Purpose: The purpose of the present study was to estimate the effect of shionone (SHI) on sepsis-induced acute lung injury (ALI).Methods: The cecal ligation and puncture (CLP) surgery was performed to induce sepsis in mice. Pulmonary hematoxylin and eosin staining, the wet/dry ratio, myeloperoxidase (MPO) activity, and the survival rate were detected. The RAW264.7 cells were treated with SHI and stimulated with lipopolysaccharide (LPS). The cells were also overexpressed by extracellular mechanism protein 1 (ECM1) adenovirus. The relative levels of granulocyte–macrophage colony-stimulating factor, IL-6, IL-1β, TNF-α, IL-10, and TGF-β in the serum and supernatant were measured by ELISA. The protein expressions of ECM1, p-STAT5, signal transducer and activator of transcription 5 (STAT5), p-NF-κB, nuclear factor kappa-B (NF-κB), Arg1, CD206, CD16/32, and iNOS in the CLP-induced lung tissues and LPS-induced cells were detected by western blot. The cell counts of Ly6G, F4/80, CD16/32, and CD206 were evaluated by flow cytometry. The ECM1 expression was also observed by immunohistochemistry and immunofluorescence staining.Results: As a result, the histopathological change, pulmonary edema, and the MPO activity were relieved by SHI. SHI treatment increased the percentage of neutrophil and macrophage in the bronchoalveolar lavage fluid. Besides, SHI administration inhibited pro-inflammatory cytokines and M1 phenotype indices, as well as augmented the anti-inflammatory cytokines and M2 phenotype indices. SHI also attenuated the ECM1/STAT5/NF-κB pathway both in vivo and in vitro. The overexpression of ECM1 confirmed that the regulated effect of SHI was due to ECM1 signaling.Conclusion: In conclusion, the present study suggests that SHI ameliorated sepsis-induced ALI by screwing M1 phenotype to M2 phenotype macrophage via the ECM1/STAT5/NF-κB pathway.

Introduction: Atrial Septal Defect/Patent Foramen Ovale (ASD/PFO) occlusion is performed to prevent paradoxical embolism and reduce the risk of recurrent ischemic stroke. Left atrial appendage (LAA) closure is used as an alternative to medical therapy of non-valvular atrial fibrillation for prevention of stroke. Multiple studies have examined performing LAA and ASD/PFO occlusion. However, the feasibility and safety of combined occlusion of the left atrial appendage and ASD/PFO are not clear, furthermore, these studies are limited by their small sample sizes and retrospective analysis. In this study, we aimed to systematically review and meta-analyze the feasibility and safety of combining left atrial appendage and ASD/PFO closure.Methods: PubMed, Web of Science, CNKI, Cochrane Library, Embase, and WanFang database were searched up to April 2022 to identify peer-reviewed human studies on assessing the feasibility, safety, and efficacy of combining left atrial appendage and ASD/PFO closure. The primary outcome was calculated: procedural feasibility outcome and procedural safety outcome.Results: A total of 10 articles, including 340 patients from multiple countries, were included in the analysis. The principal findings of our study are: compared with single LAA closure, (i) combining PFO/ASD occlusion and LAA closure had similar procedural success proportion (98.43%, 95% CI: 96.67–100.00%), (ii) similar safety event incidences developed (1.67%, 95% CI: 0.24–3.92%), subgroup analyzed safety event incidences in death was 0.00 (95% CI: 0.00–0.33%), cardiac tamponade was 0.87% (95% CI: 0.00–2.77%), device embolization was 0.00 (95% CI: 0.00–0.60%), major bleeding was 0.00 (95% CI: 0.00–0.33%), stroke was 0.00 (95% CI: 0.00–0.02%).Conclusion: Although this systematic review and meta-analysis demonstrate the technical feasibility and safety of combining closure of PFO/ASD and LAA, further studies of sufficient sample size, long-term follow-up, and rigor endpoint criteria are yet needed to fully evaluate this combination procedure for its role in clinical outcomes.

Alzheimer’s disease (AD) is the leading cause of dementia worldwide and significantly impacts the essential functions of daily life and social activities. Research on AD has found that its pathogenesis is related to the extracellular accumulation of amyloid-beta (Aβ) plaques and intracellular neurofibrillary tangles in the cortical and limbic areas of the human brain, as well as cerebrovascular factors. The detection of Aβ or tau can be performed using various probes and methodologies. However, these modalities are expensive to implement and often require invasive procedures, limiting accessibility on a large scale. While magnetic resonance imaging (MRI) and computed tomography (CT) are generally used for morphological and structural brain imaging, they show wide variability in their accuracy for the clinical diagnosis of AD. Several novel imaging modalities have emerged as alternatives that can accurately and vividly display the changes in blood flow and metabolism in each brain area and enable physicians and researchers to gain insights into the generation and progression of the cerebro-microvascular pathologies of AD. In this review, we summarize the current knowledge on microvascular perfusion imaging modalities and their application in AD, including MRI (dynamic susceptibility contrast-MRI, arterial spin labeling-MRI), CT (cerebral CT perfusion imaging), emission computed tomography (positron emission tomography (PET), single-photon emission computed tomography (SPECT)), transcranial doppler ultrasonography (TCD), and retinal microvascular imaging (optical coherence tomography imaging, computer-assisted methods for evaluating retinal vasculature).