Covid and Didier Raoult (supporter of hydroxychloroquine): analyzes on the pandemic

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Adrien (ex-nico239)
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by Adrien (ex-nico239) » 12/07/20, 15:48

How many deaths out of 5 people with remdesivir in Lescure's study, Gilead's employee?

2 deaths
2 in serious condition

You talk about efficiency
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by GuyGadebois » 12/07/20, 16:22

izentrop wrote:It is weak but better than the Raoult protocol which has proved nothing to it. :P

And are you still there to dirty your bib? It is precisely this type of protocol used by Raoult that proves it. Not your rigged double blind shit.: roll:

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“It is better to mobilize your intelligence on bullshit than to mobilize your bullshit on intelligent things. (J.Rouxel)
"By definition the cause is the product of the effect". (Tryphion)
"360 / 000 / 0,5 is 100 million and not 72 million" (AVC)
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by Obamot » 12/07/20, 17:05

What an eagerness to want to understand nothing for yourself Izentrop!

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Adrien (ex-nico239)
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by Adrien (ex-nico239) » 12/07/20, 17:16

Would like more interesting than these idiots a comparative table of raw figures produced by an individual which allows to see in real time how many deaths could have been avoided by country and in relation to the IHU and between countries by applying the case fatality rates of each to each.

This comparison should not be taken for a truth but as a basis for reflection on the links between protocols and results.
The best result that emerges from this table is that of the Protocol Screening, Selective Isolation, Treatment applied at the IHU with Hydroxychloroquine +/- Azithromicine


view the comparative table

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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by GuyGadebois » 12/07/20, 18:09

Oh, that's crazy, with the Raoult protocol, we could have saved practically 100% of people! Ah well then ... : Mrgreen:
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“It is better to mobilize your intelligence on bullshit than to mobilize your bullshit on intelligent things. (J.Rouxel)
"By definition the cause is the product of the effect". (Tryphion)
"360 / 000 / 0,5 is 100 million and not 72 million" (AVC)
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by sicetaitsimple » 12/07/20, 18:19

Adrien (ex-nico239) wrote:More interesting than these idiots is a comparative table of raw figures produced by an individual ......


Excel drives you crazy .....
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by Obamot » 12/07/20, 18:34

sicetaitsimple wrote:Me is "Kiki"


... yes, yes, and he doesn't need Excel to drive him crazy : Cheesy:
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by Adrien (ex-nico239) » 12/07/20, 23:05

A review of the cytokine storm


What kills in Covid-19?
Posted on July 11, 2020 by Gérard Maudrux
What kills in Covid-19?


Why do people die from Covid-19? Why, with modern means of resuscitation, in our country, 50% of patients in intensive care die, when they are no longer carriers of the virus? Why these differences in mortality from one country to another, for the same virus? Different resuscitations? What is this "cytokine storm" we are talking about?

I never broached these subjects, because to explain things well, you must first master the subject, and the least we can say is that we are in a fairly specialized field, and even for explain clearly only one part, you have to dominate the rest.

Doctor Jean Louis Thillier is an international scientific consultant, member of the French Society of Toxicology. His colleagues, in a collective work, asked him to write the physiopathology-immunopathology section of COVID-19. We have made a simplified summary of this problem of cytokine shock. Sorry if it remains a little complex, that's the subject that wants it. Here is this text:

COVID-19 illustrates the duality of the effects of inflammatory cytokines. In the body, faced with an attack, there is an inflammatory reaction with accumulation of cytokines which activate the immune system, attracting the actors of the response to the attacked site. Too strong a reaction itself leads to damage such as destruction not only of the aggressor, but of other cells (necrosis).

The main inflammatory cytokines are interleukin 1 and TNF alpha (the tumor necrosis factor, which also belongs to the interleukin family).

To avoid too strong a reaction, there is, as always, in many human functions, a balance between facilitating and restraining factors.

To avoid too much interleukin, there are therefore interleukin 1 antagonists which act in competition with the membrane interleukin receptors.

Among them, 1) the interleukin 1 receptor antagonist, which binds to the interleukin receptor by mimicry (resemblance), without activating this receptor, 2) the type 2 receptor of interleukin 1, which acts as a decoy, without transmitting the activating signal to the cell, and 3) the soluble receptors, expressed by the cells following an enzymatic cleavage, and binding to interleukin 1.

The cytokine storm of COVID-19 is the equivalent of septic shock.

The cytokines released by interleukin 1 act locally, but many of the antagonist systems, such as soluble receptors, diffuse throughout the body.

If in general the inflammatory reaction remains localized at the site of production of inflammatory cytokines (interleukin 1 and TNF alpha), while the anti-inflammatory components re-establish a distant equilibrium, in the cytokine storm of COVID-19 this equilibrium at distance is broken, the quantity of inflammatory cytokines which suddenly flows into the blood is such that the neutralization systems of these cytokines are saturated.

Inflammatory cytokines that act on the endothelium, normally limited to the site of production, diffuse throughout the body. causing failure of many organs such as the liver, kidneys, lungs, heart.

Under their action, the blood vessels suddenly dilate (by the release of nitric oxide), their permeability increases and the liquid they contain leaks into the extravascular space. This leads to a sudden drop in blood pressure, organs like the kidneys are no longer sufficiently oxygenated (dialysis), disturbances of consciousness appear and in the lungs, the liquid which leaves the blood vessels, invades the pulmonary alveoli, creating pulmonary edema, which disrupts gas exchange, further aggravating the poor oxygenation of tissues.
The anarchic reactions of the endothelium trigger a coagulation disseminated in all the small vessels of the organism, the capillaries are blocked, and the surrounding tissues are no longer oxygenated (endothelial cells activated by TNF alpha synthesizing coagulation factors).
Finally, inflammatory cytokines have a direct toxicity on the heart by reducing the contractile force of the heart muscle (drop in flow due to hypotension and lack of oxygen), an action wrongly put on the action of hydroxychloroquine by some!

While interleukin-1 and TNF alpha are deleterious when they spread throughout the body, they are essential for activating the immune system and fighting the infectious agent at the site of the coronavirus attack. . The treatment of the cytokine storm of COVID-19, which is the equivalent of septic shock, can only be triple therapy, the antiviral being sometimes still necessary (if PCR still positive) but incidental.

Cytokines are therefore the targets of new drugs and today we better understand their role in human pathologies. It has been discovered that certain substances which modulate the immune system and which have been used for a long time, such as corticosteroids (given back to the honor by the English), act on this network, by reinforcing or by mimicking the action of certain cytokines, or, on the contrary, by blocking their production or their effects.

Since the early 1980s, it has been known that alpha interferon has antiviral and antiproliferative properties, so this other cytokine, produced by genetic engineering, began to be used in people with chronic viral hepatitis.

In patients with COVID-19 in intensive care, the total number of T lymphocytes, cytotoxic T lymphocytes (CD8 T killer T) and helper T lymphocytes (TCD4 or T helper) is significantly reduced, and there is a correlation between total T cells and patient survival. Interleukin 2 activates Rateiliary lymphocytes and killer T lymphocytes.

It is also noted that the reduction in the number of T lymphocytes is prior to clinical signs. T cell count is negatively associated with increased serum IL-6, IL-10 and TNFalpha concentrations, and low level of interferons, antiviral factors (IFNs)

The production of IFN-I (or IFN-α / β) is the main cause of immune response against viral infections, it is a key molecule that plays an antiviral role in the early stages of viral infection. Delayed release of IFNs in the early stages of SARS-CoV and MERS-CoV infection hampers the antiviral response.

Considerable progress has been made with antagonists of cytokines, in particular TNF alpha: these are either specific monoclonal antibodies which muffle TNF alpha and prevent it from acting, or soluble receptors for TNF alpha (which trap this factor) .

When the disease resolves, the concentrations of IL-6, IL-10 and TNF-alpha are reduced and the number of T lymphocytes restored.

In the case of the cytokine storm of septic shock or COVID-19, substances which neutralize TNF alpha have been shown to prevent the occurrence of this shock provided they are administered at the onset of massive cytokine release. .

The attempts on Covid-19, which did not have the expected results, can be explained by too late administration, once the cytokine storm is already advanced.

The antiviral treatments used ensure a noticeable reduction in the concentration of viral particles in the blood, but the recovery of the functions of the immune system is slow and incomplete.

I advised to speed up this recovery. This is because interleukin 2 is normally synthesized by helper T lymphocytes, but the latter are destroyed by the virus. In addition, it is known that this cytokine stimulates the proliferation of T lymphocytes, in vitro.

Conclusion: let the general practitioners prescribe hydroxychloroquine + azithromycin to avoid arriving at the cytokine storm, by reducing the viral load, and consequently the excessive reaction of the organism, which can be fatal, for lack of being able to better control it.
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by Christophe » 12/07/20, 23:07

Adrien (ex-nico239) wrote:Would like more interesting than these idiots a comparative table of raw figures produced by an individual which allows to see in real time how many deaths could have been avoided by country and in relation to the IHU and between countries by applying the case fatality rates of each to each.

This comparison should not be taken for a truth but as a basis for reflection on the links between protocols and results.
The best result that emerges from this table is that of the Protocol Screening, Selective Isolation, Treatment applied at the IHU with Hydroxychloroquine +/- Azithromicine


view the comparative table



Another dirty conspiratorial shit !!! : Mrgreen: : Mrgreen: : Mrgreen: : Mrgreen:
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Adrien (ex-nico239)
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Re: Resignation of Dr Raoult, supporter of Chloroquine, from the Covid Scientific Council19




by Adrien (ex-nico239) » 13/07/20, 00:26

Molecular dynamics simulation study argues for the combined action of hydroxychloroquine and azthromicin

Synergistic antiviral effect of hydroxychloroquine and azithromycin in combination against SARS-CoV-2: what studies of the molecular dynamics of virus-host interactions reveal
Synergistic antiviral effect of hydroxychloroquine and azithromycin ... etc

In conclusion, ATM and CLQ-OH have synergistic antiviral effects on SARS-CoV-2 infection, which supports the use of this combination therapy for the COVID-19 pandemic. In this dual therapy, one molecule (ATM) is directed against the virus, while the other (CLQ-OH) is directed against the cofactors of cellular attachment. However, the two drugs should work together to prevent the first stage of SARS-CoV-2 infection in the plasma membrane, where the therapeutic intervention is likely to be most effective. The conserved QFN triad of the SARS-CoV-2 spike protein, recognized by both gangliosides and ATM, should be considered a target for antibody neutralization in vaccine strategies. The molecular modeling approaches used here are based on the search for mimicry of saccharide gangliosides and could be useful for identifying other ATM binding sites on viral proteins, and more generally for predicting the efficacy of any potential drug candidate. and reused and / or innovative before clinical evaluation. In this regard, we suggest testing the antiviral association of ATM with short synthetic peptides specifically designed to target gangliosides without toxicity [17,33].
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