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Obsessive compulsive disorder (OCD) is characterized by intrusive thoughts or images (obsessions) and/or rigid rituals that may be driven by obsessions (compulsions). Controlled outcome studies investigating the efficacy of psychological treatments for OCD and exposure and response prevention (ERP) has been found to be the “treatment of choice” for OCD. Moreover, mindfulness-based approaches have been proven-effective in treating OCD and anxiety disorders. In this study combination of mindfulness and exposure with response prevention in the treatment of OCD had been investigated. The aim of this research was to study the effectiveness of mindfulness based exposure therapy (MET) for OCD. In this research, single subject design with base line and 3 months follow-up was used. Participants were selected from clients of psychiatry hospital and received 8 sessions of MET. The patient was a 45 years man who suffered from OCD. Yale-Brown obsessive compulsive scale, Beck anxiety and depression inventories and SUD and process of treatment questionnaire were used in this study for analysis. Results showed that the patients acquired clinically significant change on outcomes measures. MET is effective for OCD, anxiety and depressive symptoms and SUD. Weekly analyses of process of treatment showed that distress, reaction to obsession moderated. The treatment gains were maintained at 3 month follow-up. Combination of mindfulness and exposure with response prevention can led to improvement of obsessive-compulsive symptoms. Our primary study showed mindfulness based exposure therapy can be useful for anxiety and depressive symptoms in OCD. Further research is needed for study the effectiveness of MET for OCD.

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Antisocial personality‌has some clear symptoms as impulsivity, unstable emotions, aggression, drinking, use of drugs, early initiation of sexual behavior make some difficulties and problems in their relations with family members and those who have interaction with them and at least in society. According to the mentioned symptoms of this personality disorder in this research project, it has been tried to solve its problems by comparing the effectiveness of dialectical behavior therapy on anxiety and depression among young male prisoners who have antisocial personality in Ilam prison. This semi experimental project has been done by pre and post-test. 32 subjects have been selected purposely between 18-40 years among male prisoners in Ilam prison. Three questionnaires have been used the Millon clinical questionnaire, Beck anxiety questionnaire and depression questionnaire. In the study of the effectiveness of the treatment of anxiety (P=0.014 (is not effective in treating depression (P=0.955). According to the findings obtained appears to be a dialectical therapy, due to the nature of the treatment that the acceptance and credibility of the person making the attempt to change a person's psychological stresses therapeutic efficacy in the treatment of some of the characteristics of people with antisocial personality disorder.

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Anxiety and depression are very common in population and occur in a wide range of clinical states and is very common in epileptic patients. Many recent epidemiological studies have found a high prevalence of depression and anxiety in epileptic patients. These studies found that epileptic patients suffered from depression and anxiety than those without epilepsy. The prevalence of depression or anxiety is higher in drug refractory epilepsy, especially temporal-lobe epilepsy. Depression and anxiety have been associated with increased adverse events in response to anti-epileptic drugs in epileptic patients. Structural abnormalities, monoamine pathways, cerebral glucose metabolism, the hypothalamic pituitary adrenal axis and interleukin-1β all plays a crucial role in the common pathogenesis of these conditions. Studies that have examined depressed patients using high-resolution brain MRI have shown reductions in the volumes of various areas, including the frontal, temporal, limbic regions and hippocampus (the left and right hippocampus in temporal-lobe epilepsy and depression). Findings of reductions in hippocampal volume suggest that depression and epilepsy reflect common structural abnormalities. The symptoms of depressive disorders in epileptic patients can be classified according to their temporal relationship with seizures. The psychiatric and clinical effects of depression and anxiety can impair the quality of life of epileptic patients. Therefore, early detection and management of depression and anxiety are critical for the management of epileptic patients.

