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the autonomic nervous system has a branch that does not use acetylcholine or noradrenaline as transmitters. instead it uses other things, like nitric oxide, ATP, serotonin, neuropeptide-Y, etc…

some thoughts RE #MECFS #LongCovid #teamclots #dysautonomia 🧵
Nitric oxide gets released (depleted?) in ischaemia reperfusion injuries

Dysmetabolism is commonly reported in #MECFS…

(Circulating) Serotonin may get depleted with platelet activation…
Appetite gets dysregulated in #LongCovid and ME, often (not always) causing lower appetite. ME may be associated with higher neuropeptide Y
Read 5 tweets
Thanks to a very kind collaborator, i have some copeptin (marker of AVP) data, compared to my pre-vaccine measures👇🏻👇🏻👇🏻

Whilst not all samples were taken in ideal conditions, it is clear something funky is (or was) going on with my AVP. some thoughts🧵
#postvac #LongCovid #POTS Graph showing serum copepti...
First a bit of background about copeptin (AVP)

AVP is part of the HPA ("stress") axis. briefly, high AVP = high ACTH = high cortisol

AVP also regulates hydration: low fluid/high salt = high AVP = kidney reabsorption of water = pee less = stay hydrated
1. What i find MOST interesting is that under the most controlled conditions (9am, no fluid), my copeptin was much lower than pre-vaccine on the same day my cortisol came back much lower than pre-vaccine
Read 31 tweets
🍒 Put 'Em on the Glass 🍒

An interesting article about the SARS2 spike binding to Estrogen Receptor-α (ERα) and causing severe coagulopathy in Acute Covid and COVID 💉.

This leads to a question about spike ERα binding and cancer. >…
These researchers designed a spike protein with point mutations which eliminate the ERα binding, improving AE outcomes in the vaxxed.

(Because improvements are urgently needed in a 💉 with "extremely rare effects" in a "minority" of patients.)🙄 #ShibbolethsOfTheDamned > Image
Read 11 tweets
Latest paper from Dr Robin Kerr & me:
#LongCovid is primarily a Spike protein Induced Thrombotic Vasculitis…
Here we proposed that long covid is primarily a spike protein-induced thrombotic vasculitis, & we use Robin as a supporting case study 🧵
#TeamClots a U-shaped blood vessel. at...
We start by discussing the highly thrombotic nature of acute COVID & how this pathology doesnt cease in those with long COVID. in other words, long COVID is a continuation of the pathology accompanying acute COVID. Importantly, we cant rehabilitate until the pathology is treated
we highlight the role of microclots in capillary occlusion, that coagulopathic outcomes occur after acute covid (e.g. ↑ stroke risk), that there is platelet hyperactivation and endotheliitis, and all this leads to impaired oxygen extraction (and more)
Read 17 tweets

The COVID 💉 is comprised of mRNA encased in a lipid nanoparticle.
The mRNA is codon optimized with n1-methy-pseudoU and codes for a more durable spike protein.
It also contains dsDNA bacterial contaminants and an SV40 promoter.
See research of Kevin McKernan. >
Read 17 tweets
PEG supports prolonged circulation of the LNPs, and their payload, the spike protein mRNA.
Spike protein is then expressed on the surface of cells in the endothelium all over the body.
This causes amyloid fibrin micro clots to form in response. See #TeamClots research > Image
The immune system reacts to the expression of the foreign spike protein, and in the process, damages the endothelial wall, releasing collagen.
The collagen and the PEG from the LNPs act like a Hemopatch™️ to strengthen the amyloid fibrin clots. This creates a durable matrix.
Read 4 tweets
If other diseases were treated like #LongCovid:

"You expect me to believe blood sugar is the reason we needed to amputate your leg?"

"Riiiiggghhht, so the lump in your lung has just *moved* to your liver..."

"And how exactly do you think shellfish made your throat swell up?!"
"Youre saying the virus has been hiding in your body and has now come back to life and given you shingles?"

"Really, you think your own immune system is 'attacking' you"

"There's no evidence a head injury can make you thirsty"
Physiology is complex.

It utterly baffles me that so many doctors seem to think we know and understand it all, that what they learnt at med school is fact and final, that things they cant imagine happening *might actually be happening*.

