A UK ME/CFS advocate has contacted Dr Gow for details of how donations may be made for his research fund.

The ME Association has recently made funds available to ensure that Dr Gow's research assistant could be retained by his department for the months of April and May but funds are urgently required now if this important work by Dr Gow and his team is to continue. Please send whatever you can.

See media coverage at:

http://newsscotsman.com/scotland.cfm?id=550752005

(you will need to register with The Scotsman for free to view the article)

http://www.eveningtimes.co.uk/hi/news/5039240.html


Dr Gow writes:

Thank you for your interest in our research on CFS/ME. If you would like to send a donation to help us continue our research we would be extremely grateful. Please send a cheque directly to myself at the address below and made payable to "The University of Glasgow" and my secretary will ensure that the cheque goes into our research account. The University will, of course, send you a receipt.

I have attached a copy of the abstract which I presented both orally and in poster form in Japan in February 2005. We have submitted the data for publication in a peer-reviewed journal and hope to have the data published later this year.

The University of Glasgow patented the novel biomarkers and triple drug treatment on Feb 1st 2005 "Materials and Methods for Diagnosis and Treatment of Chronic Fatigue Syndrome" application number GB 0502042.5

We have generated a "gene signature" of patients with CFS/ME but we emphasise that we require extensive further trials, including a larger number of patients with CFS/ME and controls (healthy controls and patients with a variety of disorders), of the diagnostic test prior to the test becoming widely available.

Thank you again for your interest in our work.

Kind regards,
Dr John W Gow

Senior Lecturer in Clinical Neuroscience
University Dept. of Neurology
Southern General Hospital
1345 Govan Rd
Glasgow, G51 4TF
Scotland

Tel: 44 (0)141 201 2465
Fax: 44 (0)141 201 2993


Attachment:

Whole-Genome (33,000 genes) Affymetrix DNA Microarray Analysis of Gene Expression in Chronic Fatigue Syndrome

Gow JW, Cannon C, Behan WMH, Herzyk P, Keir S, Riboldi-Tunnicliffe G, Behan PO & Chaudhuri A.

University of Glasgow Department of Neurology, Southern General Hospital, 1345 Govan Rd, Glasgow G51 4TF, Scotland, UK. email: j.gow@clinmed.gla.ac.uk

Background:

Chronic fatigue syndrome (CFS) is a complex disorder characterised by persistent fatigue, musculoskeletal pain and post-exertional malaise. The mechanism of fatigue in CFS is not known and as no reliable diagnostic test is available, misdiagnosis is common and treatment regimes vary. As CFS symptoms are multi-systemic and are often preceded by infections, gene expression in peripheral blood mononuclear cells (PBMC) was examined. The study was carried out to determine if any characteristic changes in biochemical pathways could be identified. This would identify biomarkers and provide a rational
basis for targeted pharmacotherapy.

Methods:

Whole human genome DNA microarray analysis was performed on RNA isolated from PBMC. Affymetrix HG-U133 (A+B) DNA chips which include probe sequences for the entire human genome, 33,000 genes, were used. Eight male patients with CFS (18-54 years, mean 36 years) and seven age-matched male healthy controls (22-58 years, mean 34 years) were included in the initial microarray study. An additional twenty patients with CFS and twenty age and sex matched controls were recruited for RT-PCR and western blot assays in order to verify the microarray data for a number of putative biomarkers.

Findings: Iterative group analysis of the differentially expressed genes indicate that in CFS:

(a) there is a shift of immune response with preferential antigen presentation to MHC class II receptors, downregulation of the MHC class I system with a consequential suppression of Natural Killer cells and fÑT-cell receptors,

(b) increased cell membrane prostaglandin-endoperoxide synthase activity with downstream changes in oxygen transport and

(c) macrophage activation with phagocytosis of apoptotic neutrophils.

Interpretation:

A comprehensive map of gene expression has been generated by whole-genome DNA microarray assay for patients with CFS. Several biomarkers have been identified by the microarray assay and confirmed by RT-PCR and western blot analysis. Functional changes affected by altered gene regulation offer an explanation of the fatigue experienced by patients with CFS. Western blot/ELISA assays of key biomarker genes can be used to support the clinical diagnosis and identify candidates for treatment trials in CFS.


Abstract S7-03/P2-19 (oral and poster presentations)

In:

International Conference on Fatigue Science, Karuizawa, Japan, February 9-11, 2005