Previously, young children had limited respiratory support options during interfacility transport. Recently, high-flow nasal cannula (HFNC) and noninvasive ventilation (NIV) have become available for pediatric transport. We hypothesized that the implementation of HFNC and NIV on interfacility transport decreases the rate of intubation in infants and toddlers before and after transport to a tertiary-care pediatric intensive care unit (PICU).

We conducted a retrospective chart review of children aged 30 days to < 36 months transported to a tertiary-care PICU from a referring hospital with respiratory distress from 2014 to 2019. Groups were analyzed before (2014-2017) and after the implementation (2017-2019) of HFNC and NIV during transport. NIV was defined as positive pressure ventilation delivered through nasal cannula. The primary outcome was to compare the pre- and postimplementation groups with regard to the rate of intubation before transport and within 48 hours of PICU admission. Secondary outcomes were the association between intubation rate and comorbidities and the comparison of length of respiratory support and hospital length of stay between the pre- and postimplementation groups.

A total of 262 patients met criteria, 133 before and 129 after the intervention. The rate of intubation before PICU admission was 44% in the preintervention group versus 36% in patients transported after the implementation of HFNC and NIV, a trend that was not statistically significant (P = .19). The rate of intubation within 48 hours of PICU admission was 8% (before) and 11% (after) with no statistical significance (P = .48). Comorbidities were not associated with an increased rate of intubation before transport (P = .09) or within 48 hours of admission (P = .45). Hospital length of stay and length of respiratory support were not different between pre- and postintervention groups (P = .18 and P = .3, respectively). The availability of HFNC/NIV was associated with a significant decrease in the proportion of patients who received oxygen via nasal cannula or face mask during transport (46% before vs. 13% after the intervention; P < .01).

After the introduction of HFNC/NIV during transport to a large tertiary-care hospital in a major metropolitan area, fewer nasal cannula/face masks were used during transport in favor of HFNC/NIV but no significant change in intubation rates was found.

Evidence supporting the use of sugammadex as a rescue strategy in prehospital "cannot intubate, cannot oxygenate" (CICO) situations remains sparse and indirect. Although contemporary airway guidelines prioritize front-of-neck access (FONA) as the definitive intervention, discussion of pharmacological reversal persists in prehospital practice, predominantly within gray literature, local protocols, and educational materials. This persistence reflects an ongoing hypothesis in prehospital airway management that warrants critical appraisal. We performed a narrative synthesis of perioperative, emergency department, and prehospital literature, including case reports, expert consensus documents, and contemporary airway guidelines, to assess whether pharmacological reversal can plausibly modify outcomes in airway failure. Across these sources, no outcome-level data support sugammadex as an effective rescue maneuver in established CICO. Perioperative CICO case series further indicate that reversal of neuromuscular blockade does not reliably resolve airway obstruction or obviate the need for surgical airway access. In the prehospital environment, rapid desaturation and limited monitoring further reduce the plausibility of pharmacological rescue once CICO has developed. For helicopter and ground emergency medical service systems, current evidence supports emphasis on early recognition of CICO, structured airway algorithms, and timely performance of FONA, rather than reliance on pharmacological reversal.

Hepatopulmonary hydatidosis (HPH) is a clinically relevant presentation of hepatic cystic echinococcosis (CE) in which pulmonary involvement is present at the time of diagnosis. Reliable identification of patients at risk remains challenging, and indiscriminate thoracic imaging may lead to unnecessary investigations. This study aimed to identify hepatic predictors associated with concomitant pulmonary involvement and to develop a simple risk stratification model to support selective thoracic imaging.

We conducted a retrospective cohort study of patients with confirmed hepatic CE followed at a single tertiary center. Cyst activity was classified according to the World Health Organization (WHO) staging system, and anatomical distribution was assessed using a segment-based classification. Multivariable logistic regression was performed to identify predictors of HPH. A point-based clinical risk score (HepatoMAP) was derived by combining cyst activity and anatomical distribution. Model discrimination and calibration were assessed using receiver operating characteristic (ROC) analysis, bootstrap validation, and calibration plots.

Among 292 patients, 23 (7.8%) had hepatopulmonary hydatidosis (HPH) at initial diagnosis. Active cysts (WHO CE1-2) were strongly associated with HPH (91.3% in HPH vs. 33.2% in hepatic-only disease, p < 0.001) and remained the only independent predictor in multivariable analysis. The HepatoMAP score demonstrated good discrimination (AUC 0.83) with good calibration (bootstrap-corrected slope 0.97). No cases of HPH were observed in patients with low-risk scores (0-1 points), whereas HPH occurred predominantly in patients with scores ≥ 3.

