Lifestyles and the risk of an asthma attack in adult asthma patients: a cross-sectional study using NHANES database.

BACKGROUND: The influence of physical activity, diet and sleep on asthma has been well documented by recent studies respectively. However, few studies focus on the relationship between asthma attack and the overall lifestyle, which comprises interrelated lifestyle factors. This study aims to investigate the influence of lifestyles on the ratio of asthma attack. Data were extracted from the NHANES database (2017 to May 2020). METHODS: A total of 834 asthmatic patients were enrolled and divided into non-asthma attack (N.=460) and asthma attack (N.=374) groups. The risk factors for asthma attacks were preliminarily identified by univariate logistic analysis, then multivariate logistic analysis was employed to select independent risk factors other than lifestyles and further determine the association between lifestyles and asthma attacks. RESULTS: After multivariate logistic analysis, engagement of vigorous activity (Model 1 P=0.010, Model 2 P=0.016, Model 3 P=0.012), engagement of moderate activity (Model 1 P=0.006, Model 2 P=0.008, Model 3 P=0.003) and sleep disorder (Model1 P=0.001, Model 2 P<0.001, Model 3 P=0.008) were determined as independent risk factors of lifestyles for an asthma attack in the past year. CONCLUSIONS: This research documented that, for asthmatic patients, engagement of vigorous activity, engagement of moderate activity, and sleep disorder will make an asthma attack more likely to happen.

Exploration of the optimal pulse oximetry-derived oxygen saturation target for critically ill AECOPD patients: a retrospective cohort study.

Background: Appropriate levels of blood oxygen are crucial for critically ill patients. However, the optimal oxygen saturation has not been confirmed for AECOPD patients during their ICU stays. The purpose of this study was to determine the optimal oxygen saturation range target to reduce mortality for those individuals. Methods: Data of 533 critically ill AECOPD patients with hypercapnic respiratory failure from the MIMIC-IV database were extracted. The association between median SpO2 value during ICU stay and 30days mortality was analyzed by LOWESS curve, and an optimal range of SpO2(92-96%) platform was observed. Comparisons between subgroups and linear analyses of the percentage of SpO2 in 92-96% and 30days or 180 days mortality were performed to support our view further. Methods: Although patients with 92-96% SpO2 had a higher rate of invasive ventilator than those with 88-92%, there was no significant increase in the adjusted ICU stay duration, non-invasive ventilator duration, or invasive ventilator duration while leading to lower 30days and 180days mortality in the subgroup with 92-96%. In addition, the percentage of SpO2 in 92-96% was associated with decreased hospital mortality. Conclusion: In conclusion, SpO2 within 92-96% could lead to lower mortality than 88-92% and > 96% for AECOPD patients during their ICU stay.

Azithromycin use prior to ICU admission is associated with a lower short-term mortality for critically ill acute exacerbations of chronic obstructive pulmonary disease patients: A retrospective cohort study.

Azithromycin was thought to prevent acute exacerbations of chronic obstructive pulmonary disease (AECOPDs) by anti-microbial and anti-inflammatory effects. However, it's value in the treatment of critically ill patients with AECOPD before ICU admission remains unclear. Our study aimed to find whether azithromycin use prior to ICU admission leads to better clinical outcomes for those individuals. 533 critically ill patients with AECOPD from the MIMIC-IV database were included. Univariate followed multivariate logistic regression was used to select risk factors for short-term mortality. The multivariable logistic regression models were implemented to investigate the association between azithromycin use before ICU admission and short-term mortality. Lower short-term mortality was observed in the azithromycin group (p = .021), independent of differences in demographic data and other clinical outcomes (p>.05). Azithromycin use before ICU admission was proved to have a decreased short-term mortality by multivariable logistic regression (p<.05). The results remained consistent after being stratified by age, SOFA scores, pH, and cancer diagnosis. Azithromycin use prior to ICU admission was associated with lower short-term mortality for critically ill AECOPD patients.

Digoxin Ameliorates Glymphatic Transport and Cognitive Impairment in a Mouse Model of Chronic Cerebral Hypoperfusion.

The glymphatic system plays a pivotal role in maintaining cerebral homeostasis. Chronic cerebral hypoperfusion, arising from small vessel disease or carotid stenosis, results in cerebrometabolic disturbances ultimately manifesting in white matter injury and cognitive dysfunction. However, whether the glymphatic system serves as a potential therapeutic target for white matter injury and cognitive decline during hypoperfusion remains unknown. Here, we established a mouse model of chronic cerebral hypoperfusion via bilateral common carotid artery stenosis. We found that the hypoperfusion model was associated with significant white matter injury and initial cognitive impairment in conjunction with impaired glymphatic system function. The glymphatic dysfunction was associated with altered cerebral perfusion and loss of aquaporin 4 polarization. Treatment of digoxin rescued changes in glymphatic transport, white matter structure, and cognitive function. Suppression of glymphatic functions by treatment with the AQP4 inhibitor TGN-020 abolished this protective effect of digoxin from hypoperfusion injury. Our research yields new insight into the relationship between hemodynamics, glymphatic transport, white matter injury, and cognitive changes after chronic cerebral hypoperfusion.

