#1   Report Post  
Old 26-04-2003, 01:22 PM
Torsten Brinch
 
Posts: n/a
Default UK vCJD October 2002

Updated statistics of vCJD in UK (will soon be)
available at

http://www.doh.gov.uk/cjd/stats/nov02.htm

until they are, you may wish to use the press release at
http://www.info.doh.gov.uk/doh/intpr...6?OpenDocument

Changes from previous month to this month
in definite or probable vCJD

Total deaths 117 -- 117 (no change)
Total cases (dead or alive) 128 -- 128 (no change)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 102 - 117 (+15)
Total cases (dead or alive) 111 - 128 (+17)


On Tue, 08 Oct 2002 18:05:55 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/oct02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 115 -- 117 (+2)
Total cases (dead or alive) 127 -- 128 (+1)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 101 - 117 (+16)
Total cases (dead or alive) 107 - 128 (+21)


On Mon, 02 Sep 2002 21:04:13 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/sep02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 115 -- 115 (no change)
Total cases (dead or alive) 125 -- 127 (+2)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 101 - 115 (+14)
Total cases (dead or alive) 106 - 127 (+21)



On Mon, 05 Aug 2002 14:33:09 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/aug02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 115 -- 115 (no change)
Total cases (dead or alive) 124 -- 125 (+1)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 99 - 115 (+16)
Total cases (dead or alive) 106 - 125 (+19)

On Mon, 01 Jul 2002 17:54:27 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/jul02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 113 -- 115 (+2)
Total cases (dead or alive) 122 -- 124 (+2)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 96 - 115 (+19)
Total cases (dead or alive) 102 - 124 (+22)

..http://www.doh.gov.uk/cjd/stats/jun02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 111 -- 113 (+2)
Total cases (dead or alive) 121 -- 122 (+1)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 94 - 113 (+19)
Total cases (dead or alive) 101 - 122 (+21)

..
http://www.doh.gov.uk/cjd/stats/may02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 110 -- 111 (+1)
Total cases (dead or alive) 117 -- 121 (+4)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 93 - 111 (+18)
Total cases (dead or alive) 99 - 121 (+22)



  #2   Report Post  
Old 26-04-2003, 01:22 PM
Gordon Couger
 
Posts: n/a
Default UK vCJD October 2002

Torsten,

Has a trend devolved yet that would indicate that a peak is nearing if there
are no suppresses such as a genotype that has a lot longer resistance to the
disease and is sitting out there waiting to start to show up. Or is it still
just trending to the low side of estimates.

I realize with such a sparse data set random chance can play hell with the
results.

I have seen a crap shooter make 8 passes in a row. The extremes of
probability do occur.
--
Gordon

Gordon Couger
Stillwater, OK
www.couger.com/gcouger
"Torsten Brinch" wrote in message
...
Updated statistics of vCJD in UK (will soon be)
available at

http://www.doh.gov.uk/cjd/stats/nov02.htm

until they are, you may wish to use the press release at
http://www.info.doh.gov.uk/doh/intpr...6?OpenDocument

Changes from previous month to this month
in definite or probable vCJD

Total deaths 117 -- 117 (no change)
Total cases (dead or alive) 128 -- 128 (no change)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 102 - 117 (+15)
Total cases (dead or alive) 111 - 128 (+17)


On Tue, 08 Oct 2002 18:05:55 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/oct02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 115 -- 117 (+2)
Total cases (dead or alive) 127 -- 128 (+1)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 101 - 117 (+16)
Total cases (dead or alive) 107 - 128 (+21)


On Mon, 02 Sep 2002 21:04:13 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/sep02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 115 -- 115 (no change)
Total cases (dead or alive) 125 -- 127 (+2)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 101 - 115 (+14)
Total cases (dead or alive) 106 - 127 (+21)



On Mon, 05 Aug 2002 14:33:09 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/aug02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 115 -- 115 (no change)
Total cases (dead or alive) 124 -- 125 (+1)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 99 - 115 (+16)
Total cases (dead or alive) 106 - 125 (+19)

On Mon, 01 Jul 2002 17:54:27 +0200, Torsten Brinch
wrote:

Updated statistics of vCJD in UK available at

http://www.doh.gov.uk/cjd/stats/jul02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 113 -- 115 (+2)
Total cases (dead or alive) 122 -- 124 (+2)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 96 - 115 (+19)
Total cases (dead or alive) 102 - 124 (+22)

..http://www.doh.gov.uk/cjd/stats/jun02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 111 -- 113 (+2)
Total cases (dead or alive) 121 -- 122 (+1)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 94 - 113 (+19)
Total cases (dead or alive) 101 - 122 (+21)

..
http://www.doh.gov.uk/cjd/stats/may02.htm

Changes from previous month to this month
in definite or probable vCJD

Total deaths 110 -- 111 (+1)
Total cases (dead or alive) 117 -- 121 (+4)

Changes from previous year same month to this month
this year in definite or probable vCJD

Total deaths 93 - 111 (+18)
Total cases (dead or alive) 99 - 121 (+22)




  #3   Report Post  
Old 26-04-2003, 01:22 PM
Torsten Brinch
 
Posts: n/a
Default UK vCJD October 2002

On Thu, 7 Nov 2002 03:48:45 -0600, "Gordon Couger"
wrote:

Torsten,

Has a trend devolved yet that would indicate that a peak is nearing ..


You are making reference to some thought imagine of a 'normal'
epidemic curve, I think, more or less bell-shaped with a tail. I don't
think our knowledge of the disease gives us basis for assuming such a
model.

Anyhow, if it is assumed, there is no clear indication in data where
we are in this assumed progressive development in relation to a peak.
Said otherwise, one can find support in data for us being as well
past, on, or nearing a peak. Past-peakers might note the decreasing
trend in vCJD deaths since about autumn 2000; on-peakers and
nearing-peakers, that the current incidence does not stand out
as particularly high or particularly low compared to the incidence
the previous 3-4 years.


  #4   Report Post  
Old 26-04-2003, 01:22 PM
Gordon Couger
 
Posts: n/a
Default UK vCJD October 2002


"Torsten Brinch" wrote in message
...
On Thu, 7 Nov 2002 03:48:45 -0600, "Gordon Couger"
wrote:

Torsten,

Has a trend devolved yet that would indicate that a peak is nearing ..


You are making reference to some thought imagine of a 'normal'
epidemic curve, I think, more or less bell-shaped with a tail. I don't
think our knowledge of the disease gives us basis for assuming such a
model.

Anyhow, if it is assumed, there is no clear indication in data where
we are in this assumed progressive development in relation to a peak.
Said otherwise, one can find support in data for us being as well
past, on, or nearing a peak. Past-peakers might note the decreasing
trend in vCJD deaths since about autumn 2000; on-peakers and
nearing-peakers, that the current incidence does not stand out
as particularly high or particularly low compared to the incidence
the previous 3-4 years.

It wouldn't be bell shaped. I am exactly sure what the curve of an emerging
diseases looks like it would be different for each one, but the fear was
that it would be like growth curve of bacteria with a slow early phase and
very rapid log phase. Other diseases have shown this kind of explosive out
break. So the early predictions have a very wide range of out comes and of
course the press picked up on the one that sold the most papers.

Fortunately humans appear to poor hosts for vCJD. It face cattle don't
appear to be very good hosts for it either.

Flat curves are good for vCJD declining would be better.
--
Gordon

Couger
Stillwater, OK
www.couger.com/gcouger




  #5   Report Post  
Old 26-04-2003, 01:22 PM
Torsten Brinch
 
Posts: n/a
Default UK vCJD October 2002

On Thu, 7 Nov 2002 16:38:18 -0600, "Gordon Couger"
wrote:


"Torsten Brinch" wrote in message
.. .
On Thu, 7 Nov 2002 03:48:45 -0600, "Gordon Couger"
wrote:

Torsten,

Has a trend devolved yet that would indicate that a peak is nearing ..


You are making reference to some thought imagine of a 'normal'
epidemic curve, I think, more or less bell-shaped with a tail. I don't
think our knowledge of the disease gives us basis for assuming such a
model.

Anyhow, if it is assumed, there is no clear indication in data where
we are in this assumed progressive development in relation to a peak.
Said otherwise, one can find support in data for us being as well
past, on, or nearing a peak. Past-peakers might note the decreasing
trend in vCJD deaths since about autumn 2000; on-peakers and
nearing-peakers, that the current incidence does not stand out
as particularly high or particularly low compared to the incidence
the previous 3-4 years.

