Our aim is to further delineate the relationship between UV exposure, lens aging and cataractogenesis at the molecular level and correlate these data with our other methods of evaluation (optical spectroscopy, morphology, and the CCRG photographic classification system) and with the in vivo methods we have developed (UV slit lamp densitography and surface scanning NMR spectroscopy). We have further refined the UV slit lamp densitographic technique to permit widespread clinical application. An automated program has now been developed which can measure both corneal and lenticular fluorescence levels and provide biometric data as well. This program will be further tested on at least 100 patients during the coming year. In addition to the foregoing biophysical techniques, we are expanding our efforts to perform multiprobe NMR spectroscopy on whole eyes (fresh donor specimens) and on live monkeys and rabbits. We are currently performing 23Na as well as 31P analyses and proton imaging in order to develop specific parameters for in vivo NMR spectroscopy. These two in vivo biophysical approaches will enable us to correlate changes in the living lens with our ongoing multifaceted in vitro spectroscopic analyses. We have also expanded our program in which we perform the Schiempflug photos (with the UV-visible slit lamp apparatus) on patients prior to cataract surgery, and correlate these data with our laboratory analyses on the extracted lens or lens matter from these patients. A similar pilot study involving NMR spectroscopy will be instituted this year. Aside from our ongoing studies on the effects of direct UV radiation exposure on the ocular lens, we are continuing our investigations on (UV) photosensitized damage as exemplified by our work on the Psoralens and Allopurinol. The biophysical (fluorescence) in vivo approach is being applied to such patients, and our in vitro spectroscopic analysis (involving fluorescence, phosphorescence, and NMR spectroscopy) are being utilized to further delineate the types of mechanisms involved in such damage (Type I or Type II reaction).
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