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1. Full Text Neutrophil histone modification by peptidylarginine deiminase 4 is critical for deep vein thrombosis in mice
by Kimberly Martinod and Melanie Demers and Tobias A. Fuchs and Siu Ling Wong and Alexander Brill and Maureen Gallant and Jing Hu and Yanming Wang and Denisa D. Wagner
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2013, Volume 110, Issue 21, pp. 8674 - 8679
Deep vein thrombosis and pulmonary embolism are major health problems associated with high mortality. Recently, DNA-based neutrophil extracellular traps (NETs)... 
Chromatin | Pathologic constriction | Neutrophils | Histones | Venous thrombosis | Mice | Leukocytes | Chimeras | Platelets | Thrombosis | Histone citrullination | Inflammation | Programmed cell death | Nuclear swelling | Venous thromboembolism | LOCALIZATION | DNA TRAPS | PAD4 | MULTIDISCIPLINARY SCIENCES | PLATELET-ADHESION | VON-WILLEBRAND-FACTOR | MOUSE MODELS | nuclear swelling | histone citrullination | inflammation | venous thromboembolism | IN-VIVO | programmed cell death | EXTRACELLULAR TRAP FORMATION | INNATE IMMUNITY | Hydrolases - metabolism | Hydrolases - genetics | Venous Thrombosis - enzymology | Neutrophil Activation | Neutrophils - enzymology | Venous Thrombosis - therapy | Chromatin Assembly and Disassembly | Mice, Knockout | Animals | Histones - genetics | Venous Thrombosis - genetics | Histones - metabolism | Venous Thrombosis - pathology | Platelet Aggregation - genetics | Neutrophils - pathology | Pulmonary embolism | Genetic aspects | Models | Properties | Biological Sciences
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2. Full Text Neutrophil elastase‐deficient mice form neutrophil extracellular traps in an experimental model of deep vein thrombosis
by Martinod, K and Witsch, T and Farley, K and Gallant, M and Remold‐O'Donnell, E and Wagner, D. D
Journal of Thrombosis and Haemostasis, ISSN 1538-7933, 03/2016, Volume 14, Issue 3, pp. 551 - 558
Neutrophil elastase (NE) plays a role in extracellular trap formation (NETosis) triggered by microbes. The contribution of NE was evaluated in mouse NETosis... 
extracellular traps | neutrophils | serine proteases | venous thrombosis | eukocyte elastase | Serine proteases | Venous thrombosis | Eukocyte elastase | Extracellular traps | Neutrophils | DNA TRAPS | PAD4 | MOUSE | RELEASE | PERIPHERAL VASCULAR DISEASE | INHIBITOR | HEMATOLOGY | PULMONARY-FIBROSIS | INNATE IMMUNITY | Venous Thrombosis - enzymology | Tetradecanoylphorbol Acetate - pharmacology | Neutrophil Activation | Neutrophils - enzymology | Extracellular Traps - metabolism | Mice, Inbred C57BL | Neutrophils - drug effects | Venous Thrombosis - blood | Cells, Cultured | Leukocyte Elastase - genetics | Genotype | Mice, Knockout | Phenotype | Animals | Ionomycin - pharmacology | Venous Thrombosis - genetics | Leukocyte Elastase - deficiency | Disease Models, Animal | Histones | Mice | Proteases | Analysis | Thrombosis | Rodents | Index Medicus
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3. Full Text Defective thrombus formation in mice lacking endogenous factor VII activating protease (FSAP)
by Subramaniam, Saravanan and Thielmann, Ina and Morowski, Martina and Pragst, Ingo and Sandset, Per Morten and Nieswandt, Bernhard and Etscheid, Michael and Kanse, Sandip M
Thrombosis and Haemostasis, ISSN 0340-6245, 07/2015, Volume 113, Issue 4, pp. 870 - 880
Summary Factor VII (FVII) activating protease (FSAP) is a circulating protease with a putative function in blood coagulation and fibrinolysis. Genetic... 
