§ɦṛɛɗɗịɛ ßịⱺ𝔩ⱺɠịᵴŧ

“I would rather have questions that can’t be answered than answers that can’t be questioned.” - Rich Feynman

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Joined 3 years ago
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Cake day: March 19th, 2022

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  • In part, according to one of the head researchers, “compared to prior studies that relied solely on epidemiological data, we integrated multiple layers of information, including epidemiological data, conventional metabolic biomarkers, and cutting-edge metabolomics”.

    So in addition to finding the metadata, they also dug into the biomarkers present, which the molecular pathways are already known in detail. On top of this, metabolomics interpreted the chemical processes involving metabolites, the small molecule substrates, intermediates, and products of cell metabolism. Together, these aspects helped demonstrate the molecular consequences of ingesting animal products. The epidemiological layer assessed the incidence rate of developing T2D and then investigated how many involved the consumption of animal products for the individuals.

    This being the case, it appears to be more than just correlation, as once the metadata was found, the team investigated the causation of the metadata’s findings.


  • This is wild, TLR4 is associated with our immune system’s identification of LPS, which is found in the outer layer of gram-negative bacterial cells. So why it’s associated with the SARS-CoV-2 virus is mind-bending. For anyone interested in the TLR’s found in the immune system, here you go:

    It’s well-known NF-kB is directly associated with NOD-Like-Receptors, which produces inflammation as an inflammasome. This is what allows immune cells to target the area in numbers. But the TLR4 involvement here is puzzling, would have 100% bet against its involvement in the immune response to SARS-CoV-2!

    Edit: For clarity, S100 proteins are only found in vertebrates, and Heparan Sulfate is expressed by mammals on cell surfaces and in the surrounding extracellular matrix. HMGB1 works as a chromatin binding factor in our bodies. HSP60 + HSP70 (known as Heat Shock Proteins) are found in both prokaryotes and eukaryotes and are a response to stressful conditions. They’re basically chaperones and help control protein folding, transport, degradation, cell differentiation, and translocation. But viruses aren’t prokaryotes, so the HSPs they’re using during an infection are from the host. This helps show why I’m soo blown away with TLR4 being involved here!!











  • Ya, feedback loops are everywhere in the body. It’s basically the default for any reaction involving enzymes, which is most of them. But since heart attacks are a clogging of the passage and only result in tissue damage, I could only see this being used afterwards. But with spinal injuries, it maybe a different story.

    I’d bet the collagen is there to ensure it’s well received in the heart. As collagen is the main structural protein in the extracellular matrix of a body’s various connective tissues. It could also be a guide to ensure it goes to the right location.

    Well, it’s definitely not an antagonist, it’s more the activator of healing if anything. When used for spinal cords, it was “injected as a liquid, the therapy immediately gels into a complex network of nanofibers that mimic the extracellular matrix of the spinal cord. By matching the matrix’s structure, mimicking the motion of biological molecules and incorporating signals for receptors, the synthetic materials are able to communicate with cells.” So the motion is just used to active the tissue repair process.

    When it comes to immune cells, Th2 is only found as the primary immune pathway in the heart after cardiac arrest. Beforehand it’s mainly Th1, which is ideal to eliminate forien bacteria as well as viruses. Th2 is primarily for parasite defense, while also resulting in allergies and the regeneration of mucus. This is a contributing factor in being more likely to have a 2nd cardiac arrest after the 1st.

    Th2 vs Th1 is a complex relationship, and it’s primarily formed earlier in life. This is why some folks in the 70s used tape worms to cure aliments. It shifted the Th1 response to Th2, providing some relief, yet you had a tape worm in you…


  • The dancing molecules lead to gene expression which then starts regenerating the cartilage. They are basically an on switch for the repair. This is massive as it could prevent cardiac arrest from occurring down the road. When cardiac arrest takes place, the chances of it happening again drastically increase due to an alternation of the immune cells made in the heart.

    For my fellow nerds, cardiac arrest leads to Th2 immune cell production in the heart instead of Th1, and Th2 is great against parasites, but that’s not very helpful at keeping the heart safe. Th2 is also involved in most allergies, which isn’t ideal here either. Meaning, by turning on repair genes in the heart before things get more out of line, it will decrease the chances of cardiac arrest, which has numerous benefits immediately as well as down the road.

    Like most biological reactions, tissue repair is regulated in a feedback loop. So the dancing molecules get the process started, and once complete the body then stops, as this allows for energy conservation.