Are you Reza Akbarzadeh Najar?

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Publications (16)22.09 Total impact

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    ABSTRACT: PURPOSE: The high rate of p16 gene alterations in malignant neoplasms suggests the important effect of this tumor-suppressor gene mutation on the malignant behavior of tumoral lesions. The present study investigated the possible methylation of the p16 tumor in ameloblastic carcinoma, ameloblastoma, and dental follicles. MATERIALS AND METHODS: Eighteen samples of ameloblastic carcinoma, ameloblastoma, and dental follicles of mandibular impacted third molar were selected from available documents in the archives of the Department of Oral and Maxillofacial Pathology, Taleghani Hospital and the Department of Oral and Maxillofacial Pathology, Shahid Beheshti University of Medical Sciences, Tehran, Iran. After confirming the initial diagnosis, 6-μm sections were used for DNA extraction. A CpG island methylation of p16 was identified by polymerase chain reaction. RESULTS: Although CpG methylation of p16 was observed in all ameloblastic carcinoma samples, only 1 ameloblastoma specimen exhibited the mutation. The mutation was not detected in other ameloblastoma specimens or in any dental follicle sample. CONCLUSIONS: The p16 alteration might play a role in the malignant progression of ameloblastic carcinoma. It is worth mentioning that ameloblastoma can be further differentiated from ameloblastic carcinoma based on molecular observations.
    Journal of oral and maxillofacial surgery: official journal of the American Association of Oral and Maxillofacial Surgeons 06/2012; · 1.58 Impact Factor
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    ABSTRACT: Ameloblastic carcinoma (AC) is a rare malignant epithelial odontogenic tumor that histologically retains the features of ameloblastic differentiation and exhibits cytological features of malignancy in the primary or recurrent tumor. It may develop within a preexisting ameloblastoma or arise de novo or from an odontogenic cyst. Epidemiological evidence shows that human cancer is generally caused by genotoxic factors, genes involved in the susceptibility of cancer, including those involved in metabolism or detoxification of genotoxic environment and those controlling DNA replication. Nowadays, gene polymorphism has an important role in development of malignant tumor. We report a case series study of ameloblastic carcinoma and ameloblastoma to show the role of PKM2 and MAPK8IP2 polymorphisms in these tumors. The DNA was extracted separately from specimens in paraffin sections of the tumor. Polymorphism of these genes was determined by PCR-RFLP (Polymerase Chain Reaction-Restriction fragment length polymorphism) method. The allele distributions of all samples were in Hardy-Weinberg equilibrium. The genotype and allele distribution in these genes were not statistically different between patients and controls.
    International journal of molecular and cellular medicine. 01/2012; 1(4):203-9.
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    ABSTRACT: C-reactive protein (CRP) is one of the many molecular factors involved in pathogenesis of coronary artery disease which its plasma levels are associated with increased risk of cardiovascular events. The present study designed to determine whether polymorphisms in the CRP gene are associated with plasma CRP levels and susceptibility to acute myocardial infarction (AMI). Plasma CRP levels were measured in patients with AMI and control subjects and genomic DNA and peripheral blood mononuclear cells (PBMCs) were extracted. The -717A/G and 1059G/C CRP polymorphisms were detected. The mRNA expression of CRP gene and plasma levels of CRP and interleukin-6 (IL-6) were also analyzed. The -717A/G variation was significantly associated with higher CRP levels, but 1059G/C variation was associated with lower CRP levels. The AA genotype frequency of -717A/G variation was significantly more frequent in the patients than control subjects. By contrast, the genotype and allele distribution in 1059G/C of patient were not statistically different between patients and controls. There were significant differences in circulating levels of CRP and IL-6 in the patients than in controls. The mRNA expression levels of CRP were significantly higher in the patient plasma compared with controls. Our results indicate relationship between many polymorphisms in CRP gene and risk of AMI which suggest that genetic variations in CRP might be helpful for determining susceptibility to AMI in Iranian patients. In addition, CRP gene polymorphisms are associated with plasma CRP levels and susceptibility to AMI might be related to CRP gene expression which affects its plasma levels.
