Bio

Bio


Christopher Bennett M.D. M.A. is a physician scientist in the Department of Emergency Medicine at Stanford University. He completed residency training at Harvard Medical School's program in Emergency Medicine based at Massachusetts General Hospital. Christopher previously served on the 2018-2019 Board of Directors for the Society for Academic Emergency Medicine. He also served on the Massachusetts Medical Society's 2019-2020 Committee on Publications which directs the publication and distribution of the New England Journal of Medicine. Bennett graduated with honors from Winthrop University (B.S. in Biology), earned a graduate degree from Duke University (M.A. in Genetics and Genomics), and was awarded his medical degree (M.D.) from The University of North Carolina at Chapel Hill, School of Medicine. In addition to his formal graduate training, Bennett was previously a scientist with the Lineberger Comprehensive Cancer Center, a Howard Hughes Medical Institute Fellow at Johns Hopkins?s McKusick-Nathans Institute of Genetic Medicine, and a researcher with the Emergency Medicine Network based at Harvard and Massachusetts General Hospital. His research has appeared in journals such as the New England Journal of Medicine, JAMA Surgery, the Journal of Graduate Medical Education, Nature Genetics, Annals of Emergency Medicine, Academic Emergency Medicine. His writing has appeared in The American Journal of Bioethics, STAT News, KevinMD.com, and Forbes.

Academic Appointments


Publications

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  • Factors Associated with the Discordance between Perception of Being HIV Infected and HIV Sexual Risk Taking among Social Media-Using Black, Hispanic, and White Young Men Who Have Sex with Men. Journal of the International Association of Providers of AIDS Care Bennett, C. L., Marks, S. J., Rosenberger, J. G., Bauermeister, J. A., Clark, M. A., Liu, T., Mayer, K. H., Merchant, R. C. ; 19: 2325958220919260

    Abstract

    Among HIV-uninfected, social media-using black, Hispanic, and white young men who have sex with men (YMSM) who had condomless anal sex but had not been HIV tested within the past year, we aimed to determine the extent of discordance between perception of having an undiagnosed HIV infection and HIV risk-taking behaviors. Despite reporting condomless anal sex without HIV testing, 64% of 358 YMSM participants perceived having an undiagnosed HIV infection as "unlikely" and 12% as "impossible." Having a primary care provider and being Hispanic were associated with greater discordance. Interventions to decrease the discordance between perceived and actual HIV risk are needed for this higher HIV risk population.

    View details for DOI 10.1177/2325958220919260

    View details for PubMedID 32314651

    View details for PubMedCentralID PMC7175048

  • National Study of the Emergency Physician Workforce, 2020. Annals of emergency medicine Bennett, C. L., Sullivan, A. F., Ginde, A. A., Rogers, J., Espinola, J. A., Clay, C. E., Camargo, C. A. 2020

    Abstract

    We describe the current US emergency physician workforce.We analyzed the 2020 American Medical Association Physician Masterfile data set. All physicians who designated emergency medicine as their primary or secondary specialty were included; nonactive physicians, residents, primarily research or teaching faculty, or those primarily involved in administration or nonclinical work were excluded. We calculated emergency physician population density, using 2018 Census Bureau estimates of the US population; urban-rural assignments were based on Urban Influence Codes. We compared 2020 results with our previous analysis of the 2008 emergency physician workforce. Again, we were unable to account for American Osteopathic Board of Emergency Medicine certification.There were 48,835 clinically active emergency physicians in 2020. The median age was 50 years (interquartile range [IQR] 41 to 62 years) and 28% were women. Overall density of emergency physicians per 100,000 population was 14.9. Most emergency physicians were in urban areas (92%), whereas 2,730 (6%) were in large rural areas and 1,197 (2%) in small rural areas. Urban emergency physicians were younger (median age 50 years; IQR 41 to 61 years) than those in large rural areas (median age 58 years; IQR 47 to 67 years) or small rural areas (median age 62 years; IQR 51 to 68 years), and more likely to be women (29%, 20%, and 19%, respectively). Most emergency physicians in small rural areas (71%) completed their medical training more than 20 years ago. Compared with 2008, the total number of clinically active emergency physicians has increased by 9,774, but, per 100,000 US population in 2020, emergency physician density decreased in both large rural (-0.4) and small rural (-3.7) areas.Urban emergency physicians in 2020 remain substantially younger than rural emergency physicians, with many rural ones near the US retirement age. We did not observe a continued increase in the percentage of female physicians among emergency physicians. Given the ongoing demand for physicians in all US emergency departments, this analysis provides essential information for understanding the current emergency physician workforce and the challenges ahead.

