Christine Johnson
Clinical Associate Professor, Pediatrics - Neonatology
Clinical Focus
- Neonatal-Perinatal Medicine
Administrative Appointments
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Associate Director, ANES 306N Critical Care Core Clerkship - Neonatal (2015 - Present)
Honors & Awards
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T32 Training Grant Trainee, National Institutes of Health (7/1/2011-6/30/2012)
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Harry Machen Lyon Fellow, Child Health Research Institute and Stanford CTSA (7/1/2012-6/30/2013)
Boards, Advisory Committees, Professional Organizations
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Instructor, Neonatal Resuscitation Program (2010 - Present)
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Fellow, American Academy of Pediatrics (2015 - Present)
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Member, American Academy of Pediatrics (2007 - 2013)
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Member, El Camino Hospital Neonatal Code Subcommittee (2015 - Present)
Professional Education
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Fellowship: Stanford University Neonatology Fellowship (2013) CA
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Residency: University of Minnesota Pediatric Residency Program (2010) MN
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Medical Education: University of Southern California Keck School of Medicine (2007) CA
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Board Certification: American Board of Pediatrics, Neonatal-Perinatal Medicine (2016)
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Board Certification, Neonatal-Perinatal Medicine, American Board of Pediatrics (2016)
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Board Certification: American Board of Pediatrics, Pediatrics (2012)
Clinical Trials
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Predictors of Pulmonary Hypertension Risk in Premature Infants With Bronchopulmonary Dysplasia
Not Recruiting
A lung condition called bronchopulmonary dysplasia (BPD) is a major cause of poor outcomes and death for premature infants. Infants with BPD are also at high risk for pulmonary hypertension (PH)-an important contributor to their condition. Previous research has suggested that a protein in the blood, endothelin-1 (ET-1), is associated with pulmonary disease. This study aims to investigate the incidence of PH and levels of ET-1 among premature babies with BPD. It will also potentially allow us to focus further research efforts and treatment towards these infants, some of our sickest patients at LPCH.
Stanford is currently not accepting patients for this trial.
All Publications
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A Multidisciplinary ICU Clerkship Curriculum Incorporating Simulation and Competency-Based Education: Design, Implementation, and Early Outcomes.
Advances in medical education and practice
2026; 17: 618733
Abstract
Critical care competencies are increasingly relevant across specialties, yet structured exposure in undergraduate medical education (UME) remains variable. We describe the design, implementation, and early outcomes of a four-week, modular ICU clerkship.We implemented a multidisciplinary ICU clerkship integrating clinical immersion, protected weekly didactics, asynchronous learning, high-fidelity simulation, health equity rounds, and palliative care debriefing. Objectives were aligned with Delphi-derived undergraduate critical care competencies and AAMC Entrustable Professional Activities. We compared student clerkship evaluation ratings (learner perceptions on a 5-point Likert scale) before and after a comprehensive curriculum redesign (July 2022-June 2024 vs July 2024-June 2025) using Welch two-sample t-tests.Approximately 95 students per year completed the clerkship. Following redesign, the largest improvements were observed in structural and organizational domains: orientation (+0.94), syllabus (+0.95), didactics (+0.85), and organization (+0.76) (all p < 0.001). Clinical skills (+0.36, p=0.01) and knowledge (+0.31, p=0.01) increased modestly and remained consistently high. Simulation ratings remained high (4.44 to 4.65, p=0.04). Overall clerkship rating improved from 4.00 to 4.51 (p=0.002).A modular ICU clerkship is feasible and adaptable across settings. Improvements were most pronounced in structural domains, while core clinical learning domains remained stable, suggesting that targeted curricular redesign can enhance learner experience while maintaining high perceived educational value.
View details for DOI 10.2147/AMEP.S618733
View details for PubMedID 42519589
View details for PubMedCentralID PMC13384020
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A Multidisciplinary ICU Clerkship Curriculum Incorporating Simulation and Competency-Based Education: Design, Implementation, and Early Outcomes
ADVANCES IN MEDICAL EDUCATION AND PRACTICE
2026; 17
View details for DOI 10.2147/AMEP.S618733
View details for Web of Science ID 001826666000001
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FXR agonist INT-747 upregulates DDAH expression and enhances insulin sensitivity in high-salt fed Dahl rats.
PloS one
2013; 8 (4)
Abstract
Genetic and pharmacological studies have shown that impairment of the nitric oxide (NO) synthase (NOS) pathway is associated with hypertension and insulin-resistance (IR). In addition, inhibition of NOS by the endogenous inhibitor, asymmetric dimethylarginine (ADMA), may also result in hypertension and IR. On the other hand, overexpression of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme that metabolizes ADMA, in mice is associated with lower ADMA, increased NO and enhanced insulin sensitivity. Since DDAH carries a farnesoid X receptor (FXR)-responsive element, we aimed to upregulate its expression by an FXR-agonist, INT-747, and evaluate its effect on blood pressure and insulin sensitivity.In this study, we evaluated the in vivo effect of INT-747 on tissue DDAH expression and insulin sensitivity in the Dahl rat model of salt-sensitive hypertension and IR (Dahl-SS). Our data indicates that high salt (HS) diet significantly increased systemic blood pressure. In addition, HS diet downregulated tissue DDAH expression while INT-747 protected the loss in DDAH expression and enhanced insulin sensitivity compared to vehicle controls.Our study may provide the basis for a new therapeutic approach for IR by modulating DDAH expression and/or activity using small molecules.
View details for DOI 10.1371/journal.pone.0060653
View details for PubMedID 23593273
View details for PubMedCentralID PMC3617194
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FXR agonist INT-747 upregulates DDAH expression and enhances insulin sensitivity in high-salt fed Dahl rats.
PloS one
2013; 8 (4): e60653
Abstract
Genetic and pharmacological studies have shown that impairment of the nitric oxide (NO) synthase (NOS) pathway is associated with hypertension and insulin-resistance (IR). In addition, inhibition of NOS by the endogenous inhibitor, asymmetric dimethylarginine (ADMA), may also result in hypertension and IR. On the other hand, overexpression of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme that metabolizes ADMA, in mice is associated with lower ADMA, increased NO and enhanced insulin sensitivity. Since DDAH carries a farnesoid X receptor (FXR)-responsive element, we aimed to upregulate its expression by an FXR-agonist, INT-747, and evaluate its effect on blood pressure and insulin sensitivity.In this study, we evaluated the in vivo effect of INT-747 on tissue DDAH expression and insulin sensitivity in the Dahl rat model of salt-sensitive hypertension and IR (Dahl-SS). Our data indicates that high salt (HS) diet significantly increased systemic blood pressure. In addition, HS diet downregulated tissue DDAH expression while INT-747 protected the loss in DDAH expression and enhanced insulin sensitivity compared to vehicle controls.Our study may provide the basis for a new therapeutic approach for IR by modulating DDAH expression and/or activity using small molecules.
View details for DOI 10.1371/journal.pone.0060653
View details for PubMedID 23593273
View details for PubMedCentralID PMC3617194