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This digital document is an article from Southern Medical Journal, published by Southern Medical Association on December 1, 2001. The length of the article is 987 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

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Title: Stroke after Marijuana smoking in a teenager with factor V Leiden mutation.(Brief Article)
Author: Mark A. Marinella
Publication: Southern Medical Journal (Refereed)
Date: December 1, 2001
Publisher: Southern Medical Association
Volume: 94Issue: 12Page: 1217(2)

Article Type: Brief Article

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This digital document is an article from Internal Medicine News, published by Thomson Gale on August 15, 2006. The length of the article is 691 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

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Title: Estrogen use with factor V Leiden not advised.(Women's Health)(Clinical report)
Author: Colin Nelson
Publication: Internal Medicine News (Magazine/Journal)
Date: August 15, 2006
Publisher: Thomson Gale
Volume: 39Issue: 16Page: 22(1)

Article Type: Clinical report

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This digital document is an article from Proceedings of the North Dakota Academy of Science, published by North Dakota Academy of Science on April 1, 2007. The length of the article is 816 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available immediately after purchase. You can view it with any web browser.

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Title: Factor V Leiden genetic variant in an American Indian population.(COMMUNICATIONS--PROFESSIONAL)
Author: Melanie Nadeau
Publication: Proceedings of the North Dakota Academy of Science (Magazine/Journal)
Date: April 1, 2007
Publisher: North Dakota Academy of Science
Volume: 61Page: 50(1)

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Chapters: Single Nucleotide Polymorphisms, 5-Httlpr, Factor V Leiden, Rs6265, Rs6313, Rs6295, Rs5569, Rs6311, Rs6314, Rs7997012, Rs1805054, Rs4680, Rs1801133, Rs1800955, Rs7341475, Rs1799913, Rs1800532, Asp294his, Mt-Snp, Rs1954787, Y-Snp, Rs6294, Rs28363170. Source: Wikipedia. Pages: 70. Not illustrated. Free updates online. Purchase includes a free trial membership in the publisher's book club where you can select from more than a million books without charge. Excerpt: 5-HTTLPR (serotonin-transporter-linked promoter region) is a degenerate repeat polymorphic region in SLC6A4, the gene that codes for the serotonin transporter. Since the polymorphism was identified in the middle of the 1990s, it has been extensively investigated, e.g., in connection with neuropsychiatric disorders. A 2006 scientific article stated that "over 300 behavioral, psychiatric, pharmacogenetic and other medical genetics papers" had analyzed the polymorphism. The serotonin transporter gene (SLC6A4) with the 5-HTTLPR is located on chromosome 17.The polymorphism occurs in the promoter region of the gene. Researchers commonly report it with two variations: A short ("s") and a long ("l"), but it can be subdivided further. In connection with the region are two single nucleotide polymorphisms (SNP): rs25531 and rs25532. One study published in 2000 found 14 allelic variants (14-A, 14-B, 14-C, 14-D, 15, 16-A, 16-B, 16-C, 16-D, 16-E, 16-F, 19, 20 and 22) in a group of around 200 Japanese and Caucasian people. The difference between 16-A and 16-D is the rs25531 SNP. It is also the difference between 14-A and 14-D. Some studies have found that long allele results in higher serotonin transporter mRNA transcription in human cell lines. The higher level may be due to the A-allele of rs25531, such that subjects with the long-rs25531(A) allelic combination (sometimes written LA) have higher levels while long-rs25531(G) carriers have levels more similar to short-al...More: http://booksllc.net/?id=17967841 ... Read more

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Purchase includes free access to book updates online and a free trial membership in the publisher's book club where you can select from more than a million books without charge. Chapters: Factor V Leiden, Rs6265, Rs6313, Rs6295, Rs5569, Rs6311, Rs6314, Rs7997012, Rs1805054, Rs4680, Rs1801133, Rs1800955, Rs7341475, Rs1799913, Rs1800532, Asp294his, Mt-Snp, Rs1954787, Y-Snp, Rs6294. Excerpt:SNP: Asp294His Asp294His (rs1805009) is a single nucleotide polymorphism (SNP) in the MC1R gene and it is associated with red hair and light skin type. Other SNPs in the gene, Arg151Cys and Arg160Trp, are also associated with red hair. References (URLs online) A hyperlinked version of this chapter is at factor V Leiden Factor V Leiden (sometimes factor VLeiden ) is the name given to a variant of human factor V that causes a hypercoagulability disorder. In this disorder the Leiden variant of factor V cannot be inactivated by activated protein C . Factor V Leiden is the most common hereditary hypercoagulability disorder amongst Eurasians . It is named after the city Leiden (Netherlands ), where it was first identified in 1994 by Prof R. Bertina et al. Pathophysiology In the normal person, factor V functions as a cofactor to allow factor X to activate an enzyme called thrombin . Thrombin in turn cleaves fibrinogen to fibrin , which polymerizes to form the dense meshwork that makes up the majority of a clot . Activated protein C (aPC) is a natural anticoagulant that acts to limit the extent of clotting by cleaving and degrading factor V. SNP: Factor V Leiden Factor V Leiden is an autosomal dominant condition which exhibits incomplete dominance and results in a factor V variant which cannot be as easily degraded by aPC (activated Protein C ). The gene that codes the protein is referred to as F5 . Mutation of this gene a single nucleotide polymorphism (SNP) is located in exon 10. As a missense substitution index{mi... ... Read more