In hepatic CE, concomitant pulmonary involvement at baseline was strongly associated with cyst activity and showed a structured but non-independent relationship with segmental topography. The HepatoMAP score showed promising rule-out characteristics in this cohort and may support more selective use of thoracic imaging. Prospective external validation is required before routine clinical implementation.

To investigate the electromyographic activity (sEMG) of the suprahyoid/submental (SH) muscles during swallowing in adults with different OSA severities, controlled for body mass index (BMI), and to establish predictive factors for changes in muscle activity.

This cross-sectional observational study included 37 adults diagnosed with OSA (AHI > 5). The patients were divided into two groups according to the apnea-hypopnea index (AHI): Group I (AHI = 5 ≤ 30) and Group II (AHI > 30). sEMG activity was recorded during the voluntary swallowing of 10 mL and 15 mL of thin liquid (water). The sEMG peak, integral, and maximum velocity (Vmax) were calculated. Groups were compared by general multivariate analysis of covariance, with BMI as a covariate. A general multivariate linear regression model (GRM) was applied to analyze the contribution of predictors to the EMG parameters. The significance level was set at p < 0.05.

There was a predominance of males (n = 24, 64.9%) and obese individuals (BMI > 30, n = 25, 67.6%) in the sample. Compared with Group I, Group II presented significantly lower peak, Vmax and integral values (P ≤ 0.006). The GRM revealed that the peak and integral were explained by the AHI and BMI, whereas the tongue volume and behavior during swallowing together explained the Vmax.

Activation of the suprahyoid (SH) muscles was reduced in patients with severe OSA. In addition to disease severity, BMI and the myofunctional condition of the tongue also contribute to impaired activation. Taken together, these findings indicate that muscle weakness and deficits in motor control compromise the activation of SH muscles during swallowing.

Current treatment for atherosclerotic cardiovascular diseases (ASCVD) mainly focuses on the modification of systemic risk factors, such as hyperglycemia and hyperlipidemia. Despite significant efforts and expanse, achieving early and proper diagnosis of ASCVD to improve clinical outcomes remains challenging, and vascular-targeted therapies or genetic editing, while ideal, are still limited. The development of nanomedicine-based mRNA vaccines for SARS-CoV-2 has demonstrated the potential of nanotechnology to target previously inaccessible molecules. Precision therapies by nanomedicine targeting specific tissues/molecules hold potential for new treatment paradigms by precisely modulating disease-causing molecular pathways within diseased tissues, including dysfunctional vasculature. By leveraging insights into the pathogenic contributors of atherogenesis, researchers have optimized nanoplatforms' composition, synthesis strategies, and surface design to enhance therapeutic efficacy and enable early diagnosis. Herein, we present an updated overview of therapeutic and diagnostic strategies using nanomedicine for ASCVD, and explore future research directions and innovative approaches for nanomedicine-driven theranostics in cardiovascular care.

Severe scoliosis with prior corrective spinal surgery poses significant anesthetic challenges in obstetric patients due to altered spinal anatomy and potential respiratory compromise. Conventional neuraxial or general anesthesia may be risky, making alternative approaches necessary for safe cesarean delivery. The Taylor paramedian technique provides an effective option by bypassing distorted midline anatomy.

A 35-year-old primigravida (G1P0) at 37±1 week's gestation with surgically corrected thoracolumbar scoliosis and restrictive pulmonary disease, complicated by bronchopneumonia, was admitted for cesarean delivery. Preanesthetic assessment revealed limited cervical mobility, restricted mouth opening, and challenging spinal landmarks. Initial midline puncture at L3-L4 failed, so a paramedian Taylor approach at L5-S1 using anatomical landmarks was performed. Intrathecal 12 mg plain 0.5% bupivacaine with 20 µg fentanyl achieved complete sensory and motor block. Maternal hemodynamics remained stable with normal oxygenation. Cesarean section was completed uneventfully, delivering a healthy neonate weighing 3 kg with Apgar scores 8 and 9. Postoperative recovery was smooth, and the patient was discharged on day 3.

Paramedian Taylor spinal anesthesia is a safe and effective alternative in parturients with severe scoliosis and restrictive pulmonary disease. Individualized planning, technical expertise, and careful execution allow complete sensomotor block, minimize respiratory risk, and ensure successful cesarean delivery in high-risk patients.

A 3-year-old male passenger developed acute respiratory distress approximately 30 minutes after takeoff during an international flight from the United States to Addis Ababa. Despite multiple rounds of nebulized albuterol and escalating oxygen therapy, his respiratory status progressively deteriorated. A multidisciplinary team of onboard physicians administered epinephrine and hydrocortisone from the emergency medical kit while coordinating with ground medical control. The aircraft was subsequently diverted to Athens, Greece, where the child was handed over to emergency services and later stabilized. This case highlights the challenges of managing pediatric respiratory distress in-flight and the critical importance of prompt coordination, adequate medical supplies, and crew preparedness.

