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Search Results: 1 - 10 of 1346 matches for " Ashraf Mohamadkhani "
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The TNF-α -308 Promoter Gene Polymorphism and Chronic HBV Infection
Sirous Tayebi,Ashraf Mohamadkhani
Hepatitis Research and Treatment , 2012, DOI: 10.1155/2012/493219
Abstract: Background and Aims. TNF-α -308 allele promoter polymorphism has been known to be a potential prognostic factor in patients with chronic HBV infection. We tried to determine how TNF-α -308 allele promoter polymorphism would affect the prognosis in patients with chronic HBV infection. Methods. We searched MEDLINE, EMBASE, and reference lists of relevant review articles related to the association between “TNF-α G-308A promoter polymorphism” with “chronic HBV infection”. We only focused on searching -308 locus in published studies. We reviewed 21 original articles about TNF-α -308 allele polymorphism and its effect on prognosis in patients with chronic HBV infection and discussed the results. Results. conflicting results were observed. The results were divided into 3 groups including neutral, negative, and positive associations between TNF-α -308 allele polymorphism and prognosis in patients with chronic HBV infection. We summarized the primary data as a table. Conclusions. Authors concluded that although there is an upward trend in evidence to claim that there is a positive relation between TNF-α G-308A promoter polymorphisms and resolution of chronic HBV infection, due to many biases and limitations observed in reviewed studies, an organized well-designed study is needed for clarifying the real association. 1. Introduction It is believed that during chronic hepatitis B infection, the host immune response is responsible for both hepatocellular damage and viral clearance [1, 2]. Hepatocyte damage persuades an inflammatory response through activation of tissue macrophage Kupffer cells [3]. These activated cells secrete antiviral cytokines which is thought to be central in suppression or clearance of HBV from the infected liver [4]. Cytokines are proteins or glycoproteins produced by cells acting on their specific receptors on the other cells’ surfaces. They are central mediators of inflammatory events such as infection or peripheral trauma. Several cytokines have been identified that participate in the process of viral clearance via host immune response to HBV. They include TNF-α, TGFβ, PGF, and other factors contributing towards the fibrogenesis [5, 6]. Among these, TNF-α is the most important cytokine in host immune response to viral infection [7, 8]. TNF-α is a pleiotropic cytokine, located 850?kb telomeric of class II HLA-DR locus of the short arm of chromosome 6, which induces cellular responses such as proliferation, production of inflammatory mediators, and cell death [9]. In the liver, TNF-α is involved in pathophysiology of viral hepatitis,
Impact of Lamivudine plus Adefovir therapy in chronic hepatitis B Iranian patients, resistant to Lamivudine treatment alone, on disease inhibition: A pilot study  [PDF]
Arezoo Estakhri, Ashraf Mohamadkhani, Hosein Poustchi, Ghodrat Montazeri
Open Journal of Gastroenterology (OJGas) , 2012, DOI: 10.4236/ojgas.2012.22015
Abstract: AIM: To evaluate the impact of combination therapy with Lamivudine and Adefovir for treatment of chronic hepatitis B in Lamivudine-resistant patients. METHODS: Among the 110 adult chronic hepatitis B Iranian patients whom were treated with Lamivudine, for 36 months, nineteen patients (17%) with no any biochemical and viral responses to Lamivudine alone, were selected and enrolled in the study. Due to resistancy, Adefovir was added to Lamivudine, and continued for 30 months. We measured HBV_DNA viral load and serum AST, ALT in 0, 12, 24, 30 and 0, 6, 12, 18, 24, 30 months, respectively. RESULTS: Between biochemical and viral characteristics, Repeated Measure analysis identified just biochemical markers— Aspartate Aminotransferase level (AST) (P = 0.002) and Alanine Aminotransferase level (ALT) (P = 0.007) —as predictors of response to treatment, while, viral marker—HBV DNA load—was not statistically significant (P = 0.128). CONCLUSIONS: Treatment for a long time, such as 21.5 ± 8.8 months, with Lami- vudine and Adefovir, can cause liver enzymes including AST and ALT, decreasing and being normal. But, this finding is not indicative, for HBV-DNA viral load.
