Robert E. Schwartz

The paper integrates multiple datasets to create a comprehensive human liver cell atlas, identifying new cell types and associations with demographic factors.

This paper identifies mitochondrial dysfunction as a key driver of RSV infection severity and long-term complications through multi-omic analysis across multiple datasets and systems.

This paper describes engineered liver tissue that reverses acute liver failure in mice without immunosuppression, demonstrating potential for clinical translation.

SAHA creates a multimodal, subcellular-resolution reference atlas of healthy human tissues, revealing spatial organization and disease-associated disruptions across multiple organ systems.

This study identifies a nucleosome switch that primes Hepatitis B Virus infection by driving X gene transcription and shows that CBL137 inhibits this process.

This study identifies non-canonical genes linked to RAAS overactivation in lethal COVID-19, causing multi-organ damage and mediastinal lymph node dysfunction.

The paper develops vascularized macrophage-islet organoids to study immune-mediated β cell pyroptosis during viral infection and identifies TNFSF12-TNFRSF12A as a key mechanism.

The paper investigates the effects of liver-specific Mettl14 deletion, finding it causes nuclear heterotypia and disrupts RNA export machinery.

This study shows that TDP-43 accumulation in astrocytes impairs memory by altering antiviral pathways and chemokine signaling between astrocytes and neurons.

This study investigates how SARS-CoV-2 infection affects mitochondrial gene expression in different tissues and disease stages, finding targeted inhibition in some organs and upregulation in others.

This study uses rapid diagnostics and metatranscriptomics to analyze SARS-CoV-2 infection, revealing viral evolution, host responses, and drug interactions in NYC samples.