Development and Validation of Machine Learning-Based Models for Prediction of Intensive Care Unit Admission and In-Hospital Mortality in Patients with Acute Exacerbations of Chronic Obstructive Pulmonary Disease.

Background: This present work focused on predicting prognostic outcome of inpatients developing acute exacerbation of chronic obstructive pulmonary disease (AECOPD), and enhancing patient monitoring and treatment by using objective clinical indicators. Methods: The present retrospective study enrolled 322 AECOPD patients. Registry data downloaded based on COPD Pay-for-Performance Program database from January 2012 to December 2018 were used to check whether the enrolled patients were eligible. Our primary and secondary outcomes were ICU admission and in-hospital mortality, respectively. The best feature subset was chosen by recursive feature elimination. Moreover, seven machine learning (ML) models were trained for forecasting ICU admission among AECOPD patients, and the model with the most excellent performance was used. Results: According to our findings, random forest (RF) model showed superb discrimination performance, and the values of area under curve (AUC) were 0.973 and 0.828 in training and test cohorts, separately. Additionally, according to decision curve analysis, the net benefit of RF model was higher when differentiating patients with a high risk of ICU admission at a <0.55 threshold probability. Moreover, the ML-based prediction model was also constructed to predict in-hospital mortality, and it showed excellent calibration and discrimination capacities. Conclusion: The ML model was highly accurate in assessing the ICU admission and in-hospital mortality risk for AECOPD cases. Maintenance of model interpretability helped effectively provide accurate and lucid risk prediction of different individuals.

Lonicera japonica Thunb extract ameliorates lipopolysaccharide-induced acute lung injury associated with luteolin-mediated suppression of NF-κB signaling pathway.

OBJECTIVE: Lonicera japonica Thunb (LJT) is a commonly used herbal soup to treat inflammation-related diseases. However, the effect of LJT on ALI is unknown. The present study was aimed at investigating the protective effects of LJT extract (LTE) and its active ingredient luteolin (Lut) on lipopolysaccharide (LPS)-stimulated ALI and investigate its potential mechanism. MATERIALS AND METHODS: The effects of LTE and Lut were explored in an ALI mouse model induced by intraperitoneal injection of lipopolysaccharide (LPS). Besides, the LPS-induced inflammation model in BEAS-2B cells was used to clarify the underlying mechanisms. The ALI pathological changes in lung tissues were tested through Haematoxylin and eosin (HE) staining. The apoptosis of cells in lung tissue and the cell model in vitro was evaluated by TUNEL assays, respectively. Meanwhile, the viability of cells in vitro was evaluated by Cell Counting Kit-8 (CCK-8) assay. The levels/concentrations of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1ß and IL-10 in BALF were detected by enzyme-linked immunosorbent assay (ELISA). Besides, through quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting, the expression of the above-mentioned inflammatory factors and key factors in the NF-κB signaling pathway was examined. The distribution of inflammatory factors in tissue was observed through immunohistochemistry (IHC) assays . RESULTS: In relative to LPS-stimulated group, the in vivo study showed that LTE and different concentrations of Lut dramatically alleviated LPS-evoked lung pathological injury and lung edema based on the changes in total protein levels and lung wet/dry (W/D) ratio in the bronchoalveolar lavage fluid (BALF) from ALI mice. LTE and different concentrations of Lut also suppressed the inflammatory response, as reflected by the variations of neutrophil accumulation and the production of proinflammatory and anti-inflammatory cytokines in the lung tissues and BALF of ALI mice. The in vitro research also demonstrated that LTE and Lut visibly facilitated cell viability and restrained the apoptosis of BEAS-2B cells stimulated by LPS. Lut hindered LPS-inducible activation of NF-κB pathway in BEAS-2B cells. CONCLUSION: The present study proved that LTE might suppress LPS-induced acute injury and inflammation in mice and BEAS-2B cells through the Lut-caused suppression of NF-κB signal path (Figure 1).

Circulating inflammatory cytokines and risk of idiopathic pulmonary fibrosis: a Mendelian randomization study.

BACKGROUND: The previous epidemiological and experimental evidence has implied the linkage between chronic inflammation to idiopathic pulmonary fibrosis (IPF). However, it was still unclear whether there were casual associations between circulating inflammatory cytokines and IPF development. The objective of present study was to examine whether altered genetically predicted concentration of circulating cytokines were associated with IPF development using a two-sample Mendelian randomization (MR) analysis. MATERIALS AND METHODS: The causal effects of 23 circulating inflammatory cytokines were evaluated on IPF using MR analysis. The primary approach of MR analysis was the inverse variance-weighted (IVW) method. The sensitivity analyses were conducted by simple median, weighted median, penalized weighted median and MR-Egger regression methods. RESULTS: The present MR study found suggestive evidence that a higher circulating IL-14 level was associated with an increased risk of IPF (random effects IVW method: odds ratio: 1.001, 95% confidence interval: 1.000-1.001, P = 0.026). The sensitivity analysis yielded directionally similar results for IL-14. There was no significant association found between other circulating inflammatory cytokines and IPF. CONCLUSION: The high level of IL14 predicted by genes had a casual relationship with the increased risk of IPF. This finding provided epidemiological evidence for drug therapy targeting inflammatory factors in the prevention and treatment of IPF. It's warranted further exploration to validate the clinical significance of IL14 associated with developmental risk of IPF.

