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Biomedical subjects

Cheng Jin

Publications and source records attributed to Cheng Jin.

3 recordsLinked to original sources

DeepPlaque: a scalable multimodal platform for Aβ pathology and cell analysis in Alzheimer's disease.

Histological analysis is essential for understanding disease pathology and the microenvironment, particularly in Alzheimer's disease (AD), characterized by beta-amyloid (Aβ) plaques that exist as diffuse, fibrillar, and core species, with distinct toxicity levels. However, accurate classification of Aβ plaque types in postmortem brain tissues and profiling of surrounding cells present significant challenges. To address these challenges, we developed "DeepPlaque", an integrated system featuring "PlaqueNet", a deep learning model for automated classification of Aβ plaque species from diverse imaging platforms. DeepPlaque includes automated workflows for cellular phenotyping and proteomic profiling through targeted laser microdissection. PlaqueNet achieves expert-level accuracy (AUC > 90%) in classifying the 3 major Aβ plaque species, supporting consistent and large-scale annotation. By integrating spatial cellular phenotyping with laser microdissection, DeepPlaque enables high-throughput proteomic analysis of Aβ plaque niches, revealing that microglia are more abundant around core and fibrillar Aβ plaques, with increased expression of apolipoprotein E and amyloid precursor protein in core Aβ plaques. This customizable platform enhances the molecular and cellular characterization of Aβ plaque-associated environments, providing critical insights into AD pathology.

Alzheimer Disease

Comparative Responses of Invasive and Native Plant Species to Combined Cd and Microplastic Pollution.

The co-occurrence of heavy metal contamination and biodegradable microplastic (polylactic acid, PLA) pollution poses increasing risks to terrestrial plant communities and soil functioning, yet species-specific responses to combined stress remain poorly understood. Cd and microplastics frequently co-occur in agricultural soils, where microplastics can alter cadmium mobility, bioavailability, and transport pathways, potentially modifying metal toxicity and plant stress responses compared with single-pollutant exposure. We investigated the responses of the invasive Bidens pilosa and the native Solanum nigrum grown in monoculture and mixed culture under combined cadmium (Cd) and biodegradable microplastic (PLA) stress by integrating plant growth, photosynthetic performance, oxidative physiology, and rhizosphere biochemical processes. Combined Cd-MP exposure markedly reduced plant growth, chlorophyll content (SPAD), photosystem II efficiency (Fv/Fm), nitrogen accumulation, biomass production, and rhizosphere enzyme activities associated with carbon, nitrogen, and phosphorus cycling. However, B. pilosa maintained greater physiological stability under stress, characterized by higher antioxidant enzyme activities (SOD, CAT, POD), lower reactive oxygen species (H2O2, O2˙-) accumulation, and reduced lipid peroxidation (MDA), whereas S. nigrum exhibited stronger oxidative damage and functional impairment. Multivariate analyses further revealed that root antioxidant capacity was closely associated with rhizosphere microbial enzyme activity, suggesting a root-centered regulatory mechanism linking plant stress tolerance to soil functioning. Overall, the invasive species showed greater tolerance to combined contamination and maintained relatively higher rhizosphere functional activity than the native species, indicating that multi-pollutant stress may alter competitive interactions between invasive and native plants in contaminated environments.

Cadmium

Gfa1 (glutamine fructose-6-phosphate aminotransferase) is essential for Aspergillus fumigatus growth and virulence.

BACKGROUND: Aspergillus fumigatus, the primary etiological agent of invasive aspergillosis, causes over 1.8 million deaths annually. Targeting cell wall biosynthetic pathways offers a promising antifungal strategy. Gfa1, a rate-limiting enzyme in UDP-GlcNAc synthesis, plays a pivotal role in the hexosamine biosynthetic pathway (HBP). RESULTS: Deletion of gfa1 (Δgfa1) results in auxotrophy for glucosamine (GlcN) or N-acetylglucosamine (GlcNAc). Under full recovery (FR) conditions, where minimal medium is supplemented with 5 mM GlcN as the sole carbon source, the Δgfa1 mutant shows growth comparable to the wild-type (WT). However, when supplemented with 5 mM GlcN and 55 mM glucose, growth is partially repressed, likely due to carbon catabolite repression, a condition termed partial repression (PR). Under PR conditions, Δgfa1 exhibits compromised growth, reduced conidiation, defective germination, impaired cell wall integrity, and increased sensitivity to endoplasmic reticulum (ER) stress and high temperatures. Additionally, Δgfa1 demonstrates disruptions in protein homeostasis and iron metabolism. Transcriptomic analysis of the mutant under PR conditions reveals significant alterations in carbohydrate and amino acid metabolism, unfolded protein response (UPR) processes, and iron assimilation. Importantly, Gfa1 is essential for A. fumigatus virulence, as demonstrated in Caenorhabditis elegans and Galleria mellonella infection models. CONCLUSIONS: These findings underscore the critical role of Gfa1 in fungal pathogenicity and suggest its potential as a therapeutic target for combating A. fumigatus infections.

Aspergillus fumigatus