Publications
29 results found
Moradi Marjaneh M, Challenger J, salas A, et al., 2023, Analysis of blood and nasal epithelial transcriptomes to identify mechanisms associated with control of SARS-CoV-2 viral load in the upper respiratory tract, Journal of Infection, Vol: 87, Pages: 538-550, ISSN: 0163-4453
Objectives:The amount of SARS-CoV-2 detected in the upper respiratory tract (URT viral load) is a key driver of transmission of infection. Current evidence suggests that mechanisms constraining URT viral load are different from those controlling lower respiratory tract viral load and disease severity. Understanding such mechanisms may help to develop treatments and vaccine strategies to reduce transmission. Combining mathematical modelling of URT viral load dynamics with transcriptome analyses we aimed to identify mechanisms controlling URT viral load.Methods:COVID-19 patients were recruited in Spain during the first wave of the pandemic. RNA sequencing of peripheral blood and targeted NanoString nCounter transcriptome analysis of nasal epithelium were performed and gene expression analysed in relation to paired URT viral load samples collected within 15 days of symptom onset. Proportions of major immune cells in blood were estimated from transcriptional data using computational differential estimation. Weighted correlation network analysis (adjusted for cell proportions) and fixed transcriptional repertoire analysis were used to identify associations with URT viral load, quantified as standard deviations (z-scores) from an expected trajectory over time.ResultsEighty-two subjects (50% female, median age 54 years (range 3–73)) with COVID-19 were recruited. Paired URT viral load samples were available for 16 blood transcriptome samples, and 17 respiratory epithelial transcriptome samples. Natural Killer (NK) cells were the only blood cell type significantly correlated with URT viral load z-scores (r = −0.62, P = 0.010). Twenty-four blood gene expression modules were significantly correlated with URT viral load z-score, the most significant being a module of genes connected around IFNA14 (Interferon Alpha-14) expression (r = −0.60, P = 1e-10). In fixed repertoire analysis, prostanoid-related gene expression was significantly associated with higher vir
Ahu Prah D, Dunican C, Amoah L, et al., 2023, Asymptomatic Plasmodium falciparum infection evades triggering a host transcriptomic response, Journal of Infection, Vol: 87, Pages: 259-262, ISSN: 0163-4453
Bidkhori HR, Farshchian M, Hasanzadeh H, et al., 2023, Unraveling The Effects of DICER1 Overexpression on Immune-Related Genes Expression in Mesenchymal Stromal/Stem Cells: Insights for Therapeutic Applications, Cell Journal, ISSN: 2228-5806
Moradi Marjaneh M, Kirk EP, Patrick R, et al., 2023, Quantitative trait and transcriptome analysis of genetic complexity underpinning cardiac interatrial septation in mice using an advanced intercross line, eLife, Vol: 12
<jats:p>Unlike single-gene mutations leading to Mendelian conditions, common human diseases are likely to be emergent phenomena arising from multilayer, multiscale, and highly interconnected interactions. Atrial and ventricular septal defects are the most common forms of cardiac congenital anomalies in humans. Atrial septal defects (ASD) show an open communication between the left and right atria postnatally, potentially resulting in serious hemodynamic consequences if untreated. A milder form of atrial septal defect, patent <jats:italic>foramen ovale</jats:italic> (PFO), exists in about one-quarter of the human population, strongly associated with ischaemic stroke and migraine. The anatomic liabilities and genetic and molecular basis of atrial septal defects remain unclear. Here, we advance our previous analysis of atrial septal variation through quantitative trait locus (QTL) mapping of an advanced intercross line (AIL) established between the inbred QSi5 and 129T2/SvEms mouse strains, that show extremes of septal phenotypes. Analysis resolved 37 unique septal QTL with high overlap between QTL for distinct septal traits and