About

Nadir Yehya, MD, is an Associate Professor of Anesthesiology and Critical Care at the Hospital of the University of Pennsylvania and the Children's Hospital of Philadelphia. He serves as an Attending Physician in the Division of Critical Care Medicine at the Children's Hospital of Philadelphia and is the Medical Director of Respiratory Services there. Dr. Yehya's clinical expertise includes mechanical ventilation and respiratory failure. His research focuses on acute respiratory distress syndrome, with a particular emphasis on pediatric ARDS, racial and regional disparities in outcomes, and the impact of neighborhood factors on health. He has contributed to multiple research presentations at the Critical Care Congress, exploring topics such as the trajectory of pediatric ARDS before and after COVID-19, racial/ethnic disparities in mortality, inflammatory subphenotypes after cardiopulmonary bypass, and predictors of poor outcomes in pediatric sepsis-induced ARDS. Dr. Yehya holds a BA in Molecular and Cell Biology from the University of California at Berkeley, an MD from the David Geffen School of Medicine at UCLA, and a MSCE in Clinical Epidemiology and Biostatistics from the University of Pennsylvania.

Research topics

• Medicine
• Internal medicine
• Anesthesia
• Intensive care medicine
• Surgery
• Pediatrics
• Genetics

Selected publications

• Proteomic and Metabolomic Characterization of Pediatric ARDS Inflammatory Subphenotypes

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01

  article1st authorCorresponding

  Abstract Rationale: Acute respiratory distress syndrome (ARDS) is intrinsically heterogeneous. Biomarkers and clinical variables have been used to subphenotype ARDS, with a consistent hypo- and hyperinflammatory subphenotype identified with potential differential responses to therapies. Deeper unbiased biologic profiling of subphenotypes may identify mechanistic pathways differentiating hypo- and hyperinflammatory ARDS, providing insight into drivers of heterogeneity. Therefore, we aimed to characterize the metabolomic, lipidomic, and proteomic landscape of pediatric ARDS and identify pathways differentially enriched between hypo- and hyperinflammatory ARDS. Methods: This was a secondary analysis of a cohort of children with ARDS (total n = 333) from the Children's Hospital of Philadelphia enrolled between 2014 and 2019, with plasma collected within 24 hours of ARDS onset. We performed metabolomics by NMR (n = 333), lipidomics by liquid chromatography/tandem mass spectrometry (LC-MS/MS)(n = 333), and unbiased proteomics using nanoparticle-enriched LC-MS/MS (n = 179). We also performed the above analyses on 24 intubated non-ARDS controls. Differential metabolite/protein level analyses (increase/decrease fold-change ≥ 1.5 and adjusted p < 0.05) and downstream pathway analyses were performed using gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA). The primary comparison was between (biomarker-defined) hypo- and hyperinflammatory ARDS. Results: NMR metabolomics (> 30 metabolites), lipidomics (> 800 lipids), and proteomics (> 3300 proteins) all demonstrated clear signatures differentiating ARDS from non-ARDS, and hypo- from hyperinflammatory ARDS. Hyperinflammatory ARDS had higher levels of lactate, sucrose, triglycerides, diacylglycerols, phosphatidylethanolamines, and phosphatidylcholines. GSEA of the proteomic signature showed elevation of DNA- and RNA-processing proteins in hyperinflammatory ARDS, with concurrent downregulation of complement and clotting pathways. GSVA confirmed activation of DNA repair pathways, and downregulation of coagulation and complement pathways, in hyperinflammatory ARDS. GSVA also showed upregulation of hypoxia, glycolysis, and TNF signaling in hyperinflammatory ARDS. Conclusions: ARDS and its inflammatory subphenotypes are readily differentiated using unbiased metabolomics, lipidomics, and proteomics. Hyperinflammatory ARDS shows elevation of nuclear proteins consistent with cell death and damage-associated molecular pattern (DAMP) release, which is supported by the lipid and NMR metabolomic signal. Multiomic analysis of critical illness syndrome can provide significant insight into the mechanisms underlying heterogeneity, and nanoparticle-enriched LC-MS/MS specifically shows promise for identifying an underlying protein signature.

  PublisherDOI

• Abstract 4362152: Preoperative Blood Biomarkers Outperform Clinical Variables in Predicting Poor Outcome After Neonatal Cardiopulmonary Bypass Surgery

  Circulation · 2025-11-03

  articleSenior author

  Introduction: Neonates undergoing surgery for congenital heart disease (CHD) are at risk of death, longer intensive care unit (ICU) stays, and readmissions. Current prognostic models rely predominantly on unmodifiable clinical factors. Aims: We aimed to compare machine learning methods for predicting ICU-30, a validated composite outcome after neonatal surgery with cardiopulmonary bypass (CPB), using pre-operative blood biomarkers versus clinical features. Hypothesis: Inflammatory and organ injury biomarkers will predict ICU-30 better than clinical factors alone. Methods: Plasma and clinical data were collected from consecutively enrolled neonates (<30 days of age) immediately before CPB. Twenty-eight biomarkers were measured via individual or multiplexed ELISA and tested for association with ICU-30, defined as (1) mortality within 30 days of CPB, (2) ICU stay >30 days after CPB, or (3) ICU readmission within 30 days after CPB. Predictive performance of the machine learning techniques XGBoost, LASSO, and random forest (RF) were compared based on area under the receiver operating characteristic (AUROC) curve. For XGBoost, we identified the top 20 features based on importance (gain) to the model. Results: Biomarkers were available for 144 patients. Most were male (51%), White (64%), and non-Hispanic (75%). Median age at surgery was 3.6 days (IQR 2.6-5.2). Most operations were STAT 3 (32%) or STAT 5 (28%). ICU-30 occurred in 29 (20%) subjects. Using clinical and biomarker data, XGBoost performed moderately well (AUROC 0.75) to predict ICU-30, and was superior to RF (AUROC 0.73) and LASSO (AUROC 0.71) (Figure 1). Biomarkers alone performed better (AUROC 0.72) than clinical data alone (AUROC 0.61) (Figure 2). For XGBoost, 19 of the top 20 features were biomarkers, with the top 3 being neutrophil gelatinase-associated lipocalin (NGAL), trefoil factor 3 (TTF3) and growth differentiation factor-15 (GDF-15) (Figure 3). Conclusions: This preliminary data demonstrates moderate performance of a multi-biomarker model for predicting poor outcome post-CPB for neonatal CHD. A biomarker-only model outperformed a clinical-only model. Two of the top three most important features were biomarkers for renal and gut inflammation, suggesting preoperative splanchnic inflammation may be relevant for postoperative outcomes. Further investigation may identify mechanistic pathways for improved prognostication and could offer insights for targeted therapeutic interventions.

  PublisherDOI

• Magnetic Resonance Imaging for Improved Brain Tumor Detection

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-11 · 1 citations

  preprintOpen access

  Abstract Precise demarcation of brain tumor boundaries is critical for optimizing treatment strategies and improving patient outcomes. In vivo characterization of tumor using PET/CT and MRI is clinical standard. PET/CT highlights the metabolic aspects of the tumor, while MRI provides information on functional, metabolic and structural changes. Even with technological advancements in both PET/CT and MRI, a method that can precisely delineate infiltrative tumor boundaries from normal-appearing brain regions (NABR) in vivo is still lacking. To address this limitation, we explored a relatively new MR imaging method, the Nuclear Overhauser Effect Magnetization Transfer Ratio (NOE MTR ), in conjunction with a gadolinium-based contrast agent (Gd-DOTA), to precisely delineate the tumor boundaries in a rat model of infiltrative gliosarcoma. NOE MTR imaging was performed in the rat model (n=5) before and after Gd-DOTA administration. The post-Gd-DOTA NOE MTR map was subtracted from the pre-Gd-DOTA map and compared with contrast-enhanced T 1 -weighted images and immuno-histological findings. The resulting NOE MTR difference map clearly highlighted both the tumor core and infiltrative boundaries, which was not discernible on the post-contrast T 1 -weighted images. The extended tumor boundaries observed on the NOE MTR difference map corroborated with the IHC image, which confirmed the presence of infiltrative tumor cells and macrophages in these regions. Guided by the NOE MTR difference map, regions of interest (ROI) were drawn to quantify NOE MTR signal changes in the tumor core, tumor boundaries, and NABR post-Gd-DOTA. Tumor core showed a significant ∼43% reduction in NOE MTR signal (plJ=lJ0.003), while the tumor periphery exhibited a moderate reduction of ∼10%, (plJ=lJ0.045). No appreciable change in was observed in the NABR (plJ=lJ0.371). In contrast, the post contrast T 1 -weighted signal changes in tumor core, tumor periphery and NABR were, 33.32% (p = 0.092), 3.8% (p = 0.478), and 8.7% (p = 0.464) respectively. These findings suggest that NOE MTR imaging provides enhanced tumor contrast, particularly at the infiltrative tumor margins, where conventional contrast enhanced T 1 -weighted MRI may underestimate tumor extent. Histological validation confirmed the presence of infiltrative tumor cells and macrophages in the tumor periphery, as highlighted by the NOE MTR difference map. Overall, NOE MTR imaging, in combination with Gd-DOTA administration, demonstrates superior delineation of brain tumor boundaries compared to conventional MRI. As NOE MTR imaging is a fast acquisition scan (under 10 minutes) and performed on standard 3 Tesla, it can be easily integrated into clinical protocols. By improving visualization of tumor infiltration and distinguishing tumor regions from NABR, NOE MTR imaging holds promise for advancing neuro-oncological diagnostics and treatment planning.

  PublisherOA PDFDOI

• Prearrest vital sign abnormalities are associated with adverse outcomes in pediatric ICU cardiac arrest: a get with the guidelines-resuscitation analysis

  Resuscitation · 2025-09-25

  articleOpen access

  AIM: We aimed to quantitatively describe vital sign abnormalities prior to pediatric IHCA and evaluate whether the severity of abnormalities was independently associated with survival. METHODS: In a retrospective cohort study using the American Heart Association's Get with The Guidelines-Resuscitation® registry, children with ≥1 min of cardiopulmonary resuscitation (CPR) in an Intensive Care Unit (ICU) from 2007 to 2022 with prearrest vital signs were included. Vital signs most proximate to CPR (10-120 min prior) were classified as abnormal (HR or RR >95th, SBP or DBP <5th percentile for age). Multivariable regression adjusted for age, illness category, prearrest conditions, and prearrest interventions assessed the associations between vital sign abnormalities and outcomes (primary: survival to hospital discharge, secondary: return of spontaneous circulation [ROSC]). RESULTS: Of 2875 IHCA patients meeting inclusion criteria, 1790 (62.3 %) had at least one abnormal vital sign. Patients with vital sign abnormalities were older, had non-surgical illness categories, and higher prevalence of prearrest illnesses and interventions. Low SBP (<5%) was the vital sign with the lowest odds of survival to hospital discharge (aOR 0.56 [95 %CI 0.46-0.68], p < 0.01) and ROSC (aOR 0.63 [95 %CI 0.54-0.73], p < 0.01). There was a stepwise decrease in the adjusted odds of survival for each additional abnormal vital sign (1 vs 0: aOR 0.62 [95 %CI 0.51-0.76], p < 0.01; 2 vs 1: 0.72 [95 %CI 0.53-0.97] p = 0.03; 3 vs 2: 0.53 [95 %CI 0.33-0.86] p < 0.01). CONCLUSIONS: Prearrest vital sign abnormalities are common in pediatric ICU IHCA and independently associated with worse outcomes, emphasizing the need for prompt detection and intervention to improve outcomes.

