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Give Purdey the respect he deserves..he pioneered this stuff

Kathy

Well-known member
Toxicology. 2007 Apr 6; [Epub ahead of print]

Pro-oxidant effects in the brain of rats concurrently exposed to uranium and stress.

Linares V, Sanchez DJ, Belles M, Albina L, Gomez M, Domingo JL.
Laboratory of Toxicology and Environmental Health, "Rovira i Virgili" University, San Lorenzo 21, 43201 Reus, Spain; Physiology Unit, School of Medicine, "Rovira i Virgili" University, San Lorenzo 21, 43201 Reus, Spain.

Metal toxicity may be associated with increased rates of reactive oxygen species (ROS) generation within the central nervous system (CNS). Although the kidney is the main target organ for uranium (U) toxicity, this metal can also accumulate in brain. In this study, we investigated the modifications on endogenous antioxidant capacity and oxidative damage in several areas of the brain of U-exposed rats. Eight groups of adult male rats received uranyl acetate dihydrate (UAD) in the drinking water at 0, 10, 20, and 40mg/kg/day for 3 months. Animals in four groups were concurrently subjected to restraint stress during 2h/day throughout the study. At the end of the experimental period, cortex, hippocampus and cerebellum were removed and processed to examine the following stress markers: reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), thiobarbituric acid reactive substances (TBARS), as well as U concentrations. The results show that U significantly accumulated in hippocampus, cerebellum and cortex after 3 months of exposure. Moreover, UAD exposure promoted oxidative stress in these cerebral tissues. In cortex and cerebellum, TBARS levels were positively correlated with the U content, while in cerebellum GSSG and GSH levels were positively and negatively correlated, respectively, with U concentrations. In hippocampus, CAT and SOD activities were positively correlated with U concentration. The present results suggest that chronic oral exposure to UAD can cause progressive perturbations on physiological brain levels of oxidative stress markers. Although at the current UAD doses restraint scarcely showed additional adverse effects, its potential influence should not be underrated.

PMID: 17493736

I wish to point out this study because it clearly shows that metal toxicity (in this case uranyl acetate dihydrate) caused an increase of antioxidant activity in the brain where-ever the uranium lodged. Chronic increases/up-regulation of the antioxidants CAT (catalase) and SOD (superoxide dismutase), glutathione etc. resulted from the ingestion of all levels of uranyl acetate dihydrate.

In the factory of our bodies [our cells] (or that of cattle, deer, sheep etc) the upregulation of these antioxidants (due to exposure to foreign metals, and/or chemicals ) will over-time DEPLETE the factory of beneficial metals which make up these antioxidant enzymes, unless of course, we replace them.

A deficiency in copper or zinc will severely limit the ability of Cu/Zn based SOD to function and protect cells from Reactive Oxygen Species. Another SOD based on manganese is concurrently functioning to protect the mitochondria inside of the cell from ROS. The up-regulation of these antioxidants would lead to a flood of metals transported to the brain cells. If the protein transporters of metals (such as MTT) are unable to bind to free copper .... and can only find at their disposal manganese.... the brain will be flooded with manganese.

Flooding the brain with manganese (or other metals like nickel), out of balance with copper, will allow for a precursor (PrPres) protein to form if manganese binds to the newly manufactured PrPC instead of copper.

Depending on the availability of metals in the brain, these newly mis-manufactured protein fragments will attach to PNCs (proteon nucleating centers consisiting of nanoparticles of metals) SEE Vitaly Vodyanoy's patent 7,138,255 USA patent office. [Method of isolation and self-assembly of small protein particles from blood and other biological materials.]

Only specific metal nanoclusters will allow for "reversible nucleation" of misfolded proteins; Vodyanoy high-lights copper/zinc/iron alloys...for such purposes. Rogue PNCs (including tungsten, uranium, lead...) will allow for attachment of these misfolded PrPres - but the process becomes irreversible due to the metal interactions between the PNC and the malformed protein fragment.

This study above demonstrates that chronic intoxication with uranium allowed Uranium to become lodged in the brain, and this metal contamination resulted in increased antioxidant activity localized to the very same locations of the rogue metal contaminant.

Prolonged up-regulated antioxidant activity combined with a mineral deficiency which depletes the Cu/Zn SOD activity and at the same time increases the Manganese SOD activity (due to increased bio-available manganese in the diet/environment, with well-documented Mn SOD response to ionizing radiation) is/was the basis of the late Mark Purdey's arguement for the cause(s) of prion-related disease.

It is about time Mark Purdey was given respect and credit for his tireless efforts to route out the causes of TSEs and other malformed protein-related disorders.
 

flounder

Well-known member
Kathy said:
It is about time Mark Purdey was given respect and credit for his tireless efforts to route out the causes of TSEs and other malformed protein-related disorders.


Subject: FATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE
Date: May 3, 2007 at 8:41 am PST

KEY FINDINGS

Organophosphate Studies

6. Studies using phosmet (an organophosphate pesticide) were
carried out throughout the project. No relationship between this
compound and the potential to cause a TSE were identified. In
studies with oral dosing of rats, it was shown that PrP expression
levels increased in the brain but there was no association between
this and formation of proteinase K (PK) resistant PrP.


snip...


12. A model of seed protein aggregation and fibril formation was
established using PrP charged with Mn2+. PrP-Mn2+ was found to
form small circular aggregates able to catalyse further protein
aggregation and fibrilisation of PrP. This model unlike other
published models (for example those of Baskakov et al.1) does not
require the presence of denaturants and is not an autocatalytic
process (i.e. the substrate of the reaction did not aggregate). The
results suggest that Mn2+ may play a role in the formation of prion
seeds

__although further studies showed that this material was not
infectious in mouse bioassay.__

snip...

24. The project also generated information concerning the relation of
TSEs to environmental factors:
• __Potentially no role for organophosphates in TSEs.__
• Increased Mn in the diet results in higher PrP levels in the
brain.
• No conclusion is yet possible in terms of the relationship
between environmental trace element concentrations and the
geographical occurrence of TSEs (classical scrapie or BSE).
• Some confirmation was provided that in some specific farms
occurrence of classical scrapie correlates with high Mn levels.


http://www.seac.gov.uk/papers/97-4.pdf


OP'S MEETING WITH PURDEY

http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf



Subject: Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route
after Persistence in Soil over Years
Date: May 16, 2007 at 10:01 am PST

PLoS ONE. 2007; 2(5): e435.
Published online 2007 May 9. doi: 10.1371/journal.pone.0000435.
Copyright Seidel et al. This is an open-access article distributed under the
terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.

Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after
Persistence in Soil over Years

Bjoern Seidel,#1* Achim Thomzig,#2 Anne Buschmann,#3 Martin H. Groschup,3
Rainer Peters,1 Michael Beekes,2 and Konstantin Terytze4
1Fraunhofer Institute for Molecular Biology und Applied Ecology (IME),
Schmallenberg, Germany
2P24 -Transmissible Spongiform Encephalopathies, Robert Koch-Institut,
Berlin, Germany
3Institute for Novel and Emerging Infectious Diseases,
Friedrich-Loeffler-Institut, Insel Riems, Germany
4German Federal Environmental Agency (Umweltbundesamt, UBA), Dessau, Germany
Joseph El Khoury, Academic Editor
Massachusetts General Hospital & Harvard Medical School, United States of
America
#Contributed equally.
* To whom correspondence should be addressed. E-mail:
[email protected]
Conceived and designed the experiments: MB AT MG AB BS RP KT. Performed the
experiments: AT AB BS RP. Analyzed the data: MB AT MG AB BS RP KT.
Contributed reagents/materials/analysis tools: MB AT. Wrote the paper: MB AT
MG AB BS KT.
Received March 21, 2007; Accepted April 18, 2007.


