Hossein Najmabadi

Kariminejad & Najmabadi Pathology and Genetics Center, Teheran, Tehrān, Iran

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Publications (190)597.67 Total impact

  • Hossein Najmabadi, Kimia Kahrizi
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    ABSTRACT: Hearing impairment is the most common sensory disorder, present 1 in every 500 newborns. About 80% of genetic HL is classified as non-syndromic deafness. To date, over 115 non-syndromic loci have been identified of which fifty associated with autosomal recessive non-syndromic hearing loss (ARNSHL). In this review article, we represent the 40 genes function and contribution to genetic deafness in different Middle Eastern populations as well as gene frequencies and mutation spectrum. The vide variety of mutations have so far detected in 19 countries reflects the heterogeneity of the genes involved in HL in this region. The deafness genes can cause dysfunction of cochlear homeostasis, cellular organization, neuronal transmission, cell growth, differentiation, and survival, some coding for tectorial membrane-associated proteins, and the remaining with unknown functions. Non-syndromic deafness is highly heterogeneous and mutations in the GJB2 are responsible for almost 30-50% in northwest to as low as 0 to 5% in south and southeast of the Middle East, it remain as major gene in ARNSHL in Middle East. The other genes contributing to AR/ADNSHL in some countries has been determined while for many other countries in the Middle East has not been studied or little study has been done. With the advancement of next generation sequencing one could expect in next coming year many of the remaining genes to be determine and to understand their function in the inner ear.
    International Journal of Pediatric Otorhinolaryngology. 09/2014;
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    ABSTRACT: Mutations in the SLC26A4 gene cause both Pendred syndrome and autosomal recessive nonsyndromic hearing loss (ARNSHL) at the DFNB4 locus. The SLC26A4 mutations vary among different communities. Previous studies have shown that mutations in the SLC26A4 gene are responsible for the more common syndromic hereditary hearing loss in Iran. This study assesses the possibility of a founder mutation for Pendred syndrome in northwest Iran.
    International Journal of Pediatric Otorhinolaryngology 09/2014; · 1.35 Impact Factor
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    ABSTRACT: Next-generation sequencing has greatly accelerated the search for disease-causing defects, but even for experts the data analysis can be a major challenge. To facilitate the data processing in a clinical setting, we have developed a novel Medical Re-sequencing Analysis Pipeline (MERAP). MERAP assesses the quality of sequencing, and has optimized capacity for calling variants, including Single Nucleotide Variants, insertions and deletions, Copy Number Variation, and other structural variants. MERAP identifies polymorphic and known causal variants by filtering against public-domain databases, and flags non-synonymous and splice-site changes. MERAP uses a logistic model to estimate the causal likelihood of a given missense variant. MERAP considers the relevant information such as phenotype and interaction with known disease-causing genes. MERAP compares favorably with GATK, one of the widely used tools, because of its higher sensitivity for detecting indels, its easy installation, and its economical use of computational resources. Upon testing more than 1200 individuals with mutations in known and novel disease genes, MERAP proved highly reliable, as illustrated here for 5 families with disease-causing variants. We believe that the clinical implementation of MERAP will expedite the diagnostic process of many disease-causing defects.This article is protected by copyright. All rights reserved
    Human Mutation 09/2014; · 5.21 Impact Factor
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    ABSTRACT: NDST1 was recently proposed as a candidate gene for autosomal recessive intellectual disability in two families. It encodes a bifunctional GlcNAc N-deacetylase/N-sulfotransferase with important functions in heparan sulfate biosynthesis. In mice, Ndst1 is crucial for embryonic development and homozygous null mutations are perinatally lethal. We now report on two additional unrelated families with homozygous missense NDST1 mutations. All mutations described to date predict the substitution of conserved amino acids in the sulfotransferase domain, and mutation modeling predicts drastic alterations in the local protein conformation. Comparing the four families, we noticed significant overlap in the clinical features, including both demonstrated and apparent intellectual disability, muscular hypotonia, epilepsy, and postnatal growth deficiency. Furthermore, in Drosophila, knockdown of sulfateless, the NDST ortholog, impairs long-term memory, highlighting its function in cognition. Our data confirm NDST1 mutations as a cause of autosomal recessive intellectual disability with a distinctive phenotype, and support an important function of NDST1 in human development. © 2014 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 08/2014; · 2.30 Impact Factor
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    ABSTRACT: Intellectual Disabilities (ID), defined as a state of developmental deficit, result in significant limitation of intellect and poor adaptation behavior. A number of genetic factors can result in ID, such as chromosomal abnormalities, copy number variation, and single gene defect. Karyotyping is the routine method for detecting chromosomal abnormalities in patients with ID. More recently, the Multiplex Ligation-dependent Probe Amplification (MLPA) method has been applied for detecting microdeletion/duplication in patients with dysmorphism and ID.