  PublisherDOI

• GWAS of Protein Biomarkers in Pediatric ARDS

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01

  articleSenior author

  Abstract Rationale: Acute respiratory distress syndrome (ARDS) is a significant contributor to intensive care unit admissions, morbidity, and mortality. Biomarkers have increasingly been used to dissect heterogeneity and mechanisms underlying ARDS, including in pediatrics. Genetic evaluation may identify variants associated with severity and outcomes of pediatric ARDS. Methods: A genome-wide association study (GWAS) was performed on previously-published biomarkers measured on day 0 of ARDS from a single-center cohort using linear regression models. The genetic association with longitudinal biomarker levels at day 0, 3 and 7 and 28-day survival were assessed using linear mixed-effects models and Cox proportional hazard models, respectively. Models were adjusted for sex, age at ARDS, and a minimum of 2 principal components to account for population stratification. A Bonferroni-corrected p-value of 1e-6 was considered statistically significant. Results: From a cohort of 333 children with ARDS, 297 with consent for future research and sufficient DNA underwent GWAS against 18 pre-selected protein biomarkers. 50% had ARDS attributed to viral or bacterial pneumonias while 23.3% had ARDS as a result of non-pulmonary sepsis. 71.3% were classified as hypoinflammatory phenotype and overall mortality was 19.6%. Single nucleotide polymorphisms (SNPs) were identified in SFTPD (rs2146192), associated with lower levels of surfactant protein D (SURFPD) on day 0 of ARDS, and in LDLRAD3 (rs4755439) which was associated with higher levels of C-C motif chemokine ligand 3 (CCL3) on day 0 (Figure 1). SFTPD encodes SURPFD (cis effect) and LDLRAD3 encodes a viral entry receptor protein (trans effect). Linear mixed effect modeling showed that both genotypes had differential protein levels of SURFPD and CCL3 over the first 7 days of ARDS. Survival analysis demonstrated hazard ratios suggesting a slightly decreased risk of mortality for the rs2146192 SNP (0.78 and 0.57 in heterozygous and homozygous carriers of the affect allele) and increased mortality risk with hazard ratios for heterozygous carriers of the rs4755439 SNP (1.23288), although not at statistically significant levels. Conclusion: We identified two SNPs that impact relevant biomarker levels in pediatric ARDS that may confer both protective and hazardous effect. Further characterization is needed to better understand subphenotypes in pediatric ARDS, including genetic determinants of the biomarker levels used to define them. Despite limitations due to sample size and diversity, our findings underscore the potential of GWAS in uncovering molecular heterogeneity in a complex pediatric critical illness syndrome.

  PublisherDOI

• Trial Analysis and Interpretation in Critical Care Using the Evidential (Likelihood) Approach: Rationale and Practical Considerations

  American Journal of Respiratory and Critical Care Medicine · 2025-07-01 · 3 citations

  articleOpen access

  Abstract Selecting the optimal methodological framework for evidence synthesis presents a fundamental challenge in contemporary clinical research. In critical care, in which many interventions yield inconclusive results under traditional P value–based analyses, complementary analytical approaches can enhance our understanding of trial data. Although frequentist statistics remain predominant and Bayesian methods have recently experienced a resurgence of interest, the evidential (or likelihood) framework offers a methodological perspective that potentially bridges these two inferential paradigms. In this Concise Translational Review, we introduce readers to the evidential approach. To present the evidential approach as an analytical tool for critical care trials, we demonstrate its application using data from two mechanical ventilation trials (ART [the Alveolar Recruitment Trial], N = 1,010; and STAMINA [Strategy for Community Acquired Pneumonia Trial], N = 214) and one trial evaluating balanced solutions (BaSICS [Balanced Solutions in Intensive Care Study], N = 10,520). We focus on how concepts and terminology translate across paradigms, the framework’s measures of effect (i.e., likelihood ratios, support values, and support intervals), proposals for its use in sequential analysis and trial monitoring, and how to report results from this framework in research articles. We propose that the evidential framework provides a clinically intuitive approach to trial interpretation by focusing on the relative evidence between competing hypotheses, thereby offering additional and complementary insights that align with clinical reasoning processes. To facilitate implementation by the scientific community, we have developed an interactive Shiny (open-source web-based) application (https://fzampier.shinyapps.io/Likelihood_Shiny/).

  PublisherDOI

• Presence of Families at the Bedside in the PICU: Prospective, Mixed-Methods Study of Race and Insurance Disparities

  Pediatric Critical Care Medicine · 2025-08-04

  articleSenior author

  OBJECTIVES: To determine whether patient race, ethnicity, preferred language, insurance type, and social deprivation index (SDI) are associated with differences in caregiver presence in the PICU and to explore caregiver perspectives on decision-making about time spent at and away from bedside. DESIGN: Single-center prospective, concurrent mixed-methods study including: 1) a quantitative point prevalence study of caregiver bedside presence, and 2) a qualitative study of interviews with caregivers. SETTING: Seventy-five-bed PICU in a quaternary children's hospital in Philadelphia, PA. PATIENTS: Over the period 2022-2023, we enrolled: 1) children with anticipated moderate-to-long PICU length of stay and 2) adult caregivers of children in our PICU. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Multivariable regression tested associations between caregiver presence and race, ethnicity, preferred language, insurance type, and SDI. Semi-structured interviews with caregivers were evaluated using thematic analysis. Among 159 subjects, Black patient race relative to White, and public insurance relative to private, were associated with 18 and 10 fewer hours of caregiver presence during a 48-hour period, respectively. Caregivers nearly universally shared a desire to be present, yet the ability to be present was affected by practical limitations, including job flexibility and family availability. CONCLUSIONS: Public insurance and Black patient race were associated with decreased caregiver presence, disparities that may be explained by practical limitations. Additional work is necessary to explore ways to mitigate barriers to presence and equitable family-centered care and to investigate potential impacts of caregiver presence on health outcomes.