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Mast cells are a heterogeneous population of granulocytic cells in the immune system. Mast cell granules contain numerous mediators, including neurotransmitters, cytokines, chemokines and lipid-derived factors. In addition to their well-known role in immune inflammation, the presence of mast cells in the meninges and perivascular space in the central nervous system points to their role in brain physiology and their potential involvement in the development of neurological disorders. Of interest, activation of mast cells and their interaction with glial cells have been shown to be involved in altering the permeability of blood brain barrier, a phenomenon which is a key part of neuroinflammatory/degenerative processes. Mast cells have also been reported to exert protective effects against neuroinflammation likely through releasing anti-inflammatory compounds or degrading inflammatory mediators. While diseases like multiple sclerosis, Alzheimer’s disease and stroke are considered as classical examples of neuroinflammation, the role of low-grade inflammation in the pathogenesis of psychiatric disorders has recently attracted the attention of investigators. Herein, we summarize some of the findings about the role of mast cells in the pathogenesis of psychiatric disorders including anxiety disorders.

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Mitochondria are membrane-enclosed organelle found in most eukaryotic cells, which known as power house in cells. This organelle transforms energy into forms that are usable by the cell. The most common psychiatric disorders such as depression and anxiety can be linked to mitochondrial disorders. Furthermore, mutations of mitochondrial or nuclear DNA (mtDNA and nDNA, respectively) have been linked to deprecation and anxiety. Gene sets play a crucial role in the development of personality property including also affective temperaments, in the mediation of the effects of environmental factors and in the interaction of these elements in the development ofanxiety . Mutation of mitochondrial DNA such as deletion or decreased gene expression has direct effect with psychiatric disorder that the details of this mechanism have not been detected. The aim of this study is to review the literature on the relationship between neuropsychiatric disorders especially, depression and anxiety, with DNA mutations and mitochondrial alterations.

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Spreading depression (SD), discovered by Leao in 1944, is a pathophysiological wave which propagates slowly in the brain (3 mm/min) and cause dramatic ionic and hemodynamic changes. SD appears to act through several mechanisms and receptors which have not completely understood. Here, we studied the effect of inhibitory system in animal model of SD using immunohistochemistry technique. After implanting recording electrodes and cannula over the brain, repetitive SD was induced by KCl injection (2 M) in juvenile rats for four consecutive weeks. Then all rats were decapitated and the brains removed. Mean number of dark neurons in entorhinal cortex were determined using Toluidine blue staining. To identify the prevalence and distribution of γ-aminobutyric acid A (GABA-A) subunit receptors and glutamic acid decarboxylase (GAD), immunohistochemistry technique was performed. The mean number of SD induced by KCl injection was statistically increased during four weeks of experiments (P = 0.036). The mean number of dark neurons in entorhinal cortex was significantly increased in SD group compared to sham rats (P ≤ 0.001). Also, expression of GAD 65 receptor in the Entorhinal cortex significantly increased in SD group compare to control group (P < 0.05). GABA-Aα and GABA-Aβ receptors didn’t show significant change in that region. These data suggest that SD is able to damage neural cells and also it could lead to enhancement of GAD, the enzyme which is responsible for synthesizing an important inhibitory neurotransmitter, GABA receptor, in the central nervous system.

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Traumatic spinal cord injuries (SCIs) lead to severe and permanent neurological deficits. Although no effective therapeutic option is currently available, recent other studies have shown that cell transplantation strategies hold promise to enhance functional recovery after SCI. Adipose stem cells (ADSCs) obtained from pararenal and inguinal region of rats. ADSCs were cultured and then differentiated to the neural stem cells (NSCs). Directed differentiation of stem/progenitor cells to oligodendrocytes (OLCs) lineage was done and the cell viability was assessed by trypan blue. Immunocytochemistry was carried out by NF68, NF160, fibronectin and nestin for NSCs. Also, it was done by O4, O1, and oligo2 for OLCs. Results showed that fibronectin, CD44, CD90 and CD45 expressed 94.32±0.45%, 95.48±0.24% and 97.16±0.82% respectively. Expression of O1, O4 and oligo2 showed that combination of HRG, PDGF, bFGF and T3 (25 ng/ml) have an effective role in transdifferentiation of ADSCs into OLCs. ADSCs can differentiate to mature OLCs. Our suggestion is that oligodendrocytes can be used as a therapeutic strategy for treatment of SCI in future.

