A Post Mortem Case Study: Diffuse Pulmonary Ossification and Sudden Death
Dystrophic pulmonary calcification is commonly caused by granulomatous disorders, viral infections, parasitic infections, amyloidosis, pulmonary vascular infections, coal worker’s pneumoconiosis and silicosis.
Conclusion
In conclusion, pulmonary ossification probably had some correlation with his sudden death. No discernible causes were found for this pulmonary disease either clinically or on autopsy. The pulmonary ossification is most likely not related to the cardiac findings.
Virus-driven energy theft causes all pathology. If viral infections and energy theft also are linked from calcification/ossification to the fossil record, the facts about nutrient energy-dependent life in the context of the pheromone-controlled physiology of reproduction may make even more sense to serious scientists.
Unfortunately, experimental evidence of facts based on post mortem case studies have been used by theorists to explain how mutations might somehow link virus-driven energy theft to all biodiversity. With few exceptions, theories about how dead organisms evolved into all living genera have led to beliefs in ridiculous claims that are based on de Vries 1902 definition of mutation and the assumptions of population geneticists.
This case study is available for free. If Mark Armitage was willing to cooperate in attempts to link naturally occurring DNA fluorescence from the sun’s anti-entropic virucial energy to all biodiversity, collaboration among young earth creationists might lead to convincing results in the context of the only world view that can be maintained in the context of what is known about the energy-dependent links from angstroms to ecosystems in all living genera.
See also:The identification of upregulated ebv-mir-BHRF1-2-5p targeting MALT1 and ebv-miR-BHRF1-3 in the circulation of patients with multiple sclerosis
Epstein-Barr virus (EBV) is a well-documented etiologic factor for multiple sclerosis (MS). EBV encodes at least 44 microRNAs (miRNAs) that are readily detectable in the circulation of human. Previous studies have demonstrated that EBV-encoded miRNAs regulate host immune response and may serve as biomarkers for EBV-associated diseases.
The fact that virus-driven energy theft is a well documented factor in the context of all pathology suggests that others should by now have linked nutritional epigenetics to biophysically constrained viral latency via circulating miRNAs. Clearly, the guest editors of the special issue on nutritional epigenetics in the journal “Nutrients” should not have blocked publication of this invited review:
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements.
See also: LIGHT (TNFSF14) Increases the Survival and Proliferation of Human Bone Marrow-Derived Mesenchymal Stem Cells
See also: Immunotherapeutic targeting of LIGHT/LTβR/HVEM pathway fully recapitulates the reduced cytotoxic phenotype of LIGHT-deficient T cells.