    Archives of Iranian medicine 07/2014; 17(7):471-474. · 1.22 Impact Factor
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    ABSTRACT: Bardet-Biedl syndrome (BBS) is a rare ciliopathy disorder that is clinically and genetically heterogeneous with 18 known genes. This study was performed to characterize responsible genes and mutation spectrum in a cohort of 14 Iranian families with BBS. Sanger sequencing of the most commonly mutated genes (BBS1, BBS2 and BBS10) accounting for ∼50% of BBS patients determined mutations only in BBS2, including three novel mutations. Next, three of the remaining patients were subjected to whole exome sequencing with 96% at 20 × depth of coverage that revealed novel BBS4 mutation. Observation of no mutation in the other patients represents the possible presence of novel genes. Screening of the remaining patients for six other genes (BBS3, BBS4, BBS6, BBS7, BBS9 and BBS12) revealed five novel mutations. This result represents another indication for the genetic heterogeneity of BBS and extends the mutational spectrum of the disease by introducing nine novel mutations in five BBS genes. In conclusion, although BBS1 and BBS10 are among the most commonly mutated genes in other populations like Caucasian, these two seem not to have an important role in Iranian patients. This suggests that a different strategy in molecular genetics diagnostic approaches in Middle Eastern countries such as Iran should be considered.Journal of Human Genetics advance online publication, 22 May 2014; doi:10.1038/jhg.2014.28.
    Journal of human genetics. 05/2014;
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    ABSTRACT: Coronary artery disease (CAD) is the leading cause of mortality in many parts of the world. Genome-wide association studies (GWAS) have identified several genetic variants associated with CAD in Low-density lipoprotein receptor (LDLR) locus. This study was evaluated the possible association of genetic markers at LDLR locus with CAD irrespective to lipid profile and as well as the association of these SNPs with severity of CAD in Iranian population. Sequencing of 2 exons in LDLR gene (Exon 2, 12) and part of intron 30 of SMARCA4 gene include rs1122608, was performed in 170 Iranian patients angiographically confirmed CAD and 104 healthy controls by direct sequencing. Sullivan's scoring system was used for determining the severity of CAD in cases. Our results showed that homozygote genotypes of rs1122608 (P<0.0001), rs4300767 (P<0.005) and rs10417578 (p<0.007) SNPs have strong protective effects on the CAD. In addition, we found that rs1122608 (GT or TT) was at higher risk of three vessel involvement compared to single vessels affecting (P=0.01).
    Acta medica Iranica 05/2014; 52(5):352-359.
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    ABSTRACT: GGCX mutations have been reported in patients with a pseudoxanthoma elasticum (PXE)-like phenotype, loose redundant skin, with multiple Vitamin K-dependent coagulation factor deficiencies. We report on the clinical findings and molecular results in 13 affected members of two families who had a uniform phenotype consisting of (PXE)-like skin manifestations in neck and trunk, loose sagging skin of trunk and upper limbs, and retinitis pigmentosa (RP) confirmed by ElectroRetinoGraphies in 10 affected individuals. There were no coagulation abnormalities. Molecular investigations of the ATP-Binding Cassette subfamily C member 6 (ABCC6) did not yield causative mutations. All 13 affected family members were found to be homozygous for the splice-site mutation c.373+3 G>T in the Gamma-Glutamyl carboxylase (GGCX) gene. All tested parents were heterozygous for the mutation, and healthy siblings were either heterozygous or had the wild-type. We suggest that the present patients represent a hitherto unreported phenotype associated with GGCX mutations. Di-genic inheritance has been suggested to explain the variability in phenotype in GGCX mutation carriers. Consequently, the present phenotype may not be explained only by the GGCX mutations only but may be influenced by variants in other genes or epigenetic and environmental factors.Journal of Investigative Dermatology accepted article peview online, 16 April 2014. doi:10.1038/jid.2014.191.
