No evidence of association of CTLA4 polymorphisms with Addison's disease.

BACKGROUND: Addison's disease (AD) is an autoimmune disorder caused by the destruction of the adrenal gland by the lymphocytes in genetically susceptible individuals. The contribution of HLA genes to the genetic risk to AD has been known for a long time; however, non-HLA genetic factors are likely to be required for the development of the disease. Several studies have associated the CD28/CTLA4 region on chromosome 2q33 with the disease in different populations. The cytotoxic T lymphocyte-associated antigen 4 (CTLA4) gene encodes a receptor involved in the control of T cell proliferation and mediates T cell apoptosis. AIM: To determine the contribution of two polymorphisms of the CTLA4 to the disease; the A/G dimorphism at position +49 in exon 1 and the (AT)n microsatellite in the 3' untranslated region of exon 3. PATIENTS: Fifty seven patients with autoimmune AD (autoimmunity for anti 21-hydroxylase was confirmed) and 111 unrelated healthy subjects from the general populations were analyzed as controls. METHODS: Restriction enzyme digestion of polymerase chain reaction (PCR) amplified genomic DNA for the A/G dimorphism and PCR followed by high-resolution electrophoresis for the (AT)n microsatellite. For disease association studies, the case-control approach was used. RESULTS: The frequency of the A allele of 49 A/G polymorphism was 65.79% in the patients compared with 72.07% in the control group. These differences were not significant. Analysis of the (AT)n polymorphism identified 19 different alleles, ranging from 262 to 308 bp in length, but no allele was significantly associated with the disease. CONCLUSIONS: Our results did not show any evidence of association of any of the CTLA4 gene polymorphisms with the disease. This might result from population-specific differences in genetic and environmental susceptibility to AD.

Importancia de la genética en pediatría. A propósito de la diabetes / Importance of genetics in pediatrics. Based on diabetes

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[Modulation of P-fimbriation by ciprofloxacin in uropathogenic Escherichia coli]. / Modulación de la fimbriación P por ciprofloxacina en Escherichia coli uropatógena.

BACKGROUND: The aim of this study was to determine the effect of ciprofloxacin at subinhibitory concentrations on the expression of P fimbriae of uropathogenic Escherichia coli. Thirty-nine strains of Escherichia coli isolated from out patients with urinary tract infection were studied. Thirty-nine of these strains had been previously characterized as P-fimbriated and the remaining non fimbriated strain was used as a negative control. METHODS: Fimbriation was quantitatively studied by electron microscope observation of the strains before and after treatment. To determine possible qualitative variations in the fimbrial proteins and in the external membrane (OMPs), extraction and electrophoretic separation was performed in polyacrylamide gels. RESULTS: No qualitative differences were observed in the OMPs profile and fimbrial proteins induced by ciprofloxacin in any of the strains studied. However, electron microscopic observation generally showed a decrease in the percentage fimbriated bacterial cells by the antimicrobial effect. CONCLUSIONS: The mechanism of action of ciprofloxacin at subinhibitory doses may correspond to a process of fimbrial protein synthesis inhibition secondary to the initiation of general repair mechanism of the cell exposed to the antimicrobial and not to a process of specific mutations which qualitatively affect fimbrial protein composition.