Log in

Relevant bibliographies by topics / Genomic Segmental Duplications

Contents

Journal articles
Dissertations / Theses
Book chapters
Conference papers

Academic literature on the topic 'Genomic Segmental Duplications'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Genomic Segmental Duplications.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Genomic Segmental Duplications"

1

Bosfield, Kerri, Jullianne Diaz, and Eyby Leon. "Pure Distal 7q Duplication: Describing a Macrocephalic Neurodevelopmental Syndrome, Case Report and Review of the Literature." Molecular Syndromology 12, no. 3 (2021): 159–68. http://dx.doi.org/10.1159/000513453.

Full text

Abstract:

Pure distal duplications of 7q have rarely been described in the medical literature. The term pure refers to duplications that occur without an accompanying clinically significant deletion. Pure 7q duplications of various segments have previously been reported in the literature; however, pure distal 7q duplications have only been reported in 21 cases. Twenty of these earlier reports described patients who were identified via karyotype and 1 recently by microarray. Cases have also been reported in genomic databases such as DECIPHER and the University of California Santa Cruz genome browser. We have reviewed 7 additional cases with distal 7q duplications from these databases and compared them to 7 previously reported distal 7q duplication cases to uncover common features including global developmental delay, frontal bossing, macrocephaly, seizures, kyphoscoliosis/skeletal anomalies, and microretrognathia/palatal anomalies. In this case, we describe a 4-year-old boy with a 30.8-Mb pure duplication of 7q32.1q36.3. Newly reported features associated with this duplication include intermittent dystonic posturing, increased behavioral irritability, eosinophilic esophagitis, segmental vertebral anomalies, and segmental intermittent limb cyanosis. We highlight the importance of using publicly available databases to describe rare genetic syndromes and to better characterize the features of pure distal 7q duplications and further postulate that duplication of this region represents a recognizable macrocephalic neurodevelopmental syndrome.

APA, Harvard, Vancouver, ISO, and other styles

2

Fraser, James A., Johnny C. Huang, Read Pukkila-Worley, J. Andrew Alspaugh, Thomas G. Mitchell, and Joseph Heitman. "Chromosomal Translocation and Segmental Duplication in Cryptococcus neoformans." Eukaryotic Cell 4, no. 2 (February 2005): 401–6. http://dx.doi.org/10.1128/ec.4.2.401-406.2005.

Full text

Abstract:

ABSTRACT Large chromosomal events such as translocations and segmental duplications enable rapid adaptation to new environments. Here we marshal genomic, genetic, meiotic mapping, and physical evidence to demonstrate that a chromosomal translocation and segmental duplication occurred during construction of a congenic strain pair in the fungal human pathogen Cryptococcus neoformans. Two chromosomes underwent telomere-telomere fusion, generating a dicentric chromosome that broke to produce a chromosomal translocation, forming two novel chromosomes sharing a large segmental duplication. The duplication spans 62,872 identical nucleotides and generated a second copy of 22 predicted genes, and we hypothesize that this event may have occurred during meiosis. Gene disruption studies of one embedded gene (SMG1) corroborate that this region is duplicated in an otherwise haploid genome. These findings resolve a genome project assembly anomaly and illustrate an example of rapid genome evolution in a fungal genome rich in repetitive elements.

APA, Harvard, Vancouver, ISO, and other styles

3

Emanuel, Beverly S., and Tamim H. Shaikh. "Segmental duplications: an 'expanding' role in genomic instability and disease." Nature Reviews Genetics 2, no. 10 (October 2001): 791–800. http://dx.doi.org/10.1038/35093500.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Soylev, Arda, Thong Minh Le, Hajar Amini, Can Alkan, and Fereydoun Hormozdiari. "Discovery of tandem and interspersed segmental duplications using high-throughput sequencing." Bioinformatics 35, no. 20 (April 1, 2019): 3923–30. http://dx.doi.org/10.1093/bioinformatics/btz237.

