Several single-center studies have evaluated the predictive performance of mechanical power (MP) on weaning outcomes in prolonged invasive mechanical ventilation (IMV) patients. The relationship between MP and weaning outcomes in all IMV patients has rarely been studied. A retrospective study was conducted on MIMIC-IV patients with IMV for more than 24 h to investigate the correlation between MP and weaning outcome using logistic regression model and subgroup analysis. The discriminative ability of MP, MP normalized to dynamic lung compliance (C_dyn-MP) and MP normalized to predicted body weight (PBW-MP) on weaning outcome were evaluated by analyzing the area under the receiver-operating characteristic (AUROC). Following adjustment for confounding factors, compared with the reference group, the Odds Ratio of weaning failure in the maximum MP, C_dyn-MP, and PBW-MP groups increased to 3.33 [95%CI (2.04–4.53), P < 0.001], 3.58 [95%CI (2.27–5.56), P < 0.001] and 5.15 [95%CI (3.58–7.41), P < 0.001], respectively. The discriminative abilities of C_dyn-MP (AUROC 0.760 [95%CI 0.745–0.776]) and PBW-MP (AUROC 0.761 [95%CI 0.744–0.779]) were higher than MP (AUROC 0.745 [95%CI 0.730–0.761]) (P < 0.05). MP is associated with weaning outcomes in IMV patients and is an independent predictor of the risk of weaning failure. C_dyn-MP and PBW-MP showed higher ability in weaning failure prediction than MP.

Neonatal sepsis is one of the most prevalent causes of death of the neonates. However, the mechanisms underlying neonatal sepsis remained unclear. The present study identified a total of 1128 upregulated mRNAs and 1008 downregulated mRNAs, 28 upregulated lncRNAs, and 61 downregulated lncRNAs in neonatal sepsis. Then, we constructed PPI networks to identify key regulators in neonatal sepsis, including ITGAM, ITGAX, TLR4, ITGB2, SRC, ELANE, RPLP0, RPS28, RPL26, and RPL27. lncRNA coexpression analysis showed HS.294603, LOC391811, C12ORF47, LOC729021, HS.546375, HNRPA1L-2, LOC158345, and HS.495041 played important roles in the progression of neonatal sepsis. Bioinformatics analysis showed DEGs were involved in the regulation cellular extravasation, acute inflammatory response, macrophage activation of NF-kappa B signaling pathway, TNF signaling pathway, HIF-1 signaling pathway, Toll-like receptor signaling pathway, and ribosome, RNA transport, and spliceosome. lncRNAs were involved in regulating ribosome, T cell receptor signaling pathway, RNA degradation, insulin resistance, ribosome biogenesis in eukaryotes, and hematopoietic cell lineage. We thought this study provided useful information for identifying novel therapeutic markers for neonatal sepsis.

Background. The energy delivered by a ventilator to the respiratory system in one minute is defined as mechanical power (MP). However, the effect of ventilator‐induced lung injury (VILI) in patients suffering from acute respiratory distress syndrome (ARDS) is still unknown. Our previous studies revealed that CXCL10 may be a potential biomarker of lung injury in ARDS. Therefore, the aim of this study was to compare the lung injury of rats and patients under different MP conditions to explore the involvement of CXCL10 and its receptor CXCR3 in VILI. Methods. Patients were divided into the high mechanical power group (HMPp group) and low mechanical power group (LMPp group), while rats were assigned to the high mechanical power group (HMPr group), medium mechanical power group (MMPr group), and low mechanical power group (LMPr group). CXCL10 and CXCR3 plasma content in ARDS patients and rats under ventilation at different MP was measured, as well as their protein and mRNA expression in rat lungs. Results. CXCL10 and CXCR3 content in the plasma of ARDS patients in the HMPp was significantly higher than that in the LMPp. The increase of MP during mechanical ventilation in the rats gradually increased lung damage, and CXCL10 and CXCR3 levels in rat plasma gradually increased with the increase of MP. CXCL10 and CXCR3 protein and mRNA expression in the HMPr group and MMPr group was significantly higher than that in the LMPr group (P < 0.05). More mast cells were present in the trachea, bronchus, blood vessels, and lymphatic system in the rat lungs of the HMPr group, and the number of mast cells in the HMPr group (13.32 ± 3.27) was significantly higher than that in the LMPr group (3.25 ± 0.29) (P < 0.05). Conclusion. The higher the MP, the more severe the lung injury, and the higher the CXCL10/CXCR3 expression. Therefore, CXCL10/CXCR3 might participate in VILI by mediating mast cell chemotaxis.

