Endogenous Nocardia endophthalmitis.
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Aged↗
Biomedical subjects
K Gehrs
Publications and source records attributed to K Gehrs.
Estrogenic and DNA-damaging activity of Red No. 3 in human breast cancer cells.
Exposure to pesticides, dyes, and pollutants that mimic the growth promoting effects of estrogen may cause breast cancer. The pesticide DDT and the food colorant Red No. 3 were found to increase the growth of HTB 133 but not estrogen receptor (ER) negative human breast cells (HTB 125) or rat liver epithelial cells (RLE). Red No. 3, beta-estradiol, and DDT increase ER site-specific DNA binding to the estrogen response element in HTB 133 cells and increase cyclin-dependent kinase 2 activity in MCF-7 breast cancer cells. Site-specific DNA binding by p53 in RLE, HTB 125, HTB 133, and MCF-7 cells was increased when they were treated with Red No. 3, which suggests that cellular DNA was damaged by this colorant. Red No. 3 increased binding of the ER from MCF-7 cells to the estrogen-responsive element. Consumption of Red No. 3, which has estrogenlike growth stimulatory properties and may be genotoxic, could be a significant risk factor in human breast carcinogenesis.
Animals↗
Clinical study of a large family with autosomal dominant progressive cone degeneration.
PURPOSE: Autosomal dominant cone degeneration is an uncommon disorder characterized by progressive photophobia, hemeralopia, decreased central vision, and dyschromatopsia. To better understand the variable expressivity of autosomal dominant cone degeneration, we studied a single, large family. METHODS: We performed comprehensive ophthalmic examinations, full-field electroretinography, foveal electroretinography, and color vision studies on 73 family members. RESULTS: Of the 73 family members, 34 were affected. Symptoms generally began in the first decade of life and slowly progressed into midlife. Ophthalmoscopic findings consisted primarily of macular granularity or central macular atrophy. The photopic full-field electroretinogram was important in establishing the diagnosis, although the results of the electroretinographic measurements varied across individuals. Either the foveal electroretinogram amplitudes were abnormally low or the foveal/parafoveal ratio was abnormal in all affected subjects. CONCLUSIONS: No single test or finding was completely sensitive or specific for accurate diagnosis of autosomal dominant cone degeneration. Especially in the more mildly affected subjects, a constellation of symptoms, findings, and test results were used to diagnose autosomal dominant cone degeneration accurately.
Adolescent↗
Mapping of autosomal dominant cone degeneration to chromosome 17p.
PURPOSE: We studied a single, large family with autosomal dominant cone degeneration in order to map the disease-causing gene. METHODS: Seventy-three individuals in this family were examined, and 34 were found to be affected. Blood samples from 34 affected and unaffected family members were obtained for DNA analysis and linkage mapping. Fifty-three genetic markers were analyzed in this family by using short tandem repeat markers. These markers were primarily in candidate genomic regions. RESULTS: Marker D17S796 generated a significantly positive LOD score of 4.21 (theta = .04; 10,000:1 odds in favor of linkage). Marker D17S513 gave a significant LOD score of 3.1 (theta = .096; 1,000:1 odds in favor of linkage). Other markers in the region generated suggestive findings, such as D17S786, with a LOD score of 2.7, and D17S945, with a LOD score of 2.41. CONCLUSIONS: Our results indicate that a genetic defect that causes autosomal dominant cone degeneration is located on chromosome 17p in the region of recoverin. Recoverin, a retinal expressed gene, is an appealing candidate for this disease.
Adolescent↗
Hemeralopia in an older adult.
An elderly male was referred for evaluation of hemeralopia when cataract extraction did not alleviate his symptom of difficulty seeing in bright illumination. Visual acuity was 20/40 OU. Funduscopic examination revealed marked arteriolar attenuation, disc pallor, and retinal pigment epithelial changes. Visual fields demonstrated relative paracentral scotomata. An ERG was consistent with widespread photoreceptor degeneration. A diagnosis of visual paraneoplastic syndrome was made and an extensive systemic evaluation revealed a squamous cell carcinoma of the lung. The presentation and evaluation of acquired photoreceptor dysfunction in adulthood is discussed.
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