Platelet Aggregation Inhibitors
Salivary Proteins and Peptides
Amino Acid Sequence
Molecular Sequence Data
Platelet Membrane Glycoproteins
Platelet Function Tests
Platelet Glycoprotein GPIIb-IIIa Complex
Platelet Factor 4
Platelet Activating Factor
Platelet Glycoprotein GPIb-IX Complex
Receptors, Purinergic P2Y12
von Willebrand Factor
Antigens, Human Platelet
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Prostaglandin Endoperoxides, Synthetic
Platelet Factor 3
Platelet Membrane Glycoprotein IIb
Immunoglobulin Fab Fragments
Dose-Response Relationship, Drug
Blood Coagulation Factors
Receptors, Thromboxane A2, Prostaglandin H2
Receptors, Purinergic P2Y1
Purinergic P2Y Receptor Antagonists
Dual Specificity Phosphatase 2
Carotid Artery Thrombosis
Interleukin-12 is synthesized by mesangial cells and stimulates platelet-activating factor synthesis, cytoskeletal reorganization, and cell shape change. (1/4442)Preliminary studies indicate the involvement of interleukin (IL)-12 in experimental renal pathology. In the present study, we evaluated whether cultured glomerular mesangial cells are able to produce IL-12 and whether IL-12 may regulate some of their functions, including the cytoskeletal reorganization, the change in cell shape, and the production of platelet-activating factor (PAF). The results obtained indicate that pro-inflammatory stimuli, such as tumor necrosis factor-alpha and bacterial polysaccharides, induce the expression of IL-12 mRNA and the synthesis of the protein by cultured mesangial cells. Moreover, cultured mesangial cells were shown to bind IL-12 and to express the human low-affinity IL-12 beta1-chain receptor. When challenged with IL-12, mesangial cells produced PAF in a dose- and time-dependent manner and superoxide anions. No production of tumor necrosis factor-alpha and IL-8 was observed. Moreover, we demonstrate that IL-12 induced a delayed and sustained shape change of mesangial cells that reached its maximum between 90 and 120 minutes of incubation. The changes in cell shape occurred concomitantly with cytoskeletal rearrangements and may be consistent with cell contraction. As IL-12-dependent shape change of mesangial cells was concomitant with the synthesis of PAF, which is known to promote mesangial cell contraction, we investigated the role of PAF using two chemically different PAF receptor antagonists. Both antagonists inhibited almost completely the cell shape change induced by IL-12, whereas they were ineffective on angiotensin-II-induced cell shape change. In conclusion, our results suggest that mesangial cells can either produce IL-12 or be stimulated by this cytokine to synthesize PAF and to undergo shape changes compatible with cell contraction. (+info)
The mechanism of the increasing action of TA-993, a new 1,5- benzothiazepine derivative, on limb blood flow in anesthetized dogs: selective suppression of sympathetic nerve activity. (2/4442)TA-993, (-)-cis-3-acetoxy-5-(2-(dimethylamino)ethyl)-2, 3-di-hydro-8-methyl-2-(4-methylphenyl)-1,5-benzothiazepin-4(5H)one maleate, a new 1,5-benzothiazepine derivative with l-cis configuration, has a unique and selective increasing action on limb blood flow with little influence on arterial pressure besides an antiplatelet action. We studied the mechanism of increasing action of TA-993 on limb blood flow in anesthetized dogs. In a canine blood-perfused hindlimb preparation with a donor dog, TA-993 (100 microg/kg i.v.) did not increase femoral blood flow when administered to the donor dog, but did when administered to a recipient dog. TA-993 did not show the increasing action on femoral blood flow in the presence of hexamethonium or phentolamine, whereas it did in the presence of propranolol or atropine. TA-993 also showed a weak increasing effect on heart rate, which was inhibited by any one of these blockers. TA-993 (300 microg/kg i.v.) did not alter the phenylephrine (1-100 ng/kg i.a.)- or the talipexole (3-100 ng/kg i.a.)-induced increase in perfusion pressure in an autoperfused hindlimb. These results suggest that the increasing action of TA-993 on limb blood flow is mediated by the sympathetic nervous system but that the adrenergic receptors are not likely to be the central point of action of this new agent. There is a possibility that the mechanism of the increasing action on heart rate is different from that of its increasing action on limb blood flow. (+info)
