Dr Jonathan Kerr's SNP research - anyone know if this got finished, or not?

ukxmrv

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I'm not sure why this is still on their webpage.

Dr Kerr lost his lab at St George's when his contract ended and they wouldn't renew it. Since then he has been working in a non-research NHS role. Dr Kerr said at the time that it was unlikely that he would ever be able to work in CFS research again.
 

Nielk

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As far as I know, Dr. Derek Enlander at Mt. Sinai in NYC is going to continue Dr. Kerr's work. He was collaborating with him when he was working on it.
 

snowathlete

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I'm not sure why this is still on their webpage.

Dr Kerr lost his lab at St George's when his contract ended and they wouldn't renew it. Since then he has been working in a non-research NHS role. Dr Kerr said at the time that it was unlikely that he would ever be able to work in CFS research again.

What a shame. What happened? It sounds like there is more to it...
From what ive read it looks like his research was really promissing. Im pleased to hear that someone else is taking it up.
 

Bob

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I think i've read that Kerr's research is now being following up by more than one high-profile researcher, but I'm afraid that I can't remember any details, as usual.

I also read that Jonathan Kerr was unable to repeat his own research in a follow-up study that wasn't published.
I can't remember where I read about that either, but the details are somewhere on this forum.
 

oceanblue

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I also read that Jonathan Kerr was unable to repeat his own research in a follow-up study that wasn't published.
I can't remember where I read about that either, but the details are somewhere on this forum.
I've read that too on this forum - somewhere. I'm pretty sure there's something about that unpublished follow-up study on the CFS Foundation website (incidentally, this is a perfect example of how publication bias comes about - not publishing the dud result so the published (and searchable) work looks better).
 

Bob

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I've read that too on this forum - somewhere. I'm pretty sure there's something about that unpublished follow-up study on the CFS Foundation website (incidentally, this is a perfect example of how publication bias comes about - not publishing the dud result so the published (and searchable) work looks better).

Yes, the news about Kerr's unpublished negative study was a bit of an eye-opener to me... I'd always assumed that negative follow-up studies (in science generally, not just ME-related) would always be published, but it seems that they aren't.

It might explain why there is so much novel research published that isn't followed up. In other words, it is followed up, but when it led to a dead end it wasn't published.

The CFS Foundation website rings a bell for me... I think that's where we found out about Kerr's negative study.

If Kerr couldn't successfully repeat his own research, it makes me wonder if other researchers are wasting their time following it up. I hope they aren't. From what i've read, they seem to be very enthusiastic about their research and their results so far.
 

oceanblue

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Yes, the news about Kerr's unpublished negative study was a bit of an eye-opener to me... I'd always assumed that negative follow-up studies (in science generally, not just ME-related) would always be published, but it seems that they aren't.

It might explain why there is so much novel research published that isn't followed up. In other words, it is followed up, but when it led to a dead end it wasn't published.

If Kerr couldn't successfully repeat his own research, it makes me wonder if other researchers are wasting their time following it up. I hope they aren't. From what i've read, they seem to be very enthusiastic about their research and their results so far.
I think you're right: novel findings can't be replicated but because the failure to replicate isn't published, the novel 'finding' remains, apparently never followed up. Publication bias is widespread across science. It's not just the fault of researchers - lots of journals aren't interested in publishing negative studies, and there was even talk of launching a 'journal of negative findings'!

Gene expression is particularly prone to false positives because of the vast number of genes study, and the microarray tecnique Kerr used isn't particularly accurate, adding to the problem. I gather best practice is to use microarrays to identify interesting candidates, then confirm on an independent patients sample using more accurate, smaller scale techniques eg quantitative real-time PCR used by the Lights in their work.
 

Nielk

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I just checked with Dr. Enlander and he said:


WE WILL PERFORM RESEARCH ON THE GENOME IN ME/CFS, work that was inspired by Jonathan Kerr.
 

snowathlete

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WE WILL PERFORM RESEARCH ON THE GENOME IN ME/CFS, work that was inspired by Jonathan Kerr.

Thats good enough for me. I was wondering: 23andme leverage their membership to get data, via questionares, and this combined with the dna results is potentially very useful, because you can compare the dna of people with ME to those without, and the questionares could help even more to refine based on severity of condition, and so forth.

Of course, anyone can do this if they get solid ME patients and compare their dna to controls, but i just wonder if there might be something we could do to help researchers - perhaps by creating a central ME/CFS dna database for those who have had tests done. Do you think this would actually help anyone?
 

Bob

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I think you're right: novel findings can't be replicated but because the failure to replicate isn't published, the novel 'finding' remains, apparently never followed up. Publication bias is widespread across science. It's not just the fault of researchers - lots of journals aren't interested in publishing negative studies, and there was even talk of launching a 'journal of negative findings'!

Interesting... I've not come across this subject before... A journal of negative findings would actually be very helpful.


Gene expression is particularly prone to false positives because of the vast number of genes study, and the microarray tecnique Kerr used isn't particularly accurate, adding to the problem. I gather best practice is to use microarrays to identify interesting candidates, then confirm on an independent patients sample using more accurate, smaller scale techniques eg quantitative real-time PCR used by the Lights in their work.

Is it the Lights that are following up Kerr's work (as well as Dr. Enlander)? Or is it Nancy Klimas? Or maybe both? I know it's someone high profile, but I've got an awful memory for details!
 

oceanblue

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Is it the Lights that are following up Kerr's work (as well as Dr. Enlander)? Or is it Nancy Klimas? Or maybe both? I know it's someone high profile, but I've got an awful memory for details!
The Lights came at it from an entirely different direction (they'd identified some of the molecular receptors responsible for the sensory neuron signaling of muscle fatigue and muscle pain in mice, then went looking for them in CFS).
 

biophile

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This may help, from 2011 and has Kerr's name on it:

PLoS One. 2011 Mar 30;6(3):e16872.

Assessment of a 44 Gene Classifier for the Evaluation of Chronic Fatigue Syndrome from Peripheral Blood Mononuclear Cell Gene Expression.

Frampton D, Kerr J, Harrison TJ, Kellam P.

Department of Infection, Division of Infection and Immunity, University College London, London, United Kingdom.

Chronic fatigue syndrome (CFS) is a clinically defined illness estimated to affect millions of people worldwide causing significant morbidity and an annual cost of billions of dollars. Currently there are no laboratory-based diagnostic methods for CFS. However, differences in gene expression profiles between CFS patients and healthy persons have been reported in the literature. Using mRNA relative quantities for 44 previously identified reporter genes taken from a large dataset comprising both CFS patients and healthy volunteers, we derived a gene profile scoring metric to accurately classify CFS and healthy samples. This metric out-performed any of the reporter genes used individually as a classifier of CFS. To determine whether the reporter genes were robust across populations, we applied this metric to classify a separate blind dataset of mRNA relative quantities from a new population of CFS patients and healthy persons with limited success. Although the metric was able to successfully classify roughly two-thirds of both CFS and healthy samples correctly, the level of misclassification was high. We conclude many of the previously identified reporter genes are study-specific and thus cannot be used as a broad CFS diagnostic.

PMID: 21479222

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016872
 

oceanblue

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This may help, from 2011 and has Kerr's name on it:
Thanks, glad it got published. I think this is the key line in terms of methodology:
To determine whether the reporter genes were robust across populations, we applied this metric to classify a separate blind dataset
"And our findings went up in smoke." Wish more researchers would use this approachto validate or disprove their interesting novel 'findings'.
 

Bob

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Good find biophile! So it was published after all. I think that's the first time most of us have seen that.

Maybe it's still a promising area of research, with enough funding and resources.
 
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