Marc Andre Schneider

msBayesImpute improves missing value handling in proteomics data by integrating Bayesian factorization and probabilistic dropout models, outperforming existing methods in imputation and normalization.

This study shows that loss of the Y chromosome in lung adenocarcinoma causes epigenetic and transcriptomic changes that increase lineage plasticity and poor clinical outcomes.

This study shows human airway organoids can effectively model BSL-4 virus replication and pathogenesis, offering a safe and relevant alternative to animal models.

This study identifies epigenetic changes in AT2 cells from COPD patients that disrupt IFN and WNT pathways, impairing lung regeneration.

MetAlyzer streamlines and visualizes targeted metabolomics data from biocrates, enabling interactive analysis without coding.

SAME improves multimodal spatial omics integration by allowing topological disruptions during alignment, enhancing cell-type accuracy and revealing hidden biological insights.

This study shows cancer-associated fibroblasts enhance drug resistance in ALK-driven lung adenocarcinoma by promoting lipid biosynthesis and suppressing lipid peroxidation through AKT signaling.

The paper uses rRNA modification patterns to identify tissue and tumor-specific signatures, showing their potential as diagnostic biomarkers.

The paper introduces a single-sample workflow, MTBE-SP3, for simultaneous proteomic and metabolomic analysis, showing it reduces technical variation and enables consistent results across biological matrices.

This study uses early-stage IPF patient-derived cells to identify proinflammatory and fibrotic states and assess drug responses in airway cells.

Single-cell profiling of lung and bronchial cells places ACE2 mainly in a transient secretory cell state of cultured bronchial epithelium, between goblet and ciliated cells, co-expressing TMPRSS2.