摘要:

The platelet membrane glycoproteins fulfil a vital function in platelet adhesion and aggrkgation. The advent of recombinant DNA technology has provided a wealth of new informationon the sequence, structure, expression and chromosomal location of the genes encoding these proteins and Is now permitting the detailed molecular genetic analysis of both Bernard Soulier syndrome andGlanzmann's thrombasthenia.

ISSN:0953-7104    

DOI:10.3109/09537109109113690

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Thromboxane A2(TXA2) has recently become a target of intense research because of its myriad of potent pathophysiological properties. Recent progress in TXA2research is reviewed in relation to: (1) characterisation of TXA, receptors in platelets and vasculature by kinetic analysis,with evidence for the presence of distinctive receptor subtypes; (2) actions of TXA2in platelets and vasculature via their own receptors, i.e. biochemical mechanisms of signal transduction; and (3)pathophysiological roles of TXA2and clinical perspectives of TXA2blocking therapy.

ISSN:0953-7104    

DOI:10.3109/09537109109113691

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Snake venoms contain complex mixtures of proteins with biological activities. These venom proteins affect blood coagulation and platelet function in various ways. Many inducers andinhibitors of platelet aggregation have been isolated from snake venoms, especially from the Crotalidae and Viperidae families. According to their biochemical properties and modes of action,they can be classified into ten groups: (1) thrombin-like enzymes which show higher activity towards platelets than towards fibrinogen; (2) procoagulant enzymes which generate thrombin and thenactivate platelets indirectly; (3) noncoagulant glycoproteins which activate platelets independently of ADP release or thromboxane formation; (4) lectin-like peptides which cause agglutination of plateletsthrough binding to a sugar moiety; (5) coagglutinins whose activities are dependent on the presence of von Willebrand factor (vWF); (6) membrane-active polypeptides which potentiate the aggregatingaction of other inducers by activation of platelet endogenous phospholipase A2; (7) phospholipase A2enzymes which show biphasic aggregating and inhibitory effects on platelets; (8)α-fibrinogenases which degrade theα(A) chain of fibrinogen; (9) 5'-nucleotidase or ADPase which act on the ADP released from platelet dense bodies; and (10) fibrinogen-receptor antagonists which interfere with theinteraction of fibrinogen and glycoprotein IIb/IIIa on activated platelets. These venom proteins are unique research tools for study of the haemostatic process and some of them are potentialantithrombotic agents.

ISSN:0953-7104    

DOI:10.3109/09537109109113692

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Human platelets in the presence of sera from humans with chronic Chagas' disease display cytotoxic activity againstTrypanosoma cruzi (T. cruzi)trypomastigotes. Adsorption of IgE from those sera decrease the cytotoxic effect and IgG purified from the same sera revealed a cytotoxic action similar to the whole sera. Morphological studies suggest that chagasic serum promotes adhesion between parasites and platelets. On the basis of these results it is postulated that platelets may represent a defensive mechanism in South American trypanosomiasis by killing circulating forms of the parasite and that both IgG and IgE are relevant for that action.

ISSN:0953-7104    

DOI:10.3109/09537109109113693

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

The effect of a range ofα- andβ-adrenoceptor agonists and antagonists on the in vitro uptake of [45Ca2+] by human platelets was investigated. Isoprenaline and adrenaline stimulated[45Ca2+] uptake. Isoprenaline-stimulated ([45Ca2+] uptake was inhibited byβ-adrenoceptor antagonists (mabuterol [β2]>metoprolol [β1]>atenolol [β1]>pindolol [β1/β2]), but not by yohimbine[αz] or prazosin [αll. Adrenaline-stimulated [45Ca2+] uptake was inhibited (and in this order ofpotency) by yohimbine, mabuterol, metoprolol, prazosin, atenolol and pindolol. [45Ca2+] uptake wasstimulated byβ-adrenoceptor agonists (BRL37344 [β3]>terbutaline [β2]>xamoterol [β1]>salbutamol [β2]). Ca2+ionophore A23187-stimulated [45Ca2+] uptake was unaffected bypindolol, atenolol, metoprolol or mabuterol, indicating that these antagonists were not exerting nonspecitic inhibitory effects. [45Ca2+] uptake was also stimulated by dibutyryl cAMP and by iloprost (astable prostacyclin analogue and stimulator of cAMP synthesis). It is concluded that: (1)β- adrenoceptor-linked Ca2+uptake is mediated by an atypicalβ-adrenoceptor, possibly of aβ3-subtype; (2) the stimulatory action ofβ-adrenoceptor activation and prostacyclin may be mediated by adenylate cyclase, and (3) the paradoxical finding that bothα- andβ-adrenoceptor activation, cAMP and stimulators of CAMP elicit [45Ca2+] uptake suggests that the Ca2+mobilisation monitored by the present methodology is not associated with platelet aggregation but to adrenoceptor activation perse and possibly other signal transduction mechanisms that occur at the plasmalemma.

ISSN:0953-7104    

DOI:10.3109/09537109109113694

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

FA6-152, a monoclonal antibody to platelet membrane glycoprotein IV (CP IV), was used to quantify the expression of this glycoprotein on platelets, as well as to evaluate its role inplatelet aggregation. On resting platelets, 19 400±7700 molecules of the125I-labelled IgC could bind per platelet (n = 20). Binding was not modified following stimulation of the platelets with ADP(10µmol/l) or thrombin (0.1 U/ml). Fab fragments prepared from the antibody by papain digestion also bound to the platelet surface in a saturable manner. Both the intact IgC and its Fab fragmentswere found to inhibit platelet aggregation and secretion induced by ADP or collagen in platelet-rich plasma and by thrombin in platelet suspensions. Under nonstirred conditions, whereby the releasereaction was only minimally affected, the antibody markedly inhibited thrombin-induced surface expression ofα-granule thrombospondin (TSP), whereas it did not alter the concomitant expression ofα-granule fibrinogen. In addition, electron microscopy revealed a predominant distribution of TSP and T;P IV on pseudopodia and between adherent cells on thrombin-stimulated platelets. Thesefindings thus support the hypothesis that the interaction of TSP with GP IV on the platelet surface is required for an optimal platelet aggregation/secretion process to occur.

ISSN:0953-7104    

DOI:10.3109/09537109109113695

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

An unaltered platelet aggregatory response to vasopressin (VP) with a lower number of platelet VP-receptors have been described in patients withDiabetes mellitus. A possible explanation could be that the lost receptors are related to a cellular event different from aggregation.We have explored VP-induced platelet shape change in diabetic and healthy subjects. We confirmed that VP-induced aggregation was identical in control and diabetic subjects. On the other hand, thediabetic patients tested did not respond to VP in terms of platelet shape change, or presented reduced responses with respect to both EC50and maximal shape change compared to healthy subjects. In parallel, the number of VP-receptors was reduced without any alteration in their affinity.The loss of functional shape change response to VP, combined with the decrease in the number of VP-receptors occurring in diabetic patients suggests that the two abnormalities could be related. Asplatelet aggregation was unaltered, there may be different receptors for shape change and aggregation. The loss of the VP-induced shape change response in diabetic patients might then resultfrom an alteration of shape change related receptors.

ISSN:0953-7104    

DOI:10.3109/09537109109113696

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Clinical Immunohaematology: Basic Concepts and Clinical ApplicationsF. Rosse, Blackwell Scientific Publications, Boston 1990. 677 pages. Price£95.00.

ISSN:0953-7104    

DOI:10.3109/09537109109113697

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109109113698

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor