Showing 7 results for Eskandari
Mohammad Hashemi, Zahra Zakeri, Ebrahim Eskandari-Nasab, Mahdi Atabaki, Seyed Mohammad Ebrahim Pourhosseini, Mehdi Jahantigh, Gholamreza Bahari, Mohsen Taheri,
Volume 17, Issue 4 (10-2013)
Abstract
Background: Rheumatoid arthritis (RA) is a chronic inflammatory disease with many genetic factors predisposing to disease susceptibility. The aim of the present study was to investigate the impact of CD226 rs727088 and rs763361 polymorphisms and susceptibility to RA in a sample of the Iranian population. Methods: This case-control study was carried out on 100 patients with RA and 104 healthy subjects. The polymorphisms were determined using tetra amplification refractory mutation system-polymerase chain reaction assay. Results: The rs763361 (Gly307Ser) polymorphism increased the risk of RA in codominant, dominant and recessive-tested inheritance models (odds ratio [OR] = 3.18, 95% confidence intervals [95% CI] = 1.44-7.02, P = 0.004, CC vs. TT, and OR = 1.98, 95% CI = 1.10-3.57, P = 0.023, CC vs. CT-TT, and OR = 2.61, 95% CI = 1.26-5.37, P = 0.010, CC + CT vs. TT, respectively). In addition, the rs763361 T allele increased the risk of RA (OR = 2.06, 95% CI = 1.38-3.08, P<0.001). However, no significant difference was observed among the groups regarding CD226 rs727088 polymorphism (χ2 = 3.20, P = 0.202). Conclusions: Our finding showed that CD226 rs763361, but not rs727088, gene polymorphism increased the risk of RA in a sample of the Iranian population.
Solmaz Jamali, Nasim Eskandari, Omid Aryani, Shadab Salehpour, Talieh Zaman, Behnam Kamalidehghan, Massoud Houshmand,
Volume 18, Issue 2 (4-2014)
Abstract
Background: Tay-Sachs disease (TSD), or GM2 gangliosidosis, is a lethal autosomal recessive neurodegenerative disorder, which is caused by a deficiency of beta-hexosaminidase A (HEXA), resulting in lysosomal accumulation of GM2 ganglioside. The aim of this study was to identify the TSD-causing mutations in an Iranian population. Methods: In this study, we examined 31 patients for TSD-causing mutations using PCR, followed by restriction enzyme digestion. Results: Molecular genetics analysis of DNA from 23 patients of TSD revealed mutations that has been previously reported, including four-base duplications c.1274_1277dupTATC in exon 11 and IVS2+1G>A, deletion TTAGGCAAGGGC in exon 10 as well as a few novel mutations, including C331G, which altered Gln>Glu in HEXB, A>G, T>C, and p.R510X in exon 14, which predicted a termination codon or nonsense mutation. Conclusion: In conclusion, with the discovery of these novel mutations, the genotypic spectrum of Iranian patients with TSD disease has been extended and could facilitate definition of disease-related mutations.
Mohammad Hashemi, Mohsen Omrani, Ebrahim Eskandari-Nasab, Seyed-Shahaboddin Hasani, Mohammad Ali Mashhadi, Mohsen Taheri,
Volume 18, Issue 4 (10-2014)
Abstract
Background: MDM2 (Murine Double Minute2) is an oncoprotein that inhibits the P53 activity. Overexpression of MDM2 gene has been reported in several human tumors. In the present study, we aimed to evaluate the impact of 40-bp insertion/deletion (ins/del) polymorphism on the promoter of MDM2 and susceptibility to breast cancer in a sample of Iranian population. Methods: This case-control study was carried out on 236 patients with breast cancer and 203 healthy individuals. Genomic DNA was extracted from the whole blood by the salting-out method. The 40-bp ins/del polymorphism was determined by using polymerase chain reaction. Results: The findings indicated that MDM2 ins/del variant increased the risk of breast cancer in co-dominant- (odds ratio [OR] = 2.09, 95% CI = 1.14-3.85, P = 0.018, del/del vs. ins/ins), dominant- (OR = 1.49, 95% CI = 1.02-2.18, P = 0.038, ins/del + del/del vs. ins/ins), and recessive- (OR = 1.86, 95% CI = 1.03-3.34, P = 0.038, del/del vs. ins/ins + ins/del) tested inheritance models. The del allele increased the risk of breast cancer (OR= 1.48, 95% CI=1.11-1.98, P=0.008) compared with ins allele. Conclusions: Our result revealed that 40-bp ins/del polymorphism in the promoter of MDM2 increased the risk of breast cancer in an Iranian population. Further investigations with larger sample sizes and diverse ethnicities are needed to verify our findings.
