Pulmonary, Critical Care, and Sleep Medicine Research
Min Chen, MD, PhD, is an assistant professor of internal medicine in the division of pulmonary, critical care, and sleep medicine, as well as a member of the Markey Cancer Center. Prior to joining the Gerber/Sasse laboratory, her research focused on investigating signal transduction and mechanisms underlying cancer cell migration, invasion, metastasis, and therapeutic response, particularly in breast and lung cancers. She utilized a wide range of cell biology approaches including three-dimensional (3D) culture system, immunocytochemistry, advanced imaging techniques such as confocal and total internal reflection fluorescence (TIRF) microscopy. In addition, she applied molecular biology methods such as chromatin immunoprecipitation (ChIP) and CRISPR-Cas9 gene editing, complemented by both cell line-based and patient-derived xenograft models.
Her current research interest integrates this expertise in cell biology and signal transduction with cutting-edge molecular approaches to monitor enhancer function in airway epithelial and smooth muscle cells employed by the Gerber/Sasse laboratory. Her work aims to elucidate the mechanisms and the clinical significance of gene regulation in lung diseases, including lung cancer, asthma, and chronic obstructive pulmonary disease (COPD).
Publications
Publications
Girish Nair, MD, is a physician-scientist specializing in interstitial lung disease (ILD). His research integrates clinical phenotyping, advanced imaging analytics, multi-omics profiling, and mitochondrial biology to understand disease mechanisms and accelerate translational discovery.
Dr. Nair leads a hybrid translational program that bridges:
- Electronic health record (EHR)–based natural history modeling
- High-resolution CT imaging analytics and AI-driven spatial modeling
- Multi-omics integration (metabolomics, transcriptomics, proteomics)
- Mitochondrial dysfunction and epithelial–fibroblast cross-talk in fibrosis
- Digital biomarker development for early detection and progression modeling
His work aims to move beyond correlation toward mechanism-driven prediction, developing causal disease models and precision phenotyping strategies that inform trial enrichment and therapeutic targeting.
Dr. Nair’s program operates at the intersection of clinical care and data science, leveraging large-scale datasets (10,000+ CT datasets), digital twins, and computational modeling frameworks to redefine how fibrotic lung diseases are diagnosed, monitored, and treated.
Research Interests
- Idiopathic Pulmonary Fibrosis (IPF) and Progressive Fibrotic ILD
- Mitochondrial dysfunction in epithelial fibroblast signaling
- Mitoception and intercellular metabolic communication
- Digital biomarkers and remote disease monitoring
- AI-based CT imaging modeling and spatial lung analytics
- Multi-omics integration and mechanistic pathway modeling
- Natural history modeling using EHR-linked datasets
Research Interests
- Idiopathic Pulmonary Fibrosis (IPF) and Progressive Fibrotic ILD
- Mitochondrial dysfunction in epithelial fibroblast signaling
- Mitoception and intercellular metabolic communication
- Digital biomarkers and remote disease monitoring
- AI-based CT imaging modeling and spatial lung analytics
- Multi-omics integration and mechanistic pathway modeling
- Natural history modeling using EHR-linked datasets
Main Research Projects
Integrating Metabolomics and Radiographic features in Advanced Lung Diseases
Multi-omics integration with advanced imaging and mechanistic pathway modeling in patients with ILD and COPD. Radiologic characterization of early and late complications, linking imaging signatures survival outcomes.
Mitochondrial Signaling in Fibrosis
Mechanistic studies investigating mitochondrial transfer (mitoception), metabolic reprogramming, and epithelial–fibroblast crosstalk in progressive fibrosis. This program links mitochondrial dysfunction to downstream fibrotic signaling networks.
CT Phenotyping in Advanced Lung Disease
Development of higher-order functional imaging models using convolutional and graph-based neural networks to capture spatial heterogeneity in fibrotic lung disease.
Digital Twin Modeling and Natural History of ILD
Creation of predictive disease trajectory models combining imaging, omics, and clinical data to generate individualized progression forecasts. A hybrid retrospective–prospective EHR-based study integrating imaging, lung function decline, and low-burden digital biomarkers to model disease trajectory and identify early progression signals.
Main Research Projects
Integrating Metabolomics and Radiographic features in Advanced Lung Diseases
Multi-omics integration with advanced imaging and mechanistic pathway modeling in patients with ILD and COPD. Radiologic characterization of early and late complications, linking imaging signatures survival outcomes.
