Could TSE’s Be Autoimmune Diseases?

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Could TSE’s Be Autoimmune Diseases?

Could TSE’s Be Autoimmune Diseases? 1

This is a huge post, probably have hardly any interest to anyone, about the BSE/acinetobacter hypothesis. BSE could be an autoimmune disease. Prof. Alan EBRINGER B.Sc, MD, FRCP, FRACP, FRCPath. The results of the pilot research were released in “Infection & Immunity”, a journal of the American Society of Microbiology. The mixed results of the two studies involving 157 BSE affected animals and 229 healthy ones, form the foundation of this statement. “Winter feed”, based on abattoir materials from brain, spinal cord, guts, and pancreas using their items.

The use of these “winter feed” or MBM arrangements was prohibited and since that time the incidence of BSE in British herds has significantly fallen, although never to zero levels. Several ideas have been proposed as the cause of BSE. “Normal prions” are cell-membrane proteins, which are located in all organs almost but in highest concentrations in brain cells, and are encoded with a gene found on chromosome 20 in humans.

BSE in cattle and Creutzfeldt-Jakob disease (CJD) in man. “Prions” as 3rd party, infectious particles never have been proven present in the environment. DNA, considering that many “different strains” have been explained. Similar changes were observed in patients who had died from CJD. These features of tremors, progressive loss of control of limb actions, especially hindquarters, are also quality of pets suffering from BSE.

Microscopical study of the brains of these experimental animals, demonstrated “spongiform changes” and similar observations were manufactured in the individual diseases sporadic CJD and kuru. Because the microscopical and neurological features of the condition had been sent to experimental pets, these diseases were grouped jointly under the name of “transmissible spongiform encephalopathies” or TSEs. Could be autoimmune diseases TSE? What are autoimmune diseases? “Autoimmune diseases” are characterized by the existence of antibodies, which bind to “self-tissues” and are therefore known as “autoantibodies”. In a few diseases such autoantibodies can cause injury.

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Many human being diseases, such as multiple sclerosis, juvenile diabetes, and rheumatoid arthritis are believed as types of autoimmune diseases. “Molecular mimicry” with a few of the tissues of the host. Following disease, antibodies will be produced against the invading microbe and a portion of these antibodies will bind to self-cells of the sponsor, performing as autoantibodies.

When present in high concentrations, such autoantibodies can cause injury and eventually lead to a disease relating to the organ possessing constructions resembling the invading pathogen. A classical exemplary case of such a disease is “rheumatic fever”. The microbe Streptococcus offers molecular sequences which resemble the individual heart. The patient builds up a cardiac murmur, fever, and muscle aches and is then said to suffer from “rheumatic fever”. Since autoantibodies cause injury, this can be an exemplary case of an autoimmune disease made by an infection. Rheumatic fever has pretty much vanished under western culture, over the last forty years.

Over the last thirty years, medical just work at King’s College London, has been involved with trying to find microbes, like Streptococcus in rheumatic fever, which would clarify other autoimmune diseases. The microbe Klebsiella has been found to be engaged in the condition “ankylosing spondylitis” (AS) which manifests itself as recurrent backache, especially in young people and affects some fifty percent million individuals in the U.K. When patients are in inactive stages of the condition, the known degrees of anti-bacterial antibodies fall on track levels.

Drugs which hinder cell divisions and reduce antibody production such as methotrexate, have been shown to produce therapeutic improvements in controlled studies in both diseases. Proteus in RA (10) has led to some therapeutic benefits. This was most unusual, since SCID pets readily pass away from viral and bacterial attacks, yet in this case the opposite from the expected outcome was taking place – the agent was unable to produce the condition.