    Journal of Investigative Dermatology 04/2014; · 6.19 Impact Factor
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    ABSTRACT: In the context of a comprehensive research project, investigating novel autosomal recessive intellectual disability (ARID) genes, linkage analysis based on autozygosity mapping helped identify an intellectual disability locus on Chr.12q24, in an Iranian family (LOD score=3.7). Next-generation sequencing (NGS) following exon enrichment in this novel interval, detected a nonsense mutation (p.Q1010*) in the CLIP1 gene. CLIP1 encodes a member of microtubule (MT) plus-end tracking proteins, which specifically associates with the ends of growing MTs. These proteins regulate MT dynamic behavior and are important for MT-mediated transport over the length of axons and dendrites. As such, CLIP1 may have a role in neuronal development. We studied lymphoblastoid and skin fibroblast cell lines established from healthy and affected patients. RT-PCR and western blot analyses showed the absence of CLIP1 transcript and protein in lymphoblastoid cells derived from affected patients. Furthermore, immunofluorescence analyses showed MT plus-end staining only in fibroblasts containing the wild-type (and not the mutant) CLIP1 protein. Collectively, our data suggest that defects in CLIP1 may lead to ARID.European Journal of Human Genetics advance online publication, 26 February 2014; doi:10.1038/ejhg.2014.13.
    European journal of human genetics: EJHG 02/2014; · 3.56 Impact Factor
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    Alimohammad Asgharian, Mehdi Banan, Hossein Najmabadi
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    ABSTRACT: β-Gal DNA plasmid was used as a reporter DNA for determining the rate of gene transfection into HeLa cells. To accomplish the highest gene delivery into HeLa cells, optimizing experiments were car- ried out in different volumes of FuGENE-HD, Lipofectamine(TM)2000 and X-tremeGENE. Also, we investigated tranasfection efficiency in presence of various cell densities of HeLa cells. Then, transfection efficiency and cell toxicity were measured by beta gal staining and trypan blue methods, respectively. Using FuGENE-HD in volume of 4µl along with 10(5) HeLa cells, transfection efficiency was higher (43.66 ± 1.52%) in comparison with the cationic lipids Lipofectamine(TM)2000 and X-tremeGENE. In addition, the rate of cell toxicity in presence of FuGENE-HD was less than 5%. In summary, the cationic lipid FuGENE-HD indicates a suitable potential to transfer DNA into HeLa cells and it can be an efficient reagent for gene delivery for HeLa cells in vitro. Moreover, it is worth designing and optimizing gene transfer experiments for other cell lines with FuGENE-HD due to its low toxicity and high efficiency.
    Cell Journal 01/2014; 15(4):372-377. · 0.23 Impact Factor
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    ABSTRACT: Abstract Our study aimed to determine the number of couples with normal hemoglobin (Hb) electrophoresis and low-borderline hematological values, which may come up with a clinically critical status in their offspring. The number of couples at risk for severe α-thalassemia (α-thal) needed to be estimated before recommending genetic counseling and prenatal diagnosis (PND). During the past 14 years, from at least 7000 referrals, 754 couples were investigated for α-thal by direct mutation detection methods followed by reverse strip assay and α-globin gene sequencing for inconclusive cases. Detection of silent β-thalassemia (β-thal) mutations was done in suspected cases by complete β-globin gene sequencing. We were able to provide a molecular diagnosis in 87.3% (658/754) of couples. A total of 9.1% (60/658) may have a clinically significant hemoglobinopathy in their offspring. Significant conditions included hydrops fetalis (20.0%; 12/60), certain Hb H (β4) genotypes (78.3%; 47/60) and β-thal intermedia (β-TI) (1.7%; 1/60). The diagnostic flowchart for couples with microcytic hypochromic anemia in countries with a high prevalence of hemoglobinopathies should include α and β gene sequencing. As our results indicate, every nine out of 100 of these couples will face significant hemoglobinopathies and every two out of 100 can carry Hb Bart's (γ4) hydrops fetalis in their pregnancies. For such cases, PND should be utilized to allow the carrier couples to decide whether or not to abort the fetus.
