If this is an immune problem, there is help (?)

Important Discovery of the past 10 years ... The substance Stenberg credits with saving her brother's life isn't the kind of sugar that comes in cubes or 5-pound bags. It's actually in the form of glyconutritional supplements, a combination of sugars that are said to help cells communicate, leading to better health.

When cellular communication is enhance, speeded up, corrected, intensified by "glyconutrients", enzymatic activity in the body is also enhanced, modified, accelerated, detox intensifies, virus removal intensifies, in other words.... EVERYTHING works better when the body has ample or even "extra" glyconutrients to throw around. When you take them in supplement form, your body doesn't have to manufacture them.... and THIS REMOVES a huge metabolic load off your bodily systems.... 

the benefits this can provide a person are immeasurable  -   DU Poster 4MY

Dr Reg McDaniel would work with 'gulf war vets' on this. 'Dear Maggie'

He contacted me from something he received - forwarded from someone else ... but that he wanted to work with 'gulf war vets' and do a study ... but couldn't get a group together

You say "From what you have seen ... people can get better or well"  This is very hopeful

How do you know so much about immunity issues?

e-mail

Immunology 101:

What these people are not saying, and perhaps what they don't know, is that a group of sugar/protein "whiskers" that sit on the cell surface of immune cells referred to as cluster determinant 95 or CD95 are virtually non-existent in persons who suffer with Lupus. What they don't study are the effects of natural substances on the body's ability to better form and produce these sugar/protein "whiskers". (Glycoproteins)

What they would benefit from knowing is that CD95 is responsible for letting an immune cell "know" that it has turned on the body, and that it needs to DIE. (apoptosis) This is a normal process, that is obviously not normal in persons who suffer with autoimmune conditions. A potential reason for this "autoimmunity" is that they are NOT PRODUCING ENOUGH HIGHLY SPECIFIC SUGARS to properly/sufficiently construct glycoproteins, in particular CD95.

http://www.arthritis.org/research/ResearchUpdate/03Sept_Oct/Immunology_101.asp


Death for T and B cells
The immune system is normally tightly controlled so that it is only deployed in response to foreign invaders. But sometimes, the system breaks down and mistakenly attacks the body’s own cells and organs. For instance, some immune cells called T cells attack the joint lining in rheumatoid arthritis (RA), while B cells create damaging proteins that are common in lupus. Scientists are making significant progress in determining how best to seek out and destroy just these harmful immune cells while leaving other parts of the body’s disease fighting system intact.

And the evidence that apoptosis is deficient in persons who suffer with Lupus....


www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15529575
Rom J Intern Med. 2000-2001;38-39:83-8. Related Articles, Links

Serological levels of apoptotic bodies, sFAS and TNF in lupus erythematosus.
*

Alecu M, Coman G, Alecu S.

Dermatological Reaseach Center, Scarlat Longhin Hospital for Dermatology, 216, Sos. Serban Voda, 73202, Bucharest, Romania.

In our study we have investigated the presence of apoptotic bodies, soluble FAS receptor and TNF (tumor necrosis factor) in three clinical forms of lupus erythematosus. Determinations were performed in attack period of: systemic lupus erythematosus (SLE) for 20 patients, 20 patients with subacute cutaneous lupus erythematosus (SCLE), 20 patients with chronic discoid lupus erythematosus (DLE). Determinations were performed by ELISA (for apoptotic bodies, kit Boehringer, normal values 400-800 mU), (for sFAS, kit R&D Systems, normal values 4500-17000 pg/ml) (for TNF, ELISA kit R&D Systems, normal values 0.4-3.6 pg/ml). Results in SLE: apoptotic bodies were increased in 16 cases (980-1030); sFAS in 18 cases (17000-24000 pg/ml) TNF was increased in all 20 cases (40-140 pg/ml). In SCLE with multiple cutaneous lesions and without internal organs disturbance the apoptotic bodies were increased in 10 cases (960-1030 pg/ml), sFAS in 9 cases (17000-22000 pg/ml), and TNF alpha in 9 cases. In DLE, apoptotic bodies were increased in 2 patients (980-1010 pg/ml), sFAS in 3 patients (17000-20000 pg/ml) and TNF in 2 patients (20-40 pg/mil). Investigated values were slightly correlated with immune parameters (anti dsDNA antibodies), but they were correlated with the presence of renal disturbances or extension of cutaneous lesions. We consider that the presence of increased apoptotic bodies as a result of peripheral mononuclear cells apoptosis appear as a nauto-limiting mechanism in a pathological immune response.
The increase of sFAS in lupus patients serum might be interpreted as an alteration of apoptosis respectively a deficit in apoptosis which has as a first consequence the persistence of B and T lymphocytes, activated, in the pathogen immune response.

