Nahid Ahmadian, Mahnaz Talebi, Javad Mahmoudi, Saeed Sadig Etegad, Alireza Aghili,
Volume 0, Issue 0 (3-2018)
Abstract
Dementia is a progressive disorder that leads to memory loss and cognition impairment and affects daily function. Alzheimer disease (AD) is the main cause of dementia that characterized by loss of memory and cognition. AD pathologically is demonstrated by neuronal atrophy, synapse loss and the unusual reposition of amyloid-β protein (Aβ) as senile plaques and hyperphosphorylated tau protein as neurofibrillary tangles (NFT). Tau is a microtubule associated protein mostly expressed in neurons. Site-specific phosphorylation regulates Tau function. In AD, the six adult tau isoforms are unusually phosphorylated that cause to form the paired helical filament. The different conditions of tau phosphorylation eventuate from the function of specific kinases and phosphatases. In recent years some biomarkers such as phospho tau 181, 199 and 231 had been assessed in cerebrospinal fluid (CSF) and blood and had been showed their elevation in AD. This article provides an overview of tau structure, functions, and its involvement in AD and its role as a CSF biomarker.
Shilpa Reddy Ganasyam, Manaswini Namilakonda, Sujatha Madireddy, Venkateshwari Ananthapur, Srinadh Buragadda, Sunitha Tella,
Volume 0, Issue 0 (3-2018)
Abstract
Background: Dyslexia is a typical learning disability that does not affect intelligence but causes problems with reading, writing, and spelling. It is influenced by certain genes, due to which several researchers have attempted to identify the susceptible gene. Dyslexia is incurable and diagnosis is difficult because it always overlaps with other learning disabilities. Hence, timely assessment and intervention consequently give the best results. Therefore, our aim was to find the relation between dyslexia and single nucleotide polymorphisms (SNPs) in several candidate genes like DYX1C1, KIAA0319, and DCDC2 in Indian population.
Methods: In the present study, 103 individuals with dyslexia and 100 controls in the age group between 6 to 15 years were taken. Thirteen SNPs in the KIAA gene, seven SNPs of DCDC2, and three SNPs of the DYX1C1 gene were analysed by the Mass Array technique.
Results: The association of dyslexia with SNPs rs3756821, rs6935076, rs4576240 of the KIAA gene was found significant. A significant association was found with rs600753 of the DYX1C1 gene and dyslexia and we could not find any association of the DCDC2 gene with dyslexia.
Conclusions: Prerequisite genetic analysis is necessary for the diagnosis of dyslexia as it is a crucial educational barrier. Treatment is known to be most effective if dyslexia is identified in the early stages for effective intervention for children before they experience prolonged reading failure. Further, it helps in prenatal diagnosis for early intervention.
Dr Sara Banaeeyeh, Professor Bibi Marjan Razavi, Professor Hossein Hosseinzadeh,
Volume 0, Issue 0 (3-2018)
Abstract
Purpose: Alpha-mangostin (α-MG), the most prevalent xanthone found in Garcinia mangostana Linn, has been documented to possess antioxidant and anti-inflammatory properties. This study investigated the protective effects of α-MG against cuprizone (CZ)-induced demyelination in the corpus callosum (CC) of mice, as an animal model of multiple sclerosis.
Method: A chaw containing 0.4 % (w/w) CZ was used to feed adult female C57BL/6 mice for 5 weeks. Mice were divided into 6 groups: 1) The control group was fed a normal diet. 2) CPZ group. 3,4,5) Mice were fed with CZ diet + α-MG (20, 40 and 80 mg/kg by gavage). 6) Mice fed a normal diet + 80 mg/kg α-MG. After five weeks of administration, the levels of MDA and apoptotic markers, such as Bax, Bcl2, cleaved caspase-3, and inflammation factor TNF-α, were measured in CC.
Results: Compared with the control group, the CZ group lost weight (p<0.0001). In the CZ group, there was an increased amount of MDA (p<0.01) and noticeable increases in the Bax/Bcl2 ratio, cleaved caspase-3 (p<0.0001), and TNF-α (p<0.001) compared with the control group. Compared to the CZ group, using α-MG 80 mg/kg significantly increased body weight (p<0.01). In addition, α-MG at 20, 40, and 80 mg/kg decreased the MDA content (p<0.01, p<0.001, and p<0.0001, respectively). Administration of α-MG 80 mg/kg decreased the Bax/Bcl2 ratio, cleaved caspase-3 (p<0.0001), and TNF-α levels (p<0.0001).
