Clinical Focus

  • Internal Medicine

Academic Appointments

Administrative Appointments

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

Honors & Awards

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

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)


2013-14 Courses


Journal Articles

  • Improving Communication With Patients Learning by Doing JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Chi, J., Verghese, A. 2013; 310 (21): 2257-2258

    View details for Web of Science ID 000327746300009

    View details for PubMedID 24302087

  • Outcomes of Septal Myectomy and Alcohol Septal Ablation for Obstructive Hypertrophic Cardiomyopathy American Heart Association 2009 Annual Conference Scientific Sessions Yen Tibayan, D., Jeffrey Chi, Aleksandra Pavlovic, Heidi Salisbury, Matthew Wheeler, Michael Y. Ho, Michael Sgroi, Young M. Kim, Frederick A. Tibayan, Bruce A. Reitz, Robert C. Robbins, David P. Lee, Euan A. Ashley
  • Overexpression of Constitutively Active Calcium/Calmodulin-Dependent Protein Kinases in ATRA-Induced EPRO Cells Abrogates Neutrophil Functional Responses American Society of Hematology (ASH) 2003 Annual Conference Oral Session Peter Gaines, Jeffrey Chi, Nancy Berliner
  • Characterization of the Novel Exonuclease activity of the human DNA AP Endonuclease (APE1) on L-Nucleoside terminated DNA American Association for Cancer Research (AACR) 2002 Annual Conference Scientific Sessions Kai-Ming Chou, Wing Lam, Jeffrey J. Chi, Yung-Chi Cheng
  • Heterogeneity of Functional Maturation Programs in Inducible Models of Myeloid Differentiation American Society of Hematology (ASH) 2003 Annual Conference Scientific Sessions Jeffrey Chi, Peter Gaines, Nancy Berliner
  • 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

  • Kikuchi-Fujimoto Disease: An Uncommon Presentation of Persistent Fever Journal of Hospital Medicine Jeffrey Chi, Esther Luo, Candice McNeil, Jeremy Sokolove, Vcitor Herrera, Jose Montoya, Abraham Verghese 2011; 6: S163
  • 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

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