Labeling of the internal pool of GP IIb-IIIa in platelets by c7E3 Fab fragments (abciximab): flow and endocytic mechanisms contribute to the transport. (3/4442)Abciximab is a new antiplatelet therapeutic in ischemic cardiovascular disease. The drug, chimeric Fab fragments of a murine monoclonal antibody (MoAb) (c7E3), blocks GP IIb-IIIa function. However, its capacity to reach all receptor pools in platelets is unknown. Electron microscopy and immunogold labeling were used to localize abciximab in platelets of patients receiving the drug for up to 24 hours. Studies on frozen-thin sections showed that c7E3 Fab, in addition to the surface pool, also labeled the surface-connected canalicular system (SCCS) and alpha-granules. Analysis of gold particle distribution showed that intraplatelet labeling was not accumulative and in equilibrium with the surface pool. After short-term incubations of platelets with c7E3 Fab in vitro, gold particles were often seen in lines within thin elements of the SCCS, some of which appeared in contact with alpha-granules. Little labeling was associated with Glanzmann's thrombasthenia platelets, confirming that the channels contained bound and not free c7E3 Fab. Endocytosis of abciximab in clathrin-containing vesicles was visualized by double staining and constitutes an alternative mechanism of transport. The remaining free pool of GP IIb-IIIa was evaluated with the MoAb AP-2; flow cytometry showed it to be about 9% on the surface of nonstimulated platelets but 33% on thrombin-activated platelets. The ability of drugs to block all pools of GP IIb-IIIa and then to be associated with secretion-dependent residual aggregation must be considered when evaluating their efficiency in a clinical context. (+info)
Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death. (4/4442)Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death. (+info)
Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. (5/4442)Exogenously hypercholesterolemic (ExHC) rats were fed on an atherogenic diet supplemented with 1% each of either ethyl ester docosahexaenoic acid [EE-DHA, 22:6(n-3)], ethyl ester eicosapentaenoic acid [EE-EPA, 20:5(n-3)] or safflower oil (SO) for 6 months. The rats fed on the diets containing EE-EPA or EE-DHA, compared with those fed on SO, had lower serum cholesterol and triacylglycerol levels, less aggregation of platelets and slower progress of intimal thickening in the ascending aorta. Relative to the SO-fed rats, both of the (n-3) fatty acid-fed rats had a significantly reduced proportion of arachidonic acid in the platelet and aortic phospholipids, and lower production of thromboxane A2 by platelets and of prostacyclin by the aorta. These results suggest that EPA and DHA are similarly involved in preventing atherosclerosis development by reducing hypercholesterolemia and modifying the platelet functions. (+info)
Predominant inhibition of ganodermic acid S on the thromboxane A2-dependent pathway in human platelets response to collagen. (6/4442)Ganodermic acid S (GAS), a membrane acting agent, exerts multiple effects on human platelet function (C.N. Wang et al. (1991) Biochem. J. 277, 189-197). The study reported how GAS affected the response of human gel-filtered platelets (GFP) to collagen. The agent inhibited cell aggregation by prolonging lag and shape change periods and decreasing the initial cell aggregation rate. However, the inhibitory efficiency was less than its inhibition on GFP response to U46619, a thromboxane (TX) A2 mimetic. In the agent-effect on biochemical events, GAS effectively inhibited Ca2+ mobilization, phosphorylation of myosin light chain, dense granule secretion and TXB2 generation. The inhibitions might originate from blocking Ca2+ mobilization of the TXA2-dependent pathway. GAS partially decreased the phosphorylation of most phosphotyrosine proteins from early activation to the integrin alphaIIbbeta3-regulated steps. The agent did not affect the phosphorylation of three proteins at the steps regulated by integrin alphaIIbbeta3. The results suggest that GAS inhibits the collagen response predominantly on the TXA2-dependent signaling, and the tyrosine kinase-dependent pathway in collagen response plays a major role in aggregation. (+info)
