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Movement of proteins in blood is 99% due to the heart pumping. I think they are talking about movement of proteins from one side of a cell to another - i.e. inside a cell. That is presumably due to some change in surface residues like cysteine.

I didn't think the paper was suggesting mutations in cysteine coding by DNA? I cannot yet see quite what they are suggesting but I assume some form of post-translational cysteine modification of disulphide bonds.

This looks like an echo of the proposals put out by people like Peter Paine in the UK. The question has to be why anyone should be receiving unnecessary feeding support. If such a situation exists it is almost certain that it is due to memes created by the same physicians who bemoan the...

This is a very popular excuse for not bothering even to make the diagnosis. If the diagnosis is made and the surgeon has the intelligence to advise patients well then those like me who are cured have the chance to live without hormone therapy and constant fear of what next. The real problem...

I am afraid that none of this stuff looks meaningful to me. So many things you can measure in immunology are just not close enough to what you need to know to be any help. It is a bit like trying to work out who the murderer was in a French detective novel when you don't know French. You can...

I think it is just a question of them having no idea what they are talking about. Microclots are clots not platelet clumps. The level of incompetence in this sort of work takes some believing but that is how it is.

But that isn't what the term means. It may well lead to loss of function but if we are to get anywhere we need to make sure we do not use terms both for the causes of effects and the effects of the causes - which is a mistake that has been rife in medicine but gets you nowhere. (A good example...

Absolutely agree, for trials etc. But when researchers try to find leads for identifying possible treatments I don't see thresholds as being something that can provide any clear clues. For diseases like RA you just accept that those sort of things are too unpredictable for one to be able to...

That seems to me irrelevant. If a term is defined as meaning something then that is what it means. PEM may be inadequately described as malaise, fatigue or exhaustion or whatever but the term means an increase in symptoms. I am afraid I just don't follow that. The problem is the symptoms...

This looks like a group of quacks doing a bit of communal marketing. I have no idea what they even mean by mesenchymal stem cell therapy. We all have plenty of mesenchymal stem cells so it seems unlikely that a few more would make much difference.

Not a lot from that account. It is written in typical fashionable immune-soundbites without any actual data given. They have presumably found some differences in markers that have been labelled 'markers of T cell exhaustion'. My experience of working out disease mechanisms sufficiently to devise...

A drop in neutrophil count isn't really immune suppression as normally understood. ME/CFS is not going to be due to an overactive neutrophil response.

Cytokines have short half lives but inflammation caused by cytokines does not as a rule. Getting cytokine driven inflammation started and then settled down takes a few days generally. Also, the short lived cytokines give rise to elevations in CRP that last days. It seems unlikely that this has...

I was not aware of L-D syndrome as a rheumatologist. The link to TGF beta is very interesting though. I had an interest in aortic involvement in ankylosing spondylitis and TGF beta and L-D syndrome seems to confirm that TGF beta is specially relevant to places like the aortic root. The...

The mention of inflammation seems disconnected from the study of inactivity and insulin resistance. The latter may be of interest to ME/CFS research. The Beentjes paper from Edinburgh picked out insulin resistance clues despite no increase in BMI. It may be that inactivity with shift in tissue...

But is a doctor and a scientist I do not understand that because 'PEM' is the name for an increase in symptoms over a certain time course. That is what the term means - otherwise known as post exertional symptom exacerbation. We assume that PEM is due to some part of an underlying disease...

I am a bit puzzled by this. If loss of function/disability is blamed on PEM and PEM is the name for a set of symptoms, aren't we back to the central problem being symptoms? My worry has been that researchers have not focussed enough on symptoms and tended to think they are trying to explain...

Low serum sodium.

The stuff on megakaryocytes being infected would be interesting if it pans out. But the quoted statement doesn't make sense and makes me suspicious. Microclots are protein clumps that are smaller than platelets as far as I can see, not platelet material. And nobody has any evidence for...

This illustrates a general problem we have discussed in the context of cyclophosphamide, as well as therapist delivered treatments - that it can be very tricky finding an ethical 'dummy' for things that can be predicted to produce effects that interfere with blinding. My own view is that the...