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Data regarding the association between subclinical thyroid dysfunction and clinical outcomes in ischemic stroke patients with intravenous thrombolysis (IVT) are limited. We aimed to investigate the predictive value of subclinical thyroid dysfunction in END, functional outcome and mortality at 3 months among IVT patients. We prospectively recruited 563 IVT patients from 5 stroke centers in China. Thyroid function status was classified as subclinical hypothyroidism, subclinical hyperthyroidism (SHyper) and euthyroidism. The primary outcome was END, defined as ≥ 4 point in the NIHSS score within 24 h after IVT. Secondary outcomes included 3-month functional outcome and mortality. Of the 563 participants, END occurred in 14.7%, poor outcome in 50.8%, and mortality in 9.4%. SHyper was an independent predictor of END [odd ratio (OR), 4.35; 95% confidence interval [CI], 1.86-9.68, P = 0.003], 3-month poor outcome (OR, 3.24; 95% CI, 1.43-7.33, P = 0.005) and mortality [hazard ratio, 2.78; 95% CI, 1.55-5.36, P = 0.003]. Subgroup analysis showed that there was no significant relationship between SHyper and clinical outcomes in IVT patients with endovascular therapy. In summary, SHyper is associated with increased risk of END, and poor outcome and mortality at 3 months in IVT patients without endovascular therapy.

Background and purpose: The baseline glucose-to-potassium ratio (GPR) is associated with poor outcomes in patients with acute brain injury and intracranial hemorrhage. However, the impact of serum GPR on clinical outcomes after endovascular thrombectomy (EVT) is unclear. This study aimed to evaluate the association between the GPR at admission and functional outcomes at 90 days after EVT. Methods: We retrospectively reviewed our database for patients with acute ischemic stroke involving an anterior circulation large-vessel occlusion who received EVT between October 2019 and December 2021. The baseline serum GPR was measured after admission. The primary outcome was a 90-day poor outcome, which was defined as a modified Rankin scale score of 3–6. Results: A total of 273 patients (mean age, 70.9 ± 11.9 years; 161 men) were finally included for analyses. During the 90-day follow-up, 151 patients (55.3%) experienced an unfavorable outcome. After adjusting for demographic characteristics and other potential confounders, the increased GPR was significantly associated with a higher risk of a 90-day poor outcome (odds ratio, 1.852; 95% confidence interval, 1.276–2.688, p = 0.001). Similar results were observed when the GPR was analyzed as a categorical variable. In addition, the restricted cubic spline observed a positive and linear association between the GPR and poor outcomes at 90 days (p = 0.329 for linearity; p = 0.001 for linearity). Conclusion: Our study found that ischemic stroke patients with the higher GPR at admission were more likely to have an unfavorable prognosis at 3 months, suggesting that GPR may be a potential prognostic biomarker for ischemic stroke after EVT. [ABSTRACT FROM AUTHOR]

The pathogenesis of acute lung injury is complex. Studies have demonstrated the role of neutrophil extracellular traps (NETs) in the process of lipopolysaccharide (LPS)‐induced acute lung injury (ALI). However, the underlying mechanism remains unclear. In this study, the regulation of Nrf2 in the formation of NETs, which was pathogenic in LPS‐induced ALI, was identified by analyzing the levels of Cit‐H3, lung function, lung tissue pathology, lung wet/dry ratio, the inflammatory cells, cytokines and proteins in the bronchoalveolar lavage fluid (BALF) and in addition, the activity of lung myeloperoxidase (MPO) was also measured. Results showed that the levels of Cit‐H3 measured by western blot in Nrf2‐knockout (KO) mice were higher compared with the WT mice after LPS stimulation. To further investigate the NETs formation was pathogenic during LPS‐induced ALI, the Nrf2‐KO mice were treated with DNase I. Results showed that DNase I improved lung function and lung tissue pathology and significantly reduced lung wet/dry ratio and proteins in the BALF. Besides, DNase I also attenuated the infiltration of inflammatory cells and the cytokines (TNF‐α, IL‐1β) production in the BALF and the activity of lung MPO. Therefore, these results together indicate that Nrf2 may intervene in the release of NETs during LPS‐induced ALI in mice. [ABSTRACT FROM AUTHOR]

