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How does one overcome COVID?

Discussion in 'The Kruse Longevity Center' started by Jack Kruse, Dec 19, 2021.

  1. Jack Kruse

    Jack Kruse Administrator

    If you want to prevent heart attacks and stroke from today's Rx' you should introduce yourself to the sun and its power.
    WHAT IS LUX?
    [​IMG]
    Lux is a measure of the intensity of light as seen by the human eye. Technically speaking, one “lux” is one lumen per square meter. And to put that in perspective, a typical lighted hallway in an office building would measure about 80 lux, while direct sunlight on a bright day can measure upward of 80,000-100,000 lux.
    Successful outcomes using light therapy lamps depend upon several factors: light intensity or lux, how far a lightbox is from your eyes, and how long you sit in front of it.
    https://www.sciencedaily.com/rel.../2019/08/190808115052.htm


    Become the solar storm because your power is special. There is peace in the storm. When the storm breaks, the dragons will dance. Life isn't about waiting for the storm to pass........It's about learning to dance in the lighting network of the sun.
     
  2. Jack Kruse

    Jack Kruse Administrator

  3. Thank you - Dr. @Jack Kruse for allowing us to "add" to your thread "Overcoming COVID"

    Photodynamic Therapy: A Rational Approach Toward COVID-19 Management

    Enveloped protein negatively charged biomolecules, guanine residues, and five amino acids (tyrosine, histidine, tryptophan, cysteine, and methionine), are ideal properties of viruses that are present in SARS-CoV-2. In addition, singlet oxygen could be a good radical against SARS-CoV-2 because it is destructive towards guanine residues and histidine, tryptophan, and tyrosine amino acids. Fekrazad (2020) suggested the use of blue wavelength light with green-based photosensitizer indocyanine for COVID-19 therapy.​

    Successful Reduction of SARS-CoV-2 Viral Load by Photodynamic Therapy (PDT) Verified by QPCR – A Novel Approach in Treating Patients in Early Infection Stages

    Authors include: Hans Michael Weber - Laser Therapy and Research Center, Lauenfoerde, Germany
    https://www.medclinres.org/open-acc...d-by-qpcra-novel-approach-in-treating-pat.pdf

    Hans Michael Weber has multiple degrees in Chemistry, Biology, Medical school, etc. He has chosen Riboflavin-5-Phosphate B2 as the preferred photosensitizer.

    Due to the extensive knowledge of this naturally occurring compound, Riboflavin has been qualified by the US FDA as GRAS (Generally Regarded As Safe). It binds to the nucleic acid bases of virus RNA and upon UV-irradiation, specifically oxidizes the guanine bases in nucleic acids by a single electron transfer reaction. In followup reactions, ½ O2, hydrogen peroxide and hydroxyl radicals are formed. This results in irreversible single strand breaks in nucleic acids with damaging of the pathogens.

    Riboflavin PDT has been shown to be effective against enveloped as well as a number of non-enveloped viruses – including HIV, West Nile virus, VSV, IAV, porcine parvovirus, pseudorabies virus, human hepatitis A virus (HAV), encephalomyocarditis virus, Sindbis virus, the MERS coronavirus among others [6]. Riboflavin is the active photosensitizer in the MIRASOL Pathogen Reduction Technology System (Terumo BCT, Lakewood, CO, USA), which is used to treat platelet and plasma products. Moreover, it is also in use for pathogen reduction in whole blood. A new study published in the US in April 2020 showed that Covid-19 virus in plasma products can be eliminated below the limit of detection in a short time with Riboflavin and UV light.
    So what's a good PDT device for Dr Weber's protocol - The Quantlet
    https://www.photobiomodulation-treatment-covid19.com
     
    Last edited: Dec 28, 2021
  4. Jack Kruse

    Jack Kruse Administrator

    caroline and John Schumacher like this.
  5. Penny

    Penny New Member

  6. JanSz

    JanSz Gold

    Last edited: Jan 10, 2022
    John Schumacher and Penny like this.
  7. Penny

    Penny New Member

    Firefox is now denoting JK site as a potential security risk...
     
    JanSz likes this.
  8. Richard Watson

    Richard Watson New Member

    Yes that popped up for me too
     
  9. ND Hauf

    ND Hauf Pleb

    Same here. I can only log in on laptop. iPhone not letting me in for a few days now.
     