Mitochondrial Signaling in Fibrosis
Mechanistic studies investigating mitochondrial transfer (mitoception), metabolic reprogramming, and epithelial–fibroblast crosstalk in progressive fibrosis. This program links mitochondrial dysfunction to downstream fibrotic signaling networks.
CT Phenotyping in Advanced Lung Disease
Development of higher-order functional imaging models using convolutional and graph-based neural networks to capture spatial heterogeneity in fibrotic lung disease.
Digital Twin Modeling and Natural History of ILD
Creation of predictive disease trajectory models combining imaging, omics, and clinical data to generate individualized progression forecasts. A hybrid retrospective–prospective EHR-based study integrating imaging, lung function decline, and low-burden digital biomarkers to model disease trajectory and identify early progression signals.
Publications
- Nair GB, Faizee F, Smith Z, Al-Katib S, Ashrafi N, Yilmaz A, Mimi RA, Bhogoju S, Lomeikaite V, Gordevičius J, Castillo E, Graham SF. Distinct Metabolic Signatures Linked to High-Resolution Computed Tomography Radiographic Phenotypes in Stable and Progressive Fibrotic Lung Disease. Metabolites. 2026 Jan 19;16(1):82.
- Faizee F, Smith Z, Gomez O, Alnabulsi Z, Pottmeyer G, Ashrafi N, Mimi RA, Lomeikaite V, Gabrielaitė M, Krinickis K, Gordevičius J, Yilmaz A, Castillo E, Graham SF, Nair GB. Metabolomic profiling reveals distinct lipid signatures in progressive versus stable fibrotic lung disease. Metabolomics. 2025 Oct 25;21(6):153.
- Nair G, Xing YJ, Luong A, Bashar F, Nowacki A, Stevens C, Zhao L, Castillo E. CT-derived functional imaging biomarkers combined with FEV1 for predicting 10-year all-cause mortality in COPDGene cohort. NPJ Biomed Innov. 2025;2(1):25.
- Liu YK, Cisneros J, Nair G, Stevens C, Castillo R, Vinogradskiy Y, Castillo E. Perfusion estimation from dynamic non-contrast computed tomography using self-supervised learning and a physics-inspired U-net transformer architecture. Int J Comput Assist Radiol Surg. 2025 May;20(5):959-970.
View Dr. Nair's Complete List of Publications
Publications
- Nair GB, Faizee F, Smith Z, Al-Katib S, Ashrafi N, Yilmaz A, Mimi RA, Bhogoju S, Lomeikaite V, Gordevičius J, Castillo E, Graham SF. Distinct Metabolic Signatures Linked to High-Resolution Computed Tomography Radiographic Phenotypes in Stable and Progressive Fibrotic Lung Disease. Metabolites. 2026 Jan 19;16(1):82.
- Faizee F, Smith Z, Gomez O, Alnabulsi Z, Pottmeyer G, Ashrafi N, Mimi RA, Lomeikaite V, Gabrielaitė M, Krinickis K, Gordevičius J, Yilmaz A, Castillo E, Graham SF, Nair GB. Metabolomic profiling reveals distinct lipid signatures in progressive versus stable fibrotic lung disease. Metabolomics. 2025 Oct 25;21(6):153.
- Nair G, Xing YJ, Luong A, Bashar F, Nowacki A, Stevens C, Zhao L, Castillo E. CT-derived functional imaging biomarkers combined with FEV1 for predicting 10-year all-cause mortality in COPDGene cohort. NPJ Biomed Innov. 2025;2(1):25.
- Liu YK, Cisneros J, Nair G, Stevens C, Castillo R, Vinogradskiy Y, Castillo E. Perfusion estimation from dynamic non-contrast computed tomography using self-supervised learning and a physics-inspired U-net transformer architecture. Int J Comput Assist Radiol Surg. 2025 May;20(5):959-970.
