Impact of respiratory viruses in intensive care unit patient with community-acquired pneumonia : a one-year retrospective single-centre study.

International audienc

High-flow oxygen therapy versus noninvasive ventilation: a randomised physiological crossover study of alveolar recruitment in acute respiratory failure.

High-flow nasal cannula (HFNC) oxygen therapy has recently shown clinical benefits in hypoxaemic acute respiratory failure (ARF) patients, while the value of noninvasive ventilation (NIV) remains debated. The primary end-point was to compare alveolar recruitment using global end-expiratory electrical lung impedance (EELI) between HFNC and NIV. Secondary end-points compared regional EELI, lung volumes (global and regional tidal volume variation (V (T))), respiratory parameters, haemodynamic tolerance, dyspnoea and patient comfort between HFNC and NIV, relative to face mask (FM). A prospective randomised crossover physiological study was conducted in patients with hypoxaemic ARF due to pneumonia. They received alternately HFNC, NIV and FM. 16 patients were included. Global EELI was 4083 with NIV and 2921 with HFNC (p=0.4). Compared to FM, NIV and HFNC significantly increased global EELI by 1810.5 (95% CI 857-2646) and 826 (95% CI 399.5-2361), respectively. Global and regional V (T) increased significantly with NIV compared to HFNC or FM, but not between HFNC and FM. NIV yielded a significantly higher pulse oxygen saturation/inspired oxygen fraction ratio compared to HFNC (p=0.03). No significant difference was observed between HFNC, NIV and FM for dyspnoea. Patient comfort score with FM was not significantly different than with HFNC (p=0.1), but was lower with NIV (p=0.001). This study suggests a potential benefit of HFNC and NIV on alveolar recruitment in patients with hypoxaemic ARF. In contrast with HFNC, NIV increased lung volumes, which may contribute to overdistension and its potentially deleterious effect in these patients

Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome associated with COVID-19: An Emulated Target Trial Analysis.

RATIONALE: Whether COVID patients may benefit from extracorporeal membrane oxygenation (ECMO) compared with conventional invasive mechanical ventilation (IMV) remains unknown. OBJECTIVES: To estimate the effect of ECMO on 90-Day mortality vs IMV only Methods: Among 4,244 critically ill adult patients with COVID-19 included in a multicenter cohort study, we emulated a target trial comparing the treatment strategies of initiating ECMO vs. no ECMO within 7 days of IMV in patients with severe acute respiratory distress syndrome (PaO2/FiO2 <80 or PaCO2 ≥60 mmHg). We controlled for confounding using a multivariable Cox model based on predefined variables. MAIN RESULTS: 1,235 patients met the full eligibility criteria for the emulated trial, among whom 164 patients initiated ECMO. The ECMO strategy had a higher survival probability at Day-7 from the onset of eligibility criteria (87% vs 83%, risk difference: 4%, 95% CI 0;9%) which decreased during follow-up (survival at Day-90: 63% vs 65%, risk difference: -2%, 95% CI -10;5%). However, ECMO was associated with higher survival when performed in high-volume ECMO centers or in regions where a specific ECMO network organization was set up to handle high demand, and when initiated within the first 4 days of MV and in profoundly hypoxemic patients. CONCLUSIONS: In an emulated trial based on a nationwide COVID-19 cohort, we found differential survival over time of an ECMO compared with a no-ECMO strategy. However, ECMO was consistently associated with better outcomes when performed in high-volume centers and in regions with ECMO capacities specifically organized to handle high demand. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Déterminants du cœur pulmonaire aigu et évolution au décours d’une exacerbation aiguë d’une bronchopneumopathie chronique obstructive

La bronchopneumopathie chronique obstructive (BPCO) est la quatrième cause de décès dans les pays industrialisés. Elle est fréquemment associé à de l’emphysème. Les exacerbations de BPCO entraînent une élévation des pressions pulmonaires responsable d’un coeur pulmonaire aigu (CPA). Ce dernier impacte la morbi-mortalité des patients. Objectifs : L’objectif de notre étude est de déterminer les facteurs favorisant le développement d’un CPA au cours d’une exacerbation de BPCO. Matériel et méthode : Les patients hospitalisés pour exacerbation de BPCO entre janvier 2016 et juin 2017 ont été inclus. Tous les patients ont bénéficié d’une échocardiographie au moment de l’exacerbation et à 6 mois de suivi. Une tomodensitométrie a également été réalisée pour la quantification de l’emphysème pendant l’hospitalisation ou dans le mois suivant. Résultats : 29 patients ont été inclus. Il s’agissait de patients jeunes (65 ans [61-71 ans]), plutôt des femmes, avec un trouble ventilatoire obstructif sévère (34% [27-47%]). L’incidence du CPA pendant une exacerbation aiguë de BPCO était élevée (79%) dans notre étude. L’emphysème était un facteur protecteur du développement d’un CPA (OR=0,78 [0,64-0,96], p=0,018) contrairement au tabagisme actif qui apparaissait comme un facteur favorisant (OR=11,3 [1, 3-114,8], p=0,04). Un volume pulmonaire atteint par l’emphysème inférieur à 12% permettait de prédire l’existence d’un CPA avec une sensibilité égale à 83% et une spécificité égale à 82%. L’âge, le sexe, le poids, le VEMS, la Pa02 et PaCO2 n’ont pas été identifiés comme facteur favorisant d’un CPA dans notre étude. Conclusion :Notre étude a permis de définir le profil des patients BPCO développant un CPA au cours d’une exacerbation sévère. Il s’agit de patients présentant un tabagisme actif et un emphysème affectant moins de 12% du parenchyme pulmonaire. Nous n’avons pas retrouvé d’impact de la survenue d’un CPA sur la morbi-mortalité. L’impact de l’emphysème sur le développement d’un CPC reste à définir

