Objective: The chances of surviving an out-of-hospital cardiac arrest depend on early and high-quality cardiopulmonary resuscitation (CPR). Our aim is to verify whether the use of feedback devices during laypersons' CPR training improves chest compression quality. Methods: Laypersons totalling 450 participating in Basic Life Support and Automated External Defibrillation (BLS/ AED) courses were randomly divided into three groups: group No Feedback (NF) attended a course without any feedback, group Short Feedback (SF) a course with 1-minute training with real-time visual feedback, and group Long Feedback (LF) a course with 10-minute training with real-time visual feedback. At the end of each course, we recorded 1 minute of compression-only CPR. The primary end point was the difference in the percentage of compressions performed with correct depth. Results: There was a significant improvement in the percentage of compressions with correct depth in the groups receiving feedback compared to the other (NF v. LF, p = 0.022; NF v. SF, p = 0.005). This improvement was also present in the percentage of compressions with a complete chest recoil (71.7% in NF, 86.6% in SF, and 88.8% in LF; p < 0.001), compressions with the correct hand position (93.2% in NF, 98.2% in SF, and 99.3% in LF; p < 0.001), and in the Total CPR Score (79.4% in NF, 90.2% in SF, and 92.5% in LF; p < 0.001). There were no significant differences for all of the parameters between group SF and group LF. Conclusions: Real-time visual feedback improves laypersons' CPR quality, and we suggest its use in every BLS/AED course for laypersons because it can help achieve the goals emphasized by the International Liaison Committee on Resuscitation recommendations. RÉSUMÉObjectif: Les chances de survie à la suite d'un arrêt cardiaque survenu dans la collectivité dépend de la rapidité des manoeuvres de réanimation cardiorespiratoire (RCR) ainsi que de leur qualité. L'étude décrite ici visait à vérifier si l'utilisation de dispositifs de rétroaction durant la formation des profanes en la matière pouvait améliorer la qualité des compressions thoraciques. Méthode: Ont participé à des cours de réanimation de base et de défibrillation 450 profanes en la matière, divisés au hasard en trois groupes : le premier a suivi le cours sans rétroaction (SR) aucune; le deuxième a suivi le cours avec une brève rétroaction (BR), soit 1 minute de formation avec une rétroaction visuelle en temps réel; et le troisième a suivi le cours avec une longue rétroaction (LR), soit 10 minutes de formation avec une rétroaction visuelle en temps réel. À la fin de chacun des cours, il y a eu enregistrement des compressions seules durant 1 min. Le principal critère d'évaluation était les différences de pourcentage quant aux compressions réalisées à la bonne profondeur. Résultats: Une amélioration sensible du pourcentage des compressions réalisées à la bonne profondeur a été observée dans les groupes dans lesquels il y avait eu de la rétroaction comparativement à celui qui n'en avait pas reç...
TRIM5␣ is a natural resistance factor that binds retroviral capsid proteins and restricts virus replication. The B30.2/SPRY domain of TRIM5␣ is polymorphic in rhesus macaques, and some alleles are associated with reduced simian immunodeficiency virus (SIV) SIV mac251 and SIV smE543 replication in vivo. We determined the distribution of TRIM5␣ alleles by PCR and sequence analysis of the B30.2/SPRY domain in a cohort of 82 macaques. Thirty-nine of these macaques were mock vaccinated, 43 were vaccinated with either DNA-SIV/ ALVAC-SIV/gp120, ALVAC-SIV/gp120, or gp120 alone, and all were exposed intrarectally to SIV mac251 at one of three doses. We assessed whether the TRIM5␣ genotype of the macaques affected the replication of challenge virus by studying the number of SIV variants transmitted, the number of exposures required, the SIV mac251 viral level in plasma and tissue, and the CD4 ؉ T-cell counts. Our results demonstrated that TRIM5␣ alleles, previously identified as restrictive for SIV mac251 replication in vivo following intravenous exposure, did not affect SIV mac251 replication following mucosal exposure, regardless of prior vaccination, challenge dose, or the presence of the protective major histocompatibility complex alleles (MamuA01 ؉ , MamuB08 ؉ , or MamuB017 ؉ ). The TRIM5␣ genotype had no apparent effect on the number of transmitted variants or the number of challenge exposures necessary to infect the animals. DNA sequencing of the SIV mac251 Gag gene of the two stocks used in our study revealed SIV mac239 -like sequences that are predicted to be resistant to TRIM5␣ restriction. Thus, the TRIM5␣ genotype does not confound results of mucosal infection of rhesus macaques with SIV mac251 .The simian immunodeficiency virus (SIV) SIV mac251 macaque model is widely used to evaluate the relative efficacy of human immunodeficiency virus (HIV) vaccine candidates in macaques. Thus, understanding the natural factors that confer resistance to SIV mac251 replication in rhesus macaques is important in order to minimize the overestimation of vaccine efficacy. HIV-1 does not infect macaques, and the restriction of HIV replication in Old World monkeys occurs at the postentry level (6,22,29) and is mediated, in part, by the interaction of TRIM5␣ and the viral capsid protein (10, 23). TRIM5␣ is an interferon-inducible gene that is conserved across species and encodes a cytoplasmic (4, 5) protein. Species-specific TRIM5␣ polymorphisms (22) that affect the efficiency of SIV replication in vitro and in vivo have been characterized in rhesus macaques (30). TRIM5␣ antiretroviral activity is mediated by the RING domain, which through its E3 ubiquitin ligase activity, polyubiquitinates TRIM5␣ itself. The polyubiquitinated TRIM5␣ binds to the viral capsid protein via the B30.2 (SPRY) domain, and the protein complex is degraded by the proteasome (7, 27). However, the disruption of the RING domain, the modulation of the expression of E1 ubiquitin-activating enzyme, or the inhibition of the proteasome activity only partially affe...
OBJECTIVE ST-segment elevation myocardial infarction (STEMI) patients with type 2 diabetes mellitus (DM) have higher in-hospital mortality than those without. Since cardiac and renal functions are the main variables associated with outcome in STEMI, we hypothesized that this prognostic disparity may depend on a higher rate of cardiac and renal dysfunction in DM patients. RESEARCH DESIGN AND METHODS We retrospectively analyzed 5,152 STEMI patients treated with primary angioplasty. Left ventricular ejection fraction (LVEF) and estimated glomerular filtration rate (eGFR) were evaluated at hospital admission. The primary end point was in-hospital mortality. A composite of in-hospital mortality, cardiogenic shock, and acute kidney injury was the secondary end point. RESULTS There were 879 patients (17%) with DM. The incidence of LVEF ≤40% (30% vs. 22%), eGFR ≤60 mL/min/1.73 m2 (27% vs. 18%), or both (12% vs. 6%) was higher (P < 0.001 for all comparisons) in DM patients. In-hospital mortality was higher in DM patients than in non-DM patients (6.1% vs. 3.5%; P = 0.002), with an unadjusted odds ratio (OR) of 1.81 (95% CI 1.31–2.49; P < 0.001). However, DM was no longer associated with an increased mortality risk after adjustment for cardiac and renal function (OR 1.03, 95% CI 0.68–1.56; P = 0.89). A similar behavior was observed for the secondary end point, with an unadjusted OR for DM of 1.52 (95% CI 1.25–1.85; P < 0.001) and an OR after adjustment for cardiac and renal function of 1.07 (95% CI 0.85–1.36; P = 0.53). CONCLUSIONS The study indicates that the increased in-hospital mortality and morbidity of DM patients with STEMI is mainly driven by their underlying cardio-renal dysfunction.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.