Correction: Real-time feedback improves chest compression quality in out-of-hospital cardiac arrest: A prospective cohort study.

[This corrects the article DOI: 10.1371/journal.pone.0229431.]

Real-time feedback improves chest compression quality in out-of-hospital cardiac arrest: A prospective cohort study.

BACKGROUND:Current guidelines underline the importance of high-quality chest compression during cardiopulmonary resuscitation (CPR), to improve outcomes. Contrary to this many studies show that chest compression is often carried out poorly in clinical practice, and long interruptions in compression are observed. This prospective cohort study aimed to analyse whether chest compression quality changes when a real-time feedback system is used to provide simultaneous audiovisual feedback on chest compression quality. For this purpose, pauses in compression, compression frequency and compression depth were compared. METHODS:The study included 292 out-of-hospital cardiac arrests in three consecutive study groups: first group, conventional resuscitation (no-sensor CPR); second group, using a feedback sensor to collect compression depth data without real-time feedback (sensor-only CPR); and third group, with real-time feedback on compression quality (sensor-feedback CPR). Pauses and frequency were analysed using compression artefacts on electrocardiography, and compression depth was measured using the feedback sensor. With this data, various parameters were determined in order to be able to compare the chest compression quality between the three consecutive groups. RESULTS:The compression fraction increased with sensor-only CPR (group 2) in comparison with no-sensor CPR (group 1) (80.1% vs. 87.49%; P < 0.001), but there were no further differences belonging compression fraction after activation of sensor-feedback CPR (group 3) (P = 1.00). Compression frequency declined over the three study groups, reaching the guideline recommendations (127.81 comp/min vs. 122.96 comp/min, P = 0.02 vs. 119.15 comp/min, P = 0.008) after activation of sensor-feedback CPR (group 3). Mean compression depth only changed minimally with sensor-feedback (52.49 mm vs. 54.66 mm; P = 0.16), but the fraction of compressions with sufficient depth (at least 5 cm) and compressions within the recommended 5-6 cm increased significantly with sensor-feedback CPR (56.90% vs. 71.03%; P = 0.003 and 28.74% vs. 43.97%; P < 0.001). CONCLUSIONS:The real-time feedback system improved chest compression quality regarding pauses in compression and compression frequency and facilitated compliance with the guideline recommendations. Compression depth did not change significantly after activation of the real-time feedback. Even the sole use of a CPR-feedback-sensor ("sensor-only CPR") improved performance regarding pauses in compression and compression frequency, a phenomenon known as the 'Hawthorne effect'. Based on this data real-time feedback systems can be expected to raise the quality level in some parts of chest compression quality. TRIAL REGISTRATION:International Clinical Trials Registry Platform of the World Health Organisation and German Register of Clinical Trials (DRKS00009903), Registered 09 February 2016 (retrospectively registered)

SOCS2 regulates T helper type 2 differentiation and the generation of type 2 allergic responses

The incidence of allergy and asthma in developed countries is on the increase and this trend looks likely to continue. CD4(+) T helper 2 (Th2) cells are major drivers of these diseases and their commitment is controlled by cytokines such as interleukin 4, which are in turn regulated by the suppressor of cytokine signaling (SOCS) proteins. We report that SOCS2(-/-) CD4(+) T cells show markedly enhanced Th2 differentiation. SOCS2(-/-) mice, as well as RAG1(-/-) mice transferred with SOCS2(-/-) CD4(+) T cells, exhibit elevated type 2 responses after helminth antigen challenge. Moreover, in in vivo models of atopic dermatitis and allergen-induced airway inflammation, SOCS2(-/-) mice show significantly elevated IgE, eosinophilia, type 2 responses, and inflammatory pathology relative to wild-type mice. Finally, after T cell activation, markedly enhanced STAT6 and STAT5 phosphorylation is observed in SOCS2(-/-) T cells, whereas STAT3 phosphorylation is blunted. Thus, we provide the first evidence that SOCS2 plays an important role in regulating Th2 cell expansion and development of the type 2 allergic responses