PFO as a binary trait. Whole genome sequencing of parental strains and filtering identified predicted functional variants, including in known human congenital heart disease genes. Transcriptome analysis of developing septa revealed downregulation of networks involving ribosome, nucleosome, mitochondrial, and extracellular matrix biosynthesis in the 129T2/SvEms strain, potentially reflecting an essential role for growth and cellular maturation in septal development. Analysis of variant architecture across different gene features, including enhancers and promoters, provided evidence for the involvement of non-coding as well as protein-coding variants. Our study provides the first high-resolution picture of genetic complexity and network liability underlying common congenital heart disease, with relevance to human ASD and PFO.<
Morfopoulou S, Buddle S, Torres Montaguth OE, et al., 2023, Genomic investigations of unexplained acute hepatitis in children, Nature, Vol: 617, Pages: 564-573, ISSN: 0028-0836
Since its first identification in Scotland, over 1,000 cases of unexplained paediatric hepatitis in children have been reported worldwide, including 278 cases in the UK1. Here we report an investigation of 38 cases, 66 age-matched immunocompetent controls and 21 immunocompromised comparator participants, using a combination of genomic, transcriptomic, proteomic and immunohistochemical methods. We detected high levels of adeno-associated virus 2 (AAV2) DNA in the liver, blood, plasma or stool from 27 of 28 cases. We found low levels of adenovirus (HAdV) and human herpesvirus 6B (HHV-6B) in 23 of 31 and 16 of 23, respectively, of the cases tested. By contrast, AAV2 was infrequently detected and at low titre in the blood or the liver from control children with HAdV, even when profoundly immunosuppressed. AAV2, HAdV and HHV-6 phylogeny excluded the emergence of novel strains in cases. Histological analyses of explanted livers showed enrichment for T cells and B lineage cells. Proteomic comparison of liver tissue from cases and healthy controls identified increased expression of HLA class 2, immunoglobulin variable regions and complement proteins. HAdV and AAV2 proteins were not detected in the livers. Instead, we identified AAV2 DNA complexes reflecting both HAdV-mediated and HHV-6B-mediated replication. We hypothesize that high levels of abnormal AAV2 replication products aided by HAdV and, in severe cases, HHV-6B may have triggered immune-mediated hepatic disease in genetically and immunologically predisposed children.
Ho A, Orton R, Tayler R, et al., 2023, Adeno-associated virus 2 infection in children with non-A-E hepatitis., Nature, Vol: 617, Pages: 555-563
An outbreak of acute hepatitis of unknown aetiology in children was reported in Scotland1 in April 2022 and has now been identified in 35 countries2. Several recent studies have suggested an association with human adenovirus with this outbreak, a virus not commonly associated with hepatitis. Here we report a detailed case-control investigation and find an association between adeno-associated virus 2 (AAV2) infection and host genetics in disease susceptibility. Using next-generation sequencing, PCR with reverse transcription, serology and in situ hybridization, we detected recent infection with AAV2 in plasma and liver samples in 26 out of 32 (81%) cases of hepatitis compared with 5 out of 74 (7%) of samples from unaffected individuals. Furthermore, AAV2 was detected within ballooned hepatocytes alongside a prominent T cell infiltrate in liver biopsy samples. In keeping with a CD4+ T-cell-mediated immune pathology, the human leukocyte antigen (HLA) class II HLA-DRB1*04:01 allele was identified in 25 out of 27 cases (93%) compared with a background frequency of 10 out of 64 (16%; P = 5.49 × 10-12). In summary, we report an outbreak of acute paediatric hepatitis associated with AAV2 infection (most likely acquired as a co-infection with human adenovirus that is usually required as a 'helper virus' to support AAV2 replication) and disease susceptibility related to HLA class II status.