Abstract

The persistence of infectious biomolecules in soil
constitutes a substantial challenge. This holds particularly true with
respect to prions, the causative agents of transmissible spongiform
encephalopathies (TSEs) such as scrapie, bovine spongiform encephalopathy
(BSE), or chronic wasting disease (CWD). Various studies have indicated that
prions are able to persist in soil for years without losing their pathogenic
activity. Dissemination of prions into the environment can occur from
several sources, e.g., infectious placenta or amniotic fluid of sheep.
Furthermore, environmental contamination by saliva, excrements or
non-sterilized agricultural organic fertilizer is conceivable. Natural
transmission of scrapie in the field seems to occur via the alimentary tract
in the majority of cases, and scrapie-free sheep flocks can become infected
on pastures where outbreaks of scrapie had been observed before. These
findings point to a sustained contagion in the environment, and notably the
soil. By using outdoor lysimeters, we simulated a contamination of standard
soil with hamster-adapted 263K scrapie prions, and analyzed the presence and
biological activity of the soil-associated PrPSc and infectivity by Western
blotting and hamster bioassay, respectively. Our results showed that 263K
scrapie agent can persist in soil at least over 29 months. Strikingly, not
only the contaminated soil itself retained high levels of infectivity, as
evidenced by oral administration to Syrian hamsters, but also feeding of
aqueous soil extracts was able to induce disease in the reporter animals. We
could also demonstrate that PrPSc in soil, extracted after 21 months,
provides a catalytically active seed in the protein misfolding cyclic
amplification (PMCA) reaction. PMCA opens therefore a perspective for
considerably improving the detectability of prions in soil samples from the
field.


INTRODUCTION

Transmissible spongiform encephalopathies (TSEs) comprise a group of fatal
neurodegenerative diseases such as bovine spongiform encephalopathy (BSE) in
cows [1], chronic wasting disease (CWD) in deer (Odocoileus spp.) and elk
(Cervus elaphus nelsoni) [2]–[4], scrapie in sheep and goats [5]–[7] and
Creutzfeldt-Jakob disease (CJD) in humans [1]. The exact molecular
pathomechanisms underlying TSEs have not yet been fully elucidated but it is
generally accepted that a pathologically misfolded and/or aggregated isoform
of the normal cellular prion protein (PrP), referred to as PrPSc and PrPC,
respectively, is the key pathogenic factor for this group of diseases [1].

Among the known TSEs, only scrapie and CWD are contagious diseases which
show horizontal transmissibility under natural conditions [2], [4], [8]. CWD
is the only TSE known to affect free-ranging animals [3]. The regular
occurrence of scrapie in affected areas [7] and the spread of CWD in North
America and Korea [9], [10] among mule deer, white-tailed deer and elk
indicates that a contagion in the environment is responsible for the
occurrence of these TSEs [4], [11]–[14], and even raises the possibility of
a cross-species transmission under natural conditions. Recent findings
demonstrated that saliva from deer with CWD harbours infectivity and can
transmit this TSE upon peroral uptake [15]. Other studies pointed to
transmission of scrapie among sheep by vectors like mites, fly larvae or
other ectoparasites [16]–[19]. It has also been hypothesized that
sporadically occurring TSEs may be induced by insecticides or by a
disproportion of manganese and copper in soil leading to an enrichment of
manganese in animals [20], [21]. Alternatively, an influence of the Fe/Mn
ratio in forage has been discussed in connection with TSEs [22]. However, on
the balance of all evidence available so far, contaminated soil appears as
one of the most likely sources of infection in the natural transmission of
scrapie and possibly also CWD. It has been known for decades that sheep can
become infected with scrapie while grazing on pastures where infected sheep
have been kept before, and scrapie occurs often in areas where it has
already occurred previously [7], [8], [23]. Furthermore, Brown and Gajdusek
found that scrapie agent remains infectious after persisting in soil for 3
years as evidenced by intracerebral bioassay in Syrian hamsters [24]. The
putative transmission of scrapie and CWD via soil is also corroborated by
recent studies showing that prion infectivity binds to soil components with
high affinity [25], [26], thereby retaining its pathogenic biological
activity [25]. Thus, soil-associated TSE agents in the environment represent
a potential hazard. This holds true not least since prion infectivity
exhibits an unusually pronounced resistance against both physical and
chemical methods of inactivation, as described in detail elsewhere
[27]–[37].

The contamination of soil with TSE infectivity can occur from several
sources. Since recent studies could demonstrate that scrapie infectivity is
present in various tissues and body fluids of infected animals [38], [39],
it has been assumed that the persistent prion protein enters the environment
by contaminated excrements, birth-related tissues such as placenta, or even
whole carcasses. While a similar excretion pattern appears conceivable for
the CWD agent [40] which has also been found in saliva [15], the present
knowledge about the BSE pathology in cattle does not argue for a significant
shedding of the infectivity via faeces, urine, or during birth [41], [42].
However, small ruminants infected with BSE could supposedly spread the BSE
agent throughout the environment in a similar manner as known from
scrapie-affected sheep or CWD-affected animals [43]. Moreover,
unconventional conditions like for example the burial of animal carcasses at
larger numbers as practiced for example during the foot and mouth disease
outbreak in the UK in 2001 [44], may have fostered a dissemination of BSE
agent in the soil or ground water. Once deposited there, all three TSE
agents, BSE, scrapie, and CWD, must be assumed to persist in an infectious
state for long periods of time.

So far, the oral transmission efficacy of long-term prion contaminations in
soil have not been investigated. Therefore, we have studied the persistence
of PrPSc in the environment over time and measured its oral transmissibility
by bioassay in Syrian hamsters. With outdoor lysimeter experiments we
simulated the situation on pastures using soil spiked with scrapie-infected
hamster brain homogenate over a period of 29 months and analyzed the fate of
the prion proteins by sensitive Western blotting and, in part, also by
protein misfolding cyclic amplification (PMCA). The infectivity of such
contaminated soil samples and the respective aqueous soil extracts was
tested in the hamster bioassay.


snip...

DiscussionThe results of this research project show for the first time that
the scrapie strain 263K remains persistent in soil over a period of at least
29 months and remains highly infectious after oral application to Syrian
hamsters. It has to be pointed out that the key results of our time-course
study on the fate of PrPSc in soil have been validated, in part by examining
blinded samples, at independent laboratories.

Only a few studies have addressed the question of a persistence of prions in
soil so far [24]–[26], [47], and the results from these studies are in
principle in accordance with our observations. A pioneering study was
published by Brown and Gajdusek in 1991 [24] showing that an aqueous extract
from scrapie-contaminated soil remains infectious even after an incubation
period of three years as confirmed by hamster bioassay. However, the
infectivity studies were conducted by intracerebral injection and not by
oral application. Furthermore, the PrPSc concentration was not analyzed in
this study, so that no data are available about the proteins absorption
behavior to soil particles and about the corresponding degradation kinetics.
Most recently, PrPSc has been shown to bind to soil minerals [25] but only
short-time incubation experiments of maximal one week were conducted and,
again, bioassays were performed by the intracerebral route.

In this study we show by Western blotting a strong decrease in the amount of
extractable PrPSc over an incubation period of 29 months in soil. It is not
yet clear whether this decrease resulted from a molecular degradation of
PrPSc or a tighter binding to soil particles. Stronger binding of molecules
to soil particles with increasing incubation time is a well-known phenomenon
in soil chemistry – the so called “aging” – and influences bioavailability
and re-mobilization significantly [48], [49].