View Dr. Nair's Complete List of Publications
Funding Sources
- National Institutes of Health (NIH)
- Industry-supported pulmonary research initiatives
- Institutional translational research support
Funding Sources
- National Institutes of Health (NIH)
- Industry-supported pulmonary research initiatives
- Institutional translational research support
Recent Honors
- Boehringer-Ingelheim Pulmonary Endowed Research Professor
- Invited national speaker on ILD imaging and digital biomarker modeling
- Leadership roles in ILD clinical program development
Recent Honors
- Boehringer-Ingelheim Pulmonary Endowed Research Professor
- Invited national speaker on ILD imaging and digital biomarker modeling
- Leadership roles in ILD clinical program development
Sarah Sasse, PhD, MA, is an associate professor of internal medicine in the division of pulmonary, critical care, and sleep medicine, and co-manages the Gerber/Sasse Lab with her longstanding mentor and colleague, Anthony Gerber, MD. The Gerber/Sasse Lab integrates standard techniques in molecular biology (qPCR, immunoprecipitation, reporter assays) with cutting-edge genomics tools (ChIP-seq, ATAC-seq, PRO-seq) in culture models of human airway cell populations to explore the intricate relationships between gene regulation, genetic variation, environmental exposures, therapeutics and lung disease. They have been consistently NIH/DoD funded for the last 16 years and maintain multiple, actively funded collaborative projects that span the University of Kentucky, National Jewish Health, the University of Colorado system, nationally and internationally.
Recent Publications
- Functional variant discovery identifies a novel genetic link between SPRY2, wood smoke, and asthma https://pubmed.ncbi.nlm.nih.gov/41021275/
- Enhancer RNA transcription pinpoints functional genetic variants linked to asthma https://pubmed.ncbi.nlm.nih.gov/40164603/
- Noncoding SNPs decrease expression of FABP5 during COPD exacerbations https://pubmed.ncbi.nlm.nih.gov/38113113/
- Deconvolution of multiplexed transcriptional responses to wood smoke particles defined rapid aryl hydrocarbon receptor signaling dynamics https://pubmed.ncbi.nlm.nih.gov/34520756/
- The MUC5B-associated variant rs35705950 resides within an enhancer subject to lineage- and disease-dependent epigenetic remodeling https://pubmed.ncbi.nlm.nih.gov/33320836/
- Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era https://pubmed.ncbi.nlm.nih.gov/33891947/
- Nascent transcript analysis of glucocorticoid crosstalk with TNF defines primary and cooperative inflammatory repression https://pubmed.ncbi.nlm.nih.gov/31519741/
Recent Publications
- Functional variant discovery identifies a novel genetic link between SPRY2, wood smoke, and asthma https://pubmed.ncbi.nlm.nih.gov/41021275/
- Enhancer RNA transcription pinpoints functional genetic variants linked to asthma https://pubmed.ncbi.nlm.nih.gov/40164603/
- Noncoding SNPs decrease expression of FABP5 during COPD exacerbations https://pubmed.ncbi.nlm.nih.gov/38113113/
- Deconvolution of multiplexed transcriptional responses to wood smoke particles defined rapid aryl hydrocarbon receptor signaling dynamics https://pubmed.ncbi.nlm.nih.gov/34520756/
- The MUC5B-associated variant rs35705950 resides within an enhancer subject to lineage- and disease-dependent epigenetic remodeling https://pubmed.ncbi.nlm.nih.gov/33320836/
- Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era https://pubmed.ncbi.nlm.nih.gov/33891947/
- Nascent transcript analysis of glucocorticoid crosstalk with TNF defines primary and cooperative inflammatory repression https://pubmed.ncbi.nlm.nih.gov/31519741/
Elizabeth Schroder Stumpf, PhD, is a researcher and associate professor studying circadian rhythms. Circadian rhythms are approximately 24-hour biological cycles that synchronize the timing of an organism's behavior and physiology to daily environmental changes. The importance of these rhythms to human health is highlighted by epidemiological studies of shift workers, who display circadian disturbances and a range of health problems including increased cardiovascular disease. Patients in the intensive care unit experience profound circadian disruption due to continuous light exposure, noise, sedation, and mechanical ventilation. These are all factors that disrupt normal sleep-wake cycles and dysregulate the molecular clock throughout the body. Our laboratory uses both in vitro and in vivo models, including sleep deprivation, to investigate how circadian disruption contributes to critical illness. We have demonstrated that circadian clocks in striated muscle regulate gene expression, identifying ion channels and metabolic genes expressed in a circadian manner in cardiac muscle. We have extended this work to the diaphragm in the context of acute lung injury and sepsis, where disruption of the molecular clock may represent a novel mechanism contributing to diaphragm dysfunction. Understanding how critical illness disrupts circadian rhythms in respiratory muscle, and identifying therapeutic strategies to target this disruption, represents an important and emerging area of investigation in critical care research.
