bromochloroacetic-acid has been researched along with Anemia--Hypochromic* in 4 studies
4 other study(ies) available for bromochloroacetic-acid and Anemia--Hypochromic
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A mutant mouse with severe anemia and skin abnormalities controlled by a new allele of the flaky skin (fsn) locus.
We found a novel recessive mutation in an inbred strain, INT, that was derived from an ICR closed colony. Mice homozygous for this mutation are identified by severe anemia, dysgenesis and neonatal death. This mutation was tentatively named int. Intercrosses of int heterozygotes (+/int) and the flaky skin heterozygotes (+/fsn) resulted in abnormal mice (int/fsn heterozygotes) showing anemia and flaky skin with the expected frequency for autosomal recessive mutation. The int gene was therefore named fsn(Jic) as an allele of the fsn locus on chromosome 17. We carried out phenotype analyses using B6.INT- fsn(Jic) mice to observe phenotypes of blood and skin in the embryonic and neonatal stages. Discrimination of fsn(Jic) embryos from normal embryos was performed by an indirect diagnosis of the fsn(Jic) gene using the D17Mit130 microsatellite marker tightly linked to the fsn locus. The number of fetal nucleated RBC of normal embryos decreased gradually to 17.5 dpc, but that of the abnormal embryos decreased to 14.5 dpc followed by a gradual increase to 17.5 dpc. Skin of fsn(Jic) embryos did not show any abnormalities and expressed cytokeratins normally as skin epithelial cell markers at each embryonic stage (15.5 dpc to 18.5 dpc). Time differences in the appearance of the different phenotypes observed in various tissue and organs of fsn homozygotes suggest they are caused by expression of the fsn gene at different developmental stages. Topics: Alleles; Anemia, Hypochromic; Animals; Animals, Newborn; Biomarkers; Chromosome Mapping; Epithelial Cells; Erythroblasts; Erythrocyte Count; Female; Gene Expression Regulation, Developmental; Genes, Recessive; Keratins; Male; Mice; Mice, Inbred ICR; Mice, Mutant Strains; Microsatellite Repeats; Phenotype; Rodent Diseases; Skin Diseases, Papulosquamous | 2005 |
Brittle fingernails.
In this review an attempt has been made to clarify the etiology, pathogenesis, and therapy of brittle fingernails. Hopefully, this discussion will enable the clinician to better understand, evaluate and manage patients with this disorder. Topics: Anemia, Hypochromic; Calcium; Cosmetics; Fingers; Humans; Keratins; Nail Diseases; Nails; Skin Diseases; Sulfur; Toes; Water | 1985 |
Quantitative histological analysis of the epithelium of the ventral surface of hamster tongue in experimental iron deficiency.
Quantitative analysis of the ventral tongue epithelium of iron-deficient hamsters revealed significant progressive alterations in epithelial compartment thickness. As iron deficiency developed there was an initial increase in the proportion of the epithelium made up by progenitor cells and a decrease in the proportion formed by maturing cells. With increasing degree of deficiency, the maturation compartment formed less, and the keratinized compartment more, of the epithelium until, at the stage of anaemia, there was a significant reduction in the maturation compartment and a significant increase in the keratin thickness. Topics: Anemia, Hypochromic; Animals; Cricetinae; Epithelium; Iron Deficiencies; Keratins; Male; Mesocricetus; Tongue | 1982 |
The place of iron deficiency in the Paterson-Brown Kelly syndrome.
Topics: Anemia, Hypochromic; Animals; Deglutition Disorders; Esophageal Stenosis; Gastric Mucosa; Hematocrit; Hernia, Diaphragmatic; Iron; Keratins; Larynx; Mitosis; Rats; Tongue; Vitamin B Deficiency | 1973 |