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Saturday, April 11, 2020

Are the protocols for COVID-19 at most hospitals harming patients?




A Brooklyn doctor is warning that critically ill coronavirus patients are being inadvertently harmed by the very same breathing machines being used to keep them alive.


https://nypost.com/2020/04/06/nyc-doctor-says-coronavirus-ventilator-settings-are-too-high/

Would whole blood transfusion save COVID-19 patients?



Suggestion from Andrew Dubinsky:


"Virus destroys hemoglobin. People are dying from asphyxiation. Transfuse whole blood to save lives. this will replace the damaged cells."





https://www.spot.im/s/00bZQO6Ebpwt


COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism


https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173

The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. In this study, conserved domain analysis, homology modeling, and molecular docking were used to compare the biological roles of certain proteins of the novel coronavirus. The results showed the ORF8 and surface glycoprotein could bind to the porphyrin, respectively. At the same time, orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide. The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images. The mechanism also interfered with the normal heme anabolic pathway of the human body, is expected to result in human disease. According to the validation analysis of these finds, chloroquine could prevent orf1ab, ORF3a, and ORF10 to attack the heme to form the porphyrin, and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress. Since the ability of chloroquine to inhibit structural proteins is not particularly obvious, the therapeutic effect on different people may be different. Favipiravir could inhibit the envelope protein and ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins. This paper is only for academic discussion, the correctness needs to be confirmed by other laboratories. Due to the side effects and allergic reactions of drugs such as chloroquine, please consult a qualified doctor for treatment details, and do not take the medicine yourself.

COVID-19 affects hemoglobin



COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism


https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173

The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. In this study, conserved domain analysis, homology modeling, and molecular docking were used to compare the biological roles of certain proteins of the novel coronavirus. The results showed the ORF8 and surface glycoprotein could bind to the porphyrin, respectively. At the same time, orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide. The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images. The mechanism also interfered with the normal heme anabolic pathway of the human body, is expected to result in human disease. According to the validation analysis of these finds, chloroquine could prevent orf1ab, ORF3a, and ORF10 to attack the heme to form the porphyrin, and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress. Since the ability of chloroquine to inhibit structural proteins is not particularly obvious, the therapeutic effect on different people may be different. Favipiravir could inhibit the envelope protein and ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins. This paper is only for academic discussion, the correctness needs to be confirmed by other laboratories. Due to the side effects and allergic reactions of drugs such as chloroquine, please consult a qualified doctor for treatment details, and do not take the medicine yourself.

Are ventilators killing many COVID-19 patients?


Dr. Cameron Kyle-Sidell, a doctor treating COVID-19 patients in New York City's Maimonides Medical Center, warns that the medical community may be wrong about the nature of the coronavirus and how it is said to cause acute respiratory distress syndrome (ARDS).

Transcript from a recent video: 
In treating these patients, I have witnessed medical phenomena that just don’t make sense in the context of treating a disease that is supposed to be a viral pneumonia. Nine days ago I presume that was opening intensive care unit to treat patients with a virus causing a pneumonia that was ravaging lungs across the world starting out as something mild: cough and a sore throat, and progressively increasing in severity until ultimately ending in something called Acute Respiratory Distress Syndrome or ARDS.

I don’t know the final answer of this disease, but I’m quite sure that the ventilator is not it, that is not to say that we don’t need ventilators. We absolutely need them. They are the only way at this time that we are able to get a little more oxygen to patients who need it. But when we treat people with ARDS, we typically use ventilators to treat what’s called a respiratory failure, that is  we use the ventilator to do the work that the patient muscles can no longer do because they’re too tired to do it. These patients’ muscles work fine. I fear that we are using a false paradigm to treat a new disease that the method that we program the ventilator one based on the notion of respiratory failure as opposed to oxygen failure, that this method (and they are a great many number of methods we can use with the ventilator)  but this method being widely adopted at this very moment and every hospital in the country, which aims to increase pressure on the lungs in order to open them up, is actually doing more harm than good, and that the pressure we are providing that we are providing to lungs, we may be providing to lungs that cannot stand it, that cannot take it in, and that the ARDS that we are seeing, that the whole world is seeing, maybe nothing more than lung injury caused by the ventilator.

https://americanpressassociation.com/news-and-events/dr-cameron-kyle-ny-its-not-pneumonia-but-high-altitude-pulmonary-edema/

Will Dr. Cameron Kyle-Sidell cause a revolution in our understanding of COVID-19? He is a on the COVID-19 front line in a hospital in New York. What he is seeing challenges the whole COVID-19 paradigm. Most patients never survive the ventilators. Have scientists gotten the whole thing wrong? Are the ventilators actually harming people? Should scientists be looking for cofactors in COVID-19 patients? Is there another animal virus from China partnering with the COVID-19 virus? Is China covering up the role of African Swine Fever virus or some other virus in COVID-19? Does hydroxychloroquine work in COVID-19 patients because it has been shown to be effective against African Swine Fever or some other animal virus in COVID-19 patients?






Dr. Cameron Kyle-Sidell, a doctor treating COVID-19 patients in New York City's Maimonides Medical Center, warns that the medical community may be wrong about the nature of the coronavirus and how it is said to cause acute respiratory distress syndrome (ARDS).

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