Background and purpose: Caveolin‐1 (Cav‐1) is reported to mediate blood–brain barrier integrity after ischaemic stroke. Our purpose was to assess the role of circulating Cav‐1 levels in predicting symptomatic intracranial haemorrhage (sICH) amongst ischaemic stroke patients after endovascular thrombectomy (EVT). Methods: Patients with large‐vessel occlusive stroke after EVT from two stroke centres were prospectively included. Serum Cav‐1 level was tested after admission. sICH was diagnosed according to the Heidelberg Bleeding Classification. Results: Of 325 patients (mean age 68.6 years; 207 men) included, 47 (14.5%) were diagnosed with sICH. Compared with patients without sICH, those with sICH had a lower concentration of Cav‐1. After adjusting for potential confounders, multivariate regression analysis demonstrated that the increased Cav‐1 level was associated with a lower sICH risk (odds ratio 0.055; 95% confidence interval 0.005–0.669; p = 0.038). Similar results were obtained when Cav‐1 levels were analysed as a categorical variable. Using a logistic regression model with restricted cubic splines, a linear and negative association of Cav‐1 concentration was found with sICH risk (p = 0.001 for linearity). Furthermore, the performance of the conventional risk factors model in predicting sICH was substantially improved after addition of the Cav‐1 levels (integrated discrimination index 2.7%, p = 0.002; net reclassification improvement 39.7%, p = 0.007). Conclusions: Our data demonstrate that decreased Cav‐1 levels are related to sICH after EVT. Incorporation of Cav‐1 into clinical decision‐making may help to identify patients at a high risk of sICH and warrants further consideration. [ABSTRACT FROM AUTHOR]

The Luzon Strait (LS) is a key region for estimating carbon sources and sinks in the South China Sea (SCS) and is highly influenced by the Kuroshio Current (KC) and typhoons. Understanding the variations in the sea surface partial pressure of carbon dioxide (pCO2-sw) under the combined effects of typhoons and KC in this region is crucial for estimating local and regional changes in ocean carbon flux. Based on valuable in situ pCO2-sw and remote sensing data, this study aimed to reveal the temporal variations and the physical mechanisms of pCO2-sw variations under the comprehensive effects of both typhoons and Kuroshio Intrusion (KI) in the LS. One week after the passage of the tropical cyclone (TC) Nanmadol, the concentration in the pCO2-sw and the influencing mechanisms varied in three different regions (W1–W3) on Transect A (120°E). In the region dominated by SCS waters (W1), the average pCO2-sw increased by 5.1 μatm after TC, which was mainly due to the TC "Wind Pump" inducing strong vertical mixing, which brought dissolved inorganic carbon (DIC)-rich deeper water up to the surface. In the region affected by KC (W2 and W3), pCO2-sw decreased after the TC (−8.2 μatm and −1.8 μatm, respectively) with TC-enhanced KI because the invasion of lower pCO2-sw of Kuroshio waters inhibited the TC-induced upwelling. More significant TC-induced upwelling (W3) would alleviate the decrease in pCO2-sw caused by the TC-enhanced KI. This study is a rare case providing a better understanding of the variations in pCO2-sw under TC-enhanced KI, which provides support for regional climate change prediction and carbon flux estimation in the western boundary current regions. [ABSTRACT FROM AUTHOR]

Introduction: Endothelial dysfunction (ED) may result in parenchymal injury and therefore worsen the outcomes of ischemic stroke. This study aimed to determine whether ED could predict parenchymal hematoma (PH) in ischemic stroke patients treated with endovascular thrombectomy (EVT). Methods: Patients with large artery occlusion in the anterior circulation and treated with EVT were prospectively enrolled from 2 stroke centers. Serum soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, soluble E-selectin, and von Willebrand factor (vWF) were tested and summed to a standardized score to reflect the levels of ED. PH was diagnosed according to the Heidelberg Bleeding Classification. Results: Of the 325 enrolled patients (mean age, 68.6 years; 207 men), 41 (12.6%) developed PH. Patients with PH had higher concentrations of soluble E-selectin, vWF, and ED sum score. After adjusting for demographic characteristics, National Institutes of Health Stroke Scale score, pretreatment Alberta stroke program early computed tomography score, and other potential confounders, the increased ED burden was associated with PH (odds ratio, 1.432; 95% confidence interval, 1.031−1.988; p = 0.032). Similar significant results were found in the sensitivity analysis. The multiple-adjusted spline regression model showed a linear association between the total ED score and PH (p = 0.001 for linearity). Adding the ED score to the conventional model significantly improved the risk prediction of PH (net reclassification improvement = 25.2%, p = 0.001; integrated discrimination index = 2.9%; p = 0.001). Conclusions: This study demonstrated that ED might be related to PH. Introducing the ED score could increase the reliability of the PH risk model for stroke patients treated with EVT. [ABSTRACT FROM AUTHOR]