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Kohut, A.

Publications and source records attributed to Kohut, A..

3 recordsLinked to original sources

CMVAE: Contrastive Supervision Improves Single-Omic Latent Manifold for Breast Cancer Survival Prognosis

High-dimensional omics data are vital for fore- casting patient prognosis in oncology. While deep multi-omics learning methods are increasingly popular, they suffer from data missingness and low patient overlap across modalities. Consequently, advancing single-omic representation learning re- mains a critical yet challenging research problem. Standard generative dimensionality reduction methods rely on recon- struction objectives that optimize the global manifold topology; however, overlook downstream clinical outcomes. To address these limitations, we introduce a Contrastive Masked Denois- ing Variational Autoencoder (CMVAE), a self-supervised dual- optimization framework designed to map single-omic information into a clinical outcome-aware latent space. A stochastic feature masking strategy corrupts the input omic profiles, and CMVAE is optimized to simultaneously infer missing molecular data and contrastive alignment of patient survival trajectories. We evaluate CMVAE using leak-proof five-fold stratified cross-validation on the TCGA Breast Invasive Carcinoma (BRCA) cohort. The method outperforms traditional unsupervised methods, achieving an AUROC of 0.7397 {+/-} 0.0239 on patient prognosis. Further analysis demonstrates a highly significant (p < 0.0001) risk stratification among low vs. high risk groups. Beyond comparing within single-omic methods, CMVAE outperforms six state-of- the-art multi-omics survival baselines by a minimum of 3%. Availability: All codes including data preparation scripts, training and validation recipes, and experimental configurations are available at: https://github.com/kabir-ai2bio-lab/CMVAE. Note: Accepted at the IEEE BIBM 2026 workshop RLPD-Bio (Representation Learning and Pattern Discovery for Bioinformatics and Biomedicine).

bioinformatics↗

BK Channels Orchestrate Cardiac Homeostasis Through Mitochondrial Uncoupling Proteins

BK channels, coded by the Kcnma1 gene, integrate voltage and intracellular Ca2+ signals and are recognized for their roles in smooth muscle and neuronal excitability. However, their contribution to baseline cardiac physiology remains poorly defined. Here we uncover a fundamental function for BK channels in maintaining normal cardiac performance, independent of pathological stress. Using non-invasive echocardiography, transcriptional profiling, and mechanistic analyses, we demonstrate that Kcnma1 deletion disrupts ventricular function, and remodels metabolic and stress-response pathways. Transcriptomic profiling revealed selective downregulation of mitochondrial uncoupling proteins (UCPs) and suppression of the PGC-1/FOXO3a axis, without broad loss of oxidative phosphorylation components. Enhancing UCP expression restored cardiac performance, indicating that mitochondrial uncoupling and redox control constitute key downstream effectors of BK signaling. Together, these results identify a physiological role for BK channels in maintaining myocardial function and define a mitochondrial BK-UCP axis, critical for cardiac homeostasis.

cell biology↗

Inhibition of BKCa channels protects neonatal hearts against myocardial ischemia and reperfusion injury

BKCa channels are large-conductance calcium and voltage-activated potassium channels that are heterogeneously expressed in a wide array of cells. Activation of BKCa channels present in mitochondria of adult ventricular cardiomyocytes is implicated in cardioprotection against ischemia-reperfusion (IR) injury. However, the BKCa channels activity has never been detected in the plasma membrane of adult ventricular cardiomyocytes. In this study, we report the presence of the BKCa channel in the plasma membrane and mitochondria of neonatal murine and rodent cardiomyocytes which protects the heart on inhibition but not activation. Furthermore, K+ currents measured in neonatal cardiomyocyte (NCM) was sensitive to iberiotoxin (IbTx), suggesting the presence of BKCa channels in the plasma membrane. Neonatal hearts subjected to IR when post-conditioned with NS1619 during reoxygenation increased the myocardial infarction whereas IbTx reduced the infarct size. In agreement, isolated NCM also presented increased apoptosis on treatment with NS1619 during hypoxia and reoxygenation, whereas IbTx reduced TUNEL positive cells. In NCMs, activation of BKCa channels increased the intracellular reactive oxygen species post HR injury. Electrophysiological characterization of NCMs indicated that NS1619 increased the beat period, field, and action potential duration, and decreased the conduction velocity and spike amplitude. In contrast, IbTx had no impact on the electrophysiological properties of NCMs. Taken together, our data established that inhibition of plasma membrane BKCa channels in the NCM protects neonatal heart/cardiomyocytes from IR injury. Furthermore, the functional disparity observed towards the cardioprotective activity of BKCa channels in adults compared to neonatal heart could be attributed to their differential localization.

physiology↗