Protein-x of hepatitis B virus in interaction with CCAAT/enhancer-binding protein α (C/EBPα) - an in silico analysis approach
Ashraf Mohamadkhani, Parisa Shahnazari, Zarrin Minuchehr, Armin Madadkar-Sobhani, Mahmoud Tehrani, Ferdous Jazii, Hossein Poustchi
Theoretical Biology and Medical Modelling , 2011, DOI: 10.1186/1742-4682-8-41
Abstract: The amino acid sequence of protein-x was extracted from UniProt [UniProt:Q80IU5] and the x-ray crystal structure of the partial CCAAT-enhancer α [PDB:1NWQ] was retrieved from the Protein Data Bank (PDB). Similarity search for protein-x was carried out by psi-blast and bl2seq using NCBI [GenBank: BAC65106.1] and Local Meta-Threading-Server (LOMETS) was used as a threading server for determining the maximum tertiary structure similarities. Advanced MODELLER was implemented to design a comparative model, however, due to the lack of a suitable template, Quark was used for ab initio tertiary structure prediction.The PDB-blast search indicated a maximum of 23% sequence identity and 33% similarity with crystal structure of the porcine reproductive and respiratory syndrome virus leader protease Nsp1α [PDB:3IFU]. This meant that protein-x does not have a suitable template to predict its tertiary structure using comparative modeling tools, therefore we used QUARK as an ab initio 3D prediction approach. Docking results from the ab initio tertiary structure of protein-x and crystal structure of the C/EBPα- DNA region [PDB:1NWQ] illustrated the protein-binding site interactions. Indeed, the N-terminal part of 1NWQ has a high affinity for certain regions in protein-x (e.g. from Ala76 to Ser101 and Thr105 to Glu125).In this study, we predicted the structure of protein-x of HBV in interaction with C/EBPα. The docking results showed that protein-x has an interaction synergy with C/EBPα. However, despite previous experimental data, protein-x was found to interact with DNA. This can lead to a better understanding of the function of protein-x and may provide an opportunity to use it as a therapeutic target.Human beings are the natural hosts for the hepatitis B virus (HBV), which infects approximately 350 million individuals worldwide each year. The 3.2-kb long viral genome is partially double stranded and contains four identified open reading frames (ORFs). The ORFx encodes the 154 ami
The inverse association of serum HBV DNA level with HDL and adiponectin in chronic hepatitis B infection
Ashraf Mohamadkhani, Kourosh Sayemiri, Reza Ghanbari, Elham Elahi, Hossein Poustchi, Ghodratollah Montazeri
Virology Journal , 2010, DOI: 10.1186/1743-422x-7-228
Abstract: To investigate correlation between HBV DNA level with clinical parameters in patients with chronic hepatitis B, 92 male subjects with HBV infection without any risk factors for diabetes were enrolled in this study. Age and BMI of the study population were matched and HBV DNA, ALT, tumor necrosis factor alpha (TNF-α), adiponectin and lipid levels was measured.Serum HBV DNA correlated inversely with serum HDL level (r = -0.23; P = 0.014). The median of log copies/ml for HBV DNA (3.67) was considered as cut off point. Patients with HBV DNA level higher than cut off point had lower adiponectin (8.7 ± 5.3 vs 10.7 ± 4.9 μg/ml p = 0.05). Also, adiponectin had a negative correlation with TNF-α (r = -0.21, P = 0.04) and positive correlations with HDL (r = 0.18, P = 0.043).Multivariate regression models show that serum HDL level is an independed factor to predict serum HBV DNA.Our findings showed that higher HBV DNA levels are associated with lower HDL and adiponectin but induced TNF-alpha values.The broad outcomes of hepatitis B virus (HBV) infection can be divided into acute infection and chronic hepatitis [1]. The ongoing replication of HBV in chronic hepatitis induce oxidative stress and associated with liver inflammation, which over the course of years increases risk of fibrosis, cirrhosis, and liver cancer [2,3]. Factors which determine viral replication and outcome of infection are not fully understood, although host factors are known to play a major role in this regard [4]. Among these factors, HDL, with several biological properties, including anti oxidative and anti inflammatory activities has a potential role to be a part of nonspecific immunity [5,6]. Adiponectin also attenuates inflammation, oxidative stress, and pro-inflammatory cytokine production [7].The anti-inflammatory function of HDL involves induction transforming growth factor β which might function as an important mediator of the anti-inflammatory activity [8]. In chronic hepatitis B patients, serum HDL
