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One of these additional aberrations was in a region of prognostic importance in MM and was confirmed using FISH. However, risk stratification in these particular cases was unaffected. Thus, a perfectly concordant prognostication between array-CGH and LDS was observed. This validates LDS as a novel and cost-efficient tool for the detection of CNAs in MM. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.Close contact was first identified as the primary route of transmission for most respiratory infections in the early 20th century. In this review, we synthesize the existing understanding of the mechanisms of close contact transmission. We focus on two issues the mechanism of transmission in close contact, namely the transmission of the expired particles between two people, and the physical parameters of close contact that affect the exposure of particles from one individual to another, or how the nature of close contact plays a role in transmission. We propose the existence of three sub-routes of transmission short-range airborne, large droplets, and immediate body-surface contact. We also distinguish a "body contact," which is defined with an interpersonal distance of zero, from a close contact. We demonstrate herein that the short-range airborne sub-route may be most common. The timescales over which data should be collected to assess the transmission risk during close contact events are much shorter than those required for the distant airborne or fomite routes. The current paucity of high-resolution data over short distances and timescales makes it very difficult to assess the risk of infection in these circumstances. © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.When two or more bacterial species inhabit a shared niche, often, they must compete for limited nutrients. Iron is an essential nutrient that is especially scarce in the marine environment. Bacteria can use the production, release, and re-uptake of siderophores, small molecule iron chelators, to scavenge iron. Siderophores provide fitness advantages to species that employ them by enhancing iron acquisition, and moreover, by denying iron to competitors incapable of using the siderophore-iron complex. Here, we show that cell-free culture fluids from the marine bacterium Vibrio fischeri ES114 prevent growth of other vibrio species. Mutagenesis reveals the aerobactin siderophore as the inhibitor. Our analysis reveals a gene, that we name aerE, encodes the aerobactin exporter, and LuxT is a transcriptional activator of aerobactin production. In co-culture, under iron-limiting conditions, aerobactin production allows V. fischeri ES114 to competitively exclude Vibrio harveyi, which does not possess aerobactin production and uptake genes. By contrast, V. fischeri ES114 mutants incapable of aerobactin production lose in competition with V. harveyi. Introduction of iutA, encoding the aerobactin receptor, together with fhuCDB, encoding the aerobactin importer are sufficient to convert V. harveyi into an "aerobactin cheater". This article is protected by copyright. All rights reserved.OBJECTIVE Systemic aminoglycosides remain a cornerstone of treatment for Cystic Fibrosis (CF) pulmonary exacerbations (PEx); however, the impact of aminoglycoside pharmacokinetics (PK) on outcomes is not well defined in adult CF patients. Our objective was to assess the impact of increasing PK exposures on the clinical outcomes of PEx treatment in adult CF patients receiving high-dose and standard-dose extended-interval aminoglycosides. METHODS We conducted a retrospective study of adult CF patients treated with an intravenous aminoglycoside for a PEx. Serum amikacin, gentamicin, and tobramycin levels and FEV1 data were used to evaluate exposure-response relationships. PK parameters were estimated using a Bayesian approach to obtain AUC0-24hr , Cmax0-24hr , Cmin0-24hr estimates. The primary efficacy endpoint was a 90% recovery of baseline FEV1 by 30 days post-treatment. Toxicity included signs or symptoms of ototoxicity, vestibular, or renal toxicity. Multivariate linear mixed-effects models of FEV1 were usedtrategies for this population. This article is protected by copyright. All rights reserved.BACKGROUND Torsade de pointes is a form of polymorphic ventricular tachycardia associated with heart rate-corrected QT (QTc ) interval prolongation. With approximately 24-61% of critically ill patients experiencing QTc interval prolongation, a predictive tool to identify high-risk patients could assist in monitoring and management in the intensive care unit (ICU). The Tisdale et al. Risk Score (TRS) is a predictive tool that was developed and validated in a Cardiac Critical Care Unit. OBJECTIVES The objective of this study was to evaluate the predictive validity (sensitivity and specificity) and likelihood ratios of the TRS in a medical ICU. METHODS This was a longitudinal, retrospective, cohort study of consecutive patients who met the inclusion criteria from October 2017 to June 2018 with a sample size of 264 patients. The sample size was derived based on the number of TRS covariates and an exploratory variable. Baseline characteristics and risk factors were documented from electronic health records. The first occurrence of QTc interval prolongation, defined as a QTc interval >500ms or an increase ≥60ms above baseline, was the primary endpoint. Main Results The sensitivity and specificity of the TRS for low-risk patients against the moderate-risk and high-risk patients were 97% (95% CI 91-99%) and 16% (95% CI 11-23%), respectively. These results corresponded to a