OTHERS_CITABLE
Review Paper: Polyphenolic Antioxidants and Neuronal Regeneration
Many studies indicate that oxidative stress is involved in the pathophysiology of neurodegenerative diseases. Oxidative stress can induce neuronal damages, modulate intracellular signaling and ultimately leads to neuronal death by apoptosis or necrosis. To review antioxidants preventive effects on oxidative stress and neurodegenerative diseases we accumulated data from international medical journals and academic informations' sites. According to many studies, antioxidants could reduce toxic neuronal damages and many studies confirmed the efficacy of polyphenol antioxidants in fruits and vegetables to reduce neuronal death and to diminish oxidative stress. This systematic review showed the antioxidant activities of phytochemicals which play as natural neuroprotectives with low adverse effects against some neurodegenerative diseases as Parkinson or Alzheimer diseases.
http://bcn.iums.ac.ir/article-1-492-en.pdf
2016-04-01
81
90
10.15412/J.BCN.03070201
Curcumin
Alzheimer
Resveratrol
Oxidative stress
Amin
Ataie
ataieamin@yahoo.com
1
Cellular and Molecular Research Center, Babol University of Medical Sciences, Babol, Iran.
AUTHOR
Ramin
Ataee
raminataee1349@gmail.com
2
Department of Pharmacology and Toxicology, Pharmaceutical Sciences Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
AUTHOR
Mohammad
Shadifar
shadan220@yahoo.com
3
Amol Center, Pasteur Institute of Iran, Amol, Iran.
AUTHOR
OTHERS_CITABLE
Review Paper: Association of Transforming Growth Factor Beta-1 -509C/T Gene Polymorphism with Ischemic Stroke: A Meta Analysis
Introduction: Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS.
Methods: A review of literature for eligible genetic association Studies published before October 20, 2014 was conducted in the PubMed, EMBASE, Google Scholar and Trip database. The strength of association was calculated by pooled odds ratios (ORs) with 95% confidence intervals using RevMan 5.3 software. Heterogeneity was examined using Higgins I-squared, Tau-squared, and Chi-squared tests.
Results: A total of 2 studies involving 614 cases and 617 controls were found. The overall estimates did not show any significant relation between TGF-β1-509C/T polymorphism and risk of IS under dominant (CC+CT vs. TT: OR=1.01, 95%CI=0.31 to 3.26; P=0.99), recessive (CC vs. CT+TT: OR=0.94, 95%CI=0.47 to 1.90; P=0.87), and allelic models (T vs. C: OR=1.06, 95%CI=0.55 to 2.04; P=0.86).
Conclusion: This meta-analysis showed that TGF-β1-509C/T gene polymorphism no significant association with the susceptibility of IS. Further well-designed prospective studies with larger sample size are needed to confirm these findings.
http://bcn.iums.ac.ir/article-1-552-en.pdf
2016-04-01
91
96
10.15412/J.BCN.03070202
Transforming growth factor beta
Cytokine
Inflammation
Cerebral infarction
Ischemic stroke
Single nucleotide polymorphism
Metaanalysis
Pradeep
Kumar
pradeephuptaneuro@gmail.com
1
Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.
AUTHOR
Amit
Kumar
amits52003@gmail.com
2
Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.
AUTHOR
Mukesh Kumar
Srivastava
sriwastva.mukesh6@gmail.com
3
Department of Neurobiochemistry, All India Institute of Medical Sciences, New Delhi, India.
AUTHOR
Shubham
Misra
4
Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.
AUTHOR
Kameshwar
Prasad
kp0704@gmail.com
5
Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.
AUTHOR
Awadh
Kishor Pandit
akpandit.med@gmail.com
6
Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.
AUTHOR
OTHERS_CITABLE
Effect of Gallic Acid on Dementia Type of Alzheimer Disease in Rats: Electrophysiological and Histological Studies
Introduction: To study the effect of gallic acid (GA) on hippocampal long-term potentiation (LTP) and histological changes in animal model of Alzheimer disease (AD) induced by betaamyloid (Aβ).
