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Data on surgical lung cancer cases were extracted from the German Federal Statistics on Diagnosis-related groups (DRG) and a possible association between hospital volume and surgical mortality was explored. All treatment cases documented between 2005 and 2015 with the main diagnosis of lung cancer (International Classification of Disease code C34) and the German Operations and Procedure Key (OPS) codes 5-323 to 5-328 for anatomical lung resections were analysed. The treatment cases were assigned to hospital groups, defined according to the number of procedures performed per year. The total number of anatomical lung resections for the diagnosis of lung cancer increased by 24 % from 9376 resections in 2005 to 11,614 resections in 2015. In 2015, 57 % of anatomical lung resections in patients with lung cancer were performed in 47 high volume centres (hospitals with ≥ 75 resections/year); the remaining 43 % of the resections were distributed among 271 hospitals performing fewer than 75 resections per year. In hospitals performing fewer than 25 procedures/year, hospital mortality was almost twice as high as in large centres with ≥ 75 resections per year (5.7 vs. 3.0 %, mean value 2005 to 2015). In summary, our data indicate that a small number of high-volume hospitals perform the major part of lung resections of lung cancer in Germany with better survival as compared to low-volume hospitals. Based on current nationwide data a clear association between hospital volume and surgical mortality could be demonstrated.Phenolic acids (caffeic acid, p-coumaric acid,) and carotenes (β-carotene, lycopene) were mixed in different ratios to investigate antioxidant interactions on H2O2-induced H9c2 cells with ezetimibe (inhibitor of carotenes membrane transporters). Cellular uptake of carotenes, expression of membrane transporters, reactive oxygen species (ROS), nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H dehydrogenase quinone1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC) were analyzed. Results revealed that phenolic acids increased cellular uptake of carotenes and expression of their membrane transporters. Combination groups contained more phenolic acids showed synergistic effects. I-BET151 inhibitor For example, β-carotene caffeic acid = 12 significantly suppressed the intracellular ROS (+EZT, 66.34 ± 51.53%) and enhanced the accumulation of nucleus-Nrf2 (+EZT, 30.23 ± 5.30) compared to the groups contained more β-carotene (+EZT, ROS 75.48 ± 2.55%, nucleus-Nrf2 19.48 ± 4.22). This study provided an implication of functional foods formulation and demonstrated that antioxidant synergism may due to the up-regulation of carotenes membrane transporters by phenolic acids.The distribution and prevalence of zoonotic pathogens infecting ixodid ticks in Western Europe have been extensively examined. However, data on ticks and tick-borne pathogens in Eastern Europe, particularly Ukraine are scarce. The objective of the current study was, therefore, to investigate the prevalence of Anaplasma phagocytophilum, Anaplasmataceae, Rickettsia spp., Babesia spp., Bartonella spp., and Borrelia burgdorferi sensu lato in engorged and questing ixodid ticks collected from five administrative regions (oblasts) of Ukraine, namely Chernivtsi, Khmelnytskyi, Kyiv, Ternopil, and Vinnytsia. The ticks were collected from both wild and domestic animals and from vegetation. Of 524 ixodid ticks collected, 3, 99, and 422 ticks were identified as Ixodes hexagonus, Ixodes ricinus, and Dermacentor reticulatus, respectively. DNA samples individually extracted from 168 questing and 354 engorged adult ticks were subjected to pathogen-specific PCR analyses. The mean prevalence in I. ricinus and D. reticulatus werublic health officials when diagnosing infections and when implementing measures to combat tick-borne diseases in Ukraine.FoxO1 is a crucial transcription factor involved in lipid metabolism in mouse liver through repressing a key regulator of lipogenesis, sterol regulatory element binding protein 1 (SREBP1). However, it remains elusive whether FoxO1 plays roles in the regulation of fatty acid metabolism during lactation in dairy goats. In this study, we aim to investigate the function of FoxO1 in goat mammary epithelial cells (GMECs). We found that the expression of FoxO1 is significantly upregulated during lactation compared with the dry period. FoxO1 knockdown enhanced the expression of genes related to de novo fatty acid synthesis (e.g., FASN, ELOVL6 and SCD1) and triacylglycerol (TAG) synthesis (e.g., DGAT2 and GPAM). Consistently, intracellular TAG was significantly increased in FoxO1 knockdown cells and reduced in FoxO1 overexpression cells. Immunofluorescence staining revealed that insulin suppresses FoxO1 transcription by promoting its nuclear export. Further, we found that FoxO1 inhibits insulin-induced SREBP1 promoter activities in GMECs. Moreover, FoxO1 suppresses SREBP1 transcription via the LXR response element (LXRE) and SREBP response element (SRE) located in the SREBP1 promoter. Our data reveal that FoxO1 plays critical roles in regulating the synthesis of the fatty acid and triacylglycerol (TAG) in GMECs.Tissue factor is highly expressed in sub-endothelial tissue. The extracellular allosteric disulfide bond Cys186-Cys209 of human tissue factor shows high evolutionary conservation and in vitro evidence suggests that it significantly contributes to tissue factor procoagulant activity. To investigate the role of this allosteric disulfide bond in vivo, we generated a C213G mutant tissue factor mouse by replacing Cys213 of the corresponding disulfide Cys190-Cys213 in murine tissue factor. A bleeding phenotype was prominent in homozygous C213G tissue factor mice. Pre-natal lethality of 1/3rd of homozygous offspring was observed between E9.5 and E14.5 associated with placental hemorrhages. After birth, homozygous mice suffered from bleedings in different organs and reduced survival. Homozygous C213G tissue factor male mice showed higher incidence of lung bleedings and lower survival rates than females. In both sexes, C213G mutation evoked a reduced protein expression (about 10-fold) and severely reduced pro-coagulant activity (about 1000-fold).