Stroke, Systemic or Venous Thromboembolism | Haemostasis | Fibrinolysis | FSAP | Thrombosis | HABP2 | Coagulation | LIVER FIBROSIS | RISK | PROTEOLYSIS | fibrinolysis | thrombosis | haemostasis | G534E | PERIPHERAL VASCULAR DISEASE | MARBURG-I POLYMORPHISM | HEMATOLOGY | FACTOR PATHWAY INHIBITOR | Carotid Artery Diseases - prevention & control | Serine Endopeptidases - administration & dosage | Thrombosis - chemically induced | Carotid Artery Diseases - chemically induced | Mesenteric Vascular Occlusion - genetics | Venous Thromboembolism - blood | Chlorides | Serine Endopeptidases - genetics | Carotid Arteries - enzymology | Mesenteric Vascular Occlusion - enzymology | Thrombosis - blood | Thrombosis - prevention & control | Disease Models, Animal | Genetic Predisposition to Disease | Serine Endopeptidases - deficiency | Mesenteric Vascular Occlusion - prevention & control | Mice, Inbred C57BL | Thrombosis - enzymology | Hemostasis - genetics | Lipoproteins - blood | Mesenteric Vascular Occlusion - blood | Venous Thromboembolism - enzymology | Mice, Knockout | Ferric Compounds | Phenotype | Venous Thromboembolism - genetics | Animals | Carotid Artery Diseases - enzymology | Carotid Artery Diseases - blood | Collagen | Carotid Artery Diseases - genetics | Venous Thromboembolism - chemically induced | Blood Coagulation Tests | Thrombosis - genetics | Jugular Veins - enzymology | Norepinephrine | Mesenteric Vascular Occlusion - chemically induced | Mesenteric Arteries - enzymology
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4. Full Text Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis
by Wald, David S and Law, Malcolm and Morris, Joan K
BMJ, ISSN 0959-8138, 11/2002, Volume 325, Issue 7374, pp. 1202 - 1206
Abstract Objective: To assess whether the association of serum homocysteine concentration with ischaemic heart disease, deep vein thrombosis and pulmonary... 
Homozygotes | Predisposing factors | Medical genetics | Myocardial ischemia | Venous thrombosis | Blood pressure | Prospective studies | Cardiovascular diseases | Genetic mutation | Confidence interval | METHYLENETETRAHYDROFOLATE-REDUCTASE GENE | METHYLENE-TETRAHYDROFOLATE REDUCTASE | MEDICINE, GENERAL & INTERNAL | CORONARY-ARTERY DISEASE | PLASMA TOTAL HOMOCYSTEINE | FACTOR-V-LEIDEN | SERUM TOTAL HOMOCYSTEINE | DEPENDENT DIABETIC-PATIENTS | DEEP-VEIN THROMBOSIS | ISCHEMIC-HEART-DISEASE | FOLIC-ACID SUPPLEMENTATION | Myocardial Ischemia - genetics | Pulmonary Embolism - genetics | Genetic Predisposition to Disease | Venous Thrombosis - enzymology | Prospective Studies | Pulmonary Embolism - enzymology | Humans | Risk Factors | Venous Thrombosis - blood | Myocardial Ischemia - blood | Homocysteine - blood | Oxidoreductases Acting on CH-NH Group Donors - genetics | Methylenetetrahydrofolate Reductase (NADPH2) | Myocardial Ischemia - enzymology | Mutation - genetics | Pulmonary Embolism - blood | Homozygote | Venous Thrombosis - genetics | Odds Ratio | Cohort Studies | Papers
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5. Full Text Deficiency of Superoxide Dismutase Impairs Protein C Activation and Enhances Susceptibility to Experimental Thrombosis
by Dayal, Sanjana and Gu, Sean X and Hutchins, Ryan D and Wilson, Katina M and Wang, Yi and Fu, Xiaoyun and Lentz, Steven R
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 08/2015, Volume 35, Issue 8, pp. 1798 - 1804
OBJECTIVE—Clinical evidence suggests an association between oxidative stress and vascular disease, and in vitro studies have demonstrated that reactive oxygen... 
