Luis (@lulopson) profile picture

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Joined June 2015
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Yesterday, my 15 yo daughter asked why people are so resistant to evidence that COVID is a serious threat causing widespread damage. My answer sounded a whole lot like this👇
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Die Lebenserwartung der Deutschen sinkt Die Lebenserwartung der Männer ist seit 2020 um 18 Monate gesunken, die der Frauen um 13 Monate, so die Berechnungen des Versicherungsmathematikers Axel Kleinlein. „Er sieht heute neben den Langfristfolgen von Corona noch weitere Gründe …
Laut Berechnungen des Versicherungsmathematikers Axel Kleinlein (Analyse der Daten des Statistischen Bundesamts) sinkt in DE seit 2020 die Lebenserwartung. Gründe: Langfristfolgen von Corona, Umweltfaktoren (u.a. Hitze) und unzureichende Teilhabe am Fortschritt für Ärmere. 1/2
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Bloating and food intolerances after a gut infection? Inflammation can affect digestive enzymes, while impaired motility may contribute to SIBO. Explore the mechanisms in our new animation. Follow us for more ImmunoThings!
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Brutale Daten zu ME/CFS aus der MIRACLE Studie: Je jünger die Patienten, desto kränker sind sie im Schnitt (ü60 ausgeschlossen) Siehe Diagram rechte Seite
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🎓 Tomorrow, Braeden Charlton defends his PhD on skeletal muscle abnormalities and post-exertional malaise in #LongCOVID and #MECFS. His research has made an important contribution on understanding these diseases. 📅 12 Nov | 09:45 CET 🔴 Watch live: vu.nl/nl/agenda/2026/promoti…
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6 months in Germany! 🇩🇪🔬❤️ Months of hard work & new challenges! And next week, I'll be presenting our first results at a conference! What if SARS-CoV-2 leaves more behind than we think? Millions of people are still living with #LongCOVID, and we keep fighting to understand why.
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Il-1b/ Il-6 / Tremor / Parkinson's/ Noradrenaline/ Locus Coeruleus/ Thalamus The results advance our understanding of the mechanism underlying parkinsonian-like tremor in rats. The presented data suggests that IL-1β, IL-6, and β-receptors are a potential triple-target in therapy of PT. Combination of IL-1β and IL-6 triggers parkinsonian-like tremor in rats: correlation of the effect with noradrenaline levels in the locus coeruleus and ventral anterior thalamic nucleus - PubMed share.google/MmNSBanfu9EMLKM…
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How did #SARSCoV2/#COVID go from supposedly being a dangerous bioweapon and definitely being a BSL-3 virus damaging multi-organ systems to being a virus that 99.9% of the public, including COVID experts who used to warn of the dangers, treats like a cold requiring no protection?
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Health Rising: 'A Mitochondrial Inhibitor in the Brain? WASF3 Just Got a Lot More Interesting For ME/CFS' 'Hwang, a senior intramural researcher at the NIH, first got interested in WASF3’s effects on the muscles.' healthrising.org/blog/2026/1…
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Some incredible science coming out of the Long COVID conference in France this week. Viral persistence, autoimmunity, immune dysregulation, biomarkers, and clinical trials. It’s crazy how far this field has come in just five years. academicmedicaleducation.com…
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Mice got a mild covid infection that never reached the brain. No inflammation, no neuron loss. Every check you'd run came back clean. Two weeks on - fewer synapses in the memory region, more amyloid. The protein that builds up in Alzheimer's🧵
Recurrent mild SARS-CoV-2 infection affects the lung-brain axis in wild type and Alzheimer’s mice 🚨New mouse study: two mild COVID infections (ancestral then Omicron) quietly damage hippocampal synapses and worsen amyloid plaques in Alzheimer’s models, no brain virus, no microglial activation. Lung–brain axis in action! 🚨Interesting BELGIUM study, that sparked broad MSM coverage, and that’s unique!🤔 ➡️“Even mild corona infections can leave traces in the brain: Ghent researchers discover possible link with Alzheimer's" ➡️Let’s dig into the study: - Mice received sequential mild intranasal infections: ancestral SARS-CoV-2 (10 PFU) followed 14 days later by Omicron BA.1 (7000 PFU), - Lungs showed detectable virus after each exposure, no viral RNA was found in brain (cortex/hippocampus) at the final time point (day 28), - Disease remained sublethal with low systemic/brain cytokine responses, - Two weeks after the second infection, microglia (IBA1) and astrocytes (GFAP) showed no significant changes in number, density, or reactivity in hippocampus or cortex of either genotype, - Hippocampal synaptic integrity was reduced (lower SYP+ presynaptic and SYP/PSD-95 colocalized puncta), most clearly in the Alzheimer’s disease model mice(AD mice), no neuronal loss (NeuN) was observed, - In AD mice only, repeated infection increased hippocampal Aβ plaque number (with area trend) and cortical insoluble Aβ1-40/1-42 levels. Soluble Aβ and microglial plaque association/phagocytosis were largely unchanged, - Effects appear mediated indirectly via the lung–brain axis rather than direct CNS infection. ➡️Attention: THIS STUDY IS EXPLICITLY A REINFECTION MODEL! ‼️So, even mild, repeated SARS-CoV-2 infections leave a measurable footprint on the brain, eroding hippocampal synapses and accelerating amyloid pathology in susceptible hosts, without triggering detectable neuroinflammation. And indeed, this study adds further experimental support to the idea that repeated SARSCOV2 exposures can produce lasting, subtle CNS effects relevant to longC0VID “brain fog,” cognitive complaints, and possible accelerated neurodegenerative risk. The absence of overt gliosis suggests the damage can be stealthy and cumulative rather than driven by classic neuroinflammation. For people with genetic or early Alzheimer’s risk, or those experiencing successive infections, the findings underscore the value of monitoring cognitive trajectories and considering cumulative viral burden as a potential modifier of brain health. It does not yet prove causation in humans but strengthens without any doubt the biological rationale for taking mild reinfections seriously! #AvoidSars2 #AvoidReinfections link.springer.com/article/10… hln.be/gent/zelfs-milde-coro…
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Our bodies are colonized by trillions of viruses that we live with in homeostasis. The most diverse and abundant of these viral families are anelloviruses. A new paper from us at @MSKCancerCenter explores what happens after we *all* have been infected biorxiv.org/content/10.64898… 1/n
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We carry viruses our entire lives, yet know remarkably little about how they persist. This remarkable work helps explain where anelloviruses hide, how our genetics influence their persistence, and how viral proteins can quiet immune defenses.