PAF binding to a single receptor in corneal epithelium plasma membrane. (7/4442)PURPOSE: To study the binding characteristics and the expression of platelet-activating factor receptors (PAF-R) in corneal epithelium to elucidate the site of action of PAF. METHODS: Binding of [3H]PAF was investigated in subcellular fractions of the epithelia of bovine corneas and in membranes from cultured rabbit corneal epithelial cells. Dose-response inhibition curves of [3H]PAF-specific binding were generated using increasing concentrations of several PAF-R antagonists. RNA from rabbit corneal epithelial cells was probed for PAF-R expression by reverse transcription-polymerase chain reaction (RT-PCR) with specifically designed degenerated primers. RESULTS: Scatchard analysis showed a high-affinity binding site in bovine and rabbit corneal epithelium. The dissociation constant (Kd) and the maximum binding sites (Bmax) in a bovine membrane preparation and similar rabbit fraction were 0.77+/-0.03 nM and 180+/-21 femtomoles/mg protein and 4.3 nM and 1.3 picomoles/mg protein, respectively. Specific PAF-binding sites were found in bovine preparations enriched in plasma membranes with a Kd = 69.6 pM and Bmax = 80 femtomoles/mg protein; no specific binding was found in nuclei or microsomal fractions. RT-PCR of rabbit corneal epithelium generated a single product of the predicted size (478 bp). The deduced amino acid sequence of the purified PCR product was 87% homologous to human PAF-R. The hetrazepines BN 50727 and BN 50730 and the PAF structural analogues CV 3988 and CV 6209 competitively inhibited [3H]PAF binding to corneal epithelium with similar potency. WEB 2086 BS was two orders of magnitude less active in antagonizing PAF binding. CONCLUSIONS: Corneal epithelium contains a single population of receptors localized in the plasma membrane. PAF antagonists exert their actions by blocking this PAF-R. The partial sequence deduced in rabbit corneal PAF-R show a higher homology to the human PAF-R. (+info)
Conformational changes in the A3 domain of von Willebrand factor modulate the interaction of the A1 domain with platelet glycoprotein Ib. (8/4442)Bitiscetin has recently been shown to induce von Willebrand factor (vWF)-dependent aggregation of fixed platelets (Hamako J, et al, Biochem Biophys Res Commun 226:273, 1996). We have purified bitiscetin from Bitis arietans venom and investigated the mechanism whereby it promotes a form of vWF that is reactive with platelets. In the presence of bitiscetin, vWF binds to platelets in a dose-dependent and saturable manner. The binding of vWF to platelets involves glycoprotein (GP) Ib because it was totally blocked by monoclonal antibody (MoAb) 6D1 directed towards the vWF-binding site of GPIb. The binding also involves the GPIb-binding site of vWF located on the A1 domain because it was inhibited by MoAb to vWF whose epitopes are within this domain and that block binding of vWF to platelets induced by ristocetin or botrocetin. However, in contrast to ristocetin or botrocetin, the binding site of bitiscetin does not reside within the A1 domain but within the A3 domain of vWF. Thus, among a series of vWF fragments, 125I-bitiscetin only binds to those that overlap the A3 domain, ie, SpIII (amino acid [aa] 1-1365), SpI (aa 911-1365), and rvWF-A3 domain (aa 920-1111). It does not bind to SpII corresponding to the C-terminal part of vWF subunit (aa 1366-2050) nor to the 39/34/kD dispase species (aa 480-718) or T116 (aa 449-728) overlapping the A1 domain. In addition, bitiscetin that does not bind to DeltaA3-rvWF (deleted between aa 910-1113) has no binding site ouside the A3 domain. The localization of the binding site of bitiscetin within the A3 domain was further supported by showing that MoAb to vWF, which are specific for this domain and block the interaction between vWF and collagen, are potent inhibitors of the binding of bitiscetin to vWF and consequently of the bitiscetin-induced binding of vWF to platelets. Thus, our data support the hypothesis that an interaction between the A1 and A3 domains exists that may play a role in the function of vWF by regulating the ability of the A1 domain to bind to platelet GPIb. (+info)
There are several types of thrombosis, including:
1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.
