Biomedical subjects

P Kolesar

Publications and source records attributed to P Kolesar.

3 recordsLinked to original sources

PubMed1981

A visual field screening protocol for glaucoma.

In this prospective evaluation of the reliability and efficiency of an optimized visual field screening protocol for glaucoma, we tested 145 eyes (73 patients) with increased intraocular pressures to determine the location of early glaucomatous visual field defects. The field examination, which was used as a control, and protocol testing were performed on a manual Goldmann perimeter using kinetic and suprathreshold static techniques, respectively. Of the 145 eyes tested, kinetic Goldmann perimetry detected 43 eyes with glaucomatous defects. The screening protocol detected 39 defective eyes. There were four false-negative tests and one false-positive test. The false-negative rate of just under 10% was within the range predicted from earlier data. The computer-generated optimal protocols performed as predicted and provided an excellent screening technique for the detection of early glaucomatous visual field defects.

Clinical Trials as Topic↗

PubMed1978

Mathematical optimization of glaucoma visual field screening protocols.

There is potential for significantly shortening the time required for visual field screening protocols by a precise specification of the number, exact location, and sequence of points to be tested. Through statistical and mathematical methods, protocols have been developed for maximizing the probability of detecting at least one visual field defect in a subject who is a risk for early glaucomatous field loss. The mathematical formulation was derived in a generalized manner so that it could be applied to most kinetically or statically determined visual field screening methods.

Glaucoma↗

PubMed1977

Inhibition of L-dopa induced growth hormone release in normal and diabetic subjects by glucose administration.

Administration of L-dopa 1 g induced an increase of plasma growth hormone (GH) levels in seven of ten healthy volunteers and in six of ten hyperglycemic insulin-dependent diabetic subjects; the maximal GH response was higher in normal subjects. Addition of 100 g glucose orally to the L-dopa completely abolished the GH response of both groups. The difference between the effect of endogenous hyperglycemia and the effect of a sudden increase of blood sugar after glucose administration on L-dopa induced GH release in diabetic subjects may be explain by the resetting of the hypothalamic control for pituitary GH release to higher levels of blood glucose.

Adult↗