Tuesday, May 12, 2020


MUST READ! Research Reveals That COVID-19 Attacks Hemoglobin In Red Blood Cells, Rendering It Incapable Of Transporting Oxygen. Current Medical Protocols Could All Be Wrong!
Source: COVID-19 Research  Apr 09, 2020  1 month ago
COVID-19 Research: Findings from a new study released by Chinese researchers , Dr  Wenzhong Liu from Sichuan University and Dr Hualan Li from Yibin University has revealed that the Sars-CoV-2 coronavirus attacks hemoglobin in the red blood cells through a series of cellular actions, that ultimately renders the red blood cells incapable of transporting oxygen. https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173



Though the virus is able to attack the ACE2 receptors in the lung tissues and cause damage and also while cytokine storms are creating more damage, it is most probably the body’s inability to get enough oxygen along with a carbon dioxide build-up that is creating the so-called ARDS symptoms and current protocols could be all wrong, including the usage of ventilators in a non-proper manner that could actually aggravate already ‘injured’ and inflamed lungs.

Red blood cells are critical oxygen carriers to the various cells in the body. Inside the red blood cells is a molecule called hemoglobin that contains heme groups. Each of these heme groups is a molecular “ring” (porphyrin) that holds an Iron ion or FE ion. It is the FE ions that help to transport oxygen in the bloodstream depending on states of oxidation.

Typically the red blood cells pick up oxygen from the lungs to transport to other parts of the bodies.

Once inside a human host cell, the virus’s RNA also codes for a number of non-structural proteins that are created during the replication process. These proteins are not part of the virus itself but help the virus to ‘hijack” other cellular pathways or actions to facilitate its survival in the host.



The research discovered that some of these proteins are to hijack the red blood cells and remove the Iron ions from the heme groups (HBB) and replace themselves with it. This makes the hemoglobin unable to transport oxygen.

As a result, the lungs are stressed out and inflamed while the rest of the organs are also being affected. The so-called ARDS and subsequent organ failure could be attributed to this.

It was also suggested by another virologist that perhaps the coronavirus does not produce these proteins in the early stages of infection but will do so as a certain threshold is reached and only then the proteins ORF8, ORF1ab, ORF10, and ORF3a are produced.

This could explain the observation made by various ER docs (incl this one in New York) that patients tend to have elevated ferritin. Typically ferritin is used to store excess iron. If a lot of iron is 'pushed' out of heme groups and circulating around, the body produces more ferritin.

Many ER and ICU doctors are now questioning treatment protocols and also questioning the usage of ventilators in certain cases.

Though the study has not been peer-reviewed, many ER doctors are indicating that certain clinical observations tally with the study.

An interesting video to watch is by an ER doctor in New York. https://www.youtube.com/watch?v=k9GYTc53r2o&feature=youtu.be

The implications from this new study are many as certain medical protocols being adopted could be wrong and could actually be making things worse for patients.

Thailand Medical News will be reporting further on this new development.

UPDATE! 14th April 2020: A none peer reviewed pre-print by a British medical professional who has in the past been funded by The Wellcome trusts that is backed by a huge pharmaceuctical interest, is currently challenging the study of the Chinese researchers. https://chemrxiv.org/articles/Flawed_methods_in_COVID-19_Attacks_the_1-Beta_Chain_of_Hemoglobin_and_Captures_the_Porphyrin_to_Inhibit_Human_Heme_Metabolism_/12120912

We hope that more researchers and medical experts will come forth and help clear the validity of both pre-prints and we hope that more medical doctors on the ground level will also help to put forth their observations and thoughts. Please use the live chat function to submit a message and also include  your emails or use the contact submission.

For the latest on COVID-19 research, please keep logging on to Thailand Medical News

KINDLY HAVE HEART AND HELP! Please help to sustain this site. Donations are accepted via paypal: https://www.thailandmedical.news/p/sponsorship

Another new interesting study not related : https://www.nature.com/articles/s41467-020-14825-9
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Sunday, May 10, 2020

Are Cytokine Storms fueling COVID 19 deaths?

