The sustained progression of chronic obstructive pulmonary disease (COPD) may not be independently driven by a single process such as chronic inflammation, oxidative stress, or cell death, but rather originates from a cross-amplification network among "mitochondrial dysfunction-oxidative stress-regulated cell death." In the context of mitochondrial damage, excessive generation of reactive oxygen species (ROS), damage and release of mitochondrial DNA (mtDNA), and dysregulation of mitochondrial quality control (MQC) collectively promote airway epithelial injury, sustained inflammation, alveolar destruction, and tissue remodeling. Furthermore, regulated cell death modalities such as apoptosis, necroptosis, pyroptosis, and ferroptosis are not isolated from each other but are coupled under a shared context of mitochondrial stress, exhibiting different dominant patterns across various cell types and disease stages. Adopting an integrated perspective encompassing mitochondrial dysfunction, amplified oxidative stress, and the regulated cell death (RCD) cross-network, this article synthesizes current research regarding COPD-related mechanisms, with a focus on mitochondrial damage markers, RCD activity indicators, mechanism-oriented patient stratification, and potential therapeutic strategies targeting mitochondrial homeostasis and cell death pathways. This framework facilitates the transition of COPD understanding from the traditional chronic inflammation model to a more stratified and translationally promising mitochondrial-cell death network model.

Febrile seizures (FS) affect 2-5% of children globally, causing significant caregiver anxiety and healthcare utilization. Emerging evidence implicates neuroinflammation and T-cell-mediated immunity in FS pathogenesis, suggesting potential targets for future investigation. This Review synthesizes current evidence on FS prevention, emphasizing a paradigm shift from universal pharmacological approaches toward risk-stratified, personalized strategies. The COVID-19 pandemic provided unique insights: non-pharmaceutical interventions reduced FS incidence by 54-70%, while the Omicron variant emerged as a novel trigger associated with complex FS features. Prevention is conceptualized within a three-level framework: primary prevention targets all children through vaccination (MMR, PCV13, COVID-19 vaccines) and infection control; secondary prevention focuses on high-risk children with prior FS, where risk stratification integrates clinical predictors (complex features, young age, low fever), biomarkers (hyponatremia, zinc/vitamin D deficiency, inflammatory indices), and pathogen-specific risks (influenza A, Omicron); tertiary prevention addresses complications and epileptogenesis in children with complex FS or genetic predisposition (SCN1A, PCDH19). Key immunological mechanisms include HMGB1-NLRP3 inflammasome activation, TRPV1-mediated Th17 differentiation, and IL-1β/IL-10 dysregulation. Antipyretics do not prevent FS recurrence during distant febrile episodes, while intermittent benzodiazepines (diazepam, intranasal midazolam) effectively reduce early recurrence in high-risk children (NNT = 6.8), albeit with adverse effects in up to 36%. Emerging frontiers include novel therapeutic targets (HMGB1 inhibitors, TRP channel modulators, TSP-1 pathway inhibitors) and non-pharmacological innovations (wearable sensors, chronotherapy). Crucially, caregiver education underpins all prevention levels, addressing high rates of parental anxiety (58.2%). This integrated framework guides clinical practice toward more individualized, risk-based management.

Community-acquired bacterial infections (CABIs) remain a leading cause of pediatric morbidity and mortality. This study aimed to provide a contemporary description of pediatric CABIs requiring admission to pediatric intensive care units (PICUs) in France.

The CAPRICE study is a prospective, multicenter cohort including all children with suspected CABIs who were admitted to 28 French PICUs from January to December 2024. Demographic, clinical, microbiologic, and outcome data were prospectively collected. The primary outcome was mortality at day 28 and secondary outcomes included sequelae at day 28, PICU length of stay, and total hospital stay. Independent predictors of mortality were identified by multivariable logistic regression.

Among 897 children, the median age was 1.9 years (IQR 0.2-8.8); 55% were male, and 30% had a chronic condition. The leading infections were lower respiratory tract infection (43%), meningitis (20%), and ear-nose-throat infections (13%). Septic shock occurred in 17% of cases. A pathogen was identified in 89% of cases: Bordetella pertussis (22%) and Mycoplasma pneumoniae (15%) were predominant, followed by Streptococcus pneumoniae (13%), and Staphylococcus aureus (11%). In all, 34% patients had viral co-infection and 70% required organ support. Overall mortality was 7%, increasing to 19% with septic shock. Independent predictors of death included multiple organ failure, meningitis, and B. pertussis infection. Sequelae occurred in 15% of survivors.

Severe CABIs in French PICUs in 2024 were mainly caused by B. pertussis and M. pneumoniae, followed by S. pneumoniae and S. aureus. Mortality and morbidity of these infections remain substantial.

