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2 Jan, 4 tweets, 5 min read
Cyproheptadine prevents pulmonary platelet trapping in endotoxin shocked or severely beaten dogs.

osti.gov/biblio/5502933…

Further evidence for potential efficacy against development of ARDS via pulmonary microthrombosis-- explicitly discussed.

@farid__jalali ImageImageImageImage
@cameronks @pathdoc3 @icedoc61 @Jopo_dr @Acute_Pulmo_Med @ZaidYounes9 @Geurys7 @MARYau_MCU_PH @DrBrandon55 @VectorSting @Crashcart

Interesting earlier result on cyproheptadine and pulmonary platelets.
Just found this one for pulmonary fibrosis as well-- another success for cyproheptadine in earlier animal experiments:

Ongoing thread for practitioner feedback-- feel free to report any observations noted:



Tentative indication is severe COVID-19. May (likely) also be applicable in late moderate phase.

Appears effective for pulmonary, neurological, and renal symptoms.

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More from @__ice9

ice9 Profile picture
3 Jan
@ianbirrell Comprehensive.

Only a few flaws.

The first is the 'missing researcher'-- she left years earlier, irrelevant.

The second is that you missed the EcoHealth Alliance grant, and Daszak explicitly confirmed recombinant CoV testing in humanized mice Nov 2019.

@ianbirrell You need to read this:

@ianbirrell And you *really* need to read this:

Read 4 tweets
ice9 Profile picture
3 Jan
What to expect in a COVID-19 case that progresses to the severe phase and ICU admission-- in terms of typical patient experiences.

Note this thread is 14 posts long.
The things we are discussing about 5-HT2 antagonists and plasma serotonin, about attempting to halt progression in the early severe stage, are relevant *during* these events.

Rates of PTSD following survival from severe COVID-19 exceed 30%, ditto anxiety and depression.
The ventilator settings required to keep these patients alive tend to permit blood CO2 levels to rise somewhat, in avoiding excessive mechanical damage to the lungs.

This has been repeatedly demonstrated to cause severe anxiety and promote PTSD.

Read 5 tweets
ice9 Profile picture
30 Dec 20
For anyone interested in the Baric interview on synthetic recombinant SARS-like CoVs earlier, see around 38:00 into this video.

There is also some interesting preliminary discussion starting around 36:30 or so, mostly in English.
This provides the video that went missing when a few accounts I had quoted earlier were suspended.

Here are the translations of the transcript of the Baric interview, reference via @TheSeeker268

Read 4 tweets
ice9 Profile picture
29 Dec 20
@HenkPoley Yes, am familiar with the issue.

I will see if I can locate my earlier findings on this.

So far I have only located some notes from earlier, but not the actual citation yet.

@HenkPoley This paper indicated that a single exposure to 70% ethanol largely preserved filtration efficacy, comparable to dry heat or UV sanitizing. However, further exposure events gradually worsened filtration efficacy.

medrxiv.org/content/10.110…
@HenkPoley Discussion thread here:

Read 6 tweets
ice9 Profile picture
29 Dec 20
To date, anecdotal reports from dual entry inhibition in mild acute COVID-19 remain excellent.

Recovery within 48 hours appears typical, absent significant complications (e.g. secondary infection).

Dual entry inhibition means blocking both:
- TMPRSS2/13/11
- endosomal entry
Dual entry inhibition was tested in the Ansarin et al. RCT, adding bromhexine 8mg t.i.d. to a baseline of HCQ 200mg q.d.

Mortality in hospitalized moderate COVID-19 patients fell to zero.

This remains one of the best results of any COVID-19 RCT to date.

Theoretical justification arises from the fact that endosomal entry is of only secondary importance for SARS-CoV-2 replication in the respiratory tract.

Both TMPRSS (proteases at the cell membrane) and cathepsins (proteases in endosomes) must be blocked.

Read 15 tweets
ice9 Profile picture
3 Dec 20
More evidence that endothelial cells are not directly vulnerable to infection by SARS-CoV-2.

Endothelial dysfunction in COVID-19 is entirely indirect. Image
Discussion thread on pericytes, nearby susceptible cells strongly suspected to mediate some of the damage.

Discussion on infection of pulmonary megakaryocytes, i.e. platelet-forming cells, also strongly suspected of involvement.

Read 6 tweets

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