Evidence for multiple CD95-CD95 ligand interactions in anteriorchamber-associated immune deviation induced by soluble protein antigen.
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We have investigated whether CD95-CD95 ligand interactions are important in anterior chamber-associated immune deviation (ACAID) induced by soluble protein antigen, and if so, to identify the participating cells on which these molecules are expressed. Peritoneal exudate cells as antigen-presenting cells (APC) obtained from B6.lpr/lpr, B6.gld/gld and C57BL/6 mice were cultured with ovalbumin (OVA) and transforming growth factor-beta2 (TGF-beta2) overnight, then injected intravenously into C57BL/6 or B6.lpr/lpr recipients. Some B6.lpr/lpr mice were reconstituted with naive T cells from wild-type C57BL/6 donors. In other experiments, B6. lpr/lpr and B6.gld/gld mice received an anterior chamber injection of OVA followed 7 days later by subcutaneous immunization with OVA plus adjuvant. Delayed hypersensitivity (DH) was assessed with an ear swelling assay. T cells activated in vitro with OVA-pulsed, TGF-beta-treated APC were tested in vivo for their capacity to suppress DH expression in a local adoptive transfer assay. The results indicate that when ACAID was induced by in-vitro generated ACAID-inducing cells, the APC expressed CD95L, and recipient T cells expressed CD95. The capacity of in vitro generated regulatory T cells to suppress DH expression to OVA in vivo was not governed by CD95-CD95L interactions. When OVA was injected into the anterior chamber of naive mice, CD95 expression was required for ACAID induction, although ACAID was readily induced in CD95L-deficient mice. We conclude that CD95-CD95L interactions are required in ACAID for the initial stage of APC presentation of eye-derived antigens to T cells, and that CD95-CD95L interactions participate at one or more additional step in the process by which ACAID is induced by soluble protein antigens. (+info)
A pathologic study on ocular disorders in calves in southern Kyushu, Japan.
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Of 822 calves, ranging in age between one day and six months necropsied between 1996 and 1998 at Miyazaki University, histological examination showed that 25 (3.0%) had ocular lesions. These ocular lesions consisted of suppurative inflammation (13 cases), cataract (seven cases), and retinal atrophy (five cases). Inflammatory changes were classified as suppurative keratitis (one case), keratitis and uveitis (ten cases), and uveitis and retinitis (two cases). Cataract was subclassified into three categories; cortical (three cases), nuclear (one case), and mature (three cases). These lesions were characterized by degenerative changes in the lens fibers and the appearance of eosinophilic globules known as Morganian globules. In the most severely affected case, there was capsular rupture of the lens, resulting in severe infiltration by eosinophils and histiocytes of the whole anterior chamber. Almost all the calves with retinal atrophy had been suffering from severe hydranencephaly and three had significantly raised levels of neutralization antibodies for the Akabane and/or Aino viruses. This study indicates that congenital arbovirus infections may predispose calves to ocular diseases, especially retinal atrophy. (+info)
Painful blind eye: efficacy of enucleation and evisceration in resolving ocular pain.
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AIMS: To assess the effectiveness of enucleation or evisceration in relieving pain from painful blind eyes. METHODS: 24 patients with intractable ocular pain underwent enucleation or evisceration with or without an orbital implant. RESULTS: Complete pain relief was achieved in all patients at an average time of 3 months (range 1-15 months). Seven patients required further medical or surgical treatment in addition to removal of the globe. CONCLUSION: Enucleation and evisceration were effective in relieving ocular pain in all patients with a painful blind eye in our study. However, complications of surgery and orbital implants can cause recurrent pain. (+info)
X-linked Alport syndrome: natural history in 195 families and genotype- phenotype correlations in males.
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Alport syndrome (AS) is a type IV collagen hereditary disease characterized by the association of progressive hematuric nephritis, hearing loss, and, frequently, ocular changes. Mutations in the COL4A5 collagen gene are responsible for the more common X-linked dominant form of the disease. Considerable allelic heterogeneity has been observed. A "European Community Alport Syndrome Concerted Action" has been established to delineate accurately the AS phenotype and to determine genotype-phenotype correlations in a large number of families. Data concerning 329 families, 250 of them with an X-linked transmission, were collected. Characteristics of the 401 male patients belonging to the 195 families with COL4A5 mutation are presented. All male patients were hematuric, and the rate of progression to end-stage renal failure and deafness was mutation-dependent. Large deletions, non-sense mutations, or small mutations changing the reading frame conferred to affected male patients a 90% probability of developing end-stage renal failure before 30 yr of age, whereas the same risk was of 50 and 70%, respectively, in patients with missense or splice site mutation. The risk of developing hearing loss before 30 yr of age was approximately 60% in patients with missense mutations, contrary to 90% for the other types of mutations. The natural history of X-linked AS and correlations with COL4A5 mutations have been established in a large cohort of male patients. These data could be used for further evaluation of therapeutic approaches. (+info)
Ocular changes in beagle dogs following oral administration of CGS 24565, a potential hypolipidemic agent.