    View details for DOI 10.1016/j.annemergmed.2020.06.039

    View details for PubMedID 32747085

  • Evaluation of two commercial and two non-commercial immunoassays for the detection of prior infection to SARS-CoV-2. medRxiv : the preprint server for health sciences Nilles, E. J., Karlson, E. W., Norman, M., Gilboa, T., Fischinger, S., Atyeo, C., Zhou, G., Bennett, C. L., Tolan, N. V., Oganezova, K., Walt, D. R., Alter, G., Simmons, D. P., Schur, P., Jarolim, P., Baden, L. R. 2020

    Abstract

    Background Seroepidemiology is an important tool to characterize the epidemiology and immunobiology of SARS-CoV-2 but many immunoassays have not been externally validated raising questions about reliability of study findings. To ensure meaningful data, particularly in a low seroprevalence population, assays need to be rigorously characterized with high specificity. Methods We evaluated two commercial (Roche Diagnostics and Epitope Diagnostics IgM/IgG) and two non-commercial (Simoa and Ragon/MGH IgG) immunoassays against 68 confirmed positive and 232 pre-pandemic negative controls. Sensitivity was stratified by time from symptom onset. The Simoa multiplex assay applied three pre-defined algorithm models to determine sample result. Results The Roche and Ragon/MGH IgG assays each registered 1/232 false positive, the primary Simoa model registered 2/232 false positives, and the Epitope registered 2/230 and 3/230 false positives for the IgG and IgM assays respectively. Sensitivity >21 days post symptom-onset was 100% for all assays except Epitope IgM, but lower and/or with greater variability between assays for samples collected 9-14 days (67-100%) and 15-21 days (69-100%) post-symptom onset. The Simoa and Epitope IgG assays demonstrated excellent sensitivity earlier in the disease course. The Roche and Ragon/MGH IgG assays were less sensitive during early disease, particularly among immunosuppressed individuals. Conclusions The Epitope IgG demonstrated good sensitivity and specificity. The Roche and Ragon/MGH IgG assays registered rare false positives with lower early sensitivity. The Simoa assay primary model had excellent sensitivity and few false positives.

    View details for DOI 10.1101/2020.06.24.20139006

    View details for PubMedID 32607518

    View details for PubMedCentralID PMC7325183

  • Two decades of little change: An analysis of U.S. medical school basic science faculty by sex, race/ethnicity, and academic rank. PloS one Bennett, C. L., Salinas, R. Y., Locascio, J. J., Boyer, E. W. 2020; 15 (7): e0235190