Methods: Sixty-four adult male Wistar rats (300±20 g) were divided into 8 groups: 1) Control (Cont); 2) AD; 3) Sham; 4-7) AD+GA (50, 100, and 200 mg/kg for 10 days, orally) or vehicle, 8) Cont+GA100, Aβ (1μg/μL in each site) was infused into hippocampus bilaterally. Changes of amplitude and slope of LTP induced in hippocampal dentate gyrus (DG) were evaluated by high frequency stimulation (HFS) of perforant path (PP).
Results: Data showed that LTP amplitude and area under curve significantly impaired in AD rats (P<0.001), while significantly improved in AD rats treated with GA (P<0.05, P<0.01).
Conclusion: Current findings suggest that GA reduces neural damage and brain amyloid neuropathology and improves cognitive function via free radicals scavenging and inhibiting oligomerization of Aβ but with no effect on healthy rats.
http://bcn.iums.ac.ir/article-1-579-en.pdf
2016-04-01
97
106
10.15412/J.BCN.03070203
Alzheimer disease
Beta-amyloid
Long-term potentiation
Neuronal apoptosis
Rat
Somayeh
Hajipour
1
Physiology Research Center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
Alireza
Sarkaki
sarkaki_a@yahoo.com
2
Physiology Research Center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
Yaghoob
Farbood
y_farbood@yahoo.com
3
Physiology Research Center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
Akram
Eidi
akram_eidi@yahoo.com
4
Department of Biology, Science & Research Branch, Islamic Azad University, Tehran, Iran.
AUTHOR
Pejman
Mortazavi
sp.mortazavi@gmail.com
5
Department of Pathology, Faculty of Specialized Veterinary Science, Science & Research Branch, Islamic Azad University, Tehran, Iran.
AUTHOR
Zohreh
Valizadeh
valizadeh_z@yahoo.com.
6
Department of Nursing and Midwifery, Dezfoul Branch, Islamic Azad University, Dezfoul, Iran.
AUTHOR
OTHERS_CITABLE
A Grey Box Neural Network Model of Basal Ganglia for Gait Signal of Patients with Huntington Disease
Introduction: Huntington disease (HD) is a progressive neurodegenerative disease which affects movement control system of the brain. HD symptoms lead to patient’s gait change and influence stride time intervals. In this study, we present a grey box mathematical model to simulate HDdisorders. This model contains main physiological findings about BG.
Methods: We used artificial neural networks (ANN) and predetermined data to model healthy state behavior, and then we trained patients with HD with this model. All blocks and relations between them were designed based on physiological findings.
Results: According to the physiological findings, increasing or decreasing model connection weights are indicative of change in secretion of respective neurotransmitters. Our results show the simulating ability of the model in normal condition and diferent disease stages.
Conclusion: Fine similarity between the presented model and BG physiological structure with its high ability in simulating HD disorders, introduces this model as a powerful tool to analyze HD behavior.
http://bcn.iums.ac.ir/article-1-519-en.pdf
2016-04-01
107
114
10.15412/J.BCN.03070204
Basal ganglia
Huntington disease
Neural network models
Neurotransmitters
Abbas
Pourhedayat
a.pourhh@gmail.com
1
Department of Mechatronics Engineering, School of Engineering-Emerging Technologies, University of Tabriz, Tabriz, Iran.
AUTHOR
Yashar
Sarbaz
yashar.sarbaz@tabrizu.ac.ir
2
Department of Mechatronics Engineering, School of Engineering-Emerging Technologies, University of Tabriz, Tabriz, Iran.
AUTHOR
OTHERS_CITABLE
Brain Derived Neurotrophic Factor Modification of Epileptiform Burst Discharges in a Temporal Lobe Epilepsy Model
Introduction: Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS.
