The pursuit of Artificial Intelligence (AI) that emulates human cognitive processes is a cornerstone of ethical AI development, ensuring that emerging technologies can integrate seamlessly into societal frameworks requiring nuanced understanding and decision-making. Zero-Shot Instance Retrieval (ZSIR) stands at the forefront of this endeavour, potentially providing a robust platform for AI systems, particularly large visual language models, to demonstrate and refine cognition-aligned learning without the need for direct experience. In this paper, we critically evaluate current cognition alignment methodologies within traditional zero-shot learning paradigms, using visual attributes and word embedding generated by large AI models. We propose a unified similarity function that quantifies the cognitive alignment level, bridging the gap between AI processes and human-like understanding. Through extensive experimentation, our findings illustrate that this similarity function can effectively mirror the visual-semantic gap, steering the model towards enhanced performance in zero-shot instance retrieval. This work not only benchmarks the cognition alignment of AI, but also sets a new precedent for the development of visual language models attuned to the complexities of human cognition.}

In this study, a commercial sodium butyrate protected by a new buffer salt solution (NSB) was tested to determine whether it can be used as an antibiotic alternative in broiler production. 192 1-day-old broilers were randomly allocated to three dietary treatments: soybean meal diet (CON), antibiotic diet (ANT, basal diet + 100 mg/kg aureomycin), and NSB (basal diet + 800 mg/kg NSB). The growth performance, serum anti-inflammatory cytokines, intestinal morphology, gut barrier function, antioxidative parameters, SCFAs content, and cecal microbiota were analyzed. The result showed that NSB significantly improved ADFI, ADG (p < 0.01), and decreased FCR (p < 0.01). Serum anti-inflammatory cytokine IL-10 was up-regulated (p < 0.01), and pro-inflammatory TNF-α was down-regulated (p < 0.05) by NSB supplementation. H&E results showed that VH and VH: CD ratio significantly increased (p < 0.05) in the jejunum and ileum in the NSB group. Furthermore, ZO-1 (p < 0.01), claudin-1 (p < 0.01), and occludin (p < 0.05) in the jejunum and claudin-1 (p < 0.01) and mucin-2 (p < 0.05) in the ileum significantly up-regulated in the NSB group, respectively. Additionally, SOD (p < 0.05) and T-AOC/MDA ratio (p < 0.01) in the jejunum and SOD in the ileum were significantly increased (p < 0.05) in the NSB group. The MDA level also significantly increased (p < 0.01) in the ANT group in the jejunum. Propionic acid (p < 0.05) and butyric acid (p < 0.01) content significantly increased in the NSB group in the jejunum and ileum segments. The 16S rRNA sequencing results showed no significant difference (p > 0.05) in alpha and beta diversity among the groups. LEFSe analysis also indicated that Peptostreptococcaceae, Colidextribacter, Firmicutes, Oscillospira, and Erysipelatoclostridiaceae, which promote SCFA production (p < 0.05), were identified as dominant taxon-enriched bacterial genera in the NSB group. The Spearman correlation analysis revealed that Colidextribacter with ADFI, ADG, VH, claudin-1 (p < 0.05), and unclassified_f__Peptostreptococcaceae with ADFI, IL-10, and ZO-1 were positively correlated (p < 0.05). Furthermore, ADFI and ADG with IL-10, claudin-1, SOD, T-AOC, and butyric acid (p < 0.05), and similarly, ADG with VH (p < 0.05) showed a positive correlation. In conclusion, NSB enhanced the growth performance by improving jejunum and ileum morphology, serum anti-inflammatory cytokines, regulating intestinal barrier function and antioxidant capacity, SCFAs content, and cecum microbiota, showing its potential use as an alternative to antibiotics in poultry nutrition.

Environmental arsenic exposure is closely related to nerve damage, and chronic arsenic exposure will cause neurotoxicity and damage the nervous system. Recent research suggests miR-27a-3p is required for the progression of certain neurodegenerative and neuropsychiatric disorders. Nonetheless, the precise impact of miR-27a-3p on neuron functioning in the hippocampus remains unclear. In this investigation, models were established using arsenite-treated cells and mice to investigate this aspect. After male C57BL/6J mice were exposed to arsenite (0, 0.5, 5 or 50ppm) in drinking water for 48 weeks, Nissl staining, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay, and Hematoxylin-Eosin (H&amp;E) stainingrevealed an arsenite-induced neuronal injury and apoptosis. For 6 μmol/L arsenite-treated HT22 cells, arsenite decreases miR-27a-3p levels and activated the FTO/DRP1 pathway. For arsenite-treated HT222 cells, the increases of FTO and DRP1 and p-DRP1 (Ser616) levels induced by arsenite were reversed by miR-27a-3p mimic.Furthermore, the increases of neuronal apoptosis and pro-apoptotic protein (Bax and Cleaved-caspase 3) levels as well as decreased levels of anti-apoptotic proteins Bcl-2 induced by arsenite were reversed by miR-27a-3p mimic in HT22 cells. Moreover,the decreases of MMP induced by arsenitewas reversed by miR-27a-3p mimic. Overall, in HT22 cells exposed to arsenite, miR-27a-3p mitigates neuronal apoptosis, suggesting its potential utility in addressing arsenite accumulation and associated with brain pathologies. Dysregulated expression patterns of miRNAs in the hippocampus have emerged as pivotal elements in neuronal apoptosis linked to neurological dysfunction, with miR-27a-3p specifically implicated in apoptotic pathways.