High-flow nasal cannula therapy versus conventional oxygen therapy for adult patients after cardiac surgery: A systemic review and meta-analysis.

BACKGROUND: Oxygen therapy constitutes a crucial element of post-cardiac operative care. The study assessed the effectiveness of high-flow nasal cannula (HFNC) in comparison to conventional oxygen therapy (COT). OBJECTIVES: The aim of the study was to assess the effectiveness of HFNC in comparison to COT for adult patients following cardiac surgery. METHODS: We conducted a comprehensive search of Embase, PubMed, Scopus, Cochrane Library, and Web of Science databases from inception until April 18, 2023, to identify randomized controlled trials (RCTs) and crossover studies that compared the efficacy of HFNC with COT in adult patients following cardiac surgery. RESULTS: The meta-analysis included nine studies, consisting of eight RCTs and one crossover study. Compared with COT, HFNC could reduce the need for escalation of respiratory support (RR 0.67, 95% CI: 0.48 to 0.93, P = 0.02), decrease arterial partial pressure of carbon dioxide (PaCO2) levels (MD -3.14, 95% CI: -4.90 to -1.39, P<0.001), and increase forced expiratory volume in 1 second (FEV1) levels (MD 0.08, 95% CI: 0.02 to 0.15, P = 0.02). There was no significant difference between the HFNC and COT groups in terms of mortality, intubation rate, respiratory rate, heart rate, intensive care unit and hospital length of stay, arterial partial pressure of oxygen (PaO2), forced vital capacity, and complications of atrial fibrillation and delirium. CONCLUSION: Compared with COT, HFNC could decrease the need for escalation of respiratory support, lower PaCO2 levels, and elevate FEV1 levels in patients following cardiac surgery.

Pseudorabies Virus Infection Activates the TLR-NF-κB Axis and AIM2 Inflammasome To Enhance Inflammatory Responses in Mice.

Pseudorabies virus (PRV) infection activates inflammatory responses to release robust proinflammatory cytokines, which are critical for controlling viral infection and clearance of PRV. However, the innate sensors and inflammasomes involved in the production and secretion of proinflammatory cytokines during PRV infection remain poorly studied. In this study, we report that the transcription and expression levels of some proinflammatory cytokines, including interleukin 1ß (IL-1ß), IL-6, and tumor necrosis factor alpha (TNF-α), are upregulated in primary peritoneal macrophages and in mice during PRV infection. Mechanistically, Toll-like receptor 2 (TLR2), TLR3, TLR4, and TLR5 were induced by the PRV infection to enhance the transcription levels of pro-IL-1ß, pro-IL-18, and gasdermin D (GSDMD). Additionally, we found that PRV infection and transfection of its genomic DNA triggered AIM2 inflammasome activation, apoptosis-related speckle-like protein (ASC) oligomerization, and caspase-1 activation to enhance the secretion of IL-1ß and IL-18, which was mainly dependent on GSDMD, but not GSDME, in vitro and in vivo. Taken together, our findings reveal that the activation of the TLR2-TLR3-TRL4-TLR5-NF-κB axis and AIM2 inflammasome, as well as GSDMD, is required for proinflammatory cytokine release, which resists the PRV replication and plays a critical role in host defense against PRV infection. Our findings provide novel clues to prevent and control PRV infection. IMPORTANCE PRV can infect several mammals, including pigs, other livestock, rodents, and wild animals, causing huge economic losses. As an emerging and reemerging infectious disease, the emergence of PRV virulent isolates and increasing human PRV infection cases indicate that PRV is still a high risk to public health. It has been reported that PRV infection leads to robust release of proinflammatory cytokines through activating inflammatory responses. However, the innate sensor that activates IL-1ß expression and the inflammasome involved in the maturation and secretion of proinflammatory cytokines during PRV infection remain poorly studied. In this study, our findings reveal that, in mice, activation of the TLR2-TLR3-TRL4-TLR5-NF-κB axis and AIM2 inflammasome, as well as GSDMD, is required for proinflammatory cytokine release during PRV infection, and it resists PRV replication and plays a critical role in host defense against PRV infection. Our findings provide novel clues to prevent and control PRV infection.