Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.69 (APC)
 16,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Venous valves are more frequent in distal veins and venulae, providing a protecting action against blood skin reflux. Structurally simple, collagen and endothelium, they allow a cavity to be formed by distension, when occlusion occurs. Venous angioscopy can distinguish bicuspid floating valves, reinforced, reinforcing valves with free edges and seat valves as well as the presence of apertures of small collateral vessels in the sinus, of which they play a role in the filling up. Valves are inefficient in supine and in standing among 20% of the adult population. Sinuses allow vortices to be created, low recirculating zones, where blood flow move slowly in niches, at a low shear rate, independently from the main stream. A deep vortex is located in sinus, usually empty, but likely to receive red cell aggregates and leukocytes in the condition of stasis and hyperviscosity. Such a vortex is hypoxic, cause of endothelial activation. In such areas fibrin-leucocytic nidus are created, histologically recognized, of which sub-endothelium has become thick and thrombogenic. Two stages characterized its progression: stage I: a few alteration in the valves, little thrombin generation, taken over by the coagulation inhibitors: AT III, APC and TFPI. Stage II: damaged valves, local consumption of the inhibitors and extended generation of thrombin over the platelets, through factor IXa. Hereditary inhibitor deficits increase the risk (frequent factor Leyden V). When the coagulation cascade is considered, VIIa-tissue factor complex appears to be the thrombotic pathway, leading first to wall linked thrombin, uneasily reached by AT III and facteur IXa non inhibited by TFPI, therefore explaining the platelet extension. Monocytes, which can bear tissue factor, may be "lodged" inside the niches. Besides this important role in deep venous thrombosis, incompetent venous valves are responsible for the skin venous hypertension, a subsequent ground for ulcers. Their role in chronic venous insufficiency is uncertain. In the near future, venous angioscopy will bring about new findings about the pathophysiology of venous valves.
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PMID:[Venous valves in the legs: hemodynamic and biological problems and relationship to physiopathology]. 948 Mar 31

Bicuspid aortic valve is one of the most common congenital heart valve disorders. We present the development of acute myocardial infarction (AMI) in an 18-year-old male patient with unrecognized bicuspid aortic valve and moderate aortic regurgitation. He presented with chest pain. The electrocardiogram showed ST-segment elevation in leads V2 to V6. Creatine kinase-MB level was elevated to 97 U/l and troponin I was very high (45,000 ng/ml). The diagnosis was made as anterior wall AMI. Following treatment with intravenous rt-PA, ST-segment elevation completely returned to normal. Transthoracic echocardiography showed a bicuspid aortic valve, moderate aortic regurgitation, and apical wall hypokinesia; left ventricular global systolic function was normal. The patient had no risk factors for coronary atherosclerosis, nor a history of substance addiction or a family history of coronary artery disease. Protein C, protein S and homocysteine levels were normal. He refused any further intervention. Two weeks after discharge, he presented again with chest pain. Electrocardiography, cardiac markers, and coronary arteriography were normal. He was discharged on appropriate medical treatment. The presented case is the first report of AMI in a patient with bicuspid aortic valve.
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PMID:Acute myocardial infarction in a young patient with bicuspid aortic valve. 2120 14

Apoptosis of vascular smooth muscle cells (VSMCs) is involved in bicuspid aortic valve (BAV) ascending aorta aneurysms characteristically affecting the convex site. Caspase-3 is a pivotal effector of the apoptosis machinery. The aim of this study was to investigate the impact of an inhibited caspase-3 pathway on apoptosis in convex and concave sites VSMCs of ascending aortic tissue in vitro. Specimens from the convex and concave sites of ascending aortic aneurysm were collected from nine patients with BAV (mean age 58.7+/-14.8). Cultured VSMCs were characterized morphologically and immunohistochemically. Apoptosis activity was measured in VSMCs using Annexin V-APC with propidium iodide nuclear staining in flow cytometry. To investigate apoptotic modulation, caspase-3 was inhibited by N-acetyl-Asp-Glu-Val-Asp-CHO (Ac-DEVD-CHO). Apoptosis was initiated by calcium chloride. Inhibition of caspase-3 with Ac-DEVD-CHO protected VSMCs against calcium chloride apoptosis significantly more in the concave site than in the convex site (25.8+/-9.8 versus 38.5+/-8.0% apoptotic cells, p=0.01). Morphological scanning using light microscopy revealed typical VSMCs. We provide evidence that VSMCs show a different behavior with respect to apoptosis in the concave versus the convex sites in BAV ascending aortic aneurysm. Inhibition of caspase-3 resulted in a significantly increased protection of VSMCs against apoptosis in the concave site compared with the convex site in ascending aortic aneurysm in BAV. These findings may have some implications on understanding aneurysmal formation and its potential modulation.
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PMID:Inhibition of caspase-3 differentially affects vascular smooth muscle cell apoptosis in the concave versus convex aortic sites in ascending aneurysms with a bicuspid aortic valve. 2042 68