PubMed · 14282064
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
T H SPAET, J CINTRON. 1965. STUDIES ON PLATELET FACTOR-3 AVAILABILITY.. https://doi.org/10.1111/j.1365-2141.1965.tb06587.x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
BACKGROUND AND PURPOSE: Fibrinogen, plasminogen activator inhibitor-1, and other key proteins in the coagulation cascade have been implicated in the origin of cardiovascular disease. Polymorphisms in genes encoding these proteins have been associated with variability in plasma levels of these proteins. Carotid intimal medial thickness (IMT) is a heritable, quantitative measure of atherosclerosis that is predictive of subsequent myocardial infarction and stroke. We sought to test whether carotid IMT is associated with polymorphisms in several well-characterized genes in the hemostatic factor pathways. METHODS: Here, 867 men and 911 women (mean age, 57 years) in the Framingham offspring cohort underwent B-mode carotid ultrasonography to determine the mean internal (ICA) and common carotid artery (CCA) IMT. Age-, sex-, and multivariable-adjusted linear regression was used to estimate the association of the following variants with log-transformed CCA and ICA IMT: factor V Leiden, factor VII Arg/Gln, fibrinogen HindIII beta-148, plasminogen activator inhibitor-1 4G/5G, and the glycoprotein IIIa Pl(A2) polymorphism. RESULTS: Mean ICA IMT was 0.58 mm; mean CCA IMT was 0.60 mm. There were no differences in ICA or CCA IMT by genotype for any of the candidate genes in unadjusted, age- or sex-adjusted, and multivariable-adjusted models. CONCLUSIONS: There is no evidence for an association between well-studied polymorphisms in the hemostatic factor genes and carotid IMT. Whether other common genetic variants in hemostatic factor genes are associated with subclinical atherosclerosis remains to be determined.
The demonstrated benefits of home care for haemophilia include improved quality of life, less pain and disability, fewer hospitalizations, and less time lost from work or school. Although reduced mortality has not been demonstrated, the substantial increase in longevity since the early 1980s correlates with the introduction of home treatment and prophylaxis programmes. These programmes must be designed and monitored by haemophilia treatment centres (HTC), which are staffed with professionals with broad and complementary expertise in the disease and its complications. In return, patients and their families must be willing to accept the reciprocal responsibilities that come from administering blood products or their recombinant equivalents at home. Patients with inhibitors to factors VIII or IX pose special challenges, but these complications do not obviate participation in home care programmes. Home care was an essential prerequisite to the introduction of effective prophylactic factor replacement therapy. Prophylaxis offers significant improvements in quality of life, but requires a substantial commitment. The use of implantable venous access devices can eliminate some of the difficulty and discomfort of peripheral venous access in small children, but brings additional risks. The future holds the promise of factor concentrates for home use that have longer half-lives, or can be administered by alternate routes. Knowledge of patient genotypes may allow treatments tailored to avoid complications such as inhibitor development. Gene therapy trials, which are currently ongoing, will ultimately lead to gene-based treatments as a complement to traditional protein-based therapy.
It is now recognized that the hemostatic system plays an important role in cancer growth and dissemination, processes known to be vitally dependent on new tumor blood vessel formation (angiogenesis). There is also an increasing body of evidence supporting the link between the various components of the coagulation/fibrinolysis systems and angiogenic activity in cancer patients. Tissue factor (TF), thrombin, fibrinogen, fibrin, and plasminogen activation system, as well as platelets, all are able to promote angiogenesis. On the other hand, coagulation inhibitors, as well as cryptic (proteolytically released) domains of hemostatic proteins, are also known to act as angiogenesis inhibitors. Indeed, modulation (stimulation or inhibition) of angiogenesis may result from either classical functions of various molecular components of the hemostatic cascade, their less studied "alternative" activities, or both. Although much remains to be understood about this complex circuitry these considerations support the judicious use of anticoagulants in patients with malignancy as well as encourage the search for novel antiangiogenic activities that may reside within molecular and cellular components of the hemostatic system.