Congenital lobar emphysema (CLE) presents unique anaesthetic challenges due to the risk of worsening hyperinflation with positive pressure ventilation. We describe an infant who developed rapid desaturation during induction for thoracoscopic lobectomy. In the absence of a suitable bronchial blocker or time for fibreoptic guidance, lung isolation was achieved using a rigid bronchoscope for immediate left lung ventilation, followed by bougie-assisted endobronchial intubation. This manoeuvre restored oxygenation and enabled safe surgical completion. The case highlights the life-saving potential of rigid bronchoscope-guided intubation with temporary bronchoscope ventilation in airway emergencies involving CLE.

A woman in her mid-30s presented with a 3-month history of dry cough, profound weight loss and anorexia. Evaluation revealed pulmonary tuberculosis microbiologically confirmed by bronchoalveolar lavage cartridge-based nucleic acid amplification testing (CBNAAT) together with histopathological evidence from endobronchial biopsy, with extensive dissemination involving the pleura, pericardium, peritoneum, omentum, liver and colon. Bronchoscopy demonstrated multiple nodular endobronchial lesions while bronchoalveolar lavage CBNAAT detected Mycobacterium tuberculosis without rifampicin resistance. Endobronchial biopsy showed granulomatous inflammation consistent with tuberculosis. The patient was HIV-negative and non-diabetic but had severe protein-energy malnutrition, with a body mass index of 12.9 kg/m². Cutaneous lesions over the extremities initially raised suspicion of vasculitis; however, autoimmune evaluation including antinuclear antibody testing and serum angiotensin-converting enzyme levels was unremarkable. The clinical course was further complicated by antitubercular therapy-induced hepatitis and severe left ventricular systolic dysfunction, necessitating modification of therapy. This case highlights the protean manifestations of disseminated tuberculosis, the diagnostic value of bronchoscopy and molecular testing in sputum smear-negative disease and the challenges of management in severely malnourished individuals.

This review summarizes the biological characteristics of mast cell-derived extracellular vesicles (EVs) and their roles in lung diseases involving mast cell activation and immune dysregulation, focusing on asthma, neonatal lung injury, and lung adenocarcinoma.

Published studies involving mast cell lines, animal models, and patient-derived biospecimens on mast cell-derived EVs in pulmonary inflammation were summarized.

Not applicable.

We synthesized evidence on EV biogenesis, cargo composition, target-cell interactions, immunomodulatory functions, and disease-specific roles.

Mast cells are key effector cells in pulmonary inflammation whose functions extend beyond classical degranulation. They communicate with epithelial, stromal, and immune cells via EVs carrying proteins, lipids, mRNAs, and microRNAs. These vesicles modify recipient-cell function and mediate inflammatory amplification, epithelial injury, airway remodeling, and immune-cell activation. Mast cell-derived EVs exert disease- and context-dependent effects by regulating epithelial-immune crosstalk, type 2 inflammation, tissue remodeling, and tumor microenvironmental interactions.

Mast cell-derived EVs are key mediators of intercellular communication in pulmonary inflammation. However, most evidence comes from cell and animal models, and the clinical relevance of specific EV cargoes remains unclear. Further studies are needed to clarify their disease-specific mechanisms and evaluate their potential as biomarkers and therapeutic targets.

Hypopharyngeal inflammatory masses are rare conditions that may occur in association with factors such as intubation, trauma, or reflux. Their clinical and imaging features often closely mimic those of malignant tumors, necessitating a definitive diagnosis through the histopathological examination of surgical specimens. Although surgical excision remains the primary intervention for large lesions, vigilant postoperative surveillance is imperative because of the high recurrence rates.

We detail the case of a 26-year-old female admitted for a traumatic brainstem injury. Following 21 days of endotracheal intubation and over 2 months of nasogastric tube placement, flexible laryngoscopy revealed a mass in the left pyriform sinus, prompting referral to the Department of Otolaryngology-Head and Neck Surgery. The patient exhibited dysphagia and mild hoarseness as her sole symptoms.

