Vitamin D influences immune development, but its role in childhood asthma remains unclear. Findings from studies examining vitamin D exposure from pregnancy into early childhood in relation to childhood asthma have been inconsistent, and few have assessed exposure longitudinally. We examined vitamin D status from pregnancy through early childhood to identify the critical window for physician-diagnosed asthma.

Among 205 children from the Chiba High-Risk Birth Cohort for Allergy, we analyzed serum 25-hydroxyvitamin D (25(OH)D) measured at five time points: maternal blood at 36 weeks' gestation, cord blood at birth, and child blood at 1, 2, and 5 years. Asthma was diagnosed at age 5 years using national guideline criteria and classified as no asthma, suspected asthma, or asthma. Multinomial logistic regression models assessed associations adjusted for maternal asthma, prenatal smoking exposure, and birth season.

Maternal and cord blood 25(OH)D concentrations were low (median: 12.0 ng/mL in maternal blood and 6.0 ng/mL in cord blood), whereas postnatal concentrations ranged from 21.0 to 23.4 ng/mL in ages 1-5 years. Cord blood 25(OH)D levels showed a marginal inverse association with asthma (adjusted odds ratio per 1 ng/mL, 0.801; 95% confidence interval: 0.635-1.010). Maternal and postnatal 25(OH)D concentrations showed no clear associations with asthma risk, although estimates showed a similar inverse trend.

Among measurements from late pregnancy through early childhood, cord blood 25(OH)D showed the strongest association with asthma risk at age 5 years, suggesting that fetal vitamin D exposure is a particularly relevant window for asthma development.

Vitamin D may play a role in early lung development, yet epidemiologic evidence on its association with later asthma risk is mixed. We aimed to investigate the associations of neonatal 25-hydroxyvitamin D (25(OH)D) and vitamin D-binding protein (DBP) and their corresponding genetic predictors with asthma risk.

We conducted a population-based cohort study of a random sample of individuals born in Denmark during 1991-2005 from the iPSYCH2012 study. Neonatal concentrations of 25(OH)D and DBP were measured via dried blood spots, and asthma cases were identified through diagnoses or asthma prescriptions after age 5 years. Cox regression was used to estimate hazard ratios (HRs) for asthma in relation to 25(OH)D, DBP, and polygenic scores (PGSs) for these traits and asthma to assess genetic liability to vitamin D status and asthma.

Of 14,005 individuals, 2308 (16.5%) developed asthma over a maximum follow-up of 25 years. We found no association between neonatal 25(OH)D (HR = 1.04, 95% CI: 0.99-1.09 per SD increase) or DBP (HR = 1.01, 95% CI: 0.97-1.05) and asthma risk. Analyses using tertiles to assess potential non-linear associations yielded similar null results. A higher asthma PGS was associated with increased asthma risk (HR = 1.42, 95% CI: 1.36-1.47 per SD increase), whereas PGSs for 25(OH)D (HR = 1.00, 95% CI: 0.96-1.05) and DBP (HR = 0.99, 95% CI: 0.95-1.04) were not.

Our study suggests that neonatal vitamin D status is not associated with asthma risk. Similarly, genetic liability related to vitamin D status, as reflected in PGSs for 25(OH)D and DBP, is not associated with an increased risk of asthma.

Viral load data provide critical insights into host-pathogen interactions and guide clinical and public health decisions. Because frequent testing is often infeasible, viral dynamics models are used to reconstruct infection trajectories, but optimal sampling strategies remain unclear. We compared two approaches for collecting SARS-CoV-2 viral load data: cross-sectional sampling (one measurement at symptom onset) and longitudinal sampling (every 3 days after onset) under constraints on the total number of tests and tests per individual. A viral dynamics model was first fitted to data from the National Basketball Association cohort, and the estimated parameters were treated as ground truth. Synthetic data were then generated under each sampling design, refitted, and evaluated for accuracy in estimating viral load over 30 days, peak viral load, peak time, and viral shedding duration. Longitudinal sampling consistently yielded lower root mean squared error and narrower one standard deviation interval than cross-sectional sampling. Peak timing and viral shedding duration were unbiased under both designs, but cross-sectional designs underestimated peak viral load and produced wider one standard deviation intervals. Coverage of viral load estimates was markedly higher for longitudinal designs (> 0.90) compared with cross-sectional ones (~0.10). Accuracy and coverage exceeded 0.96 even with just two tests per individual, with little additional benefit from more tests. In conclusion, longitudinal sampling-despite limited data-substantially improves accuracy and precision of viral load estimation compared with cross-sectional designs. These findings highlight efficient strategies for study design and resource allocation in infectious disease research.