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Generation neural stem cells from neurosphere-derived adipose tissue using bioactive substance ATC. Adipose tissue from rat hypodermal and pararenal fat was digested with collagenase, followed by filter and centrifugation the isolated adipose stromal cells were cultured in dishes. These cells evaluated by specific markers of adipose-derived stem cells (ADSCs) such as bioactive substance ATC and then ADSCs differentionated in to neurosphere in four groups that compared morphologically. Diameter and number of this neurosphere evaluated every day in four groups. ADSCs are mesenchymal stem cells that can be extracted from adipose tissue and obtained by a less invasive method. ADSCs markers were measured by immunocytochemistery that expressed CD90 (80%), CD44 (70%) and fibronectin while CD45 didn’t express. Diameter and number of Neurosphere by (0.1 ng/ml) was optimal dose for expansion. Then these cells evaluated by neuroectodermal markers such as nestin and NF 68 that expressed>80% and this data approved by RT-PCR technique. This study develops a simplified, efficient, and nontoxic approach by lowest factors which derives a large number of neurospheres from Adipose-derived stem cells (ADSCs). With our newly devised approach 10 to 15 passage cells were used for in vitro differentiation. Neuronal differentiation was induced by incubation of the ADSCs with bioactive substance (ATC) induction media.

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Generation neural stem cells from neurosphere–derived bone marrow stem cells using bioactive substance ATC. Bone marrow cells (BMSCs) were isolated from rat. BMSCs cultured by DMEM/F12 medium supplemented with 10% fetal bovine serum. These cells evaluated by specific markers of BMSCs such as bioactive substance ATC, B27. Then BMSCs differentionated in to neurosphere and divided in two groups which were evaluated morphologically. Diameter and number of this neurosphere evaluated daily. BMSCs markers were measured by immunocytochemistery that expressed, CD 90 (75%) CD 44 (60%) fibronectin. Diameter and number of Neurosphere by 0.1 ng/ml was optimal dose for expansion. Then these cells evaluated by neuroectodermal markers such as nestin and NF 68, NF 200 and NF160, that expressed >80 % and this data approved by RT-PCR assay. This study develops a simplified, efficient, and nontoxic approach by lowest factors which derives a large number of neurospheres from BMSCs. With our newly devised approach 10 to 15 passage cells were used for in vitro differentiation. Neuronal differentiation was induced by incubation of the BMSCs with bioactive substance (ATC) induction media.

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Traumatic central nervous system injuries lead to a severe and permanent neurological deficit. Oligodendrocytes (OLCs) are vulnerable to damage in a variety of neurologic diseases. Although no effective therapeutic option is currently available, recent other studies have shown that cell therapeutic strategies hold promise to enhance functional recovery after injury. The aim of this study is to analyze transplantation of OLCs which differentiated from bone marrow stem cells (BMSCs) in rat models of spinal cord injury. BMSCs were isolated from twenty-day old rat and were plated for differentiation to neurosphere. BMSCs were evaluated by different immunocytochemistry markers such as fibronectin, CD106, CD44, CD90 and CD45. Cell viability was assessed by trypan blue method. OLCs were assessed by immunocytochemistry for O4, oligo2 and O1 markers. Our results showed that the fibronectin, CD44, CD90 and CD45 expressed 94.32±0.45%, 95.48±0.24% and 97.16±0.82% respectively. Expression of O1, O4 and oligo2 showed that combination of HRG, PDGF, bFGF and T3 (25ng/ml) have an effective role in transdifferentiation of BMSCs into OLCs. BMSCs can differentiate mature OLCs. Our suggestion is that oligodendrocytes can be used as a therapeutic strategy for treatment of spinal injuries in future.

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Introduction: According to the previous studies, neural pathway of the basolatral amygdala plays an important role in etiology and pathophysiology of depression, anxiety, and aggression. However, the exact role of the basolateral amygdala in anxiety needs to be elucidated. Using social interaction and elevated plus maze tests, the role of AMPA glutamate subreceptors in the basolatral amygdala on aggression and anxiety-like behaviors was investigated. Materials and Methods: After anesthesia, two cannulas were implanted in the basolatral amygdala in Wistar rats. After one week recovery, anxiety levels and different forms of aggression were analyzed by elevated plus maze and social interaction tests. Results: AMPA agonist was administered at 0.25, 0.5, and 1 mg/kg doses in the basolateral amygdala. Doses of 0.5 and 1 mg/kg were significantly increased time spent in the open arms and offensive sideway compared to sham group. In addition, activation of AMPA receptor at 1 mg/kg significantly decreased the stay and entrance percentage of open arm and offensive sideway. Conclusion: Our data indicate that AMPA receptors modulate the signaling in the basolateral amygdala and may affect anxiety and aggression.