Computed tomography and neck magnetic resonance imaging demonstrated a mass measuring approximately 32 mm × 27 mm at its largest cross-section, with ill-defined borders, heterogeneous density, and multiple bilateral cervical lymph nodes. Biopsy revealed inflammatory necrosis and granulation tissue.

Given the large size of the mass, persistent dysphagia, the inability to completely exclude malignancy based on imaging findings, and limited biopsy results, complete resection was performed under general anesthesia to alleviate symptoms and establish a definitive diagnosis. Subsequent pathological examination confirmed the presence of an inflammatory mass composed of necrotic and proliferative granulation tissue.

The patient recovered well after the surgical removal of the lesion. During the 4-month follow-up period, a laryngoscopy performed 11 weeks after surgery revealed no recurrence of the mass. At the final telephone follow-up at 4 months after surgery, the patient reported no throat-related symptoms.

This case suggests that prolonged tube placement may be a potential contributing factor in the development of inflammatory masses in the pyriform sinus. In patients with a history of long-term tube placement who present with a pyriform sinus mass, inflammatory masses may be considered among the differential diagnoses.

To investigate the role of the transcription factor FOXP1 and its target gene SDHAF2 in allergic rhinitis (AR), as well as their regulatory effects on ferroptosis in nasal epithelial cells.

An AR mouse model and IL-4/IL-13-induced human nasal epithelial cells (HNEpCs) were used. Gene and protein expression, cytokine secretion, ferroptosis markers, nasal pathology, and AR symptoms were assessed via transcriptome sequencing, qRT-PCR, Western blot, ELISA, dual-luciferase reporter assay, co-immunoprecipitation, detection of Fe²⁺, ROS, GSH, MDA and lipid peroxides (LPO), and transmission electron microscopy. The biological functions of FOXP1 and SDHAF2 were explored through gene knockdown or overexpression, combined with the intervention of ferroptosis activator Erastin or inhibitor Ferrostatin-1.

Sdhaf2 was significantly upregulated in AR models and closely associated with mitochondrial function and ferroptosis. Knockdown of SDHAF2 inhibited IL-4/IL-13-induced ferroptosis and inflammation in HNEpCs, whereas overexpression of SDHAF2 aggravated these phenotypes. The above changes could be modulated by Erastin or Ferrostatin-1. FOXP1 was highly expressed in AR models and transcriptionally regulated SDHAF2, which was verified by dual-luciferase reporter assays. SDHAF2 interacted with ALOX15 to increase ALOX15 expression and promote ferroptosis. Additional overexpression of ALOX15 reversed the inhibitory effect of SDHAF2 knockdown on ferroptosis. In OVA-induced AR mice, Sdhaf2 knockdown relieved nasal symptoms, reduced inflammatory cytokines, improved nasal pathological lesions and suppressed ferroptosis, and these protective effects were partially abolished by Erastin.

FOXP1 upregulates SDHAF2. The encoded SDHAF2 protein interacts with ALOX15 to facilitate ferroptosis in nasal epithelial cells, thereby aggravating AR progression. The FOXP1/SDHAF2/ALOX15/ferroptosis axis may serve as a novel therapeutic target for AR.

