The COVID-19 pandemic has, in a matter of a few short months, drastically reshaped society around the world. Because of the growing perception of machine learning as a technology capable of addressing large problems at scale, machine learning applications have been seen as desirable interventions in mitigating the risks of the pandemic disease. However, machine learning, like many tools of technocratic governance, is deeply implicated in the social production and distribution of risk and the role of machine learning in the production of risk must be considered as engineers and other technologists develop tools for the current crisis. This paper describes the coupling of machine learning and the social production of risk, generally, and in pandemic responses specifically. It goes on to describe the role of risk management in the effort to institutionalize ethics in the technology industry and how such efforts can benefit from a deeper understanding of the social production of risk through machine learning.One in eight women develops invasive breast cancer in her lifetime. The frontline protection against this disease is mammography. While computer-assisted diagnosis algorithms have made great progress in generating reliable global predictions, few focus on simultaneously producing regions of interest (ROIs) for biopsy. Can we combine ROI-oriented algorithms with global classification of cancer status, which simultaneously highlight suspicious regions and optimize classification performance? Can the asymmetry of breasts be adopted in deep learning for finding lesions and classifying cancers? We answer the above questions by building deep-learning networks that identify masses and microcalcifications in paired mammograms, exclude false positives, and stepwisely improve performance of the model with asymmetric information regarding the breasts. This method achieved a co-leading place in the Digital Mammography DREAM Challenge for predicting breast cancer. We highlight here the importance of this dual-purpose process that simultaneously provides the locations of potential lesions in mammograms.Mitochondria modulate inflammatory processes in various model organisms, but it is unclear how much mitochondria regulate immune responses in human blood leukocytes. Here, we examine the effect of i) experimental perturbations of mitochondrial respiratory chain function, and ii) baseline inter-individual variation in leukocyte mitochondrial energy production capacity on stimulated cytokine release and glucocorticoid (GC) sensitivity. In a first cohort, whole blood from 20 healthy women and men was stimulated with increasing concentrations of the immune agonist lipopolysaccharide (LPS). Four inhibitors of mitochondrial respiratory chain Complexes I, III, IV, and V were used (LPS + Mito-Inhibitors) to acutely perturb mitochondrial function, GC sensitivity was quantified using the GC-mimetic dexamethasone (DEX) (LPS + DEX), and the resultant cytokine signatures mapped with a 20-cytokine array. Inhibiting mitochondrial respiration caused large inter-individual differences in LPS-stimulated IL-6 reactivity (Cohen'NF-α response. Respiratory chain .function, particularly Complex IV activity, was positively correlated with LPS-stimulated IL-6 levels (r = 0.45, p = 0.002). Overall, these data provide preliminary evidence that mitochondrial behavior modulates LPS-induced inflammatory cytokine signatures in human blood.Reporter cell lines based on human pluripotent stem cells (hPSCs) are highly desirable for studying differentiation, lineage tracing, and target cell selection. However, several technical bottlenecks, such as DNA transduction, low homology recombination rate (HDR), and single-cell cloning, have made this effort an arduous process in hPSCs. Here, we provide a step-by-step protocol and practical guide for generating reporter lines in hPSCs via CRISPR/Cas9-mediated HDR. We also elaborate on the process of generating a TBXT-GFP reporter line as an example.
  The current COVID 19 pandemic brings into sharp focus the global necessity of having sufficient numbers of nurses and the dire impacts of nursing shortages throughout health systems in many countries. In 2020 retaining skilled experienced nurses continues to be a major global challenge. The dominant and consistent concentration of workforce research to date has focused on attitudinal factors including job satisfaction and burnout and there is limited research on how organisational commitment in combination with job satisfaction and burnout may explain what keeps nurses in nursing.
 
  To measure how organisational commitment in combination with job satisfaction and burnout relate to the intention of Registered General Nurses' staying in nursing (ITSN).
 
  A quantitative descriptive design using a cross-sectional survey was utilised. A national postal survey of a representative sample of registered general nurses employed within the Republic of Ireland (ROI) health services was undertaken in 2010. A number of ering the increased nurse vacancy rates in many countries and the evident lack of resolution of the issues raised from this study.
 Results reveal the complex and multidimensional nature of ITSN with the majority of nurses having a strong intention to stay in nursing. Organisational commitment and low burnout represented predictors which are influential in nurses remaining in nursing throughout their career lifespan. These results remain relevant in 2020 particularly in light of the ongoing pandemic when retention and recruitment of skilled and experienced nurses to the workforce will be critical to the management of health care, considering the increased nurse vacancy rates in many countries and the evident lack of resolution of the issues raised from this study.
  Doxorubicin (DOXO) chemotherapy increases risk for cardiovascular disease in part by inducing endothelial dysfunction in conduit arteries.  https://www.selleckchem.com/products/bismuth-subnitrate.html  However, the mechanisms mediating DOXO-associated endothelial dysfunction in (intact) arteries and treatment strategies are not established.
 
  We tested the hypothesis that DOXO impairs endothelial function in conduit arteries via excessive mitochondrial reactive oxygen species (ROS) and that these effects could be prevented by treatment with a mitochondrial-targeted antioxidant (MitoQ).
 
  Endothelial function (endothelium-dependent dilation [EDD] to acetylcholine) and vascular mitochondrial ROS were assessed 4 weeks following administration (10 mg/kg intraperitoneal injection) of DOXO. A separate cohort of mice received chronic (4 weeks) oral supplementation with MitoQ (drinking water) for 4 weeks following DOXO.
 
  EDD in isolated pressurized carotid arteries was 55% lower 4 weeks following DOXO (peak EDD, DOXO 42 ± 7% vs. sham 94 ± 3%; p = 0.006). Vascular mitochondrial ROS was 52% higher and manganese (mitochondrial) superoxide dismutase was 70% lower after DOXO versus sham (p = 0.