摘要:

Fetal and neonatal thrombocytopenia (NNT) may lead to bleeding and to death or neurological sequelae. NNT affects 25-40% of the infants in intensive care units and even in the absence of bleeding, must be considered as a potentially valuable sign. There are various causes, the main one being bacterial or viral infection, followed by immune thrombocytopenia which may be due to maternal autoantibodies or alloantibodies that cross the placenta. Management during pregnancy aims to prevent fetal bleeding especially in the central nervous system, and to avoid birth trauma. Percutaneous umbilical blood sampling provides a direct measure of the fetal platelet count and makes it possible to assess the effectiveness of therapy. Other causes, such as disseminated intravascular coagulation, local platelet consumption or antenatal hypoxia, must also be considered. Finally, the accuracy of the diagnosis of the mechanism of NNT will determine the specific management for the mother, the newborn and any subsequent pregnancy.

ISSN:0953-7104    

DOI:10.3109/09537109209003389

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Human platelet cytosol contains several phosphoinositide-specific phospholipases C (PLCs) separable by stepwize ion-exchange chromatographies [Banno, Yu, Nakashima, Homma, Takenawa and Nozawa Biochem Biophys Res Commun 1990 167; 396-401]. In the present study, one type of PLC (cPIP2-PLC) for which phosphatidylinositol 4,5-bisphosphate (PIP2) was the preferred substrate, was isolated from human platelet cytosol as a truncated form (100 kDa). A mPIP2-PLC was purified to near homogeneity from the cholate extract of human platelet membranes. The purified 150-kDa mPIP2-PLC was truncated during purification, and ran as 100-kDa and 45-kDa polypeptides on SDS-polyacrylamide gel electrophoresis. The 100-kDa component of cytosolic PLC (cPIP2-PLC) and the 150-kDa, 100-kDa and 45-kDa polypeptides of mPIP2-PLC were all recognized by the antibody raised against PLC-β. The 150-kDa enzyme was immunoprecipitated by anti-PLC-βantibody from freshly prepared human platelet cytosol. The catalytic properties of the platelet 100-kDa form were observed to be very similar to those of 100-kDa form derived from bovine brain PLC-β. These results indicate thatβ-type PLC exists in both cytosol and membranes of human platelets.

ISSN:0953-7104    

DOI:10.3109/09537109209003390

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

We studied the effect of inhibition of platelet aggregation (obtained by omitting sample stirring and by the addition of ASA and GRGDS peptide) on ATP secretion and Ca2+movements. When collagen was the agonist, platelet aggregation stimulated release reaction and Ca2+movements in both the presence and absence of extracellular Ca2+. When platelets were stimulated by thrombin, ATP release and Ca2+movements were largely independent of aggregation. Our data suggest that platelet aggregation stimulates Ca2+movement, and that this phenomenon of feedback amplification of platelet activation plays an important role in platelet function when collagen is the agonist, while it has little or no role when thrombin is the stimulus.

ISSN:0953-7104    

DOI:10.3109/09537109209003391

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Platelet functions were studied in 10 patients with insulin dependent diabetes mellitus (IDDM) with vasculopathy, and in age and sex-matched normal controls. The patient group at presentation showed increased circulating platelet aggregates, greater platelet factor III availability and increased aggregation of platelets in response to various agonists (shorter latent period, greater rate of aggregation, greater degree of aggregation, p<0.05-<0.001). This platelet hyperreactivity remained unchanged even after normalisation of blood glucose. In contrast, similar platelet hyperreactivity seen by us earlier in patients with uncontrolled IDDM without vasculopathy reversed to normal after metabolic control.In view of the postulated role of hyperreactivity of platelets in the pathogenesis of vasculopathy in IDDM, our results imply that once vasculopathy sets in, a vicious cycle starts between platelet hyperreactivity and vasculopathy. Proper and early treatment of IDDM at a stage when vasculopathy is not present, would therefore be important in reversing the platelet hyper-function and may possibly delay the development of vasculopathy.

ISSN:0953-7104    

DOI:10.3109/09537109209003392

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Hydrogen peroxide (H2O2) triggers activation of platelets 'primed' by low concentrations of arachidonic acid (<20μM) or collagen (<0.2μg/ml), but has no effect on platelets exposed to low concentrations of thrombin, ADP or A23187. Platelets are not affected (they do not aggregate or produce thromboxane A2or release serotonin) by H2O2alone or by the low concentrations of arachidonic acid or collagen.The H2O2concentration used (0.15-7.5μM) induces aggregation, TA2production and dense granule content release (monitored by radiolabeled serotonin) by 'primed' platelets. Using arachidonic acid as the 'priming' stimulus, Kappof 687 nM and 560 nM are calculated for platelet aggregation and TA2formation respectively. With collagen as the 'priming' stimulus, Kappof 841 nM and 946 nM are obtained for platelet aggregation and TA2production, respectively.The effect of H2O2is dependent on arachidonic acid metabolism because aspirin prevents H2O2-mediated platelet activation. Furthermore this activation seems to be dependent on arachidonic acid mobilization from platelet phospholipids by phospholipase A2since mepacrine is able to block H2O2-mediated platelet activation.

ISSN:0953-7104    

DOI:10.3109/09537109209003393

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

A method for selective screening of platelet glycoprotein deficiencies, based on the use of antibody-coated magnetobeads and light microscopic examination is reported. The method is simple, time-saving and needs less than 1 ml of blood.

ISSN:0953-7104    

DOI:10.3109/09537109209003394

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

摘要:

Platelet aggregation is usually measured by a spectroscopic method using an aggregometer. However, when the process of platelet aggregation is followed by the changes in light transmission of platelet-rich plasma (PRP), factors such as platelet deformation or changes in plasma permeability must be taken into consideration. Thus, a better method was developed in our laboratory for measuring platelet aggregation by chronologically counting non-aggregated single platelets, one of the simplest parameters of the aggregation process, using PRP to which adenosine diphosphate (ADP) was added.1,2In the present study, we attempted to further evaluate platelet aggregability by measuring the velocity of platelet aggregation in different subjects using our single platelet counting method.

ISSN:0953-7104    

DOI:10.3109/09537109209003395

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109209003396

出版商:Taylor&Francis    

年代:1992

数据来源: Taylor