Conclusion: Our data illustrate that α-MG can eliminate destructive CZ effects in CC by decreasing oxidative stress, inflammation and apoptosis.
Dr. Maryam Nazari, Dr. Afsaneh Eliassi, Dr. Reza Saghiri, Dr. Farnaz Nikbakht, Dr. Javad Fahanikbabaei,
Volume 0, Issue 0 (3-2018)
Abstract
Several types of ion channels found in the plasma membrane have also been identified in the membranes of intracellular organelles. These ion channels, including potassium channels, play a crucial role in regulating intracellular ion homeostasis. An ATP-sensitive potassium channel (KATP) with various functional roles has been identified in the endo/sarcoplasmic reticulum membranes of both excitable and non-excitable cells. Our Previous studies have investigated the electro pharmacological and molecular properties of KATP and Bkca+2 channels in the rough endoplasmic reticulum (RER) of rat hepatocytes. In this study, for the first time, we described the electro-pharmacological and molecular properties of the RER ATP-sensitive potassium channel in rat brain cells using an incorporated single channel in the planar lipid bilayer and western blotting analysis. The results of the study revealed the presence of an ATP-sensitive potassium channel with a conductance of 306 pS, and the open probability was found to be voltage-independent at a holding potential ranging from +40 to -60 in an asymmetric solution (200/50 mM KCl; cis/trans). Additionally, we observed that adding ATP (2.5 mM) to the positive and negative potentials and 100 μM glibenclamide to the positive voltages inhibited the channel activity. Interestingly, the addition of 100 mM 5-HD and 100 nM charybdotoxin to the cis side did not affect the channel behavior. Furthermore, a western blot analysis provided evidence of the expression of Kir6.2, Kir6.1, SUR1, and/or SUR2B, but not SUR2A, in the RER of rat brain fractions. In this study, we provide strong evidence for the existence of an ATP-sensitive potassium channel on the RER membrane of rat brain cells, displaying different pharmacological properties than those classically described for the plasma membrane and other intracellular organelles.
Ms Parisa Zarei, Dr Mohammad Reza Raoufy, Dr Amir Shojaei, Dr Yaghoub Fathollahi, Dr Javad Mirnajafi-Zadeh,
Volume 0, Issue 0 (3-2018)
Abstract
Introduction: Application of deep brain stimulation (DBS) has been considered as a new therapeutic manner for neurological disorders, including epilepsy, treatment. However, the precise procedures underlying the anticonvulsant action of high-frequency stimulation (HFS) remain unclear. In this study, we explored the impact of applying high-frequency stimulation in the olfactory bulb on alterations observed in spontaneous excitatory postsynaptic currents (sEPSCs) in kindled animals.
Methods: Male rats underwent a kindling procedure involving semi-rapid electrical stimulation (six stimulations/day) of the dorsal CA1 area. HFS (130 Hz) was administered in full kindled rats at four times (i.e., 5 min, 6 h, 24 h, and 30 h) after the 6th (i.e., the last) kindling stimulation (kindled+HFS group). Subsequently, the impact of HFS on EPSCs was evaluated in pyramidal cells in CA1 area of the hippocampal slices from kindled subjects using whole cell patch clamp technique.
Results: In kindled animals sEPSC amplitude increased (p<0.001), while the sEPSC inter-event interval decreased compared to the control group (p<0.05). Application of HFS in the olfactory bulb of fully kindled rats resulted in a reduction in sEPSCs amplitude and an increase in the sEPSCs’ inter-event interval. There was not any significant difference in membrane potential and input resistance in kindled animals compared to control group. Notably, application of HFS in kindled animals restored the observed changes, so that no significant change was observed in mentioned parameters when kindled+HFS compared with the control group.
Conclusion: These findings suggested that the olfactory bulb may be considered a viable DBS target in epilepsy treatment, and HFS application may mitigate the increase in sEPSCs occurrence following seizure in kindled animals.
