Clinical Focus

  • Internal Medicine

Academic Appointments

Administrative Appointments

  • Coordinator, Stanford Hospital Nocturnist Program (2009 - 2010)
  • Committee Member, Stanford Hospital Paging/Communication Committee (2009 - 2011)
  • Committee Member, Stanford Hospital Pharmacy and Therapeutics Committee (2009 - 2012)
  • Committee Member, Department of Medicine Professional Practice Evaluation Committee (PPEC) (2011 - 2014)
  • Committee Member, Stanford Hospital Health Information Management (HIM) Committee (2010 - Present)
  • Committee Member, Stanford Hospital Quality Council (2009 - Present)
  • B1/C1 Unit Based Medical Director, Stanford Hospital and Clinics (2012 - Present)
  • Faculty Lead, School of Medicine Practice of Medicine Practicum Course (2009 - Present)
  • Faculty Lead, School of Medicine Practice of Medicine Electronic Medical Records Curriculum (2011 - Present)
  • Faculty Member, E4C (Educators For Care) Associates Program (2010 - 2012)
  • Faculty Member, E4C (Educators for Care) (2012 - Present)
  • Core Faculty, Stanford Program in Bedside Medicine (Stanford 25) (2011 - Present)
  • Associate Director, Internal Medicine Residency Clinician Educator Pathway of Distinction (2015 - Present)
  • Associate Director, Section of Hospital Medicine (2014 - Present)
  • Clinical Instructor, Hospitalist, Stanford University School of Medicine (2008 - 2010)
  • Clinical Assitant Professor of Medicine, Hospitalist, Stanford University School of Medicine (2010 - Present)

Honors & Awards

  • G.D. Hsuing Research Fellowship, Yale Medical School (May 2001 - August 2001)
  • Medical Research Fellow, Howard Hughes Medical Institute (2003)
  • Annual Conference Travel Award, American Society of Hematology (2003)
  • Franklin G. Ebaugh, Jr. Research Award, Stanford Hospital Department of Medicine (2006, 2008)
  • Department of General Internal Medicine 2009 Teaching Award, Stanford Dept General Internal Medicine (2009)
  • "Excellence in Teaching" Pin, Stanford School of Medicine (2009, 2010)
  • Semi-Finalist - Poster Presentation, Society of Hospitalist Medicine Annual National Meeting (May 2011)
  • Faculty Fellow, Rathmann Family Foundation E4C Fellowship in Patient-centered Care (2011)
  • Award Recipient, Henry J Kaiser Family Foundation Award for Excellence in Preclinical Teaching (May 2012)

Boards, Advisory Committees, Professional Organizations

  • Regional Officer - Secretary/Treasurer, Society of General Internal Medicine (2013 - Present)

Professional Education

  • Residency:Stanford University School of Medicine (2008) CA
  • Board Certification: Internal Medicine, American Board of Internal Medicine (2008)
  • Medical Education:Yale School of Medicine Appointments (2005) CT
  • BA, Yale University, Biology (2000)


All Publications

  • Internal Medicine Resident Computer Usage: An Electronic Audit of an Inpatient Service. JAMA internal medicine Ouyang, D., Chen, J. H., Hom, J., Chi, J. 2016; 176 (2): 252-254

    View details for DOI 10.1001/jamainternmed.2015.6831

    View details for PubMedID 26642261

  • Long-term outcomes of septal reduction for obstructive hypertrophic cardiomyopathy. Journal of cardiology Sedehi, D., Finocchiaro, G., Tibayan, Y., Chi, J., Pavlovic, A., Kim, Y. M., Tibayan, F. A., Reitz, B. A., Robbins, R. C., Woo, J., Ha, R., Lee, D. P., Ashley, E. A. 2015; 66 (1): 57-62


