Open Call for those wishing to publish their results

Professional Forum
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Dear all,

During the conference, I encountered many people who were sitting on results which they would like to publish at some point. There were variations in the readiness of the data to be published, with some people not having data, but wanting to start collecting it, some people having data but it being disorganized, and others having publication-quality data but unfamiliar with the path to publication or lacking time and energy.

Regardless of where you are along this path, if you have results you would like to publish, I am interested in getting your work into the scientific or medical literature (My Scholar profile ‪Matthew Thomas J Halma‬ - ‪Google Scholar‬).

If this interests you, please provide a brief description of the project, your current stage, and what would be necessary to take it to publication. I do believe that the extended FLCCC network will become a powerhouse, not only for patient-empowering care, but for science and knowledge dissemination.

Thank you,

Matt

P.S. I can be reached at matt@worldcouncilforhealth.org

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“Factor analysis of VAERS data for COVID-19 injectable products: Possible ‘causal’ evidence for separate carcinogenic and non-carcinogenic factors?” Hi all, I did an interesting analysis using the VAERS data and shared it with just a couple people. The idea is presented in the 10 minute video I’ve included, along with a preliminary analysis. I’ve done a larger analysis with considerably more variables. I’ve never seen another analysis like this one, but perhaps someone else has done something like this. I’m looking for collaborators and critics who would like to work with me to finish the analysis, if there’s interest. Best,

Dave. / David Henry Peterzell PhD, PhD

PS. I’m interested in finding out where like minded people do this sort of research and communicate.

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What didn’t work? Is it that you couldn’t view it on the site or you couldn’t download it or the format was not usable for you? I can write a summary when I have some free time … but I hope this will suffice for now.

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When I click on the download link, it just takes me back to the forum. WHen I go click-to-view, it takes me to the video viewing screen but the video won’t start.

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Here’s a Vimeo link.

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David,
This is very interesting work. This can be used to approach mechanism. If there was a general downregulation of cancer surveillance mechanisms, such as by the interaction of spike protein with tumor suppressors P53 and BRCA (Checking your browser - reCAPTCHA), you would expect to see higher rates of all cancers. Possibly this is mediated metabolically, as the spike protein damages mitochondria and impairs fatty acid metabolism (Signatures of Mitochondrial Dysfunction and Impaired Fatty Acid Metabolism in Plasma of Patients with Post-Acute Sequelae of COVID-19 (PASC) - PubMed), analogous to how diabetes impairs glucose metabolism.

I’d be interested to see a grouping by lot. I think grouping by state probably captures some of that structure, as lots are typically geographically limited. I recall McKernan and Rose showed a correlation between AE rate and DNA contamination levels. This was highly preliminary. I suspect DNA would be a carcinogenic risk factor. It would also increase persistence of spike. We still really don’t know what the reservoir of spike is, could be human genome incorporation by DNA or N1mΨRNA or possibly bacterial transfection by DNA. In principle this is testable: if bacterial transfection, changing gut microbiotal composition should alter spike levels (can measure directly or possible anti-spike antibodies).

The other hypotheses are more difficult to test, you could support either by adding the DNA plasmid sequence to cell culture and seeing if the sequence survives or gets incorporated when you sequence after using single cell sequencing, or you could just add the actual injectable product to cell culture (DNA contamination and all), sequence after a delay and see if the plasmid or the ‘vaccine’ sequence show up. Main spike sequence should be identical, but plasmid sequence will have extra genetic content on both sides of spike sequence, and lack poly-A tails.

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Hello Bluebird.

I hope we can help each other with our combined research. Main difference I can see is that neither my mother nor I have it on our hands and the history as below.

I have posted in a two forums about the rash that both my mother and I developed about 6 weeks ago.

My case study-

My initial hypothetical -

  1. shedding of Covid vax nano particles/spike as studied extensively by Dr P. Kory. (Neither my mother or myself have had Covid, nor been injected with it. I did have a bad gastic flu last year but tested negative for Covid. Four days ago I had blood drawn for Covid antibodies and the nucleocapsid privately as no Dr is likely to order them through Medicare) as per discussed here if positive to nuclecapsid then infection with virus, if not, only Covid antibodies then injection (my addition ??shedding) - https://jpsaleebymd.substack.com/p/neuropasc-aka-neurological-covid?utm_source=substack&utm_medium=email#media-6a6bf92d-f838-45cb-82a2-a11d4c6041e3

  2. Bed bugs - suggested by another member on this Forum, not found, all bedding washed etc.

  3. Rainwater - filter stopped way ahead of time, many pollutants in air that land on roof, rainwater tanks getting low as no rain all summer except one night (?January but possibly not more than would have been flushed away in first flush), red dust toxin report from Alcoa mine and refinery 20 kms to the east (prevailing summer wind is from the east). Awaiting water test & hair test report.

My 94 year old mother does not suffer allergies or ill health other than dementia (not Alzheimer’s), not on medication etc whereas I suffered over 9 months of what was possibly idiopathic chronic urticaria in September 2020. No cause found, no systemic inflammation etc and biopsy - spongiosis. (I am now having other thoughts about its origin although Covid was rare in Western Australia - highly quarantined state, and I was unlikely to have come in contact with it then & pre jabs.)