Keywords:
Homa Akhavan, Farzad Ahmadabadi, S Erfan Hosseini-Asl, S Saied Hosseini-Asl,
Volume 0, Issue 0 (3-2018)
Abstract
Background: Growth retardation, distinctive facial dysmorphism, and intellectual disability are hallmark features of Dubowitz syndrome. Pathogenic variants at the NSUN2 and LIG4 genes are related to this syndrome. Case presentation: A male patient, 8 years old, with a clinical diagnosis of Dubowitz syndrome, was referred to the Homa Medical Genetic Laboratory. WES analysis determined a novel nonsense mutation NSUN2(NM_01755.6):c.346C>T(p.Gln116Ter) has been detected as a homozygous genotype. Sanger-based PCR-Sequencing confirmed the finding. Segregation analysis revealed heterozygosity in his unaffected parents and sister, as well as homozygosity for the mutant allele in his mother’s uncle with the same phenotype. Conclusions: About 32 loss-of-function variants were reported to be responsible for Dubowitz syndrome. Being a nonsense variant leading to a truncated protein, not found in the genomic database, and finally, this variant should be categorized as pathogenic based on PVS1, PP4, PP1, and PM2, according to the segregation analysis results.
Shufei Li, Yanmei Wang, Jiali Li, Liuyuan Deng, Yilong Dong,
Volume 0, Issue 0 (3-2018)
Abstract
Introduction: Microglia-mediated neuroinflammation is one of the most striking hallmarks of Alzheimer’s disease (AD).Emerging evidence indicates that microglia can be polarized into proinflammatory M1 or anti-inflammatory M2 phenotypes, and excess activation of M1 microglia along with neuroinflammation are critically associated with the pathogenesis and progression of AD. The aim of the present study was to test the hypothesis that Galectin-1 (Gal-1), a member of endogenous β-galactoside-binding lectins family, may improve AD-related neuroinflammation and that the modulation of microglial polarization plays a role in this process.
Methods: Male Sprague-Dawley rats received a single intracerebroventricular injection of Amyloid-β1-42 peptide (Aβ) following 1, 5 or 10 μg Gal-1treatment for 14 days. Learning and memory abilities were estimated using the Morris water maze. Then, hippocampal samples were collected from rats, and the expression of M1 and M2 microglial markers was measured. The levels of inflammatory cytokines and the neuronal injury were also evaluated.
Results: At doses of 5 and 10 μg, Gal-1 exerted an effect on improving the Aβ-induced learning and memory impairments in rats (P<0.05, vs. Aβ group). Subsequently, Gal-1 efficaciously regulated microglial polarization, which evidenced by upregulating the expression of M2 microglial markers (P<0.01, vs. Aβ group) while downregulating M1 microglial markers (P<0.05, vs. Aβ group) and therefore contributed to decreasing the secretion of proinflammatory factors (P<0.01, vs. Aβ group) but increasing the production of anti-inflammatory factors (P<0.01, vs. Aβ group) as well as attenuating neuronal damage(P<0.01, vs. Aβ group) mediated by Aβ.
Conclusions: Gal-1 may exert neuroprotective effects by shifting microglia from the M1 phenotype to the M2 phenotype, which is beneficial for alleviating neuroinflammation, and it might be a potential agent to prevent AD-like neurodegeneration.
Hossein Abroodi, Mohammad Taghi Joghataei, Ehsan Shekari, Reza Nilipour, Vahid Valinejad, Mostafa Almasi-Doghaee,
Volume 0, Issue 0 (3-2018)
Abstract
Background. The purpose of the present study was to identify brain regions sensitive to emotion-specific acoustic parameters in healthy individuals.
Method. Three pseudo-words consecutively in the form of one stimulus were spoken with neutral and angry prosody. Then, we changed the acoustic parameters (mean fundamental frequency, intensity, and speech tempo) in angry prosody. The stimuli were presented in a functional magnetic resonance imaging (fMRI) experiment to detect anger or neutrality.
Results. Stronger activation in the left superior temporal gyrus (STG) and Heschl’s gyrus (HG) when the mean f0 converted from 300 Hz to 250 Hz was observed. Increased activity in the right posterior STG and posterior middle temporal gyrus (MTG) was revealed in more intensity anger prosody. Moreover, we found stronger activity in the right mid-STG, MTG, and the left STG in a faster speech tempo.
