Animal tuberculosis, caused by bacteria of the Mycobacterium tuberculosis complex (MTBC), poses major economic and socio-ecological challenges in Europe. In Mediterranean ecosystems, water scarcity co...

Tobacco smoking is a critical modifiable risk factor for age-related diseases and mortality. Although smoking cessation is known to improve health outcomes, whether smoking-induced biological aging is reversible upon cessation remains unclear. We investigated the associations of smoking status and cessation duration with epigenetic age acceleration (EAA) using multi-generational DNA methylation clocks. We analyzed data from 1,911 adults aged 50–84 years in the National Health and Nutrition Examination Survey (NHANES) 1999–2002. Participants were classified as never, former, or current smokers, with former smokers further categorized by cessation duration (< 10, 10– < 20, and ≥ 20 years). EAA was evaluated across six validated DNA methylation clocks: first-generation (HorvathAge, HannumAge, SkinBloodAge), second-generation (PhenoAge, GrimAge2), and third-generation (DunedinPoAm). In survey-weighted regression, current smokers exhibited the highest EAA across all clocks. Among former smokers, a longer duration of cessation was associated with a dose–response reduction in EAA, with the strongest associations observed for GrimAge2 and DunedinPoAm. Former smokers with ≥ 20 years of cessation showed a substantial reduction in GrimAge2 acceleration (β = -12.66 years; 95% CI: -14.56, -10.75), approaching the levels observed among never smokers (β = -13.88 years; 95% CI: -15.70, -12.05). Restricted cubic spline analysis revealed rapid initial declines in EAA during the first decade post-cessation, with continuous declines observed beyond 20 years for GrimAge2 and DunedinPoAm. These findings suggest that longer durations of smoking cessation are associated with more favorable biological aging profiles, adding biological evidence for the long-term health benefits of sustained cessation for healthy aging.

Background We aimed to explore associations between the presence of pets at one and 4–5 years of age with internalizing and externalizing problems at 7–8 years. Methods Participants comprised 1893 families from the INfancia y Medio Ambiente (INMA) project. Information was collected on the presence of (1) any pet, (2) dogs, (3) cats, (4) birds or (5) other animals. Pet ownership was categorized as never, always, only at age 1 and only at age 4–5. Internalizing and externalizing problems were measured at ages 7–8 years through the Strengths and Difficulties Questionnaire, a Likert questionnaire on children’s behavioural and emotional symptoms. Negative binomial regression models and Tukey’s multiple comparison tests were used to analyse data sets. Five sensitivity analyses were performed. Results Families that always owned a pet made up 24.4% of the sample. In addition, 11.5%, 4.5%, 3.8% and 17.6% of the families owned a dog, cat, bird or other animal, respectively. The median (P25–P75) for internalizing problems was 3 (1–5) and 5 (3–8) for externalizing problems. Owning a cat only at age 4–5 increased mental health problems: relative rate ratio (RRR) [95% confidence interval (CI)] 1.37 (1.05–1.79) for internalizing and 1.26 (1.02–1.56) for externalizing. Always having other animals was a protective factor for internalizing problems with an RRR of 0.80 (0.66–0.96). These associations remained after multiple comparison testing and sensitivity analyses. Conclusion Owning a cat only at 4–5 years of age was linked to more internalizing and externalizing problems, whereas always having other animals was a protective factor against internalizing problems. Graphical abstract

We examined the genetic underpinnings of problem behavior in children and adolescents (4–17 years old) by leveraging a within-family trio design using data of European ancestry from the Lifelines cohort (N=3,160–4,611). We estimated direct genetic effects of educational attainment (EA) polygenic indices (PGIs), as a whole and decomposed into cognitive (Cog) and non-cognitive (NonCog) components via GWAS-by-subtraction, on a comprehensive set of internalizing and externalizing behaviors assessed via self- and parental report Achenbach System of Empirically Based Assessment (ASEBA) measures. We found that higher EA PGIs, particularly their Cog component, were robustly associated with lower levels of Attention Problems and Somatic Complaints, in parental and self-report samples respectively. These associations persisted after adjusting for parental PGIs, supporting a causal interpretation under counterfactual reasoning. In contrast, the NonCog EA PGI showed weaker and less consistent associations with problem behavior, though we cannot rule out that this reflects limited power to detect smaller effects. We observed pronounced sex differences, with associations largely driven by girls, for whom the Cog component was the primary predictor. In the self-report sample in particular, associations with Somatic Complaints were significantly stronger in girls, with no significant findings observed for boys. We also found that associations with Somatic Complaints were significantly larger in the self-report than the parental report sample, while for other scales, differences across informants were statistically negligible. Our findings contribute to a more holistic understanding of how EA-related genetics manifest in socioemotional processes beyond academic achievement