Hossein Mostafavi, Narges Amoli, Elham Ghasemloo, Meysam Forouzandeh, Masoumeh Hosseini, Mehdi Eskandari,
Volume 26, Issue 5 (9-2022)
Abstract
Introduction: Brain ischemia often leads to the chloride gradient alternations, which affects volume regulation and neuronal survival. Increase in NKCC1 expression and reduction in KCC2 level under ischemic condition results in inflammation and neuronal death. In this study, we investigated the effect of mimic miRNA and coenzyme Q10 (CoQ10) on the expression of cation-chloride cotransporters (CCCs) (NKCC1 and KCC2) after cerebral ischemia.
Methods: In this study, cerebral ischemia was modeled using the middle cerebral artery occlusion method. Rats were randomly divided into six groups: sham, model, negative control, vehicle, and the first and second treatments. In the Sham group, ischemia was not induced, and no treatment was performed. In the Model group, ischemia induction was performed, and other groups, in addition to ischemia induction, received Scramble miRNA, Ethanol, mimic miRNA-149-5p and CoQ10, respectively. Each group was divided into three subgroups to assess the volume of the tissue damage and neurological deficits scores (NDS) in subgroup 1, brain water content in subgroup 2, level of miRNA-149-5p and CCC expressions in subgroup 3.
Results: Our data suggested that the use of mimic miRNA and Q10 increased the level of miRNA-149 and KCC2 expression and decreased NDS, NKCC1 expression, brain water content, and infract volume.
Conclusion: Findings of this study suggest that the mimic miRNA and Q10 may have neuroprotective effects through reducing infract volume and brain water content and modulating the expression of CCCs after brain ischemia.
Hamidreza Golian, Mohammad Amin Ghezel, Nooshin Roudbari, Morteza Eskandari, Mehrdad Hosein-Zadeh, Neda Asl Estiyari, Amir Arshiya Mohammadi Vala, Shilan Nasri,
Volume 28, Issue 0 (Supplementary 2024)
Abstract
Introduction: Formaldehyde (CH2O) poisoning causes widespread neuronal death in the central nervous system by inducing oxidative stress. This study aimed to evaluate the therapeutic effects of propofol and the antioxidant CoQ10 on the neuronal density of the entorhinal cortex, hippocampal pyramidal cells, and oxidative stress factors in the fetal forebrain following formaldehyde poisoning.
Methods and Materials: Thirty-five pregnant Wistar rats were randomly divided into seven control groups: formaldehyde + saline, formaldehyde + propofol 10 mg/kg, formaldehyde + propofol 20 mg/kg, formaldehyde + propofol 40 mg/kg, formaldehyde + CoQ10 50 mg/kg, and formaldehyde + propofol 40 mg/kg + CoQ10 50 mg/kg. To induce formaldehyde poisoning, on the 14th day of pregnancy, formaldehyde (20 mg/kg body weight) was injected intraperitoneally into pregnant rats. From the 12th to the 18th day of pregnancy, the treatment groups received propofol with different doses and coenzyme Q10 via the gavage method. After cesarean delivery of the fetuses on the 21st day of pregnancy, the neuronal density of the entorhinal cortex, CA1 and CA3 areas of the hippocampus, and the tissue levels of catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPX) in the forebrain of the fetuses were evaluated using the ELISA method.
