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Introduction: Traumatic brain injuries may cause some neurological deficits, such as altered level of consciousness or coma, sensory-motor dysfunction, and seizure attacks. The neuroprotective effect of progesterone and erythropoietin has been shown in different types of brain injuries and cerebral ischemia. This study aims to evaluate the probable additional neuroprotective effects of progesterone and erythropoietin after brain injury. Materials and Methods: The effects of progesterone, erythropoietin or the combination of these substances were investigated in 54 male Wistar rats suffering from traumatic brain injury. The effects of drugs were investigated using Modified Neurological Severity Scores as well as counting the number of dark neurons (injured cells) in the hippocampal CA1 and CA3 areas. Results: Our data revealed that the scale of neurological deficits increased by co-application of progesterone and erythropoietin in brain-injured rats. Assessment of dark neurons did not show a significant decrease in the number of dark neurons after combined treatment compared to control groups. Conclusion: Our study showed that the combination therapy did not exhibit any synergistic effect and may worsen the outcome of traumatic brain injury.

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Introduction: Epilepsy has been known as a chronic brain disorder, influences large number of population around the world. Seizures should be treated as soon as possible to avoid the development of chronic epilepsy. Furthermore, there are some complications following surgical resection of epileptic focus and drug treatment. Transcranial magnetic stimulation has been suggested to generate current flow in the brain and could be an alternative to drug treatment or surgery. We study the protective effects of repetitive transcranial magnetic stimulation (rTMS) on seizure attacks and cellular damage in the amygdala in rats. Materials and Methods: In the present study four groups of rats including intact, pentylenetetrazole, rTMS+pentylenetetrazole and rTMS were used to investigate rTMS effects on cellular activity and seizure attacks in a model of epilepsy. The rTMS was applied for a month and then seizures was induced by intraperitoneally injection of pentylenetetrazole and seizure scores were determined. Finally, rats were killed and neuronal injury was evaluated in the amygdala. Results: Seizure scores as well as histological assessment revealed a significant reduction on seizure attacks and the mean number of necrotic cells in the amygdala following rTMS application. Conclusion: This study advocated a protective effect of rTMS on cellular structure in epilepsy. However, safety of rTMS in clinical practice need further investigations.

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Genetic epidemiological studies strongly suggest that additive and interactive genes, each with small effects, mediate the genetic vulnerability for schizophrenia. With the human genome working draft at hand, candidate gene (and ultimately large-scale genome-wide) association studies are gaining renewed interest in the effort to unravel the complex genetics of schizophrenia. Linkage and fine mapping studies have established that the neuregulin 3 gene (NRG3) is a susceptibility locus for schizophrenia. Association studies of this disorder have implicated NRG3 variants in both psychotic symptoms and attention performance. These animals show increases in reaction time (RT) variability and false alarms on choice reaction time (CRT) tasks. The aims of the present study were to extend analysis of the association between NRG3 and psychotic symptoms and attention in animal model of schizophrenia. Twenty-one-day-old male Wistar rats were either reared in individual cages (isolated rats) or in group cages of six per cage (group-housed rats) for 8 weeks. After the CRT test and decapitation of brain, symptoms and performance scores were then tested for association with the NRG3 variant rs6584400 by polymerase chain reaction method. A significant association was found between the number of rs6584400 DNA and the CRT for reaction time in post weaning social isolation rats.

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Transactional analysis (TA) is a theory of personality that can be applied in virtually all fields of psychology: educational, counseling, organizational and psychotherapy. The atmosphere that supports transactional analysis is one of comfort, security and respect. A positive relationship is forged between the clinician and the client in order to provide a model for subsequent relationships that are developed outside the therapy arena. TA group therapy techniques can help the psychosocial patient such as child anxious, personality disorder. In this study reviewed post-traumatic stress disorder (PTSD) patients that had personality disorder and other psychological disorder also TA group therapy techniques on improvement of personality disorder. Post-traumatic stress disorder is classified as an anxiety disorder in the diagnostic and statistical manual of mental disorders (DSM V) the characteristic symptoms are not present before exposure to the violently traumatic event. Several interviews are available for assessing PTSD. These interviews vary in merit when compared on stringent psychometric and utility standards. Within the overarching framework of transactional analysis, more recent transactional analysts have developed several different and overlapping theories of TA: cognitive, behavioral, relational, redecision, integrative, constructivist, narrative, body-work, positive psychological, personality adaptational, self-reparenting, psychodynamic, and neuroconstructivist. Adult ego in PTSD state enables us to form a narrative self or coherent sense of identity. Trauma interferes with this integrative capacity, creating excluded ego states and a disorganized self.