Conclusion. According to the increased activity in the STG and MTG of both hemispheres following the more intense anger (lower fundamental frequency, more intensity, and faster speech tempo), it can probably be concluded that a more intense comprehension of anger is resulted from the sending different information from these regions to the inferior frontal gyrus (IFG) and orbital frontal cortex (OFC).
Zahra Mansouri, Fereshteh Motamedi, Fariba Khodagholi, Maryam Zahmatkesh,
Volume 0, Issue 0 (3-2018)
Abstract
Alzheimer’s disease (AD) is a kind of neurodegenerative disease that is associated with progressive impairment of cognitive function. The primary pathological features of AD include the aggregated amyloid-β (Aβ) and hyperphosphorylation of tau protein. Histone deacetylase enzymes (HDAC) contribute in pathophysiology of neurodegenerative diseases. This study has investigated the possible neuroprotective effects of HDAC6 and HDAC10 inhibition in a rodent-AD model.
Learning and memory deficits were induced by bilateral intra-hippocampal Aβ injection in the male Wistar rats. The Tubacin (HDAC6 inhibitor) and Bufexamac (HDAC6 and10 inhibitor) were microinjected 30 min following Aβ injection. The possible molecular changes in the hippocampus following Aβ injection, were also assessed by western blotting analysis of pCREB/CREB and Pp70/P70 ratios.
Our results revealed that Bufexamac significantly recovered learning and memory impairments induced by Aβ in the MWM task. Meanwhile, Tubacin improved memory decline without affecting learning. Bilateral intra-hippocampal injection of each of HDAC inhibitors significantly increased the pCREB/CREB and Pp70/p70 ratios compared to the Aβ group that were concurrent with behavioral alterations.
HDAC IIb treatment may be a promising strategy for improving the learning and memory impairments in an animal model of AD, suggesting that HDAC targeting is valuable strategy for further investigation.
Dr. Seyed Zanyar Athari, Dr. Fereshteh Farajdokht, Prof. Dryoush Mohajeri, Dr. Mir Alireza Nourazar,
Volume 0, Issue 0 (3-2018)
Abstract
Neurotrophic factors and physical activities have beneficial effects on neurodegenerative disorders. This study assessed the effect of physical activity (EXE) and Cerebrolysin (CBL), individually or in conjunction, in a hemiparkinsonian model (PD) caused by 6-hydroxydopamine (6-OHDA). The study utilized seventy-two male Wistar rats, which were distributed into six groups (n=12): Sham (received intra substantia nigra (SN) injection of normal saline), PD (underwent 6-OHDA (12.5 μg) injection into the left SN), PD+Levodopa (treated with levodopa; 12 mg/kg, gavage, for three weeks), PD+CBL (treated with intraperitoneal injection of CBL 2.5 ml/kg, for three weeks), PD+EXE (exercised 30 min/day for three weeks), and PD+CBL+EXE. Rotation with apomorphine and Murprogo’s test were assessed, 21 days after PD induction and after treatments. Ultimately, the levels of lipid peroxidation marker and total antioxidant capacity (TAC), glutathione peroxidase (GPx) activity, α-synuclein protein expression, and histopathological changes of the SN were evaluated ipsilateral to the lesioned side. The results showed that CBL and exercise, alone or in combination, decreased ipsilateral apomorphine rotation and muscle rigidity in the PD animals. Moreover, these behavioral changes were associated with decreased malondialdehyde levels and α-synuclein protein levels, increased TAC level and GPx activity, as well as a greater neuronal count in the SN. Notably, the combination effects were greater than single therapy and levodopa treatment. Our findings indicated that the combination of exercise and CBL ameliorated 6-OHDA-induced motor impairments by attenuating oxidative stress and protein expression of α-synuclein, and preserving neurons in the SN.
Masume Behruzi, Mehrdad Ghorbanlou, Ronak Shabani, Auob Rustamzadeh, Enam Alhagh Charkhat Gorgich, Elham Seidkhani, Farnoosh Usefi, Mehdi Mehdizadeh, Fatemeh Moradi,
Volume 0, Issue 0 (3-2018)
Abstract
Introduction: Targeting SMO has been a remarkable strategy in Shh-dependent cancers, especially medulloblastoma. In this manner, GDC-0449 or vismodegib is used as a potent SMO inhibitor with mild toxicity and high affinity. Thus, the main purpose of the present study was to investigate the anti-medulloblastoma efficacy of vismodegib on the DAOY medulloblastoma cell line.
