81. Activated Protein C Resistance And Mutations In Factor V It has been shown that APC resistance results from a mutant Factor Vamolecule, termed factor v leiden. This molecule has a specific http://www.hemex.com/apc_resistance.htm

Updated February 2, 2000 ACTIVATED PROTEIN C RESISTANCE (APC RESISTANCE) AND MUTATIONS IN FACTOR V MOLECULAR BASIS: When thrombin (IIa) is generated, it has both procoagulant activities and anticoagulant activities. Excess thrombin is washed downstream where it binds to thrombomodulin (TM) on endothelial cells of the vessel wall. Protein C from plasma binds to the IIa/TM complex and is cleaved to its active form, termed "activated Protein C" (APC). APC is one of the most physiologically important anticoagulants as it selectively degrades the coagulation cofactors, Va and VIIIa to limit thrombin generation, fibrin formation and blood clotting in vivo. It has been shown that APC resistance results from a mutant Factor Va molecule, termed Factor V Leiden. This molecule has a specific point mutation (Arg -> Gln ) which cannot be degraded by APC in more than 90% of all APC resistant patients2. The defective Va is able to clot as normal and clotting continues because of this resistance to inactivation by APC. Other APC cleavage sites in the Factor Va molecule are potential mutation sites. These sites include: Arg -> Gln and Arg -> Gln . The other 10% of APC resistance includes Acquired APC Resistance and these secondary sites. Recent studies have shown the occurrence of APC resistance to vary from 2 - 16% depending on the population studied. This data suggests that screening protocols for hereditary thrombotic disorders should include testing for APC resistance as an important genetic risk factor. Hypercoagulability has been explained by hereditary deficiencies of Protein C, Protein S and Antithrombin in only 9 to 21% of thrombotic cases in patients without the usual risk factors for thrombosis (i.e., cancer, recent surgery, lupus anticoagulant)

82. Health .nl Dè Gezondheids Zoekmachine In Nederland! Klik hier voor informatie. factor v leiden. Webgroep voor mensen met de stollingsafwijkingfactor v leiden, of dergelijke stollingsstoornissen. http://www.health.nl/Ziektebeelden/Factor_V_Leiden/

Ziektebeelden : Factor V Leiden Hoest .iedereen heeft er wel eens last van, maar wat is het eigenlijk? Klik hier voor informatie Stoelgang problemen? klik hier en breng uw natuurlijke ritme weer op gang Factor V Leiden Website met informatie over Factor V leiden en soortgelijke stollingsafwijking/problemen (apc resistentie, proteine s/c deficientie, factor II, antitrombine III, homocysteine, cardiolipine, anti fosfolipiden etc). (Gemiddeld cijfer: 10.00 Stemmen: 3) Stem! Webgroep factor-v-leiden Webgroep voor mensen met de stollingsafwijking Factor V Leiden, of dergelijke stollingsstoornissen. (Gemiddeld cijfer: 9.50 Stemmen: 4) Stem! Ziektebeelden a CRIO Company Home Adverteren Toevoegen ... Populair

83. TOTAL PLASMA HOMOCYST(E)INE LEVEL, FACTOR V LEIDEN, AND RISKS OF FUTURE VENOUS T TEKTRAN. TOTAL PLASMA HOMOCYST(E)INE LEVEL, factor v leiden, ANDRISKS OF FUTURE VENOUS THROMBOEMBOLISM. Author(s) RIDKER PAUL M http://www.nal.usda.gov/ttic/tektran/data/000007/64/0000076417.html