Moradi Marjaneh M, Challenger J, Salas A, et al., 2023, Analysis of blood and nasal epithelial transcriptomes to identify mechanisms associated with control of SARS-CoV-2 viral load in the upper respiratory tract
Moradi Marjaneh M, Kirk E, Patrick R, et al., 2022, Quantitative trait and transcriptome analysis of genetic complexity underpinning cardiac interatrial septation in mice using an advanced intercross line, Publisher: bioRxiv
Asgharzadeh F, Moradi-Marjaneh R, Marjaneh MM, 2022, The Role of Heat Shock Protein 27 in Carcinogenesis and Treatment of ColorectalCancer, Current Pharmaceutical Design, Vol: 28, Pages: 2677-2685, ISSN: 1381-6128
<jats:sec><jats:title>Abstract:</jats:title><jats:p>The incidence of colorectal cancer (CRC) has significantly increased in recent decades, which has made this disease an important global health issue. Despite many efforts, there is no useful prognostic or diagnostic biomarker for CRC. Heat shock protein 27 (Hsp27) is one of the most studied members of Hsp family. It has attracted particular attention in CRC pathogenesis, since it is involved in fundamental cell functions for cell survival. Evidence show that Hsp27 plays important roles in CRC progression and metastasis. Hsp27 overexpression has been observed in CRC and suggested to be associated with CRC poor prognosis. In the present review, we focus on the current knowledge on the role of Hsp27 in CRC carcinogenesis and the underlying mechanisms. In addition, we discuss the value of targeting Hsp27 in CRC treatment.</jats:p></jats:sec>
Asgharzadeh F, Moradi-Marjaneh R, Marjaneh MM, 2022, The Role of Heat Shock Protein 40 in Carcinogenesis and Biology of ColorectalCancer, Current Pharmaceutical Design, Vol: 28, Pages: 1457-1465, ISSN: 1381-6128
<jats:sec><jats:title>Abstract:</jats:title><jats:p>Colorectal cancer (CRC) is the third most common cancer worldwide. Despite the enormous amountof effort in the diagnosis and treatment of CRC, the overall survival rate of patients remains low. The precisemolecular and cellular basis underlying CRC has not been completely understood yet. Over time, new genesand molecular pathways involved in the pathogenesis of the disease are being identified. The accurate discoveryof these genes and signaling pathways are important and urgent missions for the next generation of anticancertherapy research. Chaperone DnaJ, also known as Hsp40 (heat shock protein 40), has been of particular interestin CRC pathogenesis, as it is involved in the fundamental cell activities for maintaining cellular homeostasis.Evidence shows that protein family members of DnaJ/Hsp40 play both roles, enhancing and reducing thegrowth of CRC cells. In the present review, we focus on the current knowledge of the molecular mechanismsresponsible for DnaJ/Hsp40 in CRC carcinogenesis and biology.</jats:p></jats:sec>
Challenger J, Foo C, Wu Y, et al., 2022, Modelling upper respiratory viral load dynamics of SARS-CoV-2, BMC Medicine, Vol: 20, ISSN: 1741-7015
Relationships between viral load, severity of illness, and transmissibility of virus, are fundamental to understanding pathogenesis and devising better therapeutic and prevention strategies for COVID-19. Here we present within-host modelling of viral load dynamics observed in the upper respiratory tract (URT), drawing upon 2172 serial measurements from 605 subjects, collected from 17 different studies. We developed a mechanistic model to describe viral load dynamics and host response, and contrast this with simpler mixed-effects regression analysis of peak viral load and its subsequent decline. We observed wide variation in URT viral load between individuals, over 5 orders of magnitude, at any given point in time since symptom onset. This variation was not explained by age, sex, or severity of illness, and these variables were not associated with the modelled early or late phases of immune-mediated control of viral load. We explored the application of the mechanistic model to identify measured immune responses associated with control of viral load. Neutralizing antibody correlated strongly with modelled immune-mediated control of viral load amongst subjects who produced neutralizing antibody. Our models can be used to identify host and viral factors which control URT viral load dynamics, informing future treatment and transmission blocking interventions.