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Information on many genetic disorders, and the frequent new findings on them, has been extremely difficult to come by—until now. The “Gale Encyclopedia of Genetic Disorders” addresses the need for current, hard-to-find facts on emerging discoveries. The two-volume Encyclopedia, presented in a single alphabetical sequence, provides clear, complete information on genetic disorders, including conditions, tests, procedures, treatments and therapies, in articles that are both comprehensive and easy to understand, in language accessible to laypersons. The articles are arranged in a standardized format for quick comparison and ease of use, while non-disorder topics are covered in detail with extended entries. Students will want to consult the “Gale Encyclopedia of Genetic Disorders” for useful information on a range of well known disorders, including Down Syndrome, Trisomy, Hemophilia and Tourette Syndrome, and rarely seen diseases such as Meckel Syndrome, Neuraminidase Deficiency and Phenylketonuria.

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Chapters: Hemoglobin, Hemocyanin, Glycated Hemoglobin, Haptoglobin, Human Serum Albumin, Fibrin, Factor V Leiden, Thyroxine-Binding Globulin, Transthyretin, Hemopexin, Cholesterylester Transfer Protein, Fetal Hemoglobin, Keyhole Limpet Hemocyanin, Serum Amyloid P Component, Fetuin, Hemoglobin C, Hemoglobin E, Macroglobulin, Fibronectin Binding Protein A, Hemoglobin Variants, Hemoglobin A, Hemoglobin A2, Barbourin. Source: Wikipedia. Pages: 128. Not illustrated. Free updates online. Purchase includes a free trial membership in the publisher's book club where you can select from more than a million books without charge. Excerpt: Hemoglobin (also spelled haemoglobin and abbreviated Hb or Hgb) is the iron-containing oxygen-transport metalloprotein in the red blood cells of vertebrates, and the tissues of some invertebrates. Hemoglobin in the blood is what transports oxygen from the lungs or gills to the rest of the body (i.e. the tissues) where it releases the oxygen for cell use. In mammals, the protein makes up about 97% of the red blood cell's dry content, and around 35% of the total content (including water) . Hemoglobin has an oxygen binding capacity between 1.36 and 1.37 ml O2 per gram of hemoglobin, which increases the total blood oxygen capacity seventyfold. Hemoglobin is also found outside red blood cells and their progenitor lines. Other cells that contain hemoglobin include the A9 dopaminergic neurons in the substantia nigra, macrophages, alveolar cells, and mesangial cells in the kidney. In these tissues, hemoglobin has a non-oxygen-carrying function as an antioxidant and a regulator of iron metabolism. The oxygen-carrying protein haemoglobin was discovered by Hünefeld in 1840. In 1851, Otto Funke published a series of articles in which he described growing haemoglobin crystals by successively diluting red blood cells with a solvent such as pure water, alcohol or ether, followed by slow evaporation of the solvent from...More: http://booksllc.net/?id=13483 ... Read more

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This digital document is an article from Journal of Nursing Scholarship, published by Thomson Gale on March 22, 2006. The length of the article is 5839 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

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Title: Factor V Leiden as a common genetic risk factor for venous thromboembolism.(Genomics to Health)
Author: McDonald K., III Horne
Publication: Journal of Nursing Scholarship (Magazine/Journal)
Date: March 22, 2006
Publisher: Thomson Gale
Volume: 38Issue: 1Page: 19(7)

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High Quality Content by WIKIPEDIA articles! Factor V Leiden (sometimes factor VLeiden) is the name given to a variant of human factor V that causes a hypercoagulability disorder. In this disorder the Leiden variant of factor V cannot be inactivated by activated protein C. Factor V Leiden is the most common hereditary hypercoagulability disorder amongst Eurasians. It is named after the city Leiden (Netherlands), where it was first identified in 1994 by Prof R. Bertina et al. ... Read more