Seroprevalence of coxiella burnetii in human and animal populations in türkiye: meta-analysis

This study aims to reveal Coxiella burnetii by examining the studies reporting Q fever seroprevalence in humans and animals in the last 25 years in Türkiye. In this study, based on PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), various databases were searched between January 1997 and October. 2022. A literature review was carried out using data analyses performed using the IBM SPSS Version 25.0 statistical package program and Comprehensive Meta-Analysis (CMA) program. Overall prevalence of C. burnetii in humans was 22.78% (95% CI: 16.43%-29.12%), overall prevalence in animals was 13.49% (95% CI: 10.04-16.93%) was detected. The mean prevalence of C. burnetii in sheep was 19.1%±10.88, 10.46±6.39% in cattle, 15.21±10.01% in studies including cattle and sheep together, 11.17±10.74 in cattle, sheep and goats, and 12.4%±1.15% in sheep and goats. As a result of this study, it was determined that the prevalence of Q fever in humans in Türkiye is high in those dealing with animals, women who had a miscarriage, and infertile individuals. Although it is known that this disease is seen in Türkiye, there are not enough case reports in the literature. Detailed studies on Q fever in humans and animals need to be conducted. Further studies are needed to evaluate Q fever risk factors and prevalence data together within the scope of One Health approach

The role of MRS in the differentiation of benign and malignant soft tissue and bone tumors

Objective: The aim of our study was to investigate the value of choline in the discrimination of benign and malignant soft tissue and bone tumors

Genotoxicity in rats treated with the antidiabetic agent, rosiglitazone

Rosiglitazone (RSG), a member of the thiazolidinedione class of antidiabetic agents, improves glycemic control by increasing insulin sensitivity. The therapeutic mode of action of RSG involves its activity as a highly selective and potent agonist for peroxisome proliferator-activated receptor-gamma. Although other drugs in this class have displayed unacceptable hepatotoxicity, RSG was approved for human use. The package insert indicates that RSG has minimal genotoxicity, but information on the genotoxicity of RSG is not available in the published literature. In this study, we used the single cell gel electrophoresis (SCGE)/Comet assay to investigate the DNA damage in peripheral blood and liver cells of rats treated with RSG. Sixteen male Sprague-Dawley rats were randomly distributed into four groups, and dosed daily by oral gavage with 0.0, 0.5, 1.0, and 2.0 mg/kg/day RSG. The rats dosed with 2.0 mg/kg/day RSG received an similar to 10-times the area under the curve concentration of the maximum recommended human daily dose. After 14 days of treatment, the rats were euthanized, and peripheral blood and liver were collected and. processed for the Comet assay. A dose-dependent increase in DNA damage (as assessed by % tail DNA and Olive Tail Moment) was observed in the hepatocytes of RSG-treated groups, with significant increases detected between rats treated with all the doses of RSG and the control, and between rats treated with different RSG doses (P < 0.05 - P < 0.0001). In contrast, DNA damage was detected in peripheral blood lymphocytes only in rats treated with the higher RSG doses (1.0 and 2 mg/kg/day). Taken together, the data indicate that RSG is able to induce primary DNA damage in rats, with greater damage being detected in liver cells than lymphocytes

Assessment of genotoxicity in rats treated with the antidiabetic agent, pioglitazone

Pioglitazone (PIO), a member of the thiazolidinedione class of antidiabetic agents, specifically targets insulin resistance. Drugs of this class act as ligands for the gamma subtype of the peroxisome proliferator-activated receptor. Although troglitazone, another drug in this class, displayed unacceptable hepatotoxicity, PIO was approved for human use by the U.S. Food and Drug Administration. To our knowledge, there are no published reports on the genotoxicity of PIO; however, the package insert indicates that it has minimal genotoxicity. In this study, we used the comet assay to investigate the DNA damage in the peripheral blood and liver cells of rats treated with PIO. Sixteen male Sprague-Dawley rats were randomly distributed into four groups, and dosed daily for 14 days by oral gavage with 0, 10, 20, and 40 mg/kg/day PIO. A dose-dependent increase in DNA damage, as assessed by % tail DNA, was observed in both hepatocytes and blood lymphocytes of the PIO-treated groups, with significant increases detected between the rats treated with all the doses of PIO and the control, and between the rats treated with different PIO doses (P < 0.005 to P < 0.0001). Treating nuclei from the exposed animals with an enzyme cocktail containing Fpg and Endonuclease III prior to performing the comet assay increased the level of DNA damage, which reflects oxidized purine and pyrimidine. Taken together, our data indicate that PIO is able to dose-dependently induce DNA damage in both the liver and blood lymphocytes of rats, which is partially due to the generation of oxidative lesions

Biological effects of tolerable level chronic boron intake on transcription factors

The mechanism of boron effect on human transcription and translation has not been fully understood. In the current study it was aimed to reveal the role of boron on the expression of certain transcription factors that play key roles in many cellular pathways on human subjects chronically exposed to low amounts of boron. The boron concentrations in drinking water samples were 1.57 +/- 0.06 mg/l for boron group while the corresponding value for the control group was 0.016 +/- 0.002 mg/l. RNA isolation was performed using PAX gene RNA kit on the blood samples from the subjects. The RNA was then reverse transcribed into cDNA and analyzed using the Human Transcription Factors RT2 Profiler (TM) PCR Arrays. While the boron amount in urine was detected as 3.56 +/- 1.47 mg/day in the boron group, it was 0.72 +/- 0.30 mg/day in the control group. Daily boron intake of the boron and control groups were calculated to be 6.98 +/- 3.39 and 1.18 +/- 0.41 mg/day, respectively. The expression levels of the transcription factor genes were compared between the boron and control groups and no statistically significant difference was detected (P > 0.05). The data suggest that boron, intake at 6.98 +/- 3.39 mg/day, which is the dose at which beneficial effects might be seen, does not result in toxicity at molecular level since the expression levels of transcription factors are not changed. Although boron intake over this level will seem to increase RNA synthesis, further examination of the topic is needed using new molecular epidemiological data. (C) 2016 Elsevier GmbH. All rights reserved