    Molecular Biology Reports 07/2011; 39(4):3705-12. · 2.51 Impact Factor
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    ABSTRACT: Transforming growth factor beta 1 (TGF-β1) gene plays an important role in acute myocardial infarction (AMI); however, little is known about the relation of variations within the gene and risk of cardiovascular diseases. In this study, the authors evaluated the influence of TGF-β1 polymorphisms on the onset and progression of AMI in Iranian patients comparing with healthy individuals. Genomic DNA and peripheral blood mononuclear cells of 900 enrolled patients with AMI and 900 control subjects were extracted. The -509 C/T, 868T/C, 913G/C and 11929C/T TGF-β1 polymorphisms were detected. The messenger RNA (mRNA) expression and serum levels of TGF-β1 were analyzed by real-time reverse-transcriptase polymerase chain reaction and ELISA, respectively. The frequency of "T" allele in -509 C/T, "C" allele in 868T/C, "C" allele in 913G/C and "T" allele in 11929C/T polymorphisms were significantly higher in the patients than control subjects (P < 0.001). There were significant differences in circulating levels of TGF-β1 in the patients than in control subjects (P < 0.001). These concentrations are associated with its gene polymorphism. The mRNA expression levels of TGF-β1 were significantly higher in the patient serums compared with controls (P < 0.001). Our results confirmed the association between the TGF-β1 polymorphisms and risk of AMI, which suggest that genetic polymorphisms in TGF-β1 might be helpful for determining susceptibility to AMI in Iranian patients. There are also significant relationship between serum TGF-β1 and occurrence of AMI. In addition, susceptibility to AMI might be related to TGF-β1 gene expression, which affects its serum levels.
    The American Journal of the Medical Sciences 06/2011; 342(5):365-70. · 1.33 Impact Factor
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    ABSTRACT: Inflammatory processes play a pivotal role in the pathogenesis of atherosclerosis. Genes coding for cytokines such as interleukin-6 (IL-6) are candidates for predisposing to the risk of coronary artery disease. The aim of this study was to investigate whether molecular polymorphism of the IL-6 gene is involved in the predisposition to acute myocardial infarction (AMI). Genomic DNA and peripheral blood mononuclear cells of patients with AMI and controls were extracted. IL-6 gene variations were evaluated by polymerase chain reaction followed by restriction enzyme analysis. The mRNA expression of IL-6 gene and plasma levels of IL-6 and C-reactive protein (CRP) were analyzed. The prevalence of 'C' allele in -174 G/C variation was higher in patients with AMI than in controls. The IL-6 -174 'C' allele is associated with high levels of IL-6 in the patients, of which the patients with CC and GC genotypes significantly have higher IL-6 concentrations, respectively. Increased CRP concentrations were associated with -174 G/C variation in the patients compared with controls. The mRNA expression levels of IL-6 were significantly higher in the patient compared with controls (P<0.001). The findings of this study indicate the relationship between IL-6 gene polymorphism and the risk of AMI, which suggests that genetic polymorphism in IL-6 gene, might be helpful for determining susceptibility to AMI in Iranian patients. In addition, susceptibility to AMI might be related to IL-6 gene expression, which affects its plasma levels. CRP plasma levels also were associated with IL-6 gene variation in the patients.
    Coronary artery disease 04/2011; 22(5):299-305. · 1.56 Impact Factor
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    ABSTRACT: Infection with Helicobacter pylori strains may result in different pathological manifestations and increased oxidative stress leading to a strong inflammatory response in gastric mucosa. The prevalence of cagA and vacA genes, proteins and the association of serum levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) with oxidative DNA damage were determined. The presence of cagA gene and vacA alleles and IgG antibodies against CagA and VacA proteins were determined. Oxidative DNA damage status was determined using serum levels of 8-OHdG. Helicobacter pylori-positive, cagA-positive, and vacA alleles (s1 and m2) were predominant in all clinical outcomes. There was no significant association between prevalence of CagA and VacA status and clinical outcomes. The serum levels of 8-OHdG was at a higher level in H. pylori-positive patients. These virulence factors are not associated with the development of PUD in Iranian patients. H. pylori infection may be associated with increased serum 8-OHdG.