MotherToBaby (MTB) is a teratogen information service that provides information about exposures during pregnancy and breastfeeding to the public and healthcare providers. During the Coronavirus Disease of 2019 (COVID-19) pandemic, MTB received an influx of queries regarding the teratogenicity of the virus and the vaccine. The purpose of this study was to assess the frequency and type of exposures asked about prior to the onset of the COVID-19 pandemic through March 2022 and to evaluate the demographics of individuals who made inquiries.

Data from MTB contacts (2018-2022) were accessed through a data-sharing agreement. The data were cleaned and standardized by coding all exposures into 11 established categories before linking demographic and exposure files into a single dataset. Analyses included descriptive statistics, chi-square tests, and logistic regression conducted in Excel and STATA 17.0, with statistical significance set at a 0.01% error rate.

The total number of contacts increased from 2019 to 2022, and the exposure category with the highest number of contacts was prescription medications, followed by COVID-19-related exposures. Peaks in the number of contacts relating to COVID-19 correlate with various pandemic milestones, such as when vaccines were approved by the U.S. Food and Drug Administration (FDA).

These data provide valuable information for healthcare providers and agencies, such as the Centers for Disease Control and Prevention (CDC), to better prepare for future pandemics and epidemics.

The escalating threat of antimicrobial resistance (AMR) and the limited efficacy of conventional antibiotics have intensified the search for alternative therapeutic strategies. Nanozymes, nanomaterials with enzyme-mimicking properties, have emerged as a promising class of antimicrobial agents due to their broad-spectrum activity, tunable catalytic functions, and resistance-independent mechanisms. This review provides a comprehensive overview of the recent advances in nanozyme-based antimicrobial applications, focusing on their classification, catalytic mechanisms, and multifaceted antimicrobial actions. We highlight the unique advantages of nanozymes, including their ability to generate reactive oxygen species (ROS), disrupt biofilms, modulate infection microenvironments, and synergize with other therapeutic modalities. Furthermore, we discuss their performance in various infection models, such as skin and soft tissue infections, oral infections, ocular infections, gastrointestinal infections, respiratory infections, urinary tract infections, systemic infections, diabetic wounds, chronic ulcers, and fungal infections. Finally, we address current challenges in clinical translation, including biosafety, dose control, and scalable production. This review underscores the transformative potential of nanozymes in combating drug-resistant pathogens and offers insights into future directions for their clinical development.

Hypervirulent Klebsiella pneumoniae (hvKp) has emerged as a significant public health threat owing to its ability to cause invasive infections. This study aimed to investigate the clinical characteristics and epidemiological associations of hypervirulent Klebsiella pneumoniae (hvKp) and classical K. pneumoniae (cKp) among patients treated at a tertiary hospital in Zhuhai City, Guangdong Province, China, during the period from January to December 2022, in the context of the ongoing COVID-19 pandemic.

A total of 97 non-duplicated K. pneumoniae isolates and corresponding clinical data were collected. Antimicrobial susceptibility testing, hypermucoviscosity phenotyping, sequence typing, capsular serotyping, and whole-genome sequencing were performed. Hypervirulent strains were identified by the presence of the rmpA, rmpA2, iucA, iroB, peg-344, and peg-589 genes.

Among the 97 isolates, 40 (41.2%) were classified as hvKp. Compared with cKp, hvKp was significantly more likely to cause bacteraemia (P < 0.05) and less likely to cause urinary tract infections (P < 0.05). The K20 capsular serotype was significantly associated with hvKp isolates (P < 0.05). The multidrug resistance rate among hvKp strains (22.5%) was markedly lower than that among cKp strains (56.63%), and extended-spectrum β-lactamase production was more common in cKp strains. Multilocus sequence typing identified 29 sequence types, including 24 novel types. Whole-genome sequencing of a multidrug-resistant hvKp isolate (Kp00198874) revealed an ST11-K64 strain resistant to all tested antibiotics.

The prevalence of hvKp increased during the COVID-19 pandemic in Guangdong, China. The isolates identified in this study represent sporadic infections, and the emergence of ST11-K64 hypervirulent carbapenem-resistant K. pneumoniae (hv-CRKp) highlights the urgent need for continued surveillance and vigilance regarding hvKp-associated bacteraemia.