    Hemoglobin 01/2014; 38(3):153-7. · 0.89 Impact Factor
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    ABSTRACT: Ethnic-specific differences in minor allele frequency impact variant categorization for genetic screening of nonsyndromic hearing loss (NSHL) and other genetic disorders. We sought to evaluate all previously reported pathogenic NSHL variants in the context of a large number of controls from ethnically distinct populations sequenced with orthogonal massively parallel sequencing methods. We used HGMD, ClinVar, and dbSNP to generate a comprehensive list of reported pathogenic NSHL variants and re-evaluated these variants in the context of 8,595 individuals from 12 populations and 6 ethnically distinct major human evolutionary phylogenetic groups from three sources (Exome Variant Server, 1000 Genomes project, and a control set of individuals created for this study, the OtoDB). Of the 2,197 reported pathogenic deafness variants, 325 (14.8%) were present in at least one of the 8,595 controls, indicating a minor allele frequency (MAF) >0.00006. MAFs ranged as high as 0.72, a level incompatible with pathogenicity for a fully penetrant disease like NSHL. Based on these data, we established MAF thresholds of 0.005 for autosomal-recessive variants (excluding specific variants in GJB2) and 0.0005 for autosomal-dominant variants. Using these thresholds, we recategorized 93 (4.2%) of reported pathogenic variants as benign. Our data show that evaluation of reported pathogenic deafness variants using variant MAFs from multiple distinct ethnicities and sequenced by orthogonal methods provides a powerful filter for determining pathogenicity. The proposed MAF thresholds will facilitate clinical interpretation of variants identified in genetic testing for NSHL. All data are publicly available to facilitate interpretation of genetic variants causing deafness.
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    ABSTRACT: Many abnormal α-chain hemoglobins (Hbs) are caused by single nucleotide mutations in α1- or α2-goblin genes. One of these Hbs is Hb Q-Iran which is resulted from a point mutation at codon 75 of the α1-globin gene (Asp→His). The identification of Hb Q-Iran was observed in two members of a family from the Central Province of Iran. In this study, Globin chain analysis on high performance liquid chromatography (HPLC) and DNA sequencing were applied. An unusual Hb variant, like HbS on alkaline pH electrophoresis was identified from samples of a father and his son from Arak city in the Central Province of Iran. The variant was further characterized by globin chain analysis and DNA sequencing methods. Globin chain analysis revealed an unknown globin chain peak after α-globin chain peak with a different retention time from βs-globin chain, as the control in both samples. Genetic analysis led to the identification of an unknown Hb variant, Hb Q-Iran. Globin chain analysis showed the presence of an unknown globin chain, and likewise DNA sequencing revealed HbQ-Iran. In other words, Globin chain analysis procedure could preliminarily detect an unknown globin chain.
    Archives of Iranian medicine. 12/2013; 16(12):739-740.
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    ABSTRACT: Mental retardation (MR) has a prevalence of 1-3% and genetic causes are present in more than 50% of patients. Chromosomal abnormalities are one of the most common genetic causes of MR and are responsible for 4-28% of mental retardation. However, the smallest loss or gain of material visible by standard cytogenetic is about 4 Mb and for smaller abnormalities, molecular cytogenetic techniques such as array comparative genomic hybridization (array CGH) should be used. It has been shown that 15-25% of idiopathic MR (IMR) has submicroscopic rearrangements detectable by array CGH. In this project, the genomic abnormalities were investigated in 32 MR patients using this technique. Patients with IMR with dysmorphism were investigated in this study. Karyotype analysis, fragile X and metabolic tests were first carried out on the patients. The copy number variation was then assessed in a total of 32 patients with normal results for the mentioned tests using whole genome oligo array CGH. Multiple ligation probe amplification was carried out as a confirmation test. In total, 19% of the patients showed genomic abnormalities. This is reduced to 12.5% once the two patients with abnormal karyotypes (upon re-evaluation) are removed. The array CGH technique increased the detection rate of genomic imbalances in our patients by 12.5%. It is an accurate and reliable method for the determination of genomic imbalances in patients with IMR and dysmorphism.
