Academic Appointments


  • Clinical Assistant Professor, Medicine

Administrative Appointments


  • Academic Physician-in-Chief, Stanford Health Care - ValleyCare (2020 - Present)
  • Research Physician Lead, Stanford Health Care - ValleyCare (2019 - Present)
  • Co-Director, Stanford Health Care - ValleyCare Clinical Summer Academy Program (2018 - Present)
  • Transfer Center Physician Lead, Stanford Health Care - ValleyCare (2018 - Present)
  • Chief, Stanford Health Care - ValleyCare section, Division of Hospital Medicine, Stanford University School of Medicine (2017 - 2020)
  • Vice Chief, Internal Medicine Department at Stanford Health Care - ValleyCare (2017 - 2019)
  • Member, Medication Error Reporting and Prevention at Stanford Health Care - ValleyCare (2016 - Present)
  • Director, Internal Medicine Elective Rotation at Stanford Health Care - ValleyCare (2016 - 2020)
  • Chair, Utilization Review Committee, Stanford Health Care - ValleyCare (2015 - Present)

Honors & Awards


  • Member, Gold Humanism Honor Society (2011)
  • Member, Alpha Omega Alpha Honor Medical Society (2011)

Boards, Advisory Committees, Professional Organizations


  • Member, SHC-VC Strategy Planning: Workforce Development Workgroup (2019 - Present)
  • Member, SHC-VC Strategy Planning: Clinical Program Workgroup (2019 - Present)
  • Participant, Stanford Leadership Development Program (2018 - 2019)

Professional Education


  • Board Certification, Internal Medicine, American Board of Internal Medicine (2015)
  • Residency, Stanford University Internal Medicine Residency, CA (2015)
  • Internship, Stanford University Internal Medicine Residency, CA (2013)
  • MD, University of Illinois College of Medicine at Chicago, IL, Medical Degree (2012)
  • MPH, University of Southern California, Los Angeles, CA, Epidemiology/Biostatistics (2008)
  • BA, University of California at Berkeley, Berkeley, CA, Molecular Cell Biology (2004)

Clinical Trials


  • Adaptive COVID-19 Treatment Trial 2 (ACTT-2) Recruiting

    ACTT-2 will evaluate the combination of baricitinib and remdesivir compared to remdesivir alone. Subjects will be assessed daily while hospitalized. If the subjects are discharged from the hospital, they will have a study visit at Days 15, 22, and 29. For discharged subjects, it is preferred that the Day 15 and 29 visits are in person to obtain safety laboratory tests and oropharyngeal (OP) swab and blood (serum only) samples for secondary research as well as clinical outcome data. However, infection control or other restrictions may limit the ability of the subject to return to the clinic. In this case, these visits may be conducted by phone, and only clinical data will be obtained. The Day 22 visit does not have laboratory tests or collection of samples and is conducted by phone. The primary outcome is time to recovery by Day 29.

    View full details

  • Adaptive COVID-19 Treatment Trial (ACTT) Not Recruiting

    This study is an adaptive, randomized, double-blind, placebo-controlled trial to evaluate the safety and efficacy of novel therapeutic agents in hospitalized adults diagnosed with COVID-19. The study is a multicenter trial that will be conducted in up to approximately 100 sites globally. The study will compare different investigational therapeutic agents to a control arm. There will be interim monitoring to introduce new arms and allow early stopping for futility, efficacy, or safety. If one therapy proves to be efficacious, then this treatment may become the control arm for comparison(s) with new experimental treatment(s). Any such change would be accompanied by an updated sample size. Because background standards of supportive care may evolve/improve over time as more is learned about successful management of COVID-19, comparisons of safety and efficacy will be based on data from concurrently randomized subjects. An independent Data and Safety Monitoring Board (DSMB) will actively monitor interim data to make recommendations about early study closure or changes to study arms. To evaluate the clinical efficacy, as assessed by time to recovery, of different investigational therapeutics as compared to the control arm.

    Stanford is currently not accepting patients for this trial. For more information, please contact NIH sponsored, (650) 493 - 5000.