thrombosis | protein C | superoxides | catalase | thrombomodulin | OXIDATIVE STRESS | VASCULAR DYSFUNCTION | MECHANISMS | INHIBITION | GENE | NITRIC-OXIDE | PERIPHERAL VASCULAR DISEASE | MICE | HEMATOLOGY | CORONARY-ARTERY-DISEASE | TISSUE FACTOR | Superoxide Dismutase - genetics | Venous Thrombosis - enzymology | Oxidative Stress | Humans | Mice, 129 Strain | Thrombomodulin - metabolism | Superoxides - metabolism | Vena Cava, Inferior - pathology | Carotid Artery Injuries - genetics | Carotid Artery Injuries - pathology | Disease Models, Animal | Oxidation-Reduction | Thrombosis - enzymology | Mice, Transgenic | Superoxide Dismutase - deficiency | Catalase - metabolism | Vena Cava, Inferior - enzymology | Thrombosis - pathology | Animals | Carotid Artery Injuries - enzymology | Carotid Artery, Common - enzymology | Carotid Artery, Common - pathology | Thrombosis - genetics | Enzyme Activation | Protein C - metabolism | Superoxide Dismutase-1 | Venous Thrombosis - pathology | methionine oxidation | superoxide
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6. Full Text The JAK2 V617F mutation in patients with cerebral venous thrombosis
by Passamonti, S.M and Biguzzi, E and Cazzola, M and Franchi, F and Gianniello, F and Bucciarelli, P and Pietra, D and Mannucci, P.M and Martinelli, I
Journal of Thrombosis and Haemostasis, ISSN 1538-7933, 06/2012, Volume 10, Issue 6, pp. 998 - 1003
Background: It is currently unclear whether or not cerebral venous thrombosis, such as splanchnic venous thrombosis, can be the first manifestation of an... 
Cerebral sinus venous thrombosis | Myeloproliferative neoplasm | Risk factors | DIAGNOSIS | risk factors | POLYCYTHEMIA-VERA | ACTIVATION | MYELOPROLIFERATIVE NEOPLASMS | JAK2V617F MUTATION | ESSENTIAL THROMBOCYTHEMIA | GRANULOCYTE | cerebral sinus venous thrombosis | DISEASE | PERIPHERAL VASCULAR DISEASE | THROMBOEMBOLISM | myeloproliferative neoplasm | HEMATOLOGY | BLOOD | Intracranial Thrombosis - genetics | Venous Thrombosis - enzymology | Prevalence | Humans | Middle Aged | Male | Incidence | Young Adult | Myeloproliferative Disorders - blood | Time Factors | Myeloproliferative Disorders - epidemiology | Adult | Female | Retrospective Studies | Genetic Predisposition to Disease | Risk Assessment | Gene Frequency | Risk Factors | Janus Kinase 2 - genetics | Venous Thrombosis - mortality | Chi-Square Distribution | Disease-Free Survival | Phenotype | Intracranial Thrombosis - enzymology | Intracranial Thrombosis - mortality | Adolescent | Blood Coagulation - genetics | Italy - epidemiology | Aged | Venous Thrombosis - genetics | Mutation | Myeloproliferative Disorders - mortality
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7. Full Text Protein disulfide isomerase inhibitors constitute a new class of antithrombotic agents
by Jasuja, Reema and Passam, Freda H and Kennedy, Daniel R and Kim, Sarah H and Van Hessem, Lotte and Lin, Lin and Bowley, Sheryl R and Joshi, Sucharit S and Dilks, James R and Furie, Bruce and Furie, Barbara C and Flaumenhaft, Robert
Journal of Clinical Investigation, ISSN 0021-9738, 06/2012, Volume 122, Issue 6, pp. 2104 - 2113
Thrombosis, or blood clot formation, and its sequelae remain a leading cause of morbidity and mortality, and recurrent thrombosis is common despite current... 
MEDICINE, RESEARCH & EXPERIMENTAL | FUNCTIONAL ASSOCIATION | ACTIVATION | LASER-SCANNING MICROSCOPY | DIETARY FLAVONOIDS | THROMBUS FORMATION | VENOUS WALL | CORONARY-HEART-DISEASE | FIBRIN GENERATION | PLASMA-MEMBRANE | TISSUE FACTOR | Recombinant Proteins - antagonists & inhibitors | Thrombosis - chemically induced | Humans | Rutin - pharmacology | Thrombosis - enzymology | Enzyme Inhibitors - pharmacology | Fibrin - genetics | Protein Disulfide-Isomerases - adverse effects | Protein Disulfide-Isomerases - antagonists & inhibitors | Recombinant Proteins - genetics | Recombinant Proteins - adverse effects | Recombinant Proteins - pharmacology | Fibrinolytic Agents - pharmacology | Protein Disulfide-Isomerases - genetics | Animals | Protein Disulfide-Isomerases - pharmacology | Blood Platelets - metabolism | Mice | Platelet Aggregation - drug effects | Thrombosis - drug therapy | Fibrin - metabolism | Identification and classification | Enzyme inhibitors | Thrombolytic drugs
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8. Full Text Should we screen for Janus Kinase 2 V617F mutation in cerebral venous thrombosis?