    Irish Journal of Medical Science 03/2011; 180(1):155-61. · 0.51 Impact Factor
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    ABSTRACT: A polymorphism within tumor necrosis factor-α (TNF-α) gene promoter and contribution of TNF-α converting enzyme (TACE) have been reported to be associated with TNF-α production which may increase susceptibility to heart failure such as acute myocardial infarction (AMI). However, the relationship between this polymorphism and susceptibility to AMI and the mechanism of TACE-TNF-α system regulation has poorly been studied. Genomic DNA and peripheral blood mononuclear cells (PBMCs) of patients with AMI and control subjects was extracted. The -308 G/A TNF-α polymorphism was detected. The mRNA transcription and protein expression levels of TNF-α and TACE were analyzed by real time RT-PCR and flow cytometry respectively as well as plasma TNF-α by ELISA. The 'A' allele frequency of TNF-α was significantly more frequent in the patients than controls (P < 0.001). There were statistically significant differences in TNF-α and TACE mRNA and protein levels as well as circulating TNF-α in the patients. However, these levels were higher in the patients who carry 'A' allele. There were significant positive correlation between these mRNAs and protein expression levels (r = 0.66, P < 0.001, r = 0.78, P < 0.001 respectively). These data suggest that genetic polymorphism in TNF-α might be helpful for determining susceptibility to AMI in Iranian patients. The TACE-TNF-α system in circulating leucocytes is stimulated which these results demonstrate that in patients with AMI, TACE expression in PBMC increases with TNF-α expression and processing of TNF-α in PBMC might be regulated by TACE at transcriptional, translational, and post-translational levels in AMI.
    Molecular Biology Reports 12/2010; 38(8):4971-7. · 2.51 Impact Factor
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    ABSTRACT: Activation of mitogen-activated protein kinases (MAPKs) signaling cascade are important pathophysiologic regulators during the development of acute myocardial infarction (AMI). In present study, we designed to monitor the activity of these MAPKs in Iranian patients with AMI comparing with controls. The degree of activation (phosphorylation) of p38 kinase, p44/42 extracellular regulated kinase, and c-Jun N-terminal kinase (JNK1/2) and their corresponding activity levels were analyzed in 258 patients with AMI and 250 normal subjects. The expression of p38α mRNA was determined. These analysis were carried out immediately and 12 h after AMI. Activity of p38 and JNK1/2 MAPKs were significantly increased in patients with AMI than controls immediately after infarction. These activities were reduced during 12 h after AMI. However, there were no statistically differences in activation and activity of p44/42 in the patients and controls. The mRNA expression of p38α was increased in the patients comparing with controls. Results of this study indicate that these MAPKs signaling pathway might be activated by AMI which signal transduction involves kinase phosphorylation and play important roles in their activity. Elevated activity of p38 and JNK1/2 MAPKs suggests that they may potentially play significant roles in AMI.
    Journal of Thrombosis and Thrombolysis 11/2010; 31(4):424-30. · 1.99 Impact Factor
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    ABSTRACT: Helicobacter pylori infection has been linked to cardiovascular diseases (CVD) and several studies have reported its positive association with inflammatory response after acute myocardial infarction (AMI). On account of the importance of the inflammatory process in the development of CVD, we decided to examine the seroprevalence of H. pylori, the prevalence of CVD risk in the more virulent strains bearing the cytotoxin-associated protein (CagA), and the changes in C-reactive protein (CRP) as an inflammatory marker in Iranian patients with AMI. A case-control study was designed to determine the seropositivity status of H. pylori and CagA in blood samples obtained from 500 patients with AMI and 500 control individuals without any evidence of clinical CVD. Serum and peripheral blood mononuclear cells were analyzed using the enzyme-linked immunosorbent assay and western blotting methods, respectively. CRP levels were also measured in all individuals. The prevalence of H. pylori infection and CagA status were significantly higher among the patients with AMI than the controls (66 vs. 20% and 75.7 vs. 30%, respectively); the odds ratio was 2.57 (95% confidence interval 1.89-3.49). CRP levels were significantly different in the patients compared with the controls (5.02±1.04 mg/l vs. 2.41±0.9 mg/l, respectively). Our results confirmed that the patients with AMI had a significantly higher prevalence of H. pylori infection and CagA seropositivity than the control population. Infection with H. pylori may influence AMI, which in our findings shows an association between H. pylori seropositivity and AMI through an inflammatory process.
    Coronary artery disease 10/2010; 22(1):6-11. · 1.56 Impact Factor
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    ABSTRACT: Matrix metalloproteinases (MMPs) play an important role in early atherosclerosis, plaque rupture, extracellular matrix remodeling, and myocardial infarction (MI). MMP gene polymorphisms contribute to the risk of developing cardiovascular disease. We designed to investigate the association of acute MI (AMI) with a polymorphism in the human MMP-1, 2, 3, and 9 genes in Iranian patients with AMI. Genomic DNA of 400 enrolled patients with AMI and 200 controls was extracted from their blood samples. The -1607 1G/2G MMP-1, -1306 C/T MMP-2, -1171 5A/6A MMP-3, -1562 C/T MMP-9 polymorphisms were detected. Plasma levels of MMPs were analyzed. There are significant differences in MMP-3 '5A' allele and genotype in the patients with AMI comparing with controls. However, no significant differences were observed in MMP-1, 2, and 9 allele frequencies between the patients and controls. Differences between plasma levels of MMPs were significant in the patients than in controls. There were statistically significant differences between plasma MMP-3 in carriers of 5A allele compared with 6A allele. MMP-9 plasma levels were significantly higher in the carriers of -1306 TT and -1306 CT than CC. However, there were no statistically significant association between genetic variation of MMP-1, 2, and 3 in the patients and their plasma levels. These data suggest that MMP genotyping such as genetic polymorphism in MMP-3 might be helpful in determining susceptibility to AMI in Iranian patients. In addition, susceptibility to AMI might be related to MMP-9 gene expression, which affects its plasma levels.