We had an overseas guest stay for three weeks in February this year. One week after their departure (approximately 4 weeks after starting to drink rainwater without filtering it) both my mother and I developed an itchy rash on chest and back and then upper legs. The rash has subsided significantly in my mother but has continued in myself. I used betamethasone cream liberally for my mother, whereas I have used a mixture of fresh aloe vera plant, healing oils, and oatmeal like anti itch creams. Systemic antihistamines were tried a few times with no lasting effect (a couple of hours maybe). My mother still has some marks on her back and scratches occasionally but is not disturbed by the rash. Up until yesterday I was going mad with the itching (varies day to day and area).

I was already taking Vit D, Quecertin, & Resveratrol more recently, and a formula for varicose veins so ordered NAC, Nattokinase, Serrapeptase. I have also ordered Ivermectin from India (hope it gets through customs). See photo - ones to be taken on empty stomach are first.

I started taking the new supplements on the 30th (now taken 10 doses) and have felt no different - tired but able to push through and do gardening, cleaning etc for a 2-3 hours per day. I have used betamethasone cream a couple of times when itch unbearable including when my left lower leg was swollen and oozing (venous insufficiency). I also started wearing support stockings again which has helped. The connection with venous insufficiency is also supported by this study information on id reactions and autoeczematisation. Note the connection to T lymphocytes, proinflammatory cytokines and the link to viruses.

Autoeczematisation

"Approximately 37% of patients diagnosed with stasis dermatitis develop an id reaction (Figure 1).

The pathogenesis of AE is uncertain, but circulating T lymphocytes play a role in this reaction. Normally, T cells are activated by a release of antigens after a primary exposure to a stimulus. However, overactivation of these T cells induces autoimmune reactions such as AE.7 Activated T lymphocytes express HLA-DR and IL-2 receptor, markers elevated in the peripheral blood of patients undergoing id reactions. After treatment, the levels of activated T lymphocytes decline. An increase in the number of CD25+ T cells and a decrease in the number of suppressor T cells in the blood may occur during an id reaction.7-9 Keratinocytes produce proinflammatory cytokines, such as thymic stromal erythropoietin, IL-25, and IL-33, that activate T cells.10-12 Therefore, the most likely pathogenesis of an id reaction is that T lymphocytes are activated at the primary reaction site due to proinflammatory cytokines released by keratinocytes. These activated T cells then travel systemically via hematogenous dissemination.

The spread of activated T lymphocytes produces an eczematous reaction at secondary locations distant to the primary site.9

…

In later stages, vesicles disseminate to the legs, arms, and trunk, where they group to form papules and nummular patches in a symmetrical pattern.5,13-15 These lesions may be extremely pruritic. The pruritus may be so intense that it interrupts daily activities and disrupts the ability to fall or stay asleep.16

…

Viral infections that can cause an id reaction are herpes simplex virus and molluscum contagiosum.27-29* *Scabies, leishmaniasis, and pediculosis capitis are parasitic infections that may be etiologic.14,30,31 In addition, noninfectious stimuli besides stasis dermatitis that can produce id reactions…"

https://www.mdedge.com/dermatology/article/245813/contact-dermatitis/autoeczematization-strange-id-reaction-skin

You may find this 2021 research helpful if getting a biopsy -

Covid and eczema

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8431833/

Here are some photos of the rash on my mother (26th February - early onset & myself on the 2nd March although I had it on the 26th as well. I think it started a few days earlier on the chest). This is my left leg last night when the itch got so bad I used betamethasone cream mainly on the right leg and today both are reduced in itch and redness especially the right leg.

References on FLCCC site

Fibrin - Nattokinase can break down fibrin to potentially prevent clots, reduce BP, blood thinning, ?amyloid fibrils, Take 2000 to 4000 FU twice a day

https://imahealth.org/wp-content/uploads/2023/11/Dr.-Carmans-Guide-to-Nattokinase-.pdf

Shedding is real

https://imahealth.org/wp-content/uploads/2024/02/conf2024-Shedding%20is%20Real-kory-slides.pdf

Skin rashes one of most common symptoms

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Cortisol steigt während des Fastens. Der Stressforsche Selye beschrieb bereits in den 50er Jahren des letzten Jahrhunderts, dass Fasten eine ähnlich gute therapeutische Wirkung wie Cortison hat – ohne die negativen Nebenwirkungen.

Dass Cortison aufgrund des Fastens gestiegen ist, konnte in Studien bestätigt werden. Fasten war erfolgreich bei chronischen Schmerzstörungen und chronisch entzündlichen Erkrankungen

Nakamura Y,Walker BR, Ikuta T (2016) Systematische Überprüfung und Metaanalyse zeigen akut erhöhten Plasmacortisolspiegel nach Fasten, jedoch nicht nach geringerer Kalorienrestriktion. Stress 19 (2) 1517 doi: 10.3109/102538 PMID: 26586092