A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, pre-eclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders.
A CXC chemokine that is found in the alpha granules of PLATELETS. The protein has a molecular size of 7800 kDa and can occur as a monomer, a dimer or a tetramer depending upon its concentration in solution. Platelet factor 4 has a high affinity for HEPARIN and is often found complexed with GLYCOPROTEINS such as PROTEIN C.

NMR structure and dynamics of monomeric neutrophil-activating peptide 2. (1/247)

Neutrophil-activating peptide 2 (NAP-2), which demonstrates a range of proinflammatory activities, is a 72-residue protein belonging to the alpha-chemokine family. Although NAP-2, like other alpha-chemokines, is known to self-associate into dimers and tetramers, it has been shown that the monomeric form is physiologically active. Here we investigate the solution structure of monomeric NAP-2 by multi-dimensional 1H-NMR and 15N-NMR spectroscopy and computational modelling. The NAP-2 monomer consists of an amphipathic, triple-stranded, anti-parallel beta-sheet on which is folded a C-terminal alpha-helix and an aperiodic N-terminal segment. The backbone fold is essentially the same as that found in other alpha-chemokines. 15N T1, T2 and nuclear Overhauser effects (NOEs) have been measured for backbone NH groups and used in a model free approach to calculate order parameters and conformational exchange terms that map out motions of the backbone. N-terminal residues 1 to 17 and the C-terminus are relatively highly flexible, whereas the beta-sheet domain forms the most motionally restricted part of the fold. Conformational exchange occurring on the millisecond time scale is noted at the top of the C-terminal helix and at proximal residues from beta-strands 1 and 2 and the connecting loop. Dissociation to the monomeric state is apparently responsible for increased internal mobility in NAP-2 compared with dimeric and tetrameric states in other alpha-chemokines.  (+info)

In vitro antibacterial activities of platelet microbicidal protein and neutrophil defensin against Staphylococcus aureus are influenced by antibiotics differing in mechanism of action. (2/247)

Thrombin-induced platelet microbicidal protein-1 (tPMP-1) and human neutrophil defensin-1 (HNP-1) are small, cationic antimicrobial peptides. These peptides exert potent in vitro microbicidal activity against a broad spectrum of human pathogens, including Staphylococcus aureus. Evidence suggests that tPMP-1 and HNP-1 target and disrupt the bacterial membrane. However, it is not yet clear whether membrane disruption itself is sufficient to kill the bacterium or whether subsequent, presumably intracellular, events are also involved in killing. We investigated the staphylocidal activities of tPMP-1 and HNP-1 in the presence or absence of pretreatment with antibiotics that differ in their mechanisms of action. The staphylocidal effects of tPMP-1 and HNP-1 on control cells (no antibiotic pretreatment) were rapid and concentration dependent. Pretreatment of S. aureus with either penicillin or vancomycin (bacterial cell wall synthesis inhibitors) significantly enhanced the anti-S. aureus effects of tPMP-1 compared with the effects against the respective control cells over the entire tPMP-1 concentration range tested (P < 0.05). Similarly, S. aureus cells pretreated with these antibiotics were more susceptible to HNP-1 than control cells, although the difference in the effects against cells that received penicillin pretreatment did not reach statistical significance (P < 0.05 for cells that received vancomycin pretreatment versus effects against control cells). Studies with isogenic pairs of strains with normal or deficient autolytic enzyme activities demonstrated that enhancement of S. aureus killing by cationic peptides and cell wall-active agents could not be ascribed to a predominant role of autolytic enzyme activation. Pretreatment of S. aureus cells with tetracycline, a 30S ribosomal subunit inhibitor, significantly decreased the staphylocidal effect of tPMP-1 over a wide peptide concentration range (0.16 to 1.25 microgram/ml) (P < 0.05). Furthermore, pretreatment with novobiocin (an inhibitor of bacterial DNA gyrase subunit B) and with azithromycin, quinupristin, or dalfopristin (50S ribosomal subunit protein synthesis inhibitors) essentially blocked the S. aureus killing resulting from exposure to tPMP-1 or HNP-1 at most concentrations compared with the effects against the respective control cells (P < 0.05 for a tPMP-1 concentration range of 0.31 to 1.25 microgram/ml and for an HNP-1 concentration range of 6.25 to 50 microgram/ml). These findings suggest that tPMP-1 and HNP-1 exert anti-S. aureus activities through mechanisms involving both the cell membrane and intracellular targets.  (+info)

