Masonic medical research laboratory mmrl presentation at florida keys masonic lodge
Masonic Medical Research Laboratory is a research organization founded by the Grand Lodge of New York. Through its Cardiac Research Institute, it studies experimental cardiology with an emphasis on cardiac arrhythmias, ischemic heart disease and sudden cardiac death.
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Masonic medical research laboratory picnic 1987
History
The MMRL was established in 1958, sponsored by the Grand Lodge of New York, for the purpose of general research in cardiology. Over the years, the MMRL was engaged in research into cardiac electrophysiology, blood substitutes, vision, muscular dystrophy, hypertension and geriatrics. The institution has been administered by three Directors of Research since its inception, Dr. Murray Steele, Dr. Gordon K. Moe followed by Dr. Charles Antzelevitch, who was named Executive Director in 1984.
MMRL established the Cardiac Research Institute, a scientific and medical research center focused on developing strategies to combat heart disease, including new heart medications and diagnostic procedures for the management of cardiac arrhythmias. Its researchers have studied the mechanisms underlying sudden cardiac death and other arrhythmia syndromes and have evaluated approaches to therapy. The institute also houses a genetic screening center for families afflicted with sudden death syndromes.
IN 2009, the MMRL initiated a stem cell research program.
In 2013 the institute's staff consisted of about 40 researchers and administrators and its budget was about $4.5 million. It received financial support from the Grand Lodges of New York, Florida, Connecticut, Massachusetts, Maryland, Rhode Island, Wisconsin, New Hampshire, and Delaware; and a, derived from individual donations, It also received corporate grants, research grants from the National Institutes of Health, as well as partnerships with pharmaceutical and biotechnology companies.
In 2015 the MMRL was in the news when its former vice president was charged and plead guilty to stealing more than $400,000 from the organization.
Current research programs
Past scientific research results
In 1960 researchers at MMRL developed a mathematical model for use in he 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 afterpotentials (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 MMRL developed a blood substitute which was patented in 1990.
In the 1990s MMRL 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 MMRL published the first gene, SCN5A, to be linked to idiopathic ventricular fibrillation (IVF). The MMRL 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.
In 2000 the MMRL 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, that some forms of early repolarization could result in the development of life-threatening arrhythmias.
During the next few years MMRL discovered several genes that when mutated give rise to the Long QT, Short QT, Brugada and Early Repolarization syndromes. They later demonstrated that, ranolazine (Ranexa), a drug approved for ischemic heart disease, was capable of suppressing both atrial and ventricular arrhythmias.
In 2007 MMRL 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 MMRL 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.
Education and Training
The MMRL 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. NNRL also operates Mentoring Programs with BOCES, tours and shadowing programs to provide information to high school students about careers in science and research.