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There are well established common causal processes for these as I understand things. In true Idiopathic Parkinson's Disease there is depletion of dopaminergic cells in the substantial nigra. In Alzheimer's Disease there is an increase in amyloid proteins in the brain and neurofibrillary tangles...

Where does it say 4000 micro chambers? That would seem to need 200ml of cell suspension, which is a crazy amount. I am afraid I am still lost with this.

I am not sure that site is particularly well informed. It obviously assumes that CFS is a syndrome since it uses CFS as an example of syndrome. It also says that a syndrome can be a condition or several diseases... It doesn't fit very well with the usage I know and doesn't seem to explain why...

I think poor Henrik has some unhelpful illness beliefs still. I am not sure how sound Diane's arguments to authority are though!

I really don't know. From what I had heard it is intended as a way to look for haemodynamic changes like increased heart rate. Not so much whether someone faints but what happens to their circulation if they do. I have to say I had never heard of it before joining ME forums!

I think 'a disease' has to imply that we know of some common causal process for all cases. That does not have to mean a common causal initiator. At the moment I don't think we can be confident that everyone with ME/CFS has some shared causal process. More people with ME/CFS may have higher TGF...

I guess it just closed. A good job well done.

Not a lot I am afraid. I was aware of it. It is just that as an immunologist familiar with suspensions of peripheral blood mononuclear cells I find it very hard to work out what was actually going on. Why didn't the cells walk off the electrodes from time to time?

Perhaps I should take John up on that. The quote sounds like twaddle to me. Diabetes is a syndrome rather than a disease and a blood sugar test is quite good. A rheumatoid factor test picks out people with swollen joints and it took fifty years to work out why the two are linked - after the...

Not really because I cannot work out the geometric relation between probe and a cell? several cells? - how do we know what the impedance is being measured across? I would also like to see the raw renormalised impedances to see how variable they were.

Absolutely not. It would still be a biomarker. Wessely has put a foot wrong there.

I suspect autonomic testing is useful for people with autonomic neuropathy, but that is a very different situation from the OI issues of ME. I am not familiar with the use of the tilt table test but I thought it was largely to look for tachycardia in POTS. That of course would be quite...

I am sorry to say that I still do not understand what they did or why. I have no idea how many cells they tested or whether they even knew how many cells they were testing. The introduction does not inspire confidence. I really would like to think this study is meaningful but so far I can get...

Sorry, but if the authors want other scientists to take them seriously they need to present the crucial data in the abstract in a watertight form. There is never any difficulty doing that if you have hard data. If the impedance results are of no clinical relevance then the study is of no...

Well to be fair that seems to be what the abstract implies.

Does anyone know how to access the paper itself? I am surprised to find that mY UCL account does not seem to access it - presumably because it is still 'e-hot'. Normally I can get access to all routine journals. The abstract is disappointing - not what I would hope of a scientific paper, but I...

'Because you're worth it.'

Seems like if colleagues don't like your studies they won't recruit to them. And quite right too.