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composition of the aqueous humour, hor monal and neuronal agents, etc., in influenc ing the morphogensis of the vacuoles re mains to be established." This subject has been discussed in greater depth more re cently.4 I have regarded the process of endothelial vacuolation as dynamic (which does not nec essarily imply that the driving force for this function can only be provided by the metab olism of the cell), (a) to distinguish it from the vacuoles that can be formed as a post mortem change or in a diseased condition, a subject fully discussed by Ashton,6 and (b) to indicate that the transcellular channels are regarded as transient stages in the develop ment of the vacuole during which it is open to both surfaces of the endothelial cell. Ramesh C. Tripathi, M.D., Ph.D., Institute of Ophthalmology, University of London Judd Street, London WC1H 9QS, England. REFERENCES
1. Tripathi, R. C. : Ultrastructure of Schlemm's canal in relation to aqueous outflow. Exp. Eye Res. 7:335,1968. 2. Tripathi, R. C : Mechanism of aqueous out flow across the trabecular wall of Schlemm's canal. Exp. Eye Res. 11:116, 1971. 3. Tripathi, R. C. : Aqueous outflow pathway in normal and glaucomatous eyes. Br. J. Ophthalmol. 56:157, 1972. 4. Tripathi, R. C. : Comparative physiology and anatomy of the outflow pathway. In Davson, H. (ed.) : The Eye, vol. 5. London, Academic Press. In press. 5. Cole, D. F., and Tripathi, R. C. : Theoretical consideration on the mechanism of aqueous outflow. Exp. Eye Res. 12:25, 1971. 6. Ashton, N. : The exit pathway of the aqueous. Trans. Ophthalmol. Soc. UK 80:397, 1960. REPLY
Editor, American Journal of Ophthalmology: We admire Dr. Tripathi's work, and ap preciate his pointing out that our interpreta tion of his concept was not exactly what he had in mind. His letter is helpful in making this clear. It is attractive to us to conceive of vital activity of the endothelial lining of
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Schlemm's canal having some modulating in fluence on outflow of aqueous and not to postulate an active outward transport requir ing much energy from the metabolism of these cells. W. Morton Grant, M.D. Murray A. Johnston, M.D. Howe Laboratory of Ophthalmology Harvard University Medical School 243 Charles Street Boston, MA 02114 DIABETIC RETINOPATHY STUDY
To the Editor, American Journal of Ophthalmology: Diabetic retinopathy has become one of the four most common causes of blindness in the United States. 1 Although photocoagulation has been employed in its treatment for more than ten years, its true value remains controversial. In spite of the need for objec tive, definitive evidence, an adequately con trolled trial of photocoagulation in proliferative diabetic retinopathy has not been per formed. This is not surprising, considering the complexity and expense of large scale clinical trials in chronic disease. However, as Inglefinger2 has aptly stated, When serious diseases are treated by serious methods .. . then ethical as well as scientific con siderations require that medicine depend on the most reliable and the best controlled data avail able^—the kind of data that is sought by ran domized clinical study.
In keeping with this admonition, a ran domized clinical trial of photocoagulation in the treatment of proliferative diabetic reti nopathy has been designed and launched. The Diabetic Retinopathy Study (DRS) in volves 16 clinical centers in various parts of the United States, a coordinating center at the University of Maryland, and a fundus photograph reading center at the Univer sity of Wisconsin, all supported by contracts from the National Eye Institute, a part of the National Institutes of Health.