Steven A. Jones
Updated: September 10, 2004
Below are the questions that I find interesting, and brief descriptions of the approaches to these questions.
Are there methods that can be used in Doppler ultrasound that will provide the spatial and temporal resolution required to measure velocity fluctuations related to turbulence, coherent structures and vortex shedding?
To answer this question, two approaches are being made. One approach is the use of multiple receivers to collect more information about the velocities of the ultrasonic scatterers (blood cells). This method helps to reduce the “coherent scattering noise” that is inherent in Doppler ultrasound. The other approach is to use “adaptive Doppler,” in which the parameters of the ultrasound system are revised as a result of previous measurements that have been made by the instrument. This approach can not only reduce coherent scattering noise, but can also narrow the Doppler spectrum, hence enhancing the frequency estimates.
What can we learn about an individual pool of platelets from studying the adhesion over a selected number of protein substrates?
We are using the layer-by-layer self assembly technique to generate well-controlled layers of different proteins on microchannel surfaces. The adhesion patterns are examined by fluorescence microscopy, and various parameters are related back to the different aspects of platelet physiology. A governing hypothesis is that changes made to the platelets, such as inhibition of glycoproteins, or alteration of granule contents, will have distinctly different affects on different substrates. Some changes may even increase adhesion over one set of substrates while decreasing it over another set. Thus, by studying the different adhesion patterns over different substrates, one may obtain a physiological description of a given sample of platelets. This type of diagnosis may be useful in the determination of conditions under which a given subject may suffer cardiac infarction.
What is the role of Nitric Oxide and Transport in the initiation, extension, and limitation of platelet thrombus?
Nitric oxide is one of the molecules that is responsible for inhibiting platelet activation. One of its unique properties is its small size, since it is a simple two-atom molecule, as opposed to a protein. The transport of this molecule is therefore extremely rapid. We propose that this rapid transport is significant to the function of NO and may be instrumental to the limitation of platelet thrombus size in vivo.
How can we determine regions of high NO concentration in an in vitro setup.
While NO is ubiquitous, its lifetime in the body is short, on the order of 5 seconds. Whereas chemical electrodes can be used to measure NO, they are limited in sensitivity, and they are used for single-point measurements. We are interested in obtaining a spatial map of the regions in which NO has been built up through the processes of production and transport. We are currently looking at the use of surfaces coated with hemoglobin to capture the NO molecules, after which a spectroscopic scan of the surface can be used to identify regions in which the concentration of NO-Hemoglobin is high.