A Nomogram Based on Comorbidities and Infection Location to Predict 30 Days Mortality of Immunocompromised Patients in ICU: A Retrospective Cohort Study.

BACKGROUND: The existing comorbidity indexes, like Charlson Comorbidity Index (CCI) and the Elixhauser Comorbidity Index (ECI), do not take infection factors into account for critically ill patients with immunocompromise, bringing about a decrease of prediction accuracy. Therefore, we attempted to incorporate infection location into the analysis to construct a rapid comorbidity scoring system independent of laboratory tests. METHODS: Data were extracted from the Multiparameter Intelligent Monitoring in Intensive Care III database. A total of 3904 critically ill patients with immunocompromise admitted to ICU were enrolled and assigned into training or validation sets according to the date of ICU admission. The predictive nomogram was constructed in the training set based on logistic regression analysis and then undergone validation in the validation set in comparison with SOFA, CCI and ECI. RESULTS: Factors eligible for the nomogram included patient's age, gender, ethnicity, underlying disease of immunocompromise like metastatic cancer and leukemia, possible infection on admission including pulmonary infection, urinary tract infection and blood infection, and one comorbidity, coagulopathy. The nomogram we developed exhibited better discrimination than SOFA, CCI and ECI with an area under the receiver operating characteristic curve (AUC) of 0.739 (95% CI 0.707-0.771) and 0.746 (95% CI 0.713-0.779) in the training and validation sets, respectively. Combining the nomogram and SOFA could bring a new prediction model with a superior predictive effect in both sets (training set AUC = 0.803 95% CI 0.777-0.828, validation set AUC = 0.818 95% CI 0.783-0.854). The calibration curve exhibited coherence between the nomogram and ideal observation for two cohorts (p>0.05). Decision curve analysis revealed the clinical usefulness of the nomogram in both sets. CONCLUSION: We established a nomogram that could provide an accurate assessment of 30 days ICU mortality in critically ill patients with immunocompromise, which can be employed to evaluate the short-term prognosis of those patients and bring more clinical benefits without dependence on laboratory tests.

Focal Solute Trapping and Global Glymphatic Pathway Impairment in a Murine Model of Multiple Microinfarcts.

Microinfarcts occur commonly in the aging brain as a consequence of diffuse embolic events and are associated with the development of vascular dementia and Alzheimer's disease. However, the manner in which disperse microscopic lesions reduce global cognitive function and increase the risk for Alzheimer's disease is unclear. The glymphatic system, which is a brain-wide perivascular network that supports the recirculation of CSF through the brain parenchyma, facilitates the clearance of interstitial solutes including amyloid ß and tau. We investigated whether glymphatic pathway function is impaired in a murine model of multiple microinfarcts induced by intraarterial injection of cholesterol crystals. The analysis showed that multiple microinfarcts markedly impaired global influx of CSF along the glymphatic pathway. Although suppression of global glymphatic function was transient, resolving within 2 weeks of injury, CSF tracers also accumulated within tissue associated with microinfarcts. The effect of diffuse microinfarcts on global glymphatic pathway function was exacerbated in the mice aged 12 months compared with the 2- to 3-month-old mice. These findings indicate that glymphatic function is focally disrupted around microinfarcts and that the aging brain is more vulnerable to this disruption than the young brain. These observations suggest that microlesions may trap proteins and other interstitial solutes within the brain parenchyma, increasing the risk of amyloid plaque formation.SIGNIFICANCE STATEMENT Microinfarcts, small (<1 mm) ischemic lesions, are strongly associated with age-related dementia. However, how these microscopic lesions affect global cognitive function and predispose to Alzheimer's disease is unclear. The glymphatic system is a brain-wide network of channels surrounding brain blood vessels that allows CSF to exchange with interstitial fluid, clearing away cellular wastes such as amyloid ß. We observed that, in mice, microinfarcts impaired global glymphatic function and solutes from the CSF became trapped in tissue associated with microinfarcts. These data suggest that small, disperse ischemic lesions can impair glymphatic function across the brain and trapping of solutes in these lesions may promote protein aggregation and neuroinflammation and eventually lead to neurodegeneration, especially in the aging brain.