  10. Richard Watson

    Richard Watson New Member

    Only once did it pop on screen and that was the laptop, closed that window, opened a new one and came back on, but had to log in and then the text size was smaller.....me better go and change the password I think....
     
    ND Hauf likes this.
  11. JanSz

    JanSz Gold

    Hearing all this, I am not even trying Firefox.
    All works fine for me when I use Edge.
    -------------
    OTOH, going by my past experience, the problems are (likely) due to the stuff Jack has done to his site.
    -------------
    In my past experience, I was still able to get to the Forum going by my personal skills.
    The worst was when I was trying to communicate about webinars or PowWow's.
    There I hit the wall.

    .
    Good idea to keep old passwords.
    Sometimes the old work when the new does not.
    ------
    [​IMG]
     
    Last edited: Jan 10, 2022
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  12. In his blog CPC #61: WHAT SHOULD WE LOOK FOR IN ADVERSE EVENTS? Dr. @Jack Kruse identified a few ideas
    Long COVID is likely related to high levels of homocysteine ... leading to DNA damage.
    • The demethylation reaction leads to the formation of SAH (S- adenosylhomocysteine). SAH is a thioether (a sulfur bonded to two alkyl or aryl groups) analogous to methionine.
    • The mRNA of the spike proteins has far too much durability and this leads to the chronic elevation of the cyclins D1, E1, and A1,… because the mRNA stays around too long effecting T cells and monocytes.
    • Since the protein p21 is another key protein regulator of DNA damage induced cell death, Dr. @Jack Kruse recommends the patient’s physician understand the p21 analysis of the patient. - https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-019-0586-x
    upload_2022-1-10_19-56-26.png

    When I look at long-COVID, I think of viral scarring.
    We know Nature uses virus to edit our mRNA genome.
    The difference now is we have a “man-made” modified virus which has a 50 year history of development. The documents are being compiled and hopefully we will be able to present the findings to the courts. Whether or not this occurs is not important to the injured.
    They need a “solution” or at least a set of things they can do to improve if possible.

    The reasoning I use for postulating the idea of viral scarring can be as simple as the question ->
    Why do skin scars seem to last a life time, regrowing the same mutation in the same location year over year?
    It is as simple as any mRNA gene editing and proliferation of those cells after injury.​

    The question maybe, when we concern ourselves with viral inflectional genome damage, -> How does the COVID virus imprint a change?

    Dr. @Jack Kruse introduced IL-6, "IL-6 destroys the redox potential everywhere it is found because it raises cortisol in the stroma of organs."

    I would like to introduce IL-10.

    Before I get started, my I apologized for being a bit long winded. If you want this just skip the rational -> go to the Bottomline.

    IL-10: A Multifunctional Cytokine in Viral Infections

    The anti-inflammatory master regulator IL-10 is critical to protect the host from tissue damage during acute phases of immune responses. This regulatory mechanism, central to T cell homeostasis, can be hijacked by viruses to evade immunity. IL-10 can be produced by virtually all immune cells, and it can also modulate the function of these cells.​

    Viral infections can cause severe complications could occur due to excessive immune activation. To prevent host tissue damage, immunoregulatory cytokines control the magnitude of these immune responses. IL-10 is a key component of this cytokine system that regulates and suppresses the expression of proinflammatory cytokines during the recovery phases of infections and consequently reduces the damage caused by inflammatory cytokines [1, 2]. IL-10 binds IL-10R, a dimeric receptor composed of a high affinity IL-10R1 chain predominantly expressed on leukocytes and unique to IL-10 recognition, and an ubiquitously expressed IL-10R2 chain involved in the recognition of other cytokines from the IL-10 family (IL-22, IL-26, IL-28A, IL-28B, and IL-29) [3, 4]. The interaction of IL-10 with IL-10R triggers the Jak-STAT signaling pathway, leading to STAT1, STAT3, and, in some instances, STAT5 activation. STAT3 is critical for IL-10 effects on immune cells.​

    IL-10 is important in controlling viral immunity. Studies using lymphocytic choriomeningitis virus (LCMV) infections with strains that provoke either acute or persistent infections have helped understand the role of IL-10 in viral infections. IL-10 acts as an immunoregulator, inhibiting proinflammatory responses from innate and adaptive immunity and preventing tissue damage due to exacerbated adaptive immune response. However, viruses have evolved mechanisms that exploit the immunoregulatory function of IL-10 for immune evasion, suppression, and tolerance, promoting their own survival. As a result, viruses can persist for life in infected hosts possessing otherwise competent immune responses. The effects of pleiotropic IL-10 during the course of infection are nonetheless multiple and the subtle IL-10-governed mechanisms that balance inflammation and immunoregulation are still subject to plenty of attention.​

