Rune Busk Damgaard

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Rune Busk Damgaard

Rune Busk Damgaard

@rbdamgaard

Associate Professor, Section for Medical Biotechnology, Technical University of Denmark. Studies ubiquitin signalling in inflammation, metabolism, and disease.

Copenhagen, Denmark Katılım Aralık 2015
1.4K Takip Edilen2K Takipçiler
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
More evidence that LUBAC has functions beyond immune signalling. Our recent study shows that LUBAC and OTULIN regulate metabolic signalling: specifically they govern AMPK signalling to control metabolic adaption, autophagy, and cell death during energetic stress. This suggests that the metabolic symptoms observed in patients with LUBAC deficiency and ORAS, including glycogen storage disease, lipodystrophy, and liver disease, may be caused directly my metabolic dysregulation rather than being secondary to the systemic inflammation. nature.com/articles/s4141…
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
@BarteltLab Overall, I agree. But the power of the programme boards/committees, who request the evaluations, are not to be underestimated.
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Alexander Bartelt
Alexander Bartelt@BarteltLab·
@rbdamgaard 🤣🤣🤣 tru dat - no frame of reference but for the most part critical difference is that reviewer #2 has more power over you 😜
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
I’d take a full review from a grumpy Reviewer #2 any day over student teaching evaluations. Students are savage.
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Jamie Timmons
Jamie Timmons@metapredict·
@rbdamgaard @BarteltLab Yet you mock the native speaker rather than admit you didn't think or perhaps recognise the nuance of 'context''. Spent nearly 5yr in Sweden & Denmark and you all absolutely do JUST (21st Century) fine with basic english. Accents are irrelevant but nice try at gaslighting👋
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
Why not cite preprints? They are published, the data are there for everyone to see. Why ignore the latest data of out of principle?
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Jamie Timmons
Jamie Timmons@metapredict·
@rbdamgaard @BarteltLab It's not; but you are nicely illustrating the issue of non-native english speakers missing nuances. Data is out there isn't a euphemism for "publishing" either - we clearly distinguish between data release and 'publishing' in science. Your last sentence lacks clarity.
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
@metapredict @BarteltLab I know what it means to publish. Your point is semantic and moot. The data is out there for everyone to see. Just assess it rather than dismiss out of principle.
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Jamie Timmons
Jamie Timmons@metapredict·
@rbdamgaard @BarteltLab That is a high school definition of "publish" - ie literal. As you know, "publish" in science implies a multi step process. English is nuanced. Preprints are accessible, should now be cited (regrettably) & I absolutely agree much of (genuinely) published work is complete shite
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
@metapredict @BarteltLab They are published. They are just not peer reviewed. A lot of what’s published by your definition of that word is 💩 too. Just read it and assess it. As you do with anything else. I find it problematic to not cite preprints just because they are preprints.
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Jamie Timmons
Jamie Timmons@metapredict·
@rbdamgaard @BarteltLab They aren't "published" - that term in science means something distinct (in english at least). Saying that the horse has bolted and now everyone cites esp in informatics. (the reason not to is obvious; u can pre-print anything including made up 💩like myokines....oh wait)
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
@KehatLab @BarteltLab I understand your point, but I don’t agree that it’s a useful way to do it. I am in favour of preprints, but not as the sole mechanism of publication. We need peer-review.
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Kehat Lab
Kehat Lab@KehatLab·
@rbdamgaard @BarteltLab Maybe we should site the pre-print even after the paper is published in a ‘conventional’ journal. The pre print is the prior science
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Rune Busk Damgaard retweetledi
Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
More evidence that LUBAC has functions beyond immune signalling. Our recent study shows that LUBAC and OTULIN regulate metabolic signalling: specifically they govern AMPK signalling to control metabolic adaption, autophagy, and cell death during energetic stress. This suggests that the metabolic symptoms observed in patients with LUBAC deficiency and ORAS, including glycogen storage disease, lipodystrophy, and liver disease, may be caused directly my metabolic dysregulation rather than being secondary to the systemic inflammation. nature.com/articles/s4141…
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WW3finalboss
WW3finalboss@WW3finalboss·
🇺🇸🇳🇴🇮🇷 Speech at the White House this morning. “If the Prime Minister of Norway had given me the Nobel Peace Prize, our submarine wouldn’t have had to sink an Iranian ship…” — Donald Trump, President of the United States
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Joakim 🌹🇳🇴🇪🇺
Joakim 🌹🇳🇴🇪🇺@joakial_·
New ad by the Norwegian Consumer Council: "A Day in the Life of an Ensh*ttificator"
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Martin Bauer
Martin Bauer@martinmbauer·
The UK sacrifices its research lead to uphold an unsustainable University funding system and the naiv view that less University research equals more growth in the private sector This is a mistake that will be much, much more expensive in the long run researchprofessionalnews.com/rr-news-uk-uni…
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
🧐 What if metabolic defects are not just a consequence of inflammatory disease - but actively contribute to it? Inflammation and metabolism are deeply intertwined, but the molecular links remain unclear. Our new paper in @cddpress uncovers one. 🧵👇 nature.com/articles/s4141…
Rune Busk Damgaard tweet media
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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
This project started with confusion 🤔 nature.com/articles/s4141… Loss of LUBAC or OTULIN causes inflammatory disease. But patients also show clear metabolic defects. Neither LUBAC nor OTULIN had been linked to metabolic regulation. So where do these metabolic symptoms come from?
Rune Busk Damgaard tweet media
Rune Busk Damgaard@rbdamgaard

🧐 What if metabolic defects are not just a consequence of inflammatory disease - but actively contribute to it? Inflammation and metabolism are deeply intertwined, but the molecular links remain unclear. Our new paper in @cddpress uncovers one. 🧵👇 nature.com/articles/s4141…

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Rune Busk Damgaard
Rune Busk Damgaard@rbdamgaard·
We turned to proteomics 📊 and found that LUBAC and OTULIN regulate AMPK. This suggests the metabolic defects may not simply be secondary to inflammation. Rather, they may be central in the pathogenesis.
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