Margarita Laczeski has been graduated from National University of Misiones of Biochemistry. She holds a PhD in biochemistry from the National University of Tucuman specializing in bacteriology. She is currently professor and researcher at the National University of Misiones with an interest in microbiology, molecular biology techniques and biotechnology.
Streptococcus agalactiae (GBS) is the leading cause of severe invasive infections in infants less than three months. Meningitis, pneumonia and sepsis are the leading cadres in these children. Infection is primarily acquired vertically from mothers colonized with GBS. GBS has many virulence factors, the capsular polysaccharide is one of the most important and are associated with different surface proteins of antigenic characteristics, such as α, β, Rib, HylB, Lmb, C5a peptidase, FbsA, FbsB and CylB which are encoded by several genes associated with virulence and host interaction acting on bacteria involved in invasiveness. The study of surface protein antigens is important for the understanding of the pathogenesis and epidemiology of infection and several these antigens have been proposed as components of multivalent conjugate vaccines. This study was carried out in order to study the molecular profiles of virulence in GBS strains. Two hundred isolates of vaginal swabs from pregnant women from Misiones (Argentina), were studied. Virulence genes those encoding: C protein (bac and bca), Rib protein (rib), laminin (lmb), hyaluronidase (hylB), c5a-peptidase (scpB), FbsA and FbsB protein (fbsA and fbsB) and β-hemolysin (cylB), were investigated by conventional PCR. Virulence genes were simultaneously identified in 73 isolates (36.5%). fbsA, fbsB and cspB genes were detected at 100% of the strains. Other genes studied were detected in these frequencies: cylB (95%), lmb (94%), bca (87,5%), rib (85,3%), hylB (81%) and bac (58%). The high frequency of detection of fbsA, fbsB and cspB genes, suggesting assessment of their inclusion in future vaccines.
Merab Beraia has been graduated from Tbilisi State Medical University in 1986, as a Medical Doctor, with the specialty of Internal Medicine and took a Diploma in Neurology from the Institute of Clinical and Experimental Neurology Tblisi, Georgia. Later he obtained his post-graduation diploma in Radiology from University of Graz, Austria and then started working at The Institute of Clinical Medicine Tbilisi, Georgia, where he has continued his research. Presently he is working at the Tbilisi.
Objectives: To study the arterial blood flow with the MRI and CT and initial factors of atherosclerosis. \r\nMethods: In 17 healthy volunteers (18-52y) at the different sites of the aorta peak velocity, net flow, flow acceleration and blood density (in Hounsfield) has been investigated. \r\nResults: At the outer curvature of the aorta in the end systole flow separates. At the isthmus, flow acceleration in the initial diastole is 11.6±0.6 times higher than that in systole. Net flow from systole to diastole increases 2.5±0.5 folds. From the end systole to the initial diastole there is a plateau on the net flow graph: here, at the outer curvature of the isthmus, group waves at the boundary reflection, changes in phase at 1800 at the sine wave oscillation frequencies -1.25Hz and 2.5Hz. Blood density, from the aortic isthmus, to the abdominal aorta, equals to -51±3HU to- 31±4HU respectively. \r\nConclusion: Pulse pressure propagating in the blood and the vessel wall, at the boundary layer, forms surface wave. Blood is viscoelastic substance. At the outer wall isthmus of the aorta and all arterial branching sites, pulse pressure, at the reflection is in resonance with the end systolic pressure drop and amplitude of the wall stress increases. In the end of systole, at the outer wall of the circular flow sites, wave packets with the different frequencies forms - flow separates. Wave packets at the frequency dispersion, destroys the flow cell aggregates increasing the blood entropy, whereas at the boundary layer of the vessel, denudate the endothelial sheet.\r\n