    Viruses typically trigger PRR engagement after pathogens-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) recognition (reviewed in). PAMP and DAMP recognition drives the antiviral state in antigen-presenting cells (APC) and type I IFN production that initiate the innate immune response. Concomitant to the proinflammatory first line of defense triggered by PRR signaling, the immunoregulatory cytokine IL-10 is induced in DCs and macrophages (Figure 1). The regulation of IL-10 production in APC is complex and depends on cell type and the integration of secondary activation signals such as type I IFN, PGE2 [39], or CD40 ligation [40] that synergize with PRR signals. Moreover, IL-10 production in APC can be antagonized by the presence of IFN-γ. In macrophages, IL-10 production can be maintained through an autocrine IFN-β feedback loop. In DC, IL-10 production depends on subtype-specific preprogrammed cytokine patterns. Kinetic studies indicate that IL-10 could be produced in late activation phase in APCs, which suggests that IL-10 balances the proinflammatory signals induced by viral PAMPs. Early IL-10 production by APCs probably limits excessive inflammation and thus potential tissue damage.​

    upload_2022-1-10_19-55-59.png

    IL-10 role in viral infections. During acute infections, proinflammatory signals are produced by DCs after recognition of pathogen patterns. In parallel, NK cells recognizing pathogen patterns and/or stimulated by proinflammatory signals further enhance inflammation. In this proinflammatory context, DC can promote antiviral T cell responses that clear the infection. Activation of DC, T cells, and NK cells also results in the production of the immunoregulatory cytokine IL-10 to balance inflammation. In this context, IL-10 expression controls immunopathology and leads to the resolution of the inflammation and T cell responses once the pathogen is cleared. During persistent infections, the virus exploits the production of IL-10 by DCs to exhaust antiviral T cells. High IL-10 levels produced by DCs suppress their antigen presenting capacity and lead to inefficient T cell activation. Chronic antigen presence further exhausts T cells and induces IL-10 production. T cells therefore become “tolerant” to viral antigens and infection persists. To establish chronicity and latent infections, the virus produces viral IL-10 homologs that favor anti-inflammatory responses. In human cytomegalovirus infection, cytomegalovirus-encoded IL-10 (cmvIL-10) and latency-associated cytomegalovirus-encoded IL-10 (LAcmvIL-10) are produced in myeloid cells and impair their function. cmvIL-10 induces hIL-10 production in DCs, macrophages, and monocytes, impairs DC differentiation, and promotes M2 polarization of macrophages. LAcmvIL-10 also promotes hIL-10 production in DCs and monocytes and impairs monocyte presenting capacity. IL-10 viral homologs induce human IL-10 (hIL-10) production in myeloid cells that contributes to impairment of their antigen presenting cell (APC) function. This in turn probably limits anti-CMV T cells responses and promotes IL-10+ T cell development. Impaired APC function permits chronic infections, while IL-10+ T cells allow latent infections to persist.​

    IL-10 production appears thus to be embedded in the activation program of T cells. Indeed, at the height of the inflammatory response and once cellular immune responses are mounted, antiviral CD4+ and CD8+ T cells become the main sources of IL-10.​

    Effector CD8+ T cells can produce IL-10 during the acute phase of influenza virus, respiratory syncytial virus, coronavirus infection, paramyxovirus simian virus 5, or vaccinia infections. The transcription factor BLIMP-1 is essential for IL-10 production in effector and memory CD8+ T cells. BLIMP-1 is induced in CD8+ T cells through T cell help and can be sustained by proinflammatory signals (IL-27), T cell growth factors (IL-2), and antiviral signaling like type I IFN. It thus appears that antiviral and inflammatory signals elicited during viral infections trigger activated T cells to produce IL-10 as a feedback regulatory mechanism that limits excessive inflammation.​

    Although T cells become the main IL-10 producers during the acute phase of infection, IL-10 effects on T cell function are usually mediated through paracrine activity on DCs and macrophages.​

    Acute and chronic LCMV infection models have been essential to comprehend IL-10’s crucial role in controlling antiviral T cell responses. IL-10 limits cytokine production and proliferation in antiviral Th1 cells.​

    It should be noted that the effects of IL-10 on CD8+ T cells could also depend on the strength of the antigenic signal, as CD8+ T cells recognizing different LCMV epitopes appear to have different IL-10 inhibition thresholds. <- This is where the COVID code sequence has been successful by limiting (reducing) or eliminating the CD8+T cell recognition antigenic signal.