Upon feeding hamsters with scrapie contaminated soil which had been
incubated for over two years in outdoor lysimeters all animals developed
terminal scrapie after relatively short incubation times (162 dpi). In other
studies it has been well established that pure 10% (w/v) brain homogenates
from 263K scrapie hamsters cause terminal scrapie in perorally challenged
hamsters after mean incubation times of about 155–165 days with an attack
rate of 100% [50]–[53]. This indicates that scrapie-contaminated soil may
represent a potential TSE hazard for ruminants in the environment. While a
considerable excretion of infectivity has to be assumed for scrapie or BSE
infected sheep and CWD infected deer [40], [43], [54], it is generally
acknowledged that the potential environmental contamination risk represented
by BSE infected cattle is marginal, if at all present [41], [42]. On the
other hand, the burial of bovine carcasses [44] might have accidentally led
to a spill of BSE prions into the environment. Furthermore, the fact that
even feeding of aqueous extracts from scrapie-contaminated soil induced a
terminal scrapie infection in four hamsters so far suggests that surface
water or groundwater from pastures of scrapie-affected flocks may provide a
potential source of scrapie infectivity.

However, the relevance of the results obtained in this study for the field
situation should be interpreted with some caution, since only one soil type
was used and only a limited number of animals were challenged in the
bioassay. Therefore, other soil types and a larger number of animals have to
be tested in future studies to allow for a robust risk assessment.
Furthermore the exact binding properties and degradation kinetics of PrPSc
should be subject to further research. In addition, all published studies
addressing the persistence of prion infectivity in soil were performed with
scrapie prions while TSE agents causing BSE and especially CWD have not been
analyzed so far.

An intensified monitoring of PrPSc (and possibly also prion infectivity) in
the soil appears mandatory for a more precise assessment of the risks
emanating for humans and animals from prions in the environment. As shown in
this report, PrPSc extracted from soil can be used as a catalytically active
seed in the protein misfolding cyclic amplification (PMCA) reaction. This
opens a promising perspective for considerably improving the detectability
of prions in the environment.


snip...

for anyone interested in the full text of this article ;


http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1855989#pone.0000435-Prusiner1


http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&blobtype=pdf&artid=1855989



it's the TSE agent, not OPs or metals kathy. Purdey pioneered nothing but a false theory, so why give him any credit at all. ...tss
 

rkaiser

Well-known member
Talk about yer Pioneer.

This fellow named Terry set out on the Oregon trail and has never ventured off. Meanwhile - Kathy has seen the world by not only taking off the blinders on her Wagon Train Team, but the blinders on the side of her Bonnet as well.

Do you wear a Bonnet Terry dear? :wink:
 

flounder

Well-known member
rkaiser said:
Talk about yer Pioneer.

This fellow named Terry set out on the Oregon trail and has never ventured off. Meanwhile - Kathy has seen the world by not only taking off the blinders on her Wagon Train Team, but the blinders on the side of her Bonnet as well.

Do you wear a Bonnet Terry dear? :wink:


come on rkaiser, your just jeolous that im not wearing a dress like you.
ill keep my bonnet ;-)


as far as kathy's continuous rant about metals causing TSEs ;



kathy wrote ;


...... is/was the basis of the late Mark Purdey's arguement for the cause(s) of prion-related disease.

It is about time Mark Purdey was given respect and credit for his tireless efforts to route out the causes of TSEs and other malformed protein-related disorders. ........end



METALS DO NOT CAUSE TSE.

please show me and everyone else here a transmission study of metals that confirm metals to be infectious ???

on the other hand, it has been proven that TSE are transmissible and infectious. ...TSS
 

Kathy

Well-known member
Terry,

The studies that you and I, and the rest of the ranchers board need to see, want to review and guess exist.... are classified.

That doesn't stop us from looking at other examples, and this is what I try to post like:

Dr. A. Hamir's lead toxicosis study on dogs which demonstrated feeding lead to dogs caused spongiform of the brain... Did Dr. Hamir continue on and try to spread the disease via "intracranial injection of brain homogenate" from these dogs to genetically modified mice expressing dog prion proteins?

If he did, its hasn't been published. BUT, it would make for an interesting paper.

As for OPs, my God your a broken record Terry....

OPs cause reactive oxygen species generation in the body and they shut down mechanisms involving cholinesterase. These scientists below, have also shown that exposure of neonatal rats at levels well below toxicity caused "significant differences for >60% of 252 genes" examined. These researchers "evaluated gene expression profiles in brainstem and forebrain."

This study may turn out to be one of the most important papers published to date, regarding low level organophosphate toxicity. Read it and weep, Flounder!


Brain Res Bull. 2007 May 30;72(4-6):232-74. Epub 2007 Jan 25.

Comparative developmental neurotoxicity of organophosphates in vivo: Transcriptional responses of pathways for brain cell development, cell signaling, cytotoxicity and neurotransmitter systems.

Slotkin TA, Seidler FJ.
Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.

Organophosphates affect mammalian brain development through a variety of mechanisms beyond their shared property of cholinesterase inhibition. We used microarrays to characterize similarities and differences in transcriptional responses to chlorpyrifos and diazinon, assessing defined gene groupings for the pathways known to be associated with the mechanisms and/or outcomes of chlorpyrifos-induced developmental neurotoxicity. We exposed neonatal rats to daily doses of chlorpyrifos (1mg/kg) or diazinon (1 or 2mg/kg) on postnatal days 1-4 and evaluated gene expression profiles in brainstem and forebrain on day 5; these doses produce little or no cholinesterase inhibition. We evaluated pathways for general neural cell development, cell signaling, cytotoxicity and neurotransmitter systems, and identified significant differences for 60% of 252 genes. Chlorpyrifos elicited major transcriptional changes in genes involved in neural cell growth, development of glia and myelin, transcriptional factors involved in neural cell differentiation, cAMP-related cell signaling, apoptosis, oxidative stress, excitotoxicity, and development of neurotransmitter synthesis, storage and receptors for acetylcholine, serotonin, norepinephrine and dopamine. Diazinon had similar effects on many of the same processes but also showed major differences from chlorpyrifos. Our results buttress the idea that different organophosphates target multiple pathways involved in neural cell development but also that they deviate in key aspects that may contribute to disparate neurodevelopmental outcomes. Equally important, these pathways are compromised at exposures that are unrelated to biologically significant cholinesterase inhibition and its associated signs of systemic toxicity. The approach used here demonstrates how planned comparisons with microarrays can be used to screen for developmental neurotoxicity.

PMID: 17452286
 

flounder

Well-known member
Kathy said:
Terry,

The studies that you and I, and the rest of the ranchers board need to see, want to review and guess exist.... are classified.
[/quote]


your kidding me right???

i suppose that all the governments around the globe would put into jeopardy there precious livestock industry with the ruminant feed theory and the ramifications from that just to cover up metals, ops, and nuclear proliferation. get real. again, when the UK and other countries stopped feeding ruminant protein, there BSE cases dramatically declined. please explain that kathy ??? i do not dispute that OPs and other pesticides, metals, are toxic to humans. i have said this before. but your argument is that you believe OPs, pesticides, metals, nuclear proliferation, and just about everything else, except ruminant to ruminant feeding cause TSEs. this is incorrect. there is not one shred of evidence to date. amplification and transmission of ruminant feed has been proven to amplify and in the end reduce the spread of TSEs. all one has to do is look at the reduction of BSE in the UK and other BSE countries that had an effective feed ban. the statistics do not lie. for you to continue to dispute these facts and your claim of everything from nuclear weapons, to OPs, to metals causing TSEs, when it's been proven otherwise, only shows how desperate you are. you sure your not a feeder/packer ;-) i applaud your efforts to bring attention to these deadly toxins, but again, they are not the cause of TSEs. you have shown us absolutely nothing (scientifically) that would support this. by arguing this nonsense, only hinders your efforts to show the real factors of these dangerous toxins, even though they do not cause TSEs. The potential for neurological effects from OPs and or metals is real, but when you lump TSEs in there, you negate any credibility to your argument, because OPs and or metals do not cause TSEs. when it comes to metals and OPs contamination, and the potential for human health risk, im on your side girlfriend, but when you try to claim that they cause any TSE, you loose me and most everyone else that has ever studied anything on these topics, unless you wear a dress like rkaiser, and then you will believe anything ;-)