Mixed forests represent the largest contributor to China’s forest carbon sink, yet their spatio-temporal changes in biomass carbon stocks remain insufficiently quantified, limiting the accuracy of national carbon sink assessments under the carbon neutrality target. Here, we integrated National Forest Inventory (NFI) data with multi-source remote-sensing products to quantify the changes in biomass carbon stocks of mixed forests across China from 1999 to 2018. The NFI dataset comprises approximately 26,000 plots nationwide, with plot sizes ranging from 600 to 800 m2. Biomass carbon changes were attributed to distinct ecological and management processes, including natural growth, succession from pure forests, afforestation-driven expansion, and conversion-related losses. We found that biomass carbon stocks in China’s mixed forests increased continuously from 968.63 ± 109.2 Tg C (1 Tg C = 1012 g C) in 1999 to 3833.39 ± 278.3 Tg C in 2018. The conversion of pure stands into mixed forests accounted for approximately 84.8% of this increase (2709.15 ± 320.2 Tg C), followed by area expansion (25.8%; 713.33 ± 136.9 Tg C) and natural growth (19.7%; 598.7 ± 122.7 Tg C), partially offset by an estimated 30.4% loss (− 929.78 Tg C) due to conversion from mixed forests to other forest types. Our findings provide empirical evidence for the dominant role of forest-type transitions in driving China’s forest carbon accumulation and underscore the necessity of incorporating mixed-forest management and dynamic forest-type transitions into national climate mitigation and carbon sink projections.

Advances in deep learning have led to significant progress in the field of speech processing, particularly in applications such as speaker recognition systems (SRSs). Additional information such as ge...

Interoception, the capacity to sense, perceive, and metacognitively appraise viscerosensory and homeostatic signals, is a growing focus in psychology and psychiatry. Adaptive psychophysical tasks now ...

When we think about risk in early childhood, certain images come easily to mind: a child climbing too high, running too fast, balancing on an unstable surface, or attempting something that might end in a scraped knee.

Hepatitis B virus (HBV) infection can lead to hepatocellular carcinoma, and HBV integration into the host genome is regularly observed in the liver of chronic HBV carriers and is speculated to trigger carcinogenesis. To detect HBV integration, PCR-based methods are sensitive but may not be effective depending on the HBV integration site. High-throughput sequencing reveals not only HBV integration but also the site. However, it is still expensive for clinical applications. In situ hybridization is efficient and allows detection of DNA and RNA in single cells and has been applied to study HBV infection and dynamics. The technique, however, has not been applied to detect HBV integration. The task is challenging because of the small copy number of integrated HBV genomes, which results in a small signal-to-noise ratio. Here, we developed a fluorescence in situ hybridization approach for examining HBV integration in each liver cell. The obtained images of cells were analyzed using a deep learning model. Using several hepatoma cell lines with and without integrated HBV DNA, we showed that our trained neural network achieved an over 90% accuracy for majority of positive and negative control cells. This is the first proof-of-concept study showing that fluorescence imaging and deep learning are useful in detecting HBV integration at the single-cell level.

Alcohol consumption is a major risk factor for cancer, particularly of the head and neck. Acetaldehyde, the main ethanol metabolite, is linked to oral carcinogenesis, but the mechanisms are not well understood. While some mutational signatures such as single-base substitution signature SBS16, doublet-base substitution signature DBS4, and indel signature ID11 have been linked to alcohol use, they are not limited to alcohol-related cancers. We examined the genome-wide in vivo mutation landscapes of rats chronically exposed to ethanol or acetaldehyde, focusing on head-and-neck tumors (involving the cheek and the Zymbal gland) and tumors of the forestomach and liver. Mutational signature analysis revealed early-onset, exposure-associated formation of signature SBS17 in ~ 38% of head-and-neck tumors, suggesting inflammation and oxidative damage may mediate carcinogenesis in these sites. We observed relative enrichment of driver-like mutations in Tp53, Mtor and Hras in exposed tumors, where all Tp53-mutated tumors were SBS17-positive, recapitulating a similar scenario from human gastro-esophageal adenocarcinomas. Next, the doublet-base, indel, copy number and structural variant changes were sporadic and not following exposure-specific patterns. No signatures previously associated with alcohol consumption in humans were observed in the exposed animals. Thus, in this animal cancer model, alcohol-related carcinogenesis across multiple organs is unlikely to be driven mainly by direct mutagenicity of ethanol or acetaldehyde. Rather, the results support a role for non-mutational processes in mediating their carcinogenic effects. Further investigation is warranted to clarify the relationship between mutational signature SBS17 and TP53 loss-of-function mutations as potential biomarkers of alcohol-related carcinogenesis in animals and humans. Graphical Abstract Ethanol or acetaldehyde exposure in rats induces limited genome-wide mutations in head-and-neck, forestomach, and liver tissues. SBS17 appears early in 38% head-and-neck tumors following exposure, implicating inflammation and oxidative damage. Tp53, Mtor, and Hras mutations are enriched upon exposure, with all Tp53-mutant tumors SBS17-positive, paralleling human cancer observations. Exposure-linked carcinogenesis is unlikely driven by direct mutagenicity of ethanol/acetaldehyde.