Taylor Sterling Adams

This study identifies a monocyte-macrophage-fibroblast axis in post-COVID-19 lung fibrosis using multi-omic profiling and shows its potential as a therapeutic target.

This study shows that sobetirome, a thyroid hormone receptor beta agonist, reduces pulmonary fibrosis in mice and human tissue by restoring mitochondrial function and modulating apoptosis.

This study identifies early alveolar niche disruption and aberrant epithelial reprogramming in IPF using multi-modal analyses of patient cohorts.

The paper identifies transcriptional programs in fibroblastic foci fibroblasts using spatial and single-cell transcriptomics, revealing MMP11 as a prognostic biomarker and potential therapeutic target.

The paper uses single-cell transcriptomics to analyze an IPF cohort, revealing a transcriptional deficit refractory to current treatments and identifying STAT3 as a key regulator in the therapeutic gap.

Single-nucleus multiomic and ex vivo lung slice profiling of human idiopathic pulmonary fibrosis identifies Alveolar Intermediate cells bridging alveolar and Aberrant Basaloid states and reveals AP-1 chromatin injury memory.

This study uses single-cell RNA sequencing to analyze sputum cells from asthma patients and controls, identifying dysregulated pathways and communication networks involved in asthma pathogenesis.

This study identifies CD103+ dendritic cell-fibroblast crosstalk via TLR9 and AHR signaling as a driver of lung fibrosis in IPF, showing that inhibiting AHR signaling reduces fibrosis.

This study examines hypoxia-induced cardiopulmonary remodeling in mice, finding that pulmonary artery stiffening due to collagen remodeling precedes and correlates with cardiac and lung dysfunction, with partial recovery observed after normoxia.

This study investigates GPR87's role in pulmonary fibrosis, finding it highly expressed in IPF lungs and protective against fibrosis when knocked down in multiple models.

This study develops an engineered whole-lung tissue model to study tissue organization and alveolar barrier function, showing improved barrier function with alveolar macrophages.

The paper identifies dedifferentiated early postnatal lung myofibroblasts that persist into adulthood and redifferentiate in response to injury.

The paper identifies cell-to-cell communication between mesothelial cells and alveolar tuft cells that regulates lung regeneration after pneumonectomy.

This study uses single-cell RNA sequencing to identify common and distinct immune aberrations in IPF and FHP, revealing shared monocyte features and disease-specific lymphocyte and receptor repertoires.

SDePER improves cell type deconvolution in spatial transcriptomic data by addressing platform effects, sparsity, and spatial correlation, achieving more accurate results than existing methods.

iDESC identifies differential expression in scRNA-seq data with multiple subjects by separating subject effects from disease effects, showing better performance than existing methods.

The paper develops a computational framework to study division of labor in tissues by analyzing cell interactions and spatial cues using single-cell RNA-seq and spatial transcriptomics data.

This study uses multi-omic data to identify age-related changes in lung cell composition and molecular programs associated with aging and senescence.

The paper identifies novel disease-associated genes for idiopathic pulmonary fibrosis using integrative genetic and transcriptomic analyses.

CINS infers differential cell-cell interactions between conditions using scRNA-Seq data and identifies the proteins involved in these interactions.

Connectome quantifies and visualizes cell-cell signaling networks from single-cell RNA-sequencing data using a software package for R.

The paper introduces MRFscRNAseq, a Markov Random Field model for identifying cell-type specific differentially expressed genes in scRNA-seq data, showing improved power over conventional methods.

This study uses single-cell RNA-seq to identify aberrant cell populations in IPF lungs, revealing novel basaloid cells and vascular endothelial changes.

Across 1,176,683 airway and lung cells from 22 datasets, ACE2 rises with age, in males and in smokers' multiciliated cells, and is lowest in young children.