Re: ms& occupations

[Guest guest]

For what it's worth....if there is an interest in polling peoples occupations...I'm a jeweler. Silver & gold fabrication(I inhale some really toxic fumes)

-------Original Message-------

From: low dose naltrexone

Date: Monday, September 06, 2004 22:20:17

low dose naltrexone

Subject: Re: [low dose naltrexone] ms

Along this same general line of thinking, there are many , many people who are or who have been involved in the medical industry, myself included, who now have MS. It's interesting, if nothing more. I think that you tend to notice that like people also have the disease. I'm not sure if there's any hidden meaning behind all of this but, you do tend to take notice more easily given the similarities you share with them. Would be further interesting to take a poll of what other MS'ers do or have done for a living.

DesinieAudrey Henry <mumpuss@...> wrote:

Tom, I just looked at the site you gave - www.mult-sclerosis.org.If you look at the bit where it says famous peoplewith MS. What do you notice?Well I noticed what an incredibly talented bunch ofpeople they were and most of them are involved in thearts.That either means that people only become famous ifthey are artistic,or they are artistic as a result of the MS, or the statistics for getting MS are high if you arean artist. I am myself an artist.Just Curious. Audrey-- Bayuk <tbayuk@...> wrote: > > > More MS news articles for March 2004> >--------------------------------------------------------------------------------> Immune system cause of multiple sclerosis questioned> > Study shows evidence that myelin-producing cells die> before there is any immune system activity > > http://www.mult-sclerosis.org > > March 18, 2004 > > All About Multiple Sclerosis > > Prevailing medical wisdom says that multiple> sclerosis is an autoimmune disease - a disease in> which the body's immune system turns in on itself.> Specifically, it attacks the myelin sheaths that> insulate the nerve cells in the brain and spinal> cord. This immune system activity produces> inflammation similar to what happens in the skin> when we get a pimple. > > Crucially, the inflammation also kills the cells> responsible for produc! ing and maintaining the> myelin. These cells are called oligodendrocytes and> they have long been known to die in large numbers> during attacks of MS. > > The majority of existing treatments for the disease> and a fair proportion of new treatments currently in> research focus on reducing the inflammation or> disabling the immune system cells responsible for> it. > > However, a dramatic piece of new research published> in The ls of Neurology threatens to turn this> understanding of multiple sclerosis on its head. > > The study examined twelve brains of people with> multiple sclerosis, concentrating on newly forming> areas of disease activity called lesions. It found> that the oligodendrocytes in these lesions were> dying before there were any signs of inflammation. > > This implies that it is not the inflammation that> causes t! he death of the oligodendrocytes in multiple> sclerosis but the other way around. The inflammation> occurs in response to the oligodendrocyte cell> death. > > The authors, Barnett and Prineas of the> Institute of Clinical Neurosciences at the> University of Sydney, Australia don't deny that the> inflammation might cause some of the damage seen in> multiple sclerosis but they do paint a radically new> picture of of the disease. > > They suggest that the first stage of the development> of a new multiple sclerosis lesion is mass suicide> of the oligodendrocytes over a relatively small> area. This process is called apoptosis or programmed> cell death and is a normal response in the human> body during growth and repair. If cells were allowed> to grow and divide without limits, they would form a> cancer. Similarily, cells infected by viruses or> cells that are no longer needed by the body will> often cell kill themselves. > > Barnett and Prineas observed oligodendrocytes in> which the central nucleus was shrivelling up - a> typical sign of a cell committing suicide. Other> cells in the brain were also changing. Microglia,> another , which are responsible for> activating the botype of maintenance cell which canswallow> up dead and dying cells, were forming long> extensions ready to engulf the dead and dying> oligodendrocytes. Additionally, a group of proteins,> called complementdy's rubbish-collecting cells, had> collected on the myelin. Crucially, the> rubbish-collecting cells of the immune system, the> macrophages, had not yet appeared in the lesion. > > Within one or two days of lesion formation, all the> oligodendrocytes had disappeared. The authors> suggest that they had been ! swallowed up by the> microglia. The spaces that they had once occupied> were now full of liquid forming what is known as> edema. > > The next stage seems to be the invasion of immune> system cells. Macrophages now start to appear,> together with T cells, the orchestrators of the> immune response. These initiate and take part in> inflammation. The macrophages start to gobble up the> myelin left over by the vanished oligodendrocytes. > > The final stage would appear to be regeneration.> Oligodendrocyte precursor cells, cells that have the> ability to develop into new oligodendrocytes, move> in to replace the lost cells. They are fed special> chemicals called trophic factors by the macrophages> and the process of remyelination can begin. > > It is important to bear in mind that this was a> study of only 12 brains and further work needs to be>! done to validate the studies findings. However, if> this work reflects what is actually happening in> multiple sclerosis, then its implications are earth> shattering: > > a.. Multiple sclerosis will no longer be an> autoimmune disease. A lot of text books are going to> have to be rewritten. > a.. Treatments that target inflammation will not> not addressing the root cause of the diease. This> does not mean that they are not effective to some> degree but that they can never be as good as> treatments that target the death of the> oligodendrocytes. > a.. All the animal models of multiple sclerosis> are poor representations of the disease in that they> are all primarily autoimmune models. Perhaps this is> why so many treatments that are so effective in> mouse models prove to make no difference to multiple> sclerosis in h! umans. For animal models to be valid,> they would need to show the kind of disease process> described by Barnett and Prineas. > a.. Researchers will need to change direction.> Whilst work on oligodendrocyte precursor cells> becomes more important than ever, work on describing> the inflammation process in multiple sclerosis needs> to take a back-seat. Importantly, researchers need> to find out why oligodendrocytes are dying and what> can be done to stop them. > Quite how the world of multiple sclerosis research> will react to this paper is unclear. Thus far,> Barnett and Prineas's paper seems to have been met> with a deafening silence which is why I decided to> write this piece. > Source: > > Relapsing and remitting multiple sclerosis:> Pathology of the newly forming lesion > H. Barnett, MBBS, W. Prinea! s, MBBS * > ls of Neurology, Feb 23, 2004 > http://www3.interscience.wiley.com/cgi-bin/abstract/107629227/ABSTRACT> ATTACHMENT part 2 image/gif name=personal.gif> ATTACHMENT part 3 image/gif name=links.gif> ATTACHMENT part 4 image/gif name=search.gif> ATTACHMENT part 5 image/gif name=about.gif ___________________________________________________________ALL-NEW Messenger - all new features - even more fun! http://uk.messenger.

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