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(11R)-N,15-dideoxo-1-deoxy-1,15-epoxy-11-hydroxy-4-0methy l-8-0-(2, 2-dimethyl-1-oxopropyl)-3-[4- inverted question mark(2,4, 6-trimethylphenyl)methyl inverted question mark-1-piperazinyl]rifamycin has been evaluated as a potential hypolipidemic agent. As part of a safety evaluation program, a 3-month oral toxicity study was performed in which CGS 24565 was administered to beagle dogs via gelatin capsules at 10, 50, or 300 mg/kg/day. Ophthalmoscopic examinations (using focal illumination and indirect opthalmoscopy) on day 83 (week 12) revealed bilateral adnexal and corneal changes affecting 5 dogs (3 males, 2 females, 300 mg/kg/day). Ophthalmoscopically, dogs from the 300 mg/kg dose level exhibited the adnexal changes characterized as ptosis, conjunctivitis, episcleritis, and relaxed membrane nictitans, while the corneal changes were characterized as posterior stromal edema (cloudy, diffuse opacity usually accompanied by deep neovascularization; the diffuse edema masked the complete evaluation of other ocular structures) and stromal infiltrates in the area of Decement's membrane (appeared to be multifocal, polymorphic changes/alterations in Decement's membrane, or endothelial swelling). No changes from normal were seen clinically in the eyes of other dogs on this experiment. In those dogs affected by the ocular changes caused by CGS 24565, a visual deficit in acuity was suspected. The corneal changes, as manifested, were suggestive of permanent, irreversible corneal damage. Subsequent ophthalmoscopic examinations performed at established intervals during weeks 15 through 26, revealed abatement of the adnexal changes, while the corneal changes, as described above, remained generally unchanged, confirming irreversibility of the corneal changes within the recovery period of 13 weeks. Light microscopy confirmed irreversible corneal neovascularization, vacuolar degeneration of the keratocytes at 300 mg/kg, and polymorphic infiltrates in the region of Decement's membrane. The results demonstrate that the cornea was the target tissue of toxicity for CGS 24565, and indicated that the findings represent a significant toxic effect. The correlation of histopathological findings support the hypothesis of the diagnosis of interstitial stromal degeneration/atrophy. The potential for a similar result to the cornea of humans does exist. Due to these changes and other toxic effects associated with this class of compound, further development was terminated. (+info)
Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review.
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BACKGROUND: The cardinal characteristics of primary hypomagnesaemia-hypercalciuria-nephrocalcinosis include renal magnesium wasting, marked hypercalciuria, renal stones, nephrocalcinosis, a tendency towards chronic renal insufficiency and sometimes even ocular abnormalities or hearing impairment. METHODS: As very few patients with this syndrome have been described, we provide information on nine patients on follow-up at our institutions and review the 42 cases reported in the literature (33 females and 18 males). RESULTS: Urinary tract infections, polyuria-polydipsia, renal stones and tetanic convulsions were the main clinical findings at diagnosis. The clinical course was highly variable; renal failure was often reported. The concomitant occurrence of ocular involvement or hearing impairment was reported in a large subset of patients. Parental consanguinity was noted in some families. CONCLUSIONS: The results indicate an autosomal recessive inheritance. The diagnosis of primary hypomagnesaemia-hypercalciuria-nephrocalcinosis deserves consideration in any patient with nephrocalcinosis and hypercalciuria. (+info)
The effect of massive doses of vitamin A on the signs of vitamin A deficiency in preschool children.
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Marked seasonal variation in the prevalence of signs of vitamin A deficiency was found in the 2nd year of a continuing study of children age 0 to 4-1/2 years in a village in West Bengal, confirming results of a previous 18-month study. Administration of 200,000 IU of vitamin A every 4 months completely eliminated night blindness and prevented the development of new cases of Bitot's spot in a statistically significant number of children. The effectiveness of massive doses of vitamin A, administered at intervals of 4 months, as a short-term measure to fight the problem, was confirmed in this village. The study yielded additional evidence of the complex etiology of Bitot's spot, since alternate day dose of vitamin A in addition to massive therapy failed to eliminate these spots. (+info)
Xerophthalmia and blindness in Northeast Brazil.
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Dietary and biochemical data have indicated that hypovitaminosis A is a public health problem in Northeast Brazil. However, there are few reports regarding clinical signs of hypovitaminosis A. Therefore, an epidemiological study was designed to study this problem. The study as done was primarily a review of hospital records of xerophthalmia in each state with attention paid to other nutrition factors. It was found that xerophthalmia is a problem in Northeast Brazil and a cause of blindness in certain areas. However, the number varied greatly from some states to others. Around 1,000 preschool-age children were recorded as blind from vitamin A deficiency in a 1-year period. It was also noted that the peak incidence of xerophthalmia and blindness was around 1 year of age. The government of Brazil is taking urgent measures to combat this deficiency with such measures as the supplementation of sugar with vitamin A and the distribution of massive doses of vitamin A. (+info)