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Test is the majority of student’s life and test anxiety is an experience that has commonly been observed during exams. In fact, anxiety is a vague feeling and very uncomfortable that so often considered to be associated with one or more physical sense, for instance, the empty feeling of heart palpitations, headache and sweating. The purpose of this study is to investigate and to compare the self-efficacy beliefs and coping styles among students with high test anxiety. This study is a cross-sectional comparison. The study population consisted of all high school students in Tehran studying in 2014. Subjects consisted of 52 students with high test anxiety and 52 students were normal using matching method (based on sex, age, school grade, school and socio-economic status). Information about the variables of interest was collected through questionnaires of general self-efficacy Sherer and colleagues and coping with stress questionnaire (CISS). Results of multivariate analysis of variance showed that the two groups of students in self-efficacy and coping style, there is a significant difference (P≤0.01). This means that students with high test anxiety are more likely to experience low levels of self-efficacy and had avoidant emotion-focused coping styles. While normal students have a higher self-efficacy and coping styles is a problem-focused. These results may have important implications in the field of education and counseling services for students with high test anxiety. Problem-focused coping skills in schools can increase self-efficacy in terms of life skills training to prevent test anxiety. A regular program of teaching them to cope properly and efficiently may help reducing anxiety and increasing the level of self-efficacy in students.

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Cerebral ischemia causes death of millions people all over the world, annually and also suffering more people from neurological deficits and neuromuscular disorders. In our country, 250 to 300 people experience mild to severe stroke, daily. In this study we reviewed 120 original paper selected from PubMED database. Our keywords were erythropoietin, anti-inflammatory, stroke, neuropathy and cerebral ischemia. Studies have been revealed that anti-inflammatory and neuroprotection effects of erythropoietin are mediated by receptors that available in cerebral cortex, spinal cord, hypothalamus and hippocampus. These effects include the ability to repair neural inflammation, prevention of neural cell death, preservation of surviving neural cells, regulation of neurogenesis, anti-apoptosis and anti-coagulation. Erythropoietin also prevents Alzheimer's disease, Parkinson's disease, epilepsy, multiple sclerosis, and other motor diseases. All studies showed that erythropoietin has anti-inflammatory and neuroprotection properties and can decrease probability of cerebral ischemia, impressively. Today, erythropoietin is considered as an attractive and effective therapeutic approach to cerebral ischemia; one of the most common causes of morbidity and mortality around the world.

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Introduction: The prenatal stress is a key factor which affects the growth and function of the brain. Several studies have shown that prenatal stress induces deficits in learning and memory of the offspring. The prenatal stress alters the activity of neurotransmitters, such as noradrenaline, dopamine and serotonin, via over-activation of the hypothalamic–pituitary–adrenal axis. In addition, the prenatal stress reduces the values of various hippocampal proteins involved in learning and memory and long-term potentiation, like brain-derived neurotrophic factor, Ca2+/calmodulin dependent protein kinase II, postsynaptic density protein 95, and cAMP response element-binding protein. It seems that exercise, environmental enrichment, and antioxidants could improve learning and memory deficits induced by the prenatal stress in offspring. Conclusion: Interventions to protect the offspring against stress is crucial to preserve their cognitive abilities.

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Introduction: Parkinson's disease is a common neurodegenerative disorder. In this disease, mitochondrial defects and oxidative stress lead to the enhancement of the free radicals and the death of dopamine neurons in the Sabstantia nigra. The clinical symptoms of this disease are including tremor, muscle stiffness, and inability to walk as well as cognition, memory and learning deficits. Aging increases the severity of Parkinson's disease. Conclusion: Any therapeutic strategy which can modulate antioxidant homeostasis and neuroprotection may increase the life expectancy and quality of life of patients with Parkinson's disease.

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Introduction: The prevalence of early symptoms of Parkinson's disease, even in middle age and adolescence, has caused widespread concern. Physical activity is known as one of the non-pharmacological methods to reduce behavioral, motor, biochemical, cardiovascular, and mitochondrial dysfunctions in Parkinson's disease. Although the basis of such biological and molecular benefits is unknown, the antioxidant and anti-inflammatory properties of physical activity may improve the symptoms of Parkinson's disease. Conclusion: Although there is no definitive cure for Parkinson's disease, the use of medications along with adjunctive therapies, such as exercise, can be resulted in promising improvements. However, more research is required to achieve an exercise program that provides optimal benefits to patients' quality of life and reduces mortality.

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Introduction: Oxidative stress (OS) is one of the main factors of neuronal damage during cerebral ischemia. OS leads to the formation of reactive oxygen species (ROS) and triggers several destructive mechanisms, including mitochondrial dysfunction, elevated calcium levels, reperfusion injury, and inflammation. This study aimed to investigate the effects of eight weeks of endurance training on the expression of malondialdehyde (MDA) and superoxide dismutase (SOD) in the hippocampus of rats following ischemic stroke. Materials and Methods: In this experimental study, 21 adult male Wistar rats were randomly assigned to three groups: control, stroke, and stroke + training. Brain ischemic stroke was induced by occluding both common carotid arteries (CCA) for 45 minutes. The training group underwent treadmill running at speeds ranging from 18 to 30 meters per minute, with sessions lasting 20 to 50 minutes, five days per week for eight weeks. Forty-eight hours after the final training session, the rats were sacrificed, and the gene expression of SOD and protein expression of MDA in the hippocampus were analyzed. Results: Ischemic stroke resulted in a significant increase in MDA protein expression and a decrease in SOD gene expression in the hippocampus of rats compared to the control group. However, endurance training significantly reduced MDA protein expression and enhanced SOD gene expression in the hippocampus of rats following ischemic stroke. Conclusion: Endurance training increased SOD gene expression and decreased MDA protein expression, leading to reduced OS and enhanced antioxidant defense in rats following brain ischemic stroke. These findings highlight the potential of physical exercise as a therapeutic strategy for reducing oxidative damage after ischemic events.