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Objective: To assess the surgical outcomes and identify predictors of surgical success in patients with positional and non‐positional obstructive sleep apnea following multilevel airway surgery. Study Design: Retrospective cohort study. Setting: Singe‐tertiary medical center. Methods: This study included 158 patients with obstructive sleep apnea who underwent multilevel airway surgery. Patients were divided into 2 groups according to position dependency: "positional patients" group (n = 100), and "nonpositional patients" group (n = 58). The characteristics and surgical outcomes of the 2 groups were compared. Results: The nonpositional group included younger and more obese patients in comparison to the positional group. Moreover, the nonpositional group had more severe disease than the positional group. Both groups showed overall improvement after surgery, and the surgical success rate did not differ significantly between the 2 groups (nonpositional, 41.4% vs positional, 48.0%; P =.424). Notably, 69.0% of patients belonging to the non‐positional group converted to positional group postoperatively. Logistic regression analysis revealed that larger tonsil size, female sex, and higher mean O2 saturation were associated with higher success rate in the positional group, whereas larger tonsil size was associated with surgical success in the nonpositional group. Conclusion: Both nonpositional and positional groups showed improvements following multilevel airway surgery, and surgery induced a transition from nonpositional to positional group. Given that the factors related to surgical success differed between the two groups, surgeons should consider position dependency and these distinct factors during decision‐making. [ABSTRACT FROM AUTHOR]

The IL-23-Th17 axis is responsible for neutrophilic inflammation in various inflammatory diseases. Here, we discover a potential pathway to inhibit neutrophilic asthma. In our neutrophil-dominant asthma (NDA) model, single-cell RNA-seq analysis identifies a subpopulation of CD39+CD9+ interstitial macrophages (IMs) suppressed by IL-23 in NDA conditions but increased by an IL-23 inhibitor αIL-23p19. Adoptively transferred CD39+CD9+ IMs suppress neutrophil extracellular trap formation (NETosis), a representative phenotype of NDA, and also Th17 cell activation and neutrophilic inflammation. CD39+CD9+ IMs first attach to neutrophils in a CD9-dependent manner, and then remove ATP near neutrophils that contribute to NETosis in a CD39-dependent manner. Transcriptomic data from asthmatic patients finally show decreased CD39+CD9+ IMs in severe asthma than mild/moderate asthma. Our results suggest that CD39+CD9+ IMs function as a potent negative regulator of neutrophilic inflammation by suppressing NETosis in the IL-23-Th17 axis and can thus serve as a potential therapeutic target for IL-23-Th17-mediated neutrophilic asthma. Interstitial macrophages (IM) are a specialised population of macrophage cells in the lungs which regulate lung inflammation. Here using mouse models, the authors show that a CD39+CD9+ IM population reduce IL-23/Th17 driven neutrophilic inflammation through suppression of NETosis. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the impact of different types of nasal inflammation on the regulation of entry‐associated genes of respiratory viruses, including severe acute respiratory syndrome coronavirus 2 (SARS CoV‐2), Middle East respiratory syndrome coronavirus (MERS‐CoV), human coronavirus 229E (HCoV‐229E), and influenza virus, in the nasal epithelium. Subjects were classified into three groups: control, eosinophilic chronic rhinosinusitis (ECRS), and noneosinophilic CRS (NECRS) groups. Angiotensin‐converting enzyme 2 (ACE2) and transmembrane protease serine subtype 2 (TMPRSS2), alanyl aminopeptidase (ANPEP), dipeptidyl peptidase 4 (DPP4), and beta‐galactoside alpha‐2,6‐sialyltransferase 1 (ST6GAL1), and beta‐galactoside alpha‐2,3‐sialyltransferase 4 (ST3GAL4) were selected as key entry‐associated genes for SARS‐CoV‐2, HCoV‐229E, MERS‐CoV, and influenza, respectively, and were evaluated. Brushing samples obtained from each group and human nasal epithelial cells cultured using an air–liquid interface system were treated for 7 days with typical inflammatory cytokines and analyzed using real‐time polymerase chain reaction. Western blot analysis and confocal microscopy were performed. The entry‐associated genes showed distinct regulation patterns in response to each interleukin‐4 (IL‐4), interleukin‐13 (IL‐13), tumor necrosis factor‐α (TNF‐α), and interferon‐γ (IFN‐γ). Specifically, ACE2 significantly decreased in type 2 cytokines (IL‐4 and IL‐13), while TMPRSS2 significantly decreased in type 1 cytokines (TNF‐α and IFN‐γ). ANPEP significantly decreased in both types of cytokines. Remarkably, DPP4 significantly increased in type 2 cytokines and decreased in type 1 cytokines. Moreover, ST6GAL1 and ST3GAL4 significantly increased in type 2 cytokines and decreased in type 1 cytokines, particularly IFN‐γ. These findings were supported by western blot analysis and confocal imaging results, especially for ACE2 and DPP4. The findings regarding differential regulation suggest that patients with ECRS, primarily mediated by type 2 inflammation, may have lower susceptibility to SARS‐CoV‐2 and HCoV‐229E infections but higher susceptibility to MERS‐CoV and influenza infections. [ABSTRACT FROM AUTHOR]