Presence of respiratory viruses in ICU patients with community acquired-pneumonia (CAP): a one-year restrospective single center study

International audienc

Une histoire sociale des langues romanes : Genèse, construction et évolution sociolinguistiques d’une famille de langues

Cette leçon raconte une histoire sociale passionnante : celle d’une langue – le latin – qui s’est transformée et a donné naissance à toute une famille linguistique : la famille romane. L’étudiant découvrira comment, à partir des différentes variétés de latin qui se sont individuées de plus en plus à la suite de la disparition de l’Empire romain, s’est constituée la configuration sociolinguistique de la Romania. Il pourra apprécier le rôle des évènements politiques (invasions, guerres, conflits divers…), religieux (Christianisme, Réforme, Contre-Réforme…) et culturels (Humanisme, Romantisme…) dans la formation des langues romanes et dans l’évolution écolinguistique de l’Europe. En définitive, à la fin de cette ressource, l’étudiant sera en mesure de relativiser ce que l’on appelle le "poids des langues" (Calvet) et de mieux comprendre pourquoi certaines langues "ont réussi", c’est-à-dire sont devenues des langues d’État, symboles d’une Nation, porteuses d’une culture internationalement reconnue tandis que d’autres sont aujourd’hui en situation de minoration (et que d’autres ont disparu). L’étudiant est guidé dans sa découverte par des contenus théoriques et interdisciplinaires, par des liens qui le dirigeront vers d’autres ressources offrant des informations complémentaires, par des cartes historiques qui lui serviront de repères, et qui montreront aussi le rapport étroit entre les différents processus de stabilisation stato-nationale et l’évolution sociolinguistique des langues d’Europe. Cela dit, le cœur de cette histoire est un important ensemble de documents historiques rédigés en langues romanes à différentes époques (dont les caractéristiques graphiques d’origine sont, presque toujours, respectées) accompagnés d’une version audio (pour certains d'entre eux), d’une traduction et d’un commentaire sociolinguistique.

Impact of respiratory viruses in intensive care unit patient with community-acquired pneumonia : a one-year retrospective single-centre study.

International audienc

Additional file 1 of ROX index performance to predict high-flow nasal oxygen outcome in Covid-19 related hypoxemic acute respiratory failure

Additional file 1: Figure S1. Receiver operating characteristic curves for HFNO failure within 28 days at different times after HFNO initiation. HFNO: high-flow nasal oxygen therapy; ROC: receiver operating characteristic; H0: ROC curve at the time of HFNO initiation; H12:12 hours after HFNO initiation; H18: 18 hours after HFNO initiation; H24:24 hours after HFNO initiation. Figure S2. Rox index performance to predict the risk of HFNO failure at different times after HFNO initiation. HFNO: high-flow nasal oxygen therapy; red line gives proportion of patients in the HFNO failure group with a ROX index ≤ a chosen cut-off value; black line gives proportion of patients in the HFNO success group with a ROX index ≤ a chosen cut-off value. For example: at H6, using a Rox index of ≤8.50 as cut-off would identify 90% of patients with HFNO failure after H6, whereas this cut-off would identify only 38% of patients with HFNO success after H6, avoiding intubation. Figure S3. Incidence of HFNO failure within 7 days after HFNO initiation. HFNO: high-flow nasal oxygen therapy. Table S4. Conditions of intubation and clinical respiratory parameters in all intubated patients and according to hemodynamic status. HFNO: high-flow nasal oxygen therapy; FiO2: fraction of inspired oxygen; SpO2: pulse oxygen saturation; RR: respiratory rate; values are expressed as n (%) or median (Q1-Q3). Table S5. Rox index at H0, HFNO outcome and duration according to each ICU center. HFNO: high-flow nasal oxygen therapy; ICU: intensive care unit; values are expressed as n (%) or median (Q1-Q3); *= logistic regression unless stated otherwise; **= Kruskall-Wallis’s test

Tetrahydrobenzimidazole TMQ0153 triggers apoptosis, autophagy and necroptosis crosstalk in chronic myeloid leukemia

By comparing imatinib-sensitive and -resistant chronic myeloid leukemia (CML) cell models, we investigated the molecular mechanisms by which tetrahydrobenzimidazole derivative TMQ0153 triggered caspase-dependent apoptosis at low concentrations accompanied by loss of mitochondrial membrane potential (MMP) and increase of cytosolic free Ca2+ levels. Interestingly, at higher concentrations, TMQ0153 induced necroptotic cell death with accumulation of ROS, both preventable by N-acetyl-L-cysteine (NAC) pretreatment. At necroptosis-inducing concentrations, we observed increased ROS and decreased ATP and GSH levels, concomitant with protective autophagy induction. Inhibitors such as bafilomycin A1 (baf-A1) and siRNA against beclin 1 abrogated autophagy, sensitized CML cells against TMQ0153 and enhanced necroptotic cell death. Importantly, TMQ153-induced necrosis led to cell surface exposure of calreticulin (CRT) and ERp57 as well as the release of extracellular ATP and high mobility group box (HMGB1) demonstrating the capacity of this compound to release immunogenic cell death (ICD) markers. We validated the anti-cancer potential of TMQ0153 by in vivo inhibition of K562 microtumor formation in zebrafish. Taken together, our findings provide evidence that cellular stress and redox modulation by TMQ0153 concentration-dependently leads to different cell death modalities including controlled necrosis in CML cell models. © 2020, The Author(s)