'Mad cow' proteins successfully detected in blood

[flounder]

the 25 year old study by the late great Dr. Gibbs is my favorite study.
i tend to like to read it from time to time to really bring this thing home.
you should too;

my point ;

''were exposed to the infectious agents only by their nonforced consumption''

TSS

 

[Kathy]

Explain this:

response from another thread, which I feel I need to repeat here.

Quote from TS's thread:
Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C.

The samples here were "completely ashed" no protein would remain. Therefore no prion, no virus. Yet 5 of 35 developed disease.

I found this explanation on the net for magnetism:

The way magnetism works is this: magnetism is all based on the simple principle of electrons and their behavior. Electrons move around the atom in a specific path. As they do this they are also rotating on their own axis. This movement causes an attraction or repulsion from the electrons that are unpaired. They are moving in two directions though causing a negative and positive charge. In the case of magnetism though we find that these elements have a lot of unpaired electrons, in the case of iron, Fe, there are four.

What happens then in the case of a natural magnet is the unpaired electrons line up around the magnet in a specific manner. That is all the atoms with unpaired electrons moving in a direction which causes a certain charge are lined up on one side, and all the atoms with the opposite charge move to the other side. The atoms then start to cancel each other out as they approach the center of the magnet. This all happens at the currie point where these atoms are free to move, and then when cooled and the metal becomes solid the atoms can
no longer move (barely) causing a "permanent" magnet (as in the diagram on the next page).

This same principle can be applied to a piece of metal that has been sitting next to a magnetized piece of metal in that over the long time they are together the very slow moving atoms in the metal situate in the same fashion also creating a magnet.

Could this not explain the cannibalistic - catalyse nature of the prion?

"After temperatures of 1000 degrees celcius, no transmission occurred."

600 C = 1112 F, 1000 C = 1832 F

Melting points of some metals:
tungsten 3410 C
molybdenum 2623 C
platinum 1772 C
titanium 1660 C
iron 1535 C
colbalt 1495 C
nickle 1455 C
silicon 1410 C
manganese 1246 C
uranium 1132 C
copper 1083 C
gold 1064 C
silver 962 C
strontium 769 C
barium 725 C
aluminum 660 C
magnesium 650 C
zinc 419 C
lead 327 C
cadmium 320 C

Melting point is of interest, as is the currie points of metals, and metal alloys such as Alnico - aluminum-nickel-cobalt, neodymium -iron-boron, Sumarium Cobalt. Since nothing is left after these high temperatures but ash, the answer to factor X must lie with the basic molecular components carbons, nitrogen and metals(minerals).

 

[TimH]

the 25 year old study by the late great Dr. Gibbs is my favorite study.
i tend to like to read it from time to time to really bring this thing home.
you should too;

my point ;

''were exposed to the infectious agents only by their nonforced consumption''

TSS

Your "favorite" study??? Isn't "favorite" kind of an emotional word for someone to be using in a scientific debate???

As far as your "point" goes........assuming that the monkeys actually contracted the diseases,which BTW is not made clear in the abstract(only the length of time that they were asymptomatic was mentioned ie. did they begin to display symptoms? was a positive diagnosis actually made?? this is not made clear).....this "favorite" study of yours only seems to show that, IN THIS INSTANCE, monkeys seem to be able to contract CJD(were they fed human brain material?), sheep scrapie, or Kuru by eating "known infective agents".
Never mind the lack of any explanation anywhere as to how this "infective agent" somehow passes unscathed through the digestive tract and the blood/brain barrier, but just HOW does this relate to BSE or vCJD? They are after all different diseases are they not?
Even if this particular study was valid, it fails to prove,beyond any reasonable doubt, that BSE in cattle is transmitted through feed. :roll: :roll:

 

[flounder]

IN fact, we are now finding that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE ;




Published online

January 27, 2005

Risk of oral infection with bovine spongiform

encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,

Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys

The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant

Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the ef.ciency of oral infection

and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral

transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a

BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the

other remained free of disease at 76 months. On the basis of these .ndings and data from other studies, we made a

preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public

health measures can prevent transmission of BSE to man.



snip...



BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the .rst positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula



snip...end



www.thelancet.com Published online January 27, 2005

TSS

 

[flounder]

1: Dev Biol Stand. 1993;80:9-13.

Transmission of human spongiform encephalopathies to experimental animals: comparison of the chimpanzee and squirrel monkey.

Asher DM, Gibbs CJ Jr, Sulima MP, Bacote A, Amyx H, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20992.

The agents of kuru and Creutzfeldt-Jakob disease have been consistently transmitted from patients with those diseases to chimpanzees and squirrel monkeys, as well as to other new-world primates, with average incubation periods of two or three years. No other animals have been found so consistently susceptible to the agents in human tissues. More rapid and convenient assays for the infectious agents would greatly facilitate research on the spongiform encephalopathies of humans.

PMID: 8270119 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8270119

1: J Med Primatol. 1976;5(4):205-9.


Experimental kuru in the gibbon and sooty mangabey and Creutzfeldt-Jakob disease in the pigtailed macaque. With a summary of the host range of the subacute spongiform virus encephalopathies.

Masters CL, Alpers MP, Gajdusek DC, Gibbs CJ Jr, Kakulas BA.

The experimental host range for the slow virus infections causing subacute spongiform virus encephalopathies is enlarged in primates to include the gibbon for kuru, the pigtailed macaque for Creutzfeldt-Jakob disease, and the sooty mangabey for both diseases. The report is based on neuropathological evidence of the diseases in animals with preclinical lesions. A table lists all the species to which the subacute spongiform virus encephalopathies have been transmitted.

PMID: 826636 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=826636

1: Brain. 1975 Dec;98(4):595-612.

Experimental kuru in the spider monkey. Histopathological and ultrastructural studies of the brain during early stages of incubation.

Beck E, Bak IJ, Christ JF, Gajdusek DC, Gibbs CJ Jr, Hassler R.

The brains of 10 spider monkeys inoculated intracerebrally with brain suspension from kuru patients have been studied histologically and ultrastructurally. The animals were killed by perfusion of fixative from four to forty-one weeks after inoculation, when healthy and free of neurological signs. Definite histopathological changes had occurred as early as four weeks after inoculation, when moderate numbers of bi-nucleated neurons were found within the limbic cortex, striatum, the hypothalamus and amongst the Purkinje cells of the cerebellum. At later stages of incubation a moderate loss of neurons in the cerebral and cerebellar cortex and a mild to moderate proliferation of fibrous astrocytes here and also in the hypothalamus were the most striking features. None of our cases showed either status spongiosus or the generalized astrocytic proliferation and hypertrophy, characteristic of fully developed experimental kuru, in any region of the brain. The principal ultrastructural abnormalities consisted of the formation of membrane-bound intracytoplasmic vacuoles, predominantly within dendrites, and of concentric laminar arrays derived from the endoplasmic reticulum. The former were seen in all regions of the brain examined and at all stages of incubation. Concentric laminar arrays were confined to the cerebellar nodulus, where they were most numerous in dendrites and neuronal perikarya four weeks after inoculation. Both changes are interpreted as an indication that the kuru agent acts upon the plasma membrane from an early stage onwards and, by stimulating its growth, leads to the formation of complex, membrane-bounded vacuoles and to hyperplasia of the endoplasmic reticulum. The formation of vacuoles is further regarded as the first sign of status spongiosus on an ultrastructural level. Attention is drawn to the great similarities between the changes observed in the present material and those described in the brains of patients dying from kuru and of primates with fully developed experimental kuru. The significance of the relatively rapid spread of the kuru agent throughout the brain is discussed in relation to the concept of "slow virus" diseases.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=814967

1: Adv Neurol. 1975;10:291-317.

Familial and sporadic chronic neurological degenerative disorders transmitted from man to primates.

Gajdusek DC, Gibbs CJ Jr.

PMID: 125030 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=125030

1: Intervirology. 1974;2(1):14-9.

Transmission of kuru and Creutzfeldt-Jakob disease to marmoset monkeys.