Comparison of the antithrombotic effect of PEG-hirudin and heparin in a human ex vivo model of arterial thrombosis. (3/247)

Polyethylene glycol (PEG)-hirudin is a derivative of hirudin with a long plasma half-life. We have compared the efficacy of PEG-hirudin with unfractionated heparin (UH) in preventing arterial thrombosis. Arterial thrombus formation was induced ex vivo in 12 healthy human volunteers by exposing a tissue factor-coated coverslip positioned in a parallel-plate perfusion chamber to flowing nonanticoagulated human blood drawn directly from an antecubital vein at an arterial wall shear rate of 2600 s-1 for 3.5 minutes. PEG-hirudin, UH, or saline (as control) were administered ex vivo through a heparin-coated mixing device positioned proximal to the perfusion chamber. Platelet and fibrin deposition was quantified by immunoenzymatic measure of the P-selectin and D-dimer content of dissolved plasmin-digested thrombi, respectively. UH was administered to a plasma concentration of 0.35 IU/mL. This concentration prolonged the activated partial thromboplastin time from 32+/-1 seconds to 79+/-4 seconds (P<0.01). UH did not significantly prevent platelet deposition. However, fibrin deposition was reduced by 39% (P<0.05). PEG-hirudin in plasma concentrations of 0.5, 2.5, and 5 microg/mL prolonged the activated partial thromboplastin time to 48+/-2, 87+/-4, and 118+/-4 seconds, respectively. In contrast to UH, PEG-hirudin prevented both platelet and fibrin deposition in a dose-dependent manner with a >80% reduction at 5 microg/mL (P<0.01). Furthermore, the plasma level of PEG-hirudin required to significantly prevent fibrin deposition (0.5 microg/mL) corresponded to a much shorter prolongation of activated partial thromboplastin time (48+/-2 seconds) than that needed for UH (79+/-4 seconds). Thus, our results are compatible with the view that thrombin is greatly involved in recruitment of platelets in evolving thrombi, and that PEG-hirudin is an effective agent for preventing arterial thrombosis in a human ex vivo experimental model.  (+info)

Large amounts of vascular endothelial growth factor at the site of hemostatic plug formation in vivo. (4/247)

Vascular endothelial growth factor (VEGF) is important for the proliferation, differentiation, and survival of microvascular endothelial cells. It is a potent angiogenic factor and a specific endothelial cell mitogen that increases fenestration and extravasation of plasma macromolecules. Recently, large quantities of VEGF were detected in human megakaryocytes. Incubation of human platelets with thrombin in vitro resulted in the release of large amounts of VEGF. To investigate whether VEGF is released from platelets during coagulation activation in vivo, we measured in human subjects VEGF at the site of plug formation, ie, in blood emerging from a standardized injury made to determine bleeding time (shed blood). VEGF was also determined in the same volunteers after treatment with the specific thrombin inhibitor recombinant hirudin (r-hirudin). In a double-blind, randomized, crossover study, 17 healthy male volunteers (aged 20 to 35 years) were investigated. VEGF concentrations were measured in venous blood and in shed blood by the use of an immunoassay 10 minutes after intravenous administration of r-hirudin (0.35 mg/kg of body weight) or physiological saline. Prothrombin fragment f1.2 (f1.2) and beta-thromboglobulin (beta-TG) were determined as indicators of coagulation and platelet activation, respectively. Concentrations of VEGF, f1.2, and beta-TG in shed blood 4 minutes after injury were significantly higher than in venous blood (VEGF, 55.8+/-9.2 versus <20 pg/mL, P<0.001; f1.2, 71.3+/-10.4 versus 0.78+/-0.03 nmol/L, P<0. 001; beta-TG, 2290+/-170 versus 53.2+/-14.0 ng/mL, P<0.001). Administration of r-hirudin caused a >50% inhibition of the beta-TG and f1.2 levels in shed blood. In a similar manner, much lower amounts of VEGF were detectable at the site of plug formation after r-hirudin treatment (69.0+/-9.5 versus 37.8+/-2.6 pg/mL per minute; P=0.0015). Our data indicate that substantial quantities of VEGF are released from platelets during the interaction with the injured vessel wall in vivo. This finding may be relevant with respect to wound healing and tissue repair, tumor vascularization, or arterial thrombus formation.  (+info)

