Penn State Faculty Research Expertise Database (FRED) , A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC).activated protein c resistance. http://fred.hmc.psu.edu/ds/retrieve/fred/meshdescriptor/D020016
Obstetrical & Gynecological Survey - UserLogin Changes of Resistance to Activated Protein C in the Course of Pregnancy and Obstetric Implications of activated protein c resistance and Factor V Leiden http://www.obgynsurvey.com/pt/re/obgynsurv/fulltext.00006254-199901000-00003.htm
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Abstract The relation of activated protein c resistance with ABO blood groups. Abstract number P0942. Ozcan* M., Kasapoglu A., Topcuoglu* P., Arslan* O. http://www.blackwellpublishing.com/isth2003/abstract.asp?id=9116
LU:research - Lund University Institutional Archive Title, Reactions to awareness of activated protein c resistance carriership a descriptive study of 270 women. Fulltext, Available as PDF http://lu-research.lub.lu.se/php/gateway.php?who=lr&method=getfile&file=archive/
LU:research - Lund University Institutional Archive Title, The discovery of activated protein c resistance. Fulltext, Not available in this archive. Author, Dahlbäck, B http://lu-research.lub.lu.se/php/gateway.php?who=lr&method=getfile&file=archive/
Protein C - Enpsychlopedia activated protein c resistance is the inability of protein C to cleave factors V and/or VIII. This may be hereditary or acquired. http://psychcentral.com/psypsych/Protein_C
Extractions: home resource directory disorders quizzes ... support forums Protein C is a major physiological anticoagulant . It is a vitamin K -dependant serine protease enzyme EC http://us.expasy.org/cgi-bin/nicezyme.pl?3.4.21.69 ) that is activated by thrombin into activated protein C (APC). The activated form (with protein S as a cofactor ) degrades Factor Va and Factor VIIIa Contents showTocToggle("show","hide") 1 Genetics edit The PROC gene is located on the second chromosome edit Protein C deficiency is a rare genetic disorder that predisposes to venous thrombosis and habitual abortion . If homozygous , this presents with a form of disseminated intravascular coagulation in newborns termed purpura fulminans ; it is treated by replacing the defective protein C. Activated protein C resistance is the inability of protein C to cleave factors V and/or VIII. This may be hereditary or acquired. The best known and most common hereditary form is Factor V Leiden . Acquired forms occur in the presence of elevated Factor VIII concentrations. Warfarin necrosis is acquired protein C deficiency due to treatment with the vitamin K inhibitor anticoagulant warfarin . In initial stages of action, inhibition of protein C may be stronger than inhibition of the vitamin K-dependant coagulation factors (II, VII, IX and X), leading to paradoxical activation of coagulation and
Thrombosis And Haemostasis activated protein c resistance (FVQ506) and Pregnancy Activated protein C (APC) resistance, due to a point mutation in the factor V gene (FVQ506), http://www.schattauer.de/zs/thromb/artikel.asp?path=/zs/thromb/1999/4/&nummer=th
Portal Toolkit Invalid Site URL activated protein c resistance Associated with Maternal Floor Infarction Factor V Leiden with activated protein c resistance is found in up to 5% of the http://ppv.ovid.com/pt/re/ajrp/fulltext.00001833-200219050-00008.htm
PHS 398 (Rev. 5/01), Biographical Sketch Format Page activated protein c resistance in ischemic stroke not due to factor V arginine506 glutamine mutation. Stroke 271163-6, 1996. 15. Macko RF, Ameriso SF, http://www.bme.ogi.edu/~trant/bme507/AndrasGruber.htm
Extractions: Follow this format for each person. DO NOT EXCEED FOUR PAGES. NAME Andras Gruber , M.D. POSITION TITLE Associate Professor of Biomedical Engineering EDUCATION/ TRAINING Begin with baccalaureate or other initial professional education, such as nursing, and include postdoctoral training.) INSTITUTION AND LOCATION DEGREE (if applicable) YEAR(s) FIELD OF STUDY Semmelweis Medical Univ., Budapest , HU MD Medicine Postgraduate Medical School Budapest , HU Board Cert. Cert. Internal Medicine The Scripps Research Institute, La Jolla CA Postdoc biochem A. Positions and Honors Positions and Employment Medical residency, and staff physician, Internal Medicine, Postgraduate Med. School Budapest , HU Staff physician , Internal Medicine, Szonyi T. County Hospital Vac , HU Postdoctoral Research Fellow The Scripps Research Institute, La Jolla CA Research Associate
Entrez PubMed Resistance to the anticoagulant action of activated protein C, APC resistance, is a highly prevalent risk factor for venous thrombosis among individuals of http://ghr.nlm.nih.gov/gene=f5/show/PubMed
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Extractions: Who should be tested? Indications include: Deep vein thrombosis and pulmonary embolism Venous thrombosis and pulmonary embolism pose a serious health problem. In this country half a million people are hospitalized each year and 50,000-100,000 deaths occur due to venous thrombosis which is also a leading cause of maternal death. The incidence of symptomatic venous thrombosis cases is approximately 1 in 1000 people per year. Venous thrombosis is a multifactorial condition caused by a combination of genetic, aquired or environmental influences. Natural anticoagulant systems (the protein C system and antithrombin III) are in place to keep coagulation in check. Excess clotting occurs when there is a disturbance in one of the coagulation inhibitor mechanisms or in natural lysis of clots.