    Coronary artery disease 09/2010; 21(6):330-5. · 1.56 Impact Factor
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    ABSTRACT: Current evidence indicates that extracellular matrix (ECM) remodeling is a component of acute myocardial infarction (AMI) and matrix metalloproteinase (MMP) has a role in early atherosclerosis, plaque rupture and myocardial infarction (MI). The necessity of inhibition of ECM remodeling and subsequent injuries in patients with AMI suggests that MMP might be involved in this task. Therefore, we investigated the activities of MMP-1, -2, -3, and -9 which play an important role in AMI. Plasma and peripheral blood mononuclear cells (PBMCs) of 50 patients with AMI were isolated from peripheral blood after the onset of AMI within 24 h, comparing with 50 control subjects. The active form of MMPs was measured by enzyme linked immunosorbent assay (ELISA); MMP proteins presence and expression by immunoblotting and zymography analysis; and mRNA expression of MMPs by real time reverse transcriptase polymerase chain reaction. Plasma concentrations of MMPs increase in patients rather than control subjects. Gel zymography revealed 43, 66, 45, and 83 kDa molecular weight bands which consistent with active MMP-1, -2, -3, and -9, respectively, exhibiting gelatin-degrading activity in both patient and control subjects. No up-regulation of mRNA expression was found. To our knowledge, it is the first monitoring of MMP gene and protein expression and also circulating active MMPs in Iranian patients with AMI and normal subjects. Up-regulation of MMPs activity is common in the falling myocardium and missing up-regulation of transcription indicates that protein levels of MMPs were regulated at the post transcriptional level.
    Journal of Thrombosis and Thrombolysis 03/2010; 30(4):404-11. · 1.99 Impact Factor
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    ABSTRACT: Although the aetiology of varicose veins remains unknown, recent studies have focused on endothelial cell integrity and function. Among the regulatory factors of vessel tone, synthesises, pro- and anti-inflammatory, adhesion molecules and the transcription factor hypoxia inducible factor-1 alpha (HIF-1alpha), which are responsible for recruiting leukocytes, are very important. Investigation in this study focused on the expression of ICAM-1, E-selectin and HIF-1alpha on endothelial cells using immunostaining and RT-PCR in varicose vein specimens compared with controls. Findings of this study showed alterations of the intima, such as focal intimal discontinuity and denudation of endothelium in varicose veins. Based on data derived from immunostaining and RT-PCR, no major differences were identified between ICAM-1 and E-selectin expression in varicose vein specimens compared with controls. In contrast, immunostaining results identified HIF-1alpha expression in five (5/20) varicose vein specimens, whereas no control saphenous vein specimens expressed HIF-1alpha. These findings could explain other evidence of hypoxia in varicose veins. Finally, results already obtained in this investigation suggest that the process of pathogenesis of varicose veins is not restricted to the role of adhesion molecules.
    Pathology 01/2010; 42(5):446-53. · 2.66 Impact Factor
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    ABSTRACT: Spermatogonia are the male germ line stem cells whose life long expansion is needed for permanent production of spermatozoa. The present study was designed to examine the effect of hCG treatment on germ cell proliferation following stem cell transplantation in mice. Spermatogonial stem cells were isolated from neonatal mice testes and characterized by alkaline phosphatase, immunoreactivity and morphological analysis. hCG was injected into normal and cell transplanted mice. We then evaluated the testosterone levels and cell number in normal mice. After that, cyclin B1 gene expression was investigated in transplanted mice. Different doses of busulfan were injected to investigate the effects of chemotherapy on morphological criteria and preparation of recipient mice for transplantation. In this report we show proliferative potential of spermatogonial stem cells after cytotoxic treatment, transplantation efficiency by semi-quantitative RT-PCR, and hCG effect on stem cell regeneration in normal mice and following cell transplantation. The results indicate that spermatogonial stem cells can proliferate after transplantation, and the efficiency of their transplantation depends on hormonal treatment. Therefore, hormonal treatment after stem cell transplantation will be a powerful avenue for increasing the efficiency of transplantation and fertility restoration.