WEBMD HEALTH NEWS

Cytokine Storms May Be Fueling Some COVID Deaths

By 
coronavirus cells illustration
April 17, 2020 -- One of the great mysteries of the new coronavirus is why it causes only mild disease in most people, but turns fatal for others. In many cases, it seems the worst damage may be driven by a deranged immune response to the infection, rather than the virus itself.
In many of the sickest patients with COVID-19, their blood is teeming with high levels of immune system proteins called cytokines.
Scientists believe these cytokines are evidence of an immune response called a cytokine storm, where the body starts to attack its own cells and tissues rather than just fighting off the virus.
Cytokine storms are known to happen in autoimmune diseases like juvenile arthritis. They also occur during certain kinds of cancer treatment, and can be triggered by infections, like the flu. One study of patients who died of H1N1 influenza, for example, found that 81% had features of a cytokine storm.
Though the virus that causes COVID-19 has been circulating for only a few months, early research shows that like other infections, it, too, may cause this kind of catastrophic immune problem, and researchers say the size of the storm it triggers is gale-force.

How Cells Die

Dozens of studies have been launched to see whether drugs and devices that sop up cytokines, or prevent their release in the first place, may keep COVID-19 patients from dying.
Mukesh Kumar, PhD, is a virologist and immunologist at Georgia State University in Atlanta. He studies how the body responds to infections. In experiments in his high-security lab, he has been infecting cells and animals with SARS-CoV-2 to learn what happens.
One thing he has observed is that the virus copies itself very quickly once it infects a cell.
“That’s a lot of stress on the cell in a small amount of time,” Kumar says.
The cell begins to send SOS signals.
“When any cell senses that there is something foreign, that there is something bad happening, the immediate response of the cell is to kill itself,” he says, “It’s a protective mechanism so it doesn’t spread to other cells.”
Certain kinds of cytokines trigger cell death. When you have many cells doing this at the same time, a lot of tissue can die. In COVID-19, that tissue is mostly in the lung. As the tissue breaks down, the walls of the lungs’ tiny air sacs become leaky and fill with fluid, causing pneumonia and starving the blood of oxygen.
“Basically, most of your cells will die because of the cytokine storm. It eats away at the lung. They cannot recover,” Kumar says. “It seems to play a role in death in a large number of cases.”
When the lung becomes greatly damaged, respiratory distress syndrome follows. Then other organs start to fail.
Kumar says the amount of cytokines he sees being produced by cells in response to a SARS-CoV-2 infection is about 50 times higher than he has seen in response to Zika or West Nile virus infections.
Researchers aren’t sure what percentage of severely ill patients will die from a cytokine storm, or even why some people who are infected will go on to have this reaction, while others won’t. COVID-19 patients die from other puzzling problems, too, like heart arrhythmias.
The haywire immune attack does seem to play a role in how severe the disease is. One study of 21 COVID-19 patients admitted to a hospital in China, for example, found that the 11 patients who were classified as severely ill because they needed oxygen were much more likely than those who were deemed to be just moderately ill to have higher levels of cytokines. A separate study of 191 COVID-19 patients from two hospitals in China found that higher levels of the cytokine IL-6 were linked to the risk of death from the disease.

Trying to Prevent the 'Storm"

For some patients, drugs that may blunt the body’s attack on itself could be lifesaving.
Ryan Padgett, MD, an emergency room doctor in Washington state, began having symptoms of COVID-19 in early March. He spent nearly 2 weeks on a ventilator and an ECMO machine, and recovered after receiving IV infusions of the rheumatoid arthritis drug Actemra, which blocks the cytokine IL-6 receptor, one of several that soar in the COVID-19 cytokine storm.
Another doctor, Jeff Brown, MD, in Richmond, VA, also recovered from a serious COVID-19 infection after several doses of Actemra. His story was reported by the Richmond Times-Dispatch.
While stories like these are encouraging, researchers caution the drugs were experimental, and the cases don’t really provide solid scientific information about whether the drugs work the way we think they should, or offer any guidance about when they should be used.
To tease out that information, you need randomized controlled clinical trials, which test a drug against a placebo. Dozens of studies are underway testing Actemra and other drugs to see if they can curb the body’s over-the-top response to the virus. Kumar is planning to test another arthritis drug, called auranofin, for example. He’s seen signs that it can eliminate the virus from infected cells.
These drugs are often expensive. Actemra can cost thousands of dollars per dose, for example. While it’s widely used to help people who have autoimmune diseases, doctors are more cautious about giving it to people with active infections since it tamps down immune functions that may be needed to fight off the virus.
Max Konig, MD, a rheumatologist at Johns Hopkins University, has paused his regular research to study cytokine storms in COVID-19 patients.
He says there’s something unique about the virus that causes COVID-19.
“This virus acts different than other viruses, especially common viruses. Most people who get infected with Epstein-Barr or influenza, they don’t mount this response,” Konig says.
Yet a significant portion of patients who are hospitalized for COVID-19 have higher cytokines.
Rather than blocking cytokines, Konig thinks it may be possible to head off the storm altogether by blocking some of the chemicals that can trigger its release, which are called catecholamines.
“In those situations, we know that before the cytokines become so excessively elevated, there is a surge of catecholamines. If you prevent that surge,” he says, “the immune response just falls flat.”
In theory, this approach might prevent more damage, he says, since the cytokines never get the chance to destroy tissue.
Konig has found some preliminary evidence to support that idea. In a recent study published to medRxiv, Konig and his colleges analyzed the medical records of more than 12,673 people with acute respiratory distress syndrome, or ARDS, the same diagnosis given to many of the severely ill COVID-19 patients. These patients were not infected with the virus that causes COVID-19, however.
He found that patients who were taking medications that block the release of catecholamines -- as some kinds of blood pressure drugs do -- in the year before their diagnosis were about 20% less likely to need to be placed on a ventilator after their diagnosis, compared to others, an effect that was statistically significant.
The study hasn’t been peer-reviewed. It’s part of an effort to get scientific findings out more quickly in the midst of a pandemic. Konig says more research will be needed to find out if this approach will help keep COVID-19 patients out of the hospital, or off ventilators, in the real world.
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Saturday, May 9, 2020

WHAT I HAVE LEARNED SO FAR.




Gentle people:

 The facts I have learned so far.

  SARS-CoV-2 which creates the Covid-19 disease, infects every organ in the body and blocks the activation of the body's immune T-cells.  (To reach every organ in the body the virus must travel via blood circulation and oxygen distribution.) T cell lymphocytes are necessary for cell-mediated immunity. If made aware of the virus, T cells actively destroy infected cells as well as signaling other immune cells to participate in the immune response. A full-blown cytokine immune response may prove dangerous to people who have SARS-coV-2 and Doctors may boost the initial cytokine immune response only to then dampen the protein's response to the virus in order to buy time and avoid large amounts of cell death. 

   This is my theory and correct me if I am wrong but I have learned that Thrombi, otherwise known as blood clots, are being linked to Covid-19 and can travel to the brain to create strokes and sudden death. If tested and diagnosed with Covid-19, immediately ask your doctor to check for Thrombi in your blood. If the doctor finds thrombi, ask him to be very careful because blood thinners may not work. It is my theory that the SARSCoV-2 enters the lungs, attaches itself inside lung cells and replaces the oxygen, then blocks the immune response and takes a ride as the still living lung cells transfer the virus into the red blood circulation system. 
  The virus may be replacing oxygen in the blood with itself and if doctors use blood thinners, they may be inadvertently releasing more virus. The SARSCoV-2 has the ability to block a cells immune response and without that response cells do not sense they are being invaded. They do not immediately commit suicide but provide a living host for the virus and that may explain why the virus multiplies and travels through the blood stream uninhibited. When the virus is finally discovered by the immune system, a full blown cytokine response may occur as T cells kill both the virus and the cell host. 

