Joined May 2009
2,544 Photos and videos
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Very honored to have given this Rising Star interview, where I could talk a bit about myself, my research, my passion for microscopy, and my dream to find a cure for #LongCovid one day 🥹 Link for the full interview: short-link.me/123uR Press release: eurekalert.org/news-releases…

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Danielle Beckman retweeted
🇧🇷🟢🟡 Brazil has officially taken over Times Square! 👏
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It's never been easier to eat enough protein. There are protein-rich options everywhere. Left: my groceries in California. Right: my groceries in Munich. Different foods, same result: ~2 g/kg of protein per day. I'm still adapting (less eggs, more yogurt), but it's very doable.
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Disclaimer: I don't live on this stuff alone 😛. I also go out with friends, drink alcohol, and make plenty of less-than-perfect food choices. This is just what I try to keep stocked at home to make hitting my protein goals easier.
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Danielle Beckman retweeted
For decades, we've asked where therapeutics go in the body. Now we can ask which cells they reach. Our new SCP-Nano platform combines whole-body imaging and AI to map nanocarrier biodistribution at single-cell resolution, revealing both intended targets and unexpected off-target destinations. A new way to accelerate the development of safer and more precise therapies. Read our paper published at @NatureBiotech nature.com/articles/s41587-0…
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Danielle Beckman retweeted
nightmare blunt rotation and i’m unfortunately the blunt
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Proudly trained in America. Proudly hired in Germany. Don't beg to stay in a place where you are no longer welcome. Build where you're valued. #BrainDrain
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Great to see @VirusesImmunity last paper highlighted at @NatRevImmunol. One of the strongest pieces of evidence yet for autoimmunity in #LongCOVID. Not proof that autoimmunity explains all neurological Long COVID, but it's getting harder to dismiss as one important mechanism.
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The Office for National Statistics estimates that around 110,000 children in England & Scotland are living with Long Covid. Friends, if you live in the UK, please help us by contacting your elected representatives. Letter template below! #LongCovidKids longcovidkids.org/post/all-p…
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Danielle Beckman retweeted
I’ve officially resigned as Associate Editor for Frontiers in Systems Neuroscience (part of @FrontNeurosci). It used to be a reputable journal, but became a case study in how forced automation destroys academic integrity. 👇
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That's my piece of art, I forgot a plastic tube rack in the water bath and gave it a suggestive name.
We all know how creative scientists can get in the lab… Tell us (or even better, show us!) your best benchside masterpieces 🧪🎨
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Danielle Beckman retweeted
Professor Of Religion Reminds People That Their Brains Are Not Part Of Their Bodies
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Bad news: many kids under 8 never received the original Wuhan #COVID vaccines. Their immunity was shaped mostly by Omicron infections. New data suggest the "Cicada" variant (BA.3.2.2), now re-emerging in several countries, may be particularly good at evading immune responses.
