Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To understand how human corneal endothelium compensates for cell loss, nuclear DNA-cytofluorometry and cell morphometry were carried out on injured corneal endothelium. The examined corneas included two cases of keratoconus complicated with acute hydrops and one without acute hydrops, two cases of herpetic keratitis, one case of post-intracapsular cataract extraction (post-ICCE) and one case of luetic keratitis. The endothelial cell layer was separated from Descemet's membrane and double-stained with Rhodamine-labeled wheat germ agglutinin-lectin (WGA) and 4',6-diamidino-2-phenylindole dihydrochloride (DAPI). The area of each cell was measured with a color image analyser and compared with its cytofluorometric nuclear DNA content. The endothelium in apparently intact regions of the diseased corneas showed the same DNA-ploidy pattern and cell area as the physiological corneas. However, endothelial cells in injured regions had greater area, even in diploidy, than in presumably normal ones and showed a larger number of hyperploid cells ranging from 4C to 36C. Hyperploid cells consisted of many multinucleates and few polyploidies and had extremely large and bizarre cytoplasm. All injured corneas were accompanied by cells with numerous micronuclei. A few asymmetrical 4C-binucleates (with DNA values such as 1.3 plus 2.6C) appeared in the case of the post-ICCE. It is concluded that damage to human corneal endothelial cells in vivo results in cell enlargement with or without DNA synthesis. Those changes appear more severe in diseased corneas than in the situation of physiological aging which we have reported previously. In severe cases, micronuclei, polyploid cells and multinucleated giant cells are frequent, thereby suggesting a possible long-persistent metabolic impairment of the endothelium after severe damage to the cornea.
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PMID:Changes in nuclear DNA content and cell size of injured human corneal endothelium. 340 92

The Galalpha1-3Galbeta1-4GlcNAc epitope is the key antigen in the hyperacute rejection of pig-to-man xenotransplantation. In the alpha-1,3-galactosyltransferase knockout (alpha-1,3GT-KO) mouse - a model for xenograft donor pigs - a targeted mutation of the alpha-1,3 galactosyltransferase gene (Ggta1) has been constructed. These mice are depleted of the carbohydrate antigen and besides the mice are also known to develop cortical cataracts. The present study aimed at evaluating the morphology and the degree of the cataract in a population of alpha-GT KO mice, its age of onset, its progression and the impact the cataract may have on aggression, anxiety and perception of light. The alpha-gal epitope could be shown in the lenses with lectin GS1 B4 in all wild-type and none of the alpha-GT KO mice. Histology showed apparent cataract in all alpha-GT KO mice from six weeks of age. Apart from a single wild-type mouse with a small degree of microscopically visible cataract without epithelial involvement at the age of 30 weeks none of the wild-type mice showed signs of cataract. Behavioural testing demonstrated significantly more mounting behaviour and a longer duration of attacking in the alpha-GT KO mice. Apart from this, the agonistic behaviour was not influenced by genotype. Neither did the genotype affect anxiety or perception of light.
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PMID:Aggression in cataract-bearing alpha-1,3-galactosyltransferase knockout mice. 1834 65