Increased formation of thromboxane in vivo in humans with mastocytosis. (5/247)

Clinical manifestations of mastocytosis are mediated, at least in part, by release of the mast cell mediators histamine and prostaglandin D2. It has been previously reported that in addition to prostaglandin D2, mast cells produce other eicosanoids, including thromboxane. Nonetheless, little information exists regarding the formation of other prostanoids in vivo. The most accurate method to examine the systemic production of eicosanoids in vivo is the quantitation of urinary metabolites. We previously developed a highly accurate assay employing mass spectrometry to measure a major urinary metabolite of thromboxane, 11-dehydro-thromboxane B2, in humans. We utilized this assay to quantitate thromboxane production in 17 patients with histologically proven mastocytosis. We report that thromboxane formation was significantly increased (>2 SD above the mean) in at least one urine sample from 65% of patients studied. Of these, 91% of patients with documented systemic involvement had elevated thromboxane generation. In addition, endogenous formation of thromboxane was highly correlated with the urinary excretion of the major urinary metabolite of prostaglandin D2 (r = 0.98) and Ntau-methylhistamine (r = 0.91), suggesting that the cellular source of increased thromboxane in vivo could be the mastocyte. Enhanced thromboxane formation in patients with this disorder is unlikely to be of platelet origin as other markers of platelet activation, platelet factor 4 and beta-thromboglobulin, were not increased in three patients with marked overproduction of thromboxane. Furthermore, the recovery of 11-dehydro-thromboxane B2 excretion in two patients after the administration of aspirin occurred significantly more rapidly than the recovery of platelet thromboxane generation. These studies, therefore, report that thromboxane production is significantly increased in the majority of patients with mastocytosis that we examined and provide the basis to elucidate the role of this eicosanoid in disorders of mast cell activation.  (+info)

Changes of hemostasis, endogenous fibrinolysis, platelet activation and endothelins after percutaneous transluminal coronary angioplasty in patients with stable angina. (6/247)

OBJECTIVES: This study investigated parameters of endogenous fibrinolysis, activation of coagulation and platelets, and endothelin levels before and after elective percutaneous transluminal coronary angioplasty (PTCA) in patients with stable coronary artery disease (CAD). BACKGROUND: Abrupt vessel closure is a serious short-term complication after PTCA and is often unforeseeable. Detailed insight into the effect of PTCA on hemostasis, platelets and the release of vasoconstrictive substances, which are among the mainly discussed mechanisms of abrupt vessel closure, is needed to enhance the safety of coronary intervention. METHODS: Plasma levels of markers of platelet activity, coagulation, endogenous fibrinolysis and endothelins were determined in 20 patients with stable CAD undergoing elective PTCA. The blood specimens were drawn before, immediately after, 1 h after intervention and on the next morning. RESULTS: All patients showed an initially uncomplicated PTCA. Regarding the efficacy of anticoagulation after receiving 15.000 IU heparin during PTCA, two groups were compared. In eight patients with ineffective anticoagulation production of thrombin and platelet activation directly after and 1 h after PTCA was significantly higher compared with 12 patients with effective anticoagulation. Despite the strong activation of coagulation, only a low fibrinolytic response could be observed. Endothelins rose significantly after PTCA in both groups but stayed longer on higher levels in patients with distinct thrombin generation. Three of the eight patients without sufficient heparin treatment suffered abrupt vessel closure. CONCLUSIONS: Initially uncomplicated dilation of coronary arteries leads to systemically measurable activation of coagulation and platelets in patients with ineffective doses of heparin and release of endothelins in all patients. Therefore, individual adjustment of anticoagulation and platelet inhibition in combination with effective antivasospastic substances are needed in every patient before, during and after initially uncomplicated PTCA to prevent this serious complication.  (+info)

Plasmid-mediated resistance to thrombin-induced platelet microbicidal protein in staphylococci: role of the qacA locus. (7/247)