The adrenal gland plays a pivotal role in the stress response via the hypothalamic-pituitary-adrenal (HPA) axis and the sympatho-adrenomedullary system (SAMS). Congenital adrenal hyperplasia (CAH) results from pathogenic variants in genes encoding adrenal steroidogenic enzymes. The most common form, 21-hydroxylase deficiency, impairs cortisol biosynthesis, leading to compensatory overproduction of adrenocorticotropic hormone (ACTH) and chronic adrenal hyperplasia.

A 40-year-old man was referred for incidentally detected bilateral adrenal lesions on abdominal computed tomography (CT). CT revealed marked bilateral adrenal enlargement with clear contours. One month before admission, he had an acute upper respiratory tract infection and recovered after treatment with a cephalosporin. On admission, physical examination showed hyperpigmentation of the nipples region, lips, gums, and buccal mucosa. Superficial lymph nodes were palpable. He reported a history of infertility and suspected precocious puberty. Endocrinology markers demonstrated an elevated ACTH level (180 ng/L; reference range 5.0-78.0 ng/L) with a cortisol level of 174 nmol/L (reference range 133.0-537.0 nmol/L). Luteinizing hormone and follicle-stimulating hormone levels were both low, whereas dehydroepiandrosterone sulfate was elevated. Markedly elevated 17α-hydroxyprogesterone levels and a blunted cortisol response were observed under ACTH-stimulated conditions. Based on the clinical phenotype and biochemical findings, CAH due to 21-hydroxylase deficiency was diagnosed and considered consistent with the simple virilizing form, which was subsequently genetically supported by the CYP21A2 I172N homozygous mutation in exon 4. Remarkably, without any specific treatment, adrenal volume decreased substantially within one month, from 61.06 cm³ to 33.47 cm³, corresponding to an approximately 1.8-fold reduction, although the adrenal glands remained enlarged compared with normal reference values. After excluding adrenal-related tumors, hemorrhage, infections and autoimmune diseases, we postulated that the transient morphological changes reflected stress-induced compensatory hypertrophy and/or hyperplasia of the adrenal cortex following the respiratory infection, aimed at augmenting cortisol production to modulate inflammation and maintain homeostasis.

In patients with 21-OHD and residual enzymatic activity, infectious stress may trigger transient enlargement of pre-existing adrenal hyperplasia, potentially as a compensatory response to increased cortisol demand, followed by partial regression after stress resolution.

Preexisting immunity to influenza confers rapid protection against antigenically matched viruses but can also constrain responses to drifted variants. This review asks when and why prior infection or vaccination is protective versus detrimental, and which biological mechanisms-epitope masking by circulating antibody, inhibitory FcγRIIb signaling, and competitive dominance by affinity-matured memory B cells-drive these outcomes. We synthesize human cohort, serological, and vaccine-effectiveness data with mechanistic mouse and fate-mapping studies to explore how vaccine formulation, antigen dose, antigenic distance and T cell help modulate the balance between memory recall and recruitment of naïve B cells. Finally, we outline strategies (higher dose, adjuvants, multivalent display, and considered strain selection) to restore de novo responses against escape epitopes and improve vaccine performance.

Whole-lung lavage (WLL) is the definitive treatment for pulmonary alveolar proteinosis (PAP), yet it carries significant perioperative risks. Precision nursing is vital to optimize outcomes.

Four PAP patients presented with progressive dyspnea and severe anxiety regarding the complex surgical procedure and its uncertain prognosis.

The diagnosis was confirmed by the characteristic "paving stone" pattern on chest computed tomography and bronchoalveolar lavage fluid analysis.

A full-cycle precision nursing protocol was implemented, encompassing preoperative pulmonary prehabilitation and psychological support, intraoperative vital-sign monitoring with multidisciplinary collaboration, and postoperative airway management coupled with structured discharge follow-up.

All patients completed WLL successfully with stable intraoperative physiology. No adverse events occurred. Postoperative respiratory function improved significantly, and therapeutic effects were sustained.

Full-cycle precision nursing ensures the safety and efficacy of WLL for PAP patients, optimizes perioperative management, prevents complications, and promotes patients' long-term functional recovery. This standardized nursing model is feasible and worthy of clinical popularization.

Community-acquired pneumonia (CAP) remains a significant cause of adult morbidity and mortality. Respiratory syncytial virus (RSV) contributes meaningfully to adult CAP, particularly in older adults and those with chronic cardiopulmonary disease, yet is frequently underdiagnosed because clinical features overlap with other respiratory infections and routine testing is limited.