  PublisherDOI

• Acute Respiratory Distress Syndrome in Veterinary Medicine—The ARDSVet Definitions

  Journal of Veterinary Emergency and Critical Care · 2025-07-01 · 5 citations

  articleOpen accessSenior author

  OBJECTIVE: To use a systematic, evidence-based consensus process to develop updated definitions for acute respiratory distress syndrome (ARDS) in veterinary medicine to facilitate its recognition and diagnosis. DESIGN: International consensus conference series involving 12 multidisciplinary international content experts from three countries, using consensus conference methodology and implementation science. A systematic review of the literature was carried out for ARDS and acute lung injury in veterinary medicine. Updated definitions of ARDS were generated based on synthesis of human and veterinary literature. Consensus on the definitions was achieved through Delphi-style surveys involving the above subject matter experts. Draft recommendations were made available through industry specialty listservs for feedback, which was incorporated in the final definitions. RESULTS: Updated definitions were developed for Veterinary Acute Respiratory Distress Syndrome (ARDSVet) in small animals (dogs and cats) and large animals (equids). For small animals, 690 publications were identified for dogs and 99 were identified for cats in the initial literature search. Seventeen cats and 103 dogs with ARDS were represented across these publications. For the initial literature search in large animals, there were 83 equid, five camelid, 158 pig, 714 sheep and goat, and 270 cattle publications identified. Additionally, 1084 publications were found across all large animals that addressed interstitial lung disease. Five adult equids and 136 foals with ARDS were represented across these publications. The updated ARDSVet definitions incorporate criteria for risk factors, origin and timing of pulmonary edema, and impaired oxygenation, with severity stratified by oxygenation and definitions for both intubated and nonintubated animals. CONCLUSIONS: The evidence review and consensus process resulted in updated definitions that can be used to improve the recognition of veterinary ARDS as well as facilitate and standardize future research, including the development of an ARDS registry and eventual treatment recommendations.

  PublisherOA PDFDOI

• Serum Proteomic Profiles in Children With Acute Respiratory Distress Syndrome Due to Lower Respiratory Tract Infection and Sepsis

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01

  articleSenior author

  Abstract RATIONALE: Acute respiratory distress syndrome (ARDS) and associated acute respiratory failure is a cause of significant morbidity and mortality in children. ARDS can be caused by multiple underlying etiologies with overlapping clinical features, including lower respiratory tract infection (LRTI) and sepsis. While individual biomarkers have been used to assess heterogeneity, unbiased proteomics remains less explored in ARDS. We therefore aimed to identify a proteomic profile for patients with ARDS caused by either LRTI or sepsis, compared to control, in order to inform mechanisms contributing to ARDS heterogeneity. METHODS: In a single-center prospective cohort of intubated pediatric patients with ARDS, we collected plasma on day 0 of ARDS diagnosis and performed proteomics analysis using nanoparticle-enriched mass spectrometry (MS) to assess relative abundance of over 3300 proteins. We compared patients with ARDS from LRTI (n = 86), ARDS from sepsis (n = 47), and non-ARDS controls (n = 24). We identified significant proteins and performed over-representation analysis and gene set enrichment analysis (GSEA) to establish a proteomic profile for patients with LRTI-associated and sepsis-associated ARDS. RESULTS: We identified a distinct plasma proteomic signature of LRTI-associated ARDS compared to controls, with 1077 proteins significantly affected between groups (adjusted p-value &amp;lt; 0.05 and fold-change &amp;gt; 1.5) including upregulation of DEFA1 (antimicrobial defensin), EWSR1 (RNA splicing and transcription), RALBP1 (receptor-mediated endocytosis), ORC2 (DNA replication). GSEA demonstrated upregulation of proteins associated with cytoplasmic translation, RNA splicing, and cellular response to DNA damage. In patients with sepsis-associated ARDS, we identified 1379 proteins that showed significant changes, including upregulation of EWSR (RNA splicing and transcription), HMGN1 and 2 (maintenance of transcriptionally active chromatin) and suppression of TPPP3 (critical for mitosis). GSEA demonstrated upregulation of proteins associated with rRNA processing in multiple parts of the cell, and suppression of proteins associated with defects of the contact activation system and kallikrein system and diseases of hemostasis. CONCLUSIONS: We used MS-based proteomics, enhanced by nanoparticles enrichment for sample preparation, to characterize plasma proteomic profile of pediatric ARDS caused by LRTI and sepsis, and identified specific proteins with potential mechanistic roles in disease severity. This unbiased proteomics method is a powerful technique for understanding ARDS heterogeneity. Figure 1: Volcano plot of significantly abundant plasma proteins between LRTI-associated ARDS and controls, with the top 23 proteins labeled based on their adjusted Pvalue.

