There are 3 things you could check in Wang's table 1. (See: Wang, et al., http://tinyurl.com/2v28tl.) This is always my first step, checking if VDR plays a role, and more often than not, it does
 
About the article:
1. There is mention of potassium channels playing a role, search table 1 with: Channel and you'll be amazed
 
2. there is also mention of the ABC transporters:  search table 1 with: ABC (the binding cassettes mentioned are also ABC transporters, in table 1, copy the Genesymbol, go to pubmed, change 'search pubmed' to 'search omim' OMIM is in the dropdown list and then paste the gene symbol)
 
3.  of course, when DeMeirleir is qouted, there is always talk of RNASE L, which can be found in table 4
 
It all almost screams VDR :-)
 
Frans

Summary: Neurological diseases with channelopathies are quite often associated with fatigue and other symptoms common to CFS. Altered neurotransmitter activity and abnormal brain scan images in CFS have provided results consonant with Chaudhuri and Behan’s predictions. Indirect evidence of a channelopathy continues to grow in CFS but there is, as yet, however, no direct evidence of a nervous system channelopathy in CFS. The resolution of that question requires the kinds of studies suggested by Chaudhuri and Behan in 1999.

Last edited on Wed Sep 9th, 2009 12:32 by Joyful

Moderate Exercise Increases Expression for Sensory, Adrenergic, and Immune Genes in Chronic Fatigue Syndrome Patients But Not in Normal Subjects.

J Pain. 2009 Jul 30. [Epub ahead of print]

Light AR, White AT, Hughen RW, Light KC.

Department of Anesthesiology, Utah, University of Utah Salt Lake City, Utah;
Department of Exercise and Sport Science, University of Utah Salt Lake City, Utah
Department of Neurobiology and Anatomy, University of Utah Salt Lake City, Utah

Chronic fatigue syndrome (CFS) is characterized by debilitating fatigue, often accompanied by widespread muscle pain that meets criteria for fibromyalgia syndrome (FMS). Symptoms become markedly worse after exercise. Previous studies implicated dysregulation of the sympathetic nervous system (SNS), and immune system (IS) in CFS and FMS. We recently demonstrated that acid sensing ion channel (probably ASIC3), purinergic type 2X receptors (probably P2X4 and P2X5) and the transient receptor potential vanilloid type 1 (TRPV1) are molecular receptors in mouse sensory neurons detecting metabolites that cause acute muscle pain and possibly muscle fatigue. These molecular receptors are found on human leukocytes along with SNS and IS genes. Real-time, quantitative PCR showed that 19 CFS patients had lower expression of beta-2 adrenergic receptors but otherwise did not differ from 16 control subjects before exercise. After a sustained moderate exercise test, CFS patients showed greater increases than control subjects in gene expression for metabolite detecting receptors ASIC3, P2X4, and P2X5, for SNS receptors alpha-2A, beta-1, beta-2, and COMT and IS genes for IL10 and TLR4 lasting from 0.5 to 48 hours (P < .05). These increases were also seen in the CFS subgroup with comorbid FMS and were highly correlated with symptoms of physical fatigue, mental fatigue, and pain. These new findings suggest dysregulation of metabolite detecting receptors as well as SNS and IS in CFS and CFS-FMS. PERSPECTIVE: Muscle fatigue and pain are major symptoms of CFS. After moderate exercise, CFS and CFS-FMS patients show enhanced gene expression for receptors detecting muscle metabolites and for SNS and IS, which correlate with these symptoms. These findings suggest possible new causes, points for intervention, and objective biomarkers for these disorders.

PMID: 19647494 [PubMed - as supplied by publisher]

Last edited on Tue Sep 15th, 2009 08:33 by Joyful