Citizendia

Denise L. Faustman, (born 1958[1]) is a U.S. physician and medical researcher. The United States of America —commonly referred to as the A physician, medical practitioner or medical doctor who practices Medicine, and is concerned with maintaining or restoring human Health An associate Professor of Medicine at Harvard University, her work specializes in Diabetes mellitus type 1 (formerly called juvenile diabetes). Diabetes mellitus type 1 (Type 1 diabetes Type I diabetes T1D T1DM IDDM juvenile diabetes is a form of Diabetes mellitus. Diabetes mellitus (ˌdaɪəˈbiːtiːz or /ˌdaɪəˈbiːtəs/ /məˈlaɪtəs/ or /ˈmɛlətəs/ often referred to simply as diabetes ( Ancient Greek: grc She has worked at Massachusetts General Hospital in Boston since 1985. Massachusetts General Hospital ( Mass General or MGH) is a Teaching hospital of Harvard Medical School and a Biomedical research Year 1985 ( MCMLXXXV) was a Common year starting on Tuesday (link displays 1985 Gregorian calendar)

Contents

Research

Faustman's research is based on the observation that autoreactive T cells, that is, T cells programmed to attack the body's own cells and tissues, are more sensitive to the effects of TNF-alpha (TNF-α), a cytokine that influences the immune system. T cells belong to a group of White blood cells known as Lymphocytes, and play a central role in Cell-mediated immunity. Tumor necrosis factor ( TNF, cachexin or cachectin and formally known as Tumor necrosis factor-alpha) is a Cytokine involved in systemic TNF-α is a strong promoter of inflammation, and several treatments have been developed to block the effects of TNF-α in chronic and autoimmune diseases, including adalimumab, infliximab, and entanercept. Autoimmunity is the failure of an organism to recognize its own constituent parts as self, which results in an immune response against its own cells and tissues Adalimumab (brand name HUMIRA) is the third TNF inhibitor, after Infliximab and Etanercept, to be approved in the United States. Infliximab (brand name Remicade) is a drug used to treat Autoimmune disorders. However, side effects of these drugs include flare-ups of autoimmune symptoms.

Under some conditions, TNF-α causes T cells to undergo apoptosis, or programmed cell death. Autoimmune T cells are more sensitive to TNF-α and undergo apoptosis more readily than normal T cells when exposed to TNF-α. Faustman's hypothesis, somewhat contrary to conventional thinking, is that blocking TNF-α actually promotes the survival of undersirable autoreactive T cells, and that autoimmune diseases should be treated by stimulating TNF-α to trigger apoptosis in self-destructive autoimmune T cells. [1]

Former Chrysler chairman Lee Iacocca, whose wife died of type 1 diabetes complications and who has declared a desire to see the disease cured in his lifetime, is a patron of her work. Chrysler LLC is an American Automobile manufacturer that has been producing Automobiles since 1925 Lido Anthony "Lee" Iacocca (born October 15, 1924) is an American businessman most commonly known for his revival of the After Faustman's application for funding was not approved by the JDRF (although she has acknowledged that her application was given a fair review), The Iacocca Foundation provided an $11. 5 million dollar grant which both supported Faustman's work, and is being used for a clinical trial to be conducted by Harvard researcher David Nathan. This trial will not use spleen cells but only bacillus Calmette-Guerin (BCG), a weakened strain of bacteria that is used in the prevention of tuberculosis and in the treatment of bladder tumors and bladder cancer. BCG induces TNF-α. In previous human trials, it has not been shown to have a therapeutic effect in type 1 diabetics. Faustman hypothesizes that the correct dosing of BCG for diabetics has not been utilized in previous trials. As part of her research, she is seeking to define a dose that might have a therapeutic effect in the clinical trial to be led by Dr. Nathan.

Faustman's research has been profiled in the New York Times on November 9, 2004 and March 24, 2006, and in the Wall Street Journal on March 24, 2006. Events 694 - Egica, a king of the Visigoths of Hispania, accuses Jews of aiding Muslims sentencing all "MMIV" redirects here For the Modest Mouse album see " Baron von Bullshit Rides Again " Events 1401 - Mongol emperor Timur sacks Damascus. 1603 - James VI of Scotland Year 2006 ( MMVI) was a Common year starting on Sunday of the Gregorian calendar.