    Surgical myectomy and alcohol septal ablation (ASA) aim to decrease left ventricular outflow tract (LVOT) gradient in hypertrophic cardiomyopathy (HCM). Outcome of myectomy beyond 10 years has rarely been described. We describe 20 years of follow-up of surgical myectomy and 5 years of follow-up for ASA performed for obstructive HCM.We studied 171 patients who underwent myectomy for symptomatic LVOT obstruction between 1972 and 2006. In addition, we studied 52 patients who underwent ASA for the same indication and who declined surgery. Follow-up of New York Heart Association (NYHA) functional class, echocardiographic data, and vital status were obtained from patient records. Mortality rates were compared with expected mortality rates of age- and sex-matched populations.Surgical myectomy improved NYHA class (2.74±0.65 to 1.54±0.74, p<0.001), reduced resting gradient (67.4±43.4mmHg to 11.2±16.4mmHg, p<0.001), and inducible LVOT gradient (98.1±34.7mmHg to 33.6±34.9mmHg, p<0.001). Similarly, ASA improved functional class (2.99±0.35 to 1.5±0.74, p<0.001), resting gradient (67.1±26.9mmHg to 23.9±29.4mmHg, p<0.001) and provoked gradient (104.4±34.9mmHg to 35.5±38.6mmHg, p<0.001). Survival after myectomy at 5, 10, 15, and 20 years of follow-up was 92.9%, 81.1%, 68.9%, and 47.5%, respectively. Of note, long-term survival after myectomy was lower than for the general population [standardized mortality ratio (SMR)=1.40, p<0.005], but still compared favorably with historical data from non-operated HCM patients. Survival after ASA at 2 and 5 years was 97.8% and 94.7%, respectively. Short-term (5 year) survival after ASA (SMR=0.61, p=0.48) was comparable to that of the general population.Long-term follow-up of septal reduction strategies in obstructive HCM reveals that surgical myectomy and ASA are effective for symptom relief and LVOT gradient reduction and are associated with favorable survival. While overall prognosis for the community HCM population is similar to the general population, the need for surgical myectomy may identify a sub-group with poorer long-term prognosis. We await long-term outcomes of more extensive myectomy approaches adopted in the past 10 years at major institutions.

    View details for DOI 10.1016/j.jjcc.2014.08.010

    View details for PubMedID 25238885

  • Clinical education and the electronic health record: the flipped patient. JAMA Chi, J., Verghese, A. 2014; 312 (22): 2331-2332

    View details for DOI 10.1001/jama.2014.12820

    View details for PubMedID 25490318

  • Medical students and the electronic health record: 'an epic use of time'. American journal of medicine Chi, J., Kugler, J., Chu, I. M., Loftus, P. D., Evans, K. H., Oskotsky, T., Basaviah, P., Braddock, C. H. 2014; 127 (9): 891-895

    View details for DOI 10.1016/j.amjmed.2014.05.027

    View details for PubMedID 24907594

  • Assigning a team-based pager for on-call physicians reduces paging errors in a large academic hospital. Joint Commission journal on quality and patient safety / Joint Commission Resources Shieh, L., Chi, J., Kulik, C., Momeni, A., Shelton, A., DePorte, C., Hopkins, J. 2014; 40 (2): 77-82


    As complexity of care of hospitalized patients has increased, the need for communication and collaboration among members of the team caring for the patient has become increasingly important. This often takes the form of a nurse's need to contact a patient's physician to discuss some aspect of care and modify treatment plans. Errors in communication delay care and can pose risk to patients. This report describes the successful implementation of a standardized team-based paging system at an academic center. Results showed a substantial improvement in nurses' perceptions of knowing how to contact the correct physician when discussion of the patient's care is needed. This improvement was found across multiple medical and surgical specialties and was particularly effective for services with the greatest communication problems.