Results: The results showed a significant increase in the activity of CAT, GPX, and SOD enzymes and a significant decrease in MDA levels in the forebrain of fetuses receiving propofol plus CoQ10 compared to the formaldehyde + saline group. Additionally, an increase in the density of neurons in the entorhinal cortex and CA1/CA3 areas of the hippocampus was observed in the groups receiving propofol + coenzyme Q10 compared to the formaldehyde + saline group.
Conclusion and Discussion: Prenatal formaldehyde poisoning, by inducing oxidative stress in the fetal forebrain, caused damage to the entorhinal cortex and hippocampus of the rat fetal brain. On the other hand, propofol improved neuronal damage in these regions of the fetal brain. Propofol can be used as an efficient and effective drug in the treatment of formaldehyde poisoning and brain surgeries. It can prevent the spread of tissue damage to nearby tissues and facilitate the treatment process by using it during the complete treatment of the poisoned individual.
Maryam Toolabi, Mahsa Akbari, , Mohammad Reza Eskandari, Mohammad Ali Shahbazi,
Volume 28, Issue 0 (Supplementary 2024)
Abstract
Introduction: Wound healing is a complicated physiological process requiring an appropriate environment to encourage healing. Herein, we develop a novel dissolving microneedle (MN) patch with an electrospun nanofiber backing layer to perform transdermal delivery and combination therapy for wound healing. A nanofibrous scaffold with poly (vinyl alcohol) and gelatin loaded with taurine and Bi2S3 nanoparticles was prepared using the electrospinning method, PGTBi. The needle of the MN, called PHA, was composed of poly methyl vinyl ether-alt-maleic acid, hyaluronic acid, and allantoin.
Methods and Materials: The PGTBi-PHA MN patches were fabricated via a molding method in a two-step casting process. All characterization assays, including size and photothermal performance of the Bi2S3 nanoparticles, morphology and mechanical properties of the fibers, and ex vivo and in vitro, insertion of the needle in the skin and parafilm, were performed to ensure the fabricated device meets desirable properties for effective wound healing.
Results: TEM image, zeta potential, and elemental analysis indicated successful synthesis of Bi2S3 NPs. The temperature of Bi2S3 NPs increased by about 50.4 °C at a concentration of 200 μg/mL after irradiation for 10 min, which is the temperature required to kill bacteria, indicating the excellent photothermal performance of Bi2S3 NPs. Investigation of tensile tests showed that Young's modulus of the nanofiber mats was 168.4 MPa, which was in the skin range. Parafilm and skin insertion tests show that the PGTBi-PHA MN patches have sufficient strength to penetrate the skin and release their contents after dissolution.
Conclusion and Discussion: In this study, an electrospun patch with photothermal properties was successfully incorporated into the backing layer of MNs for wound healing application. This technology can combine different therapeutic modalities to enhance the overall healing process of wounds on the skin.
Dr. Seyed Ebrahim Eskandari, Dr. Mojtaba Memariani, Dr. Hamed Memariani, Dr. Mehdi Mohebali, Dr. Ali Khamesipour,
Volume 28, Issue 4 (7-2024)
Abstract
Cutaneous leishmaniasis (CL) is a common form of leishmaniasis in underdeveloped countries. Although CL tends to be self-limiting, it can cause significant scars and may progress to more severe manifestations. Additionally, Leishmania species vary in susceptibility to the available treatments. The selection of treatment and clinical outcome of CL depend on the accurate determination of the Leishmania species. This mini-review aims to provide an overview of the molecular diagnosis techniques such as PCR-based assays, nucleic acid sequence-based amplification, and loop-mediated isothermal amplification utilized in the identification of Leishmania species in Iran.
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