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MALAT1 is a long non-coding transcript that affects immune reactions, thus being involved in the pathoaetiology of immune-related conditions. We investigated the associations between two genetic variants in MALAT1 and susceptibility to psoriasis in the Iranian population. The G allele of rs619586 has been shown to be less common among cases versus controls (odds ratios (OR; 95% confidence intervals (CI)) = 0.57 (0.36-0.9)), adjusted p = .02). This single nucleotide polymorphism has been associated with the risk of psoriasis in a dominant model (AG + GG vs. AA: OR (95% CI) = 0.56 (0.35-0.92), adjusted p = .04) as well as log-additive model (OR (95% CI) = 0.59 (0.38-0.92), adjusted p = .04). The rs3200401 was not associated with psoriasis in any of the supposed inheritance models. This study potentiates rs619586 as a risk locus for psoriasis in the Iranian population.

NF-κB partakes in the pathophysiology of neurologic conditions. We quantified levels of NF-κB-associated genes in 119 patients with migraine versus healthy controls.We measured levels of NF-κB-associated genes in 42 patients with migraine compared with age- and sex-matched controls.Comparison between patients without aura and controls revealed down-regulation of PACER [expression ratio (95% CI) 0.15 (0.06-0.36), P value 0.0001]. Similar results were detected when comparing expression of PACER in patients with aura and controls [expression ratio (95% CI) 0.05 (0.02-0.12), P value 0.0001]. Both DILC and CEBPA were over-expressed in patients with aura [expression ratio (95% CI) 4.9 (2.96-7.83), P value 0.0001 and expression ratio (95% CI) 3.65 (2.39-5.24), P value 0.0001, respectively] and in patients without aura compared with controls [expression ratio (95% CI) 3.6 (2.21-5.69), P value 0.0001 and expression ratio (95% CI) 4.5 (2.53-7.11), P value 0.0001, respectively]. ADINR was over-expressed in patients with aura [expression ratio (95% CI) 4.98 (3.09-8.33), P value 0.0001] as well as patients without aura compared with controls [expression ratio (95% CI) 13.15 (7.41-23.58), P value 0.0001]. Notably, ADINR levels were lower in patients with aura compared with patients without aura. When comparing ATG5 levels in patients with aura and controls, significant up-regulation was detected [expression ratio (95% CI) 4.4 (3.01-6.32), P value 0.0001]. This pattern was also detected in patients without aura compared with controls [expression ratio (95% CI) 3.5 (2.28-5.35), P 0.0001]. Finally, expression of DICER1-AS1 was elevated in patients with aura compared with patients without aura [expression ratio (95% CI) 2.47 (1.14-5.85), P = 0.03]. This lncRNA was under-expressed in patients without aura compared with controls [expression ratio (95% CI) 0.4 (0.21-1.31), P = 0.03]. CEBPA, ATG5 and ADINR had the best AUC values for distinguishing patients with aura from controls (AUC values = 0.91, 0.85 and 0.83, respectively). The AUC values for separation between patients without aura and controls were 0.90, 0.86 and 0.75 for CEBPA, ATG5 and ADINR, respectively.Taken together, several genes in the NF-κB pathway has been revealed to be dysregulated in migraineurs and expression of these genes can be used as markers for this neurological condition.

mTOR has been shown to be involved in the regulation of immune responses and differentiation of immune cells. This protein is a candidate molecule for unraveling the molecular mechanisms of autoimmune disorders such as multiple sclerosis (MS). We designed the current study to assess expression of MTOR, and four associated long non-coding RNAs (lncRNAs), namely SNHG1, SNHG3, SHNG5 and DANCR in the peripheral blood of patients with MS compared with healthy controls. Analysis of real-time PCR results has shown down-regulation of SNHG5 and DANCR in MS patients compared with controls. Sex of study participants had no significant effect on expression of either genes and the interaction of sex and disease on expression levels of all studied genes were insignificant. There was a significant negative correlation between expression levels of MTOR gene and disease duration. No other significant correlations were detected between genes expressions and clinical/demographic data. SNHG5 and DANCR transcript levels had AUC values of 0.88 and 0.68 in separation of patients with MS from healthy controls, respectively. Taken together, our study suggests participation of two mTOR-related lncRNAs, i.e. SNHG5 and DANCR in the pathophysiology of MS.