Thrombin-induced platelet microbicidal protein 1 (tPMP-1) is a small, cationic peptide released from rabbit platelets following thrombin stimulation. In vitro resistance to this peptide among strains of Staphylococcus aureus correlates with the survival advantage of such strains at sites of endothelial damage in humans as well as in experimental endovascular infections. The mechanisms involved in the phenotypic resistance of S. aureus to tPMP-1 are not fully delineated. The plasmid-encoded staphylococcal gene qacA mediates multidrug resistance to multiple organic cations via a proton motive force-dependent efflux pump. We studied whether the qacA gene might also confer resistance to cationic tPMP-1. Staphylococcal plasmids encoding qacA were found to confer resistance to tPMP-1 in an otherwise susceptible parental strain. Deletions which removed the region containing the qacA gene in the S. aureus multiresistance plasmid pSK1 abolished tPMP-1 resistance. Resistance to tPMP-1 in the qacA-bearing strains was inoculum independent but peptide concentration dependent, with the level of resistance decreasing at higher peptide concentrations for a given inoculum. There was no apparent cross-resistance in qacA-bearing strains to other endogenous cationic antimicrobial peptides which are structurally distinct from tPMP-1, including human neutrophil defensin 1, protamine, or the staphylococcal lantibiotics pep5 and nisin. These data demonstrate that the staphylococcal multidrug resistance gene qacA also mediates in vitro resistance to cationic tPMP-1.  (+info)

PDGF-AB release during and after haemodialysis procedure. (8/247)

BACKGROUND: During haemodialysis blood membrane contact causes the release of the content of platelet alpha-granules, which contain platelet-derived growth factor (PDGF). In view of its possible role in accelerated atherosclerotic processes, we evaluated the intra- and post-dialytic changes in PDGF-AB serum levels during haemodialysis sessions performed using a cellulosic membrane. METHODS: Using the ELISA method, PDGF-AB, platelet factor-4 (PF4) and beta-thromboglobulin (beta-TG) levels were determined in peripheral blood, as well as in arterial and venous haemodialyser lines, in 10 patients each of whom underwent five consecutive dialysis sessions with a CU membrane. Blood samples were taken at 0, 15, 30, 60, 120, 180 and 240 min during dialysis and at 1, 4 and 20 h after the end of the session. In the same group of patients the levels of the same molecules were also determined after a heparin bolus injection of 4500 IU, blood samples were taken at 0, 15 and 30 min after injection of the bolus. RESULTS: PDGF-AB serum levels increased, remained consistently high during the haemodialysis session (in particular +134+/-20% after 30 min, P<0.001, and +140+/-5% after 240 min, P<0.001) and returned to basal values only after 20 h following the end of the session. PF4 and beta-TG showed a similar trend to PDGF. The heparin bolus injection caused only a small increase (+15+/-5% at 30 min) in PDGF-AB serum levels. CONCLUSIONS: PDGF-AB is released during dialysis mainly as consequence of the blood-membrane contact and it returns only slowly to basal values.  (+info)

Beta-thromboglobulin is a type of protein that is released from platelets (a component of blood) when they are activated. It is often used as a marker for platelet activation, which can occur in various physiological and pathological conditions such as hemostasis, thrombosis, inflammation, and atherosclerosis.

Beta-thromboglobulin is a member of the thromboglobulin family, which also includes platelet factor 4 (PF4) and other proteins that are involved in hemostasis and thrombosis. These proteins play important roles in the regulation of blood clotting and wound healing, but their excessive release or activation can contribute to the development of various cardiovascular diseases, such as myocardial infarction (heart attack) and stroke.

Elevated levels of beta-thromboglobulin have been found in patients with thromboembolic disorders, inflammatory bowel disease, cancer, and other conditions associated with platelet activation. Therefore, the measurement of beta-thromboglobulin can be useful in the diagnosis and monitoring of these diseases.

Platelet Factor 4 (PF4), also known as CXCL4, is a chemokine that is primarily secreted by activated platelets and involved in hemostasis and inflammation. It is a small protein with a molecular weight of approximately 8 kDa and is stored in the alpha granules of resting platelets. Upon activation, platelets release PF4 into the bloodstream, where it plays a role in attracting immune cells to sites of injury or infection.