    View full details

All Publications


  • Night-time communication at Stanford University Hospital: perceptions, reality and solutions BMJ QUALITY & SAFETY Sun, A., Wang, L., Go, M., Eggers, Z., Deng, R., Maggio, P., Shieh, L. 2018; 27 (2): 156–62

    Abstract

    Resident work hour restrictions have led to the creation of the 'night float' to care for the patients of multiple primary teams after hours. These residents are often inundated with acute issues in the numerous patients they cover and are less able to address non-urgent issues that arise at night. Further, non-urgent pages may contribute to physician alarm fatigue and negatively impact patient outcomes.To delineate the burden of non-urgent paging at night and propose solutions.We performed a resident review and categorisation of 1820 pages to night floats between September 2014 and December 2014. Both attending and nursing review of 10% of pages was done and compared.Of reviewed pages, 62.1% were urgent and 27.7% were non-urgent. Attending review of random page samples correlated well with resident review. Common reasons for non-urgent pages were non-urgent patient status updates, low-priority order requests and non-critical lab values.A significant number of non-urgent pages are sent at night. These pages likely distract from acute issues that arise at night and place an unnecessary burden on night floats. Both behavioural and systemic adjustments are needed to address this issue. Possible interventions include integrating low-priority messaging into the electronic health record system and use of charge nurses to help determine urgency of issues and batch non-urgent pages.

    View details for PubMedID 29055898

  • Improving and sustaining a reduction in iatrogenic pneumothorax through a multifaceted quality-improvement approach JOURNAL OF HOSPITAL MEDICINE Shieh, L., Go, M., Gessner, D., Chen, J. H., Hopkins, J., Maggio, P. 2015; 10 (9): 599-607

    Abstract

    The Agency for Healthcare Research and Quality has adopted iatrogenic pneumothorax (IAP) as a Patient Safety Indicator. In 2006, in response to a low performance ranking for IAP rate from the University Healthsystem Consortium (UHC), the authors established a multidisciplinary team to reduce our institution's IAP rate. Root-cause analysis found that subclavian insertion of central venous catheterization (CVC) was the most common procedure associated with IAP OBJECTIVE: Our short-term goal was a 50% reduction of both CVC-associated and all-cause IAP rates within 18 months, with long-term goals of sustained reduction.Observational study.Academic tertiary care hospital.Consecutive inpatients from 2006 to 2014.Our multifaceted intervention included: (1) clinical and documentation standards based on evidence, (2) cognitive aids, (3) simulation training, (4) purchase and deployment of ultrasound equipment, and (5) feedback to clinical services.CVC-associated IAP, all-cause IAP rate.We achieved both a short-term (years 2006 to 2008) and long-term (years 2006 to 2008-2014) reduction in our CVC-associated and all-cause IAP rates. Our short-term reduction in our CVC-associated IAP was 53% (P = 0.088), and our long-term reduction was 85% (P < 0.0001). Our short-term reduction in the all-cause IAP rate was 26% (P < 0.0001), and our long-term reduction was 61% (P < 0.0001).A multidisciplinary team, focused on evidence, patient safety, and standardization, can use a set of multifaceted interventions to sustainably improve patient outcomes for several years after implementation. Our hospital was in the highest performance UHC quartile for all-cause IAP in 2012 to 2014. Journal of Hospital Medicine 2015. © 2015 Society of Hospital Medicine.

    View details for DOI 10.1002/jhm.2388

    View details for Web of Science ID 000360836000007

  • Improving and sustaining a reduction in iatrogenic pneumothorax through a multifaceted quality-improvement approach. Journal of hospital medicine Shieh, L., Go, M., Gessner, D., Chen, J. H., Hopkins, J., Maggio, P. 2015; 10 (9): 599-607

    Abstract

    The Agency for Healthcare Research and Quality has adopted iatrogenic pneumothorax (IAP) as a Patient Safety Indicator. In 2006, in response to a low performance ranking for IAP rate from the University Healthsystem Consortium (UHC), the authors established a multidisciplinary team to reduce our institution's IAP rate. Root-cause analysis found that subclavian insertion of central venous catheterization (CVC) was the most common procedure associated with IAP OBJECTIVE: Our short-term goal was a 50% reduction of both CVC-associated and all-cause IAP rates within 18 months, with long-term goals of sustained reduction.Observational study.Academic tertiary care hospital.Consecutive inpatients from 2006 to 2014.Our multifaceted intervention included: (1) clinical and documentation standards based on evidence, (2) cognitive aids, (3) simulation training, (4) purchase and deployment of ultrasound equipment, and (5) feedback to clinical services.CVC-associated IAP, all-cause IAP rate.We achieved both a short-term (years 2006 to 2008) and long-term (years 2006 to 2008-2014) reduction in our CVC-associated and all-cause IAP rates. Our short-term reduction in our CVC-associated IAP was 53% (P = 0.088), and our long-term reduction was 85% (P < 0.0001). Our short-term reduction in the all-cause IAP rate was 26% (P < 0.0001), and our long-term reduction was 61% (P < 0.0001).A multidisciplinary team, focused on evidence, patient safety, and standardization, can use a set of multifaceted interventions to sustainably improve patient outcomes for several years after implementation. Our hospital was in the highest performance UHC quartile for all-cause IAP in 2012 to 2014. Journal of Hospital Medicine 2015. © 2015 Society of Hospital Medicine.

