Don D. Sin

Systematic benchmarking reveals pseudo-bulk biases and provides practical fixes for accurate RNA deconvolution.

The paper constructs a standardized BAL scRNA-seq atlas using BAL-EA, a novel annotation framework, revealing disease-associated shifts in COPD and validating findings in COVID-19 datasets.

This study examines SARS-CoV-2 infection and repair responses in human airway epithelial cells, finding prolonged and incomplete repair linked to long-COVID pulmonary symptoms.

The paper identifies twelve novel genetic risk loci for lung cancer subtypes through multi-ancestry GWAS and shows smoking-independent genetic risk.

The paper identifies shared genetic variants between critically ill COVID-19 and idiopathic pulmonary fibrosis by integrating GWAS with context-specific eQTLs and transcriptomics.

This study investigates how lipid nanoparticles interact with mucus in healthy and cystic fibrosis conditions, identifying factors affecting their diffusivity for improved transmucosal delivery.

The paper develops a rapid, minimal-handling protocol for preparing single-cell suspensions from bronchial brush specimens for scRNA-seq to improve airway disease research.

SMART deconvolves spatial transcriptomics data without a reference, inferring cell type profiles and composition using marker genes, and outperforms existing methods when references are unavailable.

This study identifies seven age-associated ECM proteins with increased expression in human lung tissue and demonstrates age-related differences in specific lung compartments.

This study identifies eight novel genetic signals associated with asthma-COPD overlap through a genome-wide association analysis involving multiple cohorts.

The paper uses multi-omics approaches to identify genes and plasma proteins associated with COVID-19, finding ABO plasma protein as a causal risk factor.

The paper identifies proteins associated with lung function and COPD risk using integrative omics and Mendelian Randomization, finding 37 proteins with causal associations.

The paper identifies co-expressed genes with ACE2 and TMPRSS2 in lung tissue and finds many have drug interactions, suggesting potential targets for COVID-19 therapeutics.

This study uses Mendelian randomization to examine if ACE inhibitors or cardiometabolic risk factors affect lung ACE2 and TMPRSS2 expression or plasma ACE2 levels, finding no overall association.

This study uses Mendelian randomisation to show that higher serum CC-16 levels protect against COPD risk and progression, with genetic variants linked to CC-16 expression in lung tissue.

The paper identifies SNPs with sex-specific effects on lung function traits using UK Biobank data, finding a significant interaction at rs7697189 near HHIP.

The paper identifies sex-specific transcriptomic responses to smoking in human airway epithelium, revealing sexually dimorphic gene modules associated with autophagy and immune response pathways.

This study identifies three new genetic loci associated with idiopathic pulmonary fibrosis and confirms 11 previously reported ones, highlighting mTOR signaling and mitotic spindle-assembly genes in disease susceptibility.

The paper identifies 279 new genetic signals for lung function across multiple ancestries, showing associations with COPD and pleiotropic effects.

This study identifies over 50 new genetic loci associated with pulmonary function through a multiethnic meta-analysis of 90,715 individuals.

The paper identifies 12 novel COPD loci and candidate causal genes using GWAS and lung eQTL data from 129 risk loci.