  A Potassium treatment may be a life-saver.
Covid-19 Research: A research study by a medical University in Zhejiang province lead by Dr Don Chen revealed that almost all Covid-19 patients exhibited hypokalemia and that supplementation with potassium ions was one of the many factors that assisted in their recovery. 

  The virus also slowly and insidiously infects the lungs and a person who is infected with the SARS-C0V-2 is silently asphyxiated. “When any cell senses that there is something foreign, that there is something bad happening, the immediate response of the cell is to kill itself,”  says Dr. Mukesh Kumar, Ph.D.  “It’s a protective mechanism so it doesn’t spread to other cells.” 

 Certain kinds of cytokines trigger cell death. When you have many cells doing this at the same time, a lot of tissue can die. In COVID-19, that tissue is mostly in the lung. As the tissue breaks down, the walls of the lungs’ tiny air sacs become leaky and fill with fluid, causing pneumonia and starving the blood of oxygen.
“Basically, most of your cells will die because of the cytokine storm. It eats away at the lung. They cannot recover,” Kumar says. “It seems to play a role in death in a large number of cases.”

Some people do not realize they are being smothered until they start to experience shortness of breath and that is the final and most dangerous symptom of the disease. 

  It is recommended you have yourself tested if you suffer from a sore throat and repeated shaking with: chills, muscle pain, and a loss of taste and or smell. Unless you are totally asymptomatic and have completed a mile run, don't wait until you are short of breath to see your doctor because along with the other symptoms, shortness of breath means you have the last stage of the disease where your lungs are slowly filling with fluid. Many people with the virus do not feel the last stage until it is almost too late. That is the stage where doctors place a tube down your throat and into your lungs and shrug their shoulders. They have only a slight hope you will recover. Ventilators are important but one young emergency room doctor in New York is reporting that the wrong protocol is being used and that intubation may be doing more harm than good. Oxygenating is important but the manner it is being done can be the difference between life and death. 

Gentle People:

  I do not claim to be anything but a research journalist interested in presenting honest straight forward facts. What you find on my Blog is what I learn from the best scientists and research experts around the world. Information I may use to save my own life if the need should arise. Also, I do not hesitate to remove or change any research finding that does not prove relevant against the Covid-19 disease. Conflicting research is also becoming a problem! It is difficult to discern which research paper has the best information and is the most up-to-date and relevant to finding a cure for Covid-19.

1. Remember to wear a mask because the virus enters through your nose, eyes, and throat. The mask also protects others from you if you asymptomatically carry the virus.
2. Remember to wear gloves when you do your grocery shopping because you do not want to touch places where the virus may be lurking.
3. Remember to keep a six-meter distance from strangers.
4. Remember to wash your hands when entering a grocery store and when arriving home. P.S. Bananas contain Potassium.
5. If tested positive for Covi-19, remember to ask your doctor for a blood-thinning medication to counter blood thrombi's. 
6. Remember to keep a positive attitude and stay alive.

  More facts to come.
 There are now many vaccines in the trial stage and more than one are showing promise. Stay positive! 
N.J.R.

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Friday, May 8, 2020

A phase 2 clinical trial of APNO1 for treatment of COVID-19

Phase 2 Clinical Trial of APN01 for Treatment of COVID-19 Inititated

 
Phase 2 Clinical Trial of APN01 for Treatment of COVID-19 Inititated
Credit: Pixabay
 Read Time: 4 min
APEIRON Biologics AG today announced that it has received regulatory approvals in Austria, Germany, and Denmark to initiate a Phase II clinical trial of APN01 to treat COVID-19. APN01 is the recombinant form of the human angiotensin-converting enzyme 2 (rhACE2), and has the potential to block the infection of cells by the novel SARS-CoV-2 virus (COVID-19), and reduce lung injury. The Phase II trial aims to treat 200 severely infected COVID-19 patients, and the first patients are expected to be dosed shortly.