Our latest preprint is out, where we investigated a profound SARS-CoV-2 epidemiological anomaly: BA.3.2.2 is selectively infecting children. Here, we show that the lack of ancestral-strain immune imprinting is promoting BA.3.2.2 pediatric infections. 1/9 biorxiv.org/content/10.64898…
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“If the cells are frequently turning over and they are still detecting viral persistence, what other plausible explanations are there for this other than replication?” That's a very good question, and it's one of the central puzzles in the field of viral persistence. Let’s see why: If a tissue contains cells that turn over relatively quickly (intestinal epithelium, immune cells, etc.), and viral RNA or proteins are still being detected months or years after an infection, then ongoing replication is the most intuitive explanation, but it is not the only one. Other reasonable options are: 1. Persistence in long-lived reservoir cells. The tissue as a whole may turn over, but a subset of cells may not. We know this happens for neurons, some endothelial cells, tissue macrophages, lymphocytes, and others. In this case, the virus isn't replicating continuously, but instead, a long-lived infected cell survives for months or years and continues to produce low levels of viral RNA or protein. This is essentially how the HIV reservoir works, for example. 2. Defective viral genomes. A cell can also contain incomplete viral genomes incapable of producing infectious viruses, so the genome may still produce RNA transcripts and some proteins. While this stimulates innate immunity (so enough to cause symptoms and pathology), it doesn’t generate new infectious virions. 3. Protein persistence without viral persistence. The virus itself may be gone but you can have lingering viral remnants like spike protein and nucleocapsid fragments that can persist inside phagocytic cells or in extracellular compartments. In this case, what is being detected is essentially debris rather than an active infection, but their presence is enough to induce immunological responses (and again, enough to produce symptoms/pathology). 4. Continuous release from another hidden reservoir. The tissue where detection occurs may not be the reservoir. Hidden reservoir can include gut, bone marrow and lymphoid tissue, while the released is being detected in blood or peripheral immune cells. In this model, the virus replicates (or persists) in one location, while viral products continually seed other compartments. 5. Cell-to-cell transfer without productive infection. Macrophages and other immune cells can acquire viral material from neighboring cells. These cells may test positive for viral RNA or viral proteins like spike, despite never being truly infected. So a positive signal does not necessarily mean productive viral replication. From a scientific perspective, the most reasonable model may actually be a combination of different situations, like a small reservoir that exists in a long-lived cell, which can induce low-level or intermittent replication. This can induce viral proteins and RNA to be continuously released. These products can then be captured by immune cells and distributed through the body. That model can explain why viral material remains detectable despite turnover, and why it is so hard for scientists to recover large amounts of infectious virus years later. One of the key unresolved question is whether the reservoir is producing new virus, or merely old viral products that are being recycled and retained. That's one of the areas where the field is still struggling to obtain definitive evidence. #LongCovid #MECFS
If the cells are frequently turning over and they are still detecting viral persistence, what other plausible explanations are there for this other than replication? (genuinely curious, have been wondering about this for a while)
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Danielle Beckman retweeted
Excellent and biologically rich review. It brings together neuroinflammation, glia, BBB, vascular dysfunction, mast cells, the vagus nerve, and viral persistence - and adds an original hypothesis of local sleep - a state in which small groups of neurons shift into a sleep-like/silent mode even while a person is awake - which could help explain both brain fog and flares.
Happy to share that after a prolonged peer-review process, our review covering the major Neuroinflammatory events in #LongCovid was accepted today for publication at @Transl_Psych from the @NaturePortfolio! Coming soon, but preprint available here: preprints.org/manuscript/202…
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Happy birthday to @realmikefox! The @MichaelJFoxOrg invested more in Parkinson's research than the U.S. government itself. "Optimism is a political act." In a world full of uncertainty, setbacks, and reasons to give up, choosing optimism is an act of courage. Video from the Too Young for this Sh*t Podcast #Parkinson
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C'mon @WIRED, you have a chance to do better. Instead of amplifying pseudoscience, why not talk to the patients living with #LongCovid and the researchers studying its biology? Levinovitz is not a physician, neuroscientist, or virologist. His expertise is in religion. Try again!
Highly unusual for a journalism article to not be retracted when several sources and people mentioned in the article were misrepresented and have come forward about it — your move, @wired #LongCovid
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Danielle Beckman retweeted
I'm quite fond of my orbital prefrontal cortex.
The anatomical proximity and direct connection between the olfactory bulb and the orbital prefrontal cortex (OFC) make it a key neuroinvasion route for #COVID in the brain. In patients with #NeuroCovid, we observe thrombotic events, hypometabolism and atrophy in this region.
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The anatomical proximity and direct connection between the olfactory bulb and the orbital prefrontal cortex (OFC) make it a key neuroinvasion route for #COVID in the brain. In patients with #NeuroCovid, we observe thrombotic events, hypometabolism and atrophy in this region.
Let's rip the band-aid off
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