PF4 can bind to various negatively charged molecules, including heparin, DNA, and RNA, which can lead to the formation of immune complexes. In some cases, these immune complexes can trigger an abnormal immune response, resulting in conditions such as heparin-induced thrombocytopenia (HIT) or vaccine-induced immune thrombotic thrombocytopenia (VITT).

In summary, Platelet Factor 4 is a chemokine released by activated platelets that plays a role in hemostasis and inflammation but can also contribute to the development of certain immune-related disorders.

... (β-TG), or beta-thromboglobulin, is a chemokine protein secreted by platelets. It is a type of chemokine (C-X ... Kaplan KL, Owen J (February 1981). "Plasma levels of beta-thromboglobulin and platelet factor 4 as indices of platelet ... Cella G, Scattolo N, Girolami A, Sasahara AA (1984). "Are platelet factor 4 and beta-thromboglobulin markers of cardiovascular ... Cytokines & Cells Online Pathfinder Encyclopaedia --> Beta-Thromboglobulin Retrieved on August 17, 2009 Chung-Eun Ha; N. V. ...
It is an isoform of Beta-Thromboglobulin or Pro-Platelet basic protein (PPBP). It is a protein that is released in large ... Tunnacliffe A, Majumdar S, Yan B, Poncz M (1992). "Genes for beta-thromboglobulin and platelet factor 4 are closely linked and ... Majumdar S, Gonder D, Koutsis B, Poncz M (1991). "Characterization of the human beta-thromboglobulin gene. Comparison with the ... Majumdar S, Gonder D, Koutsis B, Poncz M (1991). "Characterization of the human beta-thromboglobulin gene. Comparison with the ...
... a growth factor structurally related to beta-thromboglobulin". The EMBO Journal. 7 (7): 2025-2033. doi:10.1002/j.1460-2075.1988 ... Becker S, Quay J, Koren HS, Haskill JS (March 1994). "Constitutive and stimulated MCP-1, GRO alpha, beta, and gamma expression ... capacity for immortalized melanocytes expressing melanoma growth stimulatory activity/growth-regulated cytokine beta and gamma ...
Reduced osmotic pressure will trigger the liver to produce more proteins like fibrinogen and beta-thromboglobulin, which ... Cystathionine beta synthase deficiency, also known as homocystinuria, is an autosomal recessive inherited disorder in which the ...
... beta-2 microglobulin MeSH D12.776.377.715.182.160 - beta-thromboglobulin MeSH D12.776.377.715.182.200 - complement factor h ... beta-thromboglobulin MeSH D12.776.467.374.200.100 - chemokines, c MeSH D12.776.467.374.200.110 - chemokines, cc MeSH D12.776. ... beta-crystallin a chain MeSH D12.776.306.366.300.200 - beta-crystallin b chain MeSH D12.776.331.199.750.500 - succinate ... thyroid hormone receptors beta MeSH D12.776.624.664.700.915 - RNA-binding protein FUS MeSH D12.776.624.664.700.957 - stathmin ...
... beta-2 microglobulin MeSH D12.776.124.790.223.160 - beta-thromboglobulin MeSH D12.776.124.790.223.200 - complement factor h ...
"Negative regulation of human megakaryocytopoiesis by human platelet factor 4 and beta thromboglobulin: comparative analysis in ...
... beta-thromboglobulin MeSH D23.125.300.100 - chemokines, c MeSH D23.125.300.110 - chemokines, cc MeSH D23.125.300.120 - ... beta-thromboglobulin MeSH D23.469.200.100 - chemokines, c MeSH D23.469.200.110 - chemokines, cc MeSH D23.469.200.120 - ... beta subunit, human MeSH D23.101.840.375 - hormones, ectopic MeSH D23.101.840.400 - ki-67 antigen MeSH D23.101.840.500 - ... transforming growth factor beta MeSH D23.348.479.996 - wnt proteins MeSH D23.348.479.996.500 - wnt1 protein MeSH D23.348. ...