NOW, i think you might find this study interesting kathy, NOTHING in there about TSEs and OPs causing them though, but still, a most disturbing study. ...TSS


Organophosphate Pesticide Exposure and Neurodevelopment in
Young Mexican-American Children
Brenda Eskenazi,1 Amy R. Marks,1 Asa Bradman,1 Kim Harley,1 Dana B. Barr,2 Caroline Johnson,1 Norma Morga,3
and Nicholas P. Jewell1
1Center for Children’s Environmental Health Research, School of Public Health, University of California, Berkeley, California, USA;
2National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA; 3Center for the Health
Assessment of Mothers and Children of Salinas, Clinica de Salud del Valle de Salinas, Berkeley, California, USA
BACKGROUND: Organophosphate (OP) pesticides are widely used in agriculture and homes. Animal
studies suggest that even moderate doses are neurodevelopmental toxicants, but there are few studies
in humans.
OBJECTIVES: We investigated the relationship of prenatal and child OP urinary metabolite levels
with children’s neurodevelopment.
METHODS: Participating children were from a longitudinal birth cohort of primarily Latino farmworker
families in California. We measured six nonspecific dialkylphosphate (DAP) metabolites in
maternal and child urine as well as metabolites specific to malathion (MDA) and chlorpyrifos
(TCPy) in maternal urine. We examined their association with children’s performance at 6 (n =
396), 12 (n = 395), and 24 (n = 372) months of age on the Bayley Scales of Infant Development
[Mental Development (MDI) and Psychomotor Development (PDI) Indices] and mother’s report
on the Child Behavior Checklist (CBCL) (n = 356).
RESULTS: Generally, pregnancy DAP levels were negatively associated with MDI, but child measures
were positively associated. At 24 months of age, these associations reached statistical significance [per
10-fold increase in prenatal DAPs: β = –3.5 points; 95% confidence interval (CI), –6.6 to –0.5; child
DAPs: β = 2.4 points; 95% CI, 0.5 to 4.2]. Neither prenatal nor child DAPs were associated with
PDI or CBCL attention problems, but both prenatal and postnatal DAPs were associated with risk
of pervasive developmental disorder [per 10-fold increase in prenatal DAPs: odds ratio (OR) = 2.3,
p = 0.05; child DAPs OR = 1.7, p = 0.04]. MDA and TCPy were not associated with any outcome.
CONCLUSIONS: We report adverse associations of prenatal DAPs with mental development and pervasive
developmental problems at 24 months of age. Results should be interpreted with caution
given the observed positive relationship with postnatal DAPs.
KEY WORDS: Bayley Scales of Infant Development, Child Behavior Checklist, DAPs, farmworker,
Mexican Americans, neurodevelopment, organophosphates, pervasive developmental disorder,
pesticides. Environ Health Perspect 115:792–798 (2007). doi:10.1289/ehp.9828 available via
http://dx.doi.org/ [Online 4 January 2007]

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867968&blobtype=pdf


TSS
 

Kathy

Well-known member
Brain Res Bull. 2007 May 30;72(4-6):232-74. Epub 2007 Jan 25.

Comparative developmental neurotoxicity of organophosphates in vivo: Transcriptional responses of pathways for brain cell development, cell signaling, cytotoxicity and neurotransmitter systems.

Slotkin TA, Seidler FJ.
Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.

Organophosphates affect mammalian brain development through a variety of mechanisms beyond their shared property of cholinesterase inhibition. We used microarrays to characterize similarities and differences in transcriptional responses to chlorpyrifos and diazinon, assessing defined gene groupings for the pathways known to be associated with the mechanisms and/or outcomes of chlorpyrifos-induced developmental neurotoxicity. We exposed neonatal rats to daily doses of chlorpyrifos (1mg/kg) or diazinon (1 or 2mg/kg) on postnatal days 1-4 and evaluated gene expression profiles in brainstem and forebrain on day 5; these doses produce little or no cholinesterase inhibition. We evaluated pathways for general neural cell development, cell signaling, cytotoxicity and neurotransmitter systems, and identified significant differences for 60% of 252 genes. Chlorpyrifos elicited major transcriptional changes in genes involved in neural cell growth, development of glia and myelin, transcriptional factors involved in neural cell differentiation, cAMP-related cell signaling, apoptosis, oxidative stress, excitotoxicity, and development of neurotransmitter synthesis, storage and receptors for acetylcholine, serotonin, norepinephrine and dopamine. Diazinon had similar effects on many of the same processes but also showed major differences from chlorpyrifos. Our results buttress the idea that different organophosphates target multiple pathways involved in neural cell development but also that they deviate in key aspects that may contribute to disparate neurodevelopmental outcomes. Equally important, these pathways are compromised at exposures that are unrelated to biologically significant cholinesterase inhibition and its associated signs of systemic toxicity. The approach used here demonstrates how planned comparisons with microarrays can be used to screen for developmental neurotoxicity.

PMID: 17452286

no signs of "systemic toxicity" to measure - but gene expression in the brain (brainstem and forebrain) "identified significant differences for 60% of 252 genes."

I like this study more!

flounder asked:
"when the UK and other countries stopped feeding ruminant protein, there BSE cases dramatically declined. please explain that kathy ???"

I thought you read Mark Purdey's papers. Read them again.
www.markpurdey.com and/or www.purdeyenvironment.com
 

flounder

Well-known member
Kathy said:
[
flounder asked:
"when the UK and other countries stopped feeding ruminant protein, there BSE cases dramatically declined. please explain that kathy ???"

I thought you read Mark Purdey's papers. Read them again.
www.markpurdey.com and/or www.purdeyenvironment.com


i did not think you could answer that question kathy. thanks for proving my point............tss
 

Kathy

Well-known member
Hey flounder, you are incredibly closed-minded.

I've answered your stupid question several times, at nausium. You apparently can't absorb the information.

You can't attack the papers I post, so you attach me - the messenger. So sad!

I don't need to take credit for work that Mark Purdey outlined years ago. He deserves the credit for digging up all the environmental information surrounding TSEs, and that is the purpose of this thread.

Like Randy said, you continue down the road with blinders on. You share your opinion with other webpages, like vegsource and CJD sites - which is your right. It is your lifes' work and I am sorry your family suffered from this brain wasting disorder.

Thankfully, the vast majority of people, ie: researchers, that I speak with are a lot more open-minded than you.

Brain Res Bull. 2007 May 30;72(4-6):232-74. Epub 2007 Jan 25.

Comparative developmental neurotoxicity of organophosphates in vivo: Transcriptional responses of pathways for brain cell development, cell signaling, cytotoxicity and neurotransmitter systems.

Slotkin TA, Seidler FJ.
Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.

