Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corneal inflammation with subsequent scarring and blindness occurs in the inherited human metabolic disease tyrosinemia type II, yet putative inflammatory mediators in this disorder and in the avascular cornea in general are poorly defined. In a Tyr-fed rat model of tyrosinemia type II, intracellular crystals, presumably Tyr, are hypothesized to be responsible for the increased lysosomal activity observed in corneal epithelial lesions. Because polymorphonuclear leukocytes (PMNs) are seen only at the site of these lesions, we used this model to study humoral mediators released from Tyr-fed rat corneal organ cultures. Only Tyr-fed rats developed stromal edema and linear granular opacities in gray edematous corneal epithelium, compatible with a noninfectious keratitis. Electron micrographs confirmed epithelial edema and showed focal epithelial necrosis with PMN invasion of the stroma. Only Tyr-fed rat corneal culture supernatants contained chemotactic activity that was heat labile and moderately trypsin sensitive. Four peaks with varying amounts of chemotactic activity were found on Sephadex G-75 chromatography. Although the identity of these peaks of activity has not yet been established, we suggest that they may be responsible for the PMN infiltration observed in this model of corneal inflammation.
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PMID:Corneal organ cultures in tyrosinemia release chemotactic factors. 258 Sep 25

We developed a simple and rapid semiquantitative method for the determination of alpha-1-antitrypsin (alpha-1-AT) in human tears. It is a modification of Endre's method (1974) which was originally developed for the determination of serum alpha-1-AT. A filter paper disc saturated with trypsin was placed on the light-sensitive side of a color slide that had been developed unexposed. The trypsin digested the gelatine layers containing different stains and the film under the filter paper showed various colors depending on the trypsin content of the filter paper and the duration of digestion. If the filter paper discs saturated with trypsin had been treated with 5 microliters of tears before film digestion, the trypsin inhibitors in the tears partially or totally inhibited the digestion of the layers with different stains. Four grades of tear trypsin inhibitor capacity were differentiated on the basis of the inhibition of film digestion. These grades correspond to four alpha-1-AT concentration ranges: I greater than 150 micrograms/ml; II = 50-150 micrograms/ml; III = 15-50 micrograms/ml; IV less than 15 micrograms/ml. The concentration ranges were determined by radial immune diffusion. Alpha-1-AT was determined in the tears of 14 normal and 36 pathological eyes using the film digestion method. This method has been found to be suitable for rapid clinical and screening examinations and for the diagnosis of different types of keratitis.
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PMID:[A new method for semi-quantitative alpha 1-antitrypsin determination in human tear fluid]. 262 14