Recent Controversy

Research

This approach was recently tested in non-obese diabetic mice (NOD mice), a strain of mice that spontaneously develops Type 1 diabetes. Diabetes mellitus type 1 (Type 1 diabetes Type I diabetes T1D T1DM IDDM juvenile diabetes is a form of Diabetes mellitus. Injecting the mice with a common inflammatory agent (Freund's adjuvant) and a preparation of spleen cells allowed the beta islet cells to regenerate. Freund's adjuvant is an Antigen Solution emulsified in Mineral oil, used as an Immunopotentiator (booster of the Immune system Beta cells ( beta-cells, β-cells) are a type of cell in the Pancreas in areas called the Islets of Langerhans. [2]

The adjuvant increased the production of TNF-α , which reduced the number of autoreactive T cells and allowed for islet cell regrowth. Faustman hypothesizes that this regeneration may be attributed in part to the re-differentiation of the spleen cells, a position that continues to be debated. In Developmental biology, cellular differentiation is the process by which a less specialized cell becomes a more specialized Cell type.

Type 1 Autoimmune Diabetes is caused by rogue T cells that attack healthy tissue. In the case of Type 1 Autoimmune Diabetes, the healthy tissue under attack are the beta cells that regulate and produce insulin. Faustman's protocol of Freund's adjuvant, along with the spleen cells, was effective in curing even mice with end-stage diabetes. In her human trial, scheduled for early 2008, she plans to use BCG to kill the rogue T-cells that maintain the diseased state of autoimmunity. CFA and BCG affect rogue T-cells in a peculiar way, they induce cell apoptosis, a kind of cell suicide. Normal T-cells remain unaffected. The research is promising because it is hoped that once the bad T-cells are gone, regeneration of the beta cells will ensue. However, a debate continues over the source of the islet cell regeneration.

Researchers from three laboratories funded by the Juvenile Diabetes Research Foundation confirmed her success with mice and published paper in the March 24, 2006 issue of Science, but suggest that the proliferation of existing pancreatic stem cells may have been responsible for the success of the treatment. The Juvenile Diabetes Research Foundation ( JDRF) is a Not-for-profit organization that raises money for research to find a Cure for Type 1 diabetes The pancreas is a Gland organ in the digestive and Endocrine system of Vertebrates. Adult stem cells are undifferentiated cells found throughout the body after embryonic development that divide to replenish dying cells and regenerate damaged The JDRF funded researchers did not find that adult spleen cells played a role in the regeneration of islets. However, they did find that regeneration occurred once the rogue T-cells were removed; it just wasn't obvious where the regeneration was coming from. Faustman has stated in the Wall Street Journal regarding the debated source of islet regeneration, "The pancreas is too smart to cure itself in only one way," and stated "I think there will be many sources of regeneration, and we're only at the beginning of understanding what they are. "

The New York Times, in a March 24, 2006 article titled "A Controversial Therapy for Diabetes Is Verified," states that "Three groups of scientists report today that they independently replicated a controversial finding. " [3] Similarly, The Wall Street Journal's article ran with the headline "After Initial Rejection, Scientists Back Work on Cure for Diabetes".

A newspiece that ran in Science on that same day, however, says ""Three separate attempts have failed to replicate promising results that electrified the diabetes community 2 years ago. " [4] In addition, the piece reported that ""because the three groups could not detect spleen-derived beta cells, and because treatment with CFA and islets alone yielded the same results as when spleen cells were added to the mix, the groups attribute these cures to CFA and temporary islets," and that "using CFA to cure mice is probably not relevant to humans. " But nobody has ever measured BCG dosage and autoreactive cell death in repeated dosages as Faustman plans to. A grassroots campaign to raise money through Joinleenow. org from the Iacocca Foundation plans to bring Faustman's work to human trials.

Since then, a group from the National Institutes of Health has replicated her work in mice who have type 1 diabetes and Sjogren's disease. This laboratory was also able to confirm a role for a splenic stem cell in regeneration. The results are part of a poster presentation by Tran et al. (Abstract # 1202-P) at the June 2006 American Diabetes Association (ADA) Meeting [5]. Similarly, a Japanese group also presented corroboratory findings at the ADA meeting, presented by Okubo et al (Abstract # 1193-P).

Early life

Faustman was born in Royal Oak, Michigan, in 1958. Royal Oak is a city in Oakland County of the US state of Michigan. [1] In 1978, she gained her BSc in zoology and chemistry from the University of Michigan, Ann Arbor. The University of Michigan Ann Arbor ( U of M, U-M, UM or simply Michigan) is a top-ranked Coeducational public research [1]

Partial bibliography

External links

  1. ^ a b c Biography - Dr. Denise L. Faustman. Changing the Face of Medicine - Physicians. National Library of Medicine. Retrieved on 2008-01-16. 2008 ( MMVIII) is the current year in accordance with the Gregorian calendar, a Leap year that started on Tuesday of the Common Events 27 BC - The title Augustus is bestowed upon Gaius Julius Caesar Octavian by the Roman Senate.
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