    Avicenna Journal of Medical Biotechnology 01/2010; 2(1):23-35.
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    ABSTRACT: Spermatogonia are the male germ line stem cells whose life long expansion is needed for permanent production of spermatozoa. The present study was designed to examine the effect of hCG treatment on germ cell proliferation following stem cell transplantation in mice. Spermatogonial stem cells were isolated from neonatal mice testes and characterized by alkaline phosphatase, immunoreactivity and morphological analysis. hCG was injected into normal and cell transplanted mice. We then evaluated the testosterone levels and cell number in normal mice. After that, cyclin B1 gene expression was investigated in transplanted mice. Different doses of busulfan were injected to investigate the effects of chemotherapy on morphological criteria and preparation of recipient mice for transplantation. In this report we show proliferative potential of spermatogonial stem cells after cytotoxic treatment, transplantation efficiency by semi-quantitative RT-PCR, and hCG effect on stem cell regeneration in normal mice and following cell transplantation. The results indicate that spermatogonial stem cells can proliferate after transplantation, and the efficiency of their transplantation depends on hormonal treatment. Therefore, hormonal treatment after stem cell transplantation will be a powerful avenue for increasing the efficiency of transplantation and fertility restoration.
    Avicenna journal of medical biotechnology. 01/2010; 2(1):23-35.
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    ABSTRACT: Adherence is a primary prerequisite for bacterial colonisation and has been considered as one of the main criteria for selection of probiotic bacteria. Different cell lines have been used to investigate probiotic–host interactions in vitro. The comparison of adherence properties of probiotics among different cell lines has not yet been reported. The purpose of this study was to investigate and compare the adherence level and adherence pattern of a selection of probiotic bacteria to Caco-2, HEp-2 and T84 cell lines. The methods used compared probiotic bacteria adherence level and pattern among the cell lines. Eleven lactobacilli or bifidobacteria, isolated from pharmaceutical or dairy probiotic products, and five type strains were tested. Strains of Escherichia coli with known adherence patterns were used as controls. Adhesion assays were carried out using light microscopy. According to the number of cells in each field, and the number of bacteria attached to each of those cells, the adherence level of each strain was classified and compared among cell lines. Also, it was noted that probiotic bacteria showed a localised or diffused pattern of adherence, resembling that seen with locally or diffusely adherent E. coli. Patterns were strain not species dependent. The adherence pattern and level of 14 out of 16 of the strains were similar on HEp-2 and Caco-2. The similarity observed between T84 and Caco-2 was 10 out of 16. This study suggests the potential of using easily handled, rapidly growing HEp-2 cells for primary selection of epithelial adherence of probiotic bacteria.
    Annals of Microbiology 62(1). · 1.55 Impact Factor
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    ABSTRACT: Apoptosis is implicated in unfavorable remodeling of the left ventricle during acute myocardial infarction (AMI). Both DNA damage and p53 play important roles in regulating apoptosis. Expression patterns of apoptotic regulating genes such as p53, bax, and bcl-2 highlight the importance of inhibiting ventricle remodeling and subsequent injuries. In the present study, serum levels of p53 and 8-hydroxy-2-deoxyguanosine (8-OHdG) as well as p53, bax, and bcl-2 expression were examined after the onset of AMI in Iranian patients. Serum levels of p53 and 8-OHdG were measured by enzyme-linked immunosorbent assay (ELISA) and the presence of p53 protein and mRNA expression of p53, bax, and bcl-2 were analyzed by Western blotting and real time RT-PCR methods respectively. In patients presenting with AMI, serum levels of p53 and 8-OHdG were increased in comparison to healthy controls. Likewise, transcripts of p53 and bax were also elevated in patients while bcl-2 was decreased. Collectively, our data suggest the novel use of p53 and 8-OHdG as markers of apoptosis and DNA damage following AMI. Our results also revealed that apoptosis occurs in concert with an up-regulation of p53 and bax and a down-regulation of bcl-2 which may suggest a possible therapeutic intervention in patients recovering from AMI. KeywordsApoptosis-p53-bax-bcl-2-DNA damage-8-OHdG-Acute myocardial infarction
    Central European Journal of Biology 5(4):439-445. · 0.82 Impact Factor