    View details for DOI 10.1002/jhm.2388

    View details for PubMedID 26041246

  • Structural protein 4.1R is integrally involved in nuclear envelope protein localization, centrosome-nucleus association and transcriptional signaling JOURNAL OF CELL SCIENCE Meyer, A. J., Almendrala, D. K., Go, M. M., Krauss, S. W. 2011; 124 (9): 1433-1444

    Abstract

    The multifunctional structural protein 4.1R is required for assembly and maintenance of functional nuclei but its nuclear roles are unidentified. 4.1R localizes within nuclei, at the nuclear envelope, and in cytoplasm. Here we show that 4.1R, the nuclear envelope protein emerin and the intermediate filament protein lamin A/C co-immunoprecipitate, and that 4.1R-specific depletion in human cells by RNA interference produces nuclear dysmorphology and selective mislocalization of proteins from several nuclear subcompartments. Such 4.1R-deficiency causes emerin to partially redistribute into the cytoplasm, whereas lamin A/C is disorganized at nuclear rims and displaced from nucleoplasmic foci. The nuclear envelope protein MAN1, nuclear pore proteins Tpr and Nup62, and nucleoplasmic proteins NuMA and LAP2α also have aberrant distributions, but lamin B and LAP2β have normal localizations. 4.1R-deficient mouse embryonic fibroblasts show a similar phenotype. We determined the functional effects of 4.1R-deficiency that reflect disruption of the association of 4.1R with emerin and A-type lamin: increased nucleus-centrosome distances, increased β-catenin signaling, and relocalization of β-catenin from the plasma membrane to the nucleus. Furthermore, emerin- and lamin-A/C-null cells have decreased nuclear 4.1R. Our data provide evidence that 4.1R has important functional interactions with emerin and A-type lamin that impact upon nuclear architecture, centrosome-nuclear envelope association and the regulation of β-catenin transcriptional co-activator activity that is dependent on β-catenin nuclear export.

    View details for DOI 10.1242/jcs.077883

    View details for Web of Science ID 000289621300009

    View details for PubMedID 21486941

  • Downregulation of protein 4.1R, a mature centriole protein, disrupts centrosomes, alters cell cycle progression, and perturbs mitotic spindles and anaphase MOLECULAR AND CELLULAR BIOLOGY Krauss, S. W., Spence, J. R., Bahmanyar, S., Barth, A. I., Go, M. M., Czerwinski, D., Meyer, A. J. 2008; 28 (7): 2283-2294

    Abstract

    Centrosomes nucleate and organize interphase microtubules and are instrumental in mitotic bipolar spindle assembly, ensuring orderly cell cycle progression with accurate chromosome segregation. We report that the multifunctional structural protein 4.1R localizes at centrosomes to distal/subdistal regions of mature centrioles in a cell cycle-dependent pattern. Significantly, 4.1R-specific depletion mediated by RNA interference perturbs subdistal appendage proteins ninein and outer dense fiber 2/cenexin at mature centrosomes and concomitantly reduces interphase microtubule anchoring and organization. 4.1R depletion causes G(1) accumulation in p53-proficient cells, similar to depletion of many other proteins that compromise centrosome integrity. In p53-deficient cells, 4.1R depletion delays S phase, but aberrant ninein distribution is not dependent on the S-phase delay. In 4.1R-depleted mitotic cells, efficient centrosome separation is reduced, resulting in monopolar spindle formation. Multipolar spindles and bipolar spindles with misaligned chromatin are also induced by 4.1R depletion. Notably, all types of defective spindles have mislocalized NuMA (nuclear mitotic apparatus protein), a 4.1R binding partner essential for spindle pole focusing. These disruptions contribute to lagging chromosomes and aberrant microtubule bridges during anaphase/telophase. Our data provide functional evidence that 4.1R makes crucial contributions to the structural integrity of centrosomes and mitotic spindles which normally enable mitosis and anaphase to proceed with the coordinated precision required to avoid pathological events.

    View details for DOI 10.1128/MCB.02021-07

    View details for Web of Science ID 000254181400015

    View details for PubMedID 18212055