Mahsa M. Amoli

Prof. Dr. Mahsa M. Amoli


Research Focus & Metrics

Academic Career Length

27Years (2000-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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10 December 2018 in Journal of Cellular Physiology
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RARasoul Abdollahzadeh
Rasoul Abdollahzadeh
ADAbdolreza Daraei
Abdolreza Daraei
YMYaser Mansoori
Yaser Mansoori
MSMasoumeh Sepahvand
Masoumeh Sepahvand
MAMahsa M. Amoli
Mahsa M. Amoli
JBJavad Tavakkoly Bazzaz
Javad Tavakkoly Bazzaz

1 August 2003 in Seminars in Arthritis and Rheumatism
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Journal Article
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Miguel Angel Gonzalez-GayMiguel Angel Gonzalez-Gay
Miguel Angel Gonzalez-Gay
MAMahsa M. Amoli
Mahsa M. Amoli
CGCarlos Garcia-Porrua
Carlos Garcia-Porrua
WOWilliam E.R. Ollier
William E.R. Ollier

1 June 2002 in Genes & Immunity
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Journal Article
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MAMahsa M. Amoli
Mahsa M. Amoli
SHS Hand
S Hand
AHA H Hajeer
A H Hajeer
KJK P Jones
K P Jones
SRS Rolf
S Rolf
WOW E R Ollier
W E R Ollier
Nut allergy is an important and potentially life threatening food allergy with a prevalence of one in 150 children in the UK population. STAT6 (signal transducer and activator of transcription) is an important molecule in the induction and regulation of an allergic response, which maps to chromosome 12q in a region previously linked with total serum IgE concentration and atopy in different populations. We have examined the frequency of a single nucleotide polymorphism (SNP) in the 3′UTR region of STAT6 gene in 71 UK Caucasoid patients diagnosed with nut allergy and 45 atopic patients without nut allergy using PCR-RFLP and compared these with 184 UK healthy controls. The STAT6 G allele frequency was significantly increased in nut allergy patients compared with blood donor controls (P < 0.0001, OR = 2.9, 95% CI: 1.7–4.9), which was under a recessive model (GG vs GA+AA, P = 0.0001, OR = 3.2, 95% CI: 1.7–5.8) but not in atopic patients without nut allergy. The G allele was most frequent in the severe cases and GG homozygosity was associated with the increased risk of severe reaction (OR = 3.9, 95% CI: 1.9–8.3). We conclude that STAT6 3′UTR polymorphism is associated with susceptibility and severity in nut allergic patients in our population.

8 June 2004 in Rheumatology
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Miguel Angel Gonzalez-GayMiguel Angel Gonzalez-Gay
Miguel Angel Gonzalez-Gay
JLJ. Llorca
J. Llorca
ESE. Sanchez
E. Sanchez
MAMahsa M. Amoli
Mahsa M. Amoli
CGC. Garcia-Porrua
C. Garcia-Porrua
Javier MartínJavier Martín
Javier Martín
Objective. To assess the influence of inducible and endothelial nitric oxide synthase (iNOS and eNOS) polymorphisms in susceptibility to rheumatoid arthritis (RA). Methods. Two hundred RA patients fulfilling the 1987 American College of Rheumatology classification criteria followed at the out-patient rheumatology clinic of the Hospital Xeral-Calde (Lugo, Spain) and 251 ethnically matched controls were studied. Patients and controls were genotyped by PCR-based techniques for a multiallelic (CCTTT)n repeat in the promoter region of the iNOS gene and for a T/C polymorphism at position −786 in the promoter region and a polymorphism in exon 7 (298Glu/Asp or 5557G/T) of the eNOS gene. Results. No significant difference in allele or genotype frequencies for either polymorphism in the eNOS gene was observed between RA patients and controls. The overall iNOS CCTTTn allelic or genotypic distribution did not show statistical significant differences between RA patients and controls. Interestingly, when we stratified the iNOS alleles into short (8–11) and long (12–16) repeats, significant differences were observed between RA patients and controls (P = 0.021; odds ratio = 1.37, 95% confidence interval 1.04–1.81). Of note, individuals carrying two alleles with a repeat number less than 12 (fewer than 196 base pairs) exhibited a double risk of developing RA (P = 0.005, odds ratio 2.26, 95% confidence interval 1.25–4.08). Conclusions. Significant differences in the iNOS promoter polymorphism genotype frequency between northwest Spanish RA patients and controls suggest a potential role for this polymorphism in susceptibility to RA.

26 October 2015 in Journal of Diabetes Research
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MKMehrnoosh Khodaeian
Mehrnoosh Khodaeian
SESamaneh Enayati
Samaneh Enayati
OTOzra Tabatabaei-Malazy
Ozra Tabatabaei-Malazy
MAMahsa M. Amoli
Mahsa M. Amoli
Introduction.Diabetes mellitus as the most prevalent metabolic disease is a multifactorial disease which is influenced by environmental and genetic factors. In this systematic review, we assessed the association between genetic variants and diabetes/its complications in studies with Iranian populations.Methods.Google Scholar, PubMed, Scopus, and Persian web databases were systematically searched up to January 2014. The search terms were “gene,” “polymorphism,” “diabetes,” and “diabetic complications”; nephropathy, retinopathy, neuropathy, foot ulcer, and CAD (coronary artery diseases); and Persian equivalents. Animal studies, letters to editor, and in vitro studies were excluded.Results.Out of overall 3029 eligible articles, 88 articles were included. We found significant association between CTLA-4, IL-18, VDR, TAP2, IL-12, and CD4 genes and T1DM, HNFαand MODY, haptoglobin, paraoxonase, leptin, TCF7L2, calreticulin, ERα, PPAR-γ2, CXCL5, calpain-10, IRS-1 and 2, GSTM1, KCNJ11, eNOS, VDR, INSR, ACE, apoA-I, apo E, adiponectin, PTPN1, CETP, AT1R, resistin, MMP-3, BChE K, AT2R, SUMO4, IL-10, VEGF, MTHFR, and GSTM1 with T2DM or its complications.Discussion.We found some controversial results due to heterogeneity in ethnicity and genetic background. We thought genome wide association studies on large number of samples will be helpful in identifying diabetes susceptible genes as an alternative to studying individual candidate genes in Iranian populations.

30 March 2010 in Molecular Biology Reports
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JBJavad Tavakkoly Bazzaz
Javad Tavakkoly Bazzaz
MAMahsa M. Amoli
Mahsa M. Amoli
VPVera Pravica
Vera Pravica
RCRamesh Chandrasecaran
Ramesh Chandrasecaran
ABAndrew J. M. Boulton
Andrew J. M. Boulton
IHIan V. Hutchinson
Ian V. Hutchinson