Methods: Male Wistar rats were divided into sham (receiving phosphate buffered saline within dorsal hippocampus), pilocarpine (epileptic model of TLE), single injection BDNF (epileptic rats which received single high dose of BDBF within dorsal hippocampus), and multiple injections BDNF (epileptic rats which received BDNF in days 10, 11, 12, and 13 after induction of TLE) groups. Their electrocorticogram was recorded and amplitude, frequency, and duration of spikes were evaluated.
Results: Amplitude and frequency of epileptiform burst discharges were significantly decreased in animals treated with BDNF compared to pilocarpine group.
Conclusion: Our findings suggested that BDNF may modulate the epileptic activity in the animal model of TLE. In addition, it may have therapeutic effect for epilepsy. More studies are
necessary to clarify the exact mechanisms of BDNF effects.
http://bcn.iums.ac.ir/article-1-529-en.pdf
2015-07-18
115
120
10.15412/J.BCN.03070205
Temporal lobe epilepsy
BDNF
EEG
Brain
Rat
Sanaz
Eftekhari
sanaz.eftekhari8@gmail.com
1
Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
AUTHOR
Soraya
Mehrabi
soraya.mehrabi@gmail.com
2
Shefa Neuroscience Center, Khatam-Alanbia Hospital, Tehran, Iran.
AUTHOR
Fariba
Karimzadeh
fariba_karimzade@yahoo.com
3
Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
AUTHOR
Mohammad-Taghi
Joghataei
mt.joghataei@yahoo.com
4
Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
AUTHOR
https://orcid.org/0000-0003-0492-8239
Mojtaba
Khaksarian
5
Department of Physiology, School of Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran.
AUTHOR
Mahmoud Reza
Hadjighassem
6
Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Majid
Katebi
7
Department of Anatomy, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
AUTHOR
Mansooreh
Soleimani
mansourehsoleimani@gmail.com
8
Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
AUTHOR
OTHERS_CITABLE
Pathophysiological Concepts in Multiple Sclerosis and the Therapeutic Effects of Hydrogen Sulfide
Introduction: Multiple sclerosis (MS) is generally known as a manageable but not yet curable autoimmune disease affecting central nervous system. A potential therapeutic approach should possess several properties: Prevent immune system from damaging the brain and spinal cord, promote differentiation of oligodendrocyte progenitor cells (OPCs) into mature oligodendrocytes to produce myelin, prevent the formation of fibronectin aggregates by astrocytes to inhibit scar formation, and enhance function of healthy endothelial cells (ECs).
Methods: To determine if an increase in sulfur contents through H2S, a potent antioxidant known to induce protective autophagy in cells, could provide the above desired outcomes, peripheral blood mononuclear cells (PBMNCs), OCPs, astrocytes, and ECs were treated with NaHS (50 μM) in vitro.
Results: Transmigration assay using EC monolayer showed that serotonin increased migration of PBMNC while pretreatment of EC with NaHS inhibited the migration induced by serotonin treatment. NaHS upregulated proteins involved in immune system response and downregulated PBMNCs- and EC-related adhesion molecules (LFA-1 and VCAM-1). Furthermore, it had a cell expansion inducing effect, altering EC morphology. The effects of NaHS on OPCs and astrocytes were studied compared to mTOR inhibitor rapamycin. In NaHS treated astrocytes the induced fibronectin production was partially inhibited while rapamycin almost fully inhibited fibronectin production. NaHS slowed but did not inhibit the differentiation of OCPs or the production of myelin compared to rapamycin.