Methods: Human DAOY medulloblastoma cells were cultured in DMEM.50, 80, 100, and 150μM doses of vismodegib were used to treat cells. MTT, Scratch, and trypan blue assay, and also real-time polymerase chain reaction (RT-PCR) and immunofluorescence studies were performed, 24 and 48 hours post-treatment.
Results: MTT and trypan blue assay showed a significant difference in viability, between the control group and treatment groups. Results of the scratch assay showed that in the control group, the cells managed to repair the lesion, while the scratch was disintegrated in higher doses of vismodegib. The expression of SMO, Gli1, and MYCN genes, as the main components of the SHH signaling pathway, had a significant reduction in the vismodegib-treated groups compared to the control group. Also a notable rise in the activation of metastasis-promoting genes (Bax and p53) while a reduction in metastasis-inhibiting gene (Bcl2), was observed.
Conclusion: The results of the current study confirm that vismodegib is a potent inhibitor of the Shh pathway and could be used as a drug in combination with new therapeutic methods, in order to treat medulloblastoma.
Dr Sepideh Saffarpour, Dr Arash Mehraz, Mrs Pargol Sadeghi Tehran, Dr Farinaz Nasirinezhad,
Volume 0, Issue 0 (3-2018)
Abstract
Purpose:While Genotropin, a recombinant human growth hormone (GH), may be a repositioning drug for treating neurological diseases, its effectiveness for neuropathic pain remains uncertain. The current research investigated the pain alleviating effect of Genotropin and its possible effective mechanisms.
Method: Two weeks after chronic constriction injury (CCI) of sciatic nerve, adult male rats were divided into three main experimental groups: Control, Vehicle which received normal saline, and Treatment which received Genotropin (0.3 and 0.6 mg/kg) either alone or in combination with L-arginine, L-NAME, or glutamate (n=8). Pain-related behaviors were assessed using Von Frey filaments, plantar and the Randall-Selitto tests. Blood samples were collected to evaluate relevant oxidant/antioxidant markers.
Results: GH decreased mechanical allodynia (P<0.05, F=2.7) mechanical (P<0.01, F=3.4) and thermal hyperalgesia (P<0.001, F=2.5). Also, pretreatment with 0.3 mg/kg GH abolished the nociceptive effects of L-arginine (500mg/kg) and glutamate (1000nmol) (P<0.01; F=2, F=3), while enhancing the antinociceptive effect of L-NAME (P< 0.05, F=2.8). It significantly reduced lipid peroxidation (P < 0.01, F =3.7), restored glutathione, glutathione peroxidase, and superoxide dismutase levels (P < 0.01, F =11, F = 10.52, F = 5 respectively) and increased the catalase level (P < 0.01, F =5) in plasma.
Conclusion: The current data suggests that exogenous GH, alleviates pain and enhance antioxidative factors in the peripheral neuropathic pain model. The glutamate and nitric oxide pathways are also involved in its’ antinociceptive effect. It seems that Genotropin can be effective as a repositioning drug in the treatment of neuropathic pain.
Prof. Peng Zhang, Prof. Hui Xiao,
Volume 0, Issue 0 (3-2018)
Abstract
Introduction: Alzheimer's Disease (AD) is a prevalent neurodegenerative disorder characterized by amyloid-beta (Aβ) accumulation, leading to inflammation, oxidative stress, and impaired synaptic function. This study explores the neuroprotective mechanisms of Vitis vinifera L. flavones (VTF) against Aβ-induced neurodegeneration and its potential as an AD therapeutic.
Methods: In an in vitro analysis, Aβ1-42 oligomers induced a mitophagy model in SH-SY5Y neuroblastoma cells. Cells were treated with VTF alone and in combination with chloroquine (CQ), a lysosome inhibitor, to assess Aβ1-42-induced mitophagy. Transmission electron microscopy (TEM) and Immunofluorescence (IFC) revealed Aβ1-42 effects on autophagosomes and deposition. Cellular protection against Aβ-induced damage was evaluated using the CCK-8 assay. Western blotting determined the expressions of autophagy–lysosomal pathway proteins (Beclin-1, Atg7, p62, and BACE1) and the LC3-II/LC3-I ratio as an autophagy marker.
