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Tiny research, big selections: the function regarding pilot/feasibility scientific studies in small technology along with premature scale-up regarding behavioral treatments.
OBJECTIVES To examine the impact of workplace injury on opioid dependence, abuse and overdose (opioid-related morbidity) and if severity of injury increases the hazard of these health effects. METHODS We used MarketScan databases to follow injured and propensity score matched non-injured workers, both without prior opioid-related diagnoses. Using a Cox proportional hazard model, we examined the impact of workplace injury on opioid-related morbidity. RESULTS The hazard of opioid-related morbidity for injured workers was 1.79 times than that of matched non-injured workers (95% CI 1.89 to 3.60). For medical-only and lost-time injured workers, it was respectively 1.54 (95% CI 1.02 to 2.32) and 2.91 (95% CI 1.75 to 4.84) times that of non-injured workers. CONCLUSIONS Reducing workplace injury or severity of workplace injury, as well as efforts to ensure appropriate opioid prescribing for injured workers, may help to reduce the societal costs of opioid use. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.Emergency edicine providers are responsible for ensuring the emergency department is staffed 24 hours a day. As such, providers must efficiently transition between day, swing and night shift on an almost weekly basis. There is no formal education in medical school or residency on how to approach the transition to and from night shift, remain alert and productive and maximise sleep during the day. There are a multitude of blogs and online sources discussing night shift, but few, if any, provide an evidence-based approach. This article will provide the top 10 evidence-based recommendations to increase sleep, maximise performance, decrease fatigue on shift and improve quality of life outside the workplace. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. selleck Published by BMJ.BACKGROUND Inflammation-related factors might give further insight into the pathophysiology of vessel wall inflammation and intracranial aneurysm (IA) rupture. One of these factors is the protein complex S100A8/A9, which is released by neutrophils, monocytes, and activated macrophages and is known for its role in cardiovascular disease. OBJECTIVE To determine if venous S100A8/A9 levels in patients with a ruptured IA (rIA) or unruptured IA (uIA) are elevated compared with a control group. Second, to assess differences between venous and intra-aneurysmal S100A8/A9 levels of rIA and uIA patients. METHODS A prospective case study was performed between June 2016 and May 2017 in patients harboring a ruptured or unruptured saccular IA. Primary outcome measures were individual S100A8/A9 serum concentrations as measured in venous and intra-aneurysmal blood samples during endovascular treatment. Venous serum S100A8/A9 concentrations from a healthy control group served as a reference. RESULTS We included 16 patients with either a rIA or uIA and 47 healthy controls. Venous S100A8/A9 concentrations were higher in aneurysm patients (rIA and uIA) than those of healthy controls (P≤0.001). S100A8/A9 concentrations were higher in intra-aneurysmal samples than in venous samples of rIA patients (P=0.011). This difference was not found in uIA patients (P=0.054). Intra-aneurysmal S100A8/A9 levels were higher in rIAs than in uIAs (P=0.04). CONCLUSIONS Venous S100A8/A9 levels are elevated in patients with both rIAs and uIAs compared with healthy controls and likely represents aneurysm wall inflammation. S100A8/A9 causes macrophage-induced inflammation and degeneration of the vessel wall which might explain higher intra-aneurysmal S100A8/A9 levels found in rIAs than in uIAs. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.BACKGROUND Pediatric subspecialists routinely provide procedural sedation outside the operating room. No large study has reported trends in outpatient pediatric procedural sedation. Our purpose in this study was to identify significant trends in outpatient procedural sedation using the Pediatric Sedation Research Consortium. METHODS Prospectively collected data from 2007 to 2018 were used for trending procedural sedation. Patient characteristics, medications, type of providers, serious adverse events, and interventions were reported. The Cochran-Armitage test for trend was used to explore the association between the year and a given characteristic. RESULTS A total of 432 842 sedation encounters were identified and divided into 3 4-year epochs (2007-2011, 2011-2014, and 2014-2018). There was a significant decrease in infants less then 3 months of age receiving procedural sedation (odds ratio = 0.97; 95% confidence interval, 0.96-0.98). A large increase was noticed in pediatric hospitalists providing procedural sedation (0.6%-9.5%; P less then .001); there was a decreasing trend in sedation by other providers who were not in emergency medicine, critical care, or anesthesiology (13.9%-3.9%; P less then .001). There was an increasing trend in the use of dexmedetomidine (6.3%-9.3%; P less then .001) and a decreasing trend in the use of chloral hydrate (6.3%-0.01%; P less then .001) and pentobarbital (7.3%-0.5%; P less then .001). Serious adverse events showed a nonsignificant increase overall (1.35%-1.75%). CONCLUSIONS We report an increase in pediatric hospitalists providing sedation and a significant decrease in the use of chloral hydrate and pentobarbital by providers. Further studies are required to see if sedation services decrease costs and optimize resource use. Copyright © 2020 by the American Academy of Pediatrics.CD8+ T cell-mediated immunity is critical for host defense against viruses and requires mitochondria-mediated type I IFN (IFN-I) signaling for optimal protection. Cyclophilin D (CypD) is a mitochondrial matrix protein that modulates the mitochondrial permeability transition pore, but its role in IFN-I signaling and CD8+ T cell responses to viral infection has not been previously explored. In this study, we demonstrate that CypD plays a critical extrinsic role in the survival of Ag-specific CD8+ T cell following acute viral infection with lymphocytic choriomeningitis virus in mice. CypD deficiency resulted in reduced IFN-I and increased CD8+ T cell death, resulting in a reduced antiviral CD8+ T cell response. In addition, CypD deficiency was associated with an increase in pathogen burden at an early time-point following infection. Furthermore, our data demonstrate that transfer of wild-type macrophages (expressing CypD) to CypD-deficient mice can partially restore CD8+ T cell responses. These results establish that CypD plays an extrinsic role in regulating optimal effector CD8+ T cell responses to viral infection.
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