    Abstract

    To examine changes in U.S. medical school basic science faculty over the last 20 years (1998-2018), we undertook an observational study utilizing data from the American Association of Medical Colleges Faculty Roster. Rank (Instructor, Assistant Professor, Associate Professor, and Professor), sex (Female), and race/ethnicity (Asian, Black or African American, Hispanic, Latino, Spanish Origin, or Multiple Race-Hispanic, and White) were analyzed; this reflected a population of 14,047 (1998) to 18,601 (2018) faculty. Summary percent of faculty in various gender, race/ethnicity origin categories were analyzed across years of the study using regression models. We found that females (24.47% to 35.32%) were underrepresented at all timepoints and a minority of faculty identified as Black or African American (1.57% to 1.99%), Hispanic, Latino, Spanish Origin, or Multiple Race-Hispanic (3.03% to 4.44%), or Asian (10.90% to 20.41%). The largest population at all time points was White Male Professors (30.53% to 20.85%), followed by White Male Associate Professors (15.67% to 9.34%), and White Male Assistant Professors (13.22% to 9.75%). Small statistically significant increases were observed among female faculty and faculty at multiple ranks who identified as Black or African American or Hispanic, Latino, Spanish Origin, or Multiple Race-Hispanic. We then completed secondary analyses looking at the interaction of race/ethnicity and Gender. We found: (1) a significant increase (p<0.0001) in both genders who identify as Asian although males had a higher rate of increase (6 point difference, p<0.0001); (2) a significant increase for Black or African American females (P<0.01) not found among males; (3) significant increases (p<0.0001) among both genders of faculty who identify as Hispanic, Latino, Spanish Origin, or Multiple Race-Hispanic although females had an approximately 1% higher rate of increase; and (4) among faculty who identify as White, males had a significant decrease (p<0.0001) while females demonstrated an increase (p<0.0001).

    View details for DOI 10.1371/journal.pone.0235190

    View details for PubMedID 32735593

    View details for PubMedCentralID PMC7394429

  • The Gender Gap in Surgical Residencies. JAMA surgery Bennett, C. L., Baker, O., Rangel, E. L., Marsh, R. H. 2020

    View details for DOI 10.1001/jamasurg.2020.2171

    View details for PubMedID 32725179

  • COVID-19: A Resident's Perspective AEM Education and Training Bennett, C. 2020; 4 (3)

    View details for DOI 10.1002/aet2.10457

  • Gender Differences in Faculty Rank Among Academic Emergency Physicians in the United States. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine Bennett, C. L., Raja, A. S., Kapoor, N., Kass, D., Blumenthal, D. M., Gross, N., Mills, A. M. 2019; 26 (3): 281?85

    Abstract

    The purpose of this study was to complete a comprehensive analysis of gender differences in faculty rank among U.S. emergency physicians that reflected all academic emergency physicians.We assembled a comprehensive list of academic emergency medicine (EM) physicians with U.S. medical school faculty appointments from Doximity.com linked to detailed information on physician gender, age, years since residency completion, scientific authorship, National Institutes of Health (NIH) research funding, and participation in clinical trials. To estimate gender differences in faculty rank, multivariable logistic regression models were used that adjusted for these factors.Our study included 3,600 academic physicians (28%, or 1,016, female). Female emergency physicians were younger than their male colleagues (mean [±SD] age was 43.8 [±8.7] years for females and 47.4 [±9.9] years for males [p < 0.001]), had fewer years since residency completion (12.4 years vs. 15.6 years, p < 0.001), had fewer total and first/last author publications (4.7 vs. 8.6 total publications, p < 0.001; 4.3 vs. 7.1 first or last author publications, p < 0.001), and were less likely to be principal investigators on NIH grants (1.2% vs. 2.9%, p = 0.002) or clinical trials (1.8% vs. 4.4%, p < 0.001). In unadjusted analysis, male physicians were more likely than female physicians to hold the rank of associate or full professor versus assistant professor (13.7 percentage point difference, p < 0.001), a relationship that persisted after multivariable adjustment (5.5 percentage point difference, p = 0.001).Female academic EM physicians are less likely to hold the rank of associate or full professor compared to male physicians even after detailed adjustment for other factors that may influence faculty rank.

    View details for DOI 10.1111/acem.13685

    View details for PubMedID 30636377

  • In Reply. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine Bennett, C. L., Raja, A. S., Kass, D., Gross, N., Mills, A. M. 2019; 26 (11): 1303

    View details for DOI 10.1111/acem.13828

    View details for PubMedID 31286614

  • Changes in Sex, Race, and Ethnic Origin of Emergency Medicine Resident Physicians From 2007 to 2017. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine Bennett, C. L., McDonald, D. A., Hurwitz, S., Zheng, H., Nadel, E., Ranney, M. L. 2019; 26 (3): 331?34

