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Träfflista för sökning "WFRF:(Bridges P) srt2:(2020-2021)"

Sökning: WFRF:(Bridges P) > (2020-2021)

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1.
  • 2021
  • swepub:Mat__t
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2.
  • Thoma, B, et al. (författare)
  • An international, interprofessional investigation of the self-reported podcast listening habits of emergency clinicians: A METRIQ Study
  • 2020
  • Ingår i: CJEM. - : Springer Science and Business Media LLC. - 1481-8043 .- 1481-8035. ; 22:1, s. 112-117
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectivesPodcasts are increasingly being used for medical education. A deeper understanding of usage patterns would inform both producers and researchers of medical podcasts. We aimed to determine how and why podcasts are used by emergency medicine and critical care clinicians.MethodsAn international interprofessional sample (medical students, residents, physicians, nurses, physician assistants, and paramedics) was recruited through direct contact and a multimodal social media (Twitter and Facebook) campaign. Each participant completed a survey outlining how and why they utilize medical podcasts. Recruitment materials included an infographic and study website.Results390 participants from 33 countries and 4 professions (medicine, nursing, paramedicine, physician assistant) completed the survey. Participants most frequently listened to medical podcasts to review new literature (75.8%), learn core material (75.1%), and refresh memory (71.8%). The majority (62.6%) were aware of the ability to listen at increased speeds, but most (76.9%) listened at 1.0 x (normal) speed. All but 25 (6.4%) participants concurrently performed other tasks while listening. Driving (72.3%), exercising (39.7%), and completing chores (39.2%) were the most common. A minority of participants used active learning techniques such as pausing, rewinding, and replaying segments of the podcast. Very few listened to podcasts multiple times.ConclusionsAn international cohort of emergency clinicians use medical podcasts predominantly for learning. Their listening habits (rarely employing active learning strategies and frequently performing concurrent tasks) may not support this goal. Further exploration of the impact of these activities on learning from podcasts is warranted.
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3.
  • Bridges, Hannah R., et al. (författare)
  • Structure of inhibitor-bound mammalian complex I
  • 2020
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 11:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Respiratory complex I (NADH:ubiquinone oxidoreductase) captures the free energy from oxidising NADH and reducing ubiquinone to drive protons across the mitochondrial inner membrane and power oxidative phosphorylation. Recent cryo-EM analyses have produced near-complete models of the mammalian complex, but leave the molecular principles of its long-range energy coupling mechanism open to debate. Here, we describe the 3.0-Ao resolution cryo-EM structure of complex I from mouse heart mitochondria with a substrate-like inhibitor, piericidin A, bound in the ubiquinone-binding active site. We combine our structural analyses with both functional and computational studies to demonstrate competitive inhibitor binding poses and provide evidence that two inhibitor molecules bind end-to-end in the long substrate binding channel. Our findings reveal information about the mechanisms of inhibition and substrate reduction that are central for understanding the principles of energy transduction in mammalian complex I. The respiratory complex I (NADH:ubiquinone oxidoreductase) is a large redox-driven proton pump that initiates respiration in mitochondria. Here, the authors present the 3.0 angstrom cryo-EM structure of complex I from mouse heart mitochondria with the ubiquinone-analogue inhibitor piericidin A bound in the active site and with kinetic measurements and MD simulations they further show that this inhibitor acts competitively against the native ubiquinone-10 substrate.
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5.
  • Jandrić, Petar, et al. (författare)
  • Teaching in the Age of Covid-19
  • 2020
  • Ingår i: Postdigital Science and Education. - : Springer Science and Business Media LLC. - 2524-4868 .- 2524-485X. ; 2:3, s. 1069-1230
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • A collection of 84 author's testimonies and workspace photographs between 18 March and 5 May 2020.
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6.
