutations in at least 90 genes. Mutations of the gap junction beta-2 protein (GJB2) gene located in the nonsyndromic hearing loss and deafness (DFNB1) locus (chromosome 13q11-12) are the main causes of autosomal recessive nonsyndromic hearing loss worldwide, but important differences exist between various populations. In the present article, two common mutations of the GJB2 gene are compared for ethnic-specific allele frequency, their function, and their contribution to genetic HL in different populations. The results indicated that mutations of the GJB2 gene could have arisen during human migration. Updates on the spectrum of mutations clearly show that frequent mutations in the GJB2 gene are consistent with the founder mutation hypothesis.

Lower Expression of miR-10a in Coronary Artery Disease and its Association with Pro/Anti-Inflammatory Cytokines.

BACKGROUND: Coronary artery disease (CAD) is the leading cause of death worldwide. Atherosclerosis, the main underlying cause of CAD, is a progressive inflammatory disease. microRNAs play a substantial role in the inflammatory process and pathogenesis of atherosclerosis. miR-155, a widely studied microRNA, is associated with inflammation but there are conflicting data regarding expression of miR-155 in CAD. miR-10a is also one of the key regulators of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway which have not been evaluated in peripheral blood mononuclear cells (PBMCs) of CAD patients. METHODS: This is a case-control study conducted on 69 angiography confirmed CAD patients and 65 controls. PBMC expressions of miR-155, miR-10a, interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) were evaluated by real-time PCR in the study population. Also, serum levels of IL-6, TNF-α, interleukin-10 (IL10), and adiponectin were measured by ELISA. RESULTS: No significant differences in miR-155 expression was found between CAD and control group (p = 0.059), while lower expression of miR-10a was observed in CAD individuals compared to controls (p < 0.001). An independent association of miR-10a expression with risk of CAD was also demonstrated. Higher serum levels and PBMC expressions of IL-6 and TNF-α were observed in the CAD group compared to controls (p = 0.002 and p = 0.001). However, serum concentrations of IL-10 and adiponectin were lower in CAD individuals compared to controls (p < 0.001 and p = 0.005, respectively). We found a negative association of miR-10a expression with miR155, TNF-α and IL-6 gene expression as well as serum TNF-α and IL-6 levels. A positive correlation between miR10a and serum IL-10 concentrations was also shown. CONCLUSIONS: Our findings suggested a potential role of miR-10a in the inflammatory process underlying atherosclerosis; however, more studies are needed to support these finding.

miR-342-5p Expression Levels in Coronary Artery Disease Patients and its Association with Inflammatory Cytokines.

BACKGROUND: Atherosclerosis is a progressive inflammatory disease and is the main underlying mechanism of coronary artery disease (CAD). Immune system cells and cytokines play pivotal roles in the development of atherosclerosis. Several studies have shown the role of microRNA in the inflammatory processes of atherosclerosis, and miR-342-5p has been shown to be involved in macrophage activation during atherosclerosis and cytokine secretion. But until now, there has been no data regarding the association of miR-342-5p with CAD and inflammatory cytokines. METHODS: This case control study was conducted on 82 CAD patients and 80 controls. Peripheral blood mononuclear cell (PBMC) miR-342-5p expression and gene expression of IL-6 and TNF-α were evaluated using real timePCR. Also, the serum levels of IL-6 and TNF-α were measured using ELISA kits. RESULTS: The results demonstrated a higher expression of miR-342-5p in CAD patients compared to controls (p < 0.001). Moreover, logistic regression revealed an increased risk of CAD according to the expression of miR342-5p after adjusting for CAD risk factors (OR [CI] = 6.1 [1.0 - 37.2], p = 0.048). Also, serum IL-6 and TNF-α showed higher levels in CAD patients (p = 0.003 and p = 0.004, respectively). Furthermore, there were positive correlations of miR-342-5p with gene expressions and serum levels of IL-6 and TNF-α. CONCLUSIONS: The present study demonstrated higher levels of miR-342-5p in CAD patients and showed positive correlation with inflammatory cytokines. This result is in accordance with a previous study, and suggested a regulatory role for miR-342-5p in atherosclerosis and cytokine secretion, although more studies are required in this direction.

A novel variant of SLC26A4 and first report of the c.716T>A variant in Iranian pedigrees with non-syndromic sensorineural hearing loss.

The autosomal recessive non-syndromic hearing loss (ARNSHL) can be associated with variants in solute carrier family 26, member 4 (SLC26A4) gene and is the second most common cause of ARNSHL worldwide. Therefore, this study aims to determine the contribution of the SLC26A4 genotype in the hearing loss (HL) of 40 ARNSHL pedigrees in Iran. A cohort of the 40 Iranian pedigrees with ARNSHL, having no mutation in the GJB2 gene, was selected. The linkage analysis with five short tandem repeat (STR) markers linked to SLC26A4 was performed for the 40 ARNSHL pedigrees. Then, two out of the 40 pedigrees with ARNSHL that linked to DFNB4 locus were further screened to determine the variants in all exons of SLC26A4 gene by direct DNA sequencing. The 21 exons of SCL26A4 were analyzed for the two pedigrees. A known variant (c.716T>A homozygote), it is the first reported incidence in Iran, a novel variant (c.493A>C homozygote) were detected in the two pedigrees and pathogenesis of c.493A>C confirmed in this study with review 100 hearing ethnically matched controls by PCR-RFLP analysis. The present study suggests that the SLC26A4 gene plays a crucial role in the HL occurring in Iranian pedigrees. Also, the results probably support the specificity and unique spectrum of SLC26A4 variants among Iranian HL patients. Molecular study of SLC26A4 gene may lead to elucidation of the profile of the population-specific variants which has importance in diagnostics of HL.

Health consequences of intimate partner violence against married women: a population-based study in northern Iran.

The effects of different types of intimate partner violence (IPV) on mental health are understudied. The aim of this study was to analyse the association between women's mental health and physical, psychological and sexual IPV. We invited subjects of a population-based survey conducted in 2015 in Rasht, Iran, on IPV against women to complete the General Health Questionnaire (GHQ-28). The present research study is a secondary study based on these data and archival data from the 2015 study. For analysis, multivariate analysis of covariance was used. Additionally, predictors of IPV were evaluated using linear regression. A total of 2091 married women were surveyed. The participants were divided into abused women (n = 512, 24.5%) and non-abused women (n = 1579, 75.5%). The pattern of IPV among our patients showed more instances of psychological aggression than physical assault, sexual coercion or injury. Our results show that the non-psychotic psychiatric disorders of the victims were significantly impaired in all aspects, including somatic symptoms, anxiety/insomnia, social dysfunction, and depression. Except social dysfunction, the psychological and sexual abuse were significant predictors of other aspects of mental health. Our findings suggest that risk of IPV is high in this population. They also indicate that various forms of abuse are different from each other in terms of predicting a victim's mental health. Different strategies may be required to reduce and prevent this violence. Additional research is needed to confirm and expand upon our findings.