  PublisherDOI

• Cell-free DNA Methylomics Identify Tissue Injury Patterns in Pediatric ARDS

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01

  article1st authorCorresponding

  Abstract Rationale: Cell-free DNA (cfDNA) is released into the circulation from dead and dying cells, and is elevated in critical illness syndromes including sepsis and acute respiratory distress syndrome (ARDS). Plasma cfDNA has been implicated as a damage-associated molecular pattern (DAMP) that propagates ongoing inflammation. However, the tissue source of circulating cfDNA has not been fully elucidated, and identification of the cellular origin of cfDNA may provide insight into the mechanisms underlying the early inflammatory response. As cfDNA retains the unique methylation pattern of its tissue of origin, we can leverage cfDNA methylomics to map presumed tissue of origin of these DAMPs. Therefore, we conducted a pilot study to assess the cfDNA methylation and tissue origin in pediatric ARDS. Methods: This was a secondary analysis of a cohort of children with ARDS (total n = 333) from the Children's Hospital of Philadelphia enrolled between 2014 and 2019, with plasma collected within 24 hours of ARDS onset. We aimed to recruit subjects with higher levels of plasma cfDNA to assess feasibility. We randomly selected 24 children with cfDNA levels above the median value and 6 intubated non-ARDS controls. We isolated and quantified cfDNA from plasma, and performed methylation analysis using the Infinium MethylationEPIC v2.0 BeadChip. Methylation patterns were deconvoluted by mapping against known cell methylation patterns to identify tissues of origin. Hypo- and hyperinflammatory ARDS were defined using a previously published parsimonious algorithm of protein biomarkers and clinical variables. Our primary comparison was between hypoinflammatory ARDS, hyperinflammatory ARDS, and non-ARDS controls using non-parametric statistics. Results: Total plasma cfDNA levels were higher in hyperinflammatory ARDS (n = 18) compared to either hypoinflammatory ARDS (n = 6) or non-ARDS controls (n = 6). Dimensionality reduction using t-distributed Stochastic Neighbor Embedding (tSNE) separated hypo- and hyperinflammatory ARDS. Leukocytes were the dominant source of cfDNA in both ARDS and non-ARDS, and hyperinflammatory ARDS was also characterized by higher levels of hepatocyte cfDNA. Conclusions: Pediatric ARDS, especially the hyperinflammatory subphenotype, is characterized by elevated levels of plasma cfDNA originating primarily from leukocyte turnover. Hepatocyte death may also contribute to inflammation by impairing clearance of cfDNAs and other DAMPs in sicker subjects. Plasma cfDNA methylomics is a novel approach to quantify and characterize tissue injury in critical illness syndromes.

  PublisherDOI

Recent grants

• Clinical and Proteomic Characterization of Nucleosomes in Pediatric Acute Respiratory Distress Syndrome

  NIH · $694k · 2017–2021

• Linking Endotypes and Outcomes in Pediatric Acute Respiratory Distress Syndrome

  NIH · $4.1M · 2019–2026

Frequent coauthors

• Neal J. Thomas

  Pennsylvania State University

  120 shared

• Garrett Keim

  Children's Hospital of Philadelphia

  96 shared

• Robinder G. Khemani

  76 shared

• Adam S. Himebauch

  University of Pennsylvania

  65 shared

• Courtney M. Rowan

  Indiana University School of Medicine

  62 shared

• Lincoln Smith

  49 shared

• Aline B. Maddux

  46 shared

• Scott L. Weiss

  Thomas Jefferson University

  46 shared