The Impact of a Post-Prescription Review and Feedback Antimicrobial Stewardship Program in Lebanon

Antimicrobial stewardship programs (ASPs) are effective means to optimize prescribing practices. They are under-utilized in the Middle East where many challenges exist for ASP implementation. We assessed the effectiveness of infectious disease physician-driven post-prescription review and feedback as an ASP in Lebanon. This prospective cohort study was conducted over an 18-month period in the medical, surgical, and intensive care units of a tertiary care hospital. It consisted of three phases: the baseline, intervention, and follow-up. There was a washout period of two months between each phase. Patients aged ≥16 years receiving 48 h of antibiotics were included. During the intervention phase, the AMS team reviewed antimicrobial use within 72 h post-prescription and gave alternate recommendations based on the guidelines for use. The acceptance of the recommendations was measured at 72 h. The primary outcome of the study was days of therapy per 1000 study patient days. A total of 328 patients were recruited in the baseline phase (August-October 2020), 467 patients in the intervention phase (January-June 2021), and 301 patients in the post-intervention phase (September-December 2021). The total days of therapy decreased from 11.46 during the baseline phase to 8.64 during the intervention phase (p \u3c 0.001). Intervention acceptance occurred 88.5% of the time. The infectious disease physician-driven implementation of an ASP was successful in reducing antibiotic utilization in an acute care setting in Lebanon

Clinical and functional impairment after nonoperative treatment of distal biceps ruptures

© 2018 Journal of Shoulder and Elbow Surgery Board of Trustees Background: Clinical and functional impairment after nonoperative treatment of distal biceps ruptures is not well understood. The goal of this study was to measure patients’ perceived disability, kinematic adjustment, and forearm supination power after nonoperative treatment of distal biceps ruptures. Methods: Fourteen individuals after nonoperative treatment of distal biceps ruptures were matched to a control group of 18 uninjured volunteers. Both groups prospectively completed the Disabilities of the Arm, Shoulder and Hand (DASH), Single Assessment Numerical Evaluation (SANE), and Biceps Disability Questionnaire. Both performed a new timed isotonic supination test that was designed to simulate activities of daily life. The isotonic torque dynamometer measures the supination arc, center of supination arc, torque, angular velocity, and power. Motion analysis quantifies forearm and shoulder contributions to the arc of supination. Results: The nonoperative treated group\u27s DASH (23.2 ± 10.3) and SANE (59.6 ± 16.2) scores demonstrated a clinical meaningful impairment. The control group showed no significant differences in kinematic values between dominant and nondominant arms (P =.854). The nonoperative biceps ruptured arms, compared with their uninjured arms, changed supination motion by decreasing the supination arc (P ≤.036), shifting the center of supination arc to a more pronated position (P ≤.030), and increasing the shoulder contribution to rotation (P ≤.001); despite this adaptation, their average corrected power of supination decreased by 47% (P =.001). Conclusion: Patients should understand that nonoperative treatment for distal biceps ruptures will result in varying degrees of functional loss as measured by the DASH, SANE, and Biceps Disability Questionnaire, change their supination kinematics during repetitive tasks, and that they will lose 47% of their supination power

RETRACTED: Clinical and functional impairment after nonoperative treatment of distal biceps ruptures (Journal of Shoulder and Elbow Surgery (2019) 28(4) (757–764), (S1058274618307079), (10.1016/j.jse.2018.09.017))

© 2019 Journal of Shoulder and Elbow Surgery Board of Trustees This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the corresponding author and the Human Research Protection Office of the University of Pittsburgh, in conjunction with the policies of their Institutional Review Board (IRB), because IRB Number PR 013110590 had not been granted at the University of Pittsburgh

Coronal Heating as Determined by the Solar Flare Frequency Distribution Obtained by Aggregating Case Studies

Flare frequency distributions represent a key approach to addressing one of the largest problems in solar and stellar physics: determining the mechanism that counter-intuitively heats coronae to temperatures that are orders of magnitude hotter than the corresponding photospheres. It is widely accepted that the magnetic field is responsible for the heating, but there are two competing mechanisms that could explain it: nanoflares or Alfv\'en waves. To date, neither can be directly observed. Nanoflares are, by definition, extremely small, but their aggregate energy release could represent a substantial heating mechanism, presuming they are sufficiently abundant. One way to test this presumption is via the flare frequency distribution, which describes how often flares of various energies occur. If the slope of the power law fitting the flare frequency distribution is above a critical threshold, $\alpha=2$ as established in prior literature, then there should be a sufficient abundance of nanoflares to explain coronal heating. We performed $>$600 case studies of solar flares, made possible by an unprecedented number of data analysts via three semesters of an undergraduate physics laboratory course. This allowed us to include two crucial, but nontrivial, analysis methods: pre-flare baseline subtraction and computation of the flare energy, which requires determining flare start and stop times. We aggregated the results of these analyses into a statistical study to determine that $\alpha = 1.63 \pm 0.03$. This is below the critical threshold, suggesting that Alfv\'en waves are an important driver of coronal heating.Comment: 1,002 authors, 14 pages, 4 figures, 3 tables, published by The Astrophysical Journal on 2023-05-09, volume 948, page 7

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease