Member Info for Borsaci06

ever since Professor Rademacher has left in 2016, the company is going down

JV Chamary says that

Using inhalers might sound weird, but it actually makes a lot of sense because it would be faster and more convenient than intravenous injection, notably for people with a fear of blood or needles. And delivering drugs through an inhaler might be especially effective against SARS-CoV-2, the pathogen that causes COVID-19: while injecting a drug into the bloodstream helps distribute it everywhere it may be needed around the body, inhaling a nanobody will provide a more direct route to the main site of infection

https://www.forbes.com/sites/jvchamary/2020/05/18/coronavirus-inhaler/#a8f4a5972a76

most of you would know
Lansdowne is selling DDDD as well

he is a market trader as well
??

ASBMB
@ASBMB
"The main role of #ACE2 is to break down angiotensin II into molecules that counteract angiotensin II’s harmful effects; but if the virus occupies the ACE2 ‘receptor’ on the surface of cells, then its role is blunted

https://twitter.com/ASBMB/status/1262827926002819072

https://www.asbmb.org/asbmb-today/science/051620/what-is-the-ace2-receptor

On the other hand, therapies to boost ACE2 activity or the lung regenerative capacity could be particularly promising for the treatment of COVID-19 [44], as previously described for SARS [45].

In young individuals, higher levels of ACE2 [39] and ACE2+ cells, higher regenerative capacity and a strong immune response lead to an effective viral clearance with little or no symptoms.

In older subjects, possibly with lower ACE2 levels, or in the presence of comorbidities that can affect the angiotensin system, such as hypertension [40], or impair the immune response, such as diabetes, the slower viral clearance and sustained damage to ACE2+ AT2 cells goes beyond the reparative capacity [41], causing lung inflammation, with a high risk of precipitating into ARDS because of an uncontrolled inflammatory response. This is particularly true during seroconversion, at around 7 to 14 days from the start of viral replication

https://www.sciencedirect.com/science/article/pii/S1568997220300914?via%3Dihub

Highlights

The spike protein of SARS-CoV-2 harbors a multibasic S1/S2 site
The host cell protease furin cleaves the SARS-CoV-2 spike protein at the S1/S2 site
Cleavage at the S1/S2 site is essential for spike-driven viral entry into lung cells
https://www.sciencedirect.com/science/article/pii/S1097276520302641



Telling couple of sentences... (1/2) “Even more troubling... SARS-COV-2 seems to make use of the enzyme #furin from the host to cleave the viral spike protein. This is worrying... because furin is abundant in the respiratory tract and found throughout the body” @nature
(2/3) “It is used by other formidable viruses, including HIV, influenza, dengue and Ebola to enter cells. Scientists think that the involvement of furin could explain why SARS-CoV-2 is so good at jumping from cell to cell, person to person and possibly animal to human...”
(3/3) “...estimates SARS-CoV-2 has 100–1000 times greater chance than SARS-CoV of getting deep into the lungs”
https://twitter.com/Tim_WoodfieldNZ/status/1262310362302439424

Abstract

The current SARS covid-19 epidemic spread appears to be influenced by ethnical, geographical and sex-related factors that may involve genetic susceptibility to diseases. Similar to SARS-CoV, SARS-CoV-2 exploits angiotensin-converting enzyme 2 (ACE2) as a receptor to invade cells, notably type II alveolar epithelial cells. Importantly, ACE2 gene is highly polymorphic. Here we have used in silico tools to analyze the possible impact of ACE2 single-nucleotide polymorphisms (SNPs) on the interaction with SARS-CoV-2 spike glycoprotein. We found that S19P (common in African people) and K26R (common in European people) were, among the most diffused SNPs worldwide, the only two SNPs that were able to potentially affect the interaction of ACE2 with SARS-CoV-2 spike. FireDock simulations demonstrated that while S19P may decrease, K26R might increase the ACE2 affinity for SARS-CoV-2 Spike. This finding suggests that the S19P may genetically protect, and K26R may predispose to more severe SARS-CoV-2 disease.

https://www.biorxiv.org/content/10.1101/2020.04.23.057042v1.abstract

MARY Aurélien
@MARYau_MCU_PH

Aujourd'hui, je fête les 28 jours sans aucun signe de l'ANSM pour l'étude IFN inhalé, alors que le CPP a pu gérer en 7 jours. Aux UK, 16kk $ pour un projet similaire #sng001. #Covid_19. #Treatment. #Interferon. Il est pourtant important de voir au-delà de #Hydroxychloroquine.

Translated from French by

Today, I celebrate the 28 days without any sign of the ANSM for the inhaled IFN study, while the CPP was able to manage in 7 days. In the UK, $ 16kk for a similar project #sng001 . #Covid_19 . #Treatment . #Interferon . However, it is important to see beyond #Hydroxychloroquine .
https://twitter.com/MARYau_MCU_PH/status/1262655390824697857

are they planing to join covid 19 test producers like the one below using nanogold { Collodial gold } ?

https://twitter.com/sincoherenJen/status/1262281607278473216

company is for sale
&
raise £4.3 mil for what
is it not for sale anymore?

looks like good moping up needed in the lungs eliminating those S protein with its subunits

Eric Feigl-Ding
@DrEricDing
2) NOT JUST VIRUS FRAGMENTS: “the researchers found complete strains of the virus in tissue deep in her lungs. They put tissue samples under an electron microscope to confirm the existence of the intact coronavirus enveloped in a crown-like shell.”

that is why direct delivery of medicine to the infected lungs is more important

" LURKING VIRUS - relapse not resolved yet. #COVID19 patients discharged from hospital could still carry Microbe deep in their lungs, undetected by conventional tests, study found - could explain why growing number of recovered patients had tested positive again. "

read his thread;
https://twitter.com/DrEricDing/status/1255973502362009602

Closing Date for applications: 19th May 2020
https://www.synairgen.com/contact-us/employment-opportunities/

Midatech Pharma PLC ADR (MTP) Paused due to volatility
4/30/20, 11:17 AM
(END) Dow Jones Newswires
04-30-20 1117ET
Copyright (c) 2020 Dow Jones & Company, In

reports say that TMPRSS2 prime/slice S protein, so virus can enter host cell
less of tmprss2 means less of virus entry to cell, me thinks

Pharma123

do you think that interferons increase Epithelial TMPRSS2 as well ?

I can not find
if you would please

better link here
https://www.covid19-druginteractions.org

may require alteration of drug dosing, timing of administration or close monitoring

https://liverpool-covid19.s3.eu-west-2.amazonaws.com/ppi2d0vd9lnff7sq0cjtcdiiwelp?response-content-disposition=inline%3B%20filename%3D"Covid_InteractionSummary_Web_2020_Apr09.pdf"%3B%20filename%2A%3DUTF-8%27%27Covid_InteractionSummary_Web_2020_Apr09.pdf&response-content-type=application%2Fpdf&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIAI7XER5GUPWKQNOYA%2F20200427%2Feu-west-2%2Fs3%2Faws4_request&X-Amz-Date=20200427T083937Z&X-Amz-Expires=300&X-Amz-SignedHeaders=host&X-Amz-Signature=ecbd345756387893204e06bd05cb9d141418760ca3f8faa9fe6a93222a652a89

do we know that ACE2 and TMPRSS2 coexist?
do we know that interferons increase quantity of TMPRSS2 as well as ace2?

????????