Parkinson's disease (PD) is a neurological condition that is associated with abnormal expression of several transcripts. Vitamin D receptor (VDR) is a possible participant in the pathogenesis of PD.In the present research project, we evaluated expressions of VDR and three functionally associated long non-coding RNAs with this signaling, namely SNHG6, SNHG16 and LINC00346 in PD patients versus normal controls. Level of SNHG6 transcripts was lower in total patients in comparison with total controls (Expression ratio (95% CI) 0.44 (0.17-1.08)) and in male patients compared with male controls (Expression ratio (95% CI) 0.29 (0.13-0.65)). On the other hand, expression of VDR was higher in total patients compared with total controls (Expression ratio (95% CI) 10.86 (4.37-26.72)) and in male patients compared with male controls (Expression ratio (95% CI) 22.16 (6.23-78.8)). There was no significant difference in expression of SNHG16 and LINC00346 between PD patients and controls. Amounts of SNHG6 and VDR transcripts could differentiate total PD patients from total controls with AUC values of 0.66 and 0.86, respectively.Cumulatively, the results of the present investigation imply dysregulation of VDR signaling in PD and necessitate conduction of further functional studies.

Long non-coding RNAs that regulate function of regulatory T cells can affect pathoetiology of autoimmune disorders, such as inflammatory demyelinating polyneuropathies. In the current case-control study, we compared expression of four of these lncRNAs, namely FLICR, NEST, RMRP and TH2-LCR between patients with inflammatory demyelinating polyneuropathies and healthy subjects. Expressions of RMRP, NEST and FLICR were higher in total patients compared with controls. However, there was no significant difference in their expressions between acute and chronic demyelinating polyneuropathies. In addition, interaction of gender and disease factors had significant effect on expression levels of RMRP and TH2-LCR genes in subgroups. RMRR was superior to other lncRNAs in terms of AUC, sensitivity and specificity values in total patients and both subgroups of patients. This lncRNA could separate total patients, female patients and male patients from corresponding controls with AUC values (±SD) of 0.9 ± 0.03, 0.86 ± 0.07 and 0.93 ± 0.03, respectively. FLICR ranked second in this regard, since it could separate total patients, female patients and male patients from corresponding controls with AUC values (±SD) of 0.81 ± 0.03, 0.72 ± 0.07 and 0.87 ± 0.04, respectively. Therefore, our study provides evidence for participation of regulatory T cells-related lncRNAs in the pathoetiology of inflammatory demyelinating polyneuropathies.

End-stage renal disease (ESRD) is a public health problem with a high burden. The condition is associated with abnormalities in lipid metabolism. The fatty acid desaturase (FADS) gene cluster includes three genes that are significantly correlated with a number of pathologic conditions related to abnormal lipid levels. In the current study, we genotyped rs174556, rs99780, and rs7115739 single nucleotide polymorphisms within the FADS cluster in a population of ESRD patients and healthy controls. The rs174556 of the FADS1 gene and rs99780 of the FADS2 gene were not associated with the risk of ESRD in any inheritance model. However, the rs7115739 of FADS3 was associated with the risk of ESRD in all models except for the recessive model. The T allele of this SNP was significantly less prevalent among cases compared with controls [odds ratio (OR) (95% CI) = 0.44 (0.25–0.77), P value = 0.004]. GT and TT genotypes has been shown to decrease the risk of ESRD in a codominant model [OR (95% CI) = 0.49 (0.26–0.92) and OR (95% CI) = 0.18 (0.02–1.6), respectively; P value = 0.019]. In the dominant model, GT + TT status was associated with lower risk of ESRD [OR (95% CI) = 0.45 (0.24–0.82), P value = 0.0078]. Assessment of association between this SNP and risk of ESRD in an overdominant model revealed that GT genotype decreases the risk of this condition [OR (95% CI) = 0.5 (0.27–0.94), P value = 0.029]. Taken together, the rs7115739 of FADS3 is suggested as a putative modulator of the risk of ESRD in the Iranian population.

Melanoma is the utmost fatal kind of skin neoplasms. Molecular changes occurring during the pathogenic processes of initiation and progression of melanoma are diverse and include activating mutations in BRAF and NRAS genes, hyper-activation of PI3K/AKT pathway, inactivation of p53 and alterations in CDK4/CDKN2A axis. Moreover, several miRNAs have been identified to be implicated in the biology of melanoma through modulation of expression of genes being involved in these pathways. In the current review, we provide a summary of the bulk of information about the role of miRNAs in the pathobiology of melanoma, their possible application as biomarkers and their emerging role as therapeutic targets for this kind of skin cancer.

