Pre-operative methicillin-resistant Staphylococcus aureus (MRSA) colonization has been associated with increased risk of post-operative infection and medical complications in lower-extremity arthroplasty; however, its impact on outcomes following total shoulder arthroplasty (TSA) remains poorly understood. This study aims to evaluate the association between MRSA colonization and early medical as well as mid-term implant-related complications after primary TSA. The TriNetX US Research Network was queried to identify primary TSA patients. Propensity score matching (1:1) was performed using demographic characteristics and relevant comorbidities. Ninety-day medical complications, including readmission, emergency department utilization, venous thromboembolism, pneumonia, urinary tract infection, stroke, sepsis, respiratory failure, and cardiac events, were assessed. Two-year implant-related outcomes included periprosthetic joint infection, aseptic loosening, dislocation, periprosthetic fracture, revision TSA, and all-cause mortality. Risk ratios (RRs) with 95% confidence intervals (CIs) were generated for all comparative analyses. Overall, 122,665 patients met eligibility criteria. Matching resulted in 2 well-balanced cohorts of 1,781 patients each. At two years, MRSA colonization was associated with significantly higher rates of periprosthetic joint infection (RR, 6.64; 95% CI, 3.53-12.47), aseptic loosening (RR, 1.63; 95% CI, 1.08-2.47), revision surgery (RR 1.75; 95% CI, 1.22-2.52), dislocation (RR, 1.76; 95% CI, 1.08-2.86), and mortality (RR, 1.90; 95% CI, 1.55-2.33). Ninety-day medical complications were also significantly higher among MRSA-colonized patients, with higher rates of readmission, emergency department utilization, venous thromboembolism, pulmonary embolism, pneumonia, urinary tract infection, stroke, sepsis, and respiratory failure (all P < .01). Cardiac events occurred at similar rates between cohorts (P = .390). Pre-operative MRSA colonization was associated with substantially higher risks of both 90-day medical and 2-year implant-related complications following TSA. These findings highlight the importance of routine MRSA screening, consideration of decolonization protocols, and heightened perioperative vigilance in this high-risk population.

Morbidity patterns, mortality, and antimicrobial resistance among children hospitalized in neonatal and pediatric intensive care units in a rural area of Vietnam.

Although SARS-CoV-2, the virus that causes COVID-19 has been responsible for pneumonia, recent studies indicate that it also affects the kidneys, heart, and brain, among other vital organs. Evidence suggests that this virus may travel retrogradely from the olfactory epithelium to brain stem sections, causing neurological impairments in a significant number of individuals. Individuals with severe COVID-19 frequently have elevated cytokines that promote inflammation and acute respiratory failure and require frequent supportive ventilation. These factors are believed to contribute to cognitive deterioration. Severe neurological outcomes in COVID-19 patients include- paralysis, stroke, cranial nerve deficits, delirium, encephalopathy, seizures, and meningitis. The virus, with its unique structure, and a high binding affinity for the human enzyme ACE2 (used as an entry point by the virus), contributes significantly to its deadly nature. Furthermore, to address the outbreak effectively, researchers worldwide must develop precise treatment strategies. Advancing new diagnostic and treatment methods to mitigate the long-term effects of COVID-19 on cognition requires further epidemiological research and clinical experience. Additionally, by understanding the virus's impact on cognitive functions, healthcare professionals can develop targeted treatments to alleviate these severe neurological consequences.

Immune-epithelial dual-targeting bilirubin nanoparticles for acute lung injury.

Open reduction and internal fixation vs acute total hip arthroplasty for geriatric acetabular fractures: A multicenter matched cohort study.

