XSEDE Allocations Practices and Procedures V 1.0

This document covers the tasks and activities required to administer the XSEDE allocations process. The document focuses on the tasks and efforts required by XSEDE staff to translate, interpret and implement the XSEDE allocation policies and provide researchers with allocations on resources that will help them accomplish their science objectives. The goal for the XSEDE allocations process can be summarized as ensuring that the cyberinfrastructure portfolio is used as efficiently as possible to produce the best science outcomes. This documents the current procedures XSEDE uses in pursuit of that goal.National Science Foundation OCI-1053575Ope

Diagnosis of out-of-hospital cardiac arrest by Emergency Medical Dispatch : a diagnostic systematic review

Introduction Cardiac arrest is a time-sensitive condition requiring urgent intervention. Prompt and accurate recognition of cardiac arrest by emergency medical dispatchers at the time of the emergency call is a critical early step in cardiac arrest management allowing for initiation of dispatcher-assisted bystander CPR and appropriate and timely emergency response. The overall accuracy of dispatchers in recognizing cardiac arrest is not known. It is also not known if there are specific call characteristics that impact the ability to recognize cardiac arrest. Methods We performed a systematic review to examine dispatcher recognition of cardiac arrest as well as to identify call characteristics that may affect their ability to recognize cardiac arrest at the time of emergency call. We searched electronic databases for terms related to “emergency medical dispatcher”, “cardiac arrest’, and “diagnosis,” among others, with a focus on studies that allowed for calculating diagnostic test characteristics (e.g. sensitivity and specificity). The review was consistent with Grading of Recommendations, Assessment, Development and Evaluation (GRADE) method for evidence evaluation. Results We screened 2520 article titles, resulting in 47 studies included in this review. There was significant heterogeneity between studies with a high risk of bias in 18 of the 47 which precluded performing meta-analyses. The reported sensitivities for cardiac arrest recognition ranged from 0.46 to 0.98 whereas specificities ranged from 0.32 to 1.00. There were no obvious differences in diagnostic accuracy between different dispatching criteria/algorithms or with the level of education of dispatchers. Conclusion The sensitivity and specificity of cardiac arrest recognition at the time of emergency call varied across dispatch centres and did not appear to differ by dispatch algorithm/criteria used or education of the dispatcher, although comparisons were hampered by heterogeneity across studies. Future efforts should focus on ways to improve sensitivity of cardiac arrest recognition to optimize patient care and ensure appropriate and timely resource utilizatio

2019 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations

The International Liaison Committee on Resuscitation has initiated a continuous review of new, peer-reviewed, published cardiopulmonary resuscitation science. This is the third annual summary of the International Liaison Committee on Resuscitation International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. It addresses the most recent published resuscitation evidence reviewed by International Liaison Committee on Resuscitation Task Force science experts. This summary addresses the role of cardiac arrest centers and dispatcher-assisted cardiopulmonary resuscitation, the role of extracorporeal cardiopulmonary resuscitation in adults and children, vasopressors in adults, advanced airway interventions in adults and children, targeted temperature management in children after cardiac arrest, initial oxygen concentration during resuscitation of newborns, and interventions for presyncope by first aid providers. Members from 6 International Liaison Committee on Resuscitation task forces have assessed, discussed, and debated the certainty of the evidence on the basis of the Grading of Recommendations, Assessment, Development, and Evaluation criteria, and their statements include consensus treatment recommendations. Insights into the deliberations of the task forces are provided in the Justification and Evidence to Decision Framework Highlights sections. The task forces also listed priority knowledge gaps for further research

ACCESS Resource Allocation Marketplace and Platform Services (RAMPS) PY1 Annual Report

The Carnegie Mellon University led team provides Allocation Services as part of the NSF-funded Advanced Cyberinfrastructure Coordination Ecosystem: Services & Support (ACCESS) program. This report details the team's progress in Project Year 1 from May 1, 2022 to March 31, 2023 along with data related to the current status of the ACCESS ecosystem. </p