Results: CQ and VTF demonstrated significant neuroprotection against Aβ1-42-induced neurodegeneration (P < 0.05). VTF, alone or with CQ, increased viable cell count (~1.2-fold; P < 0.05), indicating reparative capabilities. TEM and IFC showed robust protection by VTF and CQ against Aβ protein deposition and preservation of mitochondrial and autophagosomal structures. VTF and CQ treatments reduced Beclin-1, Atg7, and BACE1 levels, indicating modulation of Mitophagy and autophagy–lysosomal suppression. VTF+CQ maintained LC3-II/LC3-I balance, confirming VTF's role in preserving autophagy (P < 0.01).
Conclusions: This study unveils VTF's novel neuroprotective role, emphasizing its potential as an AD therapeutic. Future research should extend investigations to in vivo models and clinical settings, enhancing understanding of VTF's neuroprotective efficacy.
Dr. Aida Moarrefzadeh, Dr. Sadra Sarandili, Dr. Nogol Motamed-Gorji, Dr. Fatemeh Majdolashrafi, Dr. Mansour Bahardoust, Dr. Safa Mousavi, Dr. Neda Hashemi, Dr. Arash Sarveazad, Dr. Mohammadhossein Vazirizadeh-Mahabadi, Dr. Seyed Amirhassan Habibi,
Volume 0, Issue 0 (3-2018)
Abstract
Background: Parkinson's disease (PD) is a common neurodegenerative disease whose motor and non-motor complication greatly affect a person's quality of life (QoL). This study aims to investigate the QoL of these patients using the PDQ-39 questionnaire and identify the prognostic factors associated with their QoL.
Method: In the current case-control study, the QoL of two groups (211 controls and 211 cases) was investigated and compared using the PDQ-39 questionnaire. Prognostic factors associated with QoL were determined using multivariate logistic regression analysis.
Results: A number of 422 patients with the mean age of 59.8 ± 13.7 years were included in the study. The mean score of PDQ-39 in the case group was significantly higher in all subscales except Social support compared to the control group. The mean score of PDQ-39 was significantly higher in the patients with non-DBS (53.9 ± 21.1 (than those with DBS (42.22 ± 18.1(, especially in the sub-scales of Mobility, Activities of daily living, Cognition, and Communication. As the stage of the disease increases, the mean score of PDQ-39 in these patients increases significantly. The results of multivariate analysis showed that gender, patient age, smoking, education level, duration of disease, patient stage, and intervention with DBS were significantly related to patients' QoL (P<0.05).
Conclusion: In conclusion, this study highlights the significant impact of DBS on PD patients' QoL, especially in sub-scales of mobility, daily activities, emotional well-being, and cognition. Moreover, identifying the main prognostic factors in QoL (gender, age, smoking status, educational level, disease duration, and stage) can lead to avenues for improving these patients' lives.
Dr Sahar Bayat, Dr Milad Gholami, Dr Hamidreza Khodadadi, Dr Mohammadreza Ghazavi, Dr Jafar Nasiri, Dr Majid Kheirollahi,
Volume 0, Issue 0 (3-2018)
Abstract
Background: Hypomyelinating leukodystrophie-5 (HLD-5) is a rare multiple congenital anomaly with intellectual disability caused by an autosomal recessive mutation in the FAM126A gene and is characterized by bilateral congenital cataract, developmental delay, cerebellar ataxia, slowly progressive gait disturbance and cognitive impairment. This study aims to contribute to a better understanding of HLD-5 by reviewing previous patients and introducing a novel variant in a new case.
Methods and Results: We subjected a case with an initial diagnosis of HLD-5 in an Iranian family. To identify the possible genetic cause(s), whole exome sequencing (WES) was carried out to detect exon mutations and Sanger sequencing was performed to verify the DNA sequence variants and co-segregation analysis. We predicted the potential deleterious effects of the novel mutation using in silico predictive tools. WES identified a novel homozygous mutation (NM_032581: c.636_639del p.C213Dfs*7) in the FAM126A gene. The variant can cause premature termination of amino acid translation or affect mRNA expression.
Conclusions: In this study, the clinical manifestations and molecular findings of HLD-5 were explained. Additionally, we reported a novel variant and some rare clinical features, such as exophthalmos and strabismus, in our proband for the first time. Further research is needed to clarify the molecular mechanisms underlying HLD-5 pathogenesis.