    View details for DOI 10.1111/acem.13674

    View details for PubMedID 30549375

  • Annals Graphic Medicine - #ThisIsOurLane. Annals of internal medicine Bennett, C. L. 2019; 170 (4): W78?W79

    View details for DOI 10.7326/G18-0034

    View details for PubMedID 31380890

  • Association of the 2003 and 2011 ACGME Resident Duty Hour Reforms With Internal Medicine Initial Certification Examination Performance. Journal of graduate medical education Bennett, C. L., McDonald, D. A., Dorner, S. C., Nadel, E. S., McDonald, F. S., McPherson, J. A. 2017; 9 (6): 789?90

    View details for DOI 10.4300/JGME-D-17-00547.1

    View details for PubMedID 29270281

    View details for PubMedCentralID PMC5734346

  • A National Cross-Sectional Study of Surgery Residents Who Underreport Duty Hours. Journal of surgical education Bennett, C. L., McDonald, D. A., Chang, Y., Finch, A., Vuong, K., Rennie, S., Nadel, E. S. 2017; 74 (6): 928?33

    Abstract

    Previous work demonstrates that many surgery residents underreport duty hours. The purpose of this study was to identify characteristics of these residents and better understand why they exceed duty hours.During the winter of 2015 we conducted an anonymous cross-sectional survey of Accreditation Council for Graduate Medical Education accredited general surgery programs.A total of 101 general surgery residency programs across the United States.A total of 1003 general surgery residents across the United States. Respondents' mean age was 29.9 ± 3.0 years; 53% were male.Study response rate was 31.9%. Residents age <30 were more likely to exceed duty hours to complete charting/documentation (68% vs. 54%, p < 0.001). Females more often cited guilt about leaving the hospital (32% vs. 24%, p = 0.014) as to why they exceed duty hours. Programs with >40 residents had the highest rates of underreporting (82% vs. 67% in other groups p < 0.001) and residents who worked >90 hours on an average week more frequently cited external pressure (p = 0.0001), guilt (p = 0.006), and feeling it was expected of them (p < 0.0001) as reasons why they underreport compared to those who worked fewer hours.Underreporting and duty-hour violations are a complex issue influenced by many variables including age, sex, and internal and external pressures.

    View details for DOI 10.1016/j.jsurg.2017.05.008

    View details for PubMedID 28529194

  • Adult male with diffuse neck masses Visual Journal of Emergency Medicine Bennett, C. L., Hayden, E. M. 2017; 8
  • Massive hemoptysis in Loeys-Dietz syndrome. American journal of medical genetics. Part A Bennett, C. L., Aziz, H., Sparks, E., Shah, T., Yoder, M., MacCarrick, G., Dietz, H. C. 2016; 170 (3): 725?27

    Abstract

    We describe four unrelated individuals with Loeys-Dietz syndrome (LDS) who presented with massive hemoptysis of unknown etiology. LDS is an autosomal dominant connective-tissue disorder characterized by altered cardiovascular, craniofacial, and skeletal development that is attributed to mutations in the TGFBR1, TGFBR2, SMAD3, or TGFB2 genes. Massive hemoptysis (MH) is a rare and often fatal pulmonary medical emergency. This is the first report of MH in individuals with LDS and establishes it as part of the LDS spectrum. It compels providers to educate their LDS patients on MH, although much investigation needs to be done to determine etiology and appropriate treatment for this newly described LDS feature.

    View details for DOI 10.1002/ajmg.a.37487

    View details for PubMedID 26614122

  • A 15-Year-Old Male with Enlarging ?Breast Lump? Visual Journal of Emergency Medicine Bennett, C., Singh, S., Lobo, V. 2016; 3
  • White (Coat) Lies: Bending the Truth to Stay Faithful to Patients. The American journal of bioethics : AJOB Bennett, C., Finch, A., Rennie, S. 2016; 16 (9): 15?17