Shared by a poster on  democraticunderground.com forums 1-16-05

Immunology 101: Pathways to a Cure   -

From the Arthritis Research 9/03  -  Full Article

Basic research about the role of the immune system in arthritis may seem dry and hard to understand, but as shared by several conference presenters, insights gained from such research are paving the way for innovative therapies to slow down and perhaps even stop disease progression.

Death for T and B cells    
The immune system is normally tightly controlled so that it is only deployed in response to foreign invaders. But sometimes, the system breaks down and mistakenly attacks the body’s own cells and organs. For instance, some immune cells called T cells attack the joint lining in rheumatoid arthritis (RA), while B cells create damaging proteins that are common in lupus. Scientists are making significant progress in determining how best to seek out and destroy just these harmful immune cells while leaving other parts of the body’s disease fighting system intact.

John Looney, MD, of the University of Rochester, reported that several different drugs directed at B cells or T cell-B cell interactions are now being tested in clinical trials. At this time, the best studied B cell specific agent is rituximab which is directed at a subset of B cells with a marker called CD20. A large recent clinical trial demonstrated marked improvement in patients with RA who were treated with rituximab, and Dr. Looney's own study of rituximab in patients with lupus suggested that this may be a useful drug in lupus as well.

Philippa Marrack, PhD, an investigator at the National Jewish Medical and Research Center in Denver, described the many checks and balances normally in place to get rid of harmful T cells. For example, researchers have identified a population of cells called regulatory cells that are designed to immobilize any T cells that are capable of attacking self-tissues. A better understanding of how to switch these cells on will help guide the design of drugs to enhance the body's natural self-protective mechanisms.

What's the relevance to people with arthritis? Therapeutic agents that selectively remove only those immune cells involved in the harmful immune response in diseases such as RA and lupus have obvious appeal. Not only could such targeted therapy help avoid many of the side effects seen with non-specific drugs, but it also has the potential of essentially turning off the underlying disease process, leading to a remission or even cure.

Taking the “Toll Road”: Your Frontline Defense  
Much of the research conducted on diseases such as RA has focused on one arm of the body's defense system called the adaptive immune response, which provides highly specific antibodies to block foreign invaders. As described in presentations by Arthur M. Krieg, MD (Coley Pharmaceutical Group, Wellesley MA) and Maripat Corr, MD, from the University of California, San Diego, growing insights about a different arm of the immune system, the so-called innate or first response system, have implications for new therapies. 

One of the first lines of defense against invading bacteria and viruses is a family of proteins called the "toll-like receptors," which are able to distinguish markers or patterns that are unique to these foreign organisms. After recognizing these early signs of infection, the toll receptors signal other immune system players to join the attack to kill and remove the foreign invaders. According to Dr. Krieg, this "infectious-type" recognition pathway appears to also be involved in diseases such as RA and lupus. Dr. Corr reported data suggesting that certain toll receptors appear to help perpetuate the chronic inflammation in RA. 

There is evidence that antimalarial drugs such as Plaquenil, which can be used to treat RA and lupus, may actually work by blocking this innate response pathway. Dr. Krieg and his colleagues have shown that by creating vaccines that include the unique markers recognized by the toll receptors, you can "trick" the immune system into making a stronger defensive response.

What's the relevance to people with arthritis? These discoveries show that the "toll road" is not only an exciting new area of research but also that it may be possible to target this arm of the immune system to develop greatly improved therapies that redirect the faulty immune response in RA, lupus and other autoimmune diseases.