Obstructive sleep apnea (OSA), characterized by recurrent apneic/hypopneic events and intermittent hypoxia, exhibits a high yet underrecognized prevalence (40%-65%) among patients with acute myocardial infarction (MI), compounded by suboptimal performance of conventional screening modalities. A defining epidemiological feature is the pronounced nocturnal predominance of MI onset in OSA cohorts, diverging from the diurnal pattern observed in non-OSA populations.Pathophysiologically, OSA manifests a paradoxical duality in the context of MI: acute cardioprotective effects, including reduced in-hospital mortality, attenuated infarct size (evidenced by lower peak troponin levels), and enhanced coronary collateralization, are attributed to ischemic preconditioning induced by chronic intermittent hypoxia. Conversely, OSA independently exacerbates long-term post-MI risk, with severe nocturnal hypoxemia driving elevated rates of major adverse cardiovascular events (MACE), alongside maladaptive ventricular remodeling, electrical instability, and endothelial dysfunction-mechanisms underpinned by synergistic activation of inflammatory pathways and cell death signaling.Therapeutically, the role of OSA-directed interventions in post-MI management remains contentious. Observational data suggest potential benefits of continuous positive airway pressure (CPAP), but large randomized controlled trials fail to demonstrate incremental cardioprotection in broader cardiovascular cohorts. Emerging proof-of-concept evidence suggests that early adaptive servo-ventilation (ASV) may influence myocardial salvage after acute MI in carefully selected patients with sleep-disordered breathing, particularly those without reduced ejection fraction. However, these findings should be interpreted cautiously given the small trial size and prior safety concerns regarding ASV in patients with heart failure and reduced ejection fraction. Resolving these uncertainties necessitates targeted research incorporating optimized adherence strategies and enhanced screening protocols to reconcile OSA's acute phenotypic associations with its long-term prognostic implications.

To interpret and transmit biological signals, proteins use correlated motions. Experimental determination of these dynamics and the structural distributions they generate remains a key challenge. Here, using 1146 crystal structures of the main protease (M^pro) from SARS-CoV-2, we were able to infer a model of the enzyme's structural fluctuations. M^pro is regulated by concentration, becoming enzymatically active after forming a homodimer. To understand the structural changes that enable dimerization to activate catalysis, we employed our model, predicting which regions of the dimerization domain are structurally correlated with the active site. Mutations at these positions, expected to disrupt catalysis, resulted in a dramatic reduction in activity in one case, a mild effect in the second, and none in the third. Additional crystallography and biophysical experiments provide a mechanistic explanation for these results. Our work suggests that a statistical crystallography, in which numerous crystallographic datasets are analyzed, can reveal the structural fluctuations of protein native states and help uncover their biological function.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease characterized by deregulated cell death programs that drive epithelial injury, fibroblast activation, and irreversible tissue remodeling. Multiple regulated cell death (RCD) modalities, including apoptosis, autophagy, necrosis, ferroptosis, pyroptosis, and cuproptosis, are implicated in IPF pathogenesis across epithelial cells, fibroblasts, macrophages, and endothelial cells. Apoptosis leads to alveolar epithelial cell loss and fibrosis initiation, whereas autophagy modulates fibroblast proliferation and extracellular matrix turnover. Necrosis amplifies inflammation; ferroptosis promotes epithelial dysfunction through lipid peroxidation; and pyroptosis activates the inflammasome pathway. Emerging evidence links cuproptosis, a copper-dependent death mode, to fibrotic remodeling. These pathways are interconnected: apoptosis and autophagy can shift within the same cell, and epithelial apoptosis may induce macrophage pyroptosis, amplifying the profibrotic cascade. Emerging evidence indicates that these RCD modalities are coordinated through shared stress signals and regulatory nodes. Therapeutically, targeting RCD offers promising opportunities, with Bcl-2 inhibitors for apoptosis, mTOR inhibitors for autophagy, iron chelators for ferroptosis, and early interventions for pyroptosis and cuproptosis. Targeting shared regulatory mechanisms or combining pathway-directed strategies may further enhance efficacy. By balancing cell death and survival, these strategies could attenuate inflammation, restrict fibroblast-driven scarring, and restore repair capacity. This review underscores the complexity and crosstalk of RCD in IPF, and proposes a conceptual framework for their coordinated regulation, highlighting its potential for therapeutic innovation.