farideh talebi

The footprint of Neuregulin 1 (NRG1) / ERbB4 in the pathophysiology of some neurological disorders and TRPV1 regulation has been indicated. The alterations in NRG1 and ErbB4 as well as the TRPV1 signaling pathway were investigated during the development of absence epilepsy in the genetic animal model of absence epilepsy.

Male WAG/Rij and Wistar rats were divided into four experimental groups of two and six months of age. The protein levels of NRG1, ERbB4, and TRPV1 were measured in the somatosensory cortex and hippocampus. 

The cortical protein levels of NRG1 and ErbB4 in the 6-month-old WAG/Rij rats were lower than in Wistar rats. Protein levels of TRPV1 were lower in two- and six-month-old WAG/Rij rats compared to age-matched Wistar rats.Hippocampal protein levels of NRG1 in 6-month-old WAG/Rij rats were lower than two-month-old WAG/Rij rats. Low levels of ErbB4 protein in two-month-old and high levels in six-month-old WAG/Rij rats were found compared to Wistar rats. Protein levels of TRPV1 were lower in the two-month-old and higher in the six-month-old WAG/Rij rats compared to age-matched Wistar rats. Furthermore, a high correlation between NRG1/ERbB4 and TRPV1 expressions in the cortex and hippocampus was indicated. The expression of NRG1/ERbB4 and TRPV1 followed a similar pattern during the life span of Wistar and WAG/Rij rats.

Our findings indicated the potential role of the NRG1/ErbB4 pathway as well as TRPV1 in the pathogenesis of absence epilepsy. The regulatory effect of the ERbB4 receptor on the TRPV1 expression has been suggested following the similar pattern of expression.

Vitamins A, D, and microRNAs contribute to T cell differentiation into TH2 phenotypes. We investigated the molecular mechanisms and effects of vitamin A and D on the expression of GATA3 and miR-27-3p isoforms in experimental autoimmune encephalomyelitis (EAE) animal model of multiple sclerosis. EAE was induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein, mixed with Complete Freund's Adjuvant, together with injection of pertussis toxin. Treatments began one day before immunization with (200 μg and 100 ng of vitamin A and vitamin D per mouse, respectively, and vitamin A+D (100 μg+50 ng) per mouse. Expression levels of GATA3 and miR‑27‑3p isoforms were measured in the CNS and splenocytes by real-time RT-PCR. The expression level of GATA3 in the mice spinal cords and splenocytes was increased in the vitamin A and A+D-treated EAE mice at 24 h and 48 h after restimulation by 10 µg and 40 µg of myelin oligodendrocyte glycoprotein. Vitamins A and D and their combination upregulated the miR-27-3p isoforms compared with EAE mice with no treatments. We also demonstrated that miR-273p isoform expression was altered in splenocytes of vitamin-treated EAE mice. The results showed a positive correlation between splenocyte GATA3 levels and miR-27-3p isoform expression. The protective impacts of vitamins A and D in EAE mice may be mediated by the upregulation of GATA3. However, it is not specified whether suppression of GATA3-targeting miRNAs of the miR-27-3p family is involved in this effect. These results do not rule out the possibility that miR-27-3p isoforms might have beneficial effects by targeting other transcripts, such as GluA2 and NR2B.

Sulfur mustard as a chemical warfare agent causes short and long-term pulmonary complications in its victims. MicroRNAs are known to act as remarkable regulators of biological pathways, monitoring, and treatment of diseases including respiratory problems. In this study, we investigated the expression of miR-106a-5p and miR-106b-5p, two regulators of TGF-β signaling, as well as their target molecule, TGFβ1I1, in peripheral blood mononuclear cells from SM-exposed individuals. A total of 70 veterans with SM-induced pulmonary complications were examined and compared to 35 gender and age-matched healthy controls. After clinical examination and pulmonary function tests, the severity of pulmonary complications was classified. Total RNA was extracted from PBMCs and the purity of extracted RNA samples was evaluated by a NanoDrop 2000. The miR-106a-5p, miR-106b-5p, and TGFβ1I1 expression levels were measured by real-time RT-PCR. The miR-106a-5p expression levels were significantly increased in both mild (P=0.015) and severe groups compared with the control group. The miR-106b-5p expression levels were considerably elevated in the severe group TGFβ1I1 expression levels were notably reduced in the severe group compared with the control group. Although, a slight decrease in TGFβ1I1 expression levels was observed in the mild group compared with the control. Our results indicate that exposure to sulfur mustard affects the expression of miR-106a-5p, miR-106b-5p, and their target gene, TGFβ1I1, in peripheral blood mononuclear cells. Considering the role of TGFβ1I1 in the regulation of TGF-β signaling, the mentioned changes might point to a potential mechanism by which SM exposure causes chronic pulmonary complications. In a ROC analysis, miR-106a-5p and miR-106b-5p potentially turned out to be a suitable diagnostic biomarker in the mild and severe categories of patients. Although, miR-106a-5p could be considered a better biomarker than miR-106b-5p.