... beta-thromboglobulin MeSH D12.644.276.174.200.100 - chemokines, c MeSH D12.644.276.174.200.110 - chemokines, cc MeSH D12.644. ... MeSH D12.644.050.200 - defensins MeSH D12.644.050.200.050 - alpha defensins MeSH D12.644.050.200.075 - beta defensins MeSH ... beta-msh MeSH D12.644.400.460.115 - gamma-msh MeSH D12.644.400.465 - msh release-inhibiting hormone MeSH D12.644.400.470 - msh- ... gtp-binding protein beta subunits MeSH D12.644.360.375.730 - gtp-binding protein gamma subunits MeSH D12.644.360.375.940 - ...
... beta adrenergic receptor - beta sheet - beta-1 adrenergic receptor - beta-2 adrenergic receptor - beta-thromboglobulin - ... transforming growth factor beta - transforming growth factor beta receptor - transient receptor potential - translation ( ... alpha-beta T-cell antigen receptor - alpha-fetoprotein - alpha-globulin - alpha-macroglobulin - alpha-MSH - Ames test - amide ... interferon-beta - interleukin receptor - interleukin-1 receptor - interleukin-2 receptor - interleukin-3 - interleukin-3 ...
The other ADP-receptor P2Y1 couples to Gq that activates phospholipase C-beta 2 (PLCB2), resulting in inositol 1,4,5- ... B-thromboglobulin, vWF, fibrinogen, and coagulation factors V and XIII δ granules (delta or dense granules) - containing ADP or ... Platelets release platelet-derived growth factor (PDGF), a potent chemotactic agent; and TGF beta, which stimulates the ...
β-Thromboglobulin (β-TG), or beta-thromboglobulin, is a chemokine protein secreted by platelets. It is a type of chemokine (C-X ... Kaplan KL, Owen J (February 1981). "Plasma levels of beta-thromboglobulin and platelet factor 4 as indices of platelet ... Cella G, Scattolo N, Girolami A, Sasahara AA (1984). "Are platelet factor 4 and beta-thromboglobulin markers of cardiovascular ... Cytokines & Cells Online Pathfinder Encyclopaedia Beta-Thromboglobulin Retrieved on August 17, 2009 Chung-Eun Ha; N. V. ...
Beta-thromboglobulin. Low molecular weight (36 kDa) heparin-binding protein. PF4. A heparin-binding protein. ...
... and beta-thromboglobulin; decreased levels of anti-factor Xa and antithrombin III; decreased antithrombin III activity; ...
Beta thromboglobulin like protein antibody. *C-X-C motif chemokine 8 antibody ... Take a look at our BETA site and see what weve done so far. ... Switch on our new BETA site. Now available. Search and browse ...
Transforming Growth Factor beta/analysis; Trypsin/pharmacology; beta-Thromboglobulin/analysis ... results in both an increase in intracellular free calcium levels and secretion of mitogenic activity and beta-thromboglobulin. ...
... and beta-thromboglobulin; decreased levels of antifactor Xa and antithrombin III, decreased antithrombin III activity; ...
... beta-thromboglobulin-like protein; C-X-C motif chemokine 8; Chemokine (C-X-C motif) ligand 8; Emoctakin; GCP-1; GCP/IL-8 ... Protein Aliases: (Ala-IL-8)77; (Ser-IL-8)72; alveolar macrophage chemotactic factor I; ANX7; beta endothelial cell-derived ...
We have measured plasma P-selectin and beta-thromboglobulin (beta TG) concurrently in (1) patients with consumptive thrombotic ... Plasma beta-thromboglobulin: differentiation between intravascular and extravascular platelet destruction. Han P, Turpie AG, ... The increased plasma P-selectin and beta TG in patients with thrombotic disorders were likely to be the result of in vivo ... Patients with DIC, HIT, and TTP/HUS, but not ITP, had significantly elevated plasma P-selectin and beta TG levels when compared ...
Beta-thromboglobulin in diabetes: relationships with blood glucose and fibrinopeptide A.. Burrows AW. Horm Metab Res Suppl; ... Prognostic value of beta-thromboglobulin in patients with transient cerebral ischaemia.. Stewart ME; Douglas JT; Lowe GD; ... 5. [Beta-thromboglobulin and fibrinopeptide A in acute myocardial infarction].. Cassetti M; Palazzesi G; Materazzi M; Massoli ... Studies of beta-thromboglobulin, platelet factor 4, and fibrinopeptide A in erythrocytosis due to cyanotic congenital heart ...