Hamed Ekhtiari,
Volume 1, Issue 3 (5-2010)
Abstract
Behnam Zamanian, Ali Goodarzi, Hamed Ekhtiari,
Volume 1, Issue 3 (5-2010)
Abstract
A B S T R A C T
“Addiction” is a multifaceted complicated disorder with many interrelated causes, as well as environmental and genetic features. Several hereditary variables that have an effect on these features might work in together to influence vulnerability and the extent of being an addict. Molecular re-sequencing of the latest and formerly researched genes holds a crucial place with regards to the breakthrough of hereditary alternates of possible interest. This report presents a brief review of this complicated disorder through genotyping and phenotyping aspects, and examines their correlation in creating and driving this disease.
Mehdi Mehdizadeh, Majid Katebi, Mansoure Soleimani, Mohammad Hassan Farahani Pad, Ali Hoseini Tehrani, Mohammad Taghi Joghataei,
Volume 1, Issue 3 (5-2010)
Abstract
A B S T R A C T
Introduction: Even today there is no effective drug therapy to prevent neuronal loss after brain stroke. In the present study we studied the effect of mitochondrial KATP channel regulators on neuronal ultrastructure after ischemia reperfusion in the rat. Materials & Methods: Rats temporarily subjected to four vessels occlusion for 15 minutes followed by 24 hours reperfusion with or without K-ATP channel regulators.
Results: Neuronal ultrastructure significantly improved in K-ATP channel opener (diazoxide) treated ischemia-reperfusion group compared with control group.
Discussion: Our results showed that dizoxide treatment after ischemia reperfusion leads to better preservation of cortical neurons in rat.
Mohammad Amin Khoshlessan1, Sadra Sadeh, Reza Nilipour,
Volume 1, Issue 3 (5-2010)
Abstract
A B S T R A C T
Introduction: In an oddball experiment, the context in which novel stimuli are presented affects characteristics of novelty P3, i.e. as long as there is a difficult task in which the difference between standard and target stimuli is small, recurrent presentation of a highly discrepant stimulus can lead to P300 highly similar to novelty P3. Effect of stimulus properties on P300 has also been previously examined and it has been shown that it plays a significant role in P300 topography, its amplitude and latency.Here we have examined the effect of surface color of objects of high color-diagnosticity in a visual oddball paradigm.
Methods: In two separate conditions, we used pictures of fruits as target and novel stimuli. In condition one, novel stimuli were pictures of fruits in their canonical colors. In the second condition, novel stimuli were the same photo filtered to have a different non-canonical color. P300 was compared among these conditions.
Results: Both target P3 and novelty P3 were detected in the two conditions but no significant difference was evident between conditions.
Discussion: This result suggests that comparing to shape information color cue does not play a significant role in detecting context novelty.
Mohammad Reza Shahraki, Hamide Mirshikari, Elham Shahraki,
Volume 1, Issue 3 (5-2010)
Abstract
A B S T R A C T
Introduction: Aloe Vera extract is used as an anti-inflammatory and anti-bradikinin agent in laboratory animals. The aim of this survey was to evaluate the ant-nociceptive effect of A. Vera aqueous extract in fructose-fed male rats.
Methods: Forty-five Wistar-Albino male rats were equally and randomly divided into five groups including sham operated and four test groups. Sham operated group consumed tap water and the test groups consumed fructoseenriched water. Test groups 2, 3 and 4 additionally received, 0, 100, 150 and 200 mg/kg of A. Vera extract, respectively, whereas the other test group received distilled water daily. Tail flick reaction time, serum glucose and oral glucose tolerance test (OGTT) were measured. The results were analyzed by SPSS software using ANOVA and Tukey tests. Results were expressed as mean ± SD. Statistical differences were considered significant at p<0.05.
Results: The results showed that tail flick reaction time significantly increased in test group 3 which received 200 mg/kg A. Vera extract comparing with that of sham operated group. However, OGTT and serum glucose value were significantly increased in all fructose-fed male rats comparing with those of sham operated group.
Discussion: These results indicated that A. Vera aqueous extract can affect tail flick reaction time in fructose-fed male rats. Further studies are required to show the exact mechanism of anti-nociceptive effect of A. Vera extract.
