Buffalo Translational Consortium News

New i2b2 dashboard unveiled at CTSA Open House

Posted on 12/29/16 at 02:35 pm

Clinical research teams in the Buffalo Translational Consortium (BTC) have a powerful new tool for accessing the de-identified electronic health records (EHRs) of some 700,000 UBMD patients. (UBMD is the practice plan of UB’s Jacobs School of Medicine and Biomedical Sciences.) Created by UB’s Institute for Healthcare Informatics (IHI), with the support of the Clinical and Translational Science Award (CTSA), a new desktop dashboard connects investigators to the massive i2b2 (Informatics for Integrating Biology and the Bedside) database from the convenience of their own desktops.

The new data retrieval and processing system was unveiled by Jonathan Blaisure, IHI senior database architect, at the CTSA Open House held at the Clinical and Translational Research Center in December. Blaisure and colleagues -- including Daniel Rodman, an i2b2 programmer affiliated with the CTSA via the UB Office of the Vice President for Research and Economic Development -- custom-designed the dashboard and its capabilities based on CTSA priorities. The IHI team is headed up by Executive Director Peter Winkelstein, MD, MBA, professor of clinical pediatrics and chief medical informatics officer for UBMD and Kaleida Health.

Investigators throughout the BTC are now able to directly identify cohorts for clinical trials and other research projects. Demographics, providers, diagnoses, medications, lab results and procedures, among other data points, are now available in de-identified form, allowing investigators to easily add inclusionary and exclusionary search criteria in order to assess the feasibility of proposed clinical trials in the Buffalo Niagara region. With IRB approval, investigative teams will then be able to use those results to begin patient recruitment.

The project supports the CTSA’s goal of establishing a “translational science pipeline” to enhance the BTC’s ability to integrate multiple types of data and share results more effectively between researchers, and then translate the results of successful research more rapidly into practice. Standardizing data storage and retrieval methods makes it easier for investigators to collaborate with one another and disseminate best practices from research results, and it makes meta-analyses and programmatic research much easier and faster.

UB’S IHI is a secure, HIPAA-compliant academic data center that opened in 2012. Its servers in the Center for Computational Research (CCR) provide a secure environment where health care data are stored, aggregated and analyzed. All translational research pipeline data are housed on secure IHI servers in the CCR.

To register for access to the new i2b2 dashboard, go to the Institute for Healthcare Informatics home page, click on the request access link at the top of the page and fill out the form. IHI personnel will provide log-in credentials.

More than a good idea, citing the CTSA is required by the NIH

Posted on 12/22/16 at 10:19 am
NIH Image Gallery

All publications, press releases and other documents that result from the use of any University at Buffalo Clinical and Translational Science Award (CTSA) resources are required by the National Institutes of Health (NIH) to credit the CTSA. In addition, the NIH Public Access Policy requires that publications be submitted to PubMed Central and include the PMC reference number (PMCID).

Translational research and clinical studies at UB and its Buffalo Translational Consortium (BTC) partner institutions were given a powerful boost by the granting of a National Institutes of Health Clinical and Translational Science Award in 2015. Our consortium is one of just 64 university or medical center coalitions nationwide to be selected as an NIH CTSA hub. The number of publications attributed to the award is a key indicator of the CTSA’s success, and ability to obtain future funding.

You must cite the CTSA in your manuscript and any downstream publications that flow directly from the project if you are:

  1. An individual who uses CTSA resources and services for a research project
  2. An individual directly funded by pilot funding provided by the CTSA
  3. A BTC scholar funded by the CTSA.

Here is the proper wording for citing the CTSA:

Research reported in this publication was supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under award number UL1TR001412 to the University at Buffalo. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

More detailed information about the CTSA citation policy is available here.

If you have questions about citing the CTSA in your work, or linking your publications to an NIH grant using the MY NCBI My Bibliography tool, contact CTSA Chief Financial Officer Erin Bailey at .(JavaScript must be enabled to view this email address) for clarification.

Hope for MS sufferers rides on development of new drug therapies

Posted on 12/16/16 at 01:16 pm
PI Fraser J. Sim, associate professor in the Department of Pharmacology and Toxicology


“Inducing Myelin Repair by Antagonism of Muscarinic Receptor Type-3”


Multiple sclerosis (MS) and other serious neurological disorders are characterized by a loss of the protective myelin sheath that covers nerve fibers in the central nervous system (demyelination), leading to impairment of neurological functions. Researchers in the Jacobs School of Medicine and Biomedical Sciences are looking at a number of drug compounds that may reverse that process, leading to the repair of damaged fibers through a process of remyelination.

Oligodendrocyte progenitor cells (OPCs) are the precursors to oligodendrocyte cells which actually provide the myelin sheath. It’s believed that signaling of a certain subtype of receptor in OPCs (known as Muscarinic Receptor Type-3, or, M3R) has a role in regulating the differentiation of OPCs into oligodendrocytes during remyelination. More specifically, a research team led by principal investigator Fraser J. Sim, PhD, associate professor in the Department of Pharmacology and Toxicology, hypothesizes that M3R signaling directly impairs OPC differentiation and remyelination following demyelination. If that were so, highly selective and potent M3R antagonists (drugs which block M3R signaling) would be expected to improve repair to the damaged cells while minimizing negative side effects.

Genetic approaches to specifically delete and impair M3R signaling will be tested for their effects on oligodendrocyte differentiation and remyelination in a pilot study supported by a $75,000 grant awarded by the Clinical and Translational Science Award and funded by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR001412.

Sim believes the data collected may establish M3R as a key receptor for future drug development of even more potent and selective compounds that target M3R activity. Rates of MS in Western New York are twice the national average, according to the National MS Society. Sim’s innovative approach could one day provide relief to the more than 3,000 people in the region suffering from this debilitating disease.

Investigating the roots of a poorly understood immune disease

Posted on 12/15/16 at 12:05 pm
PI Jill Kramer, assistant professor in the Department of Oral Biology


“Analysis of the Source and Significance of IgM in Sjögren’s Syndrome”


Sjögren’s syndrome (SS) is an autoimmune disease characterized by dry eyes and a dry mouth. Patients with SS may also experience many serious systemic disease manifestations. Current treatments focus on relieving symptoms because there are no therapies that target the disease’s etiology.

Researchers from the University at Buffalo, headed up by principal investigator Jill M. Kramer, DDS, PhD, an assistant professor in the Department of Oral Biology, and co-PI Daniel Gaile, PhD, assistant professor in the Department of Biostatistics in the School of Public Health and Health Professions, are looking at the role that Immunoglobulin M (IgM), secreted by certain B cell subsets, plays in the course of the disease.

Immunoglobulin G (IgG) autoantibodies are known to mediate pathology in SS, but the role of IgM in the context of the disease is surprisingly limited, investigators say. Further work is needed just to determine whether IgM is primarily pathogenic or protective in SS. This pilot study, awarded by the Clinical and Translational Sciences Award (CTSA), is particularly timely, given that B cell depletion is being tested as a therapy for autoimmune diseases and is likely to be used to treat SS patients in the future.

The $25,000 study is funded by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR001412. The project represents an interdisciplinary team approach that involves several Buffalo Translational Consortium partners, with good potential for securing extramural funding from the NIH.

The team hypothesizes that some IgM+ B cell subsets are enriched for self-reactivity in SS, and that this IgM contributes to SS-like salivary gland disease. Their objective is to identify the B cell subsets in mice that are responsible for autoreactive IgM secretion and determine whether this IgM is pathogenic. Therapies which target IgM production may represent a novel therapeutic strategy for those with SS and other autoimmune diseases.

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