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Sökning: WFRF:(Ambrozaitis Arvydas)

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1.
  • Ambrozaitis, Arvydas, et al. (författare)
  • Hepatitis C in Lithuania: incidence, prevalence, risk factors and viral genotypes
  • 1995
  • Ingår i: Clinical and Diagnostic Virology. - : Elsevier BV. - 0928-0197. ; 4:4, s. 273-284
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The epidemiology of hepatitis C virus (HCV) infection has been studied in many countries. However, little is known about HCV infection in Lithuania, a Baltic country, that was part of the former Soviet Union. OBJECTIVES: The aim of this study was to determine and evaluate the etiology of acute viral hepatitis, the risk factors for acquiring HCV in comparison to hepatitis B virus (HBV), seroprevalence of anti-HCV among blood donors and risk groups of the population in Lithuania. The distribution of HCV genotypes from Lithuanian first-time blood donors was also assessed. STUDY DESIGN: Sera taken from clinical viral hepatitis patients, blood donors, risk groups of population were investigated serologically. Patients with acute viral hepatitis were interviewed to determine their risk factors for HCV and HBV. HCV genotyping was done by PCR using type specific primers. RESULTS: Acute hepatitis C accounted for 5.0-8.5% of reported viral hepatitis cases in adults in Vilnius. Of the acute hepatitis C cases, 37.0% was associated with blood transfusions before the implementation of screening of blood donors for anti-HCV and only 15.4% (2/13) after the screening was started. Anti-HCV was found in 2.2% of first-time blood donors, in 7.9% of commercial blood donors, in 13.9% of commercial blood plasma donors, in 48.3% of hemodialysis patients, in 29.4% of prisoners, in 9.4% of elderly nursing home residents, and in 7.9% of hemodialysis staff. The following distribution in genotypes were found: genotype 1b (54.3%), 3a (23.9%), 2a (10.9%) 2b (4.3%), 1a (0%), and double infection (6.5%). CONCLUSIONS: Lithuania is a country with a considerable hepatitis C problem.
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2.
  • Kalesinskas, Povilas, et al. (författare)
  • Reducing dental plaque formation and caries development : A review of current methods and implications for novel pharmaceuticals
  • 2014
  • Ingår i: Stomatologija. - : Odontologijos Studija. - 1392-6470. ; 16:2, s. 44-52
  • Tidskriftsartikel (refereegranskat)abstract
    • Dental caries remains one of the most prevalent human diseases due to uncontrolled increase of dietary sucrose consumption in modern society. Sucrose is metabolized by Streptococcus mutans and Streptococcus sobrinus to acids causing tooth decay. These streptococci produce glucosyltransferases (Gtfs) for synthesis of sticky glucan polymers from sucrose, which is important for biofilm formation on teeth. In order to reduce dental biofilm build-up and oral diseases it causes, one preventive measure could be blocking of Gtf synthesis. Therefore, aim of this study was to test antisense phosphorothioate oligodeoxyribonucleotide (PS-ODN) targeting simultaneously S. mutans gtfB, gtfC and S. sobrinus gtfI mRNAs in order to inhibit biofilm formation in vitro. Materials and methods. Mixed culture of S. mutans and S. sobrinus bacteria were grown anaerobically on glass slides inserted vertically in 24-well cell culture plates containing Todd Hewitt broth with sucrose and sterile saliva under exposure to antisense or missense PS-ODNs at final concentration of 10 microM. Untreated bacteria served as controls. After 24 h of incubation, glass slides were removed, air-dried and further used for quantitative evaluation of streptococci biofilm applying optical profilometry technique. Results. It was found that antisense PS-ODN significantly reduced biofilm surface roughness and thickness of mixed S. mutans and S. sobrinus culture suppressing the biofilm development by 1.5-fold overall in comparison to untreated and missense PS-ODN-treated bacteria. Conclusions. Data demonstrate that antisense PS-ODN considerably attenuate streptococci-induced biofilm build-up on glass slides, and might therefore significantly inhibit dental biofilm formation through simultaneous inactivation of bacterial gtf mRNAs.
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