Acidic Magnetic Biocarbon-Enabled Upgrading of Biomass-Based Hexanedione into Pyrroles

Sustainable acquisition of bioactive compounds from biomass-based platform molecules is a green alternative for existing CO_(2)-emitting fossil-fuel technologies.Herein,a core–shell magnetic biocarbon catalyst functionalized with sulfonic acid(Fe3O4@SiO_(2)@chitosan-SO_(3)H,MBC-SO_(3)H)was prepared to be efficient for the synthesis of various N-substituted pyrroles(up to 99% yield)from bio-based hexanedione and amines under mild conditions.The abundance of Bronsted acid sites in the MBC-SO_(3)H ensured smooth condensation of 2,5-hexanedione with a variety of amines to produce N-substituted pyrroles.The reaction was illustrated to follow the conventional Pall-Knorr coupling pathway,which includes three cascade reaction steps:amination,loop closure and dehydration.The prepared MBC-SO_(3)H catalyst could effectively activate 2,5-hexanedione,thus weakening the dependence of the overall conversion process on the amine nucleophilicity.The influence of different factors(e.g.,reaction temperature,time,amount of catalyst,molar ratio of substrates,and solvent type)on the reaction activity and selectivity were investigated comprehensively.Moreover,the MBC-SO_(3)H possessed excellent thermochemical stability,reusability,and easy separation due to the presence of magnetic core-shell structures.Notably,there was no activity attenuation after 5 consecutive catalytic experiments.This work demonstrates a wide range of potential applications of developing functionalized core-shell magnetic materials to construct bioactive backbones from biomass-based platform molecules.

一流本科专业建设背景下突出应用特色的多元化实践课程体系建设

在新时期教育部推动一流本科专业建设项目的背景下,作为一所地方性应用型高校,郑州轻工业大学应用化学专业在国家一流专业建设过程中,依托综合实验课程、国家级实践教学基地、产学研合作以及大学生学科竞赛等单元,建设起独具应用特色的多元化创新创业实践平台和人才培养体系,为一流专业建设中强化学科分层次发展和重点建设,提升应用化学专业人才教育质量提供了一种可供借鉴的模式。

Resolving the lineage relationship between malignant cells and vascular cells in glioblastomas

Glioblastoma multiforme(GBM),a highly malignant and heterogeneous brain tumor,contains various types of tumor and non-tumor cells.Whether GBM cells can trans-differentiate into non-neural cell types,including mural cells or endothelial cells(ECs),to support tumor growth and invasion remains controversial.Here we generated two genetic GBM models de novo in immunocompetent mouse brains,mimicking essential pathological and molecular features of human GBMs.Lineage-tracing and transplantation studies demonstrated that,although blood vessels in GBM brains underwent drastic remodeling,evidence of trans-differentiation of GBM cells into vascular cells was barely detected.Intriguingly,GBM cells could promiscuously express markers for mural cells during gliomagenesis.Furthermore,single-cell RNA sequencing showed that patterns of copy number variations(CNVs)of mural cells and ECs were distinct from those of GBM cells,indicating discrete origins of GBM cells and vascular components.Importantly,single-cell CNV analysis of human GBM specimens also suggested that GBM cells and vascular cells are likely separate lineages.Rather than expansion owing to trans-differentiation,vascular cell expanded by proliferation during tumorigenesis.Therefore,cross-lineage trans-differentiation of GBM cells is very unlikely to occur during gliomagenesis.Our findings advance understanding of cell lineage dynamics during gliomagenesis,and have implications for targeted treatment of GBMs.

Paired related homeobox 1 transactivates dopamine D2 receptor to maintain propagation and tumorigenicity of glioma-initiating cells

Glioblastoma multiforme (GBM ) 是有有限治疗学的工具和差的预后的一个高度侵略的大脑肿瘤。最近的研究显示开始 glioma cells/glioma 干细胞(GICs/GSCs ) 可能为肿瘤开始，渗入，和复发负责。GIC 能异常地采用平衡胚胎的神经先锋的自强和区别的分子的机械。这里，我们发现那配对的相关 homeobox 1 (PRRX1 ) ，以前是的一个 homeodomain 抄写因素报导了控制骨胳的开发，在外皮的神经祖先被表示并且为他们的自强和合适的区别被要求。进一步， PRRX1 是在 glioma 样品和标签 GIC 的 overrepresented。Glioma 房间和 GIC 与 PRRX1 弄空不能在 vitro 宣传或在异种皮移植老鼠模型形成肿瘤。PRRX1 调整的 GIC 自强功能被多巴胺 D2 受体(DRD2 ) 调停。PRRX1 直接在 GIC 把它的表示绑在 DRD2 倡导者和 transactivates。发信号的 DRD2 的阻塞妨碍 GIC 自强，而它的 overexpression 恢复宣传和弄空 PRRX1 的 GIC 的 tumorigenic 潜力。最后， PRRX1 加强经由调停 DRD2 的细胞外的信号相关的 kinase (英皇家空军之阶级最低之兵) 和 AKT 的 GIC 激活。因此，我们的学习建议那治疗学的指向在 GIC 的 PRRX1DRD2ERK/AKT 轴是为对待 GBM 的有希望的策略。

Long non-coding RNA LncKdm2b regulates cortical neuronal differentiation by cis-activating Kdm2b

The mechanisms underlying spatial and temporal control of cortical neurogenesis of the brain are largely elusive.Long non-coding RNAs(lncRNAs)have emerged as essential cell fate regulators.Here we found LncKdm2b(also known as Kancr),a lncRNA divergently transcribed from a bidirectional promoter of Kdm2b,is transiently expressed during early differentiation of cortical projection neurons.Interestingly,Kdm2b’s transcription is positively regulated in cis by LncKdm2b,which has intrinsic-activating function and facilitates a permissive chromatin environment at the Kdm2b’s promoter by associating with hnRNPAB.Lineage tracing experiments and phenotypic analyses indicated LncKdm2b and Kdm2b are crucial in proper differentiation and migration of cortical projection neurons.These observations unveiled a lncRNA-dependent machinery in regulating cortical neuronal differentiation.

Transcriptome Analysis Identifies SenZfp536,a Sense LncRNA that Suppresses Self-renewal of Cortical Neural Progenitors

Long non-coding RNAs(lncRNAs)regulate transcription to control development and homeostasis in a variety of tissues and organs.However,their roles in the development of the cerebral cortex have not been well elucidated.Here,a bioinformatics pipeline was applied to delineate the dynamic expression and potential cis-regulating effects of mouse lncRNAs using transcriptome data from 8 embryonic time points and sub-regions of the developing cerebral cortex.We further characterized a sense lncRNA,SenZfp536,which is transcribed downstream of and partially overlaps with the protein-coding gene Zfp536.Both SenZfp536 and Zfp536 were predominantly expressed in the proliferative zone of the developing cortex.Zfp536 was cis-regulated by SenZfp536,which facilitates looping between the promoter of Zfp536 and the genomic region that transcribes SenZfp536.Surprisingly,knocking down or activating the expression of SenZfp536 increased or compromised the proliferation of cortical neural progenitor cells(NPCs),respectively.Finally,overexpressing Zfp536 in cortical NPCs reversed the enhanced proliferation of cortical NPCs caused by SenZfp536 knockdown.The study deepens our understanding of how lncRNAs regulate the propagation of cortical NPCs through cis-regulatory mechanisms.