Our Mission

Established in 2013, the Oklahoma Clinical and Translational Science Institute serves as a catalyst for clinical and translational research that improves health and healthcare for Oklahomans, to provide training and infrastructure to help junior investigators to launch independent research careers, and to expand the opportunities of IDeA states and Oklahoma communities to participate in research that improves the health of our residents. 

Oklahoma Shared Clinical and Translational Resources

OSCTR is Oklahoma's NIH-funded IDeA-CTR that provides resources, information, and training to help individuals or communities involved in performing clinical and translational research in the state

Oklahoma Primary Healthcare Improvement Cooperative

 

OPHIC is the implementation science arm of a statewide network to help improve healthcare delivery assisting primary care practices to adopt evidence-based best practices for the care of their patients.

OCTSI Clinical Research Unit

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The OCTSI CRU assists medical providers to identify and conduct clinical research opportunities in Oklahoma.

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Recent Publications

Community risks for SARS-CoV-2 infection among fully vaccinated US adults by rurality: A retrospective cohort study from the National COVID Cohort Collaborative

PLoS One. 2023 Jan 5;18(1):e0279968. doi: 10.1371/journal.pone.0279968. eCollection 2023.

ABSTRACT

BACKGROUND: While COVID-19 vaccines reduce adverse outcomes, post-vaccination SARS-CoV-2 infection remains problematic. We sought to identify community factors impacting risk for breakthrough infections (BTI) among fully vaccinated persons by rurality.

Genetic load in incomplete lupus erythematosus

Lupus Sci Med. 2023 Jan;10(1):e000843. doi: 10.1136/lupus-2022-000843.

ABSTRACT

OBJECTIVE: Patients with incomplete lupus erythematosus (ILE) have lupus features but insufficient criteria for SLE classification. Some patients with ILE transition to SLE, but most avoid major organ involvement. This study tested whether the milder disease course in ILE is influenced by reduced SLE risk allele genetic load.

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