by Lamy, Matthias and Palazzo, Paola and Agius, Pierre and Chomel, Jean Claude and Ciron, Jonathan and Berthomet, Aline and Cantagrel, Paul and Prigent, Julia and Ingrand, Pierre and Puyade, Mathieu and Neau, Jean-Philippe
Cerebrovascular Diseases, ISSN 1015-9770, 10/2017, Volume 44, Issue 3-4, pp. 97 - 104
Background: The presence of Janus Kinase 2 (JAK2) V617F mutation represents a major diagnostic criterion for detecting myeloproliferative neoplasms (MPN) and... 
Anticoagulation | Coagulation abnormalities in cerebrovascular diseases | Hematology | Cerebral venous thrombosis | POLYCYTHEMIA-VERA | JAK2 V617F | NEOPLASMS | JAK2V617F MUTATION | ESSENTIAL THROMBOCYTHEMIA | SPLANCHNIC VEIN-THROMBOSIS | CLINICAL NEUROLOGY | SINUS THROMBOSIS | CHRONIC MYELOPROLIFERATIVE DISORDERS | PERIPHERAL VASCULAR DISEASE | THROMBOEMBOLISM | CONSECUTIVE PATIENTS | Intracranial Thrombosis - genetics | Predictive Value of Tests | Recurrence | Venous Thrombosis - enzymology | Prognosis | Prospective Studies | Humans | Middle Aged | Venous Thrombosis - diagnostic imaging | Male | Genetic Testing - methods | Time Factors | DNA Mutational Analysis | Adult | Female | Intracranial Thrombosis - drug therapy | Genetic Predisposition to Disease | Venous Thrombosis - drug therapy | Risk Factors | Janus Kinase 2 - genetics | Anticoagulants - therapeutic use | Mutation Rate | Phenotype | Intracranial Thrombosis - enzymology | Aged | Venous Thrombosis - genetics | Mutation | Intracranial Thrombosis - diagnostic imaging | Medical research | Analysis | Medicine, Experimental | Mutual fund industry | Thrombophlebitis | Genetic aspects | Thromboembolism | Medicine, Preventive | Preventive health services
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9. Full Text Next‐generation sequencing study finds an excess of rare, coding single‐nucleotide variants of ADAMTS13 in patients with deep vein thrombosis
by Lotta, L. A and Tuana, G and Yu, J and Martinelli, I and Wang, M and Yu, F and Passamonti, S. M and Pappalardo, E and Valsecchi, C and Scherer, S. E and Hale, W and Muzny, D. M and Randi, G and Rosendaal, F. R and Gibbs, R. A and Peyvandi, F
Journal of Thrombosis and Haemostasis, ISSN 1538-7933, 07/2013, Volume 11, Issue 7, pp. 1228 - 1239
Background The considerable genetic predisposition to deep vein thrombosis (DVT) is only partially accounted for by known genetic risk variants. Rare... 
deep vein thrombosis | exome | VWF | ADAMTS‐13 | venous thromboembolism | Exome | Deep vein thrombosis | ADAMTS-13 | Venous thromboembolism | CONTRIBUTE | ALLELES | MYOCARDIAL-INFARCTION | FACTOR-VIII | MARKERS | RISK | VON-WILLEBRAND-FACTOR | INCREASE | THROMBOCYTOPENIC PURPURA | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | Predictive Value of Tests | Venous Thrombosis - enzymology | Prevalence | Humans | Middle Aged | Venous Thrombosis - blood | Male | von Willebrand Factor - genetics | Case-Control Studies | ADAM Proteins - blood | Adult | Female | Odds Ratio | Genetic Predisposition to Disease | Gene Frequency | Risk Factors | Linear Models | Logistic Models | ADAMTS13 Protein | Phenotype | Venous Thrombosis - epidemiology | Italy - epidemiology | High-Throughput Nucleotide Sequencing | Polymorphism, Single Nucleotide | Venous Thrombosis - genetics | ADAM Proteins - genetics | Proteins | Medicine, Experimental | Medical research | Research | Thromboembolism | Genes
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10. Full Text Matrix metalloproteinases in peripheral vascular disease
by Hobeika, Mark J., MD and Thompson, Robert W., MD and Muhs, Bart E., MD and Brooks, Peter C., PhD and Gagne, Paul J., MD
Journal of Vascular Surgery, ISSN 0741-5214, 2007, Volume 45, Issue 4, pp. 849 - 857
Matrix metalloproteinases (MMPs) are extracellular matrix–modifying enzymes that are important in many physiologic and pathologic vascular processes.... 