Glutaminase deficiency has recently been identified as a novel inherited metabolic disorder with a broad phenotypic spectrum ranging from early-onset global developmental delay to lethal early neonatal encephalopathy. We describe three infants from two unrelated families who presented clinically with neonatal onset refractory burst-suppression epileptic encephalopathy and respiratory failure, progressing to either a persistent vegetative state or early death. One patient remains alive at the age of six years. Metabolic investigations demonstrated elevated glutamine concentrations in cerebrospinal fluid and increased serum alanine and glutamine levels, biochemical features characteristic of urea cycle disorders, while ammonia levels remained within the normal range. Notably, brain magnetic resonance imaging revealed cystic lesions resembling the neuroimaging findings typically observed in patients with urea cycle defects. Exome sequencing identified a homozygous, unreported missense variant in GLS (NM_014905.5:c.1174G>A; p.Gly392Arg) in both siblings from family 1, and a novel homozygous missense variant (NM_014905.5:c.1031T>C; p.Leu344Pro) in the proband from family 2. Functional studies of patient fibroblasts and recombinantly expressed mutant glutaminase protein, demonstrated a complete glutaminase deficiency. In addition, patient-derived fibroblasts exhibited pronounced ultrastructural abnormalities, including nuclear dysmorphisms, lysosomal dysfunction with glycogen accumulation, ER stress, Golgi disruption, and mitochondrial fragmentation, along with altered cellular bioenergetics characterized by impaired mitochondrial respiratory function. The biochemical and clinical findings in our patients support a key role for elevated glutamine in the neuropathogenesis of both glutaminase-deficient patients and individuals with hepatic encephalopathy and/or urea cycle defects.

An ensemble learning approach for predicting hospital stay in transplant patients

Prehospital high-flow nasal canula oxygen therapy in hypoxemic acute respiratory failure: an open-label, randomized controlled pilot study (PRHOXY-1).

Admission clinical features associated with disease severity in psittacosis pneumonia: A retrospective study.

The immunodynamics of pulmonary fibrosis.

Successful treatment of pneumonia due to Mycobacterium goodii in a severely underweight 45-year-old woman: case report and review of literature.

Epidemiology, treatment practices, and societal and economic burden of Duchenne muscular dystrophy in Finland: A retrospective register and chart review study.

Three disease-modifying therapies are approved for individuals with spinal muscular atrophy (SMA); however, data concerning the combination of these therapies remain limited. This study aimed to evaluate the safety and efficacy of add-on risdiplam in children who had experienced clinical deterioration despite gene therapy with onasemnogene abeparvovec. This is a retrospective case series study at two centers of children treated with risdiplam who had previously received onasemnogene abeparvovec. Therapy was evaluated by clinical examination, standardized physiotherapeutic assessments, and parent perspectives. Five patients with SMA (four male and one female), diagnosed between 0 and 8 months, were included in the study. All had 2 SMN2 copies and were started on risdiplam between five and 48 months after onasemnogene abeparvovec. Risdiplam was added due to motor regression, dysphagia, new onset of respiratory insufficiency, and/or recurrent pneumonias. Four children showed improvements in motor development, swallowing, and respiratory function. One child remained stable. Parents perceived a significant improvement in general impression, motor, and respiratory function. The add-on therapy was well tolerated without adverse events. Our results indicate an improvement in most children in a case series through add-on risdiplam. Evaluating clinical outcome parameters in clinical practice may prove challenging and should be complemented by the parental perspective. The decision regarding the use of add-on therapy in children with SMA who receive one line of treatment but show a clinical deterioration should be considered on an individual level, and assessments of predefined therapeutic goals are recommended.

