The COVID-19 pandemic exposed science's adaptive strengths and epistemic limits. In fact, in the pandemic, mRNA vaccines are attributed to have saved millions of lives. The maxim "correlation does not imply causation" is an essential safeguard against premature causal inference. However, its use may become epistemically restrictive when the absence of established causality is treated as sufficient reason not to investigate (severe) vaccine adverse events. This article examines the conditions under which a valid cautionary principle may have contributed to premature epistemic closure. Thomas Kuhn's theory of scientific paradigms is used as one interpretative lens rather than as an empirical explanation of institutional behaviour. We argue that the correlation-causation distinction can shift from a heuristic of caution to an instrument of epistemic conservatism, reinforcing prevailing frameworks and discouraging exploration of anomalies. A published autopsy case report involving multifocal necrotizing encephalitis and myocarditis after BNT162b2 vaccination is examined as an illustrative and hypothesis-generating case, not as representative evidence of systematic institutional conduct. A qualitative approach using Bradford Hill's criteria provides partial, inconclusive evidence of a causal relationship while also exposing the methodological limits of the tool employed. The results of the analysis showed that one of the nine criteria demonstrated support of causality, seven were partially supported, and one did not support causality. The analysis suggests, but does not prove, a causal relationship between the BNT162b2 vaccine and multifocal necrotizing encephalitis. The absence of the nucleocapsid protein does not provide definitive evidence to demonstrate a vaccine origin. Analytical methods are described which can distinguish between the wild-type SARS-CoV-2 spike protein and the recombinant spike protein expressed following mRNA vaccination. The absence of evidence does not mean evidence of absence and we must keep an open mind to this when reviewing such evidence on causality.

Severe pneumonia is a leading cause of morbidity and mortality in children under-five years of age. In Ethiopia, it is a priority disease under routine surveillance. Several factors have been identified as influencing the length of recovery time in children with severe pneumonia; however, evidence on recovery patterns and their predictors in Jimma, where severe pneumonia remains highly prevalent, is scarce. This study aimed to assess the time to recovery from severe pneumonia and its predictors among children under-five years of age admitted to Jimma town public hospitals.

A facility-based retrospective follow-up study was conducted among 272 under-five children admitted with severe pneumonia between July 1, 2021 and July 30, 2024, at public hospitals in Jimma town. A simple random sampling technique was used to select eligible medical records. A structured tool was used to extract data from medical records. The Kaplan-Meier method was used to estimate survival and group differences were assessed via the log-rank test. Variables with P < 0.25 in the bivariate analysis were entered into the multivariable Cox proportional hazards regression to identify independent predictors of recovery time, with significance set at p < 0.05.

A total of 272 medical records were reviewed and retained for analysis. The median age was 10 months and 152 (55.9%) patients resided in rural areas. In total, 219 (80.5%) patients achieved clinical recovery, and the total accumulated person-days at risk were 1,913 days. The overall median recovery time from severe pneumonia was 5 days (IQR: 3-9). Children who were malnourished (AHR = 0.57, 95% CI: 0.39-0.84), not exclusively breastfed (AHR = 0.49, 95% CI: 0.31-0.80), or not fully vaccinated (AHR = 0.72, 95% CI: 0.53-0.98) had a lower hazard of recovery than children with no malnutrition, exclusively breastfed and fully vaccinated, respectively.

The overall median recovery time was 5 days. Recovery from severe pneumonia was delayed among under-five children who were malnourished, not exclusively breastfed or not fully vaccinated at admission. Future efforts should focus on strengthening child nutrition, promoting exclusive breastfeeding and ensuring full vaccination coverage to reduce recovery time in under-five children with severe pneumonia.

Not applicable.

The impact of obesity and sex on asthma outcomes and inflammation in the real-world setting is not completely understood. The aim of this study was to profile obesity and other comorbidities in a cohort of male and female adults with asthma; to understand the impact of obesity on asthma outcomes; and to examine sex-specific relationships between obesity and airway inflammation.