Effect of comprehensive nursing intervention in children with respiratory failure.

OBJECTIVE: To investigate the effect of comprehensive nursing intervention in the management of pediatric patients with respiratory failure. METHODS: A total of 60 pediatric patients were selected as research subjects, and the clinical data were collected and retrospectively investigated. The patients were divided either into a control group (n=30) or an observation group (n=30) according to the nursing care methods. Pediatric patients from the observation group underwent comprehensive nursing intervention, while those in the control group received conventional nursing care intervention. The clinical effects, negative emotions, SF-36 scores, hospital stays, clinical symptom indicators, blood gas indices, lung function indicators and the nursing satisfaction rates were compared between the two groups. RESULTS: The clinical effect in the observation group was significantly better than that in the control group. Compared with those in the control group, significantly lower scores of the Self-Rating Anxiety Scale and the Self-Rating Depression Scale were observed in the observation group. The indicators associated with blood gas and lung function in the observation group were significantly improved in contrast to those in the control group. Moreover, the disappearance time of pulmonary rales, disappearance time of cyanochroia, alleviation time of dyspnea and hospital stays in the observation group were significantly shorter than those in the control group, while the SF-36 scores and the nursing satisfaction rate in the observation group were significantly higher than those in the control group (all P<0.05). CONCLUSION: Comprehensive nursing intervention significantly improved clinical treatment effects and patient satisfaction, alleviated the clinical symptoms, increased life quality and shortened hospital stay. So, it is worth being promoted in clinical practice.

Serum suPAR associated with disease severity and mortality in elderly patients with community-acquired pneumonia.

Severe community-acquired pneumonia (SCAP) in elderly has more atypical clinical presentation compared to younger patients. Timely recognition could improve clinical care. This study investigated the value of soluble urokinase-type plasminogen activator receptor (suPAR) on severity assessment and outcome prediction in elderly patients with CAP. We conducted a prospective, observational study between January 2014 and December 2016. A total of 230 patients ≥65 were enrolled in this study, of which 151 were CAP and 79 were SCAP. Serum suPAR levels were determined by ELISA essays within 24 h after hospitalization. Thirty-day and 1-year mortalities were recorded as outcomes. Serum suPAR level was significantly increased in patients with SCAP. Positive correlation was found between suPAR levels with CURB-65 and PSI score (r = 0.423 and r = 0.489; p < .001 for both). The AUC for suPAR to discriminate SCAP patients from CAP was 0.783 at a cut-off value 4.27 ng/mL. AUCs of suPAR for predicting 30-day and 1-year mortalities were 0.815 (95% CI 0.746-0.866) and 0.820 (95% CI 0.770-0.870). Regression result shows suPAR (≥8.92 ng/mL) was independent factor for 30-day mortality (HR = 2.83, 95% CI 1.04-7.69) and suPAR with cut-off value 6.18 ng/mL could predict 1-year mortality (HR = 2.44, 95% CI 1.09-5.44). suPAR was strongly associated with CAP severity and could be a prognostic indicator for 1-year survival in elderly.

Roles of macrophage stimulating protein and tyrosine kinase receptor RON in smoke-induced airway inflammation of rats.

OBJECTIVE: To investigate the roles of macrophage stimulating protein (MSP) and its tyrosine kinase receptor RON in smoke-induced airway inflammation of rats. METHODS: Inhalation of combustion smoke was administered in rats to induce airway inflammation. Alveolar macrophages (AM) of healthy and smoking rats were isolated at different time points, cultured and then treated with different concentrations of MSP for 24 h. RESULTS: When compared with healthy rats, MSP increased in the serum and bronchoalveolar lavage fluid (BALF) of smoking rats in a time dependent manner. In smoking rats, the RON expression in the lung and AM was higher than in healthy rats, and these increases were time dependent. MSP stimulated the production of malondialdehyde (MDA) and reduced superoxide dismutase (SOD) activity in rat AM cells in a dose dependent manner. MSP also stimulated the release of inflammatory factors TNF-α, IL-8, IL-1ß and IL-10 in rat AM in a dose-dependent manner. Moreover, at the same MSP concentration, the contents of MDA, TNF-α, IL-8 and IL-1ß in the AM of smoking rates were higher than in healthy rats, while the IL-10 content and SOD activity were lower than in healthy rats. CONCLUSION: MSP and its receptor RON are involved in the smoke-induced airway inflammation in rats via promoting AM to release inflammatory cytokines and inducing the increase of oxygen free radical.