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To investigate the genetic factors underlying marketed body size traits in Chinese local geese, we conducted a comprehensive study involving nine body size traits in 251 samples at 10 weeks of age from five local breeds: Taihu goose (TH), Sichuan goose (SC), Guangfeng goose (GF), Xupu goose (XP), and Youjiang goose (YJ). Genotyping data were obtained through whole-genome re-sequencing, followed by a genome-wide association analysis utilizing the fixed and random model circulating probability unification (FarmCPU) approach. Our findings revealed 88 significant SNPs associated with body size traits, with 16 SNPs surpassing the genome-wide significance threshold (p = 3.98E-09) and 72 SNPs exceeding the suggestive significance threshold (p = 5E-07). Subsequent gene annotation identified these SNPs to be located within exonic regions of 86 candidate genes, including THADA, ATP5A1, ZNF462, PRDM8, and GH14523. Notably, functional enrichment analysis employing Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways highlighted 37 significantly enriched pathways, among which the "negative regulation of transforming growth factor beta receptor signaling pathway" (GO:0030512) emerged as relevant to goose skeletal development and the phenotypic expression of body size in geese. The identification of these novel SNPs and candidate genes associated with 10-week-old body size traits in geese presents valuable insights for future molecular breeding endeavors and the elucidation of underlying mechanisms governing body size trait formation in goose. [ABSTRACT FROM AUTHOR]

Aim and Objective: This current study investigated the significance of tofactinib in improving memory functions in a memory model of β-amyloid (Aβ)-induced dementia.Material and Methods: Aβ1–42 was injected in the brain of mice using intracerebroventricular injection and after 14 days, the learning and memory was assessed on the Morris Water maze test. Mice were treated with tofactinib (10, 20, 30 mg/kg) two days prior to Aβ1–42 injection and 14 days after Aβ injection.Results: Treatment of tofactinib significantly improved the learning (decrease in day escape latency time [ELT]) and memory (increase in time spent in target quadrant). This drug also decreased the levels of T NF-α and IL-6 along with the rise in expression of p-Akt and p-GSK-3β/GSK-3β ratio in mice brain. Co-administration of LY294002 (P I3K inhibitor) or MK-2206 2HCl (Akt inhibitor) with tofactinib (30 mg/kg) obliterated the beneficial effects of the latter by increasing T NF-α and IL-6 levels along with decreasing the p-Akt expression and p-GSK-3β/GSK-3β ratio.Conclusion: It is concluded that tofactinib improves the condition of dementia of Alzheimer's type, possibly through down regulation of T NF-α and IL-6 and instigation of P I3K-Akt-p-GSK-3β signalling system in the hippocampus of Aβ-treated mice. [ABSTRACT FROM AUTHOR]