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

Eleven corneal specimens from nine patients with Salzmann's nodular degeneration of the cornea, together with all available clinical information, were collected for this study. The specimens were examined by light and electron microscopy. An antecedent keratitis was diagnosed by history and microscopic findings in every case. The corneal epithelium showed degenerative changes, its thickness varied, and in nodular areas it often consisted of only a single layer of flattened epithelial cells by light microscopy. Bowman's membrane was missing over the nodules, and in this zone there was excessive secretion of a basement membrane-like material. Hyaline degeneration of collagen, cellular debris, and electron-dense hyaline deposits were seen in the collagen of the nodules. The number of fibrocytes in the nodules varied from many that were active to a few that were degenerating. External irritation because of poor epithelial protection was interpreted as a causative factor, although other tissue repair mechanisms may also have played a role.
 ...
PMID:Salzmann's nodular degeneration of the cornea. 4 19

Uniformly severe corneal infections were produced in guinea pigs by intracorneal injection of about 10 viable Pseudomonas aeruginosa. After a brief lag period, multiplication of bacteria was rapid, reaching geometric means of 280,000 after 24 hr and of 5 million after 48 hr. Within 8 hr after inoculation, polymorphonuclear leukocytes (PMNs) began to infiltrate the anterior two thirds of the stroma. Stromal cells adjacent to the injection site became necrotic and appeared to be engulfed by PMNs. By 14 to 16 hr, an abscess containing a dense aggregate of PMNs and multiplying bacteria developed in the central stroma. By 16 to 24 hr, collagen breakdown was apparent within and around the abscess. Ultrastructural evidence of collagen breakdown included loss of intact collagen fibrils, tactoid formation, and accumulation of amorphous electron-dense material. The area of liquefactive necrosis gradually enlarged, and many corneas perforated after 3 to 4 days. Because the course of infection is highly reproducible, this model should prove useful for many studies of experimental Pseudomonas keratitis.
 ...
PMID:Pathogenesis of experimental Pseudomonas keratitis in the guinea pig: bacteriologic, clinical, and microscopic observations. 10 Apr 68

Extracellular proteases of three cornea-virulent strains of Pseudomonas aeruginosa were isolated by sequential ammonium sulfate precipitation, Ultrogel AcA 54 gel filtration, and flat-bed isoelectric focusing. The purity of the preparations was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis , thin-layer isoelectric focusing in polyacrylamide gel, immunodiffusion and immunoelectrophoretic procedures, and tests for the presence of other known pseudomonal products. Light and electron microscopic examination of rabbit corneal lesions observed 4 to 6 h after the intracorneal injection of submicrogram amounts of the proteases revealed: (i) degeneration and necrosis of epithelium, endothelium, and keratocytes, (ii) infiltration, degeneration, and necrosis of polymorphonuclear leukocytes, (iii) loss of the characteristic weblike pattern, colloidal iron staining, and ruthenium red staining of the stromal proteoglycan ground substance, (iv) dispersal of strucutrally normal appearing collagen fibrils, ground substance, (iv) dispersal of structurally normal appearing collagen fibrils, and (v) accumulation of plasma proteins and fibrin in the necrotic corneas. These structural alterations are very similar to those observed previously during experimental P. aeruginosa keratitis, and this similarity supports the idea that pseudomonal proteases are responsible, at least in part, for the rapid and extensive liquefaction necrosis characteristic of pseudomonal-induced keratitis. In addition, the results support the idea that pseudomonal proteases elicit severe corneal damage by causing the loss of the corneal proteoglycan ground substance, thus resulting in dispersal of undamaged collagen fibrils, weakening of the corneal stroma, and subsequent descemetocele formation and corneal perforation by the anterior chamber pressure.
 ...
PMID:Purification of Pseudomonas aeruginosa proteases and microscopic characterization of pseudomonal protease-induced rabbit corneal damage. 41 81