We profiled comorbidities including obesity, as well as clinical asthma outcomes and airway inflammation, in patients with asthma enrolled in the Australasian Severe Asthma Registry. Data were analysed using t-tests (parametric data) or Wilcoxon rank sum tests (non-parametric data). Analysis of covariance (ANCOVA) was used to examine the effects of obesity and asthma severity on clinical and inflammatory outcomes.

We assessed 1,019 patients with severe (n = 882) and non-severe (n = 137) asthma. Patients with severe asthma were 67% more likely to have obesity, while patients with severe asthma and obesity were more likely to be female. Obesity was associated with a higher prevalence of asthma-related hospitalisation in the previous 12 months, in both severe (26.2% vs. 15.7%, p < 0.001) and non-severe asthma (12.5% vs. 3.1%, p < 0.001). Obesity was also associated with poorer asthma control and lung function, and higher sputum neutrophils. Interestingly, sputum %neutrophils correlated with body mass index in females (r_s=0.370, p = 0.003), but not males (r_s=0.092, p = 0.495). Neutrophilic airway inflammation was associated with poorer lung function and asthma control.

This study demonstrates that obesity is associated with a significantly worse clinical asthma presentation in the real-world setting and increases the risk of asthma-related hospitalisation. Critically, our findings suggest that obesity is associated with increased neutrophilic airway inflammation in females, but not males, providing some insight into possible sex-related differences in severe asthma.

Zhejiang Province, China, has implemented a free influenza vaccination program for the elderly population for five consecutive years. However, data on real-world vaccine effectiveness against influenza among the local elderly population during the 2024-2025 influenza season are still lacking.

A multicenter, retrospective test-negative design (TND) was adopted in this study. Sentinel surveillance networks were established across designated sentinel hospitals in six cities of Zhejiang Province, covering the period from October 2024 to July 2025. On a weekly basis, all or a systematic sample of patients aged ≥ 60 years presenting with influenza-like illness (ILI) were enrolled in the study. Epidemiological data were collected, respiratory specimens were obtained, and laboratory assays were conducted to detect influenza virus types and subtypes.

Of the 4694 enrolled elderly patients with ILI, 1587 (33.81%) were influenza-positive, with A(H1N1)pdm09 being the dominant subtype (93.3%). Vaccination coverage was 32.72% (1536/4694). After adjusting for age, sex, chronic comorbidities, calendar week, and city, the overall VE was 53.3% (95% CI: 45.4-60.2). VE estimates by age group were 56.9% (95% CI: 45.8-65.8) for individuals aged 60-69 years, 51.2% (95% CI: 36.2-62.8) for 70-79 years, and 57.7% (95% CI: 37.2-71.8) for those aged ≥ 80 years. When compared with non-consecutive vaccination in the current season, VE for two, three, and four consecutive seasons was 44.6% (95% CI: 31.1-55.5), 35.5% (95% CI: 17.5-49.7), and 38.6% (95% CI: 18.8-53.6), respectively. Protection waned from 58.0% (95% CI: 37.6-71.7) within 59 days post-vaccination to 42.8% (95% CI: 33.4-50.9) between 60 and 180 days. Furthermore, vaccination provided effective protection against moderate-to-severe influenza (68.8%, 95% CI: 50.0-80.6) and influenza-associated hospitalization (53.9%, 95% CI: 37.3-66.0).

In the 2024-2025 season in Zhejiang, influenza vaccination offered moderate protection against laboratory-confirmed influenza among adults aged ≥ 60 years. While VE waned over time, consecutive vaccination maintained moderate effectiveness. The vaccine also provided substantial protection against moderate-to-severe influenza and hospitalization.

Allergic bronchopulmonary candidiasis (ABPC) is a rare pulmonary hypersensitivity disorder; diagnosis is difficult because Candida albicans is usually a respiratory commensal.

A 70-year-old man with hypertension and prior cerebral infarction was admitted for sudden right limb weakness (6.5 hours) and diagnosed with hemorrhagic cerebral infarction in the intensive care unit.