ACCESS Allocation Review Committee (AARC) Reviewer Manual

  This report details essential policies, processes, and context related to the review of allocation requests for national cyberinfrastructure resources available within the NSF-funded Advanced Cyberinfrastructure Coordination Ecosystem: Services & Support (ACCESS) program.  This manual is intended to help members of the ACCESS Allocation Review Committee (AARC) understand their role within ACCESS and within the broader allocation process, as well as help the research community understand how the AARC functions.</p

The selectivity and structural determinants of peptide antagonists at the CGRP receptor of rat, L6 myocytes

1. Potency orders were determined for a series of agonists and antagonists on the calcitonin gene-related peptide (CGRP) receptor of rat L6 myocytes. The agents tested were all shown to have been active against CGRP, amylin or adrenomedullin receptors. 2. AC187 had a pIC(50) of 6.8±0.10, making it 14 fold less potent as an antagonist than CGRP(8–37) (pIC(50), 7.95±0.14). Amyline(8–37) was equipotent to AC187 (pIC(50), 6.6±0.16) and CGRP(19–37) was 3 fold less potent than either (pIC(50), 6.1±0.24). 3. [Ala(11)]-CGRP(8–37) was 6 fold less potent than CGRP(8–37), (pIC(50), 7.13±0.14), whereas [Ala(18)]-CGRP(8–37) was approximately equipotent to CGRP(8–37) (pIC(50), 7.52±0.15). However, [Ala(11),Ala(18)]-CGRP(8–37) was over 300 fold less potent than CGRP(8–37) (pIC(50), 5.30±0.04). 4. [Tyr(0)]-CGRP(28–37), amylin(19–37) and adrenomedullin(22–52) were inactive as antagonists at concentrations of up to 1 μM. 5. Biotinyl-human α-CGRP was 150 fold less potent than human α-CGRP itself (EC(50) values of 48±17 nM and 0.31±0.13 nM, respectively). At 1 μM, [Cys(acetomethoxy)(2,7)]-CGRP was inactive as an agonist. 6. These results confirm a role for Arg(11) in maintaining the high affinity binding of CGRP(8–37). Arg(18) is of less direct significance for high affinity binding, but it may be important in maintaining the amphipathic nature of CGRP and its analogues

A mouse macrophage lipidome.

We report the lipidomic response of the murine macrophage RAW cell line to Kdo(2)-lipid A, the active component of an inflammatory lipopolysaccharide functioning as a selective TLR4 agonist and compactin, a statin inhibitor of cholesterol biosynthesis. Analyses of lipid molecular species by dynamic quantitative mass spectrometry and concomitant transcriptomic measurements define the lipidome and demonstrate immediate responses in fatty acid metabolism represented by increases in eicosanoid synthesis and delayed responses characterized by sphingolipid and sterol biosynthesis. Lipid remodeling of glycerolipids, glycerophospholipids, and prenols also take place, indicating that activation of the innate immune system by inflammatory mediators leads to alterations in a majority of mammalian lipid categories, including unanticipated effects of a statin drug. Our studies provide a systems-level view of lipid metabolism and reveal significant connections between lipid and cell signaling and biochemical pathways that contribute to innate immune responses and to pharmacological perturbations

A mouse macrophage lipidome.

We report the lipidomic response of the murine macrophage RAW cell line to Kdo(2)-lipid A, the active component of an inflammatory lipopolysaccharide functioning as a selective TLR4 agonist and compactin, a statin inhibitor of cholesterol biosynthesis. Analyses of lipid molecular species by dynamic quantitative mass spectrometry and concomitant transcriptomic measurements define the lipidome and demonstrate immediate responses in fatty acid metabolism represented by increases in eicosanoid synthesis and delayed responses characterized by sphingolipid and sterol biosynthesis. Lipid remodeling of glycerolipids, glycerophospholipids, and prenols also take place, indicating that activation of the innate immune system by inflammatory mediators leads to alterations in a majority of mammalian lipid categories, including unanticipated effects of a statin drug. Our studies provide a systems-level view of lipid metabolism and reveal significant connections between lipid and cell signaling and biochemical pathways that contribute to innate immune responses and to pharmacological perturbations