Recent evidence indicates the presence of micro- and nanoplastics in the human brain, with higher accumulation observed in patients with dementia. However, their mechanistic effects on the human brain at the cellular level remain underexplored. Astrocytes play a crucial role in repairing neurons following injury. The dysfunction of these cells can lead to chronic inflammation, a hallmark of neurodegenerative diseases. Here, we investigated the cytotoxic responses of primary human astrocytes exposed to polystyrene particles of two representative sizes, 25 nm and 1 µm, at concentrations of 1 µg/mL and 5 µg/mL for 48 h. Flow cytometry and confocal microscopy revealed the accumulation of particles of both sizes within the cytoplasm. Functional assays revealed reduced cell viability and elevated lactate dehydrogenase release, indicating cytotoxic effects following microplastic exposure. Gene expression analysis showed significant upregulation of MAPK14 and SOD2, indicating oxidative stress activation, and increased expression of pro-inflammatory mediators IL-6, TNF-α, and NF-κB1. In parallel, GLUT1 transcripts and GLUT1-positive cell populations were markedly reduced, suggesting impaired glucose metabolism. Collectively, these findings demonstrate that microplastics disrupt astrocytic homeostasis by inducing oxidative, inflammatory, and metabolic disturbances, leading to a reactive yet metabolically compromised phenotype. This study demonstrates the cellular damage caused by microplastics in astrocytes, which may contribute to a cellular mechanism linking environmental pollutant exposure to adverse effects on human health.

Background/Objectives: The original GSE283839 study characterized malignant-cell heterogeneity in atypical teratoid/rhabdoid tumor (ATRT). Building on this resource, we investigated the less-characterized glial microenvironment, focusing on astrocyte and microglial transcriptional programs and expression-supported candidate interactions with tumor cells. Methods: We reanalyzed single-nucleus RNA-sequencing data from 12 ATRT tumors using published annotations, program scoring, paired astrocyte–tumor comparisons, and conservative annotation sensitivities. CellChat analyses used 10,000 permutations and within-model Benjamini–Hochberg (BH) correction. An independent cohort comprised eight specimens from four patients. Results: The discovery dataset included 47 annotated astrocytes and 288 annotated microglia. Astrocytes expressed SLC1A2, SLC1A3, and GLUL, with higher glutamate/glutamine-module scores than matched tumor cells in two of three evaluable tumors. This difference persisted in the single tumor evaluable under conservative annotation. Microglia exhibited overlapping inflammatory, immunoregulatory, phagocytic/lipid-processing, and antigen-presentation programs. Across 12 tumors, microglial CD74 expression correlated with the antigen-presentation module score. Candidate interactions included astrocyte-to-tumor NCAM1–FGFR1 and PTN–PTPRZ1 and microglia-to-tumor SPP1-related pairs. Tumor-to-microglia APP–CD74 passed within-model BH correction in 7/10 eligible discovery tumors. External analyses supported tumor-to-myeloid APP–CD74 in at least one myeloid population in each of five evaluable specimens from four patients. Conclusions: This exploratory study highlights astrocyte metabolic expression programs and immune-related microglial programs in ATRT, prioritizing APP–CD74 and additional expression-supported glia–tumor interaction candidates for future spatial and functional investigation.

Ribosomal RNA modifications play a crucial role in bacteria, impacting function, ribosome formation, and antibiotic resistance. ModrRNA1 replaces manual methods and introduces a user-friendly, streamlined bioinformatics tool for the identification of potential rRNA modification sites and associated enzymes, across various bacteria. This tool utilizes a curated database of known bacterial rRNA modifications and enzymes, employing sequence alignment with a customized scoring system for precise site identification. High-confidence alignments generate annotated RNA sequence plots. Subsequently, enzyme detection is facilitated through structural comparisons, phylogenetics, and BLAST. ModrRNA1 boasts a user-friendly web interface hosted at https://modrrna.biotechie.org with the open-source code for customization available at https://github.com/sciguysl/ModrRNA1 . The results demonstrate ModrRNA1’s efficacy in identifying potential non-species-specific bacterial rRNA modification sites and species-specific associated enzymes.