Full text

Abstract:

Abstract Motivation Several algorithms have been developed that use high-throughput sequencing technology to characterize structural variations (SVs). Most of the existing approaches focus on detecting relatively simple types of SVs such as insertions, deletions and short inversions. In fact, complex SVs are of crucial importance and several have been associated with genomic disorders. To better understand the contribution of complex SVs to human disease, we need new algorithms to accurately discover and genotype such variants. Additionally, due to similar sequencing signatures, inverted duplications or gene conversion events that include inverted segmental duplications are often characterized as simple inversions, likewise, duplications and gene conversions in direct orientation may be called as simple deletions. Therefore, there is still a need for accurate algorithms to fully characterize complex SVs and thus improve calling accuracy of more simple variants. Results We developed novel algorithms to accurately characterize tandem, direct and inverted interspersed segmental duplications using short read whole genome sequencing datasets. We integrated these methods to our TARDIS tool, which is now capable of detecting various types of SVs using multiple sequence signatures such as read pair, read depth and split read. We evaluated the prediction performance of our algorithms through several experiments using both simulated and real datasets. In the simulation experiments, using a 30× coverage TARDIS achieved 96% sensitivity with only 4% false discovery rate. For experiments that involve real data, we used two haploid genomes (CHM1 and CHM13) and one human genome (NA12878) from the Illumina Platinum Genomes set. Comparison of our results with orthogonal PacBio call sets from the same genomes revealed higher accuracy for TARDIS than state-of-the-art methods. Furthermore, we showed a surprisingly low false discovery rate of our approach for discovery of tandem, direct and inverted interspersed segmental duplications prediction on CHM1 (<5% for the top 50 predictions). Availability and implementation TARDIS source code is available at https://github.com/BilkentCompGen/tardis, and a corresponding Docker image is available at https://hub.docker.com/r/alkanlab/tardis/. Supplementary information Supplementary data are available at Bioinformatics online.

APA, Harvard, Vancouver, ISO, and other styles

5

Nicholas, Thomas J., Ze Cheng, Katrina L. Mealey, Evan E. Eichler, and Joshua M. Akey. "The genomic architecture of segmental duplications and copy number variants in dogs." Journal of Veterinary Behavior 4, no. 2 (March 2009): 71–72. http://dx.doi.org/10.1016/j.jveb.2008.09.037.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Dang, Vinh T., Karin S. Kassahn, Andrés Esteban Marcos, and Mark A. Ragan. "Identification of human haploinsufficient genes and their genomic proximity to segmental duplications." European Journal of Human Genetics 16, no. 11 (June 4, 2008): 1350–57. http://dx.doi.org/10.1038/ejhg.2008.111.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Costantino, Lorenzo, Sotirios K. Sotiriou, Juha K. Rantala, Simon Magin, Emil Mladenov, Thomas Helleday, James E. Haber, George Iliakis, Olli P. Kallioniemi, and Thanos D. Halazonetis. "Break-Induced Replication Repair of Damaged Forks Induces Genomic Duplications in Human Cells." Science 343, no. 6166 (December 5, 2013): 88–91. http://dx.doi.org/10.1126/science.1243211.

Full text

Abstract:

In budding yeast, one-ended DNA double-strand breaks (DSBs) and damaged replication forks are repaired by break-induced replication (BIR), a homologous recombination pathway that requires the Pol32 subunit of DNA polymerase delta. DNA replication stress is prevalent in cancer, but BIR has not been characterized in mammals. In a cyclin E overexpression model of DNA replication stress, POLD3, the human ortholog of POL32, was required for cell cycle progression and processive DNA synthesis. Segmental genomic duplications induced by cyclin E overexpression were also dependent on POLD3, as were BIR-mediated recombination events captured with a specialized DSB repair assay. We propose that BIR repairs damaged replication forks in mammals, accounting for the high frequency of genomic duplications in human cancers.

APA, Harvard, Vancouver, ISO, and other styles

8

Nicholas, T. J., Z. Cheng, M. Ventura, K. Mealey, E. E. Eichler, and J. M. Akey. "The genomic architecture of segmental duplications and associated copy number variants in dogs." Genome Research 19, no. 3 (December 22, 2008): 491–99. http://dx.doi.org/10.1101/gr.084715.108.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Yoshimoto, Maisa, Olga Ludkovski, Dave DeGrace, Julia L. Williams, Andrew Evans, Kanishka Sircar, Tarek A. Bismar, Paulo Nuin, and Jeremy A. Squire. "PTEN genomic deletions that characterize aggressive prostate cancer originate close to segmental duplications." Genes, Chromosomes and Cancer 51, no. 2 (November 1, 2011): 149–60. http://dx.doi.org/10.1002/gcc.20939.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Nuttle, Xander, Andy Itsara, Jay Shendure, and Evan E. Eichler. "Resolving genomic disorder–associated breakpoints within segmental DNA duplications using massively parallel sequencing." Nature Protocols 9, no. 6 (May 29, 2014): 1496–513. http://dx.doi.org/10.1038/nprot.2014.096.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Genomic Segmental Duplications"

1

Locke, Devin Paul. "SEGMENTAL DUPLICATIONS PROMOTE GENOMIC INSTABILITY IN HUMAN CHROMOSOME 15q11-q13." Case Western Reserve University School of Graduate Studies / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=case1088114861.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

DeConti, Derrick K. "Systematic Analysis of Duplications and Deletions in the Malaria Parasite P. falciparum: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/869.

