- Joined
- Mar 1, 2020
He never published a paper on COVID-19.Do you have any good sources on Bing Liu's oxidative stress disease hypothesis and research? Searching isn't turning up much, but this matches up with the musings of another doctor I follow who specializes in oxidative stress and I want to share Bing Liu's thoughts with him.
However, based on the sort of research he used to do:

Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis - Nature Chemical Biology
Arachidonyl and adrenoyl PE phospholipids generated by ACSL4, an acyl-CoA synthase, are doubly or triply oxidized by lipoxygenases and other iron-containing sources of oxidation to promote ferroptotic cell death.

Redox lipid reprogramming commands susceptibility of macrophages and microglia to ferroptotic death - Nature Chemical Biology
Susceptibility to ferroptosis can be modulated by nitric oxide (NO•) and NO synthase iNOS and through enrichment of activated M1 macrophages. NO inhibits the lipoxygenase 15-LOX that drives production of pro-ferroptotic lipids in macrophages.
Bing Liu
Research Assistant Professor, University of Pittsburgh - Cited by 1,523 - Computational Systems Biology - Biopathway Modeling - Probabilistic Approximation - Modeling Checking - High Performance Computing
And based on what we now know to be true about the virus:

SARS-CoV-2 infection: can ferroptosis be a potential treatment target for multiple organ involvement? - Cell Death Discovery
Since the outbreak of the new coronavirus in 2019 (SARS-CoV-2), many studies have been performed to better understand the basic mechanisms and clinical features of the disease. However, uncertainties of the underlying mechanisms of multiple organ involvement remain. A substantial proportion of...

Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis?
The coronavirus 2 (SARS-CoV-2) pandemic is viciously spreading through the continents with rapidly increasing mortality rates. Current management of C…
It's easy to surmise what he would have published, if he had the opportunity.
Ferroptosis was actually a relatively new scientific discovery. The term was actually coined in 2012 by Brent Stockwell and Scott J. Dixon to describe a new type of cell death distinct from apoptosis, necroptosis, pyroptosis, et cetera. Basically, it's a form of cell death that occurs when lipid hydroperoxides accumulate due to the presence of lots and lots of unliganded iron.
Ferroptosis - Wikipedia
The hallmark feature of ferroptosis is the iron-dependent accumulation of oxidatively damaged phospholipids (i.e., lipid peroxides). This change occurs when free radicals abstract electrons from a lipid molecule (typically affecting polyunsaturated fatty acids), thereby promoting their oxidation. The primary cellular mechanism of protection against ferroptosis is mediated by glutathione peroxidase 4 (GPX4), a glutathione-dependent hydroperoxidase that converts lipid peroxides into non-toxic lipid alcohols.[1] Recently, a second parallel protective pathway was independently discovered by two labs that involves the oxidoreductase FSP1 (also known as AIFM2).[9][10] Their findings indicate that FSP1 enzymatically reduces non-mitochondrial coenzyme Q10, thereby generating a potent lipophilic antioxidant to suppresses the propagation of lipid peroxides.[9][10] A similar mechanism for a cofactor moonlighting as a diffusable antioxidant was discovered in the same year for tetrahydrobiopterin (BH4), a product of the rate-limiting enzyme GCH1.[11]
Normally, the body encloses iron atoms in a protein called ferritin that acts as a cage, keeping the iron from reacting with anything it shouldn't. Unliganded "free" iron inside the body is reactive and toxic. It's just as reactive as iron sitting and rusting on a table.

Ferritin - Wikipedia
Ferritin is a universal intracellular protein that stores iron and releases it in a controlled fashion. The protein is produced by almost all living organisms, including archaea, bacteria, algae, higher plants, and animals. It is the primary intracellular iron-storage protein in both prokaryotes and eukaryotes, keeping iron in a soluble and non-toxic form. In humans, it acts as a buffer against iron deficiency and iron overload.[3]
Ferritin is found in most tissues as a cytosolic protein, but small amounts are secreted into the serum where it functions as an iron carrier. Plasma ferritin is also an indirect marker of the total amount of iron stored in the body; hence, serum ferritin is used as a diagnostic test for iron-deficiency anemia.[4] Agregated ferritin transforms into toxic form of iron hemosiderin.[5]
Ferritin is a globular protein complex consisting of 24 protein subunits forming a hollow nanocage with multiple metal–protein interactions.[6] Ferritin that is not combined with iron is called apoferritin.
In COVID-19, this is generally happening due to the over-proliferation of NETs, or neutrophil extracellular traps:

A Multiple-Hit Hypothesis Involving Reactive Oxygen Species and Myeloperoxidase Explains Clinical Deterioration and Fatality in COVID-19
Multi-system involvement and rapid clinical deterioration are hallmarks of coronavirus disease 2019 (COVID-19) related mortality. The unique clinical phenomena in severe COVID-19 can be perplexing, and they include disproportionately severe hypoxemia ...

Neutrophil extracellular traps also promote clotting:
There's also a lot of anti-PL antibodies in COVID-19:
The formation of antiphospholipid antibodies due to NETs and oxidation is actually a hallmark of friggin' Lupus.
The interest in the role of NETs in autoimmune diseases arose with the discovery of certain mechanisms that trigger NETosis by non-infectious stimuli, such as: immune complexes, autoantibodies, cytokines, cholesterol and monosodium urate (MSU) crystals [1]. Multiple studies have shown the implication of such mechanisms in NETs formation in chronic inflammatory processes, as seen in lung [9], systemic lupus erythematosus [10], antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis [11], rheumatoid arthritis [12], gouty arthritis [13,14], familiar Mediterranean fever [15], psoriasis [16] and autoimmune coagulation disorders [17,18].
Basically, it works like this:
- Neutrophils get really irritated by something, like viruses, bacteria, fungi, or an autoimmune reaction.
- Neutrophils start suicidally hurling their guts everywhere, which consist of their own nuclear DNA, histones, highly destructive myeloperoxidase enzymes, et cetera.
- Myeloperoxidase pumps out tons of hypochlorous acid by combining hydrogen peroxide and chlorine ions in the body.
- Excess hypochlorous acid oxidizes lipids and frees iron.
- Free iron makes even more radicals, such as producing hydroxyl radicals by the Haber-Weiss and Fenton reactions.
- Oxidized lipids are recognized as foreign objects.
- Immune system attacks oxidized lipids.
Oxidation-specific epitopes (OSE), present on oxidized LDL (OxLDL), apoptotic cells, cell debris and modified proteins in the vessel wall, accumulate in response to hypercholesterolemia, and generate potent pro-inflammatory, disease-specific antigens. They represent an important class of ‘danger associated molecular patterns’ (DAMPs), against which a concerted innate immune response is directed. OSE are recognized by innate ‘pattern recognition receptors’, such as scavenger receptors present on dendritic cells and monocyte/macrophages, as well as by innate proteins, such as IgM natural antibodies and soluble proteins, such as C-reactive protein and complement factor H. These innate immune responses provide a first line of defense against atherosclerosis-specific DAMPs, and engage adaptive immune responses, provided by T and B-2 cells, which provide a more specific and definitive response. Such immune responses are ordinarily directed to remove foreign pathogens, such as those found on microbial pathogens, but when persistent or maladaptive, lead to host damage. In this context, atherosclerosis can be considered as a systemic chronic inflammatory disease initiated by the accumulation of OSE type DAMPs and perpetuated by maladaptive response of the innate and adaptive immune system. Understanding this paradigm leads to new approaches to defining cardiovascular risk and suggests new modes of therapy. Therefore, OSE have become potential targets of diagnostic and therapeutic agents. Human and murine OSE-targeting antibodies have been developed and are now being used as biomarkers in human studies and experimentally in translational applications of non-invasive molecular imaging of oxidation-rich plaques and immunotherapeutics.
The thing about oxidized lipids is that they really cause a great deal of inflammation on their own, causing adjacent cells to activate transcription factors that generate inflammatory cytokines. They're called DAMPs for a reason.
Damage-associated molecular pattern - Wikipedia
Damage-associated molecular patterns (DAMPs)[1] are molecules within cells that are a component of the innate immune response released from damaged or dying cells due to trauma or an infection by a pathogen.[2] They are also known as danger-associated molecular patterns, danger signals, and alarmin because they serve as a warning sign for the organism to alert it of any damage or infection to its cells. DAMPs are endogenous danger signals that are discharged to the extracellular space in response to damage to the cell from trauma or pathogen.[3] Once a DAMP is released from the cell, it promotes a noninfectious inflammatory response by binding to a pattern-recognition receptor.[4] Inflammation is a key aspect of the innate immune response because it is used to help mitigate future damage to the organism by removing harmful invaders from the affected area and start the healing process.[5] As an example, the cytokine IL-1α is a DAMP that originates within the nucleus of the cell, which once released to the extracellular space, binds to the PRR IL-1R, which in turn initiates an inflammatory response to the trauma or pathogen that initiated the release of IL-1α.[3] In contrast to the noninfectious inflammatory response produced by DAMPs, pathogen-associated molecular patterns initiate and perpetuate the infectious pathogen-induced inflammatory response.[6] Many DAMPs are nuclear or cytosolic proteins with defined intracellular function that are released outside the cell following tissue injury.[7] This displacement from the intracellular space to the extracellular space moves the DAMPs from a reducing to an oxidizing environment, causing their functional denaturation, resulting in their loss of function.[7] Outside of the aforementioned nuclear and cytosolic DAMPs, there are other DAMPs originated from different sources, such as mitochondria, granules, the extracellular matrix, the endoplasmic reticulum, and the plasma membrane.[3]
The tragicomedy of this is that cytokines summon more fucking neutrophils (and other granulocytes), which dump even more destructive enzymes, damaging even more lipids, generating even more cytokines, et cetera.
The reason why this was so familiar to me was because I recognized it immediately for what it was. Feedback. Feedback in mechanical systems causes jittery, weird behavior. You can see it right off, if a hydraulic system has feedback in the controls. If you put a mic up to an amplifier, you'll hear a whine because noise in the system is being recursively amplified. Same thing with these inflammatory and oxidative pathways. Without something to dampen it (and the virus removes the dampener by suppressing the body's own antioxidant defenses) the feedback could become lethal.
The people who have good endothelial health have the dampener built-in, and so, the process never reaches that point.
Living organisms are extremely complex molecular machines, and indeed, just like simple machines, we have feedback loops as well. The problem is when positive feedback loops cause us to drift away from homeostasis.