Surgery | ATHEROSCLEROTIC LESIONS | SURGERY | DIFFERENTIAL EXPRESSION | ABDOMINAL AORTIC-ANEURYSMS | DEEP VENOUS THROMBOSIS | INTIMAL HYPERPLASIA | MOUSE MODEL | TISSUE INHIBITOR | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | EXTRACELLULAR-MATRIX | VEIN WALL | Matrix Metalloproteinases, Secreted - metabolism | Recurrence | Varicose Ulcer - drug therapy | Venous Thrombosis - enzymology | Humans | Ischemia - enzymology | Matrix Metalloproteinases, Secreted - antagonists & inhibitors | Varicose Veins - drug therapy | Atherosclerosis - enzymology | Biomarkers - metabolism | Aortic Aneurysm, Abdominal - drug therapy | Atherosclerosis - drug therapy | Varicose Ulcer - enzymology | Venous Thrombosis - drug therapy | Peripheral Vascular Diseases - drug therapy | Enzyme Inhibitors - pharmacology | Enzyme Inhibitors - therapeutic use | Tissue Inhibitor of Metalloproteinases - metabolism | Peripheral Vascular Diseases - diagnosis | Animals | Aortic Aneurysm, Abdominal - enzymology | Constriction, Pathologic - drug therapy | Constriction, Pathologic - surgery | Extremities - blood supply | Ischemia - drug therapy | Varicose Veins - enzymology | Vascular Surgical Procedures - adverse effects | Peripheral Vascular Diseases - enzymology | Constriction, Pathologic - enzymology | Cardiovascular diseases | Atherosclerosis
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11. Full Text Matrix metalloproteinase-9 deletion is associated with decreased mid-term vein wall fibrosis in experimental stasis DVT
by Deatrick, Kristopher B and Obi, Andrea and Luke, Catherine E and Elfline, Megan A and Sood, Vikram and Upchurch, Gilbert R and Jaffer, Farouc and Wakefield, Thomas W and Henke, Peter K
Thrombosis Research, ISSN 0049-3848, 2013, Volume 132, Issue 3, pp. 360 - 366
Abstract Introduction Post thrombotic syndrome therapy is primarily palliative, and the associated vein wall inflammatory mechanisms are unclear. Vein wall... 
Hematology, Oncology and Palliative Medicine | Monocytes | Venous thrombosis | Inflammation | Matrix metalloproteinases | COLLAGEN | TISSUE INHIBITORS | INJURY | VENOUS THROMBOSIS RESOLUTION | MOLECULAR-WEIGHT HEPARIN | MOUSE MODEL | MUSCLE-CELL MIGRATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | POLARIZATION | Gene Expression | Venous Thrombosis - enzymology | Male | Matrix Metalloproteinase 9 - deficiency | Mice, Knockout | Leukocytes, Mononuclear - pathology | Matrix Metalloproteinase 9 - metabolism | Animals | Veins - enzymology | Fibrosis | Leukocytes, Mononuclear - enzymology | Mice | Venous Thrombosis - genetics | Venous Thrombosis - pathology | Veins - pathology | Disease Models, Animal | monocytes | inflammation | matrix metalloproteinases
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12. Full Text Influence of ADAMTS13 deficiency on venous thrombosis in mice
by Tashima, Yuko and Banno, Fumiaki and Akiyama, Masashi and Miyata, Toshiyuki
Thrombosis and Haemostasis, ISSN 0340-6245, 2015, Volume 113, Issue 1, pp. 206 - 207
Letters to the Editor | INFERIOR VENA-CAVA | INFLAMMATION | IN-VIVO | MOUSE MODEL | THROMBOGENESIS | DEEP-VEIN THROMBOSIS | THROMBOCYTOPENIC PURPURA | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | VON-WILLEBRAND-FACTOR | DOMAINS | CONTINUOUS BLOOD-FLOW | Metalloendopeptidases - genetics | Venous Thrombosis - enzymology | Metalloendopeptidases - deficiency | Venous Thrombosis - blood | Genotype | Male | Mice, 129 Strain | ADAMTS13 Protein | ADAM Proteins - administration & dosage | Recombinant Proteins - administration & dosage | Mice, Knockout | Phenotype | Animals | Venous Thrombosis - prevention & control | Fibrinolytic Agents - administration & dosage | Venous Thrombosis - genetics | Disease Models, Animal
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13. Full Text γ-Glutamyl Transferase Is an Independent Biomarker of Splanchnic Thrombosis in Patients with Myeloproliferative Neoplasm
by Görtzen, Jan and Hunka, Lena M and Vonnahme, Maria and Praktiknjo, Michael and Kaifie, Andrea and Fimmers, Rolf and Jansen, Christian and Heine, Annkristin and Lehmann, Jennifer and Goethert, Joachim R and Gattermann, Norbert and Goekkurt, Eray and Platzbecker, Uwe and Brossart, Peter and Strassburg, Christian P and Brummendorf, Tim H and Koschmieder, Steffen and Wolf, Dominik and Trebicka, Jonel
Medicine (United States), ISSN 0025-7974, 05/2016, Volume 95, Issue 20, p. e3355
Myeloproliferative neoplasms (MPNs) are associated with an increased risk of thrombotic events and constitute the major risk factor of splanchnic venous... 
