Masonic Medical Research Institute (MMRI) is a non-profit medical research center located in Utica, New York. The Institute's research and staff are independent, but gets its name from its original funding in 1958 by the Masonic Grand Lodge of New York. [1]
The institute studies experimental cardiology with an emphasis on cardiac arrhythmias, ischemic heart disease and sudden cardiac death. Research topics also include autism, Noonan Syndrome, brown fat, nano-imaging, targeted drug delivery, and more. There are five Principal Investigators at MMRI, each with their own lab, team, and area of study.
The campus of Masonic Medical Research Institute is in Utica, New York, and the facility includes several labs and advanced research equipment. The core facilities include:
Besides funding from the Grand Lodge of New York and private donations, the MMRI has recently received funding from the New York state government.
In 2019, it was granted $6 million in funding from the Empire State Development Corporation for facility upgrades. [6]
In the January 2022 State of the State address, New York Governor Kathy Hochul proposed state funding for a new 32,000-square-laboratory at MMRI, which would establish the MMRI as a "biomedical incubator to accelerate commercialization of basic research." [7] Additional state funding for MMRI is currently being proposed in the New York State Legislature in a bipartisan effort including Democrats and Republicans. [8]
The MMRI offers a Postdoctoral Fellowship Program as well as a Predoctoral Research Training Program which is administered in affiliation with SUNY Upstate Medical University at Syracuse, New York. Its ten-week Summer Fellowship Program, initiated in 1960, provides hands-on experience in research to students in the life sciences. [9]
MMRI operates Mentoring Programs with BOCES, tours and shadowing programs to provide information to high school students about careers in science and research. In addition, they have partnered with Mohawk Valley Health System for key initiatives benefiting the local community. [10] In 2020 and 2021 during the COVID pandemic, MMRI's large size and capability made it an ideal center for COVID testing. [11]
Masonic Medical Research Institute has five Principal Investigators, each with their own lab and team, they are:
Other areas of research at MMRI have included:
This section needs additional citations for verification .(August 2016) |
In 1960 researchers at MMRI developed a mathematical model for use in the study of atrial fibrillation. In 1966 they demonstrated dual pathways in the AV node and showed the basis for AV nodal tachycardia.
In 1973 Institute researchers showed that oscillatory after potentials (delayed afterdepolarizations) was the basis for arrhythmias associated with digitalis toxicity. Over the next several years later they explored modulated parasystole and reflection as mechanisms of cardiac arrhythmias.
In the 1980s research staff worked to clarify the differences between epicardium and endocardium, and found that the presence of an action potential notch in epicardium, but not endocardium, is responsible for inscription of the electrocardiographic J wave. They found differences in the response of epicardium and endocardium to a variety of drugs and neurotransmitters.
The MMRI developed a blood substitute which was patented in 1990.
In the 1990s MMRI researchers discovered the M cell, confirming that the heart is made of several different cell types. In 1998 they uncovered the cellular basis for the various waves that appear on an electrocardiogram including the J, T and U waves.
Between 1996 and 1998 MMRI published the first gene, SCN5A, to be linked to idiopathic ventricular fibrillation (IVF). The MMRI named this the Brugada syndrome in 1996, after Josep and Pedro Brugada, who first described this as a new clinical entity in 1992, and in 1999 proposed use of quinidine and isoproterenol for its treatment. [18]
In 2000 the MMRI research team uncovered evidence linking Sudden Infant Death Syndrome to a congenital heart defect, the Long QT syndrome (LQTS) published in The New England Journal of Medicine. That year they also found experimental evidence, confirmed by later research,[ citation needed ] that some forms of early repolarization could result in the development of life-threatening arrhythmias.
During the next few years MMRI discovered several genes that when mutated give rise to the Long QT, Short QT, Brugada and Early Repolarization syndromes. [19] They later demonstrated that, ranolazine (Ranexa), a drug approved for ischemic heart disease, was capable of suppressing both atrial and ventricular arrhythmias.
In 2007 MMRI researchers studied atrial-selective sodium channel block as a strategy to manage atrial fibrillation. They later demonstrated that the combination of ranolazine (Ranexa) and dronedarone (Multaq) could prevent the development of atrial fibrillation, which led to Phase 2 clinical trials.
In 2010 MMRI described “J Wave Syndromes” a subset of inherited cardiac arrhythmia syndromes characterized by accentuated J waves, including the Brugada and Early Repolarization syndromes. Soon after, the research team identified Wenxin Keli, a herbal Chinese medicine, as an atrial selective sodium channel blocker capable of suppressing atrial fibrillation in experimental models. In 2012 they also identified Wenxin Keli and Milrinone as potential pharmacological therapies for the Brugada syndrome.