    View details for DOI 10.1080/15265161.2016.1197342

    View details for PubMedID 27471929

  • Surgical Resident Duty Hours. The New England journal of medicine Bennett, C. L., Finch, A., Vuong, K., McDonald, D., Rennie, S. 2016; 374 (24): 2399?2401

    View details for DOI 10.1056/NEJMc1604659

    View details for PubMedID 27305199

  • Kaposi's Sarcoma-Associated Herpesvirus Viral Interferon Regulatory Factor 1 Interacts with a Member of the Interferon-Stimulated Gene 15 Pathway. Journal of virology Jacobs, S. R., Stopford, C. M., West, J. A., Bennett, C. L., Giffin, L., Damania, B. 2015; 89 (22): 11572?83

    Abstract

    Kaposi's sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus known to establish lifelong latency in the human host. We and others have previously shown that three KSHV homologs of cellular interferon regulatory factors (IRFs), known as viral IRFs (vIRFs), participate in evasion of the host interferon (IFN) response. We report that vIRF1 interacts with the cellular interferon-stimulated gene 15 (ISG15) E3 ligase, HERC5, in the context of Toll-like receptor 3 (TLR3) activation and IFN induction. The ISG15 protein is covalently conjugated to target proteins upon activation of the interferon response. Interaction between vIRF1 and HERC5 was confirmed by immunoprecipitation, and the region between amino acids 224 and 349 of vIRF1 was required for interaction with HERC5. We further report that expression of vIRF1 in the context of TLR3 activation results in decreased ISG15 conjugation of proteins. Specifically, TLR3-induced ISG15 conjugation and protein levels of cellular IRF3, a known ISG15 target, were decreased in the presence of vIRF1 compared to the control. vIRF1 itself was also identified as a target of ISG15 conjugation. KSHV-infected cells exhibited increased ISG15 conjugation upon reactivation from latency in coordination with increased IFN. Furthermore, knockdown of ISG15 in latently infected cells resulted in a higher level of KSHV reactivation and an increase in infectious virus. These data suggest that the KSHV vIRF1 protein affects ISG15 conjugation and interferon responses and may contribute to effective KSHV replication.The KSHV vIRF1 protein can inhibit interferon activation in response to viral infection. We identified a cellular protein named HERC5, which is the major ligase for ISG15, as a vIRF1 binding partner. vIRF1 association with HERC5 altered ISG15 modification of cellular proteins, and knockdown of ISG15 augmented reactivation of KSHV from latency.

    View details for DOI 10.1128/JVI.01482-15

    View details for PubMedID 26355087

    View details for PubMedCentralID PMC4645652

  • The viral interferon regulatory factors of kaposi's sarcoma-associated herpesvirus differ in their inhibition of interferon activation mediated by toll-like receptor 3. Journal of virology Jacobs, S. R., Gregory, S. M., West, J. A., Wollish, A. C., Bennett, C. L., Blackbourn, D. J., Heise, M. T., Damania, B. 2013; 87 (2): 798?806

    Abstract

    Kaposi's sarcoma-associated herpesvirus (KSHV) infection is correlated with three human malignancies and can establish lifelong latent infection in multiple cell types within its human host. In order to establish and maintain infection, KSHV utilizes multiple mechanisms to evade the host immune response. One such mechanism is the expression of a family of genes with homology to cellular interferon (IFN) regulatory factors (IRFs), known as viral IRFs (vIRFs). We demonstrate here that KSHV vIRF1, -2, and -3 have a differential ability to block type I interferon signaling mediated by Toll-like receptor 3 (TLR3), a receptor we have previously shown to be activated upon KSHV infection. vIRF1, -2, and -3 inhibited TLR3-driven activation of IFN transcription reporters. However, only vIRF1 and vIRF2 inhibited increases in both IFN-? message and protein levels following TLR3 activation. The expression of vIRF1 and vIRF2 also allowed for increased replication of a virus known to activate TLR3 signaling. Furthermore, vIRF1 and vIRF2 may block TLR3-mediated signaling via different mechanisms. Altogether, this report indicates that vIRFs are able to block IFN mediated by TLRs but that each vIRF has a unique function and mechanism for blocking antiviral IFN responses.