SURVIVAL | MEDICINE, GENERAL & INTERNAL | POLYCYTHEMIA-VERA | PORTAL-VEIN THROMBOSIS | INFLAMMATION | BUDD-CHIARI-SYNDROME | ESSENTIAL THROMBOCYTHEMIA | ANTICOAGULATION | Predictive Value of Tests | Venous Thrombosis - diagnosis | Venous Thrombosis - enzymology | gamma-Glutamyltransferase - blood | Humans | Middle Aged | Venous Thrombosis - blood | Polycythemia Vera - blood | Male | Alanine Transaminase - blood | Primary Myelofibrosis - blood | Young Adult | C-Reactive Protein - metabolism | Aged, 80 and over | Adult | Female | Retrospective Studies | Risk Factors | Survival Rate | Biomarkers - blood | Thrombocythemia, Essential - blood | Bilirubin - blood | Aspartate Aminotransferases - blood | Adolescent | Splanchnic Circulation | Aged | Complications and side effects | Venous thrombosis | Diagnosis | Ischemia | Myeloproliferative disorders | Risk factors
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14. Full Text IL-6-174 G>C and MMP-9-1562 C>T polymorphisms are associated with increased risk of deep vein thrombosis in cancer patients
by Malaponte, Grazia and Polesel, Jerry and Candido, Saverio and Sambataro, Daniela and Bevelacqua, Valentina and Anzaldi, Massimo and Vella, Nadia and Fiore, Valerio and Militello, Loredana and Mazzarino, Maria C and Libra, Massimo and Signorelli, Santo Salvatore
Cytokine, ISSN 1043-4666, 04/2013, Volume 62, Issue 1, pp. 64 - 69
► Evaluation of IL-6 and MMP-9 polymorphisms in cancer patients DVT+ and DVT−. ► Changes in plasma levels of IL-6 and MMP-9 in cancer patients DVT+ and DVT−. ►... 
Deep vein thrombosis | MMP-9 | Gene polymorphism | IL-6 | Cancer | MYOCARDIAL-INFARCTION | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | ATHEROSCLEROSIS | IMMUNOLOGY | CELL BIOLOGY | MATRIX METALLOPROTEINASES | VENOUS THROMBOEMBOLISM | INTERLEUKIN-6 GENE PROMOTER | INFLAMMATION | G/C POLYMORPHISM | PERIPHERAL ARTERIAL-DISEASE | SEVERITY | Confidence Intervals | Genetic Predisposition to Disease | Venous Thrombosis - enzymology | Interleukin-6 - genetics | Humans | Middle Aged | Risk Factors | Venous Thrombosis - blood | Neoplasms - enzymology | Male | Venous Thrombosis - complications | Case-Control Studies | Neoplasms - complications | Neoplasms - blood | Neoplasms - genetics | Interleukin-6 - blood | Matrix Metalloproteinase 9 - genetics | Polymorphism, Single Nucleotide - genetics | Female | Leukocytes, Mononuclear - enzymology | Aged | Venous Thrombosis - genetics | Odds Ratio | Matrix Metalloproteinase 9 - blood
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