The role of mutations in core protein of hepatitis B virus in liver fibrosis
Ashraf Mohamadkhani, Ferdous Jazii, Hossein Poustchi, Omidreza Nouraein, Shahsanam Abbasi, Masoud Sotoudeh, Ghodratollah Montazeri
Virology Journal , 2009, DOI: 10.1186/1743-422x-6-209
Abstract: Worldwide, the 350 million people with chronic hepatitis B have a 15-25% risk of dying from HBV-related liver diseases, including cirrhosis and hepatocellular carcinoma [1]. It is evident that 70-84% of cirrhotic patients and 72% of individuals with hepatocellular carcinoma in Iran have evidence of exposure to HBV [2].Naturally occurring mutations of hepatitis B virus (HBV) genome have an important role in the activity of HBV related liver diseases. Patients with long standing active liver disease are at high risk to develop liver cirrhosis or hepatocellular carcinoma [3]. The genome of hepatitis B virus encodes four overlapping open reading frames that are translated to viral core protein or HBc particle, the surface proteins, a reverse transcriptase (RT), and HBx [4]. The core protein is the major polypeptide of the nucleocapsid that during virus assembly polymerizes around a complex consisting of pregenomic mRNA and viral polymerase [5]. Core protein with genotype D which is frequent in Iran [6] holding 183 amino acids with a set of closely linked α-helices [7] and consists of two distinct domains, an N-terminal domain with 144 residues required for the assembly of the 32 nm nucleocapsid and a functional C-terminal domain [5,8]. Empty core shells made from truncated HBc at residue 149 revealed the important role of C-terminal in viral genome binding and nuclear transport of the core protein [9-11]. The C-terminal arginine-rich domain with a high similarity to protamin, consists of three repeated SPRRR motifs corresponded to the part of core protein that interact closely with RNA [5]. In this domain phosphorylated site residues located in amino acid sequences 155-183. Immature nucleocapsids which contain RNA are phosphorylated at six sites, while the mature nucleocapsids which contain DNA are completely dephosphorylated either inside cells or in extracellular virions [9]. This phosphorylation clearly plays an important role in the regulation of the function of C-t
Clinical Feature of Intrahepatic B-Lymphocytes in Chronic Hepatitis B
Ashraf Mohamadkhani,Elnaz Naderi,Masoud Sotoudeh,Aezam Katoonizadeh,Ghodratollah Montazeri,Hossein Poustchi
International Journal of Inflammation , 2014, DOI: 10.1155/2014/896864
Abstract: Humoral immunity constitutes major defense mechanism against viral infections. However, the association of hepatic injury and B-cells population in chronic hepatitis B virus (HBV) carriers has not been studied well. In this study, fifty seven hepatitis B surface antigen (HBsAg) positive and HBeAg negative patients were studied to determine the expression of CD20, a cell surface marker expressed on B-cells, in liver biopsy sections using immunohistochemistry. The patients’ clinical data at the time of liver biopsy were acquired from their medical records. There was a significant association between log HBV DNA and both ALT ( , ) and histologic activity index (HAI) total score ( , ), respectively. The CD20 was expressed in all 57 liver biopsy samples with a submembranous and membranous staining pattern and its expression was significantly associated with HAI total score ( , ) and stage of fibrosis ( , ). The susceptible B lymphocytes to hepatitis B virus might be implicated in the development of immune mediated inflammation of HBV-induced hepatic injury. The present data also support that the liver is potentially one of the secondary lymphoid organs. 1. Introduction Chronic hepatitis B (CHB) virus (HBV) infection is the principal cause of cirrhosis and hepatocellular carcinoma (HCC) [1]. The pathogenesis of HBV-related chronic liver disease is not well understood. However, it is clear that the immune mechanisms associated with the antiviral response are responsible for CHB outcome [2–4]. The existence of lymphocytes in the human liver is representing a pathological situation [5]. This concept stems from the observation that, in chronic hepatitis B, T-cells can potentially participate both in the immune clearance of HBV-infected cells and in the pathogenesis of hepatocellular injury [6]. Furthermore the numbers of B lymphocytes and plasma cells are significantly higher in patients with liver cirrhosis than of those with inactive chronic hepatitis [7, 8]. Enormous intrahepatic B-cells with massive production of IgM and IgG and infiltrating plasma cells into the hepatic lobules have also been shown in HBV-associated chronic active hepatitis [9]. B-cells contribute to immune responses through the secretion of effector cytokines and it has been suggested that naive and memory B-cell subsets preferentially produce different effector cytokines [10, 11]. Na?ve B-cells undergo maturation by somatic hypermutation in immunoglobulin variable region of the B-cell receptor (BCR) genes following contact with a specific protein accessible on dendritic cells. Then the