Hepatocellular carcinoma (HCC) is among the utmost deadly human malignancies. This type of cancer has been associated with several environmental, viral, and lifestyle risk factors. Among the epigenetic factors which contribute in the pathogenesis of HCC is dysregulation of long non-coding RNAs (lncRNAs). These transcripts modulate expression of several tumor suppressor genes and oncogenes and alter the activity of cancer-related signaling axes. Several lncRNAs such as NEAT1, MALAT1, ANRIL, and SNHG1 have been up-regulated in HCC samples. On the other hand, a number of so-called tumor suppressor lncRNAs namely CASS2 and MEG3 are down-regulated in HCC. The interaction between lncRNAs and miRNAs regulate expression of a number of mRNA coding genes which are involved in the pathogenesis of HCC. H19/miR-15b/CDC42, H19/miR-326/TWIST1, NEAT1/miR-485/STAT3, MALAT1/miR-124-3p/Slug, MALAT1/miR-195/EGFR, MALAT1/miR-22/SNAI1, and ANRIL/miR-144/PBX3 axes are among functional axes in the pathobiology of HCC. Some genetic polymorphisms within non-coding regions of the genome have been associated with risk of HCC in certain populations. In the current paper, we describe the recent finding about the impact of lncRNAs in HCC.

Coronary artery disease (CAD) is the main reason of cardiovascular mortalities worldwide. This condition is resulted from atherosclerotic occlusion of coronary arteries. MicroRNAs (miRNAs) are implicated in the regulation of proliferation and apoptosis of endothelial cells, induction of immune responses and different stages of plaque formation. Up-regulation of miR-92a-3p, miR-206, miR-216a, miR-574-5p, miR-23a, miR-499, miR-451, miR-21, miR-146a, and a number of other miRNAs has been reported in CAD patients. In contrast, miR-20, miR-107, miR-330, miR-383-3p, miR-939, miR-4306, miR-181a-5p, miR-218, miR-376a-3p, and miR-3614 are among down-regulated miRNAs in CAD. Differential expression of miRNAs in CAD patients has been exploited to design diagnostic or prognostic panels for evaluation of CAD patients. We appraise the recent knowledge about the role of miRNAs in the development of diverse clinical subtypes of CAD.

Coronary artery disease (CAD) is a common disorder caused by atherosclerotic processes in the coronary arteries. This condition results from abnormal interactions between numerous cell types in the artery walls. The main participating factors in this process are accumulation of lipid deposits, endothelial cell dysfunction, macrophage induction, and changes in smooth muscle cells. Several lines of evidence underscore participation of long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in the pathogenesis of CAD. Several lncRNAs such as H19, ANRIL, MIAT, lnc-DC, IFNG-AS1, and LEF1-AS1 have been shown to be up-regulated in the biological materials obtained from CAD patients. On the other hand, Gas5, Chast, HULC, DICER1-AS1, and MEG3 have been down-regulated in CAD patients. Meanwhile, a number of circRNAs have been demonstrated to influence function of endothelial cells or vascular smooth muscle cells, thus contributing to the pathogenesis of CAD. In the current review, we summarize the function of lncRNAs and circRNAs in the development and progression of CAD.

Migraine is a common neurovascular condition. This disorder has a complex genetic background. Several single-nucleotide polymorphisms (SNPs) or mutations within genes regulating glutamatergic neurotransmission, cortical excitability, ion channels, and solute carriers have been associated with polygenic and monogenic forms of migraine. SNPs within ACE, DBH, TRPM8, COMT, GABRQ, CALCA, TRPV1, and other genes have been reported to affect the risk of migraine or the associated clinical parameters. The distribution of some HLA alleles within the HLA-DRB1, HLA-DR2, HLA-B, and HLA-C regions have also been found to differ between migraineurs and healthy subjects. In addition, certain mitochondrial DNA changes and polymorphisms in this region have been shown to increase the risk of migraine. A few functional studies have investigated the molecular mechanisms contributing to these genetic factors in the development of migraine. Here we review studies evaluating the role of genetic polymorphisms and mRNA/miRNA dysregulation in migraine.

Long non-coding RNAs (lncRNAs) embrace a huge fraction of human transcripts and participate in the pathogenesis of human disorders especially malignant conditions. Malignant melanoma, as the most fatal type of cutaneous malignnacies, is associated with dysregulation of several lncRNAs including PVT1, H19, MALAT1, and CCAT1. Moreover, a portion of lncRNAs are exclusively expressed in melanoma cell lines. Expression levels of several lncRNAs are associated with TNM stage, tumor size and progression of melanoma. Thus, these lncRNAs are regarded as biomarkers for this malignancy. Peripheral transcript levels of a number of lncRNAs, such as PVT1, SNHG5 and SPRY4-IT1, could distinguish melanoma patients from unaffected persons with appropriate sensitivity and specificity values. Moreover, expression levels of numerous lncRNAs in tissue biopsies could differentiate malignant samples from benign samples. Based on the results of both cell line and in vivo studies, lncRNAs regulate critical pathways in the carcinogenesis of melanoma, such as the PI3K/Akt and NF-κB signaling pathways, and are involved in the modulation of response to chemotherapeutic agents. Here we review the existing information on the role of lncRNAs in malignant melanoma.

