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Biology subjects

Atanga, R.

Publications and source records attributed to Atanga, R..

3 recordsLinked to original sources

Brain Stroke Prediction: A PSO Optimized Stacked Ensemble Machine Learning Approach with SMOTEEN Data Balancing

Prediction of stroke is a critical challenge in healthcare, where early intervention can significantly reduce risks and improve patient outcomes. Traditional methods often struggle with imbalanced datasets and low prediction accuracy. This paper proposes a novel approach to address these issues by combining PSO-optimized Stacked Ensemble ML Classifiers with SMOTEEN data balancing to predict strokes effectively. The technique optimizes 3 Baseline ML Classifiers(RF, SVM, XGB) using Particle Swarm Optimization (PSO) and Stacked Ensemble approach is applied that significantly improving prediction performance. The proposed methodology achieved an impressive 95.57% accuracy, outperforming conventional models such as SVM, LR, RF, KNN, XGB. Overall, the PSO-optimized stacked ensemble approach outperforms traditional machine learning techniques in stroke prediction, providing a more accurate and robust model for early detection and intervention.

bioengineering↗

Uranium-bearing dust induces differentiation and expansion of enteroendocrine cells in human colonoids

Chronic exposure to environmental toxins and heavy metals has been associated with intestinal inflammation, increased susceptibility to pathogen-induced diseases, and higher incidences of colorectal cancer, all of which have been steadily increasing in prevalence for the past 40 years. The negative effects of heavy metals on barrier permeability and inhibition of intestinal epithelial healing have been described; however, transcriptomic changes within the intestinal epithelial cells and impacts on lineage differentiation are largely unknown. Uranium exposure remains an important environmental legacy and physiological health concern, with hundreds of abandoned uranium mines located in the Southwestern United States largely impacting underserved indigenous communities. Herein, using human colonoids, we defined the molecular and cellular changes that occur in response to uranium bearing dust (UBD) exposure. We used single cell RNA sequencing to define the molecular changes that occur to specific identities of colonic epithelial cells. We demonstrate that this environmental toxicant disrupts proliferation and induces hyperplastic differentiation of secretory lineage cells, particularly enteroendocrine cells (EEC). EECs respond to UBD exposure with increased differentiation into de novo EEC sub-types not found in control colonoids. This UBD-induced EEC differentiation does not occur via canonical transcription factors NEUROG3 or NEUROD1. These findings highlight the significance of crypts-based proliferative cells and secretory cell differentiation as major colonic responses to heavy metal-induced injury.

cell biology↗

Inflammatory macrophages prevent colonic goblet and enteroendocrine cell differentiation through Notch signaling

Inflammatory macrophages in the intestine are a key pathogenic factor driving inflammatory bowel disease (IBD). Here, we report the role of inflammatory macrophage-mediated notch signaling on secretory lineage differentiation in the intestinal epithelium. Utilizing IL-10-deficient (Il10-/-) mice, a model of spontaneous colitis, we found an increase in Notch activity in the colonic epithelium as well as an increase in intestinal macrophages expressing Notch ligands, which are increased in macrophages upon inflammatory stimuli. Furthermore, a co-culture system of inflammatory macrophages and intestinal stem and proliferative cells during differentiation reduced goblet and enteroendocrine cells. This was recapitulated when utilizing a Notch agonist on human colonic organoids (colonoids). In summary, our findings indicate that inflammatory macrophages upregulate notch ligands that activate notch signaling in ISC via cell-cell interactions, which in turn inhibits secretory lineage differentiation in the gastrointestinal (GI) tract.

immunology↗