Conclusion: The in vitro results point to the potential therapeutic application of hydrogen sulfide releasing molecules or health-promoting sulfur compounds in MS.
http://bcn.iums.ac.ir/article-1-643-en.pdf
2016-04-01
121
136
10.15412/J.BCN.03070206
NaHS
Fibronectin
Myelin
Astrocytes
Oligodendrocytes
HUVEC
Peripheral Blood Mononuclear Cells
Fatemeh
Talaei
Talaei@irimc.org
1
Novel Drug Delivery Systems Lab, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
OTHERS_CITABLE
Elevated IL-17 and TGF-β Serum Levels: A Positive Correlation between T-helper 17 Cell-Related Pro-Inflammatory Responses with Major Depressive Disorder
Introduction: Depression is a mental disorder that highly associated with immune system. Therefore, this study compares the serum concentrations of IL-21, IL-17, and transforming growth factor β (TGF-β) between patients with major depressive disorder and healthy controls.
Methods: Blood samples were collected from 41 patients with major depressive disorder and 40 healthy age-matched controls with no history of malignancies or autoimmune disorders. The subjects were interviewed face to face according to DSM-IV diagnostic criteria. Depression score was measured using completed Beck Depression Inventory in both groups. The serum concentrations of IL-21, IL-17, and TGF-β were assessed using ELISA.
Results: The mean score of Beck Depression score in the patient and control groups was 35.4±5.5 and 11.1±2.3. IL-17 serum concentrations in the patients and the control group were 10.03±0.6 and 7.6±0.6 pg/mL, respectively (P=0.0002). TGF-β level in the patients group was significantly higher than compare to the control group; 336.7±20.19 vs. 174.8±27.20 pg/mL, (P<0.0001). However, the level of IL-21 was not statistically different between the two groups 84.30±4.57 vs. 84.12±4.15 pg/mL (P>0.05).
Conclusion: Considering pro-inflammatory cytokines, current results support the associationof inflammatory response and depressive disorder. So, it seems that pro-inflammatory factors profile can be used as indicator in following of depression progress and its treatment impacts.
http://bcn.iums.ac.ir/article-1-640-en.pdf
2016-04-01
137
142
10.15412/J.BCN.03070207
Major depressive disorder
Interleukin-17
interleukin-21
Transforming growth factor-beta
Inflammatory response
Mohammad Hasan
Davami
davamimh@gmail.com
1
Department of Immunology and Microbiology, School of Medicin, Jahrom University of Medical Sciences, Jahrom, Iran.
AUTHOR
Rasoul
Baharlou
Baharlour@gmail.com
2
Department of Immunology and Microbiology, School of Medicin, Jahrom University of Medical Sciences, Jahrom, Iran.
AUTHOR
Abbas
Ahmadi Vasmehjani
a.vasmehjani23@yahoo.com
3
Department of Immunology and Microbiology, School of Medicin, Jahrom University of Medical Sciences, Jahrom, Iran.
AUTHOR
Ahmad
Ghanizadeh
ghanizad@tums.ac.ir
4
Department of Psychiatry, School of Medicin, Shiraz University of Medical Sciences, Shiraz, Iran.
AUTHOR
Mitra
Keshtkar
baharlour@hotmail.com
5
Department of Psychiatry, School of Medicin, Jahrom University of Medical Sciences, Jahrom, Iran.
AUTHOR
Iman
Dezhkam
i.dezhkam@gmail.com
6
Department of Student Research Committee, School of Medicine, Jahrom University of Medical Sciences, Jahrom, Iran.
AUTHOR
Mohammad Reza
Atashzar
mr.atashzar@yahoo.com
7
Department of Student Research Committee, School of Medicine, Jahrom University of Medical Sciences, Jahrom, Iran.