Von Willebrand factor, thrombomodulin, thromboxane, beta-thromboglobulin and markers of fibrinolysis in primary Raynauds ... Phi Beta Kappa. Disclosure: Nothing to disclose. ...
Beta-thromboglobulin content in megakaryocytes of patients with myeloproliferative diseases.. Grossi A; Vannucchi AM; Rafanelli ... 6. Aberrant expression of transforming growth factor beta-1 (TGF beta-1) per se does not discriminate fibrotic from non- ...
... and beta thromboglobulin in thin frozen sections of human blood platelets. J. Clin. Invest. 72, 1277-1287. doi: 10.1172/ ...
thromboglobulin, beta-1. Description. CTAP-III (officially named PPBP) is a platelet-derived growth factor that belongs to the ...
... and beta-thromboglobulin; decreased levels of antifactor and antithrombin III, decreased antithrombin III activity; increased ...
Thromboglobulin, beta-2. beta 2 Thromboglobulin. beta Thromboglobulin. beta-2 Thromboglobulin. Tree number(s):. D12.644.276.374 ... beta-Thromboglobulin - Preferred Concept UI. M0002428. Scope note. A platelet-specific protein which is released when platelets ... Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of ... Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of ...
Beta thromboglobulin Current Synonym true false 3737110012 Beta-thromboglobulin Current Synonym true false ... Beta-thromboglobulin (substance). Code System Preferred Concept Name. Beta-thromboglobulin (substance). Concept Status. ...
beta-2 Thromboglobulin Narrower Concept UI. M0002427. Registry Number. 0. Terms. beta-2 Thromboglobulin Preferred Term Term UI ... BETA TG. Entry Term(s). beta-2 Thromboglobulin Registry Number. 0. Previous Indexing. Beta Globulins (1966-1979). Public MeSH ... Beta-Globulins [D12.776.124.790.223] * beta 2-Microglobulin [D12.776.124.790.223.100] * beta-Thromboglobulin [D12.776.124.790. ... Beta-Globulins [D12.776.377.715.182] * beta 2-Microglobulin [D12.776.377.715.182.100] * beta-Thromboglobulin [D12.776.377.715. ...
beta-2 Thromboglobulin Narrower Concept UI. M0002427. Registry Number. 0. Terms. beta-2 Thromboglobulin Preferred Term Term UI ... BETA TG. Entry Term(s). beta-2 Thromboglobulin Registry Number. 0. Previous Indexing. Beta Globulins (1966-1979). Public MeSH ... Beta-Globulins [D12.776.124.790.223] * beta 2-Microglobulin [D12.776.124.790.223.100] * beta-Thromboglobulin [D12.776.124.790. ... Beta-Globulins [D12.776.377.715.182] * beta 2-Microglobulin [D12.776.377.715.182.100] * beta-Thromboglobulin [D12.776.377.715. ...
interleukin-8; emoctakin; interleukin 8; T-cell chemotactic factor; neutrophil-activating peptide 1; beta-thromboglobulin-like ... beta endothelial cell-derived neutrophil activating peptide. ...
... beta-thromboglobulin (β-TG) ; thromboxane B2; 6-keto-prostaglandin F1α; granulocyte elastase-αl proteinase inhibitor complex (G ...
Die Konzentration an beta-Thromboglobulin lag im BCP der Electa bei durchschnittlich 2.200 IE/ml und in jenem der Xtra® bei ... Regarding the results of the aggregometry and the concentration of beta-thromboglobulin, there were no significant differences ... beta-thromboglobulin, platelet morphology (via light microscopy), and aggregometry were evaluated a second time after 6 hours ... and morphology of platelets as well as aggregometry and concentration of beta-thromboglobulin showed no significant differences ...
27%, P < 0.0001, Δmean -48.9, 95% CI -62.5 to -35.4). Neither treatment significantly influenced beta thromboglobulin or p- ... beta thromboglobulin, p-selectin, thromboxane B2 , d-Dimer, prothrombin fragment 1.2 (f1.2), and a phospholipid-dependent ...