APN01 has a unique dual mode of action. APN01 imitates the human enzyme ACE2, which is used by the virus to enter cells. The virus binds to soluble ACE2/APN01, instead of ACE2 on the cell surface, which means that the virus can no longer infect the cells. At the same time, APN01 reduces the harmful inflammatory reactions in the lungs and protects against acute lung injury (ALI/acute respiratory distress syndrome (ARDS).

“Based on its unique dual mechanism of action, APN01 has the potential to be the first drug approved to treat COVID-19 that specifically targets the new SARS-CoV-2 virus,” said Peter Llewellyn-Davies, Chief Executive Officer of APEIRON Biologics AG. “We look forward to dosing the first patient in our Phase II trial shortly, with the goal of providing a safe and effective treatment option for severely infected COVID-19 patients in urgent need of help. We are grateful to the regulatory authorities in Austria, Germany and Denmark for rapidly approving this study, and for the commitment of the Austrian Government, which has agreed to fund a significant portion of this trial.”

The randomized, double-blind Phase II trial will compare APN01 to placebo in up to 200 patients at 10 sites in Austria, Denmark and Germany. The primary objective of the trial is to assess the clinical efficacy and safety of APN01 in severe COVID-19 patients using, among other criteria, the need for invasive mechanical ventilation. Secondary objectives include the evaluation of measurable biological biomarker changes following treatment with APN01.

APN01 has been shown to be safe and well-tolerated in a total of 89 healthy volunteers and patients with pulmonary arterial hypertension (PAH) and ALI/ARDS in previously completed Phase I and Phase II clinical trials. The product candidate is currently in Phase II development by APEIRON Biologics for the treatment of PAH and ALI/ARDS, which is a significant cause of COVID-19-related mortalities.

“Importantly, the novel coronavirus strain SARS-CoV-2 is a very close relative of the first SARS-CoV virus, which emerged globally in 2002, as it critically relies on the ACE2 receptor to infect the human cell,” explained Prof. Josef Penninger, MD, co-inventor of APN01, founder of APEIRON Biologics AG, member of its supervisory board and Professor at the University of British Columbia. “There is significant scientific evidence suggesting that treatment with the dual action recombinant human ACE2 can be used to treat patients with COVID-19. We are blocking the door for the virus and, at the same time, protecting tissues, which is what ACE2 normally does.”

“We are eager to participate in this very promising and critical study. APN01 is an advanced drug candidate with a very strong dual rationale that may provide an important therapeutic contribution to fight the COVID-19 pandemic," said Prof. Henning Bundgaard, principal investigator of the study and professor at the Faculty of Health and Medical Sciences at the University of Copenhagen.

The following centers, among others, will participate in the clinical trial: in Germany, the University Medical Center Hamburg-Eppendorf and the Klinikum rechts der Isar of the Technical University of Munich; in Austria, the Medical University of Vienna, the Kaiser Franz-Josef-Spital, Vienna, the Medical University of Innsbruck and the University Medical Center Salzburg; in Denmark, the National University Hospital, Rigshospitalet (Copenhagen), the Herlev Gentofte Hospital, the Hvidovre Hospital, and the Nordsjællands Hospital (Hillerød).

CTC North GmbH & Co. KG, a medical contract research organization at the University Medical Center Hamburg-Eppendorf, will be responsible for the study-specific organization of the clinical trial.

About APN01

APN01 is a recombinant human Angiotensin-Converting Enzyme 2 (rhACE2) and was developed by APEIRON biologics for the treatment of acute lung injury (ALI), acute respiratory distress syndrome (ARDS) and pulmonary arterial hypertension (PAH). After licensing from APEIRON in February 2010, GlaxoSmithKline (GSK) conducted several clinical trials from 2014 to 2017 to treat ALI/ARDS and PAH patients, lung injury being the major source of COVID-2019 mortalities, the disease caused by the new coronavirus SARS-CoV-2. In 2019, APEIRON obtained the APN01 licenses back from GSK for further clinical development, after their strategic refocusing of GSK to oncology.