MicroRNAs are small non-coding RNAs that regulate gene expression and involve in many cellular and physiological mechanisms. Recent studies have revealed that dysregulation of microRNAs might contribute to autoimmune disorders such as Multiple Sclerosis (MS). Based on these findings, we examined the potential role of miR-320 isoforms; miR-320-3p and miR-320-5p, in the context of autoimmune neuroinflammation and pathogenesis of EAE, which is an animal model of MS. The expression levels of miR-320-3p and miR-320-5p, and their predicted target genes, TGFBR2 and Smad2, were quantified in the CNS tissue in mice with Experimental Autoimmune Encephalomyelitis (EAE) using RT-PCR method. The expression was also examined in splenocytes macrophages and astrocytes. To examine the interaction of miR-320-3p and miR-320-5p with the 3′-UTR of potential target transcripts, the mimic sequences of both isoforms were transfected into splenocytes and then examined by RT-PCR. The expression of both isoforms of miR-320 significantly increased in different phases of EAE and activated lymphocytes, whereas the levels of their predicted target genes, Smad2 and TGFBR2 decreased in these cells. Obtained data revealed that miR-320-5p level significantly increased in activated macrophages and astrocytes; however, the miR 320-3p level did not show significant changes in these cells after Lipopolysaccharide (LPS) stimulation. The levels of TGFBR2 and Smad2 decreased in transfected splenocytes. Our findings suggest that upregulation of miR-320 isoforms might be involved in the neuroinflammation and pathogenesis of MS through targeting and suppression of TGFBR2 and Smad2, i.e. protective genes in MS.

The purpose of this study was to investigate the relationship between entrepreneurship education and social capital of female headed households under the well-being of Alborz province. The method of this research has been quasi-experimental. The statistical society in this research was selected from 1257 cases of rehabilitation of women headed by households under the welfare of Alborz province in 1395. 120 samples were selected randomly from the social capital of Nahapit and Goshall and entrepreneurship questionnaires from a t-test on spss software on subjects.Sub-goals based on       -The recognition of the relationship between entrepreneurial education and the subsequent structural capital of social capital (expansion of the social network, increasing social relations). -The recognition of the relationship between post-graduate entrepreneurial education and social capital (increased cooperation, promotion of values). -The recognition of the relationship between entrepreneurship education and the social dimension of social capital (increasing mutual understanding, increasing trust, increasingcommitment).  The results of this study, with regard to the level of significance achieved, can be said that entrepreneurship education has a significant effect on social capital among female headed households under well-being. According to the significance level achieved, which is 0.024 and less than 0.05 , Therefore, it can be said that entrepreneurship education has a significant effect on social capital among female headed households covered by well-being. The comparison of the average social capital before and after the training shows that the holding of these courses has increased the social capital of these people. Also, entrepreneurship education has a significant effect on the social dimension (structural, cognitive, and communicative) of women under the supervision of well-being households. The comparison of the mean (structural, cognitive, and communicational) dimension of social capital before and after the course shows that the subsequent courses (structural, cognitive, and communicative) have increased the social capital of these individuals

Discovering the enzymes involved in steroid biosynthesis in the central nervous system and the ability of neurons and glial cells to produce steroids is one of the major findings of neurobiology over the last two decades. Unlike classical steroids, these neurosteroids influence neuronal function through direct interactions with neurotransmitter receptors at the cell surface.
Extensive studies have shown diverse physiological and pharmacological effects for these compounds. Moreover, neurosteroids have been shown to be involved in different pathological procedures, including neurodegenerative and neuro inflammatory disorders as well as neuropsychiatric diseases. Herein, we will review different aspects of neurosteroid biosynthesis and functions as well as their involvement in the pathogenesis of brain diseases.

Gene expression regulation is essential for correct functioning of the cell. Complex processes such as development, apoptosis, cell differentiation, and cell cycling require a fine tuning of gene expression. microRNAs (miRNAs) are small RNAs that have been recognized as key components of the gene expression regulatory machinery. microRNAs are a class of small RNA regulators that are involved in numerous cellular processes, including development, proliferation, differentiation, neurogenesis, and plasticity. miRNAs are critical contributors to the regulation of gene expression in the nervous system.
Emerging evidence indicates that microRNAs regulate both the development and function of the nervous system. Deficiency in microRNA function has also been implicated in a number of neurological disorders. Understanding the roles of microRNAs will provide new insights into the complexity and operation of the nervous system.

Although central nervous system (CNS) has long been known as an immune privileged site, in common with all other tissues, it requires effective immune mechanisms to protect against infections. More recent data support that certain areas of healthy CNS are continuously monitored by resident microglia and blood-borne immune cells such as macrophage and T-cell to sustain CNS immune surveillance. Interruption of CNS surveillance by lymphocyte traffic inhibition results in injury and infection by viruses such as JC virus, herpes simplex virus, etc. CNS Immune system has to be regulated in a unique way in order to prevent inflammation and autoimmune reactions against CNS derived antigens, which there is no tolerance for them.
Here, we discuss the anatomical and cellular aspects of immune surveillance in the CNS. Moreover, we review a new model to explain how antigen-specific T-cell responses occur in the CNS.