Khozoie C, Fancy N, Moradi Marjaneh M, et al., 2021, scFlow: A Scalable and Reproducible Analysis Pipeline for Single-Cell RNA Sequencing Data
Moradi-Marjaneh R, Asgharzadeh F, Khordad E, et al., 2021, Diabetes and COVID-19; a Review of Possible Mechanisms, Current Pharmaceutical Design, Vol: 27, Pages: 2522-2527, ISSN: 1381-6128
<jats:sec><jats:title /><jats:p>Coronavirus disease 2019 (SARS-CoV-2) (COVID-19) has recently raised worldwide public healthconcerns. The available data on COVID-19 in patients with diabetes is limited but generally indicate that thereis an increased risk of developing COVID-19 infection in diabetic patients, which ultimately impacts the overallpatient’s survival. Various aspects might be involved; however, the exact mechanisms and interrelationshipsbetween diabetes and the novel COVID-19 have not yet been fully elucidated. This review summarizes the possiblemechanisms by which present diabetes predispose individuals to COVID-19 infection, modulates the hostviralinteractions and increases the risk of mortality. We hope this review can provide beneficial information forfurther studies and contribute to improved disease management of diabetic patients with COVID-19.</jats:p></jats:sec>
Moradi-Marjaneh R, Asgharzadeh F, Khordad E, et al., 2021, The Clinical Impact of Quantitative Cell-free DNA, KRAS, and BRAF Mutations on Response to Anti-EGFR Treatment in Patients with Metastatic Colorectal Cancer, Current Pharmaceutical Design, Vol: 27, Pages: 942-952, ISSN: 1381-6128
<jats:sec><jats:title>:</jats:title><jats:p>Colorectal cancer (CRC) is one of the most common leading causes of cancer death in the world. AlthoughEGFR inhibitors have established efficacy in metastatic colorectal cancer (mCRC), some patients do notrespond to this treatment. The EGFR inhibitors' failure and acquired resistance are partly due to KRAS andBRAF mutations. Thus, prognostic biomarkers that help to select eligible patients are highly in demand. To improvepatient selection, assessment of mutational status in circulating cell free DNA (cfDNA), which possiblyrepresents the dynamicity of tumor genetic status better than tumor tissue, could be advantageous. This reviewsummarizes the current knowledge of the prognostic value of cfDNA in patients with mCRC treated withEGFR inhibitors with emphasis on the clinical importance of identification of KRAS and BRAF mutations.</jats:p></jats:sec>
Miranda M, Saunus JM, Akgül S, et al., 2021, A short ERK5 isoform modulates nucleocytoplasmic shuttling of active ERK5 and associates with poor survival in breast cancer
Moradi Marjaneh M, Beesley J, OMara TA, et al., 2020, Non-coding RNAs underlie genetic predisposition to breast cancer, Genome Biology, Vol: 21
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Genetic variants identified through genome-wide association studies (GWAS) are predominantly non-coding and typically attributed to altered regulatory elements such as enhancers and promoters. However, the contribution of non-coding RNAs to complex traits is not clear.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Using targeted RNA sequencing, we systematically annotated multi-exonic non-coding RNA (mencRNA) genes transcribed from 1.5-Mb intervals surrounding 139 breast cancer GWAS signals and assessed their contribution to breast cancer risk. We identify more than 4000 mencRNA genes and show their expression distinguishes normal breast tissue from tumors and different breast cancer subtypes. Importantly, breast cancer risk variants, identified through genetic fine-mapping, are significantly enriched in mencRNA exons, but not the promoters or introns. eQTL analyses identify mencRNAs whose expression is associated with risk variants. Furthermore, chromatin interaction data identify hundreds of mencRNA promoters that loop to regions that contain breast cancer risk variants.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>We have compiled the largest catalog of breast cancer-associated mencRNAs to date and provide evidence that modulation of mencRNAs by GWAS variants may provide an alternative mechanism underlying complex traits.</jats:p></jats:sec>
Beesley J, Sivakumaran H, Moradi Marjaneh M, et al., 2020, Chromatin interactome mapping at 139 independent breast cancer risk signals, Genome Biology, Vol: 21
<jats:title>Abstract</jats:title><jats:sec> <jats:title>Background</jats:title> <jats:p>Genome-wide association studies have identified 196 high confidence independent signals associated with breast cancer susceptibility. Variants within these signals frequently fall in distal regulatory DNA elements that control gene expression.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>We designed a Capture Hi-C array to enrich for chromatin interactions between the credible causal variants and target genes in six human mammary epithelial and breast cancer cell lines. We show that interacting regions are enriched for open chromatin, histone marks for active enhancers, and transcription factors relevant to breast biology. We exploit this comprehensive resource to identify candidate target genes at 139 independent breast cancer risk signals and explore the functional mechanism underlying altered risk at the 12q24 risk region.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Our results demonstrate the power of combining genetics, computational genomics, and molecular studies to rationalize the identification of key variants and candidate target genes at breast cancer GWAS signals.</jats:p> </jats:sec>
Beesley J, Sivakumaran H, Marjaneh MM, et al., 2020, eQTL Colocalization Analyses Identify <i>NTN4</i> as a Candidate Breast Cancer Risk Gene, AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 107, Pages: 778-787, ISSN: 0002-9297
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- Citations: 19
Fachal L, Aschard H, Beesley J, et al., 2020, Fine-mapping of 150 breast cancer risk regions identifies 191 likely target genes, Nature Genetics, Vol: 52, Pages: 56-73, ISSN: 1061-4036
Genome-wide association studies have identified breast cancer risk variants in over 150 genomic regions, but the mechanisms underlying risk remain largely unknown. These regions were explored by combining association analysis with in silico genomic feature annotations. We defined 205 independent risk-associated signals with the set of credible causal variants in each one. In parallel, we used a Bayesian approach (PAINTOR) that combines genetic association, linkage disequilibrium and enriched genomic features to determine variants with high posterior probabilities of being causal. Potentially causal variants were significantly over-represented in active gene regulatory regions and transcription factor binding sites. We applied our INQUSIT pipeline for prioritizing genes as targets of those potentially causal variants, using gene expression (expression quantitative trait loci), chromatin interaction and functional annotations. Known cancer drivers, transcription factors and genes in the developmental, apoptosis, immune system and DNA integrity checkpoint gene ontology pathways were over-represented among the highest-confidence target genes.