Respiratory viruses impose a substantial health burden worldwide, with viral internalization into host cells being the initial step for infection establishment. This process is tightly regulated by the host cellular machinery through two major pathways: receptor-mediated endocytosis and direct membrane fusion. To clarify the role of host factors in these steps, we present human adenovirus and respiratory syncytial virus as representative non-enveloped and enveloped viruses, respectively, as models to elucidate their life cycles, focusing on how host factors mediate their distinct internalization processes. We further categorized the host factors involved in the internalization of other common respiratory viruses, including coronaviruses, influenza A virus, and human metapneumovirus. By analyzing the virus-host interaction mechanisms underlying these processes, this review provides critical insights for developing broad-spectrum antiviral therapies targeting conserved host factors that govern viral internalization.

Liu Shen Wan (LSW) can modulate sphingolipid metabolism, which is a key pathway in inflammatory regulation, yet the precise mechanistic actions remain elusive. This study aimed to elucidate the mechanism by which LSW regulates sphingolipid metabolism to mitigate influenza-induced inflammatory responses.

The potential mechanisms of LSW were initially predicted and validated via network pharmacology and lipidomics. A549 cells were infected with influenza A/Puerto Rico/8/34 (H1N1) (PR8) or transfected to overexpress sphingosine kinase-1 (SPHK1), then treated with LSW. In vivo, mice were infected with PR8 or challenged with rAAV9-SPHK1 and administered LSW for 5 days. Inflammatory factors and sphingolipid pathway-associated proteins were evaluated.

Network pharmacology identified sphingolipid signaling as a primary target of LSW. Lipidomics revealed LSW significantly reduced the levels of sphingomyelin (SM), ceramide, CerG2GNAc1, CerG3GNAc1, Ceramide phosphate and GM1 in lungs. In PR8-infected A549 cells, LSW significantly reduced sphingomyelinase (ASMase) and Ceramide (Cer) secretion. It also inhibited the expression of SPHK1 and sphingosine-1-phosphate (S1P) in A549 cells and in mice. Pharmacological inhibition of SPHK1 mirrored these anti-inflammatory effects. In SPHK1-overexpressing or TNF-α-stimulated A549 cells, LSW significantly attenuated the expression of SPHK1, CXCL10, and MCP-1. In the rAAV9-SPHK1 overexpression mouse model, LSW ameliorated lung pathological changes and reduced the expression of SPHK1, IFN-γ, and TNF-α.

LSW alleviates influenza virus-induced inflammation by inhibiting the overactivation of the sphingolipid signaling pathway, specifically through targeting the SPHK1-S1P axis and ceramide-derived lipid mediators.

Nasal inflammatory disease has a complex pathogenesis, high incidence and long disease course. Complete resolution is often challenging, and these diseases are closely related to upper and lower respiratory tract diseases. For common nasal inflammatory diseases, such as chronic rhinosinusitis (CRS), allergic rhinitis (AR), and fungal rhinosinusitis (FRS), adverse outcomes, such as repeated inflammation, AR combined with asthma, and postoperative recurrence, often occur despite standardized treatments, causing great distress to patients and increasing societal costs due to the need for long-term and repeated treatments. Therefore, the identification of early predictors of unfavorable outcomes of nasal inflammatory diseases is important for achieving early diagnosis, intervention and treatment of nasal inflammatory diseases. This paper summarizes the progress in research on the role of indicators, such as inflammatory cytokines, inflammatory cells, metabolites, nasal flora, and clinical parameters, in predicting poor outcomes in patients with nasal inflammatory diseases.

Post-COVID-19 syndrome (PCS) is frequently associated with fatigue and cognitive dysfunction, while underlying mechanisms remain unclear. We report a 44-year-old male with persistent symptoms following SARS-CoV-2 infection, including severe cognitive and motor fatigue, word-finding difficulties, and impaired concentration. Neuropsychological testing revealed marked deficits in alertness, attention, fluency, and processing speed. Serum analysis demonstrated anti-VGLUT2 autoantibodies. IVIG therapy yielded subjective but no objective improvement. This appears to be the first PCS case associated with VGLUT2 autoantibodies and raises the hypothesis of a potential pathophysiological link that requires confirmation in larger cohorts.