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EN
EPR spectroscopy was used to the examination of free radicals evolution in cancer G361 cells during photodynamic therapy. The cancer cells were cultured with photosensitizer ALA and irradiated with 635 nm light by laser. The number of cells was determined microscopically. The decrease in the cell number and the increase in free radicals, obtained for G361 cells cultured with ALA and irradiated with laser, were stronger than relevant changes for the cells which were only irradiated with laser. The studied melanotic cells susceptible for photodynamic therapy differ from the other melanotic SK human cancer cells by fast spin-lattice relaxation processes. Slow spin-lattice relaxation processes exist in the studied earlier non susceptible for photodynamic therapy SK cells.
EN
Utilizing animals as organ donors for humans may cause transmission of foreign species pathogens to the recipient. To minimize the risk of transmission of infectious diseases from animals to humans, the strategy of appropriate animal selection is being assessed. The aim of the selection of specific pathogen-free pigs was the differentiation of active viruses from latent ones in both the recipients and donors in search of the host gene expression profiles which would differentiate the beginning of transplant rejection from an active infection. Additionally, the researchers searched for gene profile expressions indicating the type of infection which would considerably reduce the time of detection, and the cause of disease in the recipient which would offer a better chance of a positive result of the surgery.
EN
Mutations in SCN5A lead to a broad spectrum of phenotypes, including the Long QT syndrome, Brugada syndrome, Idiopathic ventricular fibrillation (IVF), Sudden infant death syndrome (SIDS) (probably regarded as a form of LQT3), Sudden unexplained nocturnal death syndrome (SUNDS) and isolated progressive cardiac conduction defect (PCCD) (Lev-Lenegre disease). Brugada Syndrome (BS) is a form of idiopathic ventricular fibrillation characterized by the right bundle-branch block pattern and ST elevation (STE) in the right precordial leads of the ECG. Mutations of the cardiac sodium channel SCN5A cause the disorder, and an implantable cardioverter-defibrillator is often recommended for affected individuals. In this study sequences of the coding region of the SCN5A gene were analysed in patients with the LQT3, Brugada Syndrome and other arrythmogenic disorders. Different mSSCP patterns are described with no disease-related SSCP conformers in any sample. Direct sequencing of the SCN5A gene confirmed the absence of mutations. This suggests that the analysed region of the SCN5A gene is not commonly involved in the pathogenesis of the Brugada Syndrome and associated disorders.
EN
Paramagnetic centers in melanin existing in pigmented soil fungi Cladosporium cladosporioides cultured at acidic (4, 5, 6), neutral (7), and alkaline (8) pH were studied by EPR method. o-semiquinone free radicals (g: 2.0032-2.0040) concentration in melanin biopolymer increased for pH from 4 to 6, decreased at pH 7, and reached the maximum value at pH 8. It may be expected that melanin free radicals reactions with small molecules (metal ions, drugs) are the most effective at pH between 6 and 8. Slow spin-lattice relaxation processes exist in the all studied melanin samples.
EN
The long QT syndrome (LQTS) is a disorder of ventricular repolarization that exposes affected individuals to cardiac arrhythmias and sudden death. The first gene for LQTS has been mapped to chromosome 11 p.15.5 by genome-wide linkage analysis. This gene, originally named KVLQT1 (and later KCNQ1), is a novel potassium channel gene. Mutations in the human KVLQT1 gene, encoding the a-subunit of the KVLQT1 channel, cause the long QT syndrome. In this work, we analysed the sequence of six KVLQT1 exons in patients with various heart pathologies. We describe 6 different mSSCP patterns with no disease-related SSCP conformers in any sample. Direct sequencing of exons 2 to 7 confirmed the absence of mutations. This suggests that the analysed region of the KVLQT1 gene is not commonly involved in pathogenesis of the long QT syndrome.
EN
DOPA-melanin-dihydrostreptomycin complexes with drug concentrations 1×10^{-4}-1×10^{-2} M were examined by the use of electron paramagnetic resonance spectroscopy at X-band (9.3 GHz). Dihydrostreptomycin was chosen for studies, because this aminoglycoside antibiotic causes strong toxic effects in organism. It was stated that dihydrostreptomycin generates o-semiquinone free radicals with g=2.0038 in melanin. Free radicals formation increases with increase in the antibiotic concentration. Changes of EPR lines with microwave powers pointed out that slow spin-lattice relaxation processes exist in DOPA-melanin and in its complexes with dihydrostreptomycin. The measured EPR lines were homogeneously broadened.
EN
Familial hypertrophic cardiomyopathy has a complex multigenic background. Previous work allowed to determine one of the gene loci responsible for this disease on chromosome 14 band q11-q12, and linked it to the a and b-cardiac myosin heavy chains. In this study we demonstrate changes in exon 21, coding for b-myosin heavy chain. We described 4 patients from different families with an unequivocal diagnosis of hypetrophic cardiomyopathy based on the clinical picture. Direct sequencing of exon 21 revealed the presence of 5 novel mutations. Two of the mutations in codons 771 and 781 revealed in our study did not result in any changes in amino acid sequence. The next three were as follows: in codon 782 (AGC > GAC) transition responsible for Ser?Asp substitution; in codon 779 (GAG > TAG) mutation that results in replacement of Glu?Stop; in codon 774 (GAG > GTG) which is expressed as substitution of Glu?Val. These mutations are located close to mutations identified and described in the literature, so they are likely to cause similar sumptoms.
EN
Familial hypertrophic cardiomyopathy (FHC) is characterised by autosomal dominant transmission, left ventricular hypertrophy and myocardial disarray. Genetic assessment is of special importance in this disease. Missense mutations of the gene coding for the b-myosin heavy chain (bMHC) have been identified as statistically the most important cause of the disease. Identification of specific mutations may be difficult, thus a simpler method of disease carrier identification is needed. We performed haplotype analysis of six Polish families (47 individuals) with three microsatellite markers located at the bMHC locus. Linkage of the disease locus to the bMHC gene was excluded in 4 out of the 6 families analysed. In 2 families particular haplotypes were coinherited with the disease phenotype. Microsatellite markers allowed identification of 2 carriers of the disease gene in these families among children of the patients.
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