Identification of Candida species and investigating antifungal susceptibility in Turkey

WOS: 00020970400060

Repair of gaps opposite lesions by homologous recombination in mammalian cells

Damages in the DNA template inhibit the progression of replication, which may cause single-stranded gaps. Such situations can be tolerated by translesion DNA synthesis (TLS), or by homology-dependent repair (HDR), which is based on transfer or copying of the missing information from the replicated sister chromatid. Whereas it is well established that TLS plays an important role in DNA damage tolerance in mammalian cells, it is unknown whether HDR operates in this process. Using a newly developed plasmid-based assay that distinguishes between the three mechanisms of DNA damage tolerance, we found that mammalian cells can efficiently utilize HDR to repair DNA gaps opposite an abasic site or benzo[a]pyrene adduct. The majority of these events occurred by a physical strand transfer (homologous recombination repair; HRR), rather than a template switch mechanism. Furthermore, cells deficient in either the human RAD51 recombination protein or NBS1, but not Rad18, exhibited decreased gap repair through HDR, indicating a role for these proteins in DNA damage tolerance. To our knowledge, this is the first direct evidence of gap-lesion repair via HDR in mammalian cells, providing further molecular insight into the potential activity of HDR in overcoming replication obstacles and maintaining genome stability

Letter to the editor: Primary cardiac rhabdomyosarcoma

WOS: 000173435400022PubMed ID: 1181319

Comparison of antiviral effect of lamivudine with interferon-?2a versus -?2b in children with chronic hepatitis B infection

PubMed ID: 15040533Aim: To compare additive efficacy of combination therapy including interferon (IFN)-?2a+lamivudine (3TC) to IFN-?2b+3TC in children with chronic hepatitis B virus (HBV) infection. Material and methods: Chronic hepatitis B infection was determined by presence of HBsAg, HBeAg and HBV DNA in serum screened at 3 months intervals for at least 1 year, serum alanine transaminase (ALT) levels more than 1.5-times the upper normal limit and chronic hepatitis with histological activity index (HAI) more than 6 by liver biopsy. Sixty-three children with chronic hepatitis B infection were treated randomly with thrice-weekly subcutaneous injections of 5 MU/m2 recombinant IFN-?2a (n=29) or recombinant IFN-?2b (n=34) with the same dose, intervals for 6 months. Patients also received 3TC (4 mg/kg/day, max 100 mg/day) orally daily combined with IFN and continued for 12 months. End of therapy response was defined as ALT normalization, HBV DNA clearance and HBe/anti-HBe seroconversion. Breakthrough infection was determined as re-emergence of HBV DNA in serum after its clearance. Response rate, incidence of side effects and breakthrough infection were compared between IFN-?2a+3TC- and IFN-?2b+3TC-treated patients. Results: Response rate was 44.8% (n=13) with IFN-?2a+3TC and 47.1% (n=16) with IFN-?2b+3TC (P=1.0). No significant difference was found in respect to the DNA clearance (P=0.32), anti-HBe (P=1.0), anti-HBs (P=0.09) seroconversion and response rates (P=1.0) between the groups. Breakthrough infection was detected in 1 (3.4%) case on IFN-?2a and none of the cases on IFN-?2b (P=0.46). All of the patients experienced flu-like symptoms, malaise and fatigue; however, side effect interfering with therapy was not encountered. Conclusion: No significant difference was found in response rates achieved by combination therapies based on IFN-?2a and IFN-?2b. Clinical efficacy of 3TC and two different IFN subtypes was found similar