Persistent fever and pulmonary infiltrates developed despite broad-spectrum antibiotics. Total immunoglobulin E (IgE) was 2181 IU/mL; sputum grew C albicans + carbapenem-resistant Pseudomonas aeruginosa; bronchoalveolar lavage fluid metagenomic next-generation sequencing detected C albicans, P aeruginosa, Klebsiella pneumoniae, EBV, and HSV-1. ABPC was suspected alongside multidrug-resistant bacterial pneumonia.

Ceftazidime-avibactam (2.5 g q8h) + nebulized polymyxin B (0.5 M IU q12h); oral voriconazole (400 mg q12h loading, then 200 mg q12h); IV methylprednisolone 40 mg/d.

Clinical improvement on combined therapy; respiratory stabilization within 2 weeks; intensive care unit transfer out. Follow-up chest computed tomography showed resolution of infiltrates; total IgE fell from 2181 to 995 IU/mL (-54%). Discharged with hemorrhagic cerebral infarction, hypertension, carbapenem-resistant Pseudomonas pneumonia, K pneumoniae co-infection, and ABPM.

Persistent infiltrates with high IgE and Candida isolation should suggest ABPM, not intensified antibiotics. ABPC can occur in older patients without asthma. Early corticosteroids plus antifungals yield rapid improvement. Metagenomic next-generation sequencing complements conventional testing but cannot confirm ABPC alone.

Long COVID syndrome (LCS) is characterized by persistent multi-system manifestations with an unclear underlying pathophysiology. Identifying the genetic and immunological factors associated with LCS is essential for improved risk stratification and clinical management. This study investigated whether incorporating HLA-DRB1* and HLA-DQB1* genotyping data could enhance the predictive value of laboratory parameters for identifying individuals at higher risk of developing LCS. Demographic characteristics and relevant clinical history data were extracted from the medical records of 88 individuals diagnosed with LCS (LCS+) and 96 individuals without LCS (LCS-). Serum levels of anti-receptor binding domain IgG (anti-RBD IgG), anti-β2-glycoprotein I IgG (anti-β2GPI IgG), and C-reactive protein (CRP) were measured. Low-resolution genotyping was performed to identify HLA-DRB1* and HLA-DQB1* alleles. Logistic regression analysis was employed to examine the associations between HLA alleles and LCS status. Subsequently, mediation analysis was conducted to explore the potential mechanistic roles of anti-RBD IgG, CRP, and anti-β2GPI IgG in these observed relationships. The LCS+ group exhibited a significantly higher frequency of the HLA-DRB1*01 allele and a lower frequency of the HLA-DRB1*11 than the LCS- cohort. Serum levels of both CRP and anti-β2GPI IgG were substantially higher in the LCS+ cohort, whereas anti-RBD IgG levels were significantly lower. After adjusting for key variables, HLA-DRB1*01 and HLA-DRB1*11 remained significantly associated with LCS. Mediation analysis suggested that these HLA associations might be partially mediated by CRP, anti-RBD IgG, and anti-β2GPI IgG levels. Our findings indicate that the combination of HLA-DRB1*01 and HLA-DRB1*11 allele screening with serological profiling (anti-RBD IgG, CRP, and anti-β2GPI IgG) may contribute to refining predictive models of LCS susceptibility, though clinical utility requires validation in larger, independent cohorts.

A growing number of literatures explores the diagnostic role of serum eosinophil-to-lymphocyte ratio (ELR) and platelet-to-lymphocyte ratio (PLR) in patients with allergic rhinitis (AR), yielding variable findings and lacking control of potential confounding variables and standardized cut-offs for clinical application. We aim to clarify their role through a systematic review and meta-analysis. Web of Science, PubMed, Embase, Scopus, Cochrane Central Register of Control Trials, Google Scholar, and Medline were systematically searched up to October, 2025. The search strategy was described by a combination of relevant medical subheadings (MeSH) and keywords. Eligible English language studies were reviewed, and their quality was appraised. This review adhered to Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. A total of 12 studies, including 3 449 individuals, met the inclusion criteria. AR group had significantly higher ELR (SMD: 0.64) and insignificantly lower PLR (SMD-0.02) than control. Patients with persistent AR had, numerically but not significantly, higher ELR (SMD: 1.19) and PLR (SMD: 0.58) compared to intermittent AR. ELR value of greater than 0.085 had a pooled AUC of 67% in discrimination of patients with AR from control. This AUC rate was statistically significant. This review investigated that no clear correlation was found between mean PLR and AR. However, mean ELR was found to be significantly increased in patients with a diagnosis of AR, and a numerical trend toward higher ELR with greater disease severity was observed. Though further research is necessary to determine its clinical utility.