Read 5 tweets
1 of 5) Excited to share our new LongCOVID paper with co-authors @dbkell @PutrinoLab Asad Khan, Ashley Woodcock and Simone Turner.…
2 of 5) We discuss LongCOVID classifications: Post Acute Covid: 3 to 12 weeks and Chronic Covid: symptoms beyond 12 weeks up to 3 years. We also discuss manifestations of the symptoms and risk factors and predictors.
3 of 5) We discuss vaccination and LongCOVID and the various pathologies including viral factors, bacteriophage-like actions of SARS-Cov-2, host factors, including autoimmunity, mast cell activation and down-stream impacts.
Read 6 tweets
A tour de force review in @RPTHjournal of NETosis and its contribution to immunothrombosis. Neutrophils cast out NETs to catch bugs (including SARS-CoV-2) but they are highly proinflammatory and thrombogenic. #TeamClots
The original form of NETosis described by the Brinkmann & Zychlinsky labs was when neutrophils “dump their guts”, committing suicide by spilling out their nucleus, forming a fishnet-like structure. Read the @RPTHjournal review for updates on non-suicidal NETosis.……
A previous review from Denisa Wagner, with a strong emphasis on the role of NETosis, “Thromboinflammation: From Atherosclerosis to COVID-19”.…
Read 6 tweets
“Antiphospholipid syndrome (APS) is a paradigmatic thromboinflammatory disease. Thromboinflammation is a pathophysiological mechanism coupling inflammation and thrombosis, which contributes to the pathophysiology of cardiovascular disease.” #immunothrombosis @isth
There has also been some suggestion that aPL antibodies may be pathogenic rather than just a transient secondary response to infection. #TeamClots #LongCovid…
From the @JTHjournal article: “Dysregulation of protective immunothrombosis may have detrimental effects, eg in severe COVID-19. This is termed thromboinflammation and can lead to collateral damage to local tissues. The existence of a systemic proinflammatory and prothrombotic……
Read 4 tweets
#TeamClots preprinted an important milestone in the microclot theory of Long Covid etiology. 🧵on the implications, as I understood them. TLDR: it looks like microclot burden will struggle as a standalone biomarker for LC; we should look deeper!…
First, why is this an important milestone? This paper uses imaging flow cytometry to quantify the microclot burden in patients, which, AFAIK, is the first time that microclots have been measured in an objective and statistically robust way.
The flow cytometry method captured the following measurements: number of microclot objects per milliliter, mean microclot area, microclot count in area range.
Read 8 tweets
Sneak peek at our latest #LongCovid preprint about microclot detection using imaging flow cytometry

By Simone Turner, Jaco Laubscher, @resiapretorius & @dbkell

These are 1st results from the instrument YOU funded by donating to @givewithkernls


Grey columns are using brightfield microscopy; black are using Thioflavin T

See the difference in size between #LongCovid & control microclots

There were statistically significant differences in mean size, number & other variables

More in the paper!

2/n Image
Why is this important?
Because flow cytometry is already accessible in clinical settings, unlike fluorescence microscopy which is mainly a research tool.

Big thanks to @gezmedinger @HarryLeeming @fearnley_k @Geraint6Jones @clarejdaly @loscharlos @ShaneyWright @j_b_kennedy 3/n
Read 7 tweets
Sharing out some results from our ai-powered #LongCovid site:
* Most popular
* Most effective overall
* Most effective for POTS, Fatigue, Brain Fog, and more

These results are *directional*, but in the spirit of empowering patients with more information, we wanted to share.

1/ Sources
* Twitter
* Reddit: 2 LC subs, plus r/cfs, r/pots, r/mcas, r/eds, and r/dysautonomia

We collected >35k treatment reports, and read them w/ an AI model to (imperfectly) see if people improved/worsened.

We show all raw data and inferences in case you want to vet!
2/ Top 20 most popular

This helps us gut check the data. Indeed, we see some familiar faces - antihistamines, nattokinase, LDN, probiotics, etc.

The beta blocker reports are mostly coming from r/pots, and the steroid reports are largely from r/mcas.
Read 13 tweets
As I reflect today on #InternationalLongCovidAwarenessDay I know that there is a lot of suffering, loss and grief to account for, but I wanted to offer a message of hope. Today, we:
1) Categorically know more about #LongCovid than we did last year
2) Have educated thousands of 1/
clinicians on basic care and management strategies
3) Have some good-quality drug trials in the mix (thanks @hmkyale and @VirusesImmunity among many others)
4) Have #MECFS and #vaccineinjury cohorts being added to clinical trials (finally!)
5) Microclot research is being taken 2/
seriously by all serious scientists (and major journals: thanks @doctorasadkhan, @dbkell, @resiapretorius and all #teamclots fam)
6) viral persistence research is being taken seriously by all serious scientists (thanks @microbeminded2, @MBVanElzakker and many others)
Read 5 tweets
I posted this in May 2021.

4 trips to Germany & 12 months of treatment, she has managed to do a handstand again (3 seconds!)

Not exercising yet, but otherwise able to live her life carefree.

With the right support and care recovery is possible (1/3)

This was filmed just over a year ago (Jasmin from 3 mins), she has since started High School full time and had no time off.

This time last year she was largely housebound and needing a wheelchair for distance (2/3)
Here’s a 10min talk I did for @TheWHN outlining her journey and how we got here.
Key points; there’s lots we can do with the right tests, expertise, courage & a leap of faith.