The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation
Malihe Moradzadeh,Sirous Tayebi,Hossein Poustchi,Kourosh Sayehmiri,Parisa Shahnazari,Elnaz Naderi,Ghodratollah Montazeri,Ashraf Mohamadkhani
Advances in Virology , 2013, DOI: 10.1155/2013/780319
Abstract: Recognition mechanisms of innate immune response help to improve immunotherapeutic strategies in HBeAg-negative chronic hepatitis B (CHB). Toll-like receptor 2 (TLR2) is an important component of innate immunity. In this study, the frequency of precore mutations of the hepatitis B virus (HBV) and serum TLR2 were evaluated in CHB patients. Fifty-one patients with chronic hepatitis B, negative for HBeAg and detectable HBV DNA, were examined for the presence of mutations in pre-core region of HBV genome by direct sequencing. Serum TLR2 was measured by enzyme-linked immunosorbent assay. Interactions of truncated HBeAg and TLR2 proteins were evaluated with molecular docking software. The G1896A pre-core mutation were detected in 29 (57%) which was significantly associated with higher concentration of serum TLR2 in comparison with patients without this mutation (4.8 2.9 versus 3.4 2.2?ng/mL, ). There was also a significant correlation between serum ALT and TLR-2 ( ; ). Docking results illustrated residues within the N-terminus of truncated HBeAg and TLR2, which might facilitate the interaction of these proteins. These findings showed the dominance of G1896A pre-core mutation of HBV variants in this community which was correlated with serum TLR2. Moreover TLR2 is critical for induction of inflammatory cytokines and therefore ALT elevation. 1. Introduction Hepatitis B virus (HBV) infection is an important cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC) [1]. The transmission of HBV from infected mothers to neonates causes persistent infection [2]. Chronic infection of HBV is a global health problem. However, the prevalence and genotype distribution of HBV are different among the geographical areas [3]. The majority of chronic hepatitis B patients lose HBe antigen (HBeAg) and develop anti-HBe antibody, which is generally associated with a decrease in serum HBV DNA levels and a gradual accumulation of precore or core promoter mutations [4]. HBeAg-negative chronic hepatitis B is the predominant type of CHB in Mediterranean inhabitants [3]. Two types of precore and core promoter HBV mutations that reduce HBeAg formation are more frequent in regions where patients are predominantly infected with HBV genotype D [4, 5]. Infection with wild-type strains of HBV often induces mild symptoms and responds well to interferon alpha therapy, but patients infected with precore mutant variants may show clinical evidence of elevated or fluctuating ALT and HBV DNA [6]. The reason that precore negative mutants become predominant in some patients during
Detection of TP53 R249 Mutation in Iranian Patients with Pancreatic Cancer
Ashraf Mohamadkhani,Elnaz Naderi,Maryam Sharafkhah,Hamid Reza Fazli,Malihe Moradzadeh,Akram Pourshams
Journal of Oncology , 2013, DOI: 10.1155/2013/738915
Abstract: The TP53 gene encodes tumor protein p53 which play a major role in the etiology of pancreatic cancer. The important role of codon 249 of TP53 for binding of p53 to its sequence-specific consensus site in DNA has been revealed by crystallography’s studies, and mutation at this codon was detected in the plasma of some human cancers. The TP53 Mut assessor software within the International Agency for Research on Cancer (IARC) TP53 Database was performed to evaluate every possible mutation at codon 249. DNA was extracted from the plasma of 133 pancreatic cancer patients and 85 noncancer-bearing individuals. Exon 7 in TP53 was amplified, and mutation at R249 was identified by the endonuclease cleavage of HaeIII. The group of patients showed a frequency of 11% (22 of 133 samples) R249 mutation compared to 3.5% (3 of 85 samples) in the group of control which was significant ( ). This mutation demonstrated statistically significant association with pancreatic cancer risk in unadjusted odds ratio (OR: 3.74, 95% CI: 1.1–13.2; ); however when adjusted for confounding factors, it was marginally significant because of lower control samples. These findings demonstrate that mutation at R249 of TP53 can be considered for increasing risk of pancreatic cancer that needs more research. 