The ACE2 receptor is expressed in human airway epithelia as well as lung parenchyma and was previously identified as the essential gateway used by the first SARS-CoV virus to infect human cells. ACE2 is also the critical receptor for the new virus SARS-CoV-2 to enter human cells. Thus, treatment with recombinant human ACE2 could be used to not only block viremia but also protect the lungs and other organs from injury. The drug candidate is administered intravenously as an infusion and has already shown safety and tolerability in 89 patients and volunteers.

This article has been republished from the following materials. Note: The material may have been edited for length and content. For further information, please contact the cited source.
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Thursday, May 7, 2020

Heparin or Dabigatran? That is the question?

CNN)Blood thinning drugs could help save some patients who are the most severely affected by the new coronavirus, doctors reported Wednesday.
The findings from a team at Mount Sinai Hospital could help with a troubling problem that has shocked and horrified doctors treating coronavirus patients around the world -- blood clots throughout the body that complicate an already hard-to-treat disease.
The team now says it is running experiments to see which anticoagulants may work best, and at which doses.
Covid-19 causes sudden strokes in young adults, doctors say
Covid-19 causes sudden strokes in young adults, doctors say
"The patients who received anticoagulants did better than those who didn't," Dr. Valentin Fuster, director of Mount Sinai Heart and physician-in-chief of The Mount Sinai Hospital, told CNN.
    "This has implications already. People, I believe, should treat these patients with antithrombotics," he added.

    The findings are not clear enough yet to make solid recommendations. The team noted that patients who were already severely ill were more likely to be given the blood thinners.

    Outcomes improved

    Fuster and colleagues looked at more than 2,700 patients treated at Mount Sinai in New York City, which has been hit hard by the coronavirus. Starting in March, some patients were given anti-clotting drugs based on bedside decisions made by doctors.
    The team started taking a systematic look at whether the drugs made a difference. They did, especially for patients who were put on ventilators to help them breathe.
    Doctors try to untangle why they're seeing 'unprecedented' blood clotting among Covid-19 patients
    Doctors try to untangle why they're seeing 'unprecedented' blood clotting among Covid-19 patients
    They found 29% of patients on ventilators who were given blood thinners died, compared to 63% of patients on ventilators who were not given blood thinners.
    "Our findings suggest that systemic anticoagulants may be associated with improved outcomes among patients hospitalized with Covid-19," they wrote in their report, published in the Journal of the American College of Cardiology.
    The researchers did not find that the patients who received blood thinners were significantly more likely to develop bleeding problems -- one of the risks of the drugs.
    Different patients received different doses and different types of blood thinners, so it will be important to systematically study which combination of dose and drug works best, Fuster said.

    'Clotting is a problem, without any question'

    New Covid-19 crisis hits ICUs as more patients need dialysis
    New Covid-19 crisis hits ICUs as more patients need dialysis
    His team has started such a study and going forward will test varying doses of either the classic blood thinner heparin or one of the newer, oral anticoagulant drugs such as dabigatran, a direct thrombin inhibitor.
    There's no doubt that blood clotting is a major factor in the deaths of patients with Covid-19, Fuster said.
    "We have done 75 autopsies and clotting is a problem, without any question," he said.
    "It starts with the lungs, followed by the kidneys, the heart and it ends up in the brain."
    The consequences, he said, are devastating. "It is so dramatic for all of us. You feel that you can do very little except to sustain the life of the patient," Fuster said.
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      Fuster would also like to study whether blood thinners could help patients who are not sick enough to be hospitalized. Some hospitals have reported a troubling increase in strokes among people under age 50 who would normally not be at risk. Many of these patients have later been found to be infected with the coronavirus.
      It's not yet clear why the virus is causing blood to clot, but increased clotting can be a side effect of the severe inflammation caused by some viral infections.
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