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Thrombosis

The antibody fragment also binds to vitronectin receptors (av integrin) that are present on a number of tissues including vessel wall endothelial cells, smooth muscle cells and platelets. These receptors are involved in the proliferative properties of endothelial and smooth muscle cells and the procoagulant properties of the platelets. [Pg.115]

Abciximab is indicated in patients with heart disease caused by poor blood flow in the arteries of the heart (ischemic cardiac complications). It is also used in patients with unstable angina not responding to conventional treatment and for precutaneous coronary intervention. It can reduce the incidence of abrupt closure and restenosis [Pg.115]

This is commonly thought of as intravascular clotting. There is however an important difference between what happens to blood in a test-tube and what can happen to blood in the circulation, since in the latter, the blood is in constant movement or flow. In the test-tube, only what is already present [Pg.168]

Thrombosis is a condition occurring in the cardiovascular system related to the normal, physiological function of haemostasis. Clinically, thrombosis is thought of as those situations where formation of thrombi has proceeded to the point where, by interfering with the circulation to an organ or part, there is interference with function and therefore symptoms result. The thrombus may produce these effects in situ or as an embolus produces such effects elsewhere. Arteriosclerotic changes in the arterial wall are the most common cause of thrombi forming in the heart and arteries. [Pg.169]

Clinical effects produced by thrombi and emboli are (1) no serious effects, the silent thrombus or embolus (2) oedema of a limb, venous thrombus and perivenous lymphangitis (3) post-thrombotic ulceration (4) gangrene of a limb (thrombosis of main artery or embolus from heart or aorta) (5) gangrene of bowel (thrombosis of mesenteric artery or vein, arterial embolism)  [Pg.169]

ACS Symposium Series American Chemical Society Washington, DC, 1980. [Pg.125]

Ga were obtained with low levels of 68(je breakthrough. At this [Pg.126]

In the area of bifunctional chelates, the method of Krejcarek and Tucker (J ) has been utilized to attach galllum-68 to proteins (51). In this approach DTPA is coupled to proteins by the formation of an amide bond. It has been shown that [Pg.127]

Ga-protelns can be formed and that the labeled protein is stable for a time period of several hours. The same type of linkage has also been used to attach galllum-68 to human serum microspheres (51). [Pg.127]


H2N(CH2)jCOOH, C H,3N02. Prepared from -benzoylaminocapronitrile or from l-hydroxycyclohexylhydroperoxide, m.p. 205 0. Aminocaproic acid is an antifibrinolytic agent, used to treat thrombosis in the deep veins. amiDoethyl alcohol. See ethanolamines. [Pg.29]

R. G. Macfadane, in R. Biggs, ed.. Human Blood Coagulation, Haemostasis and Thrombosis, 2nd ed., Blackwell Scientific PubHcations, Oxford, 1976, pp. 1-31. [Pg.539]

The primary advantages of implantable ports are no maintenance between uses other than periodic flushing with heparinized saline every 28 days to ensure patency, lower incidence of clotting and thrombosis, no dressing changes, insignificant infection incidence, unobtmsive cosmetic appearance, and no restriction on physical activity. [Pg.184]

General trends in radiopharmaceutical research emphasize the use of small peptides. These molecules, of which the agents mentioned for thrombosis localization are an example, exhibit rapid and specific binding, and rapid blood clearance, two important parameters for a successflil radiopharmaceutical. Peptides are readily labeled with Tc and lend themselves to formulation as lyophilized kits that can be rapidly and rehably reconstituted. Possible targets for these molecules are quite varied, ranging from atherosclerotic plaque to P-amyloid (for Alzheimer s disease), to a variety of somatic receptors the populations of which are increased or decreased in disease. [Pg.485]

Homocysteine arises from dietary methionine. High levels of homocysteiae (hyperhomocysteinemia) are a risk factor for occlusive vascular diseases including atherosclerosis and thrombosis (81—84). In a controlled study, semm folate concentrations of <9.2 nmol/L were linked with elevated levels of plasma homocysteiae. Elevated homocysteine levels have beea associated also with ischemic stroke (9). The mechanism by which high levels of homocysteine produce vascular damage are, as of yet, aot completely uaderstood. lateractioa of homocysteiae with platelets or eadothehal cells has beea proposed as a possible mechanism. Clinically, homocysteine levels can be lowered by administration of vitamin B, vitamin B 2> foHc acid. [Pg.42]

