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When 2018 is compared with 2017 in term of soil loss, in the amended plots, 2018 reduced soil loss by 7.4, 20, and 73.5%, respectively, for 10, 20, and 30 t ha-1biochar, whereas there was an increase of 2.7% soil loss in the control plot in 2018 compared with 2017. Therefore, application rate of 30 t ha-1 biochar is considered as suitable for severely degraded soil because this application rate efficiently improves cocoyam yield and soil properties and reduces soil loss. Copyright © 2020 Aruna Olasekan Adekiya et al.In this study, using new approach (laser diffraction + biological dyes), we have demonstrated the decrease of cells viability in vitro in the deuterated growth medium, whereas in the deuterium-depleted medium, there was an increase of cell viability. We have also found that not all dyes are equally sensitive to the D/H ratios in the culture medium (system) as well as to the different cell types (cancer vs normal cells). Copyright © 2020 I. A. Zlatskiy et al.Eddy Correlation (EC) is a technique that can be used to measure transport of substances in aquatic ecosystems between bottom sediments and the overlying water (i.e. benthic fluxes). Based on high-speed, simultaneous, and co-located velocity and concentration measurements, EC has been successfully used in a variety of freshwater and marine settings to determine benthic fluxes of dissolved oxygen. Application to a larger range of compounds is limited, however, by the lack of suitable chemical sensors. Here, we describe FACT, a novel, high-speed, multi-function sensor created to expand the range of benthic fluxes that can be measured with EC. An optical fiber spectrofluorometer with a proximally located conductivity cell and thermistor, FACT enables benthic flux measurements of fluorescing compounds, such as fluorescent dissolved organic matter, as well as of heat and salinity which can be used as tracers for submarine groundwater discharge. The high bandwidth and open-beam geometry of the fluorescence sensor are particularly beneficial for EC measurements. FACT was integrated with a velocity sensor into a full EC system capable of simultaneous benthic flux measurements of fluorescing compounds, heat, and salinity. Tested in a laboratory tank, fluxes measured by all three sensors were found to track each other as well as compare favorably with expected values. Furthermore, the ability to measure fluxes of multiple substances both extends the applicability of EC to a wider range of natural sites, and can provide insight into issues of sensing volume and time responses as they affect the application of EC to natural waters.In this paper, we propose a novel and simple method for discovery of Granger causality from noisy time series using Gaussian processes. More specifically, we adopt the concept of Granger causality, but instead of using autoregressive models for establishing it, we work with Gaussian processes. We show that information about the Granger causality is encoded in the hyper-parameters of the used Gaussian processes. The proposed approach is first validated on simulated data, and then used for understanding the interaction between fetal heart rate and uterine activity in the last two hours before delivery and of interest in obstetrics. Our results indicate that uterine activity affects fetal heart rate, which agrees with recent clinical studies.Background Estrogen sulfotransferase catalyzes conjugation of sulfuryl-group to estradiol/estrone and regulates E2 availability/activity via estrogen-receptor or non-receptor mediated pathways. Sulfoconjugated estrogen fails to bind estrogen-receptor (ER). High estrogen is a known carcinogen in postmenopausal women. Reports reveal a potential redox-regulation of hSULT1E1/E2-signalling. Further, oxidatively-regulated nuclear-receptor-factor 2 (Nrf2) and NFκβ in relation to hSULT1E1/E2 could be therapeutic-target via cellular redox-modification. Methods Here, oxidative stress-regulated SULT1E1-expression was analyzed in human breast carcinoma-tissues and in rat xenografted with human breast-tumor. Selleck CPI-203 Tumor and its surrounding tissues were obtained from the district-hospital. Intracellular redox-environment of tumors was screened with some in vitro studies. RT-PCR and western blotting was done for SULT1E1 expression. Immunohistochemistry was performed to analyze SULT1E1/Nrf2/NFκβ localization. Tissue-histoarchitecture/DNA-stability (comet assay) studies were done. Results Oxidative-stress induces SULT1E1 via Nrf2/NFκβ cooperatively in tumor-pathogenesis to maintain the required proliferative-state under enriched E2-environment. Higher malondialdehyde/non-protein-soluble-thiol with increased superoxide-dismutase/glutathione-peroxidase/catalase activities was noticed. SULT1E1 expression and E2-level were increased in tumor-tissue compared to their corresponding surrounding-tissues. Conclusions It may be concluded that tumors maintain a sustainable oxidative-stress through impaired antioxidants as compared to the surrounding. Liver-tissues from xenografted rat manifested similar E2/antioxidant dysregulations favoring pre-tumorogenic environment. © The Author(s) 2020.Background Glucose metabolic reprogramming is a significant hallmark of malignant tumors including GBM. Previous studies suggest that microRNAs play key roles in modulating this process in GBM cells. miR-181b acts as a tumor suppressor miRNA in influencing glioma tumorigenesis. Our previous results showed that miR-181b was down-regulated in glioma cells and tissues. Methods The extracellular acidification rate (ECAR), colony formation assay and levels of Glut1 and PKM2 were measured to assess the glucose metabolic and proliferation changes in GBM cells overexpressing miR-181b. Immunoblotting and luciferase reporter assay were performed to confirm the expression and role of SP1 as a direct target of miR-181b. ChIP assay was used to figure out the transcriptional regulation of SP1 on Glut1 and PKM2. In vivo study was examined for the role of miR-181b in GBM cells. Results MiR-181b overexpression significantly reduced the glucose metabolic and colony formation ability of GBM cells. And, SP1 was confirmed as a direct target of miR-181b while upregulation of SP1 could reverse the influence of overexpression of miR-181b.

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