Diagnostic tests in children with atopic dermatitis and food allergy

BACKGROUND: Skin testing is a common diagnostic procedure in food allergy. The skin prick test is the test of first choice for investigating the immediate IgE-mediated reaction. The skin application food test (SAFT) has been developed on the basis of the mechanism of the contact urticaria syndrome (CUS). METHODS: We studied the relevance of the SAFT in children younger than 4 years with atopic dermatitis and (suspected) food allergy as compared with the prick-prick test, the radioallergosorbent test (RAST), and the oral challenge. In the skin tests, we used fresh food, in the same state as it was consumed. RESULTS: There was a good agreement between the SAFT and the prick-prick test. A moderate agreement was observed between the SAFT and the serologic test (RAST). Significantly more positive results in the RAST were observed than in the SAFT. There was very good agreement between the SAFT and the oral challenge (kappa = 0.86). CONCLUSIONS: The SAFT is a reliable and child-friendly skin test for evaluating (suspected) food allergy in children younger than 4 years with atopic dermatitis. The very good correlation with the oral challenge indicates that one may probably consider the SAFT a "skin provocation" in children younger than 4 years.     

Bacterial and human cell mutagenicity study of some C18H10 cyclopenta-fused polycyclic aromatic hydrocarbons associated with fossil fuels combustion

Maximal activity of NADP.H-cytochrome c reductase was found in the liver, the lowest one--in the retina. On the contrary, the highest activity of aldose reductase was observed in the retina, the lowest one--in the liver. The activity of NADP.H-cytochrome c reductase in the retina of rats with hereditary degeneration of the retina increased to the 60th day of postnatal life by 33%, the increase reaching 273% to the 90th day. In the brain cortex, the increase in the activity to the 45-60th days amounted to 22-34%, whereas at the age of 90 days the difference between healthy and patient rats, as well as the difference between males and females became less significant. The activity of aldose reductase in the cortex and retina in patient rats at the 20th day was 35% lower than in healthy animals. In the liver of patient rats, to the age of 45 days, the activity of aldose reductase decreased by 38%. At other periods, no significant differences were observed between healthy and patient animals with respect to the activity of this enzyme.     

cDNA cloning of a human homologue of the Caenorhabditis elegans cell fate-determining gene mab-21: expression, chromosomal localization and analysis of a highly polymorphic (CAG)n trinucleotide repeat

The two most consistent features of the diseases caused by trinucleotide repeat expansion-neuropsychiatric symptoms and the phenomenon of genetic anticipation-may be present in forms of dementia, hereditary ataxia, Parkinsonism, bipolar affective disorder, schizophrenia and autism. To identify candidate genes for these disorders, we have screened human brain cDNA libraries for the presence of gene fragments containing polymorphic trinucleotide repeats. Here we report the cDNA cloning of CAGR1, originally detected in a retinal cDNA library. The 2743 bp cDNA contains a 1077 bp open reading frame encoding 359 amino acids. This amino acid sequence is homologous (56% amino acid identify and 81% amino acid conservation) to the Caenorhabditis elegans cell fate-determining protein mab-21. CAGR1 is expressed in several human tissues, most prominently in the cerebellum, as a message of approximately 3.0 kb. The gene was mapped to 13q13, just telomeric to D13S220. A 5'-untranslated CAG trinucleotide repeat is highly polymorphic, with repeat length ranging from six to 31 triplets and a heterozygosity of 87-88% in 684 chromosomes from several human populations. One allele from an individual with an atypical movement disorder and bipolar affective disorder type II contains 46 triplets, 15 triplets longer than any other allele detected. Though insufficient data are available to link the long repeat to this clinical phenotype, an expansion mutation of the CAGR1 repeat can be considered a candidate for the etiology of disorders with anticipation or developmental abnormalities, and particularly any such disorders linked to chromosome 13.