Doxycycline stops Prion Protein Infections

Topics with scientific, medical or general health related information and discussion that is not specifically related to Lyme disease.
Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Mon 19 May 2014 6:22

Lipopolysaccharide induced conversion of recombinant prion protein.
http://www.ncbi.nlm.nih.gov/pubmed/24819168

we discovered that lipopolysaccharide (LPS),+++ a component of gram-negative bacterial membranes+++ interacts with recombinant prion proteins and induces conversion to an isoform richer in β sheet at near physiological conditions as long as the LPS concentration remains above the critical micelle concentration (CMC).

What the people have been saying is being PROVEN over and over......
viewtopic.php?f=5...

viewtopic.php?f=6&t=4840&p=36246#p36246

http://www.actionlyme.org/101016.htm
THE REAL CAUSE OF AIDS IMMUNE SUPPRESSION THEY GAVE US IN VACCINES!!!

WHY ALL VACCINES ARE INFECTIVE!!!

BECAUSE YOU ARE ALREADY INFECTED WITH IMMUNE SUPPRESSING STEALTH OF EPSTEIN BORRELIOSIS!

AND so called "Normal" Prion protein.

http://www.asianscientist.com/.../scien ... er-ebv.../

http://www.ncbi.nlm.nih.gov/pubmed/24831943
---
Extensive diversity of prion strains is defined by differential chaperone interactions and distinct amyloidogenic regions.
http://www.ncbi.nlm.nih.gov/pubmed/24811344

Henrietta Lacks/IMMORTAL HeLa Cells--"The Turd in the Punchbowl" used for all vaccines for decades-- had Syphilis and they knew spirochetal prion proteins could not be killed as testified before Congress.

Coexistence of ribbon and helical fibrils originating from hIAPP20–29 revealed by quantitative nanomechanical atomic force microscopy

Uncontrolled misfolding of proteins leading to the formation of amyloid deposits

is associated with more than 40 types of diseases,

such as neurodegenerative diseases and type-2 diabetes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3581879/

SO WHEN THE CDC TRIES TO TELL YOU THE STATE OF OUR LYMEAIDS NATIONS YOU CAN TELL THEM YOU ALREADY KNOW!!!
http://www.cdc.gov/lyme/resources/May20 ... in_508.pdf
Last edited by Pandora on Sat 19 Jul 2014 18:00, edited 3 times in total.

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Mon 9 Jun 2014 20:04

Well the CDC admitted Spirochetal disease causes chronic symptoms in their lecture on persistence and called it Immunomodulatory "Complex" or some such bologna. Let's take a look at the history of Spirochetal disease and what they KNEW.

Ultrastructure of amyloid fibrils in Alzheimer's disease and Down's syndrome.
Virchows Arch B Cell Pathol Incl Mol Pathol. 1986;52(2):99-106.
Miyakawa T, Watanabe K, Katsuragi S.
Abstract

Amyloid fibrils in brains of patients with Alzheimer's disease and Down's syndrome

were examined by light and electron microscopy. In addition, replicas of amyloid fibrils produced by a quick freezing method from the brain of a patient with Down's syndrome were examined by electron microscopy.

+++++++++++++The amyloid fibrils were shown to consist of hollow rods.+++++++++++++++

These were composed of filaments arranged as a tightly coiled helix, each turn of which consisted of

+++ five globular subunits.+++

This structure appears to be similar to the prion filament observed in Creutzfeldt-Jakob disease (CJD).

The possibility therefore arises that amyloid fibrils in Alzheimer's disease and Down's syndrome may be related to the transmissible agents responsible for diseases such as CJD, kuru and Gerstmann-Sträussler Syndrome (GSS).
http://www.ncbi.nlm.nih.gov/pubmed/2878535

THEY KNEW DOWN'S, ALZHEIMERS AND AUTISM WAS CAUSED BY SPRIOCHETAL DISEASE IN 1985 AND DID NOTHING TO SAVE LIVES.
----------------------
Hollow Rods caused by spirochetal disease they were too criminal to treat or tell the truth.
http://molecularalzheimer.org/files/Cel ... tic_Bb.pdf
===
Many will not remember the early AIDS days when IT was originally called AIDS Psychosis.....
Ann Neurol. 1986 Jun;19(6):517-24.
The AIDS dementia "complex": I. Clinical features.
Navia BA, Jordan BD, Price RW.
Abstract

Of 70 autopsied patients with the acquired immune deficiency syndrome (AIDS), 46 suffered progressive dementia

that was frequently accompanied by motor

and behavioral dysfunction.

Impaired memory and concentration with psychomotor slowing represented the most common early presentation of this disorder,

but in nearly one half of the patients

"""either""" """ motor""" or """behavioral""" changes predominated.

Early motor deficits commonly included ataxia, leg weakness, tremor, and loss of fine-motor coordination,

while behavioral disturbances were manifested most commonly as apathy or withdrawal,

+++but occasionally as a frank organic psychosis.+++

The course of the disease was steadily progressive in most patients, and at times was punctuated by an abrupt acceleration.

However, in 20% of patients a more protracted indolent course was observed. In the most advanced stage of this disease, patients exhibited a stereotyped picture of severe dementia, mutism, incontinence, paraplegia, and in some cases, myoclonus. The high incidence and unique clinical presentation of this AIDS dementia complex is consistent with the emerging concept that this complication

is due to direct brain infection by the retrovirus that causes AIDS.
http://www.ncbi.nlm.nih.gov/pubmed/3729308
------------
Nor do they remember it in the over 8000 US soldiers suicides with over 2000 this yr. alone!

They gave us a make believe world of psych disease that never existed denying us the fact that over 85% of our body is loaded with assorted bacteria and never once offering you evidence of HOW those antigens used in the name of protection behaved in all the infections they knew we had. OR in those they gave us for decades!

They refuse to treat soldiers psych they caused by adding infectious junk DNA activating latent infections, just like they refuse to treat your Autism kids or those suffering Cataracts,
Gastritis from HELIcoil Bacteria, Sindumbs, and Cancers.

Bacterial tick-borne diseases caused by Bartonella spp., Borrelia burgdorferi sensu lato, Coxiella burnetii, and Rickettsia spp. among patients with cataract surgery.
http://www.ncbi.nlm.nih.gov/pubmed/24902636
Same reason they give you little purple pills instead of treating your gastritis' for the real cause!

1965 US Army -- they knew all spirochetal disease was simply "Relapsing Fever".
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC441260/
Last edited by Pandora on Mon 28 Jul 2014 2:31, edited 7 times in total.

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Mon 9 Jun 2014 21:28

In the past few years, the lab of Christian Häring, Group Leader in the Cell Biology and Biophysics Unit at EMBL Heidelberg, has found that cells use a specialised protein complex called condensin to organise the stringy chromosomes so that they can be moved around the cell.

Christian and colleagues have shown that when the cell needs to divide its genome up, condensin complexes form a ring around chromosomes and prevent the strands of DNA tangling up.


If the condensin rings are artificially cut open,
the cell still divides, but the chromosomes end up being split apart, with each daughter cell inheriting an unusable mish-mash of genetic material.
http://www.embl.de/aboutus/communicatio ... index.html

Together, the scientists found that DNA binds to condensin through unusual DNA-binding sites on the protein complex. Unlike many other DNA-binding sites, the ones on condensin do not recognise specific sequences of DNA,

and can bind anywhere on a chromosome. The team also found that when condensin binds DNA,

+++this activates the enzyme portion of one of the condensin proteins,+++

which seems to open up the ring to allow the DNA to enter (a hypothesis Christian says needs further confirmation). Then the ring closes up, leaving the DNA entrapped within the condensin ring.
-----------------
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434759/
EbfC homodimers form a structure that has been described as a pair of tweezers (56, 74).

Site-directed mutagenesis-based studies defined the extended alpha-helical “tweezers” as the DNA-binding domain,

with the space between the “tweezers” being appropriate to fit around double-stranded DNA (74).

The EbfC/YbaB orthologs of E. coli and H. influenzae bind DNA,

but their preferred binding sequences are distinct from that of B. burgdorferi EbfC (21). B. burgdorferi EbfC preferentially binds to a palindromic DNA sequence, 5′-GTnAC-3′,

where “n” can be any nucleotide (74).

The B. burgdorferi genome contains a consensus EbfC-binding site approximately every 1 kb (74). Binding by EbfC induces bending in DNA (74). The protein primarily exists as a homodimer but can also form higher-ordered structures such as tetramers and octamers, giving EbfC the potential to aggregate/bridge DNA (74). Altogether, the functional features of EbfC resemble those of many nucleoid-associated proteins (23, 74).
-----------------------------------------------------------
SIMPLY PHENOMENAL!!!
How we got HepA,B,C,D,E.F. G........from fake viral infections.