Background and Objective. During mechanical ventilation, the energy delivered by a ventilator to the respiratory system in one minute is defined as mechanical power (MP). It describes the combined effects of several mechanical factors, including tidal volume, driving pressure, transpulmonary pressure, flow rate, positive end‐expiratory pressure, and respiratory rate on lung ventilation. As such, MP may be useful for evaluating the severity and prognosis of acute respiratory distress syndrome (ARDS), as improvements in pulmonary ventilation directly affect a patient’s prognosis. Recent advances in lung ultrasound technology make it possible to evaluate lung ventilation at the bedside. In this study, MP was monitored in ARDS patients, and its correlation with lung ultrasound scores (LUS) was evaluated. Further analysis also explored the value of MP in evaluating the severity and prognosis of ARDS. Methods. A total of 121 patients with moderate to severe ARDS admitted to the intensive care unit (ICU) from June 2017 to April 2020 and treated with invasive mechanical ventilation were sequentially included in this study. Their general information was collected, and MP was recorded at 0 h, 24 h, 48 h, and 72 h after admission to the ICU. Professionally trained researchers performed the LUS assessments. Patients were divided into the death and survival groups according to their 28‐day prognosis. The trend of MP and LUS at the four time points was analyzed. A receiver operating characteristic curve (ROC) was used to analyze the predictive value of MP and LUS scores at 0 h and 72 h for the prognosis (28‐day mortality rate) of patients with moderate to severe ARDS. Results. 121 patients were included in the analysis, of which 73 were male and 48 were female. When patients entered the ICU, their oxygenation index (t: 30885, P < 0.01), APACHE II score (t: 2.105, P < 0.05), and SOFA score (t: 4.134, P < 0.001) were higher in the death group than the survival group. The death group had significantly higher MP and LUS at each time point (0 h, 24 h, 48 h, and 72 h) compared to the survival group (all P < 0.05). There was a significant upward trend over time in the MP and LUS of the death group, contrasting to a significant downward trend in the survival group (all P < 0.05). The Pearson correlation analysis showed that MP and LUS were significantly positively correlated at each time point (r values: 0 h: 0.3027; 24 h: 0.3705; 48 h: 0.3902; 72 h: 0.5916; all P < 0.01). The ROC curves showed that MP and LUS at 72 h were of significant value in predicting the prognosis of ARDS patients, with areas under the curve of 0.866 ± 0.032 and 0.839 ± 0.037, respectively. Conclusion. There was a significant correlation between the MP and LUS of ARDS patients at four time points from 0 to 72 h, which has a clinical value in evaluating severity and prognosis.

Objective. To analyze the differentially expressed genes (DEGs) in rats with endogenous acute respiratory distress syndrome (ARDS) lung injury and explore the pathogenesis and early diagnostic molecular markers using whole transcriptomic data. Methods. Twelve 8-week-old male Sprague Dawley rats were selected and randomly and equally divided into ARDS lung injury group and normal control group. RNA was extracted from the left lung tissues of both the groups and sequenced using the paired-end sequencing mode of the Illumina Hiseq sequencing platform. The DEGs of miRNA, cirRNA, lncRNA, and mRNA were screened using DESeq2 software, and the ceRNA regulatory network was constructed using Cytoscape. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed using the mRNA DEGs. STRING and Cytoscape software were used to construct the protein interaction network and identify the 15 key genes, which were verified using quantitative real-time polymerase chain reaction (qRT-PCR). Results. Based on different screening conditions, and compared with the control group, the ARDS lung injury group showed 836 mRNA DEGs (386 upregulated and 450 downregulated), 110 lncRNA DEGs (53 upregulated and 57 downregulated), 19 circRNA DEGs (3 upregulated and 16 downregulated), and 6 miRNA DEGs (5 upregulated and 1 downregulated gene). GO showed that the DEGs of mRNA were mainly involved in biological processes, such as defense response to lipopolysaccharide and other organisms, leukocyte chemotaxis, neutrophil chemotaxis, and cytokine-mediated signaling. KEGG enrichment analysis showed that the DEGs played their biological roles mainly by participating in IL-17, TNF, and chemokine signaling pathways. The PPI analysis showed a total of 281 node proteins and 634 interaction edges. The top 15 key genes, which were screened, included Cxcl10, Mx1, Irf7, Isg15, Ifit3, Ifit2, Rsad2, Ifi47, Oasl, Dhx58, Usp18, Cmpk2, Herc6, Ifit1, and Gbp4. The ceRNA network analysis showed 69 nodes and 73 correlation pairs, where the key gene nodes were miR-21-3p, Camk2g, and Stx2. Conclusions. The chemotaxis, migration, and degranulation of inflammatory cells, cytokine immune response, autophagy, and apoptosis have significant biological functions in the occurrence and development of endogenous acute lung injury during ARDS. Thus, the camk2g/miR-21-3p/lncRNA/circRNA network, CXCL10/CXCR3, and IL-17 signaling pathways might provide novel insights and targets for further studying the lung injury mechanism and clinical treatment.

Objective. To explore the effect of pulse-induced contour cardiac output (PiCCO) monitoring on the survival and prognosis of patients with myocardial injury and septic shock. Methods. A total of 400 patients with MI and septic shock who were treated in our hospital from May 2018 to June 2021 were included in the study. They were randomly grouped into the PiCCO group ( ) and the control group ( ) according to whether PiCCO was used for monitoring during the treatment period. The clinical baseline characteristics of all the patients were recorded. For comparison, we recorded hemodynamic parameters including mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), troponin I (TnI), brain natriuretic peptide (BNP), oxygen metabolism parameters including systemic central venous oxygen saturation (ScvO₂), and lactate before and 6 h after intervention. In addition, white blood cell count (WBC) and C-reactive protein (CPR) levels before and 6 h, 24 h, 48 h, and 72 h after intervention were measured in both groups. Finally, the survival and prognostic parameters were compared between the two groups. Results. At 6 h after monitoring intervention, the hemodynamic parameters of the patients in the PiCCO group were significantly increased. Additionally, compared with the control group, the ScvO₂ level was higher while the lactate level was lower in the PiCCO group. An intergroup comparison on inflammation also showed that WBC and CPR levels recovered better in the PiCCO group than in the control group. Moreover, patients with PiCCO monitoring showed better performance in outcome measures such as mortality, duration of invasive mechanical ventilation, length of hospital stay, duration of ventilator use, acute physiology and chronic health scores, and postoperative complications. Conclusion. With the monitoring and guidance of the PiCCO technique, the nursing outcomes, survival rate, and prognosis of patients with myocardial injury and septic shock can be improved.