Extractions: This Article Full Text Full Text (PDF) Alert me when this article is cited ... Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Rights and Permissions PubMed PubMed Citation Articles by Male, C. Articles by Andrew, M. E. Related Collections Plenary Papers Blood, 15 February 2001, Vol. 97, No. 4, pp. 844-849 PLENARY PAPER Christoph Male Lesley Mitchell James Julian Patricia Vegh Penny Joshua Margaret Adams Michelle David and Maureen E. Andrew Acquired activated protein C resistance (APCR) has been hypothesized as a possible mechanism by which antiphospholipid antibodies (APLAs) cause thrombotic events (TEs). However, available evidence for an association of acquired APCR with APLAs is limited. More importantly, an association of acquired APCR with TEs has not
Extractions: This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted ... Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Rights and Permissions PubMed PubMed Citation Articles by Tripodi, A. Articles by Mannucci, P. Blood, 1 November 2000, Vol. 96, No. 9, pp. 3295-3296 CORRESPONDENCE Activated protein C (APC) resistance due to the factor V (FV) gene mutation G1691A (single-letter nucleotide codes) and the prothrombin gene mutation G20210A are the most common genetic disorders associated with venous thrombosis. APC resistance not due to the FV gene mutation G1691A, and the hyperprothrombinemia secondary to the prothrombin gene mutation G20210A, are also independent risk factors for venous thrombosis. Although it has been surmised that high levels of prothrombin in plasma may result in an increased rate of thrombin generation or increased thrombin potential
Haema/Áßìá activated protein c resistance in the absence of factor V Leiden mutation is associated with an increased risk of thrombotic complications in patients http://www.mednet.gr/eae/haema/h81-18.htm
Extractions: Vol Page [Advanced] This Article Extract Full Text (PDF) Submit a response ... Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Download to citation manager PubMed PubMed Citation Articles by Granel, B Articles by Weiller, P-J Related Collections Other Rheumatology Annals of the Rheumatic Diseases B Granel J Serratrice N Ene P E Morange P Disdier and P-J Weiller Accepted 12 May 2003 Keywords: giant cell arteritis; juvenile temporal arteritis; vasculitis; protein C resistance Juvenile temporal arteritis (JTA) is a rare benign vascular lesion limited to the branches of the external carotid artery, first recognised by Lie et al Histological features of JTA include vasculitis (without giant cells and granulomas), lymphocytes
Extractions: Vol Page [Advanced] This Article Full Text Full Text (PDF) Submit a response ... Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Download to citation manager PubMed PubMed Citation Articles by Granel, B Articles by Weiller, P-J Related Collections Other Rheumatology Annals of the Rheumatic Diseases B Granel J Serratrice N Ene P E Morange P Disdier and P-J Weiller patrick.disdier@ap-hm.fr Accepted 12 May 2003 Keywords: giant cell arteritis; juvenile temporal arteritis; vasculitis; protein C resistance The first 150 words of the full text of this article appear below. Juvenile temporal arteritis (JTA) is a rare benign vascular lesion limited to the branches of the external carotid artery
Extractions: (PDFs free after 6 months) Figures/Tables List Related articles in Annals Services Send comment/rapid response letter Notify a friend about this article Alert me when this article is cited Add to Personal Archive ... ACP Search PubMed Articles in PubMed by Author: Rodeghiero, F. Tosetto, A. Related Articles in PubMed PubMed Citation ... PubMed Francesco Rodeghiero, MD and Alberto Tosetto, MD Background: Resistance to activated protein C due to the factor V R506Q (Leiden) mutation is the most common clotting abnormality in patients with venous thromboembolism. Objective: To evaluate the risk for venous thromboembolism associated with the factor V Leiden mutation or with resistance to activated protein C in the general population. Design: Cross-sectional survey. Setting: General community of Vicenza, Italy.
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