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Yes this is all over the news on CNN and newspapers. It is a huge

finding. CFS is finally being recginized in mainstream as a severe

disease.

> Found this while scurrying about looking for other stuff. It was

hiding in

> a professional health group I am in. Hope it is interesting.

>

>

>

> Kaushik N, Fear D, s SCM, et al. Gene expression in

peripheral blood

> mononuclear cells from patients with chronic fatigue syndrome.

>

> J Clin Path 2005;58:826-832.

>

> Narendra Kaushik, Fear, Selwyn CM s, Clare R

McDermott, Emile F

> Nuwaysir, Kellam, Tim J on, J Wilkinson,

AJ Tyrrell,

> T Holgate, R Kerr Fritz E, J, Kerr JR, et

al.

> Association of chronic fatigue syndrome with human leukocyte

antigen class

> ii alleles. Clin Path 2005;58:860-863.

>

>

>

> Chronic fatigue is not all in the mind

>

>

>

> 21 July 2005

>

> NewScientist.com news service

>

> Rowan Hooper

>

>

>

> AT LONG last, we are beginning to get to grips with chronic fatigue

> syndrome. Differences in gene expression have been found in the

immune cells

> of people with the disease, a discovery that could lead to a blood

test for

> the disorder and perhaps even to drugs for treating it.

>

>

>

> The symptoms of chronic fatigue syndrome have been compared to

those of a

> really bad hangover: extreme weakness, inability to think straight,

> disrupted sleep and headache. But unlike a hangover, the symptoms

linger for

> years, devastating people's lives.

>

>

>

> While nobody doubts CFS exists, just about every aspect of it is

> controversial. Some say it is the same as myalgic

encephalomyelitis, or ME;

> others disagree. Many specialists are convinced it does have a

biological

> basis, but pinning down physical abnormalities common to all

patients has

> proved tough. People with CFS have often received little sympathy

from

> doctors who dismiss it as " all in the mind " .

>

>

>

> Now Kerr's team, which is moving to St 's

University of

> London, has compared levels of gene expression in the white blood

cells of

> 25 healthy individuals with those in 25 patients diagnosed as

having CFS

> according to strict criteria. The researchers found differences in

35 of the

> 9522 genes they analysed using DNA chip technology.

>

>

>

> The few similar studies done in the past have produced conflicting

results,

> so the team double-checked their results using a more accurate

method called

> real-time PCR. That confirmed that 15 of the genes were up to four

times as

> active in people with CFS, while one gene was less active. The

results will

> appear in the Journal of Clinical Pathology next month.

>

>

>

> Kerr is repeating the study in 1000 CFS patients and healthy

controls, this

> time looking at 47,000 gene products. So far, the larger study

backs up the

> earlier results, he told New Scientist.

>

>

>

> If Kerr really has succeeded where many have failed, and

identified clear

> physical changes in people with CFS, the lingering opinion that it

is " all

> in the mind " could finally be laid to rest. " This exciting new

work shows

> that some aspects of this complex illness may be understandable in

molecular

> terms, and that CFS is not a 'made up'

>

> illness, " says Lane, a neurologist at Charing Cross

Hospital in

> London.

>

>

>

> It should also be possible to develop a blood test for CFS. The

team has

> already discovered differences in blood proteins related to the

changes in

> gene expression.

>

>

>

> Kerr hopes the work might even lead to treatments. " We have shown

that a

> significant part of the pathogenesis resides in the white blood

cells and in

> their activity, " he says. " It will open the door to development of

> pharmacological interventions. "

>

>

>

> Several of the genes identified by the team in CFS play important

roles in

> mitochondria, the power factories of our cells. " The involvement

of such

> genes does seem to fit with the fact that these patients lack

energy and

> suffer from fatigue, " Kerr says.

>

>

>

> One of these gene products, EIF4G1, is involved in protein

production in

> mitochondria. It is hijacked by some viruses, so cells may

compensate by

> ramping up gene expression. " I am excited by the paper, " says

Basant Puri, a

> CFS expert at Hammersmith Hospital in London. " The group's finding

of

> upregulation of EIF4G1 is consistent with subclinical persistent

viral

> infection. "

>

>

>

> This fits in with the idea that CFS is sometimes triggered by

viruses such

> as Epstein-Barr, Q fever, enteroviruses and parvovirus B19. " CFS

often

> begins with a flu-like illness which never goes away, " Kerr says.

>

>

>

> Of the other genes whose expression varies in CFS patients, some

are

> involved in regulating the activity of the immune system. Others

play

> important roles in nerve cells, including a gene called NTE, which

codes for

> an enzyme affected by organophosphates and nerve gases.

>

>

>

> Journal reference: Journal of Clinical Pathology (vol 58, p 823,

860) From

> issue 2509 of New Scientist magazine, 21 July 2005, page 9

> http://www.newscientist.com/article.ns?id=mg18725093.700

>

>

>

> Bruce Guilmette, Ph.D.

>

> Survive Cancer Foundation, Inc.

>

> http://www.survivecancer.net

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