MoradiMarjaneh R, Paseban M, Moradi Marjaneh M, 2019, Hsp70 inhibitors: Implications for the treatment of colorectal cancer, IUBMB Life, Vol: 71, Pages: 1834-1845, ISSN: 1521-6543
<jats:title>Abstract</jats:title><jats:p>Colorectal cancer (CRC) is one of the most common malignancies in the world. Despite intensive advances in diagnosis and treatment of CRC, it is yet one of the leading cause of cancer related morbidity and mortality. Therefore, there is an urgent medical need for alternative therapeutic approaches to treat CRC. The 70 kDa heat shock proteins (Hsp70s) are a family of evolutionary conserved heat shock proteins, which play an important role in cell homeostasis and survival. They overexpress in various types of malignancy including CRC and are typically accompanied with poor prognosis. Hence, inhibition of Hsp70 may be considered as a striking chemotherapeutic avenue. This review summarizes the current knowledge on the progress made so far to discover compounds, which target the Hsp70 family, with particular emphasis on their efficacy in treatment of CRC. We also briefly explain the induction of Hsp70 as a strategy to prevent CRC.</jats:p>
Moradi Marjaneh M, Sivakumaran H, Hillman KM, et al., 2019, High-throughput allelic expression imbalance analyses identify candidate breast cancer risk genes
Betts JA, Moradi Marjaneh M, Al-Ejeh F, et al., 2017, Long Noncoding RNAs CUPID1 and CUPID2 Mediate Breast Cancer Risk at 11q13 by Modulating the Response to DNA Damage, The American Journal of Human Genetics, Vol: 101, Pages: 255-266, ISSN: 0002-9297
Ghoussaini M, French JD, Michailidou K, et al., 2016, Evidence that the 5p12 Variant rs10941679 Confers Susceptibility to Estrogen-Receptor-Positive Breast Cancer through FGF10 and MRPS30 Regulation, The American Journal of Human Genetics, Vol: 99, Pages: 903-911, ISSN: 0002-9297
Darabi H, Beesley J, Droit A, et al., 2016, Fine scale mapping of the 17q22 breast cancer locus using dense SNPs, genotyped within the Collaborative Oncological Gene-Environment Study (COGs), Scientific Reports, Vol: 6
<jats:title>Abstract</jats:title><jats:p>Genome-wide association studies have found SNPs at 17q22 to be associated with breast cancer risk. To identify potential causal variants related to breast cancer risk, we performed a high resolution fine-mapping analysis that involved genotyping 517 SNPs using a custom Illumina iSelect array (iCOGS) followed by imputation of genotypes for 3,134 SNPs in more than 89,000 participants of European ancestry from the Breast Cancer Association Consortium (BCAC). We identified 28 highly correlated common variants, in a 53 Kb region spanning two introns of the <jats:italic>STXBP4</jats:italic> gene, that are strong candidates for driving breast cancer risk (lead SNP rs2787486 (OR = 0.92; CI 0.90–0.94; <jats:italic>P</jats:italic> = 8.96 × 10<jats:sup>−15</jats:sup>)) and are correlated with two previously reported risk-associated variants at this locus, SNPs rs6504950 (OR = 0.94, <jats:italic>P</jats:italic> = 2.04 × 10<jats:sup>−09</jats:sup>, r<jats:sup>2</jats:sup> = 0.73 with lead SNP) and rs1156287 (OR = 0.93, <jats:italic>P</jats:italic> = 3.41 × 10<jats:sup>−11</jats:sup>, r<jats:sup>2</jats:sup> = 0.83 with lead SNP). Analyses indicate only one causal SNP in the region and several enhancer elements targeting <jats:italic>STXBP4</jats:italic> are located within the 53 kb association signal. Expression studies in breast tumor tissues found SNP rs2787486 to be associated with increased <jats:italic>STXBP4</jats:italic> expression, suggesting this may be a target gene of this locus.</jats:p>