    Indian Journal of Human Genetics 10/2013; 19(4):443-8.
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    ABSTRACT: Mental retardation/Developmental delay (MR/DD) is present in 1 - 3% of the general population (1, 2). MR is defined as a significant impairment of both cognitive (IQ < 70) and social adaptive functions, with onset before 18 years of age. The purpose was to determine the results of subtelomeric screening by the Multiplex Ligation Dependent Probe Amplification (MLPA) Technique in 100 selected patients with idiopathic mental retardation (IMR) in Iran. A number of 100 patients with IMR, normal karyotypes and negative fragile-X and metabolic tests were screened for subtelomeric abnormalities using MLPA technique. Nine of 100 patients showed subtelomeric abnormalities with at least one of the two MLPA kits. Deletion in a single region was found in 3 patients, and in two different subtelomeric regions in 1 patient. Duplication was only single and was present in 2 patients. Three patients were found to have both a deletion and duplication.MLPA testing in the parental samples of 7 patients which was accessible showed that 4 patients were de novo, 2 patients had inherited from a clinically normal mother, and one had inherited from a clinically normal father. Screening with the two MLPA kits (SALSA P036 and SALSA P070) proved abnormality in only five of the 9 patients. So, the prevalence rate of abnormal subtelomeres using MLPA technique in patients with idiopathic MR in our study was 5 - 9%, the higher limit referring to the positive results of one of the two MLPA kits, and the lower limit representing the results of positive double-checking with the two MLPA kits.
    Iranian Red Crescent medical journal. 10/2013; 15(10):e8221.
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    ABSTRACT: Succinic semialdehyde dehydrogenase (SSADH) deficiency is a disorder of the catabolism of the neurotransmitter gamma-aminobutyric acid (GABA) with a very variable clinical phenotype ranging from mild intellectual disability to severe neurological defects. We report here on a large Iranian family with four affected patients presenting with severe intellectual disability, developmental delay and generalized tonic-clonic seizures. Molecular genetic analysis revealed a missense mutation c.901A>G (p.K301E, RefSeq number NM_001080) in ALDH5A1 co-segregating with the disease in the family. The missense mutation affects an amino acid residue that is highly conserved across the animal kingdom. Protein modeling showed that p.K301E most likely leads to a loss of NAD(+) binding and a predicted decrease in the free energy by 6.67 kcal/mol furthermore suggests a severe destabilization of the protein. In line with these in silico observations, no SSADH enzyme activity could be detected in patient lymphoblasts. © 2013 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 07/2013; · 2.30 Impact Factor
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    ABSTRACT: Osteoarthritis (OA) is a degenerative disease of the joints characterized by degradation of the hyaline articular cartilage and remodeling of the subchondral bone with sclerosis. The asporin (ASPN) gene encodes a cartilage extracellular protein belonging to the small leucine-rich proteoglycan family. Polymorphisms in the aspartic acid (D) repeat region in the second exon of this gene, which consist of GAT repeats, are associated with OA susceptibility. The D14 allele, which contains 14 D-repeats, is associated with increased OA susceptibility in the Japanese and the Han Chinese but is not an important factor in OA etiology among Caucasians, though the D15 allele is a risk allele for the Greek population. To examine the possibility of this controversial association, we explored the effect of ASPN on Iranians with knee OA. The D-repeat polymorphism was genotyped in 100 knee OA patients and 100 controls, and the allelic association of the D-repeat was examined. Our data suggest that the D15 allele could be considered a risk allele significant only for women (P = .045, odds ratio = 1.73, 95% confidence interval [CI] = 1.01-2.94) in the Iranian population. This association is in part similar to that found for the Greek population.
    American journal of orthopedics (Belle Mead, N.J.) 07/2013; 42(7):313-6.