Extracorporeal membrane oxygenation (ECMO) is a life-saving intervention for patients with severe cardiac or respiratory failure, but it is associated with a high risk of thrombotic and bleeding complications. Unfractionated heparin (UFH) remains the most frequently used anticoagulant, largely due to historical practice and longstanding clinical familiarity, despite the absence of robust evidence from randomized controlled trials. Alternative strategies-including direct thrombin inhibitors (DTIs), low-molecular-weight heparins (LMWHs), nafamostat mesylate (NM), and no anticoagulation-are increasingly being explored. However, a comprehensive and contemporary comparison of these approaches has been lacking. We conducted a comprehensive search of PubMed/MEDLINE, EMBASE, and CENTRAL through March 2025, supplemented by manual searches of reference lists. We included randomized controlled trials and observational studies including patients 16 years or older receiving ECMO for ≥ 24 h that compared any anticoagulation strategy with another or with no anticoagulation. The primary outcome was thromboembolic events; secondary outcomes included bleeding and mortality. Risk of bias was assessed using validated tools. Meta-analyses were performed using a multivariable random-effects model, with prespecified subgroup analyses by ECMO modality (venoarterial [VA], venovenous [VV], or mixed) and subsequent sensitivity analyses. Twenty-one observational studies involving 2 775 adult ECMO patients were included, with UFH serving as the comparator in all studies. DTIs showed reduced thromboembolism (OR 0.73; 95% CI: 0.53-0.99) and were associated with significantly lower bleeding (OR 0.51; 95% CI: 0.39-0.67) and mortality (OR 0.70; 95% CI: 0.52-0.94), confirmed in a sensitivity analysis. LMWH was associated with significantly reduced odds of thromboembolic events (OR 0.26; 95% CI: 0.13-0.55), as well as showing a favorable bleeding profile (OR 0.46; 95% CI: 0.25-0.87), yet no significant difference in mortality (OR0.80; 95% CI: 0.30-2.14). While no anticoagulation reduced the odds for bleeding (OR 0.17; 95% CI: 0.07-0.38) and NM showed no significant differences, both had wide confidence intervals, limiting interpretation. Heterogeneity for LMWH was low for efficacy and bleeding, yet substantial for mortality; for DTI, low to moderate; for no anticoagulation, low; and for NM, substantial to high on all comparisons. In this systematic review and meta-analysis, DTIs and LMWH appear to be effective and safe alternatives to UFH in adult ECMO, with consistent reductions in thromboembolic and bleeding events and a survival benefit observed for DTIs. These findings support reconsideration of UFH as the default anticoagulant and favor a more prominent role for alternative strategies in clinical practice. PROSPERO CRD42022363588.

Pediatric acute respiratory distress syndrome (PARDS) remains one of the most complex and clinically significant forms of acute respiratory failure (ARF) in pediatric intensive care. High variability of the clinical course, limited effectiveness of standard respiratory strategies, and unfavorable outcomes in a subset of patients indicate the insufficiency of traditional pathogenetic concepts predominantly based on the alveolar-inflammatory model. This article considers PARDS as a systemic pathological process driven by the sequential involvement of microcirculatory, energetic and regulatory mechanisms. Particular attention is paid to endothelial dysfunction, impaired tissue perfusion, and mitochondrial dysfunction as key factors underlying the development of energy deficiency and the limitation of process reversibility. It is shown that hypoxemia and ARF within this paradigm represent clinical manifestations of a deeper hypoxic-ischemic cascade affecting both the lungs and the central nervous system. The proposed concept has practical significance for improving the understanding of pathogenesis, stratifying disease severity, and assessing prognosis in PARDS.

A 3-year-old boy with speech delay presented with fever and choreoathetosis, progressing to cardiogenic shock and respiratory failure. He met diagnostic criteria for multisystem inflammatory syndrome in children (MIS-C) and improved with treatment, which included intravenous immune globulin (IVIG), methylprednisolone, and anakinra per hospital protocol. Following sedation weaning, choreoathetosis recurred. Repeat brain MRI revealed new symmetric T2 hyperintensity and restricted diffusion in the globi pallidi. He was discharged with persistent developmental regression, hypotonia, and choreoathetosis. Four months later, he was readmitted with respiratory failure from a human metapneumovirus infection and died from refractory cardiogenic shock and multiorgan failure. Posthumous exome sequencing identified a homozygous variant of unknown significance in MDH2 (malate dehydrogenase 2). A sibling with chronic encephalopathy and myocarditis shared this genotype. MDH2 deficiency is associated with movement disorders and cardiomyopathy. MIS-C plausibly triggered clinical decompensation in our patient. Genetic or metabolic causes should be considered in children with a history of developmental delay, acute neurologic symptoms, and symmetric basal ganglia lesions.

Effects of inflammatory phenotypes in acute respiratory distress syndrome on mortality and partitioning of lung and chest wall mechanics in patients in the USA and Canada: a retrospective cohort study.

