Reduction of quantization error in measurement of frequency

Method reduces quantization errors using new digital circuit. Circuit provides very high resolution (10 to the minus 2nd power to 10 to the minus 3rd power Hz) without high-speed counters. It lends itself to microminaturization and is simple to construct. Unknown frequency is compared to standard frequency by means of zero-crossing coincidence-detecting circuit

One way Doppler extractor. Volume 1: Vernier technique

A feasibility analysis, trade-offs, and implementation for a One Way Doppler Extraction system are discussed. A Doppler error analysis shows that quantization error is a primary source of Doppler measurement error. Several competing extraction techniques are compared and a Vernier technique is developed which obtains high Doppler resolution with low speed logic. Parameter trade-offs and sensitivities for the Vernier technique are analyzed, leading to a hardware design configuration. A detailed design, operation, and performance evaluation of the resulting breadboard model is presented which verifies the theoretical performance predictions. Performance tests have verified that the breadboard is capable of extracting Doppler, on an S-band signal, to an accuracy of less than 0.02 Hertz for a one second averaging period. This corresponds to a range rate error of no more than 3 millimeters per second

Atherothrombosis and plaque heterology: different location or a unique disease?

Formation of unstable plaques frequently results in atherothrombosis, the major cause for ischaemic stroke, myocardial infarction and peripheral arterial disease. Patients who have symptomatic thrombosis in one vascular bed are at increased risk of disease in other beds. However, the development of the disease in carotid, coronary and peripheral arteries may have different pathophysiology suggesting that more complex treatment protocols may have to be designed to reduce plaque development at different locations. In this review we describe the known risk factors, compare the developmental features of coronary and carotid plaque development and determine their association with end-point ischaemic events. Differences are also seen in the genetic contribution to plaque development as well as in the deregulation of gene and protein expression and cellular signal transduction activity of active cells in regions susceptible to thrombosis. Differences between carotid and coronary artery plaque development might help to explain the differences in anatomopathological appearance and risk of rupture