The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:
1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic
Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.
Some common types of blood platelet disorders include:
1. Thrombocytopenia: This is a condition in which there are too few platelets in the blood. It can be caused by a variety of factors, including autoimmune disorders, bone marrow disorders, and certain medications.
2. Bernard-Soulier syndrome: This is a rare inherited disorder that affects the function of platelets and causes easy bruising and prolonged bleeding.
3. Glanzmann's thrombasthenia: This is a rare inherited disorder that affects the platelets' ability to clot properly, leading to excessive bleeding.
4. Platelet dysfunction: This can be caused by a variety of factors, including certain medications, infections, and autoimmune disorders. It can lead to excessive bleeding or prolonged bleeding after injury or surgery.
5. Congenital amegakaryocytic thrombocytopenia: This is a rare inherited disorder that affects the development of platelets in the bone marrow, leading to a lack of platelets in the blood.
6. Grey platelet syndrome: This is a rare inherited disorder that affects the structure of platelets, making them more prone to rupture and lead to easy bruising and prolonged bleeding.
7. Platelet-type von Willebrand disease: This is a mild bleeding disorder caused by a deficiency of von Willebrand factor, a protein that helps platelets stick together to form clots.
8. acquired platelet dysfunction: This can be caused by various conditions such as infections, medications, and autoimmune disorders.
These disorders can be diagnosed through blood tests, including a complete blood count (CBC) and a platelet function test. Treatment options vary depending on the specific disorder and may include medication, surgery, or lifestyle changes.
There are several possible causes of thrombocytopenia, including:
1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.
Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.
In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.
The term "thrombasthenia" comes from the Greek words "thrombos," meaning clot, and "basis," meaning foundation. It was first used by the British physician Sir William Osler in the late 19th century to describe a group of rare bleeding disorders characterized by abnormal platelet function.
There are three main types of thrombasthenia:
1. Bernard-Soulier syndrome: This is the most common type of thrombasthenia and is caused by a defect in the gene that codes for the protein known as platelet membrane glycoprotein (PMG) IIb. People with this condition have large, fragile platelets that are prone to bleeding.
2. Glanzmann's thrombasthenia: This is a rare type of thrombasthenia caused by a defect in the gene that codes for the protein known as platelet membrane glycoprotein (PMG) IIIa. People with this condition have small, irregular platelets that are unable to form proper blood clots.
3. Gray platelet syndrome: This is a rare type of thrombasthenia caused by a defect in the gene that codes for the protein known as alpha-granule membrane protein (AGM). People with this condition have small, gray-colored platelets that are prone to bleeding.
Thrombasthenia can be diagnosed through blood tests that evaluate platelet function and genetic testing to identify the specific defect responsible for the disorder. Treatment typically involves avoiding medications that can exacerbate bleeding, using platelet transfusions to increase platelet numbers, and in some cases, undergoing surgery to repair or remove affected blood vessels.
Carotid artery thrombosis is often caused by atherosclerosis, which is the buildup of plaque in the arteries that can lead to the formation of blood clots. Other risk factors for carotid artery thrombosis include high blood pressure, smoking, high cholesterol, diabetes, and obesity.
Diagnosis of carotid artery thrombosis typically involves imaging tests such as ultrasound, CT or MRI scans, and Doppler studies to visualize the blood flow in the neck and brain. Treatment options for carotid artery thrombosis include anticoagulation medications to prevent further clotting, medications to dissolve the clot, and surgery to remove the clot or repair the affected artery.