This article discusses the role of exosomes, which are small vesicles released by cells, in regulating mucus hypersecretion in airway inflammatory diseases such as allergic rhinitis. The researchers isolated exosomes from nasal lavage fluid and found that they contained specific microRNAs (miRNAs) that were differentially expressed in patients with allergic rhinitis compared to control subjects. They focused on one particular miRNA, let-7a-5p, and found that it inhibited the expression of MUC5AC, a gene associated with goblet cell hyperplasia and mucus production. These findings suggest that exosomal let-7a-5p could be a potential therapeutic target for treating allergic rhinitis. [Extracted from the article]

The automotive industry has experienced remarkable growth in recent decades, with a significant focus on advancements in autonomous driving technology. While still in its early stages, the field of autonomous driving has generated substantial research interest, fueled by the promise of achieving fully automated vehicles in the foreseeable future. High-definition (HD) maps are central to this endeavor, offering centimeter-level accuracy in mapping the environment and enabling precise localization. Unlike conventional maps, these highly detailed HD maps are critical for autonomous vehicle decision-making, ensuring safe and accurate navigation. Compiled before testing and regularly updated, HD maps meticulously capture environmental data through various methods. This study explores the vital role of HD maps in autonomous driving, delving into their creation, updating processes, and the challenges and future directions in this rapidly evolving field. [ABSTRACT FROM AUTHOR]

This article discusses the role of nasal tissue-resident memory T (TRM) cells in chronic rhinosinusitis (CRS) with nasal polyps. The study found that non-eosinophilic CRS (NECRS) is characterized by an abundance of CD69+CD103+ TRM cells, which produce type 1 and type 17 cytokines. These TRM cells may contribute to NECRS pathogenesis and could indicate difficult-to-treat cases. The findings provide new insights into the role of nasal-resident T cells in CRS and suggest potential therapeutic targets. [Extracted from the article]

Obstructive sleep apnea (OSA) is characterized by cyclic normoxic and hypoxic conditions (intermittent hypoxia, IH) induced by the repeated closure of the upper-airway respiratory tract. As a pathomechanism of OSA, IH results in various comorbidities via chronic inflammation and related pathways. However, the role of other inflammatory cells, such as lymphocytes, has not been well-explored. This study aimed to examine the effects of IH on the distribution and balance of T cell subsets and other related cytokines, and mechanisms in the immune system. We modified OSA mouse model (male C57BL/6N male) using our customized chamber that controls specific sleep and oxygenic cycles. To induce hypoxia, the IH group was repeatedly exposed to 5% O2 and 21% O2 lasting for 120 s each for 7 h daily for 4 weeks. Mice were then subjected to a recovery period of 4 weeks, in which IH stimulation was ceased. T cells and related cytokines were analyzed using flow cytometry and immunohistochemistry. Compared with the control group, the IH group had significantly lower levels of CD4+CD25+Foxp3+ regulatory T cells but higher levels of Th 17, IL-4, HIF-1, and inflammatory cytokines. After the recovery period, these altered changes in the immune cells were recovered, and we found no significant difference in their levels between the control and recovery groups. This study revealed that the Th17/Treg ratio is increased by intermittent hypoxia, and this imbalance can explain immune-related diseases, including recently reported allergies, autoimmune, and even cancer diseases, arising from OSA. [ABSTRACT FROM AUTHOR]