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Chirality is a ubiquitous phenomenon in nature. The advent of nanomaterials has led to a gradual evolution of chiral studies from the molecular scale to the nanoscale. The emergence of carbon dots (CDs) has inaugurated a novel domain in the scientific and technological realms of carbon nanomaterials. In recent years, CDs have attracted increasing attention due to their luminescent properties, excellent biocompatibility and remarkable bioactivity. However, little attention has been paid to the chirality of the CDs and, in particular, the differences between CDs synthesized from racemic compounds and other chiral CDs, as well as the differences in the biological effects of chiral CDs, remain to be explored. Here, chiral CDs were synthesized from L -/ D -/ DL -arginine, and the differences in various aspects of chiral CDs were evaluated. We found that L -CDs without extreme differences in structure had brighter fluorescence and a more significant ability of NO generation and lipid droplet inhibition than the other two chiral CDs. Combined with its better drug loading and release ability, we validated its superior efficacy in tumor treatment. Therefore, this study provides a basis for further research on chiral carbon dots and their differences. [ABSTRACT FROM AUTHOR]

Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing pancreatic islet beta cells. Despite significant advancements, the precise pathogenesis of the disease remains unknown. This work integrated data from expression quantitative trait locus (eQTL) studies with Genome wide association study (GWAS) summary data of T1D and single-cell transcriptome data to investigate the potential pathogenic mechanisms of the CTSH gene involved in T1D in exocrine pancreas. Using the summary data–based Mendelian randomization (SMR) approach, we obtained four potential causative genes associated with T1D: BTN3A2 , PGAP3 , SMARCE1 and CTSH. To further investigate these genes'roles in T1D development, we validated them using a scRNA-seq dataset from pancreatic tissues of both T1D patients and healthy controls. The analysis showed a significantly high expression of the CTSH gene in T1D acinar cells, whereas the other three genes showed no significant changes in the scRNA-seq data. Moreover, single-cell WGCNA analysis revealed the strongest positive correlation between the module containing CTSH and T1D. In addition, we found cellular ligand–receptor interactions between the acinar cells and different cell types, especially ductal cells. Finally, based on functional enrichment analysis, we hypothesized that the CTSH gene in the exocrine pancreas enhances the antiviral response, leading to the overexpression of pro-inflammatory cytokines and the development of an inflammatory microenvironment. This process promotes β cells injury and ultimately the development of T1D. Our findings offer insights into the underlying pathogenic mechanisms of T1D. [ABSTRACT FROM AUTHOR]

Tumor protein P53 ( TP53 ) is an important tumor suppressor gene in humans. Under normal circumstances, TP53 can help repair mutated genes, or promote the death of cells with severe gene mutations (specifically, TP53 prevents cells from arrest in the G1/S phase when deoxyribonucleic acid (DNA) is damaged and promotes apoptosis if not repaired), and prevents normal cells from becoming malignant cells. TP53 mutations affect its tumor suppressor function, leading to the development of malignant tumors. In this study, using a public database, we explored the pan-cancer expression of TP53 , its impact on patient survival and prognosis, the types of gene mutations, its correlation with immunity, and its regulation of other transcription factors and micro RNA (miRNA). The docking sites of therapeutic drugs and key amino acid sites of action provide a basis for future targeted therapies. TP53 has important biological functions in the human body. This study provides a theoretical basis for clinical TP53 gene therapy.