The purpose of this study is to objectively quantify physical activity and sedentary behaviour in children and adolescents during hospital admission using device-based monitoring and investigate the association between sedentary behaviour and pain, constipation, surgery status, movement restrictions, 30-day readmission, and length of stay. Children and adolescents aged 2 ≤ 17 years admitted between March and September 2025 to three paediatric departments at a Danish hospital were eligible for this prospective observational study. Children and adolescents scheduled for day surgery and wheelchair users were excluded. All participants wore two triaxial accelerometers throughout their hospital stay. In total, 103 hospitalised children and adolescents were included. The participants spent 45 min per day (interquartile range 20–125) in upright position (standing and walking time combined) and were sedentary (sitting and lying time combined) for 23.3 h per day (21.8–23.7). Adolescents undergoing spine surgery were sedentary for 23.6 h per day (23.5–23.7), of which 22.6 h (21.8–23.0) were spent lying in bed. Sedentary behaviour was significantly associated with higher age (p < 0.001), opioid consumption beyond standardised analgesia (p = 0.028), and orthopaedic procedures (p < 0.001). No associations between sedentary behaviour and length of stay (p = 0.391), 30-day readmission (p = 0.467), laxative use (p = 0.695), and postoperative movement restrictions (p = 0.637) were found. Conclusion: Hospitalised children and adolescents in this study exhibited high levels of sedentary behaviour. The findings highlight that mobilisation strategies are needed across all paediatric surgical procedures, but adolescents, patients undergoing orthopaedic or spine procedures, and those prescribed opioids beyond standardised analgesia require particular attention. There is a need for further evidence of the consequences of sedentary behaviour during hospitalisation among children and adolescents.
To assess temporal changes in the timing of pulmonary valve replacement (PVR) among patients with tetralogy of Fallot and to determine whether temporal shifts toward earlier PVR were accompanied by differences in ventricular volumes, ventricular function and exercise capacity after PVR. The timing of PVR was evaluated in a national, retrospective cohort using the Aalen-Johansen method to estimate cumulative incidence while accounting for death as competing risk. Trends in ventricular volumes, ventricular function and exercise capacity were assessed in patients with prior PVR, who underwent cardiac imaging and exercise testing in a cross-sectional study using robust linear regression. Among 463 potential candidates for PVR in the retrospective cohort, estimated time from repair to PVR was 34 years, 22 years and 16 years in patients born in 1940–1976, 1977–1999, and 2000–2021, respectively (p < 0.001). In total, 153 patients with prior PVR born between 1942 and 2009 were examined in the cross-sectional study. Estimated right ventricular end-systolic volume index was lower by 5.43 mL/m2 per decade (p = 0.02), estimated right ventricular ejection fraction increased by 2.08 Overview of temporal changes in the timing of pulmonary valve replacement and impact on outcomes. The median time from repair to pulmonary valve replacement for each birth era was based on a nationwide cohort of patients with tetralogy of Fallot and estimated using the cumulative incidence function. The temporal trends in ventricular volumes, ventricular function and exercise capacity were estimated based on the results from patients who underwent cardiac magnetic resonance imaging, transthoracic echocardiography and cardiopulmonary exercise testing as part of a national multicentre cross-sectional study and estimated using robust regression methods
To assess the long-term economic and welfare burden of Ménière’s disease, focusing on healthcare costs, income, and reliance on social benefits before and after the first hospital-recorded diagnosis. We conducted a nationwide matched cohort study in Denmark, involving 5,434 patients with a hospital-recorded Ménière’s disease diagnosis later confirmed by an otorhinolaryngologist and 16,302 matched controls based on age, sex, civil status, municipality, and index year defined by the first hospital registration of Ménière’s disease. The mean age was 59 years, and 56
To investigate the association between multimorbidity level, all-cause 30-day readmissions, and 30-day mortality in a cohort of patients hospitalised with an ambulatory care sensitive condition. Older patients with moderate or severe multimorbidity had higher 30-day readmission and mortality compared with those without multimorbidity, increasing with the level of multimorbidity. Multimorbidity increases 30-day readmission and mortality risk. Identifying high-risk patients and tailoring care during and after hospitalisation is therefore crucial. We investigated the association between multimorbidity level, all-cause 30-day readmissions, and post-discharge 30-day mortality. Using Danish national registries, we identified patients aged ≥ 65 years hospitalized for ambulatory care-sensitive conditions between 2013–2018. Multimorbidity was defined as having 2–3 (moderate) or ≥ 4 (severe) of 39 chronic conditions. We estimated 30-day cumulative incidence of readmission after discharge and used Cox regression to calculate hazard ratios (HRs) for readmission and mortality. Among 178,445 patients, median age was 78 years (IQR: 71–85), 59
Inflammation, aberrant proteostasis, and energy depletion are hallmarks of neurodegenerative diseases such as multiple sclerosis (MS). However, the interplay between inflammation, proteasomal dysfunction in neurons, and its consequences for neuronal integrity remains unclear. Using transcriptional, proteomic, and functional analyses of proteasomal subunits in inflamed neurons, we found that interferon-γ-mediated induction of the immunoproteasome subunit, proteasome 20S beta 8 (PSMB8) impairs the proteasomal balance, resulting in reduced proteasome activity. This reduction causes the accumulation of phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a key metabolic regulator, leading to enhanced neuronal glycolysis, reduced pentose phosphate pathway activity, oxidative injury, and ferroptosis. Neuron-specific genetic and systemic pharmacological targeting of PSMB8 or PFKFB3 protected neurons in vitro and in a mouse model of MS. Our findings provide a unifying explanation for proteasomal dysfunction in MS and possibly other neurodegenerative diseases, linking inflammation to metabolic disruption, and presenting an opportunity for targeted neuroprotective therapies.