C112892 Q9Y5Z0 Beta-Secretase 2 C159262 Q16143 Beta-Synuclein C20468 P02775 Beta-Thromboglobulin C21199 P55957 BH3-Interacting ... C96911 P05556 Integrin Beta-1 C28489 P05107 Integrin Beta-2 C38955 P05106 Integrin Beta-3 C28490 P16144 Integrin Beta-4 C53962 ... C113551 P52757 Beta-Chimaerin C26216 P60022 Beta-Defensin 1 C91757 P81534 Beta-Defensin 103 C107438 P16278 Beta-Galactosidase ... C119645 Q86Z14 Beta-Klotho C21161 P08118 Beta-Microseminoprotein C20444 P01138 Beta-Nerve Growth Factor C112895 P56817 Beta- ...
... and beta-thromboglobulin; decreased levels of antifactor Xa and antithrombin III, decreased antithrombin III activity; ...
... platelet factor-4 and beta-thromboglobulin. Inflamm Res. 1999;48:171-5. ... β-thromboglobulin [40], soluble P selectin [40], and endogenous cannabinoids, were also observed [44]. ...
Plasma beta-thromboglobulin and platelet factor 4 are not increased in insulin-dependent diabetic patients with ... Mechanical stretch induces fibronectin production in human podocytes via a TGF-beta 1-dependent mechanism.. https://iris.unito. ... P38-mitogen activated protein kinase mediates hexosamine-induced TGF beta 1 mRNA expression in human mesangial cells.. https:// ...
... and beta- thromboglobulin; decreased levels of anti-factor Xa and antithrombin III, decreased antithrombin III activity, ...
  • β-Thromboglobulin (β-TG), or beta-thromboglobulin, is a chemokine protein secreted by platelets. (wikipedia.org)
  • Are platelet factor 4 and beta-thromboglobulin markers of cardiovascular disorders? (wikipedia.org)
  • Elevated platelet factor 4 and beta-thromboglobulin plasma levels in depressed patients with ischemic heart disease. (medhelp.org)
  • We measured the platelet counts, platelet factor 4 (PF4), β-thromboglobulin (β-TG), and CD41 and CD42b platelet surface markers at 30, 120, and 240 min. (biomedcentral.com)
  • The circuit was immersed in a thermostatic bath and maintained at 37 °C. We measured the platelet counts, CD41 and CD42b platelet surface markers, β-thromboglobulin (β-TG), and platelet factor 4 (PF4) at 30, 120, and 240 min after the initiation of blood circulation. (biomedcentral.com)
  • Chronic psychological stress causes significant platelet function impairment, including increased platelet reactivity and platelet production releases, such as platelet factor 4 and Beta-thromboglobulin [7,8]. (biomedgrid.com)
  • Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants. (lookformedical.com)
  • Beta-crystallins exist as oligomers formed from acidic (BETA-CRYSTALLIN A CHAIN) and basic (BETA-CRYSTALLIN B CHAIN) subunits. (lookformedical.com)
  • Alpha, beta, and delta crystallins occur in avian and reptilian lenses, while alpha, beta, and gamma crystallins occur in all other lenses. (lookformedical.com)
  • Gamma-crystallins are similar in structure to BETA-CRYSTALLINS in that they both form into a Greek key-like structure. (lookformedical.com)
  • Two small peptide chains removed from the N-terminal segment of the beta chains of fibrinogen by the action of thrombin. (bvsalud.org)
  • Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. (lookformedical.com)
  • An antioxidant action of the combinations alpha-tocopherol+ascorbic acid and alpha-tocopherol+beta-carotin was much more potent than that of each of the component alone. (ter-arkhiv.ru)
  • 6. Aberrant expression of transforming growth factor beta-1 (TGF beta-1) per se does not discriminate fibrotic from non-fibrotic chronic myeloproliferative disorders. (nih.gov)
  • 14. Beta-thromboglobulin content in megakaryocytes of patients with myeloproliferative diseases. (nih.gov)
  • 16. Prognostic value of beta-thromboglobulin in patients with transient cerebral ischaemia. (nih.gov)
  • Thrombin treatment of CHRF-288-11 cells results in both an increase in intracellular free calcium levels and secretion of mitogenic activity and beta-thromboglobulin. (nih.gov)