Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1069871 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27748271_1.fastq.gz | Fastqsanger.gz | |||
| SRR27748271_2.fastq.gz | Fastqsanger.gz | |||
| SRR27748272_1.fastq.gz | Fastqsanger.gz | |||
| SRR27748272_2.fastq.gz | Fastqsanger.gz | |||
| SRR27748273_1.fastq.gz | Fastqsanger.gz |
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Project description:The functional diversity of soil microbial communities was explored for a poplar plantation, which was treated solely with biogas slurry, or combined with biochar at different fertilization intensities over several years.
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Project description:Oncolytic adenoviruses (AdVs) represent a promising immunotherapeutic approach against cancer, yet their clinical translation is hindered by rapid systemic clearance, poor tumor accumulation, limited extravasation across the endothelial barrier, and an immunosuppressive tumor microenvironment. To overcome these challenges, we developed a biomimetic nanocomplex, AdV-iCD47-Fe₃O₄@PACM, consisting of an oncolytic adenovirus chemically conjugated with chemically modified CD47 siRNA and loaded with Fe₃O₄ nanoparticles, all encapsulated within a palmitoylated cancer cell membrane (PACM). Upon intravenous administration, the PACM coating enables immune evasion and prolonged circulation. Application of an external magnetic field promotes active tumor targeting via Fe₃O₄, while palmitic acid moieties transiently increase vascular permeability by downregulating tight junctions, facilitating nanocomplex extravasation into the tumor interstitium. Once inside tumor cells, the oncolytic AdV induces direct cytolysis, and the released chemically modified siRNA achieves sustained CD47 silencing, blocking the “don’t eat me” signal and enhancing macrophage-mediated phagocytosis. This dual mechanism—direct oncolysis combined with innate immune checkpoint blockade—elicits a robust antitumor immune response. Both in vitro and in vivo evaluations demonstrate that the AdV-iCD47-Fe₃O₄@PACM platform effectively overcomes key barriers of systemic delivery and immunosuppression, offering a promising strategy for enhanced cancer immunotherapy.
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Project description:Introduction Colored rice is recognized for nutritious function due to its flavonoid compounds. Flavonoid aglycones are conjugated with various sugar moieties. Iron (Fe) is an essential mineral nutrient for plants; however, the regulatory mechanisms by which Fe influences flavonoid accumulation dynamics and sugar metabolism remain unclear. Methods FeSO4 was foliar-applied to black rice cultivar Nanheinuo and red rice cultivar Yuhongdao 5815 to study regulatory mechanisms by which Fe influences flavonoid accumulation dynamics and sugar metabolism Results and discussion The content of anthocyanins, proanthocyanidins, and total flavonoids in the grains decreased throughout the later filling stages. Fe application delayed their degradation during this phase. The differential expression of numerous genes associated with flavonoid transformation may be the primary reason. Genes annotated as key enzymes involved in phenylpropanoid and flavonoid biosynthesis were significantly upregulated in Nanheinuo. Additionally, foliar Fe application significantly impacted sugar and sugar alcohol content by regulating the expression of genes involved in polysaccharide decomposition, phosphorylation and dephosphorylation processes, and sugar interconversion. A close relationship was observed between sugar content and flavonoid-related compound content in the grains of colored rice. Multiple hub genes annotated as glycoside hydrolases in KEGG occupied central nodes within the co-expression network, suggesting that glycoside hydrolases may mediate the crosstalk between sugar and flavonoid metabolism in colored rice grains under Fe treatment, although glycosyltransferases primarily function in flavonoid glycosylation. Foliar Fe application delays flavonoid degradation during the later filling stage and regulates sugar metabolism in colored rice, thereby influencing flavonoid enrichment and eating quality.
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