Full text

Abstract:

Duplications and deletions are a major source of genomic variation. Duplications, specifically, have a significant impact on gene genesis and dosage, and the malaria parasite P. falciparum has developed resistance to a growing number of anti-malarial drugs via gene duplication. It also contains highly duplicated families of antigenically variable allelic genes. While specific genes and families have been studied, a comprehensive analysis of duplications and deletions within the reference genome and population has not been performed. We analyzed the extent of segmental duplications (SD) in the reference genome for P. falciparum, primarily by a whole genome self alignment. We discovered that while 5% of the genome identified as SD, the distribution within the genome was partition clustered, with the vast majority localized to the subtelomeres. Within the SDs, we found an overrepresentation of genes encoding antigenically diverse proteins exposed to the extracellular membrane, specifically the var, rifin, and stevor gene families. To examine variation of duplications and deletions within the parasite populations, we designed a novel computational methodology to identify copy number variants (CNVs) from high throughput sequencing, using a read depth based approach refined with discordant read pairs. After validating the program against in vitro lab cultures, we analyzed isolates from Senegal for initial tests into clinical isolates. We then expanded our search to a global sample of 610 strains from Africa and South East Asia, identifying 68 CNV regions. Geographically, genic CNV were found on average in less than 10% of the population, indicating that CNV are rare. However, CNVs at high frequency were almost exclusively duplications associated with known drug resistant CNVs. We also identified the novel biallelic duplication of the crt gene – containing both the chloroquine resistant and sensitive allele. The synthesis of our SD and CNV analysis indicates a CNV conservative P. falciparum genome except where drug and human immune pressure select for gene duplication.

APA, Harvard, Vancouver, ISO, and other styles

3

DeConti, Derrick K. "Systematic Analysis of Duplications and Deletions in the Malaria Parasite P. falciparum: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/869.

Full text

Abstract:

Duplications and deletions are a major source of genomic variation. Duplications, specifically, have a significant impact on gene genesis and dosage, and the malaria parasite P. falciparum has developed resistance to a growing number of anti-malarial drugs via gene duplication. It also contains highly duplicated families of antigenically variable allelic genes. While specific genes and families have been studied, a comprehensive analysis of duplications and deletions within the reference genome and population has not been performed. We analyzed the extent of segmental duplications (SD) in the reference genome for P. falciparum, primarily by a whole genome self alignment. We discovered that while 5% of the genome identified as SD, the distribution within the genome was partition clustered, with the vast majority localized to the subtelomeres. Within the SDs, we found an overrepresentation of genes encoding antigenically diverse proteins exposed to the extracellular membrane, specifically the var, rifin, and stevor gene families. To examine variation of duplications and deletions within the parasite populations, we designed a novel computational methodology to identify copy number variants (CNVs) from high throughput sequencing, using a read depth based approach refined with discordant read pairs. After validating the program against in vitro lab cultures, we analyzed isolates from Senegal for initial tests into clinical isolates. We then expanded our search to a global sample of 610 strains from Africa and South East Asia, identifying 68 CNV regions. Geographically, genic CNV were found on average in less than 10% of the population, indicating that CNV are rare. However, CNVs at high frequency were almost exclusively duplications associated with known drug resistant CNVs. We also identified the novel biallelic duplication of the crt gene – containing both the chloroquine resistant and sensitive allele. The synthesis of our SD and CNV analysis indicates a CNV conservative P. falciparum genome except where drug and human immune pressure select for gene duplication.

APA, Harvard, Vancouver, ISO, and other styles

4

Zody, Michael C. "Investigation of Mechanics of Mutation and Selection by Comparative Sequencing." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl.[distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-108266.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Johnson, Matthew Eric. "PRIMATE GENE AND GENOME EVOLUTION DRIVEN BY SEGMENTAL DUPLICATION ON CHROMOSOME 16." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1190140658.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Iseric, Hamza. "BISER: fast characterization of segmental duplication structure in multiple genome assemblies." Thesis, Schloss Dagstuhl -- Leibniz-Zentrum für Informatik, 2021. http://hdl.handle.net/1828/13343.

