ABSTRACT
The database of imprinted genes and parent-of-origin effects in animals (http://www.otago.ac.nz/IGC ) is a collation of genes and phenotypes for which parent-of-origin effects have been reported. The database currently includes over 220 entries, which describe over 40 imprinted genes in human, mouse and other animals. In addition a wide variety of other parent-of-origin effects, such as transmission of human disease phenotypes, transmission of QTLs, uniparental disomies and interspecies crosses are recorded. Data are accessed through a search engine and references are hyperlinked to PubMed.
Subject(s)
Databases, Factual , Genes/genetics , Genomic Imprinting , Alleles , Animals , Humans , InternetABSTRACT
The effects of carbon dioxide (CO2) and pH on platelet aggregation in vitro have been studied to simulate pH changes observed in tissue fluid stasis and inflammation. Platelet aggregation induced by the 7-oxabicycloheptane mimetic of thromboxane A2 (TxA2) showed increased sensitivity in CO2-treated platelet-rich plasma (PRP). This effect is similar to that previously reported for arachidonate-induced aggregation. In contrast, aggregation of washed platelet suspensions (i.e. protein-free), in response to both arachidonate and TxA2 mimetic, was inhibited under acid conditions. These results confirm the importance of plasma proteins in the control of platelet function and support the hypothesis that the pH effects are dependent on these proteins.
Subject(s)
Arachidonic Acids/metabolism , Blood Platelets/metabolism , Hydrogen-Ion Concentration , Thromboxane A2/pharmacology , Arachidonic Acid , Carbon Dioxide/pharmacology , Humans , In Vitro Techniques , Platelet Aggregation/drug effectsABSTRACT
The effects of carbon dioxide on citrated human platelet-rich plasma (PRP) have been studied as a means of imitating the changes in pH and PCO2 observed in inflammation and tissue fluid stasis. Adenosine diphosphate (ADP)-induced platelet aggregation was inhibited in CO2-treated PRP. In contrast, CO2-treated platelets were rendered up to eight times more sensitive to sodium arachidonate and this effect could be imitated by the addition of exogenous calcium 1 min before the addition of arachidonate. The effects of CO2 on ADP-induced and arachidonate-induced aggregation were abolished if the CO2 was allowed to disperse from treated PRP subsequently exposed to air, suggesting no permanent alteration in platelet metabolism. The increased sensitivity of arachidonate-induced aggregation with lowered pH may be a significant factor in influencing platelet behaviour in haemostasis.
Subject(s)
Arachidonic Acids/pharmacology , Carbon Dioxide/pharmacology , Platelet Aggregation/drug effects , Adenosine Diphosphate/pharmacology , Arachidonic Acid , Humans , Hydrogen-Ion Concentration , In Vitro Techniques , Inflammation/bloodABSTRACT
A collaborative study on prekallikrein activator (PKA) has been carried out involving four laboratories for the purpose of establishing a British reference preparation for PKA. Samples of two plasma protein fractions (PPF) were assayed against participants' own supplies of the Bureau of Biologics Reference Preparation No. 2 (BoB 2). There was good agreement on the relative PKA activities of the two preparations. One of the preparations, coded 79/572, was established as the 1st British Reference Preparation for Prekallikrein Activator, with an assigned potency of 78.9 units/ml.