TEKTRAN TOTAL PLASMA HOMOCYST(E)INE LEVEL, FACTOR V LEIDEN, AND RISKS OF FUTURE VENOUS THROMBOEMBOLISM Author(s): RIDKER PAUL M HENNEKENS CHARLES H SELHUB JACOB MILETICH JOSEPH P MALINOW M R STAMPFER MEIR J Interpretive Summary: Homocysteine is an amino acid with an important function in the body, but it becomes harmful when its level in the blood becomes high. High levels of homocysteine in blood increase the risk of heart disease. This study is based on reports that high homocysteine in the blood also increases the risk of thrombosis (blood clots). Our data indicates that this risk is particularly high in those individuals who also carry an inherited (or genetic) malfunction in getting rid of (dissolving) blood clots. These data support the possibility that increased vitamin intake (folic acid and B6, B12) is beneficial to these patients because these vitamins lower homocysteine levels in the blood. Keywords: folate vitamin b12 vitamin b6 pyridoxal-5-phoshate homocysteine homocysteinemia sulphur amino acid b vitamins affinity hplc folate bioavailability dysplasia arteriosclerosis Contact: JEAN MAYER HUMAN NUTR. RE

84. Factor V - Leiden Mutation factor V leiden Mutation. Code and size EMK011050 - 50 tests, BACK.INTRODUCTION. It has recently been demonstrated Bertina M., 1994 http://www.euroclone.net/mol_biology/factor5.htm

FACTOR V- Leiden Mutation Code and size: EMK011050 - 50 tests BACK INTRODUCTION It has recently been demonstrated [Bertina M., 1994] that the single mutation G->A at nucleotide position 1691 in the exon 10 of the gene coding for factor V, determines an aminoacid change from Arg(R) to Gln(Q) at position 506 of the protein sequence (FV R506->FVQ506).This mutation is defined as the Leiden mutation and a study performed on different European populations, demonstrates that it is present at a frequence of 3-5% in normal populations [Dahlback B., 1995]. It has been proved that the inactivation of Factor V by the activated protein C (APC), is 10 times faster in FVArg 606 (wild-type) compared to the FVGln506 (mutant) [Heeb M.J., 1995]. Due to the presence of this mutation at a high frequency in normal population and since this mutation confers a predisposition to thrombotic events, recent reports suggest to perform a screening of people with recurrent thrombotic episodes or with subjects exposed to risk factors such as the use of oral contraceptives. The traditional laboratory assay to test this alteration, is the APC resistance test. This test evaluates the function of the factor V but it is not able to determine neither the nucleotide sequence nor the differences between the homozygous and the heterozygous mutant carriers. The traditional molecular screening for this mutation, is based on a PCR amplification followed by digestion with an appropriate restriction enzyme.

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86. Thrombosis: Factor V-Leiden And Prothrombin G20210A Gene Mutations Heighten Misc OBGYN.net Banner Ad (468x60) factor Vleiden and prothrombin G20210A genemutations heighten miscarriage risk. Thrombosis January 30, 2003 http://www.obgyn.net/newsheadlines/womens_health-Thrombosis-20030130-54.asp

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87. Fattore V Leiden - Trombofilia - Associazione Italiana Pazienti Anticoagulati - Translate this page o transitorie di resistenza alla proteina C attivata, ma essenzialmente essaè riconducibile ad una condizione ereditaria nota come Fattore V leiden. http://utenti.tripod.it/aipalink/F-Leiden.html

Resistenza alla proteina C attivata E' una causa frequente di trombofilia. Possono esserci ragioni acquisite o transitorie di resistenza alla proteina C attivata, ma essenzialmente essa è riconducibile ad una condizione ereditaria nota come Fattore V Leiden . Si tratta della mutazione di un gene che codifica per il fattore V della coagulazione, mutazione che causa una risposta insufficiente alla proteina C (un anticoagulante naturale) nella sua forma attiva, e di conseguenza un rischio maggiore di trombosi rispetto alla popolazione generale. Un fattore V mutato è inattivato con maggiore lentezza e resta in circolo più a lungo, producendo a volte alterazione in alcuni indici di coagulazione. Il rischio è molto maggiore per i portatori della mutazione in forma omozigote (presente su entrambi i geni) rispetto a quella eterozigote (un solo gene mutato). Sebbene questa alterazione sia riscontrata con una certa frequenza nelle persone che hanno avuto episodi trombotici con o senza altre cause concomitanti, buona parte dei portatori di fattore V Leiden resta asintomatico. Resistenza alla proteina C attivata Fattore V Leiden Fattore V Leiden Fattore V Leiden, proteina C attivata

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