This review summarizes key virological and immunological characteristics of RSV, highlights diagnostic challenges in adults, and discusses clinical consequences beyond respiratory illness, including cardiovascular complications, severe in-hospital outcomes, and secondary bacterial infection with antibiotic exposure. Using Korean and international data, we emphasize the value of multi-specimen molecular testing to improve detection and discuss the implications for antimicrobial stewardship in CAP management. We also provide an overview of vaccine efficacy in phase 3 trials and early real-world effectiveness in older adults.

Reducing the adult RSV burden will require a feasible diagnostic pathway during periods of RSV circulation, strengthened surveillance that captures clinically meaningful outcomes, and targeted vaccination of high-risk populations. Ongoing post-authorization evaluation and research in immunocompromised and other high-risk groups are needed to optimize vaccination strategies and inform next-generation prevention.

Observational studies indicate that children born by caesarean section (CS), have an increased risk of long-term adverse health outcomes such as allergy, obesity and autoimmune disorders. A small proportion of twin pregnancies have discordant mode of delivery, where the first twin is delivered vaginally and the second twin by CS. This provides a unique opportunity to study long-term health outcomes according to mode of birth. The aim of this study was to investigate if birth by CS is associated with cardiovascular-, metabolic-, autoimmune- or allergic disorders, by using a natural experiment with combined twin birth.

Pairs of twins with discordant mode of delivery between 1973 and 2020 were identified by the Swedish Medical Birth Register. Adverse long-term outcomes were captured by diagnosis and medical prescriptions identified in national registers. Associations between mode of delivery and adverse outcomes were analyzed with logistic regression and reported as odds ratios (ORs) with 95% confidence intervals (CIs). Vaginal birth (first twin) was defined as the reference group.

3196 twins were included. Most discordant twin births occurred from 1990 and onward (86.5%). There was no association between mode of delivery and cardiovascular- (OR: 0.88, 95% CI 0.63-1.23), metabolic- (OR 1.06, 95% CI 0.74-1.52) or allergic disorders (OR 0.99, 95% CI 0.86-1.14). Autoimmune disorders were more common after CS than vaginal delivery (4.3% vs 2.5%), OR 1.72 (95% CI 1.15-2.55).

In twins with discordant birth modes, CS was associated with an increased likelihood of autoimmune disorders later in life, compared with vaginal birth.

To prospectively evaluate the effects of transcutaneous tibial nerve electrical stimulation (TTNS) on urinary symptoms and quality of life in women with neurogenic overactive bladder (nOAB) secondary to ischemic stroke (IS).

This was a prospective case series with a six-month follow-up. Women with clinically and radiologically confirmed IS who developed nOAB symptoms persisting for more than six months after the cerebrovascular screened for eligibility. TTNS was administered twice weekly for six weeks, with 30 minute-minute sessions. Electrical stimulation was delivered at the sensory threshold using a fixed frequency of 10Hz and a pulse width of 250 µs. Outcomes were evaluated at baseline, immediately after treatment, and at six months using a one-week bladder diary and the King's Health Questionnaire (KHQ). Statistical analysis was performed using the Friedman test for repeated measures, with a significance threshold of p < 0.05.

Among 236 screened women with IS, 34 (21%) reported persistent nOAB symptoms; 31 completed the study protocol and were included in the final analysis. Mean age was 59.3 ± 13.6 years, and 67.7% were postmenopausal. Detrusor overactivity was identified in 51.6% of urodynamic studies. TTNS produced significant reductions in daytime frequency (11.95 to 6.99 voids/day post-treatment; 7.21 at follow-up), urgency episodes (13.32 to 0.97; 1.35 at follow-up), urge incontinence (9.19 to 0.26; 0.58 at follow-up), and nocturia (2.99 to 0.40; 0.64 at follow-up) (all p < 0.001). Significant improvements were observed across all KHQ domains, including general health perception (58.06 ± 24.48 to 30.65 ± 22.09), incontinence impact (60.22 ± 24.97 to 11.83 ± 22.02), physical and social limitations, emotional well-being, sleep and energy, and severity measures (all p < 0.001). Improvements were sustained at six months, with partial symptom recurrence in 19.6% and complete recurrence in 6.7% of participants.

TTNS was associated with significant and sustained improvements in urinary symptoms and quality of life in women with post-stroke nOAB.

Severe aortic stenosis (AS) is most often caused by progressive valve calcification; however, rare cases occur with little or no calcification. We report a 79-year-old man with a trileaflet aortic valve and progressive, hemodynamically severe AS despite an almost complete absence of valve calcification (aortic valve calcium score of 76.5 Agatston units). Multimodality imaging confirmed the severity of obstruction, and the patient underwent successful surgical bioprosthetic aortic valve replacement with good postoperative outcomes. This case demonstrates that severe AS can occur in elderly patients with trileaflet valves through fibrosis-predominant remodeling without significant calcification, and that computed tomography-based calcium scoring may underestimate disease severity in this rare phenotype.