Extracorporeal membrane oxygenation (ECMO) is a technique increasingly used in the practice of intensive therapy for extracorporeal gas exchange and/or circulatory support in patients with acute respiratory and/or cardiac failure, when conventional treatment modalities are ineffective. We aimed to investigate the association of antithrombin III with clinical outcomes in patients with cardiogenic shock caused by acute myocardial infarction undergoing ECMO. We retrospectively studied patients with acute myocardial infarction complicated by cardiogenic shock undergoing ECMO in four hospitals in China. The in-hospital mortality rate was 47.8% (194/406). The antithrombin III at admission of the in-hospital death group (n = 194) and the survival group (n = 212) were 45.70 ± 21.57 and 50.97 ± 25.37%, respectively. In-hospital mortality and acute kidney injury, and serum creatinine in the antithrombin III at admission < 46% group were significantly higher than that in the antithrombin III at admission ≥ 46% group. By univariate and multivariate analysis, serum albumin < 30g/L, low AT III at admission, and serum lactate were found to be related to in-hospital mortality. Our investigation demonstrated that low antithrombin III at admission was associated with in-hospital in cardiogenic shock secondary to acute myocardial infarction on ECMO, suggesting that antithrombin III may be an indicator of shock severity.

In the delivery room, newborn respiratory failure precedes cardiac failure, emphasizing the importance of effective ventilation. Face masks for ventilation may cause air leakage around the mask with subsequent suboptimal lung pressure, and intubation requires skilled providers. Laryngeal mask airways (LMA) may provide a more stable airway interface, with improved seal and more consistent ventilation that is less dependent on provider technique. An evaluation of the feasibility, acceptability, and initial outcomes of implementing the laryngeal mask airway as the first-line approach for ventilation in late preterm and term infants was conducted in a high-resource, urban safety-net hospital with a level III neonatal intensive care unit (NICU). The LMA was introduced and promoted as the firstline for delivery room ventilation in infants ≥35 weeks gestational age and ≥1.5 kg from August 2023 to August 2024. Implementation was supported by comprehensive training, survey feedback, and multidisciplinary involvement. The program evaluation spanned a 2-year period from August 2022 to August 2024. Feasibility and acceptability data were collected via provider surveys, and neonatal outcomes were compared pre- and post-implementation from electronic health record data. During implementation, LMAswereused as first-line in 58.7% of eligible neonates indicated for delivery room ventilation. Provider surveys showed increased knowledge and confidence in LMA use after education and high comfortability with LMA implementation in the delivery room. NICU admission rates, delivery room endotracheal intubations, chest compressions, and epinephrine use were similar across groups. Providers across experience levels successfully inserted LMAsafter brief training. LMA as first-line ventilation yielded similar outcomes to face mask in an urban safety-net hospital. Future research should explore broader applicability.

Pulmonary fibrosis represents one of the most challenging frontiers in respiratory medicine, characterized by progressive scarring that ultimately leads to respiratory failure and death. Despite decades of research, therapeutic options remain frustratingly limited, with only three Food and Drug Administration (FDA)-approved agents that merely slow disease progression without reversing established fibrosis. This therapeutic impasse stems largely from the translational disconnect between traditional preclinical models and human disease complexity. Animal models fail to recapitulate the chronic, progressive nature of human fibrosis, while conventional cell culture systems cannot capture the intricate three-dimensional (3D) architecture and multicellular interactions that drive fibrotic remodeling. The emergence of new approach methodologies (NAMs) has catalyzed a paradigm shift in pulmonary fibrosis research, offering unprecedented opportunities to model human disease with greater fidelity. This review examines three revolutionary platforms that are reshaping our understanding of fibrotic mechanisms: precision-cut lung slices that preserve native tissue architecture, self-organizing lung organoids that enable patient-specific disease modeling, and microfluidic lung-on-chip systems that recreate physiological breathing mechanics. We critically evaluate the unique capabilities and inherent limitations of each technology, explore their applications in mechanistic studies and drug discovery, and discuss emerging hybrid approaches that promise to accelerate therapeutic development. By synthesizing current evidence and identifying future directions, this review provides a roadmap for leveraging these innovative technologies to finally break through the therapeutic ceiling in pulmonary fibrosis.