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Schizophrenia is a severe psychiatric illness with a lifetime prevalence of ˜1% that imposes a huge toll on patients, their families and public health services worldwide. Delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior and negative symptoms constitute the core symptoms of schizophrenia. Although the neurotransmitter dopamine plays a prominent role in the pathogenesis and treatment of schizophrenia, the dopamine hypothesis of schizophrenia fails to explain all aspects of this disorder. Neuropsychopharmacological studies have focused on the role of different neurotransmitter systems in schizophrenia and led to hypotheses as to the causes of this disorder. Since the beginning of the last century, acetylcholine has been recognized as a neurotransmitter both in the CNS as well as the peripheral nervous system. Acetylcholine is synthesized in neurons from acetyl-CoA and choline in a reaction catalyzed by the enzyme choline acetyl transferase, an enzyme that is almost exclusively located in high concentrations in cholinergic neurons. Evidence for an involvement of the muscarinic cholinergic receptors in schizophrenia has been gained from the study of CNS tissue obtained postmortem. Few studies have so far assessed the distribution of cholinergic neurons in schizophrenia. This review will focus on evidence that supports the hypothesis that the muscarinic system is involved in the pathogenesis of schizophrenia and that muscarinic receptors may represent promising novel targets for the treatment of this disorder.

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Obsessive-compulsive disorder (OCD) is a psychiatric disorder manifested by thoughts and impulses that produce anxiety and result in patients performing repetitive rituals. Treatment generally consists of cognitive behavioral intervention and serotonin reuptake inhibitors. Up to 40% of patients will have functional impairment that significantly affects their quality of life. In the late 1990’s, based on positive research results in anterior capsulotomies, deep brain stimulation (DBS) researchers first implanted electrodes in the anterior capsule of treatment-resistant OCD patients. The early results were promising. Three of the first four patients experienced benefit. A worldwide study found that out of 26 patients with treatment-resistant OCD, 61.5% responded positively to DBS. This response rate is similar to the other surgeries described above. However, comparisons must be tentative since the number of patients treated with DBS is still relatively small. In this review we discuss about the target area of DBS in OCD. Since then, larger trials have been done and the target area of the brain has moved slightly to an overlapping part of the brain called the ventral capsule/ventral striatum.

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Traumatic brain injury (TBI) initiates a cascade of numerous pathophysiological events that evolve over time. Despite the complexity of TBI, research aimed at therapy development has almost exclusively focused on single therapies, all of which have failed in multicenter clinical trials. A variety of brain insults, including traumatic brain injury, encephalitis, stroke, and status epilepticus (SE), have the potential to induce the development of epilepsy, particularly temporal lobe epilepsy (TLE) in humans and rodent models of TLE. The mechanisms underlying this process, which is termed epileptogenesis, are only incompletely understood, but include inflammation, neurodegeneration, blood–brain barrier disruption, alterations in expression and function of diverse receptors and ion channels, and development of hyperexcitability of neurons and neuronal circuits. The goal of the present study was to directly address this hypothesis by treating rats with the NKCC1 inhibitor bumetanide after a TBI. For the present experiments, Wistar rats, weighing 200–230 gr must be used. As previous studies on animal model of TBI treat by co-administration of dose dependent bumetanide and dexamethasone. Predict result: the result may show dexamethasone can inhibition second injury also combination of these two drugs may have reduction and inhibition of neural injury and inflammatory process. Co-administration of dose dependent bumetanide and Dexamethasone may have therapeutic role in traumatic brain injury.

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Traumatic brain injuries may cause some neurological deficits, such as altered level of consciousness or coma, sensory-motor dysfunction, and seizure attacks. The neuroprotective effect of progesterone and erythropoietin has been shown in different types of brain injuries and cerebral ischemia. This study aims to evaluate the probable additional neuroprotective effects of progesterone and erythropoietin after brain injury. The effects of progesterone, erythropoietin or the combination of these substances were investigated in 54 male Wistar rats suffering from traumatic brain injury. The effects of drugs were investigated using modified neurological severity scores as well as counting the number of dark neurons (injured cells) in the hippocampal CA1 and CA3 areas. Our data revealed that the scale of neurological deficits increased by co-application of progesterone and erythropoietin in brain-injured rats. Assessment of dark neurons did not show a significant decrease in the number of dark neurons after combined treatment compared to control groups. Our study showed that the combination therapy did not exhibit any synergistic effect and may worsen the outcome of traumatic brain injury. Details of this study were published (Nourzad, et al. 2014).

