Guest guest Posted August 20, 2005 Report Share Posted August 20, 2005 Heres a cross-post from a thread where the Gow and Kerr work was being discussed, which gives a vague/loose account of what this method of study is all about. ===================================================== I havent read this stuff in full text and dont understand how a DNA microarray can demosntrate phagocytosis of apoptotic nuetrophils, but I can say: This work is not primarily about what alleles [particular versions of each gene] we have. It is not showing CFS to be a result of genetic heritage. Instead, it measures the rate at which each human gene (yup every single one, all ~33,000) is being " used. " Differences in those rates of use come also from the changing condition of the body, not just from heritage, and can change hourly. Almost every chemical reaction in the body is accomplished by proteins. THe information for making proteins is " copied " from RNA, which is in turn copied from DNA (ie, genes). When the body needs more of a certain protein to do a certain job, one way to get more of that protein is to make more RNA from the DNA that codes for that protein. The increased amount of that particular RNA will cause more of the corresponding protein to be made. I'm not too sure how it all works, but DNA microarrays measure the amount of RNA present in a cell by using it to construct artificial DNA. What this research demonstrates is inflammation (activated macrophages) and some particular charecteristics of the state of the CFS immune system. Activated macrophages are cytokine-spewing maniacs, and that means suffering. Ergo, CFS is caused by non-resolving inflammation, not by a phobia of doing the dishes, nor by " accidentally " seeing your mom naked at age 4 (lil dig at Sigmund Fraud there). Surprise surprise! Hopefully this stuff will be nicely replicable. These data do not show what fundamentally causes the inflammation. > Whole human genome DNA microarray analysis was performed on RNA > isolated from PBMC. Affymetrix HG-U133 (A+ 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, > > ( increased cell membrane prostaglandin-endoperoxide synthase > activity with downstream changes in oxygen transport and > > © macrophage activation with phagocytosis of apoptotic neutrophils. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 20, 2005 Report Share Posted August 20, 2005 ERic said, " Ergo, CFS is caused by non-resolving inflammation, not by a phobia of doing the dishes, nor by " accidentally " seeing your mom naked at age 4 (lil dig at Sigmund Fraud there). Surprise surprise! Hopefully this stuff will be nicely replicable. These data do not show what fundamentally causes the inflammation. " , Thanks for reposting here. It still cracks me up, but also it's a huge finding...the conclusion that CFS is caused by non-resolving inflammation. Yikes! I hope the CFS community takes heed. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 21, 2005 Report Share Posted August 21, 2005 I'd like to see the whole discussion where this was posted. Can you provide a linky-winky please? > Heres a cross-post from a thread where the Gow and Kerr work was > being discussed, which gives a vague/loose account of what this > method of study is all about. > > ===================================================== > > I havent read this stuff in full text and dont understand how a DNA > microarray can demosntrate phagocytosis of apoptotic nuetrophils, but > I can say: > > This work is not primarily about what alleles [particular versions of > each gene] we have. It is not > showing CFS to be a result of genetic heritage. Instead, it measures > the rate at which each human gene (yup every single one, all ~33,000) > is being " used. " Differences in those rates of use come also from the > changing condition of the body, not just from heritage, and can > change hourly. > > Almost every chemical reaction in the body is accomplished by > proteins. THe information for making proteins is " copied " from RNA, > which is in turn copied from DNA (ie, genes). > > When the body needs more of a certain protein to do a certain job, > one way to get more of that protein is to make more RNA from the DNA > that codes for that protein. The increased amount of that particular > RNA will cause more of the corresponding protein to be made. > > I'm not too sure how it all works, but DNA microarrays measure the > amount of RNA present in a cell by using > it to construct artificial DNA. What this research demonstrates is > inflammation (activated macrophages) and some particular > charecteristics of the state of the CFS immune system. Activated > macrophages are cytokine-spewing maniacs, and that means suffering. > > Ergo, CFS is caused by non-resolving inflammation, not by a phobia of > doing the dishes, nor by " accidentally " seeing your mom naked at age > 4 (lil dig at Sigmund Fraud there). Surprise surprise! > > Hopefully this stuff will be nicely replicable. > > These data do not show what fundamentally causes the inflammation. > > > > Whole human genome DNA microarray analysis was performed on RNA > > isolated from PBMC. Affymetrix HG-U133 (A+ 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, > > > > ( increased cell membrane prostaglandin-endoperoxide synthase > > activity with downstream changes in oxygen transport and > > > > © macrophage activation with phagocytosis of apoptotic > neutrophils. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 21, 2005 Report Share Posted August 21, 2005 olmesartan > I'd like to see the whole discussion where this was posted. Can you > provide a linky-winky please? > Quote Link to comment Share on other sites More sharing options...
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