Research Interests
Our laboratory is interested in how circadian rhythms regulate physiology in health and how their disruption contributes to disease, with a specific focus on acute lung injury, sepsis, and diaphragm dysfunction. We investigate the molecular mechanisms linking clock disruption to mitochondrial dysfunction and muscle weakness and use sleep deprivation models to understand how the circadian disturbances common in critically ill patients worsen outcomes.
Research Interests
Our laboratory is interested in how circadian rhythms regulate physiology in health and how their disruption contributes to disease, with a specific focus on acute lung injury, sepsis, and diaphragm dysfunction. We investigate the molecular mechanisms linking clock disruption to mitochondrial dysfunction and muscle weakness and use sleep deprivation models to understand how the circadian disturbances common in critically ill patients worsen outcomes.
Main Research Projects
Our currently funded work (NIH NHLBI R01HL172813-01) investigates how the cardiac molecular clock regulates the circadian expression of ion channel genes and how this regulation impacts arrhythmia susceptibility and sudden cardiac death. Using an inducible cardiomyocyte-specific Bmal1 knockout model, we have shown that disruption of the myocardial clock reduces the functional expression of cardiac potassium and sodium channels and alters cardiac electrophysiology. Current studies employ promoter analyses, chromatin immunoprecipitation, mRNA sequencing, and ribosome profiling (Ribo-seq) to define the circadian mechanisms controlling both the transcription and translation of ion channel genes in the heart. To model circadian disruption, we use time-restricted feeding misaligned with the light-dark cycle.
This paradigm uncouples peripheral clocks from the central clock in the suprachiasmatic nucleus and recapitulates the circadian misalignment experienced by shift workers and critically ill patients. Our laboratory also has an established record of investigating diaphragm dysfunction in sepsis and critical illness, including work demonstrating that mitochondrial oxidative stress is a central driver of sepsis-induced diaphragm weakness and that mitochondrial-targeted antioxidant strategies can prevent this dysfunction. Understanding how disruption of the diaphragm molecular clock during acute lung injury and sepsis contributes to mitochondrial dysfunction and muscle weakness is a question with important implications for how we care for the sickest patients in the ICU.
Main Research Projects
Our currently funded work (NIH NHLBI R01HL172813-01) investigates how the cardiac molecular clock regulates the circadian expression of ion channel genes and how this regulation impacts arrhythmia susceptibility and sudden cardiac death. Using an inducible cardiomyocyte-specific Bmal1 knockout model, we have shown that disruption of the myocardial clock reduces the functional expression of cardiac potassium and sodium channels and alters cardiac electrophysiology. Current studies employ promoter analyses, chromatin immunoprecipitation, mRNA sequencing, and ribosome profiling (Ribo-seq) to define the circadian mechanisms controlling both the transcription and translation of ion channel genes in the heart. To model circadian disruption, we use time-restricted feeding misaligned with the light-dark cycle.
This paradigm uncouples peripheral clocks from the central clock in the suprachiasmatic nucleus and recapitulates the circadian misalignment experienced by shift workers and critically ill patients. Our laboratory also has an established record of investigating diaphragm dysfunction in sepsis and critical illness, including work demonstrating that mitochondrial oxidative stress is a central driver of sepsis-induced diaphragm weakness and that mitochondrial-targeted antioxidant strategies can prevent this dysfunction. Understanding how disruption of the diaphragm molecular clock during acute lung injury and sepsis contributes to mitochondrial dysfunction and muscle weakness is a question with important implications for how we care for the sickest patients in the ICU.
Publications
Zhang X, Procopio SB, Semel MG, Schroder EA, Seward TS, Du P, Wu K, Johnson SR, Prabhat A, Schneider DJ, Stumpf IG, Rozmus ER, Huo Z, Delisle BP, Esser KA. “New role for cardiomyocyte Bmal1 in the regulation of sex specific heart transcriptomes.” Function, 2025 Feb12;6(1)zqae053.
****Selected as an APSselect article****
- Delisle BP, Prabhat A, Burgess DE, Stumpf IG, McCarthy JJ, Procopio SB, Zhang X, Esser KA, Schroder EA. “Circadian influences on sudden cardiac death and cardiac electrophysiology.” J Mol Cell Cardiol. 2025 Jan 27;200:93-112.