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To determine whether teenagers and young adults with attention deficit hyperactivity disorder (ADHD) have more motor vehicle citations and crashes and are more careless drivers than their normal peers. In fact, studies have found that teenagers and adults with attention deficit disorder are nearly twice as likely as the general population to have had their licenses suspended. People with ADHD have serious difficulties planning ahead, following through, and staying on task things you need to do to drive safely. Parent ratings of current symptoms of ADHD, oppositional defiant disorder, and conduct disorder, a survey of various negative driving outcomes, and a rating scale of driving behavior. ADHD, and especially its association with oppositional defiant disorder/conduct disorder, is associated with substantially increased risks for driving among teenagers and young adults and worthy of attention when clinicians counsel such patients and their parents.

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The paper discusses the use of modern information technologies, and in particular geographic information systems (GIS), in the management and control of major accident risk. For this purpose, the regulatory framework of the recent “Seveso II” Directive is briefly described. The referencing in space of the phenomena may be defined in terms of a geometrically exact or a relative location. The former uses local or world coordinate systems defined using a standard system of spheroids, projections, and coordinates which give an approximation of the form of the earth (a spheroid) onto a flat surface. The coordinate system may be purely local, measured in tens of meters, or it may be a national grid or an internationally accepted projection that uses geometrical coordinates of latitude and longitude. This paper places the concept of transportation GIS in the broader perspective of research in GIS and Geographic Information Science. The emphasis is placed on the requirements specific of the transportation domain of application of this emerging information technology as well as on core research challenges.

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Introduction: A typical absence epilepsy is a type of nonconvulsive and generalized epilepsy. The main feature of these attacks is a sudden brief impairment of consciousness. The disturbances in thalamocortical loop play an important role in pathogenesis of absence seizures. However, it is not clear that which part of this network triggers the seizure. This study was aimed to investigate the role of latrodorsal (LD) thalamic neurons during spike and wave discharges (SWDs) in WAG/Rij rats, as the most valid animal model of absence epilepsy. Materials and Methods: Single unit activities in the LD thalamic nucleus and electrocorticogram of somatosensory cortex were simultaneously recorded in six-month-old WAG/Rij rats. Results: During SWDs, unit activity in the LD thalamic nucleus showed burst-like discharges, which were started before the peak component of SWDs. In SWD-free periods, burst like activity in the LD was reduced. Conclusion: Our findings suggest that the burst firing of LD may stimulate the neocortex to exhibit SWDs. It can be concluded that inhibition of burst firing of LD neurons may reduce the frequency of SWDs.

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Long-term potentiation (LTP) is a process that certain types of synaptic stimulation lead to a long-lasting enhancement in the strength of synaptic transmission. Studies in recent years indicate the importance of molecular pathways in the development of memory and learning. Tropomyosin receptor kinase B (TrkB) is a member of the neurotrophin receptor tyrosine kinase family, that its ligand is brain-derived neurotrophic factor (BDNF). In recent years, Research has been shown that TrkB has an important role in LTP formation in hippocampus and after ligand binding activates several intracellular signaling cascades. Three important intracellular signaling cascades are triggered by the TrkB receptor includes: Ras–mitogen activated protein kinase (MAPK) pathway, phosphatidylinositol 3‑kinase (PI3K)-Akt pathway and PLCγ-Ca 2+ pathway.
 

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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 stimulation. The role of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in excitatory synaptic transmission and LTP formation uncovered over recent decades. The activity regulation of AMPA receptors (AMPARs) has a significant role in the LTP induction. AMPARs are homomeric or heteromeric receptors combined of four subunits GLUA1 to GLUA4. GluR1 have a critical role in LTP formation in the CA1 region of hippocampus and is necessitated for synaptic delivery of AMPA receptors.