In severe cases, carotid artery thrombosis can lead to stroke or brain damage if not treated promptly. Therefore, it is important to seek medical attention immediately if symptoms persist or worsen over time.
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- When anticoagulants or platelet aggregation inhibitors are indicated, they are resumed early. (bvsalud.org)
- At 30 days, net adverse cardiovascular results were significantly reduced in the bivalirudin versus the heparin/heparin plus tirofiban-inhibitor groups. (acc.org)
- Further, with the use of a routine post-PCI bivalirudin infusion, the rates of stent thrombosis were similar with bivalirudin, heparin, and heparin plus a glycoprotein IIb/IIIa inhibitor. (acc.org)
- Antiplatelets, such as aspirin and clopidogrel, prevent blood cells called platelets from clumping together to form a clot. (medlineplus.gov)
- Clopidogrel reduces the chances of these events by preventing platelets from forming into clumps. (medbroadcast.com)
- Whole blood dynamic platelet aggregation counting and 1-year clinical outcomes in patients with coronary heart diseases treated with clopidogrel. (cdc.gov)
- Evidence shows that antiplatelet agents, antioxidant therapies, amino acid supplementation, angiotensin converting enzyme (ACE) inhibitors, and angiotensin-receptor blockers may be able to prevent or slow the progression of atherosclerosis. (medscape.com)
- Inhibitors of the tyrosine kinase Btk have been proposed as novel antiplatelet agents. (haematologica.org)
- Potential cellular targets include vascular smooth muscle cells, monocyte/macrophage cell lines, platelets, and endothelial cells. (medscape.com)
- If MPN patients are also considered to be cancer patients in many countries, the pathophysiology of thrombosis is quite specific (hyperviscosity, platelet abnormalities, clonality, specific cytokines…) and they are exposed to a lower risk of digestive hemorrhages. (clinicaltrials.gov)
- Integrin receptors are involved in cell-cell and cell-extracellular matrix interactions, serving as the final common pathway leading to aggregation via formation of platelet-platelet bridges, which are essential in thrombosis and haemostasis. (embl.de)
- Increased intake of linoleic acid is known to interfere with the incorporation of EPA and DHA (which have the most potent inflammatory effects) in cell membrane lipids, and causes platelet aggregation and oxidation of low-density lipoprotein. (researchgate.net)
- A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A . It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II , a vasoconstrictor and important regulator of arterial blood pressure . (lookformedical.com)
- Ticagrelor, a purinergic P2Y12 receptor blocker, is a potent platelet antagonist and an important component in the treatment for acute coronary syndromes identified to have a potential risk to cause bradyarrhythmias. (manipal.edu)
Percutaneous Coronary Int1
- Effects of aging on clinical outcomes in patients receiving genotype-guided P2Y12 inhibitor selection after percutaneous coronary intervention. (cdc.gov)
- Aspirin and HMG-CoA reductase inhibitors may reduce plaque inflammation. (medscape.com)
- P-selectin, soluble endothelial protein C receptor, soluble thrombomodulin, plasminogen activator inhibitor 1, ADAMTS-13, von Willebrand factor, tissue factor, soluble intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 were more elevated in LF patients than in controls. (cdc.gov)
- Endothelial protein C receptor, thrombomodulin, intercellular adhesion molecule 1, plasminogen activator inhibitor 1, D-dimer, and hepatocyte growth factor were higher in fatal than nonfatal LF cases. (cdc.gov)
- The C-type lectin receptor CLEC-2 is expressed at high levels on platelets and at low levels on a subpopulation of hematopoietic cells. (haematologica.org)
- 7-9 This hemITAM signaling pathway is similar to that used by the YxxL-containing platelet ITAM receptors such as the collagen receptor GPVI-FcRγ complex and the low affinity immune receptor FcγRIIA 10 . (haematologica.org)
