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Coronary artery inflammation is a critical process in the pathogenesis of myocardial infarction (MI). The chemokine CCL5/RANTES (regulated upon activation, normal T cells expressed and secreted) is expressed in advanced atherosclerotic lesions. Functional polymorphisms of the RANTES gene can, therefore, be involved in the pathogenesis of coronary artery disease. We examined the association of polymorphisms in the RANTES gene with myocardial infarction in Slavonic populations of Czech and Russian origin. A total of 467 post-MI patients and 337 control subjects were genotyped for RANTES promoter G-403A (rs2107538) and intron 1.1 T/C (rs2280789) variants by PCR-SSP. Both RANTES genotypes and allele frequencies did not differ between case and control groups. Haplotype-based analysis also failed to reveal an association between MI and investigated markers. Strong linkage disequilibrium was detected between particular RANTES alleles. The data do not support an association between RANTES G-403A polymorphism and MI, as reported previously.

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The Werdnig-Hoffmann syndrome is an infantile form of hereditary spinal progressive muscle atrophy with an autosomal recessive mode of inheritance with a frequency of 1 per 10,000 population. The data on the complex ultramicroscopic study of the spinal cord and deltoid muscle of a clinical case of Verdnig-Hoffmann syndrome in a newborn male child who died at the age of 1 month are given. Rubella virus patterns of the RNA were isolated in serum and spinal cord tissue samples. Changes in the structure of the spinal cord and deltoid muscle are described. An ultrastructural study showed the presence of a virus in the tissue of the spinal cord and vascular endothelial cells of the muscle. In the tissue of the spinal cord against the destruction of neurons was detected rubella virus. Viral particles were localized both in the cytoplasm of preserved oligodendrocytes and diffusely in destructively altered tissue of the spinal cord. The number of cells in the spinal cord tissue was reduced, the structure of their mitochondria was disturbed, and vacuolization of the cytoplasm was detected. For myelin fibers there is inherent heterogeneity of the thickness of the membranes, uneven distribution, deformation of the contours, and variability of diameters. Myelin fibers stratified, fragmented, osmiophilia lost. In the study of muscle samples prevailed destructively modified muscle fibers. At the same time, against the background of an unevenly pronounced atrophy of muscle fibers, the reproduction of the rubella virus in the cytoplasm of capillary endotheliocytes and pericytes of muscle vessels was detected. The etiological role of the rubella virus in the onset of the clinical symptoms constituting spinal muscular atrophy syndrome as a variant of congenital rubella has been suggested. .