- Delisle BP, Rozmus E, Prabhat A, Procopio SB, Zhang X, Entcheva E, Esser KA, Schroder EA. “BMAL1 mediates sex-specific circadian regulation of cardiac ion channels and temporal arrhythmia vulnerability.” Heart Rhythm. 2025 Oct 9: S1547-5271(25)02946-7.
- Prabhat A, Naidu S, Stumpf IG, Seward T, Schroder EA, Delisle BP. “Dim Light at Night Worsens Cardiac Autonomic Dysregulation in Female Diabetic Mice.” Heart Rhythm. 2026 Jan 7:S1547-5271(26)00025-1.
View Dr. Stumpf's Complete List of Publications
Publications
Zhang X, Procopio SB, Semel MG, Schroder EA, Seward TS, Du P, Wu K, Johnson SR, Prabhat A, Schneider DJ, Stumpf IG, Rozmus ER, Huo Z, Delisle BP, Esser KA. “New role for cardiomyocyte Bmal1 in the regulation of sex specific heart transcriptomes.” Function, 2025 Feb12;6(1)zqae053.
****Selected as an APSselect article****
- Delisle BP, Prabhat A, Burgess DE, Stumpf IG, McCarthy JJ, Procopio SB, Zhang X, Esser KA, Schroder EA. “Circadian influences on sudden cardiac death and cardiac electrophysiology.” J Mol Cell Cardiol. 2025 Jan 27;200:93-112.
- Delisle BP, Rozmus E, Prabhat A, Procopio SB, Zhang X, Entcheva E, Esser KA, Schroder EA. “BMAL1 mediates sex-specific circadian regulation of cardiac ion channels and temporal arrhythmia vulnerability.” Heart Rhythm. 2025 Oct 9: S1547-5271(25)02946-7.
- Prabhat A, Naidu S, Stumpf IG, Seward T, Schroder EA, Delisle BP. “Dim Light at Night Worsens Cardiac Autonomic Dysregulation in Female Diabetic Mice.” Heart Rhythm. 2026 Jan 7:S1547-5271(26)00025-1.
View Dr. Stumpf's Complete List of Publications
Funding Sources
- Circadian and Sleep for a Healthy KY (CASH-KY) pilot funding, ChronoCulture: Anticipating Homeostasis in a Dish
- NIH NHLBI R01HL172813-01, Circadian Regulation of Cardiac Electrophysiology
Funding Sources
- Circadian and Sleep for a Healthy KY (CASH-KY) pilot funding, ChronoCulture: Anticipating Homeostasis in a Dish
- NIH NHLBI R01HL172813-01, Circadian Regulation of Cardiac Electrophysiology
Recent Honors
- APS Select, May 2025 for distinction in scholarship in the journal Function for the article: Zhang X, Procopio SB, Semel MG, Schroder EA, Seward TS, Du P, Wu K, Johnson SR, Prabhat A, Schneider DJ, Stumpf IG, Rozmus ER, Huo Z, Delisle BP, Esser KA. “New role for cardiomyocyte Bmal1 in the regulation of sex specific heart transcriptomes.” Function, 2025 Feb12;6(1)zqae053. Doi: 10.1093/function/zqua053. https://pubmed.ncbi.nlm.nih.gov/39658371/
- Third-place award ($500) in the NSF Mid-South Hub Micro Pitch Competition (12/2025)
- First-place recognition ($5,000) from the Kentucky Science and Engineering Foundation (KSEF) Innovation Acceleration Award for technology commercialization (12/2025)
- Completion of the UAccel Launch Blue program
Recent Honors
- APS Select, May 2025 for distinction in scholarship in the journal Function for the article: Zhang X, Procopio SB, Semel MG, Schroder EA, Seward TS, Du P, Wu K, Johnson SR, Prabhat A, Schneider DJ, Stumpf IG, Rozmus ER, Huo Z, Delisle BP, Esser KA. “New role for cardiomyocyte Bmal1 in the regulation of sex specific heart transcriptomes.” Function, 2025 Feb12;6(1)zqae053. Doi: 10.1093/function/zqua053. https://pubmed.ncbi.nlm.nih.gov/39658371/
- Third-place award ($500) in the NSF Mid-South Hub Micro Pitch Competition (12/2025)
- First-place recognition ($5,000) from the Kentucky Science and Engineering Foundation (KSEF) Innovation Acceleration Award for technology commercialization (12/2025)
- Completion of the UAccel Launch Blue program