Professional Education


  • Bachelor of Science, Stanford University, BIOL-BSH (2002)
  • MPH, Johns Hopkins Bloomberg School of Public Health, Public Health (2007)
  • MD, Yale University School of Medicine, Medicine (2008)

Stanford Advisors


Community and International Work


  • Bangladesh National Hygiene Survey - Hospital Hand Hygiene, Bangladesh

    Location

    International

    Ongoing Project

    No

    Opportunities for Student Involvement

    No

  • Promoting mother-mother networking for child health and immunizations in Bangladesh slums, Bangladesh

    Location

    International

    Ongoing Project

    Yes

    Opportunities for Student Involvement

    No

Graduate and Fellowship Programs


All Publications


  • Use of mobile phones for improving vaccination coverage among children living in rural hard-to-reach areas and urban streets of Bangladesh. Vaccine Uddin, M. J., Shamsuzzaman, M., Horng, L., Labrique, A., Vasudevan, L., Zeller, K., Chowdhury, M., Larson, C. P., Bishai, D., Alam, N. 2016; 34 (2): 276-283

    Abstract

    In Bangladesh, full vaccination rates among children living in rural hard-to-reach areas and urban streets are low. We conducted a quasi-experimental pre-post study of a 12-month mobile phone intervention to improve vaccination among 0-11 months old children in rural hard-to-reach and urban street dweller areas. Software named "mTika" was employed within the existing public health system to electronically register each child's birth and remind mothers about upcoming vaccination dates with text messages. Android smart phones with mTika were provided to all health assistants/vaccinators and supervisors in intervention areas, while mothers used plain cell phones already owned by themselves or their families. Pre and post-intervention vaccination coverage was surveyed in intervention and control areas. Among children over 298 days old, full vaccination coverage actually decreased in control areas - rural baseline 65.9% to endline 55.2% and urban baseline 44.5% to endline 33.9% - while increasing in intervention areas from rural baseline 58.9% to endline 76*8%, difference +18.8% (95% CI 5.7-31.9) and urban baseline 40.7% to endline 57.1%, difference +16.5% (95% CI 3.9-29.0). Difference-in-difference (DID) estimates were +29.5% for rural intervention versus control areas and +27.1% for urban areas for full vaccination in children over 298 days old, and logistic regression adjusting for maternal education, mobile phone ownership, and sex of child showed intervention effect odds ratio (OR) of 3.8 (95% CI 1.5-9.2) in rural areas and 3.0 (95% CI 1.4-6.4) in urban areas. Among all age groups, intervention effects on age-appropriate vaccination coverage were positive: DIDs +13.1-30.5% and ORs 2.5-4.6 (p<0.001 in all comparisons). Qualitative data showed the intervention was well-accepted. Our study demonstrated that a mobile phone intervention can improve vaccination coverage in rural hard-to-reach and urban street dweller communities in Bangladesh. This small-scale successful demonstration should serve as an example to other low-income countries with high mobile phone usage.

    View details for DOI 10.1016/j.vaccine.2015.11.024

    View details for PubMedID 26647290

  • Endocarditis due to Coccidioides spp: The Seventh Case. Open forum infectious diseases Horng, L. M., Yaghoubian, S., Ram, A., Johnson, R., Castro, L., Kuo, J., Deresinski, S. 2015; 2 (3): ofv086-?

    Abstract

    Coccidioides, a dimorphic fungus endemic within the Americas, primarily causes pulmonary disease but may disseminate. We describe a case of confirmed Coccidioides endocarditis, the seventh reported in literature. Coccidioides endocarditis often requires tissue diagnosis and combined surgical and medical treatment.

    View details for DOI 10.1093/ofid/ofv086

    View details for PubMedID 26180835

  • Receptor tyrosine phosphatase-dependent cytoskeletal remodeling by the hedgehog-responsive gene MIM/BEG4 JOURNAL OF CELL BIOLOGY Gonzalez-Quevedo, R., Shoffer, M., Horng, L., Oro, A. E. 2005; 168 (3): 453-463

    Abstract

    During development, dynamic remodeling of the actin cytoskeleton allows the precise placement and morphology of tissues. Morphogens such as Sonic hedgehog (Shh) and local cues such as receptor protein tyrosine phosphatases (RPTPs) mediate this process, but how they regulate the cytoskeleton is poorly understood. We previously identified Basal cell carcinoma-enriched gene 4 (BEG4)/Missing in Metastasis (MIM), a Shh-inducible, Wiskott-Aldrich homology 2 domain-containing protein that potentiates Gli transcription (Callahan, C.A., T. Ofstad, L. Horng, J.K. Wang, H.H. Zhen, P.A. Coulombe, and A.E. Oro. 2004. Genes Dev. 18:2724-2729). Here, we show that endogenous MIM is induced in a patched1-dependent manner and regulates the actin cytoskeleton. MIM functions by bundling F-actin, a process that requires self-association but is independent of G-actin binding. Cytoskeletal remodeling requires an activation domain distinct from sequences required for bundling in vitro. This domain associates with RPTPdelta and, in turn, enhances RPTPdelta membrane localization. MIM-dependent cytoskeletal changes can be inhibited using a soluble RPTPdelta-D2 domain. Our data suggest that the hedgehog-responsive gene MIM cooperates with RPTP to induce cytoskeletal changes.

    View details for DOI 10.1083/jcb.200409078

    View details for Web of Science ID 000226925500011

    View details for PubMedID 15684034

  • MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription GENES & DEVELOPMENT Callahan, C. A., Ofstad, T., Horng, L., Wang, J. K., Zhen, H. H., Coulombe, P. A., Oro, A. E. 2004; 18 (22): 2724-2729

    Abstract

    Sonic hedgehog (Shh) signaling plays a critical role during development and carcinogenesis. While Gli family members govern the transcriptional output of Shh signaling, little is known how Gli-mediated transcriptional activity is regulated. Here we identify the actin-binding protein Missing in Metastasis (MIM) as a new Shh-responsive gene. Together, Gli1 and MIM recapitulate Shh-mediated epidermal proliferation and invasion in regenerated human skin. MIM is part of a Gli/Suppressor of Fused complex and potentiates Gli-dependent transcription using domains distinct from those used for monomeric actin binding. These data define MIM as both a Shh-responsive gene and a new member of the pathway that modulates Gli responses during growth and tumorigenesis.

    View details for DOI 10.1101/gad.1221804

    View details for Web of Science ID 000225170900004

    View details for PubMedID 15545630