Positive and Negative Feedback Loops in Biology
Feedback loops are a natural mechanism to maintain homeostasis, by increasing the response to an event (positive feedback) or (negative feedback).

@Derka Derka
It came from the Wuhan Institute of Virology, without a doubt. That means that Fauci quite literally funded it.
Peter Daszak Eco-Fascist Who Orchestrated Global Pandemic
Peter Daszak's EcoHealth Alliance repurposed grants to Wuhan Insistitue of Virology for the Gain-of-Threat experiments on bat viruses causing Covid-19 Pandemic.

They took a bat coronavirus from caves in Yunnan province and made it more infectious to humanized hACE2 mice, which have the human version of the gene for Angiotensin Converting Enzyme 2.
That's all it would take to make a highly infectious monster SARS strain capable of ripping across the globe.
But wait, it gets worse.

SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration
The post-infection of COVID-19 includes a myriad of neurologic symptoms including neurodegeneration. Protein aggregation in brain can be considered as one of the important reasons behind the neurodegeneration. SARS-CoV-2 Spike S1 protein receptor binding ...

The post-infection of COVID-19 includes a myriad of neurologic symptoms including neurodegeneration. Protein aggregation in brain can be considered as one of the important reasons behind the neurodegeneration. SARS-CoV-2 Spike S1 protein receptor binding domain (SARS-CoV-2 S1 RBD) binds to heparin and heparin binding proteins. Moreover, heparin binding accelerates the aggregation of the pathological amyloid proteins present in the brain. In this paper, we have shown that the SARS-CoV-2 S1 RBD binds to a number of aggregation-prone, heparin binding proteins including Aβ, α-synuclein, tau, prion, and TDP-43 RRM. These interactions suggests that the heparin-binding site on the S1 protein might assist the binding of amyloid proteins to the viral surface and thus could initiate aggregation of these proteins and finally leads to neurodegeneration in brain. The results will help us to prevent future outcomes of neurodegeneration by targeting this binding and aggregation process.
Do people realize that the proline substitution that makes the SARS-CoV-2 Spike in the mRNA vaccines "safe" is on the S2 side of the S1/S2? Do they know that S1 can be proteolytically cleaved from S2 by various means? Do they know that S1 can penetrate the blood-brain barrier on its own?

The S1 protein of SARS-CoV-2 crosses the blood–brain barrier in mice - Nature Neuroscience
Rhea at al. show that intravenously injected, radiolabeled SARS-CoV-2 spike 1 protein crosses the mouse blood–brain barrier, likely through the mechanism of adsorptive transcytosis and is also taken up by peripheral tissues.

Yeah. A lot of people who took this vaccine are going to have premature Alzheimer's and dementia in a few years.
Wait a minute. What did that SPARS drill paper from 2017 say?
Reports of Corovax side effects began to gain traction. Several parents of children who experienced neurological symptoms after receiving the vaccination sued the federal government and CynBio. The lawsuit was dropped when they learned of compensation funds available through the PREP Act and the National Vaccine Injury Compensation Trust Fund.
Huh, that's interesting.

Fauci: ‘No doubt’ Trump will face surprise infectious disease outbreak
Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said there is “no doubt” Donald J. Trump will be confronted with a surprise infectious disease outbreak during his presidency. Fauci has led the NIAID for more than 3 decades, advising the past five...

Fauci: ‘No doubt’ Trump will face surprise infectious disease outbreak
archived 13 Jul 2021 23:31:20 UTC
Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said there is “no doubt” Donald J. Trump will be confronted with a surprise infectious disease outbreak during his presidency.
Fauci has led the NIAID for more than 3 decades, advising the past five United States presidents on global health threats from the early days of the AIDS epidemic in the 1980s through to the current Zika virus outbreak.
During a forum on pandemic preparedness at Georgetown University, Fauci said the Trump administration will not only be challenged by ongoing global health threats such as influenza and HIV, but also a surprise disease outbreak.
“The history of the last 32 years that I have been the director of the NIAID will tell the next administration that there is no doubt they will be faced with the challenges their predecessors were faced with,” he said.
That's very interesting.
Time to lock the motherfuckers up.