Summary The tick Ixodes ricinus is responsible for the transmission of a number of bacterial, protozoan and viral diseases to humans and animals in Europe and Northern Africa. Female I. ricinus from England, Switzerland and Italy have been found to harbour an intracellular α-proteobacterium, designated IricES1,

within the cells of the ovary. IricES1 is the only prokaryote known to exist within the mitochondria of any animal or multicellular organism.

To further examine the distribution, prevalence and mode of transmission of IricES1, we performed polymerase chain reaction screening of I. ricinus adults from 12 countries across its geographic distribution, including tick colonies that have been maintained in the laboratory for varying periods of time.

IricES1 was detected in 100% of field-collected female ticks from all countries examined (n = 128),

while 44% of males were found to be infected (n = 108). Those males that are infected appear to harbour fewer bacteria than females. Sequencing of fragments of the 16S rRNA and gyrB genes revealed very low nucleotide diversity among various populations of IricES1. Transmission of IricES1 from engorged adult females to eggs was found to be 100% (n = 31). In tick colonies that had been maintained in the laboratory for several years, a relatively low prevalence was found in females (32%; n = 25). To our knowledge, IricES1 is the most widespread and highly prevalent of any tick-associated symbiont.
http://onlinelibrary.wiley.com/doi/10.1 ... 921.f04t04

Title: Candidatus Midichloria mitochondrii, formerly IricES1, a symbiont of the tick Ixodes ricinus that resides in the host mitochondria
Authors: BANDI, CLAUDIO
SASSERA, DAVIDE (First author)
EPIS, SARA
GENCHI, CLAUDIO
MIUR subjects: VET/06 - Parassitologia e Malattie Parassitarie degli Animali
Publication date: 2010

Citation: Candidatus Midichloria mitochondrii, formerly IricES1, a symbiont of the tick Ixodes ricinus that resides in the host mitochondria

/ D. Sassera, T. Beninati, S. Epis, C. Bandi, L. Beati, M. Montagna, M. Alba, C. Genchi, L. Sacchi, N. L - In: Trends in Acarology : Proceedings of the 12th International Congress / [a cura di] M.W. Sabelis, J. Bruin. - Dordrecht : Springer, 2010. - ISBN 978-90-481-9836-8. - pp. 527-531
http://air.unimi.it/handle/2434/222868


---------------------------------------

Numerous attempts were made to develop specific serologic tests, but none of these was successful. Saline extracts of normal liver and liver from fatal cases of hepatitis were used as antigens in complement fixation82 and precipitin tests.83

Although positive tests were found in as many as one-third of the patients, they were of no practical value. A heterophile antibody absorbable on boiled guinea pig kidney and human liver was found in the acute phase serums of some patients,84

and falsely positive Wassermann and Kahn85 reactions were also described

in as many as 20 percent of some groups of patients.86

http://history.amedd.army.mil/booksdocs ... pter13.htm
---
Among the interesting phenomena encountered were tiny motile spirochetal-like filaments visualized by dark-field microscopy in the serums of patients with hepatitis.89

More than 1 hour was spent convincing their observers that they were artifacts and not the causative organisms of hepatitis.
------------------------------

You do not have to wait to get treatment for the infections they gave us, but as Christians you do have to consider those who are less fortunate and cannot afford treatment. And you do have to consider the future of all life on this planet. Big and Small.
Last edited by Pandora on Mon 28 Jul 2014 18:54, edited 2 times in total.

admin
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Re: Doxycycline stops Prion Protein Infections

Postby admin » Sat 21 Jun 2014 13:24

Topic moved from "Science" to "General Health".

Reason: not closely related to Lyme disease.

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Sat 21 Jun 2014 15:35

Prion IS Spirochetal disease. AIDS, MadCow, Lyme are all caused by the exact same thing. Stealth infections.

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Sat 28 Jun 2014 3:52

Curr Opin Cell Biol. 2014 Jun 21;29C:116-125. doi: 10.1016/j.ceb.2014.05.004. [Epub ahead of print]
Biogenesis and secretion of exosomes.
Kowal J1, Tkach M1, Théry C2.
http://www.ncbi.nlm.nih.gov/pubmed/24959705
Abstract

Although observed for several decades, the release of membrane-enclosed vesicles by cells into their surrounding environment has been the subject of increasing interest in the past few years, which led to the creation, in 2012, of a scientific society dedicated to the subject: the International Society for Extracellular Vesicles.

Convincing evidence that vesicles allow exchange of complex information fuelled this rise in interest. But it has also become clear that different types of secreted vesicles co-exist,

with different intracellular origins and modes of formation,

and thus probably different compositions and functions.