Organophosphates affect mammalian brain development through a variety of mechanisms beyond their shared property of cholinesterase inhibition. We used microarrays to characterize similarities and differences in transcriptional responses to chlorpyrifos and diazinon, assessing defined gene groupings for the pathways known to be associated with the mechanisms and/or outcomes of chlorpyrifos-induced developmental neurotoxicity. We exposed neonatal rats to daily doses of chlorpyrifos (1mg/kg) or diazinon (1 or 2mg/kg) on postnatal days 1-4 and evaluated gene expression profiles in brainstem and forebrain on day 5; these doses produce little or no cholinesterase inhibition. We evaluated pathways for general neural cell development, cell signaling, cytotoxicity and neurotransmitter systems, and identified significant differences for 60% of 252 genes. Chlorpyrifos elicited major transcriptional changes in genes involved in neural cell growth, development of glia and myelin, transcriptional factors involved in neural cell differentiation, cAMP-related cell signaling, apoptosis, oxidative stress, excitotoxicity, and development of neurotransmitter synthesis, storage and receptors for acetylcholine, serotonin, norepinephrine and dopamine. Diazinon had similar effects on many of the same processes but also showed major differences from chlorpyrifos. Our results buttress the idea that different organophosphates target multiple pathways involved in neural cell development but also that they deviate in key aspects that may contribute to disparate neurodevelopmental outcomes. Equally important, these pathways are compromised at exposures that are unrelated to biologically significant cholinesterase inhibition and its associated signs of systemic toxicity. The approach used here demonstrates how planned comparisons with microarrays can be used to screen for developmental neurotoxicity.

PMID: 17452286


no signs of "systemic toxicity" to measure - but gene expression in the brain (brainstem and forebrain) "identified significant differences for 60% of 252 genes."
 

flounder

Well-known member
Kathy said:
no signs of "systemic toxicity" to measure - but gene expression in the brain (brainstem and forebrain) "identified significant differences for 60% of 252 genes."


no sign of TSE either :lol:


TSS
 

Kathy

Well-known member
TSS

no sign of TSE either (happy face)

The animals were killed at 5 days of age.... your compasion and insight are clearly lacking....your "joy" in the lack of specific evidence (evidence not even being considered here)... is very cynical....

It's like you don't want to find an answer.... just blame the "infectious prion protein" .... that's your story and your sticking to it....

Maybe we should be encouraging these doctors and others working on related research to dig deeper and continue their research further along the path they have started. I know Dr. F. Paquet has published several papers based on one ongoing lab experiment with depleted uranium. Maybe he'll test his rats for prions?

All I know is I've encouraged where I can!

I learned at the prion symposium in Calgary last January, that researchers can't get time in various labs/facilities eg. light synchrotron at the Saskatchewan University... because of the so-called infectious nature of the prion protein... This is another road-block in the way of using available tools to "characterize" the composition of prions and other amyloid forming plaques.

The researchers at one meeting would raise their hands and do the "quote unquote" symbol when referring to "infectious" prions.... they also questioned the validity of the infectious classification... It is a "convenient road-block" - in my opinion.
 

rkaiser

Well-known member
Terry -
when it comes to metals and OPs contamination, and the potential for human health risk, im on your side girlfriend, but when you try to claim that they cause any TSE, you loose me and most everyone else that has ever studied anything on these topics, unless you wear a dress like rkaiser, and then you will believe anything ;-)

Believe anything Terry? Are you refering to women with your statement or just men who wear dresses. Either way you are walking the thin line of judgement of a minority rather than the simple manner in which I am explaining how you admit that you are lost. Your studying is only one book bud and your translation is like a Catholic reading the Bible. Take a good honest look at Mark's findings and the multitude of scientist who also study TSE's but know that he story is not completely told yet.

Continuing to sarcastically refer to Mark and Kathy's work as bunk is getting you ----- where?

My sarcasm come from my lesser amount of study on the topic than either you or Kathy and I will admit that. I simply cannot see how continually knocking a theory that has as much merit or more than the "bumping up against" and magical infection theory, is gaining you ground in the saving of lives.
 

flounder

Well-known member
J. Anim Sci., doi: 10.2527/jas.2007-0215
©Copyright, 2007, The American Society of Animal Science


ARTICLE

Exposure to low dietary copper or low copper coupled with high dietary
manganese for one year does not alter brain prion protein characteristics in
the mature bovine

L. R. Legleiter 1, H. C. Liu 1, K. E. Lloyd 1, S. L. Hansen 1, R. S. Fry 1,
J. W. Spears 1*
1 Department of Animal Science and Interdepartmental Nutrition Program,
North Carolina State University, Raleigh, NC



* To whom correspondence should be addressed. E-mail: [email protected]


Abstract


It is now widely accepted that abnormal prion proteins are the likely
causative agent in bovine spongiform encephalopathy (BSE). Cellular prion
proteins (PrPc) bind copper (Cu), which appears to be required to maintain
functional characteristics of the protein. The replacement of Cu on PrPc
with manganese (Mn) has resulted in loss of function and increased protease
resistance. Twelve mature cows were used to determine the effects of Cu
deficiency, alone and coupled with high dietary Mn, on brain Cu and Mn
concentrations, and PrPc functional characteristics. Copper-adequate cows
were randomly assigned to treatments: 1) control (adequate in Cu and Mn), 2)
Cu-deficient (-Cu), and 3) Cu-deficient plus high dietary Mn (-Cu+Mn). Cows
assigned to treatments -Cu and -Cu+Mn received no supplemental Cu and were
supplemented with molybdenum (Mo) to further induce Cu deficiency. After 360
d, Cu-deficient cows (-Cu and -Cu+Mn) tended to have less concentrations of
Cu (P = 0.09) in the obex region of the brainstem. Brain Mn tended (P =
0.09) to be greater in -Cu+Mn cattle vs. -Cu cattle. Western blots revealed
that PrPc relative optical densities, proteinase K degradability, elution
profiles, molecular weights, and glycoform distributions were not different
among treatments. The concentration of PrPc, as determined by ELISA, was
similar across treatment groups. Brain tissue (obex) Mn superoxide dismutase
activity was greatest (P = 0.04) in cattle receiving -Cu+Mn, while
immunopurified PrPc had similar superoxide dismutase-like activities among
treatments. Immunopurified PrPc had similar Cu concentrations across
treatments while Mn was undetectable. We conclude that Cu deficiency coupled
with excessive Mn intake in the bovine may decrease brain Cu and increase
brain Mn. Copper deficiency, alone or coupled with high dietary Mn, did not
cause detectable alterations in PrPc functional characteristics.

http://jas.fass.org/cgi/content/abstract/jas.2007-0215v1


Subject: FATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE
Date: May 3, 2007 at 8:41 am PST

KEY FINDINGS

Organophosphate Studies

6. Studies using phosmet (an organophosphate pesticide) were
carried out throughout the project. No relationship between this
compound and the potential to cause a TSE were identified. In
studies with oral dosing of rats, it was shown that PrP expression
levels increased in the brain but there was no association between
this and formation of proteinase K (PK) resistant PrP.


snip...


12. A model of seed protein aggregation and fibril formation was
established using PrP charged with Mn2+. PrP-Mn2+ was found to
form small circular aggregates able to catalyse further protein
aggregation and fibrilisation of PrP. This model unlike other
published models (for example those of Baskakov et al.1) does not
require the presence of denaturants and is not an autocatalytic
process (i.e. the substrate of the reaction did not aggregate). The
results suggest that Mn2+ may play a role in the formation of prion
seeds

__although further studies showed that this material was not
infectious in mouse bioassay.__

snip...

24. The project also generated information concerning the relation of
TSEs to environmental factors:
• __Potentially no role for organophosphates in TSEs.__
• Increased Mn in the diet results in higher PrP levels in the
brain.
• No conclusion is yet possible in terms of the relationship
between environmental trace element concentrations and the
geographical occurrence of TSEs (classical scrapie or BSE).
• Some confirmation was provided that in some specific farms
occurrence of classical scrapie correlates with high Mn levels.


http://www.seac.gov.uk/papers/97-4.pdf



a) As regards the involvement of organophosphates in the origin of BSE, no
new scientific
information providing evidence or supporting the hypothesis by valid data
became
available after the adoption of the last opinion of the SSC on this issue.
Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for
registration of
plant protection products and veterinary medicines – addressed in the
enquiries – provide
the basis for safe use of registered compounds and their formulations.
Regarding the
alleged intoxication cases reported and OP exposure it must be concluded
that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R.,
Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar,
H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs
Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant
Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE
and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and
transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf



OP'S MEETING WITH PURDEY

http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf



transmission studies do not lie, amplification and transmission!