In a test series with 15 rabbits a so-called central keratitis by means of a redhot needle was set in the left and right eye. The cornea of the left eye was immediately extirpated under sterile conditions and was observed in the tissue culture for 6 days. The corresponding right eye of the first rabbit was left within the animal's body, later it was extirpated after 1/2, 1, 1 1/2, 2 hours etc. up to 11 days histologically examined. In the explants following results were obtained. After the lesion is set the puncture site is devoid of epithelium. A double wall of cells lies closely around the crater. One-and-one-half hours later these large cells with more or less variably segmented nuclei demonstrate a strong proliferation. The characteristic nucleus form, the weakly positive naphthol-ASD-chloracetateesterase-reaction and the variable peroxydase-reaction of these cells resemble quite closely leucocytes in phenomenology and ferment-histochemistry. We have therefore chosen the description leucocytoid cells. They are not leucocytes, but cells which originate from basal pluripotent epithelia of the cornea. The so-called central keratitis is not an inflammation in the sense of Marchand, it is rather a regenerative process. The thesis of Busse-Grawitz, that leucocytes in the cornea originate from collagen and elastic fibers or less than coccisized transitional forms, cannot be verified.
 ...
PMID:The reaction of the cornea in vivo and in vitro to thermal stimulation: a contribution to the thesis by Busse-Grawitz. 80 59

Collagen shields applied to the corneas of patients with bacterial keratitis degrade rapidly, often within a few hours. Once treatment brings the infection under control, subsequently applied collagen shields degrade more slowly. In vitro models were established to evaluate the significance of these observations. Twenty-four and 72-hour collagen shields were incubated with collagenase from Clostridium histolyticum. The in vitro rate of digestion of the shields was directly proportional to the concentration of collagenase, with the rate of digestion of the 24-hour shields being greater than that of the 72-hour shields. Therefore, the rate of collagen shield degradation may be a clinically useful index of collagenase activity on the ocular surface. Ultrastructural studies of collagen shields from patients with acute bacterial keratitis revealed irregular degradation of shield matrix with no evidence of adherence of microorganisms or inflammatory cells. Co-incubation of deepithelialized rabbit corneas and collagen shields resulted in inhibition of the digestion of the rabbit corneas when the weight:weight ratio of collagen shield:rabbit cornea was increased to greater than or equal to 2:1. Collagen shields may inhibit corneal collagen degradation in infectious ulceration and melting disorders by effectively competing for collagenase on the ocular surface.
 ...
PMID:The collagen shield as a collagenase inhibitor and clinical indicator of collagenase activity on the ocular surface. 131 47

It is necessary to know the specific pathobiology of a persistent epithelial defect to determine the strategy to be employed to assist in its repair. Lid position and function must be normal and any deficiency in the quantity and quality of the tears enhanced by tear preparations and closure of the lacrimal canaliculi. Adverse drug effects must be eliminated. Multiple corneal punctures and excision of reduplicated basal lamina have virtually eliminated the problem of recurrent corneal erosions. Control of any inflammatory process also speeds healing. Vitamin supplements, especially A, reverse defects associated with xerophthalmia. In any of these diseases, mechanical treatments consisting of soft contact lenses for persistent epithelial defects and collagen shields for the delivery of antibiotics or steroids to the eye may be employed. Tarsorrhaphy relieves the problem of persistent epithelial defects in neurotrophic keratitis and a variety of other conditions characterized by persistent surface breakdown. Preliminary data from open label studies of epidermal growth factors and fibronectin are encouraging but not yet conclusive.
 ...
PMID:Clinical measures to promote corneal epithelial healing. 132 15

We compared collagen shields hydrated in 1.36% tobramycin with topical 1.36% tobramycin for sustained treatment of experimental Pseudomonas keratitis in rabbits. Antibiotic therapy for a total of 24 hours was initiated 14 hours after an intrastromal injection of 10(3) logarithmic phase Pseudomonas aeruginosa. Seven groups were treated as follows: groups 1-3, collagen shields hydrated in tobramycin supplemented with topical 1.36% tobramycin drops at 4, 6, or 8 hour intervals; group 4, collagen shields hydrated in tobramycin without any further topical supplementation; group 5, topical tobramycin therapy, initially every half-hour for 4 hours, then hourly; group 6, collagen shields hydrated in balanced saline solution; and group 7, no treatment. Each group contained four eyes. The groups treated with collagen shields supplemented every 4 or 6 hours with topical tobramycin had significantly fewer colony forming units (CFU) than those receiving topical or collagen shield therapy alone (P < 0.001). The group treated with collagen shields hydrated in sterile saline had 10(7) CFU per cornea, which was not significantly different from the untreated group (P > 0.2). Collagen shields hydrated in tobramycin and supplemented with topical tobramycin were effective in sustained treatment of experimental Pseudomonas keratitis.
 ...
PMID:Collagen shields containing tobramycin for sustained therapy (24 hours) of experimental Pseudomonas keratitis. 142 60

