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As many as 50% of hospitalised patients are estimated to be malnourished or at risk of malnutrition on hospital admission, but this condition often goes unrecognised, undiagnosed and untreated. Malnutrition is associated with an elevated need for continued medical interventions, higher costs of care and increased patient safety risks. Tampa General Hospital (TGH), a large teaching hospital in the southeastern USA, initiated a project to improve the quality of patient care at its institution. They did this first by focusing on improving the care quality for their malnourished patients (or patients who were at risk of malnourishment) and by using elements of the national Malnutrition Quality Improvement Initiative (MQii) Toolkit as a mechanism to measure and improve quality. The aim of this study was to evaluate the impact of quality improvement interventions on patient length of stay (LOS), infection rates and readmissions, particularly for malnourished patients. The structure of the MQii and the use of the MQand a 35.7% reduction in infection rates (from 14% to 9%, p less then 0.01). No statistically significant changes in readmission rates were observed. This study adds to a growing body of literature on quality improvement processes hospitals can undertake to better identify and treat malnourished patients. Hospitals and health systems can benefit from adopting similar institution-wide, quality improvement projects, while policy-makers’ support for such programmes can spur more rapid uptake of nutrition-focused initiatives across care delivery settings. © Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.Bone loss in response to alcohol intake has previously been hypothesized to be mediated by excessive production of reactive oxygen species (ROS) via NADPH oxidase (Nox) enzymes. Nox4 is one of several Nox enzymes expressed in bone. We investigated the role of Nox4 in the chondro-osteoblastic lineage of the long bones in mice during normal chow feeding and during chronic ethanol feeding for 90 days. We generated mice with a genotype (PrxCre +/- Nox4 fl/fl) allowing conditional knockout of Nox4 in the limb bud mesenchyme. Adult mice had 95% knockdown of Nox4 expression in the femoral shafts. For mice on regular chow, only whole-body Nox4 knockout mice had clearly increased cortical thickness and bone mineral density in the tibiae. When chronically fed a liquid diet with and without ethanol, conditional Nox4 knockout mice had slightly reduced dimensions of the cortical and trabecular regions of the tibiae (P less then 0.1). The ethanol diet caused a significant reduction in cortical bone area and cortical thiccs.Colonies of valuable inbred and transgenic laboratory-reared Xenopus frogs maintained for research constitute naïve populations of animals susceptible to some opportunistic infectious diseases. Therefore, it is prudent to characterize any new animal acquisitions before introduction into an existing colony as a biosecurity measure to preclude the concurrent introduction of an infectious microorganism associated with the new animal(s). In addition, some pathogens of Xenopus, such as Chlamydia and Mycobacterium spp, are zoonotic diseases, placing frog aquarists at risk for acquiring an infection. Because it is not cost effective to test for all diseases of Xenopus frogs, we have defined a subset of prevalent infectious microorganisms and developed TaqMan polymerase chain reaction (PCR) assays to detect these agents. The specific pathogens in our test panel were selected from relatively recent publications where they reportedly caused morbidity and/or mortality in Xenopus laevis and/or X. tropicalis The assays herein do not constitute a comprehensive list of infectious diseases of Xenopus frogs. Therefore, a frog devoid of the infectious agents in our test panel are characterized as “specific pathogen-free.” Three of the described quantitative polymerase chain reaction (qPCR) assays detect many species within their genus (i.e., qPCRs for ranaviruses, Chlamydia spp, and Cryptosporidia spp). © 2020 Cold Spring Harbor Laboratory Press.BRCA1 gene mutations impair homologous recombination (HR) DNA repair, resulting in cellular senescence and embryonic lethality in mice. Therefore, BRCA1-deficient cancers require adaptations that prevent excessive genomic alterations from triggering cell death. RNF168-mediated ubiquitination of γH2AX at K13/15 (ub-H2AX) serves as a recruitment module for the localization of 53BP1 to DNA break sites. Here, we found multiple BRCA1 mutant cancer cell lines and primary tumors with low levels of RNF168 protein expression. Overexpression of ectopic RNF168 or a ub-H2AX fusion protein induced cell death and delayed BRCA1 mutant tumor formation. Cell death resulted from the recruitment of 53BP1 to DNA break sites and inhibition of DNA end resection. Strikingly, re-introduction of BRCA1 or 53BP1 depletion restored HR and rescued the ability of cells to maintain RNF168 and ub-H2AX overexpression. Thus, downregulation of RNF168 protein expression is a mechanism for providing BRCA1 null cancer cell lines with a residual level of HR that is essential for viability. Overall, our work identifies loss of RNF168 ubiquitin signaling as a proteomic alteration that supports BRCA1 mutant carcinogenesis. We propose that restoring RNF168-ub-H2AX signaling, potentially through inhibition of de-ubiquitinases, could represent a new therapeutic approach. Copyright ©2020, American Association for Cancer Research.Obesity is associated with increased risk of many types of cancer and can be induced by various high-fat diets (HFD) from different fat sources. It remains unknown whether fatty acid composition in different HFD influences obesity-associated tumor development. Here we report that consumption of either a cocoa butter or fish oil HFD induced similar obesity in mouse models. selleck kinase inhibitor While obesity induced by the cocoa butter HFD was associated with accelerated mammary tumor growth, consumption of the fish oil HFD uncoupled obesity from increased mammary tumor growth and exhibited a decrease in pro-tumor macrophages. Compared to FA components in both HFD, n-3 FA rich in the fish oil HFD induced significant production of reactive oxygen species (ROS) and macrophage death. Moreover, A-FABP expression in the pro-tumor macrophages facilitated intracellular transportation of n-3 FA and oxidation of mitochondrial FA. A-FABP deficiency diminished n-3 FA-mediated ROS production and macrophage death in vitro and in vivo. Together, our results demonstrate a novel mechanism by which n-3 FA induce ROS-mediated pro-tumor macrophage death in an A-FABP dependent manner.