1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of
known infectious tissues. The asymptomatic incubation period in the one
monkey exposed to the virus of kuru was 36 months; that in the two monkeys
exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months,
respectively; and that in the two monkeys exposed to the virus of scrapie
was 25 and 32 months, respectively. Careful physical examination of the
buccal cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has remained
asymptomatic during the 39 months that it has been under observation.

snip...


The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides
further grounds for concern that scrapie-infected meat may occasionally give
rise in humans to Creutzfeldt-Jakob disease. ...end

(from full text study pdf...TSS)

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE

This is provided by the statistically significant increase in the incidence
of sheep scrape from 1985, as determined from analyses of the submissions
made to VI Centres, and from individual case and flock incident studies.
........


http://www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf



look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

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
Summary 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 efficiency 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 findings 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 (ic ip 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 first positive animal (%). The accuracy of

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

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


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


SHORT COMMUNICATION

Oral Transmission of Chronic Wasting Disease in Captive Shira’s Moose

Terry J. Kreeger1,3, D. L. Montgomery2, Jean E. Jewell2, Will Schultz1 and Elizabeth S. Williams2

1 Wyoming Game and Fish Department, 2362 Highway 34, Wheatland, Wyoming 82201, USA;
2 Department of Veterinary Sciences, University of Wyoming, Laramie, Wyoming 82071, USA
3 Corresponding author (email: [email protected] )

ABSTRACT: Three captive Shira’s moose (Alces alces shirasi) were orally inoculated with a single dose (5 g) of whole-brain homogenate prepared from chronic wasting disease (CWD)–affected mule deer (Odocoileus hemionus). All moose died of causes thought to be other than CWD. Histologic examination of one female moose dying 465 days postinoculation revealed spongiform change in the neuropil, typical of transmissible spongiform encephalopathy. Immunohistochemistry staining for the proteinase-resistant isoform of the prion protein was observed in multiple lymphoid and nervous tissues. Western blot and enzyme-linked immunosorbent assays provided additional confirmation of CWD. These results represent the first report of experimental CWD in moose.
Key words: Alces alces shirasi, chronic wasting disease, enzyme-linked immunosorbent assay, immunohistochemistry, moose, oral inoculation, prion, PrPCWD.


http://www.jwildlifedis.org/cgi/content/abstract/42/3/640




http://www.usaha.org/committees/reports/2005/report-wd-2005.pdf



-------- Original Message --------

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: [email protected]



Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability

Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back to ruminants including cattle, sheep, goat, deer, elk and mink,
chickens, fish (all farmed animals for human/animal consumption),
this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump or ass muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state
(especially ''sporadic'' cjd), and that a CJD Questionnaire must
be issued to every family of a victim of TSE. only checking death
certificates will not be sufficient. this has been proven as well
(see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make
the same mistakes...

REFERENCES


Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
[email protected]

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757



Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L
To: BSE-L

8420-20.5% Antler Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm


DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box 117
Sandy Lake, PA 16145
PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:

Food and Drug Administration Investigator Gregory E. Beichner conducted
an inspection of your animal feed manufacturing operation, located in
Sandy Lake, Pennsylvania, on March 23,
2001, and determined that your firm manufactures animal feeds including
feeds containing prohibited materials. The inspection found significant
deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE) . Such deviations cause products being manufactured at this
facility to be misbranded within the meaning of Section 403(f), of the
Federal Food, Drug, and Cosmetic
Act (the Act).

Our investigation found failure to label your
swine feed with the required cautionary statement "Do Not Feed to cattle
or other Ruminants" The FDA suggests that the statement be
distinguished
by different type-size or color or other means of highlighting the
statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal
feeds containing prohibited material. This
flushed material is fed to wild game including deer, a ruminant animal.
Feed material which may potentially contain prohibited material should
not be fed to ruminant animals which may become part of the food chain.

The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...tss

http://www.fda.gov/foi/warning_letters/g1115d.pdf


SNIP...FULL TEXT ;


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm


TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;

*********************************

e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;

*********************************

f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html

snip...end...tss



NOW, please note what the FDA claims was a safe level ;



FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html



then you have to worry more from the friendly fire, there of ;




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





http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf



http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf



TSS
 

Kathy

Well-known member
Spears study lacks all important contamination with radionuclides!

They provide the energy to transform the protein fragments, induce metabolic changes and damage DNA.

Close but no cigar! Recipe incomplete!
 

flounder

Well-known member
Kathy said:
Spears study lacks all important contamination with radionuclides!

They provide the energy to transform the protein fragments, induce metabolic changes and damage DNA.

Close but no cigar! Recipe incomplete!


:lol2: :lol2: :p :cowboy:
 

bse-tester

Well-known member
It is the fool who dismisses that which may have some truth to it!

With respect to Mark purdey, it is a fact that he has raised some very interesting and extremely good ideas relating to the events that bring about and/or causes TSE manifestation in animals and humans. To blatantly discount his theories would be akin to accepting that the early maps of the world stating the flatness of it were, indeed, true.

PrP studies are still very much in their infancy and any plausible ideas or theories are to be considered as potentially factual until proven to be either possible or not possible. To simply discount any potential as being false or otherwise along with the thoughts of those who are to be considered outside of the mainstream scientific community simply because of a lack of PHD's and/or years of lab work, is tantramount to inviting disaster.

Ask yourself what level of education Einstein had??

Is it not possible that the theories, thoughts, ideas and writings of people like Mark Purdey may indeed hold more water than those of others who have made it their goal in life to be recognized as the only viable voices to be listened to in the world of PrP and PrPsc studies? Mark Purdey was indeed a force and to lose his tenacious approach to this field we are in was truly sad. Metals, no matter what the current evidence may show in the studies being done by some, will possibly come to theforefront and should have every consideration afforded to the potential therein of metals being a player in the causes of TSE infection or manifestation in animals and humans. But of course, that is only my opinion. I write this not get in the middle of a 'vest-pocket-war' here, but to offer the entire idea that ideas and theories are to be embraced and given every possible chance to be explored - not dismissed out of hand without first being allowed to be proven one way or the other.

Consider the lowly postal office assistant who showed the world the meaning of relativity and the theories surrounding much of what we now take for granted in the exploration of space and time???
 

Kathy

Well-known member
First, ... bse-tester, your comments are appreciated.

Second, Dr. Spears has challenged mature animals. These animals should be impregnated and see how the diet affects the calf.

The study, even though it used mature cows, states:

We conclude that Cu deficiency coupled with excessive Mn intake in the bovine may decrease brain Cu and increase brain Mn.

The recipe is incomplete, as this disease is multifactoral, and it requires a rogue metal to challenge the brain (stress it out, destroy cells, oxidative damage - like the damage caused by releasing an alpha or beta particle inside the brain ie: 4 million electron volts).

Internal ionizing radiation localized to the brain will cause a rush of manganese superoxide dismutase production, as well as other anti-oxidants, to defend the mitochondria, DNA and other cellular mechanisms.

J Radiat Res (Tokyo). 2007 Jul;48(4):263-72. Links

A radiobiological review on melatonin: a novel radioprotector

Shirazi A, Ghobadi G, Ghazi-Khansari M.
Department of Biophysics/University of Tehran.