We report the etiological profile and management with simple patch, tarsorrhaphies, conjunctival flaps, tissue adhesive, or penetrating keratoplasty of 104 chronic corneal perforations in a North India population. Chronic corneal perforations were observed in infective keratitis, degenerative keratolysis, neurotrophic keratitis, chemical burns, dry eyes, collagen vascular diseases, and following cataract extraction. A two-stage tissue adhesive application and adhesive-assisted debridement of epithelial lining at the cornea surface of perforation were important factors in healing. Although penetrating keratoplasties brought comparable anatomical and functional success in these cases, in developing countries, where facilities for keratoplasty and availability of corneal donor is poor, detection and management of small perforations in diseased cornea with tissue adhesive is recommended.
 ...
PMID:Chronic corneal perforations. 151 36

We evaluated the effect of collagen shields presoaked with amphotericin B on the treatment of experimental Candida albicans-induced keratitis. Treatment results were compared to those of amphotericin B eyedrops instilled hourly. Forty-eight albino rabbits received intrastromal injections of 10(8) C. albicans organisms. Twenty-four hours later, eyes were treated for eight hours each day with hourly instillation of 0.15% amphotericin B drops, hourly instillation of saline drops, or application of a collagen shield presoaked in 0.5% amphotericin B for one hour. The rabbits were killed after one, three, or five days of treatment. Quantitation of fungi in the cornea was achieved by culturing homogenates and counting colony-forming units. Treatment with amphotericin B applied either as hourly instilled drops or absorbed in collagen shields significantly (P less than .05) reduced corneal fungal counts at all time points when compared to saline-treated control eyes. Rabbit eyes treated with amphotericin B-soaked collagen shields had significantly lower fungal counts compared with hourly instilled amphotericin B drops at Days 1 (P = .02) and 3 (P = .04), but not at Day 5. The collagen shields were as effective in reducing the number of colony-forming units as were amphotericin B drops at Day 5. These data suggest that collagen shields soaked in amphotericin B could be a useful and convenient treatment device in keratomycosis such as that caused by C. albicans.
 ...
PMID:Use of collagen shields containing amphotericin B in the treatment of experimental Candida albicans-induced keratomycosis in rabbits. 154 24

We compared the efficacy of a fortified tobramycin-soaked collagen shield to the efficacy of a single loading dose (four 50-microliters drops) of fortified tobramycin eyedrops in the treatment of New Zealand White rabbits with Pseudomonas aeruginosa-induced keratitis. Eyedrop loading-dose efficacy was evaluated with and without lateral tarsorrhaphy. Six hours after a single treatment, significantly fewer Pseudomonas colonies were present in the corneas of all three drug-treated groups as compared to the number of colonies in the corneas of balanced salt solution-treated control rabbits (P less than .006). Although no significant difference was observed between any of the drug-treated groups, lateral tarsorrhaphy was associated with a greater than tenfold decrease in the number of colony-forming units (P = .073). We found no significant difference in efficacy between a collagen shield presoaked in tobramycin, and a single loading dose of tobramycin eyedrops, in the treatment of rabbits with P. aeruginosa-induced keratitis.
 ...
PMID:Efficacy of tobramycin-soaked collagen shields vs tobramycin eyedrop loading dose for sustained treatment of experimental Pseudomonas aeruginosa-induced keratitis in rabbits. 155 16


1 2 3 4 5 6 7 8 9 10 Next >>