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Introduction: Spreading depression (SD), discovered by Leao in 1944, is a pathophysiological depolarization wave that propagates slowly in the brain (3 mm/min) and causes dramatic ionic and hemodynamic changes. SD appears to act through several mechanisms and receptors, which have not completely understood. Here, we studied the effect of inhibitory system in animal model of SD using immunohistochemistry technique. Materials and Methods: After implanting recording electrodes and cannula over the brain, repetitive SD was induced by KCl injection (2 M) in juvenile rats for four consecutive weeks. Then all rats’ brains removed. The mean number of dark neurons in the entorhinal cortex (EC) were determined using toluidine blue staining. To identify the prevalence and distribution of GABAA subunit receptors as well as glutamic acid decarboxylase (GAD), the GABA biosynthetic enzyme, immunohistochemistry technique was performed. Results: The mean number of SD induced was statistically increased during four weeks of experiments. The mean number of dark neurons in EC was significantly increased in SD group compared to sham rats. Furthermore, expression of GAD 65 in EC significantly increased in SD group compared to sham group. However, both GABA-A&alpha and GABA-A&beta subunit receptors didn’t significantly change in that region after SD. Conclusion: These data suggest that SD is able to damage the neuronal cells in neural tissues in juvenile rats and parallelly lead to enhancement of GAD 65 in the central nervous system.

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Introduction: Glioblastoma multiforme (GBM) is the most common and deadliest of malignant primary brain tumors in adults and is one of a group of tumors referred to as gliomas. The National Cancer Institute estimates that 23,000 adults were diagnosed with GBM every year in USA, and less than 5% survive 5 years post-diagnosis. ­Thus, novel therapeutic strategies to target and kill GBM cells are desperately needed to increase the efficiency of therapy. Immunotherapy has the potential of inducing the immunity to remove GBM cells that might have spread throughout the central nervous system. Conclusion: In current review,  the latest developments in preclinical immunotherapy for glioma will be discussed, which involve the local delivery of pro-inflammatory cytokines, such as Flt3L, Type I IFNs, IL-2, IL-4, and IL-12 using gene therapy carriers and neural stem cells, or the blockade of immune-suppressive mediators, such as TGF beta, FasL and phosphorylated STAT3. New immunotherapeutic strategies have also been evaluated in clinical trials applied in GBM patients, which makes it a promising tool in the future treatments for GBM.

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Introduction: Rabies is a fatal neurological disease caused by rabies virus, the prototype of the Lyssavirus genus. Rabies virus (RABV) has tropism to the central nervous system (CNS) and its ability for replication leads to rabies disease. RABV replication in the CNS of majority of mammalian species, including humans, leads to fatal encephalomyelitis. The combination of virulence and pathogenicity factors enables RABV transmission from peripheral bite site to the neurons through the neuro-muscular route and leads to infection of the spinal cord and the brain. Prophylactic or therapeutic vaccine-induced antibodies are able to prevent the virus from entering the CNS. In the absence of neutralizing antibodies induced by the vaccine, the immune system is unable to control the virus after entering the nerve cells. RABV has the innate ability to evade the host immune defense responses and is able to enhance the efficiency of its entry into nerve cells, control host immune responses, and inhibit the antiviral immune stimulation. RABV delays apoptosis by controlling the expression of its proteins and adjusts the survival of infected cells according to its metabolic requirements. These mechanisms enable RABV to escape the host immune system and to proliferate in the neuronal cells. Conclusion: This study review show the different immune mechanisms involved in clearing the CNS from RABV infection and strategies that the virus uses against the host immune system in the CNS. In addition, mechanisms that the virus uses to replicate as well as the interaction of the virus with the host immune system are discussed.

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Developing and promoting self-directed learning, as an one of the goals in higher education is important because it expected from students to reach the high level of individual capabilities, and able to identify their training needs in order to fix it and evaluate their own learning, without being in a special education system. Conclusion: The literature review showed that self-directed learning is growing upward in trend development. Because of the benefits of self-directed learning, paying attention to this type of learning is fundamental for improving it and it is necessary as an important program in higher education.
 

