Daily Ards Research Analysis

AIM: This review was done to evaluate diagnostic accuracy of LUS against established ARDS reference standards in adult populations. MATERIAL AND METHODS: Four electronic databases were searched through June 2025 without language restrictions. Two reviewers independently screened studies, extracted data, and assessed quality using QUADAS‑2. Bivariate random‑effects models generated pooled sensitivity, specificity, likelihood ratios, diagnostic odds ratios (DORs), and hierarchical summary receiver‑operating characteristic (HSROC) curves. Subgroup analyses explored pattern‑ versus score‑based protocols and prospective study designs. Publication bias was assessed via Deeks' funnel‑plot test. RESULTS: Fourteen studies (531 ARDS-positive; 1354 ARDS-negative; pre‑test probability=28%) met inclusion criteria. Overall pooled sensitivity was 0.84 (95%CI: 0.69-0.92) and specificity 0.94 (95%CI: 0.83-0.98), with an AUROC of 0.95 (95%CI: 0.93-0.96). The positive likelihood ratio was 13.3 (95%CI: 5.0-35.9) and negative likelihood ratio 0.17 (95%CI: 0.09-0.34), corresponding to a DOR of 77 (95%CI: 26-227). Pattern‑based protocols achieved sensitivity 0.82 and specificity 0.96 (AUROC=0.96), while score‑based approaches yielded sensitivity 0.90 and specificity 0.83 (AUROC=0.93). Deeks' test indicated potential publication bias (p=0.004).

Acute lung injury (ALI)/Acute Respiratory Distress Syndrome (ARDS) is a life-threatening condition marked by severe inflammatory responses and disruption of the alveolar-capillary barrier, leading to high mortality rates and lack of effective treatments. Recent research has underscored the crucial role of programmed cell death pathways-pyroptosis, apoptosis, and necroptosis-in exacerbating inflammation and barrier dysfunction in ALI/ARDS. However, effective therapeutic agents targeting this process remain scarce. In this study, we reveal that PANoptosis, which integrates these cell death pathways through the PANoptosome complex, plays a central role in the pathogenesis and progression of ALI/ARDS. The levels of PANoptosis-related molecules were significantly elevated in both the ALI mice and the clinical ARDS patient samples, highlighting it as a novel therapeutic target. Building on this insight, we developed a multifunctional nanomedicine, TPNs/Sal B, which integrates tea polyphenol-based nanoparticles (TPNs), a bioactive nanomaterial with anti-pyroptotic and anti-necroptotic properties, with salvianolic acid B (Sal B), known for its anti-apoptotic effects. Our results demonstrate that the nanomedcine TPNs/Sal B effectively inhibit PANoptosis, thereby attenuating lung tissue pathological damage, reducing inflammation, and improving lung epithelial barrier function in ALI models. Moreover, we identified LIM and SH3 protein 1 (LASP1) which may play an critical role in modulating alveolar epithelial barrier function during ALI/ARDS progression, and treatment with TPNs/Sal B effectively restored LASP1 levels. Our findings underscore the therapeutic potential of TPNs/Sal B as a targeted treatment for ALI/ARDS, offering a promising strategy for modulating PANoptosis and preserving lung function.

BACKGROUND: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are prevalent and severe respiratory conditions with high morbidity and mortality rates, and specific treatment modalities are lacking. Garlic oil (GO), which is rich in sulfur compounds, has diverse biological properties, including anti-inflammatory and antioxidant effects; nonetheless, its utility is hindered by its limited water solubility and bioavailability. Nanotechnology-based formulations offer a promising solution to enhance GO efficacy. The aim of this investigation was to elucidate the protective effect and underlying mechanism of GO nanodisks (GO-nanodisks) on lipopolysaccharide (LPS)-induced acute lung injury. METHODS: We developed a novel prescription utilizing GO-nanodisks. An acute lung injury model was induced in mice through LPS administration. The mice were randomly allocated into groups: healthy untreated, positive control, GO (50 mg/kg), and GO-nanodisks (50 mg/kg). Tail vein injections were administered accordingly. Subsequent assessments included lung histopathology; inflammatory cytokine (TNF-α, IL-6, IL-4, and IL-10) levels; oxidative stress marker (MDA, SOD, T-AOC, NO, and CAT) levels; and protein expression analyses. RESULTS: This study successfully developed GO-nanodisks using a novel fabrication method. The GO-nanodisks demonstrated favorable physicochemical characteristics, with a mean particle diameter of 148 ± 3 nm, a polydispersity index (PDI) of 0.15 ± 0.02, a zeta potential of -0.2 ± 0.1 mV, and an encapsulation efficiency of 55.26% ± 0.04%. Compared with the positive control group, the GO-nanodisk group presented significantly reduced lung tissue pathology, lower inflammatory factor levels, and an improved oxidative stress status. Furthermore, the GO-nanodisk group displayed Keap1/Nrf2 signaling pathway activation and NF-kappa B pathway inhibition, surpassing the efficacy of the GO group. CONCLUSION: The results of this study demonstrate that the nanodisks formulation developed in this work effectively enables stable encapsulation of GO, enhances its bioavailability, and improves its protective efficacy against LPS-induced ALI. Furthermore, this formulation provides a promising theoretical foundation for the encapsulation of oil-based pharmaceuticals.