In spite of the fact that radiotherapy is a common and effective tool for cancer treatment; the radio sensitivity of normal tissues adjacent to the tumor which are unavoidably exposed to radiation limits therapeutic gain. For the sake of improvement in radiation therapy, radiobiology- the study of the action of ionizing radiation on living things- plays a crucial role through explaining observed phenomena, and suggesting improvements to existing therapies. Due to the damaging effects of ionizing radiation, radiobiologists have long been interested in identifying novel, nontoxic, effective, and convenient compounds to protect humans against radiation induced normal tissue injuries. In hundreds of investigations, melatonin (N-acetyl-5-methoxytryptamine), the chief secretory product of the pineal gland in the brain, has been documented to ameliorate the oxidative injuries due to ionizing radiation. This article reviews different features that make melatonin a potentially useful radioprotector. Moreover, based on radiobiological models we can hypothesize that melatonin may postpone the saturation of repair enzymes which leads to repairing more induced damage by repair system and more importantly allows the use of higher doses of radiation during radiotherapy to get a better therapeutic ratio. The implications of the accumulated observations suggest by virtue of melatonin's radioprotective and anticancer effects; it is time to use it as a radioprotector both for radiation workers and patients suffering from cancer either alone for cancer inhibition or in combination with traditional radiotherapy for getting a favorable efficacy/toxicity ratio during the treatment. Although compelling evidence suggests that melatonin may be effective for a variety of disorders, the optimum dose of melatonin for human radioprotection is yet to be determined. We propose that, in the future, melatonin improve the therapeutic ratio in radiation oncology.

PMID: 17641465

So, melatonin protects cells from ionizing radiation, interesting. In the next study, researchers found that chronic contamination with Cesium 137 caused severe changes in the sleep-wake cycle of experimental rats. Melatonin is a major factor in sleep cycles.

The researches, listed below, conclude the problems may be the result of Cesium 137 accumulating in the brain stem. Yes, that would be the "brain stem". Chronic exposure to levels of Cesium 137, similar to those experienced by people living in zones contaminated by, for example, Chernobyl.

Toxicology. 2006 Sep 21;226(2-3):118-25. Epub 2006 Jun 10.

Evaluation of the effect of chronic exposure to 137Cesium on sleep-wake cycle in rats.

Lestaevel P, Dhieux B, Tourlonias E, Houpert P, Paquet F, Voisin P, Aigueperse J, Gourmelon P.
Institut de Radioprotection et de Sûreté Nucléaire, Direction de la RadioProtection de l'Homme, Service de Radiobiologie et d'Epidémiologie, Laboratoire de Radiotoxicologie Expérimentale, BP 17, 92262 Fontenay-aux-Roses, France.

Since the Chernobyl accident, the most significant problem for the population living in the contaminated areas is chronic exposure by ingestion of radionuclides, notably (137)Cs, a radioactive isotope of cesium. It can be found in the whole body, including the central nervous system. The present study aimed to assess the effect of (137)Cs on the central nervous system and notably on open-field activity and the electroencephalographic pattern. Rats were exposed up to 90 days to drinking water contaminated with (137)Cs at a dosage of 400 Bq kg(-1), which is similar to that ingested by the population living in contaminated territories. At this level of exposure, no significant effect was observed on open-field activity. On the other hand, at 30 days exposure, (137)Cs decreased the number of episodes of wakefulness and slow wave sleep and increased the mean duration of these stages. At 90 days exposure, the power of 0.5-4 Hz band of (137)Cs-exposed rats was increased in comparison with controls. These electrophysiological changes may be due to a regional (137)Cs accumulation in the brain stem. In conclusion, the neurocognitive effects of (137)Cs need further evaluation and central disorders of population living in contaminated territories must be considered.

PMID: 16876929
 

flounder

Well-known member
bse-tester said:
It is the fool who dismisses that which may have some truth to it!

With respect to Mark purdey, it is a fact that he has raised some very interesting and extremely good ideas relating to the events that bring about and/or causes TSE manifestation in animals and humans. To blatantly discount his theories would be akin to accepting that the early maps of the world stating the flatness of it were, indeed, true.

PrP studies are still very much in their infancy and any plausible ideas or theories are to be considered as potentially factual until proven to be either possible or not possible. To simply discount any potential as being false or otherwise along with the thoughts of those who are to be considered outside of the mainstream scientific community simply because of a lack of PHD's and/or years of lab work, is tantramount to inviting disaster.

Ask yourself what level of education Einstein had??

Is it not possible that the theories, thoughts, ideas and writings of people like Mark Purdey may indeed hold more water than those of others who have made it their goal in life to be recognized as the only viable voices to be listened to in the world of PrP and PrPsc studies? Mark Purdey was indeed a force and to lose his tenacious approach to this field we are in was truly sad. Metals, no matter what the current evidence may show in the studies being done by some, will possibly come to theforefront and should have every consideration afforded to the potential therein of metals being a player in the causes of TSE infection or manifestation in animals and humans. But of course, that is only my opinion. I write this not get in the middle of a 'vest-pocket-war' here, but to offer the entire idea that ideas and theories are to be embraced and given every possible chance to be explored - not dismissed out of hand without first being allowed to be proven one way or the other.

Consider the lowly postal office assistant who showed the world the meaning of relativity and the theories surrounding much of what we now take for granted in the exploration of space and time???


i give up, it's all nuclear proliferation, metals, ops, and the damn ruminant mad cow feed ban was for naught. amplification, and proven transmission studies mean absolutely nothing. all those cases of BSE in the UK, and the ramifications from feed ban there, and decline in BSE cases thereof, again, means nothing. i guess bse-tester and kathy have solved the problem. case closed. go ahead and feed mad cows to cows, no problem. even add some cwd deer and elk into the recipe, with scrapie infected sheep. it was all a hoax. :roll: :roll: :???:




Bovine spongiform encephalopathy: the effect of oral exposure dose on attack
rate and incubation period in cattle
G. A. H. Wells1, T. Konold1, M. E. Arnold1, A. R. Austin1,, S. A. C.
Hawkins1, M. Stack1, M. M. Simmons1, Y. H. Lee2, D. Gavier-Widén3, M.
Dawson1, and J. W. Wilesmith1,

1 Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey
KT15 3NB, UK
2 National Veterinary Research and Quarantine Service, Anyang, Republic of
Korea
3 National Veterinary Institute (SVA), SE-75189 Uppsala, Sweden


Correspondence
G. A. H. Wells
[email protected]

The dose–response of cattle exposed to the bovine spongiform encephalopathy
(BSE) agent is an important component of modelling exposure risks for
animals and humans and thereby, the modulation of surveillance and control
strategies for BSE. In two experiments calves were dosed orally with a range
of amounts of a pool of brainstems from BSE-affected cattle. Infectivity in
the pool was determined by end-point titration in mice. Recipient cattle
were monitored for clinical disease and, from the incidence of
pathologically confirmed cases and their incubation periods (IPs), the
attack rate and IP distribution according to dose were estimated. The dose
at which 50 % of cattle would be clinically affected was estimated at 0.20 g
brain material used in the experiment, with 95 % confidence intervals of
0.04–1.00 g. The IP was highly variable across all dose groups and followed
a log-normal distribution, with decreasing mean as dose increased. There was
no evidence of a threshold dose at which the probability of infection became
vanishingly small, with 1/15 (7 %) of animals affected at the lowest dose (1
mg).

Present address: Oak Farm, Harpsden Bottom, Henley-on-Thames, Oxon RG9 4HY,
UK.

Present address: NSPAC, Defra, Whittington Road, Worcester WR5 2SU, UK.

Present address: Defra, 1a Page Street, London SWIP 4PQ, UK, and Department
of Infectious and Tropical Diseases, London School of Hygiene and Tropical
Medicine, University of London, Keppel Street, London WC1E 7HT, UK.



http://vir.sgmjournals.org/cgi/content/abstract/88/4/1363


BSE INQUIRY
Volume 2: Science
3. The nature and cause of BSE
Dose
Dose-related experiments (including the attack rate experiment)
Summary


Transmission of BSE and scrapie to sheep and goats by intracerebral and oral
routes
3.165 Initiated in June 1988 at the NPU, this experiment set out to compare
transmission of both BSE and scrapie to two breeds of sheep, one
susceptible, the other resistant to scrapie infection, and to goats which
are rarely susceptible to natural scrapie. Its aim was to determine,
firstly, if BSE behaved differently from scrapie in these animals and,
secondly, if BSE transmission was influenced by the route of challenge.