#TeamClots doing what we can to drive research. Making good progress 🤞🏽(3/3)

Read 4 tweets
1. Acute COVID led to maximal levels of P-selectin dependent platelet-neutrophil aggregation. There was reduced phosphatidylserine exposure and integrin αIIbβ3 activation. It means less primary aggregation and more leukocyte-mediated thromboinflammatory signalling. @JTHjournal
2. #Microclots are typically positive on staining for P-selectin (also known as CD62P). Selective activation of platelet P-selectin may be a feature of acute COVID. Whether the same feature is found in #longCOVID remains unconfirmed. #TeamClots
3. P-selectin binds to PSGL-1 (P-selectin glycoprotein ligand). It is found on leukocytes eg neutrophils, macrophages and T-cells. PSGL-1 is a mediator of immunothrombosis. In chronic viral infection, PSGL-1 promotes T-cell exhaustion. @fitterhappierAJ…
Read 5 tweets
Important news about XXB1.5 pointing out that infection is more via the ACE2 receptor than previous Omicron variants.
But … the mouth is not mentioned as an important site of infection….…
A thread … 1/
2/ Minor salivary glands over the surface of the tongue, inner surface of the lips, the fauces and soft palate are highly susceptible to infection and replication. Epithelial cells in these areas express the ACE2 receptor.…
3/ The mouth can be considered a viral factory with viral entry into saliva in high quantity - 100 million per ml (equivalent to half a billion viruses in a single 5 ml teaspoon).…
Read 22 tweets
“We’re very early,' @PutrinoLab says.. But every sample from #LongCovid patients has revealed #MicroClots."

"They are not capable of clogging large vessels.. but they can significantly affect organ function."…
"@resiapretorius has been studying such #MicroClots for more than a decade & has observed them in type 2 diabetes, #MECFS, Alzheimers, Parkinsons... The main difference.. in diabetes & other conditions is they break up quite easily.. COVID microclots are harder to disintegrate"
"Trapped inside the #MicroClots, @resiapretorius team found high levels of inflammatory molecules & protein called alpha 2-antiplasmin that prevents their breakdown. Such blockages in tiny vessels throughout body could hinder supply of oxygen & nutrients to organs & tissues"
Read 18 tweets
Could PolyP be a key player in COVID contact-pathway thromboinflammation-driven microthrombi? Some thoughts from an emerging area of molecular wizardry. 🧵
#LongCOVID #TeamClots #PolyP
There is evidence in COVID of immunothrombosis being driven through the kallikrein-kinin-contact pathway—we'll just call it the “contact system”. It feeds into the renin-angiotensin system (SARS-CoV-2 binds to ACE2). @JTHjournal…
The still mysterious contact system, once mistaken for a haemostatic pathway, is now regarded as an immunothrombosis pathway. It may yet hold some secrets to how #longCOVID leads to #microclots.…
Read 13 tweets
I find the assertion that COVID-conscious people somehow want to be in a "forever pandemic" really presumptuous. I haven't met a single person who ACTIVELY WANTS to remain in isolation forever. That's actually the opposite of what we want!
There ARE options between "zero COVID" and letting it rip. Harm reduction is the approach here - COVID may be here to stay, but the constant floods of infections don't have to be. There are simple and effective ways to mitigate transmission and make our environments safer!
Every COVID-conscious and high-risk person I know understands the consequences of isolation. We have all been forced to make choices between our health and our desire to be a part of our communities. These two things don't have to be mutually exclusive.
Read 6 tweets
Serum Amyloid A has been found in Spike Protein produced #microclots. SAA amyloidosis has a 10 year median survival rate. It has not been established that Spike amyloids only affect some people. Indeed, it may be a ticking time bomb of #diedsuddenly in billions. #teamclots
If untreated, AA amyloidosis is a serious disease with a significant mortality due to end-stage kidney disease, infection, heart failure, bowel perforation, or gastrointestinal bleeding [3-5].
Patients with persistently high circulating levels of serum amyloid A protein (SAA) are at particular risk of these complications [6,7].
Read 5 tweets
wee update:
had a couple of pretty good weeks which has surprised me. everything in life is tolerable. still worse than before my last relapse, but if life stays like this, i can work around it. tho i usually feel "good" pre-relapse, so hoping it's not the calm before the storm
had TWO dr apps this week:
1. at the nutrition clinic: anaemia has resolved so i can stop iron supps, just got some follow up apps to check my haemoglobin, B12 etc stay stable

2. GP: spoke to advanced nurse practitioner. i was sorta ready to put up a bit of a fight as it was...
to discuss tests & meds recommended by a private dr. she was absolutely lovely tho, & shocked how much ive been suffering

- agreed to D-dimer: if elevated 1 month after anticoagulation ends I may be indicated for longer term anticoagulation as i have a high risk of further clots
Read 11 tweets
In 1961 the @ACSNews, @AHAScience, the National TB Association & @APHA sent a joint letter to @POTUS Kennedy asking to appoint a national commission to investigate the link between smoking and health, without wanting to threaten the freedom of the tobacco industry. 🧵
2/ He assigned this seemingly impossible task to his @SurgeonGeneral, Luther Terry. Terry appointed an expert advisory committee to summarize the links between smoking and lung cancer. Over 13 months they met for 9 sessions.…
3/ The 387 page report was released on January 11, 1964 and was one of largest cohorts ever analyzed by an epidemiological report. The truth was, people had already known about health risks of smoking for almost 15 years. It wasn’t interesting news anymore despite ongoing harm. Title: Smoking and Health: Report of the Advisory Committee
Read 19 tweets

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