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1.  Innovation Networks for Improving Access and Quality Across the Healthcare Ecosystem 
Telemedicine Journal and e-Health  2010;16(1):107-111.
Partnerships between patient communities, healthcare providers, and academic researchers are key to stepping up the pace and public health impact of clinical and translational research supported by the National Institutes of Health. With emphasis shifting toward community engagement and faster translation of research advances into clinical practice, academic researchers have a vital stake in widening the use of health information technology systems and telehealth networks to support collaboration and innovation. However, limited interaction between academic institutions and healthcare providers hinders the ability to form and sustain the integrated networks that are needed to conduct meaningful community-engaged research that improves public health outcomes. Healthcare providers, especially those affiliated with smaller practices, will need sustainable infrastructure and real incentives to utilize such networks, as well as training and additional resources for ongoing technical assistance.
PMCID: PMC3016866  PMID: 20043702
business administration/economics; distance learning; e-health; home health monitoring; policy
2.  The Role of Translational Research in Addressing Health Disparities: a Conceptual Framework 
Ethnicity & disease  2008;18(2 Suppl 2):S2-155-60.
Translational research has tremendous potential as a tool to reduce health disparities in the United States, but a lack of common understanding about the scope of this dynamic, multidisciplinary approach to research has limited its use. The term “translational research” is often associated with the phrase “bench to bedside,” but the expedited movement of biomedical advances from the laboratory to clinical trials is only the first phase of the translational process. The second phase of translation, wherein innovations are moved from the bedside to real-world practice, is equally important, but it receives far less attention. Due in part to this imbalance, tremendous amounts of money and effort are spent expanding the boundaries of understanding and investigating the molecular underpinnings of disease and illness, while far fewer resources are devoted to improving the mechanisms by which those advances will be used to actually improve health outcomes. To foster awareness of the complete translational process and understanding of its value, we have developed two complementary models that provide a unifying conceptual framework for translational research. Specifically, these models integrate many elements of the National Institutes of Health roadmap for the future of medical research and provide a salient conceptualization of how a wide range of research endeavors from different disciplines can be used harmoniously to make progress toward achieving two overarching goals of Healthy People 2010—increasing the quality and years of healthy life and eliminating health disparities.
PMCID: PMC2705204  PMID: 18646340
Translational Research; Health Disparities
3.  Addressing Health Disparities through Multi-institutional, Multidisciplinary Collaboratories 
Ethnicity & disease  2008;18(2 Suppl 2):S2-161-7.
The national research leadership has recently become aware of the tremendous potential of translational research as an approach to address health disparities. The Research Centers in Minority Institutions (RCMI) Translational Research Network (RTRN) is a research network that supports multi-institutional, multidisciplinary collaboration with a focus on key diseases and conditions for which disproportionately adverse racial and ethnic health disparities exist. The RTRN is designed to facilitate the movement of scientific advances across the translational research spectrum by providing researchers at different institutions with the infrastructure and tools necessary to collaborate on interdisciplinary and transdisciplinary research projects relating to specific health outcomes for which major racial/ethnic disparities exist. In the past, the difficulty of overcoming the restrictions imposed by time and space have made it difficult to carry out this type of large-scale, multilevel collaboration efficiently. To address this formidable challenge, the RTRN will deploy a translational research cluster system that uses “cyber workspaces” to bring researchers with similar interests together by using online collaboratory technology. These virtual meeting environments will provide a number of tools, including videoconferences (seminars, works in progress, meetings); project management tools (WebCT, Microsoft Share Point); and posting areas for projects, concepts, and other research and educational activities. This technology will help enhance access to resources across institutions with a common mission, minimize many of the logistical hurdles that impede intellectual exchange, streamline the planning and implementation of innovative interdisciplinary research, and assess the use of protocols and practices to assist researchers in interacting across and within cyber workspaces.
PMCID: PMC2705198  PMID: 18646341
Translational Research; Health Disparities; Conceptual Framework
4.  Inhibition of TATA-Binding Protein Function by SAGA Subunits Spt3 and Spt8 at Gcn4-Activated Promoters 
Molecular and Cellular Biology  2000;20(2):634-647.
SAGA is a 1.8-MDa yeast protein complex that is composed of several distinct classes of transcription-related factors, including the adaptor/acetyltransferase Gcn5, Spt proteins, and a subset of TBP-associated factors. Our results indicate that mutations that completely disrupt SAGA (deletions of SPT7 or SPT20) strongly reduce transcriptional activation at the HIS3 and TRP3 genes and that Gcn5 is required for normal HIS3 transcriptional start site selection. Surprisingly, mutations in Spt proteins involved in the SAGA-TBP interaction (Spt3 and Spt8) cause derepression of HIS3 and TRP3 transcription in the uninduced state. Consistent with this finding, wild-type SAGA inhibits TBP binding to the HIS3 promoter in vitro, while SAGA lacking Spt3 or Spt8 is not inhibitory. We detected two distinct forms of SAGA in cell extracts and, strikingly, one lacks Spt8. Conditions that induce HIS3 and TRP3 transcription result in an altered balance between these complexes strongly in favor of the form without Spt8. These results suggest that the composition of SAGA may be dynamic in vivo and may be regulated through dissociable inhibitory subunits.
PMCID: PMC85153  PMID: 10611242

Results 1-4 (4)