Deficiency of Factor VII is relatively rare and inherited as an autosomal recessive disorder. Deficiency of Factor VII has been reported to be associated with bond abnormal bleeding and thrombotic tendencies. Deep vein thrombosis and pulmonary emboli have been reported in affected individuals. There is a very high frequency of Factor VII deficiency in people with the Dubin-Johnson syndrome, which is a congenital disorder of Hver function. [Pg.174]

Two types of Protein S deficiency have been described. In type I deficiency there is tittle to no free Protein S but normal amounts of bound Protein S are present. In type II Protein S deficiency both free and bound Protein S are very low to absent. Deficiency of free Protein S is associated with venous and arterial thrombosis. [Pg.175]

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. [Pg.309]

Carrell, R.W., Evans, D.F., Stein, RE. Mobile reactive centre of serpins and the control of thrombosis. Nature 353 576-578, 1991. [Pg.119]

NS AIDs Cyclooxygenases (COX-1, COX-2) l Prostaglandins l Thromboxanes l Sensitization of sensory neurons f Inhibition of spinal neurons Nonselective gastrointestinal ulcers, perforation, bleeding, renal impairment COX-2 thrombosis, myocardial infarction, stroke... [Pg.76]

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). [Pg.108]

The two most widely used coumarins are warfarin (US, Canada, and UK) and phenprocoumon (continental Europe). The long half-life (60 h) of prothrombin means that coumarin cannot achieve therapeutic anticoagulation for at least 5 days following initiation. Thus, for patients with acute thrombosis, oral anticoagulants are usually started only when the patient is receiving a rapidly active agent, usually UFH or LMWH. [Pg.109]

Mousa SA, Bozarth JM, Edwards S et al (1998) Novel technetium 99m-labeled GPIIb/IIIa receptor antagonists as potential imaging agents for venous and arterial thrombosis. Coron Artery Dis 9 131-141... [Pg.147]

Platelets play a central role in primary hemostasis. They are also important in pathological processes leading to thrombosis. Antiplatelet drugs are primarily directed against platelets and inhibit platelet activation by a number of different mechanisms. They are used for the prevention and treatment of thrombotic processes, especially in the arterial vascular system. [Pg.167]

Due to the pivotal role of platelets in thrombus formation, especially in the arterial system, inhibition of platelet function has become a central pharmacological approach. Antiplatelet drugs are given in order to prevent and treat thromboembolic diseases such as coronary heart disease, peripheral and cerebrovascular disease. They have also revolutionized the procedures of invasive coronary interventions as they reduce the risk of restenosis and thrombosis. [Pg.170]


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A Client with Deep Vein Thrombosis

Acute arterial thrombosis

Acute coronary thrombosis

Angiogenesis thrombosis

Animal models of thrombosis

Animal models thrombosis

Anticoagulants thrombosis

Antiplatelet therapy thrombosis

Arterial thrombosis

Arterial thrombosis assay

Arterial thrombosis, treatment

Arteriovenous fistula thrombosis

Arteriovenous shunt thrombosis

Artery thrombosis

Aspirin thrombosis

Aspirin thrombosis prophylaxis

Asymptomatic deep vein thrombosis

Atherosclerosis Thrombosis

Atrial thrombosis

Basilar thrombosis

Blood thrombosis

Brain thrombosis

Cardiovascular diseases thrombosis

Catheter-related venous thrombosis

Catheters for Thrombosis Sample Exfoliation in Blood Vessels Using Piezoelectric Polymer Fibers