Exosomes are one sub-type of secreted vesicles.

They form inside eukaryotic cells in multivesicular compartments, and are secreted when these compartments fuse with the plasma membrane.

Interestingly, different families of molecules have been shown to allow intracellular formation of exosomes and their subsequent secretion,

which suggests that even among exosomes different sub-types exist.

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Sat 28 Jun 2014 3:55

To date, three vCJD cases and one vCJD infected but asymptomatic individual have been identified in the United Kingdom (UK), in patients that received Red Blood Cell units from donors who developed symptoms of vCJD 17 months to 3,5 years after donation [4], [5]. More recently, one preclinical vCJD case was reported in the UK in a haemophiliac patient. This patient had been treated with one batch of FVIII that was manufactured using plasma from a donor who developed vCJD six months after donating blood [6].

The total number of vCJD clinical cases identified so far remains limited (225 patients worldwide at the time of writing). However the prevalence of vCJD infected and asymptomatic individuals in the BSE exposed population remains extremely uncertain [7].

A first retrospective analysis of stored lymphoid tissues indicated that vCJD prevalence in the UK could approach 1 out of 4000 individuals, though with wide confidence intervals [8].

More recently 32,441 appendix samples, collected during surgery on patients born between 1941 and 1985 were tested for abnormal prion protein accumulation.

This study indicated a likely vCJD prevalence estimate of 1 in 2,000 in these age cohorts (95% Confidence Interval ranging from 1 in 3,500 to 1 in 1,250) [9].

http://www.plospathogens.org/.../10.../ ... at.1004202
Preclinical Detection of Variant CJD and BSE Prions in Blood
http://www.plospathogens.org

They started giving KNOWN spirochetal disease in the 1930's with the Yellow Fever Spirochetal vaccines to soldiers that won them hundreds of TB and Psych Sanitoriums and from there moved on to HeLa cells "IMMORTAL" cells used for all vaccines that came from a woman who died of Syphilis induced "seronegative" cancers.
http://www.embl.de/aboutus/communicatio ... index.html

When they added Ecoli normally found in the gut, and never should have been injected into the skin, is when they caused the REAL seronegative AIDS----Multiple Chronic Infections in immune suppression spirochetal stealth causes.

The Cellular Prion Protein Negatively Regulates Phagocytosis and Cytokine Expression in Murine Bone Marrow-Derived Macrophages.
http://www.ncbi.nlm.nih.gov/pubmed/25058617
E. coli infection induced an increase in the PRNP mRNA level.

Want to guess what causes Eboli?

Massive Chromosome shattering caused by infections and immune suppression.---
In the 1950s, doing his army service, Gajdusek helped show that the haemorrhagic fever killing US soldiers in South Korea was spread by migrating birds.

In 1954, the US Centers for Disease Control (CDC) sent him to a camp in Bolivia for native American Okinawans transported there by the US navy after the second world war.

There were so many deaths it was rumoured to be an extermination camp;

but he showed that the deaths were by natural causes and fighting.

The CDC offered him a job. "You're a screwball", said his boss, "but you're my kind of screwball."
http://www.theguardian.com/.../25/carle ... k-obituary
+++++++++++++++++++
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC280256/

Proc Natl Acad Sci U S A. May 1988; 85(10): 3575–3579.
PMCID: PMC280256

Evidence that DNA is present in abnormal tubulofilamentous structures found in scrapie.

H K Narang, D M Asher, and D C Gajdusek

-----

Lyme is closest to African Bird Borreliosis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187102/
Last edited by Pandora on Sun 27 Jul 2014 2:56, edited 6 times in total.

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Sun 29 Jun 2014 2:10

What in the world happened in and around 1985 that caused doctors and researchers to forget SCIENCE in favor of SINDUMbS, PSYCH, AND CANCER and a vaccine agenda that never offered us anything but immune suppression?

And when did chronic Meningitis become Syndromes?

http://jcm.asm.org/content/21/5/819.full.pdf

An elevated spirochete-CSF titer index was found in a
total of 91% of 45 CM patients

and also in 1 of 4 patients with
tuberculous meningitis. Two of the four patients with tuberculous
meningitis also had positive titers to our spirochete
strain in their serum samples.

This finding might indicate
some degree of antigenic cross-reactivity between this spirochete
strain and Mycobacterium sp.

A cross-reactivity between sera from patients with syphilis
and patients with CM was found in this study.