SARS-CoV-2 infection causes significant acute and long-term morbidity, including persistent pulmonary and muscular dysfunction in athletes. Physical exercise alters circulating microRNA (miR) profiles, and specific microRNAs have documented roles in inflammation, immune regulation, muscle metabolism, and regeneration. This study characterizes circulating microRNAs relevant to COVID-19 pathogenesis and post-viral recovery, including miR-155, miR-146a, the let-7 family, miR-21, miR-424, miR-1, miR-133, miR-499, miR-208, miR-486, and miR-22, and examines how different exercise modalities may modulate these microRNAs to support pulmonary and muscular function in post-COVID-19 athletes. miR-155 and miR-146a are highlighted as modulators of innate and adaptive inflammatory signaling and as mediators of cytokine responses implicated in severe COVID-19. Moreover, several microRNAs, such as miR-21, miR-155, miR-146a, and the let-7 family, converge on NF-κB and related pathways, linking altered miR expression to immune dysregulation and cytokine-driven tissue injury. Additionally, muscle-enriched and metabolism-associated microRNAs regulate myogenesis, mitochondrial biogenesis, and key metabolic pathways (PGC-1α, AMPK, mTOR)-processes essential for muscle repair, endurance recovery, and respiratory muscle support after SARS-CoV-2 infection. Different types of exercise produce distinct miR signatures; notably, moderate-intensity exercise consistently promotes anti-inflammatory and pro-repair miR patterns. We emphasize the therapeutic potential of moderate-intensity exercise as a non-pharmacological strategy to regulate miR expression, reduce cytokine-mediated damage, and support functional recovery in post-COVID-19 athletes. To our knowledge, this is the first study to link exercise-driven miR changes with functional pulmonary and muscular recovery in athletic populations recovering from COVID-19, supporting moderate-intensity exercise as a promising strategy for rehabilitation and performance restoration.

A 42-year-old female sustained multiple unilateral rib fractures and a hemopneumothorax following a motor vehicle collision. A paravertebral catheter was placed for analgesia; however, extensive subcutaneous emphysema obstructed ultrasound visualization, necessitating landmark‑guided placement. A continuous ropivacaine infusion produced excellent analgesia; however, the patient subsequently developed a pleural effusion. Computed tomography revealed a segment of the catheter migrated into the pleural cavity, resulting in inadvertent intrapleural local anesthetic infusion. This case highlights the limitations of landmark-based paravertebral catheter placement in the setting of distorted anatomy and underscores the need to consider catheter malposition when evaluating unexplained pleural effusions during continuous infusions.

Asthma is the most prevalent chronic inflammatory airway disease in children and is characterized by chronic airway inflammation, airway hyperresponsiveness (AHR), and airway remodeling. In traditional Chinese medicine (TCM), spine-pinching manipulation (SP) is a widely used pediatric massage technique for managing asthma and other childhood diseases. Despite a history of clinical use spanning more than 1,000 years, SP remains largely unfamiliar outside China. Moreover, the mechanisms underlying SP remain insufficiently characterized. This article describes a feasible and standardized protocol for SP that replicates the essential procedures used in clinical practice. Application of the protocol improved airway inflammation, AHR, and airway remodeling in a juvenile rat model of asthma. To enhance reproducibility, key procedural parameters were standardized, including finger pressure, manipulation frequency, number of repetitions, and intervention duration. The standardized protocol in this study may serve as a reference for further research on SP standardization and its underlying mechanisms in experimental pediatric asthma.