Dunning AM, Michailidou K, Kuchenbaecker KB, et al., 2016, Breast cancer risk variants at 6q25 display different phenotype associations and regulate <i>ESR1</i>, <i>RMND1</i> and <i>CCDC170</i>, NATURE GENETICS, Vol: 48, Pages: 374-+, ISSN: 1061-4036
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- Citations: 98
Hedayati-Moghaddam MR, Marjaneh MM, Mashhadi IE, 2012, Knowledge and attitudes of physicians in private practice towards HIV/AIDS in Mashhad, Iran, International Journal of STD & AIDS, Vol: 23, Pages: e11-e16, ISSN: 0956-4624
<jats:p> Being responsible for providing care for HIV/AIDS in a society, physicians should be knowledgeable and have favourable attitudes. We designed a cross-sectional study to assess knowledge and attitudes towards HIV/AIDS of private practicing physicians in Mashhad, Iran. A total of 346 general practitioners and specialists completed anonymous self-administered questionnaires with response rate of 91.1%. For knowledge questions, the mean proportion of correct responses was 53.5% (±13.2). Misconceptions about HIV transmission were the main areas of insufficient knowledge. Surprisingly only 20% knew how to manage a patient who had experienced sexual contact with an HIV-positive partner. While 84% disagreed that ‘HIV-infected individuals deserved to catch infection’ owing to high-risk behaviours, 38% sympathized less with people who were infected via extramarital sex. It seems that knowledge and attitudes towards HIV/AIDS among the studied physicians is not favourable and is an area that requires attention to enable effective management of the disease in Iran. </jats:p>
Moradi Marjaneh M, Martin ICA, Kirk EP, et al., 2012, QTL mapping of complex binary traits in an advanced intercross line, Animal Genetics, Vol: 43, Pages: 97-101, ISSN: 0268-9146
<jats:title>Summary</jats:title><jats:p>An advanced intercross line (AIL) is an easier and more cost‐effective approach compared to recombinant inbred lines for fine mapping of quantitative trait loci (QTL) identified by F<jats:sub>2</jats:sub> designs. In an AIL, a complex binary trait can be mapped through analysis of either continuously distributed proxy traits for the liability of the binary trait or the liability itself, the latter presenting the greater statistical challenge. In another work, we successfully applied both approaches in an AIL to fine map previously identified QTL underlying anatomical parameters of the cardiac inter‐atrial septum including patent foramen ovale. Here, we describe the statistical methods that we used to analyse complex binary traits in our AIL design. This is achieved using a likelihood‐based method, with the expectation–maximisation algorithm allowing use of standard logistic regression methods for model fitting.</jats:p>
Moradi Marjaneh M, Kirk EP, Posch MG, et al., 2011, Investigation of Association between PFO Complicated by Cryptogenic Stroke and a Common Variant of the Cardiac Transcription Factor GATA4, PLoS ONE, Vol: 6, Pages: e20711-e20711
Mehdikhani Karimabad H, Shabestari M, Baharvand H, et al., 2011, Lack of benefi cial eff ects of granulocyte colony-stimulating factor in patients with subacute myocardial infarction undergoing late revascularization: a double-blind, randomized, placebo-controlled clinical trial, Acta Cardiologica, Vol: 66, Pages: 219-224, ISSN: 0001-5385
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