    View details for PubMedID 24716330

  • Improving communication with patients: learning by doing. JAMA-the journal of the American Medical Association Chi, J., Verghese, A. 2013; 310 (21): 2257-2258

    View details for DOI 10.1001/jama.2013.281828

    View details for PubMedID 24302087

  • A piece of my mind. The road back to the bedside. JAMA-the journal of the American Medical Association Elder, A., Chi, J., Ozdalga, E., Kugler, J., Verghese, A. 2013; 310 (8): 799-800

    View details for DOI 10.1001/jama.2013.227195

    View details for PubMedID 23982364

  • A cascade of Ca2+/calmodulin-dependent protein kinases regulates the differentiation and functional activation of murine neutrophils EXPERIMENTAL HEMATOLOGY Gaines, P., Lamoureux, J., Marisetty, A., Chi, J., Berliner, N. 2008; 36 (7): 832-844


    The function of neutrophils as primary mediators of innate immunity depends on the activity of granule proteins and critical components of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex. Expression of their cognate genes is regulated during neutrophil differentiation by a complex network of intracellular signaling pathways. In this study, we have investigated the role of two members of the calcium/calmodulin-dependent protein kinase (CaMK) signaling cascade, CaMK I-like kinase (CKLiK) and CaMKKalpha, in regulating neutrophil differentiation and functional activation.Mouse myeloid cell lines were used to examine the expression of a CaMK cascade in developing neutrophils and to examine the effects of constitutive activation vs inhibition of CaMKs on neutrophil maturation.Expression of CaMKKalpha was shown to increase during neutrophil differentiation in multiple cell lines, whereas expression of CKLiK increased as multipotent progenitors committed to promyelocytes, but then decreased as cells differentiated into mature neutrophils. Expression of constitutively active CKLiKs did not affect morphologic maturation, but caused dramatic decreases in both respiratory burst responses and chemotaxis. This loss of neutrophil function was accompanied by reduced secondary granule and gp91(phox) gene expression. The CaMK inhibitor KN-93 attenuated cytokine-stimulated proliferative responses in promyelocytic cell lines, and inhibited the respiratory burst. Similar data were observed with the CaMKKalpha inhibitor, STO-609.Overactivation of a cascade of CaMKs inhibits neutrophil maturation, suggesting that these kinases play an antagonistic role during neutrophil differentiation, but at least one CaMK is required for myeloid cell expansion and functional activation.

    View details for DOI 10.1016/j.exphem.2008.02.009

    View details for Web of Science ID 000257349400010

    View details for PubMedID 18400360

  • Heterogeneity of functional responses in differentiated myeloid cell lines reveals EPRO cells as a valid model of murine neutrophil functional activation JOURNAL OF LEUKOCYTE BIOLOGY Gaines, P., Chi, J., Berliner, N. 2005; 77 (5): 669-679


    Mature neutrophils display multiple functional responses upon activation that include chemotaxis, adhesion to and transmigration across endothelial cells, phagocytosis, and pathogen destruction via potent microbicidal enzymes and reactive oxygen species. We are using myeloid cell line models to investigate the signaling pathways that govern neutrophil functional activation. To facilitate these studies, we have performed a direct comparison of functional responses of human and murine myeloid cell line models upon neutrophil differentiation. Our results show that EPRO cells, promyelocytes that undergo complete neutrophil maturation, demonstrate a full spectrum of functional responses, including respiratory burst, chemotaxis toward two murine chemokines, and phagocytosis. We also extend previous studies of granulocyte-colony stimulating factor-induced 32Dcl3 cells, showing they demonstrate chemotaxis and phogocytosis but completely lack a respiratory burst as a result of the absent expression of a critical oxidase subunit, gp91(phox). Induced human leukemic NB4 and HL-60 cells display a respiratory burst and phagocytosis but have defective chemotaxis to multiple chemoattractants. We also tested each cell line for the ability to up-regulate cell-surface membrane-activated complex-1 (Mac-1) expression upon activation, a response mediating neutrophil adhesion and a surrogate marker for degranulation. We show that EPRO cells, but not 32Dcl3 or NB4, significantly increase Mac-1 surface expression upon functional activation. Together, these data show that EPRO and MPRO cells demonstrate complete, functional activation upon neutrophil differentiation, suggesting these promyelocytic models accurately reflect the functional capacity of mature murine neutrophils.

    View details for DOI 10.1189/jlb.1004567

    View details for Web of Science ID 000228875500008

    View details for PubMedID 15673544