- Disintegrins contain an RGD (Arg-Gly-Asp) or KGD (Lys-Gly-Asp) sequence motif that binds specifically to integrin IIb-IIIa receptors on the platelet surface, thereby blocking the binding of fibrinogen to the receptor-glycoprotein complex of activated platelets. (embl.de)
- To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II , patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS . (lookformedical.com)
- In this study we show that low concentrations of the Btk inhibitor ibrutinib block CLEC-2-mediated activation and tyrosine phosphorylation including Syk and PLCγ2 in human platelets. (haematologica.org)
- An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE . (lookformedical.com)
- Thrombocytopenia is a common feature of hemorrhagic fevers and vascular permeability disorders ( 8 ), but the decrease in platelet counts in acute LF is not low enough to cause spontaneous hemorrhage. (cdc.gov)
- Selective serotonergic reuptake inhibitors (SSRIs) may decrease platelet aggregation. (duke.edu)
- The American Heart Association (AHA) has promulgated its Get With the Guidelines program, which involves an Internet-based checklist of discharge medications to ensure that coronary artery disease (CAD) patients are started on aspirin, beta-blockers, ACE inhibitors, and statins (if needed) in the hospital. (medscape.com)
- Platelet aggregation time was significantly (P less than 0.01) decreased in female rabbits treated with oral contraceptive (a preparation containing low dose of estrogen) as also by injection of diethylstilbestrol (10 mg/kg), while in animals that received indomethacin (10 mg/kg) or aspirin (30 mg/kg) (PG synthetase inhibitors) along with oral contraceptives or diethylstilbestrol there was no significant alteration in platelet aggregation time. (who.int)
- Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system. (bvsalud.org)
- The collagen-induced platelet aggregation of platelet-rich plasma samples from 14 healthy rabbits was measured turbidometrically using a platelet aggregometer, before and 1 hour after intravenous injection of alum. (who.int)
- Collagen-induced platelet aggregation was significantly reduced after alum injection. (who.int)
- contradiction in the mechanism of action of alum, we evaluated the in vivo effect of Alum (aluminium potassium sulfate) is a alum in terms of collagen-induced platelet food additive and traditional remedy used to aggregation and bleeding time. (who.int)
- Angiotensin converting enzyme inhibitors. (lookformedical.com)
- The impaired homeostasis and platelet dysfunction implicate alterations in the protein C pathway, which might contribute to the loss of endothelial barrier function in fatal infections. (cdc.gov)
- Normally, platelets help the blood to clot when needed, such as after an injury. (medbroadcast.com)
- In Sierra Leone during 2015-2018, we assessed LF patients' day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function. (cdc.gov)
- Platelet aggregation study on the blood. (who.int)
- Ces résultats semblent indiquer que l'utilisation de l'alun en tant qu'antiplaquettaire oral pourrait faire l'objet d'études complémentaires, en tenant compte des effets secondaires éventuels notamment chez les patients dont la fonction rénale est altérée. (who.int)
- These results show that Btk inhibitors selectively block activation of human platelets by CLEC-2 relative to GPVI suggesting that they can be used at 'low dose' in patients to target CLEC-2 in thrombo-inflammatory disease. (haematologica.org)
- This feedback role is not seen in mouse platelets and, consistent with this, CLEC-2-mediated activation is blocked by high but not by low concentrations of ibrutinib. (haematologica.org)
- Platelet disaggregation occurred only in samples from fatal LF cases. (cdc.gov)
- 11 Another difference between CLEC-2 and GPVI signaling in human platelets is the critical dependence of CLEC- 2 on positive feedback signaling through ADP and thromboxane A2 (TxA2), actin polymerization, and the small GTPase Rac. (haematologica.org)
- adults and adolescents weighing at least 35 kg who have previously been treated with a protease inhibitor (`protease inhibitor-experienced') or in children and adolescents from the age of 3 years with a body weight of at least 14 kg. (who.int)