Targeting Complement  
The complement system is a series of proteins that "complement" the work of antibodies in destroying foreign invaders. John Atkinson, MD, from Washington University in St. Louis, presented an update on recent progress in understanding of the complement system and how it plays an important role in the inflammation and tissue damage that occurs in diseases like lupus and RA. Interestingly, inherited deficiencies of certain complement proteins are associated with an increased risk of developing lupus. As noted by Craig Gerard, MD, PhD, from Harvard Medical School, several drugs that block the complement pathway are currently in clinical trials in patients with RA and lupus.

What's the relevance to people with arthritis? Therapies that block the complement pathway provide a new way to inhibit inflammation and tissue damage in people with RA and lupus. Recent studies supported by the Alliance for Lupus Research and the Arthritis Foundation have found that in a mouse model, such therapies might also prevent pregnancy losses. If this work can be extended to humans, complement proteins would become an important new target for preventing miscarriages in women with lupus and the antiphospholipid syndrome.

 

Research Update is compiled by Michele Boutaugh, BSN, MPH, Medical and Scientific Affairs Department, National Office.

Source

 
Rom J Intern Med. 2000-2001;38-39:83-8. Related Articles, Links

Serological levels of apoptotic bodies, sFAS and TNF in lupus erythematosus.

Alecu M, Coman G, Alecu S.

Dermatological Reaseach Center, Scarlat Longhin Hospital for Dermatology, 216, Sos. Serban Voda, 73202, Bucharest, Romania.


In our study we have investigated the presence of apoptotic bodies, soluble FAS receptor and TNF (tumor necrosis factor) in three clinical forms of lupus erythematosus. Determinations were performed in attack period of: systemic lupus erythematosus (SLE) for 20 patients, 20 patients with subacute cutaneous lupus erythematosus (SCLE), 20 patients with chronic discoid lupus erythematosus (DLE). Determinations were performed by ELISA (for apoptotic bodies, kit Boehringer, normal values 400-800 mU), (for sFAS, kit R&D Systems, normal values 4500-17000 pg/ml) (for TNF, ELISA kit R&D Systems, normal values 0.4-3.6 pg/ml). Results in SLE: apoptotic bodies were increased in 16 cases (980-1030); sFAS in 18 cases (17000-24000 pg/ml) TNF was increased in all 20 cases (40-140 pg/ml). In SCLE with multiple cutaneous lesions and without internal organs disturbance the apoptotic bodies were increased in 10 cases (960-1030 pg/ml), sFAS in 9 cases (17000-22000 pg/ml), and TNF alpha in 9 cases. In DLE, apoptotic bodies were increased in 2 patients (980-1010 pg/ml), sFAS in 3 patients (17000-20000 pg/ml) and TNF in 2 patients (20-40 pg/mil). Investigated values were slightly correlated with immune parameters (anti dsDNA antibodies), but they were correlated with the presence of renal disturbances or extension of cutaneous lesions. We consider that the presence of increased apoptotic bodies as a result of peripheral mononuclear cells apoptosis appear as a nauto-limiting mechanism in a pathological immune response. The increase of sFAS in lupus patients serum might be interpreted as an alteration of apoptosis respectively a deficit in apoptosis which has as a first consequence the persistence of B and T lymphocytes, activated, in the pathogen immune response.

PMID: 15529575 [PubMed - indexed for MEDLINE]

Source

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oil
MCA Home Video. ... PG-13 Lorenzo's Oil

... and the film have had an impact on research: the Odones are authors of scientific papers and the term "Lorenzo's Oil" can now be ... Video VHS or DVD
Drama - 1993
Based on a true 1985 story, "Lorenzo's Oil" chronicles a couple's search for a cure for their son's fatal disease. After diagnosing 5-year-old Lorenzo Odone's condition as an extremly rare degeneration of the nervous system known as Adrenoleukodystrophy (ALD), the doctors tell his parents that there is nothing that can be done, and that he has only two years to live. Refusing to accept the word of the medical establishment, the Odones begin researching ALD themselves. As her husband desperately seeks a cure, the boy's mother devotes herself to keeping her child alive with a single-minded fanaticism that alienates everyone around her, including, at times, her husband. Academy Award Nominations: 2, including Best (Original) Screenplay, Best Actress--Susan Sarandon.