AUTHOR
OTHERS_CITABLE
Methodological Note: Neurofeedback: A Comprehensive Review on System Design, Methodology and Clinical Applications
Neurofeedback is a kind of biofeedback, which teaches self-control of brain functions to subjects by measuring brain waves and providing a feedback signal. Neurofeedback usually provides the audio and or video feedback. Positive or negative feedback is produced for desirable or undesirable brain activities, respectively. In this review, we provided clinical and technical information about the following issues: (1) Various neurofeedback treatment protocols i.e. alpha, beta, alpha/theta, delta, gamma, and theta; (2) Different EEG electrode placements i.e. standard recording channels in the frontal, temporal, central, and occipital lobes; (3) Electrode montages (unipolar, bipolar); (4) Types of neurofeedback i.e. frequency, power, slow cortical potential, functional magnetic resonance imaging, and so on; (5) Clinical applications of neurofeedback i.e. treatment of attention deficit hyperactivity disorder, anxiety, depression, epilepsy, insomnia, drug addiction, schizophrenia, learning disabilities, dyslexia and dyscalculia, autistic spectrum disorders and so on as well as other applications such as pain management, and the improvement of musical and athletic performance; and (6) Neurofeedback softwares. To date, many studies have been conducted on the neurofeedback therapy and its effectiveness on the treatment ofmany diseases. Neurofeedback, like other treatments, has its own pros and cons. Although it is a non-invasive procedure, its validity has been questioned in terms of conclusive scientific evidence. For example, it is expensive, time-consuming and its benefits are not long-lasting. Also, it might take months to show the desired improvements. Nevertheless, neurofeedback is known as a complementary and alternative treatment of many brain dysfunctions. However, current research does not support conclusive results about its efficacy.
http://bcn.iums.ac.ir/article-1-608-en.pdf
2016-04-01
143
158
10.15412/J.BCN.03070208
Brain diseases
Brain waves
Complementary therapies
Electroencephalography
Neurofeedback
Hengameh
Marzbani
marzbani_88@gmail.com
1
Department of Biomedical Engineering, Faculty of Engineering, University of Isfahan, Isfahan, Iran.
AUTHOR
Hamid Reza
Marateb
h.marateb@eng.ui.ac.ir
2
Department of Biomedical Engineering, Faculty of Engineering, University of Isfahan, Isfahan, Iran.
AUTHOR
Marjan
Mansourian
j_mansourian@hlth.mui.ac.ir
3
Department of Biostatistics and Epidemiology, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran.
AUTHOR
OTHERS_CITABLE
Case Report: Iatrogenic Seeding of Tumor Cells in Thigh Soft Tissue Upon Surgical Removal of Intracranial Meningioma
Introduction: Meningioma is a benign and slowly-growing tumor that is responsible for 20% of brain neoplasms. It can be accompanied by some genetic disorders such as neurofibromatosis type 2 and is more common among women. As a space occupying lesion, it produces a wide range of signs and symptoms by compressing the adjacent and underlying tissues in the brain. Trauma and viruses are possible etiologies for meningioma. The ideal treatment of benign meningioma is surgical resection.
Case Presentation: In this case report, we present a middle-aged man with a seeding metastasis of the cranial meningioma (after its removal) in the left thigh. During the removal operation, fascia lata had been used to repair the dura mater and the skin defect was repaired primarily.
Conclusion: We believe that the occurrence of meningioma at the site of incision in the thigh is related to using the same surgical instruments for the removal of the brain tumor.
http://bcn.iums.ac.ir/article-1-444-en.pdf
2016-04-01
159
164
10.15412/J.BCN.03070209
Meningioma
Seeding
Implantation
Ghodratollah
Maddah
1
Endoscopic and Minimally Invasive Surgery Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Hossein
Shabahang
2
Endoscopic and Minimally Invasive Surgery Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Vahid
Zehi
emis@mums.ac.ir
3
Endoscopic and Minimally Invasive Surgery Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Nouriyeh
Sharifi Sistani
4
Department of Pathology, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
Hossein
Mashhadi Nejad
5
Department of Neurosurgery, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
AUTHOR
OTHERS_CITABLE
Case Report: Hallervorden–Spatz Syndrome with Seizures
Hallervorden-Spatz syndrome is a disorder characterized by dystonia, parkinsonism, and iron accumulation in the brain. The disease is caused by mutations in gene encoding pantothenate kinase 2 (PANK2) and patients have pantothenate kinase-associated neurodegeneration. We present an 8-year-old boy with progressive muscle dystonia, neuroregression, frequent fall and
multiple injury marks of different stages. Seizures are rare with PANK2. This child had seizure onset at 4 years of age and seizure free on valproate and levetricetam. The CT scan showed tiger eye appearance and mutations on PANK2 gene.