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The term synaptic plasticity points to a series of persistent changes related to the activity of synapses. Long-term potentiation (LTP) is a reflection of synaptic plasticity that has an important role in learning and memory. LTP is a long-lasting increase of synaptic activity due to enhancement of excitatory synaptic transmission after a high-frequency train of electrical stimulations. Different types of LTP have been observed in distinctive areas of the central nervous system of mammals, such as the amygdala, cortex, stratum, cerebellum, and nucleus accumbens. LTP can be divided into N-methyl-D-aspartic acid (NMDA) receptor dependent and NMDA receptor independent (by voltage-dependent calcium channels type L). The LTP process can be differentiated into Early (E-LTP) and Late (L-LTP) phases.The early phase of LTP induced by a single train of stimulation. This phase doesn’t lead to new protein synthesis. The late phase of LTP produced by repeated trains; results in gene expression. Since, the nervous system is a complex network of neurons and glial cells that are communicated with each other, so the molecular communication between these cells requires further studies.
 

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Measuring individual talent is a prerequisite of talent management. In order to do so, there are methods which have been established such as intelligence tests, general and individual tests, ratings scale and the literature of educational performance. Applying these methods are effective, if measurement error is low and validity is high. All current available methods are faced with issues related to inaccurate talent measurement. Issues of methodology in tools for talent identification will be discussed, such as ambiguity in the conceptual definition of talents, how to design a question, how to estimate reliability, and how to collect evidence of validity. Through an investigation of these theories, a solution for accurate talent measurement emerges.
 

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Introduction: Long-term potentiation (LTP) is a generic term that applies to a form of activity-dependent plasticity that induced by high-frequency or theta burst stimulation and results in enhancement of synaptic transmission. LTP has a key role in learning and memory. Different types of LTP have been observed in distinctive areas of the central nervous system. Hippocampal CA1 area is vital for the formation of long-term memory. Conclusion: Several studies have been shown the importance of signaling pathways in the development of memory and learning. In this review is intended to present an overview of the role of synaptic ion channels, ionotropic and metabotropic glutamate receptors as well as TrkB receptor in LTP formation of learning and memory.

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All humans experience anxiety in your life and it is natural that people get anxious when facing stressful situations threatening, but severe and chronic anxiety in the absence of clear cause, is uncommon. Studies show that anxiety in men and a young person are less privileged economic classes and in women, low-income people and the elderly and children and teenagers are more common. When locating of the new situation as many children face new people, feel anxious. One of the most common anxiety disorders in children and adolescents is social phobia (Social Phobia). This phobia of late childhood or early adolescence begins. They feel ashamed in the face of others, they are worried that their voice Nlrzd and not red. Generally speaking and eating in public, assertiveness off, criticize; comment and mistakes are Trsnd.dr a new study to reduce your anxiety aware of the mechanisms used. Such as efforts to control anxiety, self-conscious way of dealing with anxiety, personal plans are changing philosophies of life, the application of physical and mental exercises and instructions on the basis of defense mechanisms based psychiatrists.

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Introduction: Asymptomatic carotid artery stenosis is one of the factors that causes stroke. Other factors such as high blood pressure, cardiac diseases, smoking, diabetes, and physical inactivity may also cause the disease. Understanding and identifying the factors that cause carotid artery stenosis will help in prevention of acute stroke. Using data mining techniques, this study was aimed to discover the rules and relations that are effective in identifying asymptomatic carotid artery stenosis. Materials and Methods: To find the best approach, logistic regression (LR), genetic algorithm (GA), and chi-square test were used to predict carotid artery stenosis in patients. Results: 372 participants, 173 women (% 46.5) and 199 men (% 53.5), with an average age of 70.74± 5.29 were investigated. The results showed gender, smoking, coronary artery disease, high blood pressure, inactivity, prevention of pregnancy by medication, uremia (excessive amounts of urea and other nitrogenous compounds in the blood), and pulse rate environment are the significant risk factors for asymptomatic carotid artery. In addition, GA was a better method for this approach compared to LR. Conclusion: Our study revealed that coronary artery disease and hypertension are important factors in predicting and prognosis of asymptomatic carotid artery stenosis.