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Phagocytosis Is What Ultimately Destroys These Now Unprotected Cells
With the Salicinium-triggered re-lease of the enzyme nagalase from the surface of any fermenting anaerobic cell, the anaerobe becomes immediately discernible to innate Immune responses. When discovery occurs, natural killer (NK) cells are rallied by the now unimpeded immune system to move in and phagocytize the obvious dysfunctioning anaerobic cell.
 In the case of a circulating tumor cell (CTC) or cancer stem cell (CSC), when phagocytosis commences, the injuring of the surface of the cell immediately brings on the signal for the voltage dependent anion channel (VDAC). In cancer cells, the HK2 enzyme is functional with VDAC, which is an outer mitochondrial membrane protein that integrates cellular energy metabolism through the regulation of the influx and efflux of metabolites and ions.32 Important: Notice the terminology "Voltage Dependent Anion Channel." This is an activity governed by electrons and protons and the importance of electrons and protons was mentioned earlier. VDAC is overexpressed in many cancer cells and it is thought to increase cancer cell survival.32,33
Also during phagocytosis, a protease known as caspase-9 is released into the cytoplasm causing apoptosis.30,34 This same reaction happens exactly the same way when a normal cell is injured. In years past there has been conjecture as to the demise of fermenting cells brought on by Salicinium. Did it kill the cancer cell as chemotherapy does or did it create an environment whereby cancer cells could be killed? The following Figure 1 showing Salicinium (liquid version – Orasal™) tested against six different lines of cells shows undeniably Salicinium disrupts the metabolic activity of the cell allowing the cell to self destruct and be phagocytized. This disruption would bring on a concomitant release of its nagalase coating, leaving the cell unprotected from outside influences and no possibility of correction from the inside. Salicinium does not "kill" fermenting cells; it exposes them for what they are.
Salicinium's Effects on Glycolysis
Glycolysis is the process by which the body produces the energy molecule ATP along with NAD and NADH. It occurs in the cells of all living organisms. The enzyme HK, mentioned earlier, is the first enzyme of the glycolysis pathway.
At the point where Salicinium enters the cell, the cytoplasm of the anaerobe has just invested ALL the energy (ATP) available to maintain its function. In the absence of Salicinium, the investment of two ATP would normally go forward to produce four ATP, two of which are recycled back into the glycolytic cycle and two of which are used to produce pyruvate, which is essential for cellular respiration in the mitochondria.
However, in the presence of the glyco benzaldehyde Salicinium, this process is altered. As mentioned earlier, Salicinium changes electrical potential. All cells exist through the movement of electrons and protons generating life. The potential of every cell is in constant flux to reach its full chemical, electrical, or bio-chemical potential.24,25 By virtue of its ability to add or take away an electron or proton to or from a cell, Salicinium halts the glycolytic pathway, disrupting NAD, NADH, and ATP development. Because only two ATPs are available at this stage, just two molecules of Salicinium are required to shutdown the glycolytic pathway.
Without glycolysis the dysregulated anaerobic cell can no longer maintain the enzymatic coating of nagalase, the enzyme blocking the development of GcMAF. Without inhibition by nagalase, the immune system once again can resume the function of joining GcMAF to a de-activated macrophage, becoming NK cells that accomplish what nature intended all along – enhancing immunity. This has been well brought out in past Salicinium articles in the Townsend Letter using graphs from BioFocus Laboratory in Germany and RGCC Laboratory in Greece.
Nagalase can easily be measured in the blood and falls concurrently as the anaerobic cells are necrosing. By the time the nagalase level reaches well into the normal range (.32-.95 nmol/ml/min) tumor markers will also be returning to normal. PET scans will show no uptake and imaging will be clear or may still show some tumor scar, which the body will break down over time.
Case Study
In the introduction to this article, I mentioned the case of a man (WW) who received his initial treatment with Salicinium in May of 2014 for diagnosis of prostate cancer. This previous prostate diagnosis was alleviated as was determined by his oncologist through biopsy.
This case continues with a recent diagnosis of bone metastasis missed on initial oncology visits. The test (PSMA PET/CT) was obtained through University of California, Davis, which noted small cellular uptake in the pelvic, rib, and scapula areas. All are Prostate 4+ metastatic primary sites, and being of a slower metabolizing tissue had not been completely resolved. Patient returned to continue oral Salicinium and IV infusions with a continued treatment plan for the metastatic diagnosis.
Testing
For Improved immune response and reactionary immune globulins, physiological targeting of Salicinium has been noted in laboratory testing with BioFocus of Germany and RGCC of Greece as well as nagalase testing from the European Lab of Nutrients in the Netherlands. All of these tests are beneficial for the screening of pathogenic cell development and reducing the development of circulating tumor and stem cells. Further viral testing should be done to rule out co-morbidities
Treatment
Commitment of 15 days IV infusion with oral on non IV days, then continuance of oral until testing shows clear. Side effects may be localized fever with improved immune function.
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References .pdf
 Virginia Osborne, ND, graduated from the accredited National College of Naturopathic Medicine (NCNM) in Portland, Oregon, following a career as an RN in critical, emergency, and cardiac experience. She is an IV therapy academic instructor and clinical department supervisor at NCNM/Natural Health Centers. She is a co-founder of International IV Nutritional Therapy for Physicians; she lectures and develops workshops on IV nutrition, anti-aging, chelation, and clinical emergency medicine; and she is the co-author of Parenteral Micronutrient Therapy. Her private practice is in Grass Valley, California, with a focus on IV treatment modalities for environmentally induced diseases. She can be reached at IVnutritionaltherapy.com.
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