Clinical Focus

  • Neonatal-Perinatal Medicine

Academic Appointments

Administrative Appointments

  • Associate Director, ANES 306N Critical Care Core Clerkship - Neonatal (2015 - Present)

Honors & Awards

  • T32 Training Grant Trainee, National Institutes of Health (7/1/2011-6/30/2012)
  • Harry Machen Lyon Fellow, Child Health Research Institute and Stanford CTSA (7/1/2012-6/30/2013)

Boards, Advisory Committees, Professional Organizations

  • Instructor, Neonatal Resuscitation Program (2010 - Present)
  • Fellow, American Academy of Pediatrics (2015 - Present)
  • Member, American Academy of Pediatrics (2007 - 2013)
  • Member, El Camino Hospital Neonatal Code Subcommittee (2015 - Present)

Professional Education

  • Medical Education: LACplusUSC Medical Center Internal Medicine Residency (2007) CA
  • Board Certification: American Board of Pediatrics, Neonatal-Perinatal Medicine (2016)
  • Board Certification, Neonatal-Perinatal Medicine, American Board of Pediatrics (2016)
  • Board Certification: American Board of Pediatrics, Pediatrics (2012)
  • Fellowship: Stanford University (2013) CA
  • Residency: University of Minnesota (2010) MN
  • Internship: University of Minnesota (2008) MN

Contact

  • Clinical (Primary)  El Camino Health 2485 Hospital Dr Mountain View, CA 94040 (650) 988-7661 (fax)

Additional Clinical Info

Additional Info

  • Mail Code: 5731

Clinical Trials

  • 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. For more information, please contact Christine Johnson, MD, 650 723-5711.

    View full details

All Publications

  • FXR agonist INT-747 upregulates DDAH expression and enhances insulin sensitivity in high-salt fed Dahl rats. PloS one Ghebremariam, Y. T., Yamada, K., Lee, J. C., Johnson, C. L., Atzler, D., Anderssohn, M., Agrawal, R., Higgins, J. P., Patterson, A. J., Böger, R. H., Cooke, J. P. 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

  • FXR agonist INT-747 upregulates DDAH expression and enhances insulin sensitivity in high-salt fed Dahl rats. PloS one Ghebremariam, Y. T., Yamada, K., Lee, J. C., Johnson, C. L., Atzler, D., Anderssohn, M., Agrawal, R., Higgins, J. P., Patterson, A. J., Böger, R. H., Cooke, J. P. 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