Psoriasis is a complex disorder with genetic background. Previous studies have reported the presence of some genetically-influenced factors for this disorder. In the current study, we genotyped rs2067079 and rs6790 polymorphisms of GAS5 lncRNA in Iranian patients with psoriasis and healthy controls. Genotype frequencies of rs2067079 and rs6790 were in accordance with the Hardy-Weinberg equilibrium both in cases and controls. Distributions of alleles/genotypes of rs2067079 and rs6790 polymorphisms were similar between patients with psoriasis and healthy controls. None of these SNPS were associated with risk of psoriasis in any inheritance model. We also appraised association between GAS5 haplotypes and risk of psoriasis. Frequencies of CG, TG, CA and TA haplotypes (rs2067079 and rs6790) were statistically similar between patients with psoriasis and healthy controls. Thus, mentioned polymorphisms are not associated with risk of psoriasis in Iranian population.

Head and neck squamous cell carcinomas (HNSCCs) are human malignancies associated with both genetic and environmental factors. MicroRNAs (miRNAs) as a group of small non-coding RNAs have prominent roles in the development of this kind of cancer. Expressions of several miRNAs have been demonstrated to be increased in HNSCC samples vs. non-malignant tissues. In silico prediction tools and functional analyses have confirmed the function of some miRNAs in the modulation of cancer-associated targets, thus indicating these miRNAs as onco-miRs. Moreover, numerous miRNAs have been down-regulated in HNSCC samples. Their targets mostly enhance cell proliferation or inhibit apoptosis. miRNAs signature has practical implications in the diagnosis, staging, and management of HNSC. Most notably, numerous miRNAs have been shown to alter response of tumor cells to anti-cancer drugs such as cisplatin and doxorubicin. Circulating levels of these small transcripts have been suggested as promising biomarkers for diagnosis of HNSCC. In the present manuscript, we sum up the available literature regarding the miRNAs signature in HNSCC and their role as diagnostic/prognostic biomarkers., Bioinformatics; Cell biology; Cancer research; Epigenetics; Genetics; Gene expression; Gene regulation; Genomics; Squamous cell carcinoma; miRNA; Biomarker; Expression; Cancer.

Objective: Glucocorticoids are one of the most important drugs in the treatment of acute lymphoblastic leukemia for children. It is very important to response to glucocorticoid in the prognosis of these patients. Therefore, resistance to treatment is a major problem in lymphoid leukemia cases. In, this study, CCRF-CEM cell line was selected as a chemotherapy-resistant model. The aim of this study was to evaluate the effect of high dose prednisolone on induction of apoptosis and changes in BAX and BCL-2 gene expression at different times. Methods: CCRF-CEM cell lines were grown in standard conditions. Based on previous studies, a dose of 700 µM as subtoxic dose was selected. Changes in gene expression of BAX and BCL-2 were evaluated by using real time PCR techniques. Also stained with annexin V and the induction of apoptosis was assessed by FACS machine. Results: In this study it was found that prednisolone in high doses at different times significantly increased the gene expression of BAX and on the other hand the amount of BCL-2 expression was reduced. Cells that treated for 48 hours had more significant changes in gene expression. Based on flowcytometry data, prednisolone can induce apoptosis in a time dependent manner on this cancerous resistant cell line. Conclusions: Apoptosis induced by high-dose prednisolone in the CCRF-CEM cells, which is almost resistant, and possibly mediated by reducing the expression of BCL-2 and BAX up-regulation.

One of the most important developments in the field of quality improvement approaches that have been occurred in the last decade of the twentieth century is issue of measuring customer satisfaction as one of the core requirements of quality management system in all institutions and business enterprises. Nowadays, there are many efforts to improve the quality of management tools and customer-oriented culture by scholars, experts and managers of organizations that all show that customer satisfaction is the most important factor in determining organization’s success and profitability. Electronic services with competitive opportunities for organizations help the creation of customer satisfaction. This study aims to assess the relationship between electronic services quality and satisfaction of policyholder so that service improvement and availability are as indicators of electronic services, and reliability is used as an indicator of customer satisfaction. Questionnaires were used to collect data and then data was analyzed using statistical methods. It is concluded that there is a significant relationship between electronic service quality and customer satisfaction.

In this paper we propose a novel method to improve seam carving based on the method meta-heuristic algorithms combining simulated annealing (SA) and genetic algorithm (GA). SA is a single solution method which searches locally while GA belongs to population based algorithms that globally search to find the best answer. By this strategy, both speed and quality of the seam carving method can be increased simultaneously. First, SA is performed to find near optimum seams, which form initial population of GA. Then genetic algorithm develops this initial population to find optimum seam. Experimental results show that search for optimum seams by our proposed method successfully improves the retargeting results of seam carving.