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    ABSTRACT: Recently, five genetic modifiers [β-globin mutations, coinheritance of α-thalassemia (α-thal), XmnI polymorphism and single nucleotide polymorphisms (SNPs) in the BCL11A and HBS1L-MYB loci] were used to predict the β-thal major (β-TM) or β-thal intermedia (β-TI) types in 106 French patients with 83.2% accuracy. The dichotomous grouping was based on the age when the patient received his/her first transfusion (4 years). Here, a similar study was conducted in a cohort of 306 Iranian β-thal patients having distinct β-globin mutations and minor allele frequencies of key SNPs in these loci. Multivariate regression analyses and a simple scoring system were used to predict the β-TM/β-TI types using three scenarios: 1) when considering only the severe β-TM and the mild β-TI cases, 2) using clinical parameters for β-thal typing, and 3) using age at first transfusion as the basis for classification. Using these scenarios, the β-thal types could be correctly predicted in 77.6, 75.5 and 68.0% of cases, respectively.
    Hemoglobin 06/2013; · 0.89 Impact Factor
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    ABSTRACT: Several studies have implicated the 5-HTTLPR polymorphism in treatment outcomes of selective serotonin re-uptake inhibitors in patients with major depression. The aim of this study was to examine the association between polymorphism in the serotonin transporter gene and citalopram effectiveness in Iranian patients suffering from major depressive disorder (MDD). The sample consisted of 104 patients, with Fars ethnic background, who were diagnosed according to DSM-IV-TR criteria. Beck Depression inventory was used to evaluate the severity of the symptoms during the follow-up, and to determine clinical response of the patients at 4th and 8th week, respectively. Our results showed a correlation between the genotype and response to antidepressant drug citalopram, (odds ratios for L/S and L/L were 3.90 (95 percent CI: 1.29- 11.80) and 1.90 (95 percent CI: 0.72-5.08), respectively). In conclusion, our results reveal that genetic variation of serotonin transporter is involved in clinical remission of major depressive episodes in Iranian patients after citalopram treatment.
    Iranian journal of psychiatry. 06/2013; 8(2):86-91.

Publication Stats

2k Citations
597.67 Total Impact Points

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  • 2004–2014
    • Kariminejad & Najmabadi Pathology and Genetics Center
      Teheran, Tehrān, Iran
    • Tehran University of Medical Sciences
      • School of Medicine
      Tehrān, Ostan-e Tehran, Iran
  • 2002–2014
    • University of Social Welfare and Rehabilitation Sciences
      • Genetics Research Center
      Teheran, Tehrān, Iran
  • 2013
    • Freie Universität Berlin
      • Department of Biology, Chemistry, and Pharmacy
      Berlin, Land Berlin, Germany
  • 2006–2012
    • Max Planck Institute for Molecular Genetics
      • Department of Human Molecular Genetics
      Berlín, Berlin, Germany
  • 2011
    • Iran University of Medical Science
      Teheran, Tehrān, Iran
    • Emory University
      • Department of Cell Biology
      Atlanta, GA, United States
    • ETH Zurich
      • Institute of Cell Biology
      Zürich, ZH, Switzerland
  • 2004–2011
    • Ludwig-Maximilian-University of Munich
      • Department of Neurology
      München, Bavaria, Germany
  • 2007–2010
    • University of Iowa
      • Department of Otolaryngology-Head and Neck Surgery
      Iowa City, IA, United States
    • Charité Universitätsmedizin Berlin
      Berlín, Berlin, Germany
    • University of Antwerp
      • Medische Genetica (MEDGEN)
      Antwerpen, VLG, Belgium
  • 2009
    • University of Dohuk
      Duhuk, Dahūk, Iraq
    • University of Michigan
      • Department of Human Genetics
      Ann Arbor, MI, United States
    • Babol University of Medical Sciences
      Barfrush, Māzandarān, Iran
  • 2008
    • Ahvaz Jondishapour University of Medical Sciences
      • Thalassemia and Hemoglobinopathy Research Center
      Ahvāz, Ostan-e Khuzestan, Iran
    • Zahedan University of Medical Sciences
      Dowzdāb, Sīstān va Balūchestān, Iran
    • National Institute of Genetic Engineering and Biotechnology
      Teheran, Tehrān, Iran