  • Markmann, James F., et al. (författare)
  • Phase 3 trial of human islet-after-kidney transplantation in type 1 diabetes
  • 2021
  • Ingår i: American Journal of Transplantation. - : John Wiley & Sons. - 1600-6135 .- 1600-6143. ; 21:4, s. 1477-1492
  • Tidskriftsartikel (refereegranskat)abstract
    • Allogeneic islet transplant offers a minimally invasive option for beta cell replacement in the treatment of type 1 diabetes (T1D). The CIT consortium trial of purified human pancreatic islets (PHPI) in patients with T1D after kidney transplant (CIT06), a National Institutes of Health-sponsored phase 3, prospective, open-label, single-arm pivotal trial of PHPI, was conducted in 24 patients with impaired awareness of hypoglycemia while receiving intensive insulin therapy. PHPI were manufactured using standardized processes. PHPI transplantation was effective with 62.5% of patients achieving the primary endpoint of freedom from severe hypoglycemic events and HbA(1c) <= 6.5% or reduced by >= 1 percentage point at 1 year posttransplant. Median HbA(1c)declined from 8.1% before to 6.0% at 1 year and 6.3% at 2 and 3 years following transplant (P < .001 for all vs baseline), with related improvements in hypoglycemia awareness and glucose variability. The improved metabolic control was associated with better health-related and diabetes-related quality of life. The procedure was safe and kidney allograft function remained stable after 3 years. These results add to evidence establishing allogeneic islet transplant as a safe and effective treatment for patients with T1D and unstable glucose control despite intensive insulin treatment, supporting the indication for PHPI in the post-renal transplant setting.
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7.
  • Pinto, Cathy Anne, et al. (författare)
  • Comparing Patient Preferences for Antithrombotic Treatment During the Acute and Chronic Phases of Myocardial Infarction: A Discrete-Choice Experiment
  • 2021
  • Ingår i: Patient. - : Springer Science and Business Media LLC. - 1178-1653 .- 1178-1661.
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundAntithrombotic drugs are used as preventive treatment in patients with a prior myocardial infarction (MI) in both the acute and chronic phases of the disease. To support patient-centered benefit–risk assessment, it is important to understand the influence of disease stage on patient preferences.ObjectiveThe aim of this study was to examine patient preferences for antithrombotic treatments and whether they differ by MI disease phase.MethodsA discrete-choice experiment was used to elicit preferences of adults in the acute (≤ 365 days before enrolment) or chronic phase (> 365 days before enrolment) of MI for key ischemic events (risk of cardiovascular [CV] death, non-fatal MI, and non-fatal ischemic stroke) and bleeding events (risk of non-fatal intracranial hemorrhage and non-fatal other severe bleeding). Preference data were analyzed using the multinomial logit model. Trade-offs between attributes were calculated as the maximum acceptable increase in the risk of CV death for a decrease in the risk of the other outcomes. To assess the potential effect of sociodemographic and clinical characteristics on patient preferences, subgroups were introduced as interaction terms in logit models.ResultsThe evaluable population included 155 patients with MI in the acute phase of disease and 180 in the chronic phase. The overall population was 82% male, mean age was 64.2 ± 9.6 years, and 93% had not experienced bleeding events or key ischemic events other than MI. Patients valued reduction in the risk of non-fatal intracranial hemorrhage more than CV death (p < 0.01) and CV death more than non-fatal ischemic events (p < 0.01). Preferences were similar in the acute and chronic populations (p = 0.17). However, older patients valued reduction in risk of MI more than younger patients (p = 0.04), and patients with bleeding risk factors valued reduction in the risk of CV death (p = 0.01) and MI (p = 0.01) less than patients without bleeding risk factors. Also, patients who were at high risk of future ischemic events valued reduction of the risk of CV death less than those at low risk (p = 0.01).ConclusionPatient preferences for antithrombotic treatments were unaffected by disease stage but varied by bleeding risk and other factors. This heterogeneity in preferences is an important consideration because it can affect the benefit–risk balance and the acceptability of antithrombotic treatments to patients.Key PointsPatient preferences for antithrombotic treatment attributes were similar between the acute and chronic phases of myocardial infarction.Patients with myocardial infarction are willing to accept significant increases in the mortality risk to avoid increases in non-fatal bleeding events.
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8.
  • Yin, Z., et al. (författare)
  • Structural basis for a complex I mutation that blocks pathological ROS production
  • 2021
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 12:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Mitochondrial complex I is central to the pathological reactive oxygen species (ROS) production that underlies cardiac ischemia–reperfusion (IR) injury. ND6-P25L mice are homoplasmic for a disease-causing mtDNA point mutation encoding the P25L substitution in the ND6 subunit of complex I. The cryo-EM structure of ND6-P25L complex I revealed subtle structural changes that facilitate rapid conversion to the “deactive” state, usually formed only after prolonged inactivity. Despite its tendency to adopt the “deactive” state, the mutant complex is fully active for NADH oxidation, but cannot generate ROS by reverse electron transfer (RET). ND6-P25L mitochondria function normally, except for their lack of RET ROS production, and ND6-P25L mice are protected against cardiac IR injury in vivo. Thus, this single point mutation in complex I, which does not affect oxidative phosphorylation but renders the complex unable to catalyse RET, demonstrates the pathological role of ROS production by RET during IR injury. © 2021, The Author(s).
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