http://bcn.iums.ac.ir/article-1-535-en.pdf
2016-04-01
165
166
10.15412/J.BCN.03070210
Pantothenate Kinase-Associated Neurodegeneration
Autosomal recessive
Seizures
Sunil
Gothwal
dr.sunilgothwal@gmail.com
1
Department of Pediatrics, All India Institute of Medical Sciences, New Delhi, India.
AUTHOR
Swati
Nayan
dr.swatigothwal@gmail.com
2
Department of Obstetrics and Gynecology, Sawai Man Singh Medical College, Jaipur, Rajasthan, India.
AUTHOR
OTHERS_CITABLE
Case Report: The Effect of Neurofeedback Therapy on Reducing Symptoms Associated with Attention Deficit Hyperactivity Disorder: A Case Series Study
Introduction: This study aimed to evaluate the effectiveness of neurofeedback on attention deficit hyperactivity disorder.
Methods: This is a quasi-experimental study without a control group. The study population included all children aged 5 to 12 years old affected with attention deficit hyperactivity disorders in Tehran, Iran who were referred to psychiatric clinics and given the diagnosis. The sample included 12 children with attention deficit hyperactivity disorder who were selected based on their availability (non-random sampling). They received 30 sessions of neurofeedback treatment, 2 times per week. Before and after neurofeedback training, the children were evaluated and compared with the use of cognitive assessment system test. Data were analyzed using dependent T-test.
Results: The total mean score for pretest was 88.81 while the total mean score for the post test was 82.23. The mean in pretest for attention hyperactivity disorder was higher than the mean in the post test. Moreover, The difference of pretest and post test scores of children affected with learning disorder associated with ADHD was calculated that showed significant (P=0.003).
Conclusion: Neurofeedback is effective in the improvement of attention deficit hyperactivity disorder.
http://bcn.iums.ac.ir/article-1-596-en.pdf
2016-04-01
167
171
10.15412/J.BCN.03070211
Attention deficit
Das–Naglieri cognitive assessment system test
Hyperactivity disorder
Neurofeedback
Mostafa
Deilami
1
Deputy of Research and Technology, Ministry of Health and Medical Education, Tehran, Iran.
AUTHOR
Asghar
Jahandideh
2
Deputy of Research and Technology, Ministry of Health and Medical Education, Tehran, Iran.
AUTHOR
Yousef
Kazemnejad
3
Deputy of Research and Technology, Ministry of Health and Medical Education, Tehran, Iran.
AUTHOR
Yousef
Fakour
4
Deputy of Research and Technology, Ministry of Health and Medical Education, Tehran, Iran.
AUTHOR
Shiva
Alipoor
5
Department of Educational Psychology, Islamic Azad University, Saveh Branch, Saveh, Iran.
AUTHOR
Fatemeh
Rabiee
6
Department of General Psychology, Islamic Azad University, Tonekabon Branch, Tonekabon, Iran .
AUTHOR
Ghazal Saadat
Pournesaie
7
Department of General Psychology, Islamic Azad University, Tonekabon Branch, Tonekabon, Iran .
AUTHOR
Rosemarie
Noot Heidari
8
Center for Development of Research & Technology, Deputy of Research & Technology, Ministry of Health and Medical Education, Tehran, Iran.
AUTHOR
Seyed Aliasghar
Mosavi
a.a.mosavi@gmail.com
9
Department of Ophthalmology, Bina Eye Hospital Research Center, Tehran, Iran.
AUTHOR