Full text

Abstract:

The increasing availability of high-quality genome assemblies raised interest in the characterization of genomic architecture. Major architectural elements, such as common repeats and segmental duplications (SDs), increase genome plasticity that stimulates further evolution by changing the genomic structure and inventing new genes. Optimal computation of SDs within a genome requires quadratic-time local alignment algorithms that are impractical due to the size of most genomes. Additionally, to perform evolutionary analysis, one needs to characterize SDs in multiple genomes and find relations between those SDs and unique (non-duplicated) segments in other genomes. A na ̈ıve approach consisting of multiple sequence alignment would make the optimal solution to this problem even more impractical. Thus there is a need for fast and accurate algorithms to characterize SD structure in multiple genome assemblies to better understand the evolutionary forces that shaped the genomes of today. Here we introduce a new approach, BISER, to quickly detect SDs in multiple genomes and identify elementary SDs and core duplicons that drive the formation of such SDs. BISER improves earlier tools by (i) scaling the detection of SDs with low homology (75%) to multiple genomes while introducing further 10–34× speed-ups over the existing tools, and by (ii) characterizing elementary SDs and detecting core duplicons to help trace the evolutionary history of duplications to as far as 300 million years.
Graduate

APA, Harvard, Vancouver, ISO, and other styles

7

Newman, Tera. "Complex evolution of the 7E segmental duplications and 7E olfactory receptor genes /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10848.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Antonell, Boixader Anna. "Evolució molecular i estudi funcional de gens localitzats a les duplicacions segmentàries de la regió 7q11.23." Doctoral thesis, Universitat Pompeu Fabra, 2006. http://hdl.handle.net/10803/7151.

Full text

Abstract:

En aquest treball es presenta l'evolució molecular i estudi funcional de gens localitzats a les duplicacions segmentàries de la regió 7q11.23, implicada en la Síndrome de Williams-Beuren (SWB). S'ha datat l'aparició d'aquestes duplicacions en els últims 25 milions d'anys d'evolució i s'ha proposat un model evolutiu amb reordenaments específics i mecanismes de generació. Correlacions clínico-moleculars en els pacients amb la SWB han permès determinar que l'haploinsuficiència per NCF1, un gen localitzat a les duplicacions, és un factor protector per hipertensió. S'ha proposat un model patogènic per la hipertensió, implicant l'oxidasa NAD(P)H i estrès oxidatiu, suggerint que noves estratègies terapèutiques podrien ser utilitzades. A més, s'ha caracteritzat parcialment la funció de GTF2IRD2, un altre gen de les duplicacions. GTF2IRD2 interacciona amb altres factors de transcripció relacionats, té una localització subcel·lular variable i no s'uneix a ADN. Aquests resultats contribueixen a conèixer millor els mecanismes mutacionals i patogènics de la SWB.
This work presents the molecular evolution along with the functional analysis of the genes located in the segmental duplications flanking the 7q11.23 region, involved in Williams-Beuren syndrome (WBS). The generation of the segmental duplications has been dated to the last 25 million years of evolution and an evolutionary model with specific rearrangements and mechanisms has been proposed. Clinical-molecular correlations in WBS patients have allowed to determine that haploinsufficiency at NCF1, a gene located in the duplications, is a protective factor for hypertension. A pathogenic model for hypertension has been proposed, implicating NAD(P)H oxidase and oxidative stress, and suggesting that novel therapeutic strategies could be used. In addition, the functional characterization of another gene of the duplications, GTF2IRD2, has been partially achieved. GTF2IRD2 has been shown to interact with other related transcription factors, to display variable subcellular localization and to lack DNA binding properties. These results contribute to a better knowledge of the mutational and pathogenic mechanisms of the WBS.

APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Genomic Segmental Duplications"

1

Kahn, Crystal L., Shay Mozes, and Benjamin J. Raphael. "Efficient Algorithms for Analyzing Segmental Duplications, Deletions, and Inversions in Genomes." In Lecture Notes in Computer Science, 169–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-04241-6_15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Jun, Jin, Paul Ryvkin, Edward Hemphill, Ion Măndoiu, and Craig Nelson. "Estimating the Relative Contributions of New Genes from Retrotransposition and Segmental Duplication Events during Mammalian Evolution." In Comparative Genomics, 40–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-87989-3_4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Vallente, Rhea U., and Evan E. Eichler. "Segmental duplications and the human genome." In Encyclopedia of Genetics, Genomics, Proteomics and Bioinformatics. Chichester: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/047001153x.g203205.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Kirov, George, Michael C. O’Donovan, and Michael J. Owen. "Genomic Syndromes in Schizophrenia." In Neurobiology of Mental Illness, edited by Pamela Sklar, 247–55. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0019.