positive likelihood ratio of 1.15 (95% CI 1.07-1.24) and a negative likelihood ratio of 0.20 (95% CI 0.06-0.65). CONCLUSIONS In this study, the TRS showed high sensitivity, making it useful in identifying patients at low risk of QTc interval prolongation. However, the low specificity of the TRS suggests that it should not be used to identify patients at moderate or high risk of QTc interval prolongation. Future studies should explore a tool with improved specificity in critically ill patients to identify and manage those at risk of QTc interval prolongation. This article is protected by copyright. GX15-070 nmr All rights reserved.BACKGROUND Liver transplant (LT) presents early complications, such as allograft dysfunction and acute kidney injury, which contribute significantly to morbidity and mortality. High mobility group box 1 protein (HMGB1) has been identified as mediator in ischemia-reperfusion injury. Nucleosomes are complexes formed by DNA and histone proteins, and histones contribute to organ failure and death during sepsis. METHODS HMGB1 and nucleosome plasma levels were measured, by enzyme-linked immunosorbent assays, during LT and in the first 48 post-operative hours in 22 LT patients. The association between HMGB1 and nucleosome levels and the complications and survival within 6 months after LT were investigated. RESULTS We observed peak HMGB1 and nucleosome levels after graft reperfusion. HMGB1 and nucleosome levels were associated with the occurrence of acute kidney injury, early allograft dysfunction and early survival after LT. Nucleosome levels after graft reperfusion were associated with the occurrence of systemic inflammatory response syndrome. CONCLUSIONS HMGB1 and nucleosome levels increased after liver reperfusion in human LT setting and were associated with early complications and survival. New studies are necessary to explore their role as early markers of hepatocellular injury in human LT and the risk of graft and organs dysfunction and death. This article is protected by copyright. All rights reserved.To become a good doctor, medical students are required to continuously improve their performance. That performance is systematically monitored and those who are not able to achieve professional standards can be dismissed from medical school. What if the standards themselves, however, cause students so much stress they cannot perform to their full capability? This article is protected by copyright. All rights reserved.The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has evolved into an emergent global pandemic. Coronavirus disease 2019 (COVID-19) can manifest on a spectrum of illness from mild disease to severe respiratory failure requiring intensive care unit (ICU) admission. As the incidence continues to rise at a rapid pace, critical care teams are faced with challenging treatment decisions. There is currently no widely accepted standard of care in the pharmacological management of patients with COVID-19. Urgent identification of potential treatment strategies is a priority. Therapies include novel agents available in clinical trials or through compassionate use, and other drugs, repurposed antiviral and immune modulating therapies. Many have demonstrated in vitro or in vivo potential against other viruses that are similar to SARS-CoV-2. Critically ill patients with COVID-19 have additional considerations related to adjustments for organ impairment and renal replacement therapies, complex lists of concurrent medications, limitations with drug administration and compatibility, and unique toxicities that should be evaluated when utilizing these therapies. The purpose of this review is to summarize practical considerations for pharmacotherapy in patients with COVID-19, with the intent of serving as a resource for health care providers at the forefront of clinical care during this pandemic. This article is protected by copyright. All rights reserved.Inclusion body myositis (IBM) is a disease with a poor prognosis and limited treatment options. This study aimed at exploring gene expression profile alterations, investigate the underlying mechanisms, and identify novel targets for IBM. We analyzed two microarray datasets (GSE39454 and GSE128470) derived from the Gene Expression Omnibus (GEO) database. The GEO2R tool was used to screen out differentially expressed genes (DEGs) between IBM and normal samples. Gene Ontology（GO）function and Kyoto Encyclopedia of Genes and Genomes（KEGG）pathway enrichment analysis were performed using the Database for Annotation, Visualization and Integrated Discovery to identify the pathways and functional annotation of DEGs. Finally, protein-protein interaction (PPI) networks were constructed using STRING and Cytoscape, in order to identify hub genes. A total of 144 up-regulated DEGs and 1 down-regulated DEG were identified. The GO enrichment analysis revealed that the immune response was the most significantly enriched term within the DEGs. The KEGG pathway analysis identified 22 significant pathways, the majority of which could be divided into the immune and infectious diseases. Following the construction of PPI networks, ten hub genes with high degrees of connectivity were picked out, namely PTPRC、IRF8、CCR5、VCAM1、HLA-DRA、TYROBP、C1QB、HLA-DRB1、CD74 and CXCL9. Our research hypothesizes that autoimmunity plays an irreplaceable role in the pathogenesis of IBM. The novel DEGs and pathways identified in this study may provide new insight into the underlying mechanisms of IBM at the molecular level. This article is protected by copyright. All rights reserved.
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