Small interfering RNA (siRNA) therapeutics have emerged as a transformative approach for sequence-specific gene silencing, offering the potential to treat a broad spectrum of diseases by selectively suppressing disease-associated genes. However, the clinical translation of siRNA remains limited by rapid enzymatic degradation, poor cellular uptake, inadequate endosomal escape, and off-target effects, necessitating the development of efficient delivery systems. Extracellular vesicles (EVs) have gained considerable attention as natural nanocarriers owing to their excellent biocompatibility, low immunogenicity, intrinsic targeting capability, and ability to protect therapeutic cargo while traversing complex biological barriers. This review comprehensively discusses the biological characteristics of EVs, the molecular basis of RNA interference, and the major challenges associated with siRNA delivery [Fig. 1]. Recent advances in EV engineering, including cargo-loading strategies such as electroporation, sonication, extrusion, parent-cell engineering, and microfluidic approaches, together with surface functionalization using peptides, antibodies, aptamers, and hybrid nanoplatforms, are critically evaluated for improving targeting specificity and intracellular delivery. Furthermore, the therapeutic applications of engineered EV-mediated siRNA delivery in cancer, neurological disorders, liver diseases, cardiovascular diseases, inflammatory disorders, and infectious diseases are systematically summarized, highlighting their potential to enhance gene silencing while minimizing systemic toxicity. Current challenges related to large-scale manufacturing, cargo-loading efficiency, standardization, quality control, regulatory approval, and clinical translation are also discussed, together with emerging technologies involving synthetic biology, genome engineering, artificial intelligence, and multifunctional hybrid vesicles. Overall, engineered extracellular vesicles represent a highly versatile and biologically inspired platform for targeted siRNA delivery, providing a promising foundation for the development of next-generation precision RNA therapeutics and accelerating the clinical translation of gene-silencing strategies.

Subarachnoid hemorrhage (SAH) disproportionately affects young adults aged 15-49 years, yet prior global studies have rarely focused on this population and may obscure age-specific patterns by combining all-age data. We therefore quantified the global burden of SAH in young adults and explored disparities by sex and socio-demographic index (SDI) level.

Using Global Burden of Disease 2021 data from 204 countries (1990-2021), we estimated the age-standardized incidence rates (ASIR), age-standardized prevalence rates, age-standardized death rates, and age-standardized disability-adjusted life-year (DALY) rates. Temporal trends were assessed using estimated annual percentage changes and age-period-cohort models. We further evaluated cross-country disparities by SDI, examined risk attribution using population attributable fractions, projected future burden to 2050 using Bayesian age-period-cohort models, and conducted an exploratory machine learning analysis with SHapley Additive exPlanations.

In 2021, SAH caused 55,012 deaths and 3.19 million DALYs among young adults globally. Although the ASIR declined over time, the absolute burden remained substantial. High-SDI regions showed higher incidence, whereas lower-SDI regions bore a greater mortality and DALY burden. Males had a higher DALY burden, whereas females had higher prevalence. Metabolic risks were the leading contributors globally, while environmental and occupational risks remained more prominent in low-SDI settings. Projections suggested a continued decline in burden through 2050, although uncertainty widened after 2040.

SAH in young adults represents a non-uniform burden-transition pattern, with declining age-standardized rates but persistent premature mortality and DALYs, higher incidence in high-SDI settings, and greater fatal and disabling burden in lower-resource settings. These findings support stronger metabolic-risk reduction in high-SDI settings and improved blood pressure screening, referral, and acute-care access in lower-resource regions.

Cardiac troponin I (cTnI), the most sensitive and specific biomarker of myocardial injury, enables early detection of subclinical cardiotoxicity. Highly sensitive cTnI testing is therefore crucial for early safety assessment of TCM. This study developed an electrochemical immunosensor for cTnI using a carboxylated multi-walled carbon nanotube/poly(o-phenylenediamine) (MWCNTs-COOH/PoPD) composite sensing membrane. This design leverages the large surface area and high conductivity of MWCNTs-COOH along with PoPD's biocompatibility to enhance electrochemical performance. Antibodies achieved controllable covalent immobilization with preferential orientation via 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide/N-hydroxysuccinimide (EDC/NHS) cross-linking, facilitating specific recognition of cTnI. Under optimized conditions, the sensor exhibited excellent linearity across the ranges of 0.2-40 pg/mL and 0.05-50 ng/mL, with detection limits of 0.06 pg/mL and 4.17 pg/mL, respectively, demonstrating high sensitivity, specificity, and stability. Successfully applied to screen cardiotoxic TCM components, the sensor accurately detected cTnI released from cardiomyocytes, enabling precise quantification of toxins such as aconitine. It was also extended to evaluate myocardial protectants such as baicalin and their synergistic detoxification effects. This work establishes an efficient, sensitive platform for early TCM cardiotoxicity warning and toxic substance identification based on cTnI, while also supporting the screening of protective components. It is crucial for safeguarding the clinical safety of TCM and fostering the sustainable development of its industry.