Full text

Abstract:

Several submicroscopic genomic deletions and duplications known as copy number variants (CNVs) have been reported to increase susceptibility to schizophrenia. Those for which the evidence is particularly strong include deletions at chromosomal segments 1q21.1, 3q29, 15q11.2, 15q13.3, 17q12 and 22q11.2, duplications at 15q11.2-q13.1, 16p13.1, and 16p11.2, and deletions atthe gene NRXN1. The effect of each on individual risk is relatively large, but it does not appear that any of them is alone sufficient to cause disorder in carriers. These CNVs often arise as new mutations(de novo). Analyses of genes enriched among schizophrenia implicated CNVs highlight the involvement in the disorder of post-synaptic processes relevant to glutamatergicsignalling, cognition and learning. CNVs that contribute to schizophrenia risk also contribute to other neurodevelopmental disorders, including intellectual disability, developmental delay and autism. As a result of selection, all known pathogenic CNVs are rare, and none makes a sizeable contribution to overall population risk of schizophrenia, although the study of these mutations is nevertheless providing important insights into the origins of the disorder.

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Genomic Segmental Duplications"

1

Sadler, J. Evan. "THE MOLECULAR BIOLOGY OF VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643930.

Full text

Abstract:

Human von Willebrand factor (vWF) is a plasma glycoprotein that is synthesized by endothelial cells and megakaryocytes, and perhaps by syncytiotrophoblast of placenta. The biosynthesis of vWF is very complex, involving proteolytic processing, glycosyla-tion, disulfide bond formation, and sulfation. Mature vWF consists of a single subunit of ∼ 250,000 daltons that is assembled into multimer ranging from dimers to species of over 10 million daltons. vWF performs its essential hemostatic function through several binding interactions, forming a bridge between specific receptors on the platelet surface and components of damaged vascular subendothelial connective tissue. Inherited deficiency of vWF, or von Willebrand disease (vWD), is the most common genetically transmitted bleeding disorder worldwide. The last two years has been a time of very rapid progress in understanding the molecular biology of vWF. Four research groups have independently isolated and sequenced the 9 kilobase full-length vWF cDNA. The predicted protein sequence has provided a foundation for understanding the biosynthetic processing of vWF, and has clarified the relationship between vWF and a 75-100 kilodalton plasma protein of unknown function, von Willebrand antigen II (vWAgll)/ vWAgll is co-distributed with vWF in endothelial cells and platelets, and is deficient in patients with vWD. The cDNA sequence of vWF shows that vWAgll is a rather large pro-peptide for vWF, explaining the biochemical and genetic association between the two proteins. vWF has a complex evolutionary history marked by many separate gene segment duplications. The primary structure of the protein contains four distinct types of repeated domains present in two to four copies each. Repeated domains account for over 90 percent of the protein sequence. This sequence provides a framework for ordering the functional domains that have been defined by protein chemistry methods. A tryptic peptide from the amino-terminus of vWF that overlaps domain D3 binds to factor VIII and also appears to bind to heparin. Peptides that include domain A1 bind to collagens, to heparin, and to platelet glycoprotein Ib. A second collagen binding site appears to lie within domain A3. The vWF cDNA has been expressed in heterologous cells to produce small amounts of functionally and structurally normal vWF, indicating that endothelial cells are not unique in their ability to process and assemble vWF multimers. Site-directed mutagenesis has been used to show that deletion of the propeptide of vWF prevents the formation of multimers. Cloned cDNA probes have been employed to isolate vWF genomic DNA from cosmid and λ-phage libraries, and the size of the vWF gene appears to be ∼ 150 kilobases. The vWF locus has been localized to human chromosome 12p12—pter. Several intragenic RFLPs have been characterized. With them, vWF has been placed on the human genetic linkage map as the most telomeric marker currently available for the short arm of chromosome 12. A second apparently homologous locus has been identified on chromosome 22, but the relationship of this locus to the authentic vWF gene is not yet known. The mechanism of vWD has been studied by Southern blotting of genomic DNA with cDNA probes in a few patients. Three unrelated pedigrees have been shown to have total deletions of the vWF gene as the cause of severe vWD (type III). This form of gene deletion appears to predispose to the development of inhibitory alloantibodies to vWF during therapy with cryoprecipitate. During the next several years recombinant DNA methods will continue to contribute our understanding of the evolution, biosynthesis, and structure-function relationships of vWF, as well as the mechanism of additional variants of vWD at the level of gene structure.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!