    The subject of CD8+ T cell memory differentiation in LCMV infections shows it is a delicate process.​

    The Generation of an Engineered Interleukin-10 Protein With Improved Stability and Biological Function

    Interleukin-10 (IL-10) is an immunoregulatory cytokine that plays a pivotal role in modulating inflammation.​

    IL-10 is a pleiotropic cytokine that is produced by different cell types, including myeloid cells (dendritic cells, macrophages, eosinophils, neutrophils, and mast cells) and lymphoid cells (NK, B cells, and T cells) with broad anti-inflammatory activity. Macrophages and myeloid dendritic cells express IL-10 upon activation of MyD88 and TRIF-dependent TLR pathways such as TLR3 and TLR4, by stimulation with dsDNA and LPS, respectively.​

    The IL-10 showed to have an immunoregulatory effect during an infection with Toxoplasma gondii , Mycobacterium spp. , Herpes simplex virus , and malaria by ameliorating the exaggerated T helper 1 and CD8+ T cells response including.​

    Orf virus IL-10 accelerates wound healing while limiting inflammation and scarring

    Quantitative polymerase chain reaction analysis confirmed that ovIL-10 reduced the expression of key mediators of inflammation and granulation tissue formation.​

    Bottomline:

    • IL-10 on CD8+ T cells is depended on the strength of the antigenic signal, as CD8+ T cells recognizing different LCMV epitopes appear to have different IL-10 inhibition thresholds. <- This is where the COVID code sequence has been successful by limiting (reducing) or eliminating the CD8+T cell recognition antigenic signal.
    • Since the sequenced code of the COVID virus has shown the capacity to infect human cells without the detection of the CD8+ T cell recognition, the IL-10 response is not activated "well enough" to the invasion.
    • Thus, the editing of the human mRNA occurs without hindrance
    • The cell's replication code is permanently written, reducing the cell's future cells' response to this specific virus
    • All future cells will have a decrease response to COVID infection
    • The question is -> Is that a good thing?
    • What was the COVID code designed for...
    Ok so now what? Long-COVID how to treat.

    As Dr. @Jack Kruse at the bottom his blog -> to be continued.
     
    Last edited: Jan 19, 2022
    ND Hauf likes this.
  13. When we concern ourselves with viral inflectional genome damage -> We may have an idea as to How does the COVID virus imprint a change, but what can we do about it?

    The viral editing of the human genome is commonly referred as Host Single Nucleotide Polymorphisms (SNPs) “damage”. Once completed the encoded SNPs have the potentiation to affect gene expression and protein folding. Here is where we link multiple human diseases to medical relevance. Thus, the identification and analysis of different kinds of polymorphisms in the human genome has gained high importance in the research community, and an increasing number of studies have been published. These studies specifically are funded to find and manufacture vaccines. Vaccines marketed as potential agents to interrupt the editing process of a virus. “Vaccine protection” is a preemptive approach which focuses on the idea of “training” the immune system how to detect and remove the pathogen “virus” before human host cell become infected. This is where Dr. @Jack Kruse has informed his tribe -> The sun is your “vaccine”.

    This sunlight “vaccine” maybe why it is possible for a person to be exposed to COVID virus, never have symptoms nor build antibodies to the virus. We can say, “damn she’s lucky,” or was her immune system alert, ready with an offensive move against -> name the pathogen. Dr. @Jack Kruse has repeated, ‘if your “vitamin” D and melatonin levels are high enough, you won’t get -> name the disease -> cancer.’ And what was the genius of COVID development? -> cancer.

    Ok great, thanks lots… Is it possible the Long-COVID could eventually express its modified SNP as a cancer? Potentiality is not deterministic; medical probabilities of gene originating diseases only justify more funding toward the next vaccine manufacturing. We know from Dr. @Jack Kruse’s “teachings” that following his protocols just may reduce your destined fate by turning off the expression of these modified SNPs. So how long will it take, if you can’t do all of the protocols, are there some more important than others, when will you know you’re “cured?” And of-course the answer is -> It depends.