    View details for DOI 10.1128/JVI.01851-12

    View details for PubMedID 23115281

    View details for PubMedCentralID PMC3554052

  • KIF7 mutations cause fetal hydrolethalus and acrocallosal syndromes. Nature genetics Putoux, A., Thomas, S., Coene, K. L., Davis, E. E., Alanay, Y., Ogur, G., Uz, E., Buzas, D., Gomes, C., Patrier, S., Bennett, C. L., Elkhartoufi, N., Frison, M. S., Rigonnot, L., Joyé, N., Pruvost, S., Utine, G. E., Boduroglu, K., Nitschke, P., Fertitta, L., Thauvin-Robinet, C., Munnich, A., Cormier-Daire, V., Hennekam, R., Colin, E., Akarsu, N. A., Bole-Feysot, C., Cagnard, N., Schmitt, A., Goudin, N., Lyonnet, S., Encha-Razavi, F., Siffroi, J. P., Winey, M., Katsanis, N., Gonzales, M., Vekemans, M., Beales, P. L., Attié-Bitach, T. 2011; 43 (6): 601?6

    Abstract

    KIF7, the human ortholog of Drosophila Costal2, is a key component of the Hedgehog signaling pathway. Here we report mutations in KIF7 in individuals with hydrolethalus and acrocallosal syndromes, two multiple malformation disorders with overlapping features that include polydactyly, brain abnormalities and cleft palate. Consistent with a role of KIF7 in Hedgehog signaling, we show deregulation of most GLI transcription factor targets and impaired GLI3 processing in tissues from individuals with KIF7 mutations. KIF7 is also a likely contributor of alleles across the ciliopathy spectrum, as sequencing of a diverse cohort identified several missense mutations detrimental to protein function. In addition, in vivo genetic interaction studies indicated that knockdown of KIF7 could exacerbate the phenotype induced by knockdown of other ciliopathy transcripts. Our data show the role of KIF7 in human primary cilia, especially in the Hedgehog pathway through the regulation of GLI targets, and expand the clinical spectrum of ciliopathies.

    View details for DOI 10.1038/ng.826

    View details for PubMedID 21552264

    View details for PubMedCentralID PMC3674836

  • A transition zone complex regulates mammalian ciliogenesis and ciliary membrane composition. Nature genetics Garcia-Gonzalo, F. R., Corbit, K. C., Sirerol-Piquer, M. S., Ramaswami, G., Otto, E. A., Noriega, T. R., Seol, A. D., Robinson, J. F., Bennett, C. L., Josifova, D. J., García-Verdugo, J. M., Katsanis, N., Hildebrandt, F., Reiter, J. F. 2011; 43 (8): 776?84

    Abstract

    Mutations affecting ciliary components cause ciliopathies. As described here, we investigated Tectonic1 (Tctn1), a regulator of mouse Hedgehog signaling, and found that it is essential for ciliogenesis in some, but not all, tissues. Cell types that do not require Tctn1 for ciliogenesis require it to localize select membrane-associated proteins to the cilium, including Arl13b, AC3, Smoothened and Pkd2. Tctn1 forms a complex with multiple ciliopathy proteins associated with Meckel and Joubert syndromes, including Mks1, Tmem216, Tmem67, Cep290, B9d1, Tctn2 and Cc2d2a. Components of this complex co-localize at the transition zone, a region between the basal body and ciliary axoneme. Like Tctn1, loss of Tctn2, Tmem67 or Cc2d2a causes tissue-specific defects in ciliogenesis and ciliary membrane composition. Consistent with a shared function for complex components, we identified a mutation in TCTN1 that causes Joubert syndrome. Thus, a transition zone complex of Meckel and Joubert syndrome proteins regulates ciliary assembly and trafficking, suggesting that transition zone dysfunction is the cause of these ciliopathies.

    View details for DOI 10.1038/ng.891

    View details for PubMedID 21725307

    View details for PubMedCentralID PMC3145011

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