Abstract: A method and apparatus for fault detection of series diodes in rectifiers is disclosed, wherein the voltages across one or both of the individual diodes, and/or the voltage across the pair of diodes are measured to determine a ratio between two of those voltages. The ratio is then analyzed to determine if a fault (e.g., a short circuit or an open circuit) is present. In some embodiments, circuitry can be included to compensate for the normal variations in diode characteristics (e.g., reverse leakage current, reverse recovery charge) between the pair of series diodes to minimize the potential for erroneous fault detection.

Abstract: A method is provided of determining whether an individual has reduced ability to form platelet thrombi due to inhibition of platelet activation initiation, signal transduction and/or GPIIb/IIIa blockade. A blood sample is obtained from the individual being assessed. The blood sample is mixed in combination with 1) an anticoagulant; 2) sufficient buffer to maintain the pH and salt concentration of the anticoagulated blood within a range suitable for platelet aggregation; 3) a platelet GPIIb/IIIa receptor ligand immobilized on a solid surface; 4) one or more agents to enhance a signal transduction pathway and 5) a receptor activator. The combination is incubated under conditions for agglutinating particles. Platelet-mediated agglutination is assessed in the agitated mixture. The absence of agglutination indicates that the individual has a reduced ability to form platelet thrombi.

Abstract: A method is provided of determining whether an individual has reduced ability to form platelet thrombi. An ADP platelet activator and one or platelet inhibitors are provided. At least one of the platelet inhibitors is Prostaglandin E1 (PGE1). An alternate signal transduction pathway is produced. A final concentration of ADP is 2 to 35 ?M and a final concentration of PGE1 is 2 to 30 nM, preferably 20 to 25 nM.

Abstract: A method for obtaining a percent aggregation or inhibition of platelets resulting from anti-platelet using a single blood sample is achieved. An assay device is provided. The assay device has multiple channels, each coupled to a common introduction port. A first platelet activator is sensitive to activation pathway targeted by the anti-platelet drug. A second platelet activator is insensitive to the activation pathway targeted by the anti-platelet drug. An anti-coagulated sample is introduced simultaneously to the first and second channels. A level of platelet aggregation is simultaneously made in both channels.

Abstract: Methods and systems for rapidly determining the level of platelet inhibition in whole blood, due to aspirin usage, with a single use arachidonic based assay device that can be stored at room temperature is provided. A lyophilized assay reagent that contains arachidonic acid at sufficient concentration to maximally activate platelets is utilized. An antioxidant within the same lyophilized assay reagent reduces the oxidation rate of arachidonic acid but does not interfere with platelet function. An oxygen absorber within the single use assay device packaging creates an inert environment within a short period of time after package is sealed. The assay device can have a housing with a plurality of channels and a common blood sample introduction port coupled to each of a channel of the plurality of channels. The assay device can also include a lyophilized assay reagent that contains arachidonic acid at sufficient concentration to maximally activate platelets.

Abstract: Methodology which avoids the problems associated with interference from whole blood is provided for instrumented determination of platelet binding function. Particularly, small particles to which fibrinogen is bound, and which contain an infrared light absorbing dye, are used to determine the binding of platelets in a whole blood sample to the fibrinogen. Agglutination of the platelets with the coated particles is determined by a change in infrared light absorption characteristics.