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

Experimental investigation of time-dependent clear water scour around bridge pier due to a trapezoidal hydrograph

Environ. Water Resour. Inst. (EWRI) Am. Soc. Civ. Eng.World Environmental and Water Resources Congress 2012: Crossing Boundaries -- 20 May 2012 through 24 May 2012 -- Albuquerque, NM -- 92565Local scours around bridge piers influence their stabilities and play a key role in bridge failures. In this study, the local scours around a bridge pier resulting from unsteady flow are investigated. The experiments are carried out in a rectangular flume 80 cm wide and 18.6 m long by using uniform sediment with median diameter of 3.5 mm and geometric standard deviation of 1.4. The unsteady flow is generated by means of a trapezoidal hydrograph. The bridge pier with circular cross section has a diameter of 8 cm. The flow depth is monitored by ultrasonic sensors and the flow rate is measured by electromagnetic flow meter. The temporal variations of scour depth are measured indirectly, by placing Ultrasonic Velocity Profiler (UVP) transducers downward vertically. Three transducers of 4 MHz are located around the bridge pier. The local scours due to input hydrograph are obtained by registering the distances from the tip of the transducer to the top level of the sediment layer in the course of unsteady flow experiments. The temporal evolution of local scours as well as the final depths and configurations of the local scours are obtained. The experimental findings are interpreted in the light of present classical knowledge. This study constitutes the first part of the researches planned to investigate the time dependent local scours due to various trapezoidal hydrographs. Keywords: trapezoidal hydrograph, bridge pier, local scour, UVP, temporal evolution © ASCE 2012

Positive association of macrophage migration inhibitory factor gene-173G/C polymorphism with biliary atresia

WOS: 000234437900018PubMed ID: 16385258Background: Macrophage migration inhibitory factor (MIF) is a pleiotrophic lymphocyte and macrophage cytokine; it is likely to play an important role in innate immunity. Its expression was increased in several inflammatory diseases, and MIF gene polymorphisms have an effect on disease outcome and response to glucocorticoid treatment. Aim: To investigate the role of the 173G/C polymorphism of the MIF gene for susceptibility to biliary atresia (BA). Method: Between February 2002 and November 2004, 18 patients (mean age 1 +/- 0.4 years) diagnosed as having BA were studied. After informed consent, blood was collected, and DNA was obtained. MIF 173C/G polymorphism was detected using the polymerase chain reaction-restriction fragment length polymorphism based method. BA patients were compared with a group of chronic liver disease patients (CLD) (n = 36) and a group of unrelated healthy controls (n = 103). Results: MIF-173C allele frequency was significantly higher than both the CLD and healthy control groups (P = 0.03, odds ratio [OR] 4.4, 95% confidence interval [CI] 1.3-15.1; P = 0.000, OR 4.1, 95% CI 2.3-7.6, respectively). Univariate analysis showed that MIF-173G/C polymorphism was significantly associated with BA (for GC genotype, OR = 6, 95 % CI 2.8-11.5, P = 0.000). There was no significant correlation between pediatric end stage liver disease score and MIF genotypes both in BA and CLD groups. Conclusion: Our results suggest that the -173C allele of the MIF gene might be associated with the susceptibility to BA

Clinical significance of basal core promoter and precore mutations in chronic hepatitis B