    When we evaluate, we like to know what environmental pressures are we under which potentiate a continual expression of these unfavorable SNPs’ expressions? Most likely, the environment where we “contracted” and developed Long-COVID may not be the best for our recovery. Is it possible to chart a path to “wellness?” Are Dr. @Jack Kruse’s protocols of light-water-magnetism prescriptive for Long-COVID?

    We know light has two main inputs to our health: one - direct stimulus and second - indirect energy transference. Each are driven by the cyclical rhythms and intensity of the EMFs from our sun, depending on where the stimulus occurs on our planet. Each of our hormones respond directly under these different light and darkness stimuli. Thus, light’s strength quotient and duration determine hormonal secretion. Each of our organ’s function “prescriptively”. Just as we know, “vitamin” D and melatonin hormone levels are created under different zeitgeber color spectrum, all our hormones programs’ potential success are dependent the strength of these stimuli.

    upload_2022-1-13_12-45-59.png

    We also know, secondary light inputs are indirect energy transference embodied within what we eat. Plants (including sea plants and land herbs) and animals receive direct light, convert it to their needs, which we transform to food for us. <- taking a moment here for deep respect & gratitude… Plants use melanin photosynthesis, as we do, transforming biomass with light-water-magnetism into biological life. Science tells us the most important biproducts from plants are oxygen and carbohydrates. I believe the most important product from plants are “its hormones.” These “hormone” secretions in plants are phospholipid proteins. Most of these oily “lectins” are storage in the plants’ seeds, where preserving future “off-spring” are protected using biochemical warfare. Most plants are not eatable for this reason, some may be tolerated by humans like “night-shade”: potatoes, peppers, eggplant; oxalate rich: spinach, kale, beets; and most grains: wheat, corn, etc., which also carry high levels of aflatoxins. The secondary benefit of vegetables are their enzymatic and organic mineral compounds, (when these are not destroyed by high heat cooking). These enzymes are essential for most of our biochemical processes, not just proteases in synthesis of digestion. The organic minerals are not just carbon compounds but are bond to proteins and carbohydrates, synthesized into glucosinolate isothiocyanates, for example, found in cruciferous foods.

    When we metabolize these isothiocyanates, initially through conjugation with glutathione (GSH) by glutathione S-transferases (GSTs) which forms isothiocyanate-Cys-Gly by gamma glutamyltranspeptidase (GTP). The mercapturic acid, isothiocyanate-N-acetyl cysteine (isothiocyanate-NAC) is ultimately formed by the sequential reactions catalyzed by cysteinylglycinase (CGase) and acetyltransferase (AT). Isothiocyanate-N-acetyl cysteine (isothiocyanate-NAC) inhibits the growth of cancer by inducing apoptosis.

    The success of plants are their “hormones”, not just for protecting their future off-spring, but these are the origin of most drug inhibitory effects and herbal “medicinal” stimulating attributes. The ancient white willow bark salicin acid COX inhibitor of the prostaglandin pathway, protests the tree from invasion. Medical “advancement” salicin derived aspirin to NSAIDs -> to meloxicam derived from enolic acid -> to ramatroban an antagonist immunosuppressive and potential anti-thrombotic by inhibiting the prostaglandin D2 (PGD2) in the cyclooxygenase-2 (COX-2) pathway. <- Ramatroban as a novel immunotherapy for COVID-19 - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7500620/ Since the focus of medicine is the reduction of symptoms, this may seem as a logical road to “medical” success; however, inhibiting this pathway is littered with issues for COVID -> https://journals.asm.org/doi/10.1128/JVI.00014-21

    What would happen if we asked a different question? -> Instead of inhibiting the prostaglandin mechanism of action, what would happen is we enhanced it? What plant “hormone” would facilitates this process and what would be the results?

    Prostaglandin stimulates both thromboxane and prostacyclin by the cyclooxygenase COX isoenzyme pathway, which generating its own electron-chain-transport "energy" (through proton coupled electron transfer in cyclooxygenase) from within the vascular endothelial cells, providing potential "energy" to local cells. The naturally occurring bioflavonoids from the myricaceae plant family produce myricetin. Myricetin stimulates the prostacyclin COX enzyme pathway. Thus, myricetin have been found to inhibit the secretion of inflammatory cytokines IL-6, IL-1α, TNF-α and IFN-γ as well as anti-platelet aggregation, antihypertensive, immunomodulatory, anti-inflammatory, anti-allergic, analgesic, anticancer actions and an inhibitor of SARS-CoV-2 viral replication. - https://www.frontiersin.org/articles/10.3389/fphar.2021.669642/full

    If we went head-to-head –> a new drug inhibitor of the prostaglandin pathway -> ramatroban an antagonist immunosuppressive which shuts down the COX electron-chain-transport "energy" and interferes with the mitochondria ATP production pathway, thus starving local cells of the needed energy to handle the onslaught of COVID (however, claiming anti-thrombotic receptor effects); compared with myricetin’s simulating cyclooxygenase COX isoenzyme electron-chain-transport "energy" production to its local cells. I believe myricetin will provide better therapeutic benefit to the Long-COVID patient.