This finding is in agreement with other studies showing crossreactivity
between sera from patients with Lyme disease,
syphilis, and relapsing fever (7, 11, 14).
===================

Well I'll tell ya. When AIDS broke out in Africa and additions of vaccines activated latent infections they knew what they had done. So they just gave us more immune suppression in HepB and other vaccines so the people could suffer neurological syndromes, psych, and cancers making little to no antibodies to say pos on criminal tests and called it done.

They gave you steroids to smooth over the symptoms as you die of multiple chronic infections in immune suppression, chemo to treat the cancers they caused, and psychotherapy to convince you nothing could be done--and loads of overflowing prison's to put all the psychAIDS-- so just suck it up!

One little problem though.....Autism babies are now at the rate of 1 in 29 with every child being born with IT. Some are just more infected than others. WHO will pay to light the streets of Washington and London when there is no economy from taxes coming in?
Last edited by Pandora on Sat 19 Jul 2014 18:06, edited 3 times in total.

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Sun 29 Jun 2014 4:36

Biomolecules. 2014 May 8;4(2):510-26. doi: 10.3390/biom4020510.
Prion Fragment Peptides Are Digested with Membrane Type Matrix Metalloproteinases and Acquire Enzyme Resistance through Cu2+-Binding.
http://www.ncbi.nlm.nih.gov/pubmed/24970228
Kojima A1, Konishi M2, Akizawa T3.
Author information
Abstract

+++++++Prions are the cause of neurodegenerative disease in humans and other mammals.+++++++
----------
Coexistence of ribbon and helical fibrils originating from hIAPP20–29 revealed by quantitative nanomechanical atomic force microscopy

Uncontrolled misfolding of proteins leading to the formation of amyloid deposits

is associated with more than 40 types of diseases,

such as neurodegenerative diseases and type-2 diabetes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3581879/

Well there is at least 2 who have some.....

Pandora
Posts: 252
Joined: Tue 20 Mar 2012 14:58

Re: Doxycycline stops Prion Protein Infections

Postby Pandora » Mon 7 Jul 2014 17:54

http://www.ncbi.nlm.nih.gov/pubmed/24995389
Brain Pathol. 2014 Jul 4. doi: 10.1111/bpa.12168. [Epub ahead of print]

The brainstem pathologies of Parkinson's disease and dementia with Lewy bodies.

Seidel K1, Mahlke J, Siswanto S, Krüger R, Heinsen H, Auburger G, Bouzrou M, Grinberg L, Wicht H, Korf HW, den Dunnen W, Rüb U.
Abstract

Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are among the human synucleinopathies, which share the neuropathological features of alpha-synuclein immunoreactive neuronal and/or glial aggregations, as well as progressive neuronal loss in select brain regions (e.g. dopaminergic substantia nigra and ventral tegmental area, cholinergic pedunculopontine nucleus).

Despite a number of studies about brainstem pathologies in PD and DLB, there is currently no detailed information available regarding the presence of alpha-synuclein immunoreactive inclusions (a) in the cranial nerve, precerebellar, vestibular and oculomotor brainstem nuclei and (b) in brainstem fiber tracts and oligodendroctyes.

Therefore, we performed a detailed analysis of the alpha-synuclein immunoreactive inclusion pathologies in the brainstem nuclei

(Lewy bodies, LB; Lewy neurites, LN; coiled bodies, CB) and fiber tracts (LN, CB) of clinically diagnosed and neuropathologically confirmed PD and DLB patients.

As also reported in previous studies, LB and LN were most prevalent in the substantia nigra, ventral tegmental area, pedunculopontine and raphe nuclei, periaqueductal gray, locus coeruleus, parabrachial nuclei, reticular formation, prepositus hypoglossal, dorsal motor vagal, and solitary nuclei.

However, we for the first time demonstrated LB and LN

+++in all cranial nerve nuclei, premotor oculomotor, precerebellar and vestibular brainstem nuclei, as well as LN in all brainstem fiber tracts.+++

++++++++CB were present in nearly all brainstem nuclei and brainstem fiber tracts containing LB and/or LN.++++++

These novel brainstem findings can account for or contribute to a large variety of less well-explained PD and DLB symptoms (e.g. gait and postural instability, impaired balance and postural reflexes, falls, ingestive and oculomotor dysfunctions), and point to the occurrence of disturbances of intra-axonal transport processes

and a transneuronal spread of the underlying pathological processes of PD and DLB along anatomical pathways

+++ in a prion-like manner.+++


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