WOS: 000251892800030PubMed ID: 18265656Background/Aims: The mutations in the basal core promoter and precore region of hepatitis B virus genome in hepatitis B e antigen-positive and -negative chronic hepatitis B patients have been described. The reports about their prevalence and clinical significance in the Mediterranean region where D is the predominant genotype, are very limited. Methodology: The serum samples were collected from 44 naive chronic hepatitis B patients. For detection of the mutations basal core promoter and precore regions of HBV genome were amplified and sequenced. Results: All samples were determined as genotype D. Before initiation of treatment basal core promoter mutations were found as 55% (11/20) and 46% (11/24) in HBeAg-positive and -negative patients, respectively (p > 0.5). HBeAg-negative samples were associated with precore mutations (G1896(A) and G1899(A)). Three of 20 (15%) patients of HBeAg-positive and seven of 24 (29%) of HBeAg-negative populations showed sustained response to therapy at the 24th month of initiation. Conclusions: The presence of precore stop codon mutant in those with sustained response was 89%, overall at the end of therapy. At initiation of therapy basal core promoter mutations were more common in non-responders than responders (65% vs. 20%; p < 0.001). While 23% of cases totally showing sustained response, absence of mutations in the basal core promoter region of hepatitis B virus genotype D may be related to sustained response in patients with chronic hepatitis B

Synthetic routes to manganese oxoborate and correlations between experimental parameters and properties

This study examines manganese oxoborate synthesis in three different routes and the role of process parameters on structure and morphology of the products. Borax or boric acid and simple manganese salts were used as raw materials. In this regard, the samples prepared by hydrothermal, solid-state, and solution combustion methods were characterized by powder X-ray diffraction (XRD), vibrational spectroscopy (FT-IR and Raman), thermal analysis (DSC and TGA), scanning and transmission electron microscopy (SEM and TEM), chemical analysis and BET surface area measurements. It was found that all three strategies yielded warwickite-type Mn2OBO3 nanoparticles, but with significant changes in morphology, size, and surface characteristics. The hydrothermal approach has proven to be a general approach for synthesizing manganese oxoborate nanorods at pH 7.5. Solution combustion technique appeared the most practical and promising not only as a time-saving route but also in the production of ca. 100 nm, quasi-spherical, mesoporous manganese oxoborate nanoparticles

Determination of intracellular Th1/Th2 type cytokines in lymphocytes of chronic hepatitis B patients treated with interferon-alpha

WOS: 000287286100011PubMed ID: 21331994Background/aims: Host-related immune factors in childhood chronic hepatitis B and change in the initial profile with interferon (IFN)-alpha treatment need to be clarified. Methods: Sixteen patients were included in the study, and 10 million units of IFN-alpha treatment 3 times per week for 6 months was initiated. Pre- and post-treatment percentages of interleukin (IL)-2 and IFN-gamma in CD4+ T cells were assessed to determine intracellular T helper cell 1 (Thl) type cytokine expression. Similarly, percentages of intracellular IL-2 and IFN-gamma were detected to verify cytotoxic T cell 1 (Tc1) type cytokine expression in CD8+ T cells. Percentages of Th2 and Tc2 type cytokine expression (IL-4 and IL-13) were determined in CD4+ and CD8+ T cells, respectively. Resuts: Six (50%) of these were evaluated as having no response and the other half with partial complete response. All patients had higher percentages of Th2 cells with respect to healthy controls pre-treatment. Tc percentages, both Tc1 and Tc2, were significantly different between these groups, being higher in the patient group. When values of the nonresponder group were compared with healthy controls, IL-4 expression was higher and the percentages of Th1 type cells were significantly low. IL-13 expression in Th2 and Tc2 cells decreased after 6 months of treatment in the unresponsive group. The decrease we observed in Th1 percentages with treatment, in the responsive group, may be due to Thl deposition shifting from the periphery to liver tissue, as reported before. Intracellular cytokine profiles of treatment responders and normal controls were not different. Results: This is the first study in children comparing baseline and post-treatment intracellular cytokine profiles with values in healthy controls

Plasma levels of thrombin activatable fibrinolysis inhibitor in normal and preeclamptic pregnant women.

To explain the pathogenesis of preeclampsia with coagulation induction or a defective fibrinolysis, various hemostatic parameters were studied and different treatment modalities targeting these parameters were evaluated. Considering the role of TAFI in down-regulation of fibrinolysis, in our study we have investigated whether TAFI contributes to impaired fibrinolysis in patient with preeclampsia