Peterson DA, Wolfe LG, Deinhardt F, Gajdusek DC, Gibbs CJ Jr.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=4207302


Gibbs CJ Jr, Gajdusek DC.
No abstract Experimental subacute spongiform virus encephalopathies in primates and other laboratory animals.
Science. 1973 Oct 5;182(107):67-8. No abstract available.
PMID: 4199733 [PubMed - indexed for MEDLINE]
35: Beck E, Daniel PM, Asher DM, Gajdusek DC, Gibbs CJ Jr.
No abstract Experimental kuru in the chimpanzee. A neuropathological study.
Brain. 1973 Sep;96(3):441-62. No abstract available.
PMID: 4200638 [PubMed - indexed for MEDLINE]
36: Gajdusek DC, Gibbs CJ Jr.
No abstract Transmission of kuru from man to rhesus monkey (Macaca mulatta) 8 and one-half years after inoculation.
Nature. 1972 Dec 8;240(5380):351. No abstract available.
PMID: 4632275 [PubMed - indexed for MEDLINE]

Gajdusek DC, Gibbs CJ Jr.
No abstractTransmission of two subacute spongiform encephalopathies of man (Kuru and Creutzfeldt-Jakob disease) to new world monkeys.
Nature. 1971 Apr 30;230(5296):588-91. No abstract available.
PMID: 4994933 [PubMed - indexed for MEDLINE]

Gajdusek DC, Rogers NG, Basnight M, Gibbs CJ Jr, Alpers M.
No abstract

1: Ann N Y Acad Sci. 1969 Jul 3;162(1):529-50.

Transmission experiments with kuru in chimpanzees and the isolation of latent viruses from the explanted tissues of affected animals.

Gajdusek DC, Rogers NG, Basnight M, Gibbs CJ Jr, Alpers M.

PMID: 5257421 [PubMed - indexed for MEDLINE]


45: Lampert PW, Earle KM, Gibbs CJ Jr, Gajdusek DC.
No abstract Experimentak kuru encephalopathy in chimpanzees and spider monkeysElectron microscopic studies.
J Neuropathol Exp Neurol. 1969 Jul;28(3):353-70. No abstract available.
PMID: 4978020 [PubMed - indexed for MEDLINE]
46: Beck E, Daniel PM, Alpers M, Gajdusek DC, Gibbs CJ Jr.
No abstract Neuropathological comparisons of experimental kuru in chimpanzees with human kuru.
Int Arch Allergy Appl Immunol. 1969;36:Suppl:553-62. No abstract available.
PMID: 5392818 [PubMed - indexed for MEDLINE]
47: Gibbs CJ Jr, Gajdusek DC, Alpers MP.
No abstract Attempts to transmit subacute and chronic neurological diseases to animals.
Int Arch Allergy Appl Immunol. 1969;36:Suppl:519-52. No abstract available.
PMID: 5392817 [PubMed - indexed for MEDLINE]
48: Gajdusek DC, Gibbs CJ Jr, Asher DM, David E.
No abstract Transmission of experimental kuru to the spider monkey (Ateles geoffreyi).
Science. 1968 Nov 8;162(854):693-4. No abstract available.
PMID: 5687819 [PubMed - indexed for MEDLINE]
49: Gibbs CJ Jr, Gajdusek DC, Asher DM, Alpers MP, Beck E, Daniel PM, Matthews WB.
No abstract Creutzfeldt-Jakob disease (spongiform encephalopathy): transmission to the chimpanzee.
Science. 1968 Jul 26;161(839):388-9. No abstract available.
PMID: 5661299 [PubMed - indexed for MEDLINE]
51: Gajdusek DC, Gibbs CJ Jr, Alpers M.
No abstract Transmission and passage of experimenal "kuru" to chimpanzees.
Science. 1967 Jan 13;155(759):212-4. No abstract available.
PMID: 6015529 [PubMed - indexed for MEDLINE]

53: Beck E, Daniel PM, Alpers M, Gajdusek DC, Gibbs CJ Jr.
No abstract Experimental "kuru" in chimpanzees. A pathological report.
Lancet. 1966 Nov 12;2(7472):1056-9. No abstract available.
PMID: 4162508 [PubMed - indexed for MEDLINE]

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract

TSS