Robot-assisted gait training (RAGT) is well established for post-stroke gait rehabilitation, but its potential effects on psychological and behavioral outcomes are less clear. This study investigated the effects of adding RAGT to conventional rehabilitation on balance, gait, kinesiophobia, and movement confidence in individuals with post-stroke hemiparesis.

This single-blind, parallel-group randomized controlled trial included 60 individuals with post-stroke hemiparesis (50-75 years), randomly allocated to an RAGT group (n = 30) or control group (n = 30). Ethical approval was obtained from the Clinical Research Ethics Committee of Istanbul Yeni Yüzyıl University (Approval No. 20.01.2022/05; approval date: 20 January 2022). Both groups received conventional rehabilitation for 8 weeks; the RAGT group additionally received 24 sessions of RAGT. Kinesiophobia was a prespecified study outcome assessed using the Kinesiophobia Causes Scale (KCS); balance, gait, and balance confidence were also assessed. All 60 randomized participants completed follow-up and were analyzed in their assigned groups.

Significant group × time interactions were observed for several outcomes, including BBS, TUG duration, 10MWT walking speed, ABC, and KCS total score (p < 0.05). The between-group difference in change for KCS total score was -0.36 (95% CI: -0.51 to -0.21; partial eta squared = 0.292). In post hoc analyses adjusting each outcome for its baseline value, significant group effects remained for BBS, TUG duration, 10MWT walking speed, ABC, KCS biological domain, and KCS total score (p< = 0.031), whereas 10MWT step count and the KCS psychological domain were no longer statistically significant.

Adding RAGT to conventional rehabilitation was associated with greater improvements in several balance, mobility, walking-speed, balance-confidence, and kinesiophobia outcomes compared with conventional rehabilitation alone. These findings suggest potential additional physical and psychological benefits of incorporating RAGT into post-stroke rehabilitation. However, because the RAGT group received greater overall treatment exposure, the observed between-group differences cannot be attributed solely to the robotic component. The principal contribution of this study is the concurrent evaluation of kinesiophobia and movement confidence alongside physical outcomes.

The weight-adjusted waist index (WWI), a recently proposed marker reflecting central fat distribution independent of body weight, has emerged as a potential indicator of metabolic and cardiovascular risk. Considering the high burden of inflammation and metabolic disturbance in chronic kidney disease (CKD), we examined whether elevated WWI is associated with all-cause and cardiovascular disease (CVD) mortality among CKD patients and whether systemic inflammation, assessed by the neutrophil-to-lymphocyte ratio (NLR), mediates this relationship. Data were obtained from the National Health and Nutrition Examination Survey 1999 to 2018 cycles. WWI was calculated based on anthropometric measurements. Weighted multivariate Cox proportional hazards models were applied to examine the associations of WWI with mortality. Robustness was verified through WWI quartile-based survival curves and subgroup analyses. Mediation analysis was used to evaluate the indirect effect of NLR on the WWI-mortality relationship. A total of 5582 CKD participants were included. WWI levels were significantly and independently associated with increased risks of all-cause mortality (adjusted hazard ratio = 1.17, 95% confidence interval (CI): 1.09-1.26, P < .001) and CVD mortality (adjusted hazard ratio = 1.24, 95% CI: 1.09-1.41, P = .001). WWI showed a linear positive relationship with both outcomes (nonlinearity P > .05). Mediation analysis indicated that NLR exerted a modest but significant indirect effect on all-cause mortality (β = -9.94, 95% CI:-20.90--2.85, P < .001), explaining 6.66% of the total effect. Elevated WWI was independently associated with higher risks of all-cause and CVD mortality in CKD. NLR partially mediated these associations. Therefore, assessing both central adiposity and inflammatory burden may aid in identifying high-risk CKD patients and guide clinical strategies for improving long-term outcomes.