Catheters thrombosis sample exfoliation

Cavernous sinus thrombosis

Central retinal vein thrombosis

Cerebral vein thrombosis, with oral contraceptives

Cerebral venous and sinus thrombosis

Cerebral venous sinus thrombosis

Cerebral venous thrombosis

Cerebral venous thrombosis causes

Cerebral venous thrombosis diagnosis

Cerebral venous thrombosis treatment

Cilostazol thrombosis

Clinical trials venous thrombosis

Coagulation/Thrombosis

Coronary arteries platelet thrombosis inhibition

Coronary artery thrombosis, treatment

Coronary thrombosis

Coronary thrombosis treatment

Coronary thrombosis, platelet-dependent

Deep vein thrombosis

Deep vein thrombosis case study

Deep vein thrombosis concentrate

Deep vein thrombosis derivatives

Deep vein thrombosis diagnosis

Deep vein thrombosis prevention

Deep vein thrombosis treatment

Deep vein thrombosis with oral contraceptives

Deep vein thrombosis, anticoagulation

Deep venous thrombosis

Deep venous thrombosis anticoagulants

Deep venous thrombosis thrombolytics

Desmopressin thrombosis

Effect of anticoagulants on thrombosis

Electrical-Induced Thrombosis

Embolism/thrombosis

Embolism/thrombosis derivatives

Embolization and thrombosis

Enoxaparin deep vein thrombosis

Eversion-graft induced thrombosis

Extracorporeal Thrombosis Models

Fatty Acids in Coagulation and Thrombosis

Femoral Thrombosis

Fibrinogen thrombosis

Fibrinolysis thrombosis

Fibrinolytic enzyme in thrombosis treatment

Fibrolase thrombosis model systems

Focal cerebral thrombosis

Folic acid thrombosis

Gene therapy thrombosis

Genetic models of hemostasis and thrombosis

Graft thrombosis

Haemorrhage and thrombosis

Hemodialysis thrombosis

Hemostasis thrombosis

Hemostasis, Thrombosis, and Coagulation

Heparin deep vein thrombosis

Heparin-induced thrombocytopenia with thrombosis

Heparins arterial thrombosis

Heparins cerebral venous thrombosis

Hepatic thrombosis

Human diseases Thrombosis

In vitro Models of Thrombosis

In-stent thrombosis

Inferior thrombosis

Internal thrombosis

Intravenous immunoglobulin venous thrombosis

Laser-induced thrombosis

Late stent thrombosis

Liver portal vein thrombosis

Medicinal plants for thrombosis

Mesenteric vein thrombosis

Models of thrombosis

Multisystem venous thrombosis

Natural products in thrombosis

Neonatal aortic thrombosis

Orbital vein thrombosis

Ovarian vein thrombosis

Peripheral arterial thrombosis, treatment

Photochemical-induced thrombosis

Plantar Vein Thrombosis

Platelet aggregation arterial thrombosis due

Platelet coronary artery thrombosis

Platelets and thrombosis

Portal thrombosis

Prevention of Clinical Thrombosis by Aspirin

Prostaglandins arterial thrombosis

Prostaglandins clinical thrombosis

Puerperal vein thrombosis

Pulmonary thrombosis

Pulmonary thrombosis treatment

Renal thrombosis

Renal vein thrombosis

Retinal vein thrombosis

Risk factors thrombosis

Rofecoxib thrombosis

Saphenous Thrombosis

Saturated fatty acids thrombosis

Segmental thrombosis

Sinus thrombosis

Stasis-Induced Thrombosis (Wessler Model)

Stent thrombosis factors related

Stents subacute thrombosis

Stents thrombosis

Surface thrombosis

Thread-induced venous thrombosis

Thrombosis A Dark Side of Hemostatic System Function

Thrombosis Calf Veins

Thrombosis Factor

Thrombosis Superficial Veins

Thrombosis abnormal hemostasis

Thrombosis adrenaline

Thrombosis and

Thrombosis and Haemostasis

Thrombosis cerebral vein

Thrombosis coagulation cascade

Thrombosis coronary heart disease

Thrombosis deep cerebral venous

Thrombosis definition

Thrombosis described

Thrombosis development

Thrombosis drugs affecting

Thrombosis eicosanoids

Thrombosis endothelial cell products

Thrombosis factors regulating

Thrombosis heparin-induced

Thrombosis homocysteine

Thrombosis in Myocardial Infarction

Thrombosis inhibitors

Thrombosis molecular mechanisms

Thrombosis phases

Thrombosis platelets

Thrombosis protein-coated surfaces

Thrombosis proteins)

Thrombosis risk reduction

Thrombosis role of natural products

Thrombosis supplementation trials

Thrombosis surgery

Thrombosis symptoms

Thrombosis synthesis

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Thrombosis treatment abciximab

Thrombosis, anticoagulation

Thrombosis, cerebral

Thrombosis, portal vein

Thrombosis, propagating

Thrombosis, prostaglandins

Thrombosis, protective effects

Thrombosis, renal venous

Use of Aspirin to Prevent Thrombosis

Vascular thrombosis

Vein Thrombosis

Vein thrombosis oral contraceptives

Venous sinus thrombosis

Venous thromboembolism thrombosis Pulmonary embolism

Venous thromboembolism vein thrombosis Pulmonary embolism

Venous thrombosis

Venous thrombosis Subject

Venous thrombosis immunoglobulin

Venous thrombosis intravenous

Venous thrombosis model

Venous thrombosis parenteral nutrition

Venous thrombosis, treatment

Vitamin thrombosis

Warfarin thrombosis

Wire-Coil Induced Thrombosis

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