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The revision of the writing section in the unified junior high school Chinese textbook aligns with the ideas, goals, and requirements of the new Chinese curriculum standard. It follows the principle of "adhering to tradition while innovating, and seeking progress while maintaining stability."Adjustments have been made to various aspects such as writing perspectives, writing types, topic setting, and writing guidance, retaining the strengths and characteristics of the original textbooks meanwhile. Specific revisions include adding five writing themes, merging some repeated content, removing outdated themes, improving writing topics, and further refining the writing guidance system. The new textbook particularly emphasizes new forms of writing, such as situational task writing, critical thinking writing, and creative writing, aiming to comprehensively enhance students' new writing skills. To adapt to the new textbook, it is recommended to recognize the importance of writing instruction and establish a specialized awareness; adhere to a competency-oriented approach and foster new writing concepts and teaching perspectives; enhance the professionalism of writing instruction with evidence-based practice; adopt corresponding teaching strategies based on different writing types; focus on writing process guidance, writing strategies, and writing scaffold design; and fully utilize the textbook as the primary channel for curriculum resources.

UHRF1 maintains DNA methylation by recruiting DNA methyltransferases to chromatin. In mouse, these dynamics are potently antagonized by a natural UHRF1 inhibitory protein STELLA, while the comparable effects of its human ortholog are insufficiently characterized, especially in cancer cells. Herein, we demonstrate that human STELLA (hSTELLA) is inadequate, while mouse STELLA (mSTELLA) is fully proficient in inhibiting the abnormal DNA methylation and oncogenic functions of UHRF1 in human cancer cells. Structural studies reveal a region of low sequence homology between these STELLA orthologs that allows mSTELLA but not hSTELLA to bind tightly and cooperatively to the essential histone-binding, linked tandem Tudor domain and plant homeodomain (TTD-PHD) of UHRF1, thus mediating ortholog-specific UHRF1 inhibition. For translating these findings to cancer therapy, we use a lipid nanoparticle (LNP)-mediated mRNA delivery approach in which the short mSTELLA, but not hSTELLA regions are required to reverse cancer-specific DNA hypermethylation and impair colorectal cancer tumorigenicity. There is growing evidence indicating the different roles of natural UHRF1 inhibitory protein STELLA in mouse-derived cells from its human ortholog. Here, the authors report the differences of hSTELLA versus mSTELLA in inhibiting the maintenance or de novo DNA methylation functions of UHRF1 in human cancer cells, and lipid nanoparticle-delivered mSTELLA reversing cancer-specific DNA hypermethylation thereby impairing colorectal cancer tumorigenicity. [ABSTRACT FROM AUTHOR]