Our bodies are colonized by trillions of viruses that we live with in homeostasis. The most diverse and abundant of these viral families are anelloviruses. A new paper from us at @MSKCancerCenter explores what happens after we *all* have been infected biorxiv.org/content/10.64898… 1/n
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BioVie presented new findings from our Phase 2 ADDRESS-LC trial that suggest two distinct biomarker-defined #LongCOVID endotypes are associated with different patient responses to bezisterim treatment. See details about our presentation at the @FNIH_Org @NIH RECOVER-TLC workshop here: investors.bioviepharma.com/n… #LongCOVID $BIVI
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There’s something that has always struck me about ME/CFS and Long COVID. Many patients experience a worsening of their symptoms after physical exertion, an infection, a poor night’s sleep, or a stressful situation. And for years, this worsening has sometimes been used to suggest that the illness has a psychological origin. But did you know that some of these very same factors can also trigger flares in inflammatory diseases whose biological mechanisms we understand quite well? I want to share a study that I find particularly interesting, because I think it challenges the way we interpret symptom flares in ME/CFS and Long COVID. What if we’ve spent years confusing what triggers a flare with what actually causes the disease? 1/
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Incredible to see this $15M philanthropic investment into @polybioRF & the complex chronic illness space. Thank you @pagsceltics and family for supporting innovative research. This is how the needle gets moved and people receive meaningful help - with substantive funding dedicated to high quality research that begins to match the scale of those impacted.
WCVB: 'Philanthropist, former Celtics co-owner Steve Pagliuca backs $15M long COVID research effort' "It’s really hard to watch if one of your children is sick and one of your friends is sick," Pagliuca said. "And so this really needs to be done." wcvb.com/article/former-celt…
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A subset of individuals with depression (1), sleep disorders (2), bipolar disorder (3), or mood disorders (1) have all been found to have elevated pro-inflammatory cytokines in their blood. The study referenced in the infographic is yet another example of why immunopsychiatry remains an active area of research. We recently removed the paywall from a recent Substack article explaining how inflammation in the body can affect our mental health. Access it for free here: buff.ly/o0wpjRp (For those of you who are paid Substack members, keep an eye out for our next article examining the crosstalk between myofibroblasts and mast cells in those with hypermobility spectrum disorder (HSD) and hEDS.) Literature Cited: 1. Felger JC. Curr Neuropharmacol. 2018. PMID: 29173175 2. Zielinski MR, Gibbons AJ. Front Cell Infect Microbiol. 2022. PMID: 35392608 3. Dolsen MR, Soehner AM, Harvey AG. Psychosom Med. Jan 2018. PMID: 28914726
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Could CAR-T therapy become a future treatment for certain patients with Long COVID or ME/CFS? For those who missed my recent thread, I’ve now published a more detailed article on Substack. I’ve included additional research on EBV, autoreactive B cells, HLA class II, and the potential of resetting the immune system. Could this approach help specific autoimmune subgroups? The evidence is promising, but important questions remain. Read the full article here: manruipa.substack.com/p/coul…
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Highest level of cancer diagnosis in history. It's suggested that better diagnosis is the reason (may be true) but no mention of an airborne virus (SARS2) circulating and re-infecting which degrades T-Cells, NK cells and the P53 protein, all of which help protect against cancers.
JUST IN: 🇬🇧 England now records 1,000 new cancer diagnoses every day, the highest level in history.
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Hab gerade mit einer Immunologin gesprochen, die recht amüsiert war von der neurologischen Eminenzenmeinung, dass eine immunologische Ursache von ME/CFS nicht mehr State of the Art zu hypothetisieren sei.
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