    Ok, we have reviewed some basic ideas: light has two main inputs to our health: one - direct stimulus and second - indirect energy transference. So let’s make a note about light’s indirect energy transference -> Dr. @Jack Kruse’s food protocol ->

    The basic nutritional building blocks starting with fatty acids, specifically DHA; every human cell requires it. Protein folding require DHA for its building phospholipid bilayer membranes; thus, cold water “sea food”. Minerals are used with fatty acids and proteins to build every human cell; thus Dr. Jack Kruse recommends oysters. Enzymes are required in most molecular transformation; these are by plants; thus "sea weed".


    Just a note on what’s missing from his list -> foods which produce advance glycation end-products.

    Long-COVID how to treat -> to be continued.
     
    Last edited: Jan 19, 2022
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  14. ND Hauf

    ND Hauf Pleb


    Myricaceae a family of dicotyledonous plants, including evergreen and deciduous bushes and low trees, growing on acid swampy soils and in coastal regions. The leaves are sequential and simple; they range from solid forms with large or small teeth to feathery incised forms, usually lacking stipules.

    Some say yes and some say no to the benefits of white pine needle tea...I drank 3-4 glasses a day during my big C trip. No idea if it helped but the old timers in my hometown like the suramin benefits when brewed properly. See article below with some embedded links.

    Is pine needle tea the answer to covid vaccine shedding / transmission? - Nexus Newsfeed
     
  15. JanSz

    JanSz Gold

    From the study:

    Shikimic acid, when separated by HPLC, exhibited a dose-dependent inhibitory effect on platelet aggregation induced by adenosine diphosphate and collagen in rabbits. Because of the relative high content and good antiplatelet-aggregating activity of shikimic acid, the Masson pine needles can be used as a potential source of shikimic acid.
    ================================

    The same argument was used in support of ClO2 to fight existing Covid infection.
    That includes video, shoving clumps of RBC Red Blood Cells, (immediately) flying apart when in contact with Chlorine Dioxide.
    --------------------------------------------
    Later on, he extended that to a (possible) removal of the vaccines from the body.


    ...
    How to remove jab? | Jack Kruse Optimal Health Forum
    ......................................
     
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  16. During the infectious stage of COVID, Shikimic acid has interesting biological properties,displaying activity as antioxidant, anticoagulant and antithrombotic, antibacterial, antiinflamatory and analgesicagent. However, besides being important itself from the pharmacological point of view, shikimic acid has also a key
    role in the synthesis of a number of relevant compounds in the pharmacological industry and there are reports on the shikimic acid-based synthesis of anticancer agents, antibacterials, hormones or herbicides.

    Shikimic acid has inhibitory effects of on platelet aggregation and blood coagulation, and it shows antagonistic effects of shikimic acid against focal cerebral ischemia injury in rats subjected to middle cerebral artery thrombosis by affecting the metabolism of arachidonic acid.
    https://www.researchgate.net/publication/230563702_The_Medicinal_Chemistry_Of_--Shikimic_Acid
    The derivative, the 3,4-oxo-isopropylidene-shikimic acid (ISA), have an interesting biological profile. This derivative has anti-thrombosis effect, increasing the prostacyclin PGI2 release and inhibiting anti-platelet-aggregation. ISA have some protective effect on focal cerebral ischemia, decreasing the the size of cerebral infarction and the brain edema and improving the abilities of learning and memory. ISA also have significant anti-inflammatory effects which might be related to reducing the production of PGE2 and inhibiting free radical oxidation.​

    However, the mechanism of action (metabolic pathway) that shikimic acid uses seems to be still researched. What is encourages me is this molecule increasing the prostacyclin PGI2 release. ;)

    For me, I would prefer to understand the pathway within humans so we can predict if shikimic acid is an option for Long-COVID treatment.
     
    Last edited: Jan 12, 2022
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  17. caroline

    caroline Moderator

    me too
     

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