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Long-term potentiation (LTP) is a form of activity dependent plasticity that induced by high-frequency stimulation or theta burst stimulation and results in synaptic transmission. Several Studies have been shown that LTP is one of the most important processes in the CNS that plays an important role in learning and memory formation. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a major synaptic protein that involved in many signaling cascades and has an important role in the induction of LTP and certain forms of learning. This kinase consist of 12 subunits (alpha and beta) and activated by calcium-calmodulin and expressed presynaptically and postsynaptically. In one of the most important pathways, CaMKII is phosphorylated α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) and increased conductance of the ion-channels. On the other hand, CaMKII increased the insertion of AMPARs at the postsynaptic membrane and enhanced the density of receptors at the neurons. Therefore, CaMKII seems prone to be a mediator of essential significance in connecting transient calcium signs to neuronal plasticity.

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Spinal cord injury (SCI)-induced systemic inflammatory response affects multiple organs outside the spi­nal cord. Treatment options for such complications are lacking. Valproic acid (VPA) is a histone deacetylase inhibitor, acting directly at the level of gene transcription by inhibiting histone deacetylation and making transcription sites more accessible. Acetylation of histones is critical to cellular inflammatory and repair processes. A recent study demonstrated that VPA has effects on neuroprotection and neurogenesis for the treatment of the injured spinal cord. VPA can decreases glial apoptosis, neruoinflammation, neurotoxicity and autophagy during the secondary injury period, and upregulates prosurvival neurotrophic factors. The neuroprotective effects of VPA are interdepend and mediated by HDAC inhibition and GSK-3 inhibition. VPA increased several stages of neurogenesis, including the proliferation of endogenous neural stem cells, neuronal differentiation and maturation, neurite outgrowth, and synaptic integration. In addition, VPA can promote neurogenesis even after spinal cord cells are damaged, by controling the expression of important transcriptional factors and the activation of multiple signaling pathways. Furthermore, the effects and mechanisms of VPA on neuronal excitation mediated neuroprotection and neurogenesis are cooperated and interconnected in treating SCI. It is necessary to optimize VPA treatment processes for SCI on aspects of therapeutic timing, effective dosage, and reliable administration route. Combinatory strategies should be established to maximize the benefits of VPA and to reduce adverse events. Specific criteria must be met prior to translating VPA treatment for SCI from animal experiments to clinical trials.

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Post traumatic stress disorder (PTSD) is a disorder of emotional and mental stress occurring as an outcome of injury or severe emotional shock. Yoga may be useful in decrease of PTSD symptomology. New studies demonstrate that people suffering from PTSD can find actual relief with yoga. Yoga decreases stress-induced allosteric load in three reactive systems of stress: the autonomic nervous system, the hypothalamic-pituitary adrenal axis and the GABAergic system. It is hypothesized that yoga-based practices correct under-activity of the peripheral nerveos system and GABA systems, the primary inhibitory neurotransmitter system, in part through stimulation of the vagus nerves, the main peripheral pathway of the PNS. the decreased PNS and GABAergic activity that underlies stress-related disorders can be corrected by yoga practices resulting in enhancement of disease symptoms. Yoga practice can increase resilience and improve mind-body awareness, which may contribute to changing cognitions and activities. These findings are critical as they address the physiology associated with PTSD. Yoga may develop the functioning of traumatized individuals by assisting them to tolerate physical and sensory experiences associated with distress and helplessness and to increase emotional awareness and affect tolerance.

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Traumatic brain injury (TBI) is a disruption in the brain functions as a result of an external force. To date, the main problem is that no direct effective therapies exist for brain injury treatment. It is thought that stem Cell therapy may provide a promising treatment for TBI. The use of human-derived stem/progenitor cells seeded in three- dimensional (3D) micro-environments have shown as a promising novel method for cell replacement therapy in TBI. The project aims here were to investigate the effects of human neural stem/progenitor cells (hNS/PCs) derived from the resected mesial temporal lobe brain tissues and human adipose-derived stromal/stem cells (hADSCs) cultured in PuraMatrix hydrogel (PM) on brain function in animal models of TBI. By comparing the results of doubling time characteristics of hNS/PCs and hADSCs, revealed that hNS/PCs doubling time was significantly longer than hADSC. Transplantation of hNS/PCs and hADSCs seeded in PM after TBI does seem to improved functional recovery, decreased lesion volume, inhibited neuroinflammation, and reduced the reactive gliosis at the injury site in rats. The data suggest the hNS/PCs derived from epileptic human brain seeded in PM scaffold can be used for the potential cell therapy for neurological disorders, such as TBI.