3.166 Sheep of both breeds and goats were inoculated either intracerebrally
with 0.05 g of infected BSE brain material, or orally with 0.5 g of infected
material. The size of the intracerebral inoculations was based on that used
for standard scrapie transmissions and was effectively limited by the volume
of material that could be introduced into the brain. 6 Amounts used for oral
administration were limited by the physical quantity of bovine material
available, and so, in order to inoculate several animals, it was necessary
to use a smaller quantity of inoculum (0.5 g) than if the available material
had been administered to one animal.

3.167 BSE was found to transmit to both scrapie-resistant and susceptible
sheep breeds as well as to goats following intracerebral inoculation. This
result was significant in that it showed that BSE transmitted to animals
which were not susceptible to scrapie infection. BSE was also found to
transmit orally to these animals, showing that the amount of infectivity
contained in 0.5 g of brain material was sufficient to cause disease. The
results also showed that the two inoculation routes were similarly efficient
in transmitting disease, when it had been commonly accepted that the
intracerebral route was much more efficient than the oral route.

3.168 Results of positive oral transmission to scrapie-susceptible sheep
were known to scientists conducting the experiment by November 1990, 7
although it was not clear if the sheep had succumbed to infection with
natural scrapie or BSE. This was more than a year before the start of the
attack rate experiment. Oral transmission of BSE to negative-line sheep was
not recorded until October 1991. 8

3.169 It is not clear when MAFF officials became aware of the oral
transmission of BSE to sheep, let alone the amount of material that was
sufficient to cause disease. Results were supplied periodically by the NPU
to the CVL in the form of a data sheet which contained updates of all NPU
experiments. It is not clear who received these reports, though it appears
that they were distributed prior to the NPU/CVL R&D meetings. 9 The quantity
of material administered orally to the animals was not recorded on these
data sheets, so those not familiar with the design of the experiment would
not necessarily have appreciated the significance of the oral transmission.
Interim results of this experiment were published in the Veterinary Record
in 1993. 10

3.170 These results showed that a small amount of infectious material
administered orally was sufficient to cause BSE, even across a species
barrier. This information could have usefully guided decisions made on the
design of the attack rate experiment in cattle. ...END


TSS
 

rkaiser

Well-known member
i give up, it's all nuclear proliferation, metals, ops, and the damn ruminant mad cow feed ban was for naught. amplification, and proven transmission studies mean absolutely nothing. all those cases of BSE in the UK, and the ramifications from feed ban there, and decline in BSE cases thereof, again, means nothing. i guess bse-tester and kathy have solved the problem. case closed. go ahead and feed mad cows to cows, no problem. even add some cwd deer and elk into the recipe, with scrapie infected sheep. it was all a hoax.

Whenever you post your own words here Terry, you prove what a simple case of human fixation you really are. Has anyone ever promoted the feeding of cattle parts to other cattle? Have you ever read anything that anyone else ever posts about TSE's? Have you ever tried Vitamin B12. It is a wonder drug for an unhealthy - focused mind. You can't imagine the amount of information available to each and every human being that is stored in these things we carry around on our shoulders when we allow them to work in an unfettered, unfocused way. Where so you get your beef Terry? You may be showing early signs of a metal contaminated noodle and Kathy might be able to help you trace the product you are consuming to your local army base.
 

flounder

Well-known member
rkaiser said:
i give up, it's all nuclear proliferation, metals, ops, and the damn ruminant mad cow feed ban was for naught. amplification, and proven transmission studies mean absolutely nothing. all those cases of BSE in the UK, and the ramifications from feed ban there, and decline in BSE cases thereof, again, means nothing. i guess bse-tester and kathy have solved the problem. case closed. go ahead and feed mad cows to cows, no problem. even add some cwd deer and elk into the recipe, with scrapie infected sheep. it was all a hoax.

Whenever you post your own words here Terry, you prove what a simple case of human fixation you really are. Has anyone ever promoted the feeding of cattle parts to other cattle? snip.



What Do We Feed to Food-Production Animals? A Review of Animal Feed
Ingredients and Their Potential Impacts on Human Health


Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker1
1Johns Hopkins Center for a Livable Future, Bloomberg School of Public
Health, Baltimore, Maryland, USA; 2Maryland Institute for
Applied Environmental Health, College of Health and Human Performance,
University of Maryland, College Park, Maryland, USA;
3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA


snip...



Table 1. Animal feed ingredients that are legally used in U.S. animal feeds



Animal


Rendered animal protein from Meat meal, meat meal tankage, meat and bone
meal, poultry meal, animal the slaughter of food by-product meal, dried
animal blood, blood meal, feather meal, egg-shell production animals and
other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and
animal animals digest from dead, dying, diseased, or disabled animals
including deer and elk Animal waste Dried ruminant waste, dried swine waste,
dried poultry litter, and undried processed animal waste products


snip...


Conclusions


Food-animal production in the United States has changed markedly in the past
century, and these changes have paralleled major changes in animal feed
formulations. While this industrialized system of food-animal production may
result in increased production efficiencies, some of the changes in animal
feeding practices may result in unintended adverse health consequences for
consumers of animal-based food products. Currently, the use of animal feed
ingredients,
including rendered animal products, animal waste, antibiotics, metals, and
fats, could result in higher levels of bacteria, antibioticresistant
bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting
animal-based food products intended for human consumption. Subsequent human
health effects among consumers could include increases in bacterial
infections (antibioticresistant and nonresistant) and increases in the risk
of developing chronic (often fatal) diseases
such as vCJD. Nevertheless, in spite of the wide range of potential human
health impacts that could result from animal feeding practices, there are
little data collected at the federal or state level concerning the amounts
of specific ingredients that are intentionally included in U.S. animal feed.
In addition, almost no biological or chemical testing is conducted on
complete U.S. animal feeds; insufficient testing is performed on retail meat
products; and human health effects data are not appropriately linked to this
information. These surveillance inadequacies make it difficult to conduct
rigorous epidemiologic studies and risk assessments
that could identify the extent to which specific human health risks are
ultimately associated with animal feeding practices. For example, as noted
above, there are insufficient data to determine whether other human
foodborne bacterial illnesses besides those caused by S. enterica serotype
Agona are associated with animal feeding practices. Likewise, there are
insufficient data to determine the percentage of antibiotic-resistant human
bacterial infections that are attributed to the nontherapeutic use of
antibiotics in animal feed. Moreover, little research has been conducted to
determine whether the use of organoarsenicals in animal feed, which can lead
to elevated levels of arsenic in meat products (Lasky et al. 2004),
contributes to increases in cancer risk. In order to address these research
gaps, the following principal actions are necessary within the United
States: a) implementation of a nationwide reporting system of the specific
amounts and types of feed ingredients of concern to public health that are
incorporated into animal feed, including antibiotics, arsenicals, rendered
animal products, fats, and animal waste; b) funding and development of
robust surveillance systems that monitor biological, chemical, and other
etiologic agents throughout the animal-based food-production chain “from
farm to fork” to human health outcomes; and c) increased communication and
collaboration among feed professionals, food-animal producers, and
veterinary and public health officials.


REFERENCES...snip...end


Sapkota et al.
668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives


http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf



BANNED MAD COW PROTEIN IN COMMERCE

http://ranchers.net/forum/viewtopic.php?t=19155



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