1. Introduction Pancreatic ductal adenocarcinoma (PDAC), the most common cancer of the pancreas, is the fifth commonest cause of cancer-related mortality among industrialized countries [1]. There is not much data regarding incidence and mortality of pancreatic cancer in Middle East. However the cancer of pancreas is not in the top 10 of cancer-related deaths in Iran [2]. The aggressive nature of the PDAC is related to poor prognosis; therefore, most of the patients at the time of diagnosis are harboring unsuitable cancer that is extremely resistant to chemotherapy [3]. The incidence rate of pancreatic cancer has been stabilizing over the past two decades in many developed countries; however, this continues to increase in countries where the rate of pancreatic cancer was relatively low four decades ago, such as Japan [4]. In Iran, pancreatic cancer is diagnosed in advanced stage with no identified risk factors. Pancreatic cancer is primarily an environmental disease and attributed mostly to cigarette smoking [5]; however the pathogenesis of this cancer also involves various genetic alterations particularly genes that controlled the cell cycle [6, 7]. The TP53 (tumor protein p53) as a main tumor suppressor gene is mutated in most of the tumors [8, 9]. The p53 protein inhibits cancer formation
The Impact of Illicit Drug Use on Spontaneous Hepatitis C Clearance: Experience from a Large Cohort Population Study
Hossein Poustchi, Saeed Esmaili, Ashraf Mohamadkhani, Aghbibi Nikmahzar, Akram Pourshams, Sadaf G. Sepanlou, Shahin Merat, Reza Malekzadeh
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023830
Abstract: Background and Aims Acute hepatitis C infection usually ends in chronic infection, while in a minority of patients it is spontaneously cleared. The current population-based study is performed on a large cohort in Golestan province of Iran to examine the demographic correlates of Spontaneous Hepatitis C Clearance. Methods Serum samples used in this study had been stored in biorepository of Golestan Cohort Study. These samples were evaluated for anti hepatitis C Virus by third generation Enzyme-linked immunosorbent assay (ELISA). Subjects who tested positive were then invited and tested by Recombinant Immunoblot Assay (RIBA) and Ribonucleic Acid Polymerase Chain Reaction test (PCR). If tested positive for RIBA, subjects were recalled and the two tests were re-done after 6 months. Those subjects who again tested positive for RIBA but negative for PCR were marked as cases of spontaneous clearance. Results 49,338 serum samples were evaluated. The prevalence of Chronic Hepatitis C Virus (CHCV) infection based on PCR results was 0.31%. Among those who had acquired hepatitis C, the rate of SC was 38%. In multivariate analysis, illicit drug use both Injecting Use (OR = 3.271, 95% CI: 1.784–6.000, p-value<0.001) and Non-Injecting Use (OR = 1.901, 95% CI: 1.068–3.386, p-value = 0.029) were significant correlates of CHCV infection versus SC. Conclusions Illicit drug use whether intravenous or non-intravenous is the only significant correlate of CHCV, for which several underlying mechanisms can be postulated including repeated contacts with hepatitis C antigen.
Prediction of Future Configurations of a Moving Target in a Time-Varying Environment Using an Autoregressive Model  [PDF]
Ashraf Elnagar
Intelligent Control and Automation (ICA) , 2011, DOI: 10.4236/ica.2011.24033
Abstract: In this paper, we describe an algorithm for predicting future positions and orientation of a moving object in a time-varying environment using an autoregressive model (ARM). No constraint is placed on the obstacles motion. The model addresses prediction of translational and rotational motions. Rotational motion is represented using quaternions rather than Euler representation to improve the algorithm performance and accuracy of the prediction results. Compared to other similar systems, the proposed algorithm has an adaptive capability, which enables it to predict over multiple time-steps rather than fixed ones as reported in other works. Such algorithm can be used in a variety of applications. An important one is its application in the framework of designing reliable navigational systems for autonomous mobile robots and more particularly in building effective trajectory planners. Simulation results show how significantly this model could reduce computational cost.
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