It wouldn't be bell shaped. I am exactly sure what the curve of an emerging
diseases looks like it would be different for each one snip


Yes,exactly and the shape is not known a priori unless one has a
reasoned model -- which in this case we most certainly do not have.

As you probably know, some think it is caused by the chronic effect of
exposure to toxic proteins from BSE affected cows. Quite a bit like
that Minamata disease in Japan caused by exposure to methylmercury,
just slower. But that can't be right, since the US EPA has determined
in connection with their approvals of genetically modified crops, that
when proteins are toxic they act by acute toxicity mechanisms and in
very small doses.

If there were to be toxic protein in the brains of BSE cows,
there should be at least sproadic reports of acute cases of dementia
in humans caused by the sunday dinner, and there should be huge
masses of supporting animal evidence for the acute toxic effects of
BSE brain muck. But quite on the contrary, there is a vast body of
evidence proving beyond any doubt, that experimental animals tolerate
large acute doses of BSE muck with no ill effect. IOW, we do not have
a clue what vCJD is caused by, and to be worse very many people think
it is caused by something that the EPA has determined that it cannot
be caused by.



  #6   Report Post  
Old 26-04-2003, 01:23 PM
Oz
 
Posts: n/a
Default UK vCJD October 2002

Gordon Couger writes

It wouldn't be bell shaped. I am exactly sure what the curve of an emerging
diseases looks like it would be different for each one, but the fear was
that it would be like growth curve of bacteria with a slow early phase and
very rapid log phase.


That's a pretty good description of what happened in cattle if you take
birth date and adjust for seasonality, up until the first MBM ban. Of
course it would have been bell shaped simply because there would have
been few if any unaffected cattle without the ban.

Other diseases have shown this kind of explosive out
break. So the early predictions have a very wide range of out comes and of
course the press picked up on the one that sold the most papers.


The fact that it resulted in substantial grants to the researchers had
nothing to do with the stories of course.

Fortunately humans appear to poor hosts for vCJD. It face cattle don't
appear to be very good hosts for it either.


So far only about 40% of the UK genotype seems to be susceptible (met-
met). Interestingly it's the genotype considered resistant to CJD. If
work on scrapie and sheep genetics is followed in humans then we ought
to expect little or none in the (not-met)(not-met) group (probably about
30% of the population) and considerably lower incidences in the
(met)(not-met) group (about 30%). GM mice with these genotypes did not
succumb to exposure to BSE (in the brain).

Since we do not know the exposure we do not know how susceptible humans
are. Cats, pigs and dogs in the UK had heavy exposure and the incidence
is small for cats, zero for dogs and pigs. I would point out that the
'species barrier' is misunderstood by many in that it is typically not a
total barrier but represents how hard it is to infect a species with a
particular prionic disease. Under extreme enough exposure (like
injecting it directly into the brain) most species can be infected by
most prionic diseases.

We do know for SURE that BSE is hugely less infective to humans than
human-strains of CJD. We know that invisibly microscopic traces of CJD
on stainless surgical implements can infect many subsequent people and
that post mortems on CJD patients carry a high risk of infection to
those doing the work. However thousands (probably tens of thousands) of
people, from farmers and vets, through abattoir workers, butchers,
knackers, renderers and hauliers are known for sure to have been
regularly exposed to high levels of known highly infectious material for
many years with not a single one of these groups so far succumbing to v-
CJD (although sooner of later it will happen).

Flat curves are good for vCJD declining would be better.


If we can get the data on dates of onset for this year (I'll probably
get the question asked in january) then I suspect the evidence will be
pretty clear, one way or the other. I have a horrible suspicion it's
going to match a flat curve. This would make me increasingly suspicious
that v-CJD is a low-incidence human CJD unrelated to BSE.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

  #7   Report Post  
Old 26-04-2003, 01:23 PM
Oz
 
Posts: n/a
Default UK vCJD October 2002

Torsten Brinch writes

Yes,exactly and the shape is not known a priori unless one has a
reasoned model -- which in this case we most certainly do not have.


We have data from the UK cattle epidemic, which should be a reasonable
guide until more information is available (if ever).

As you probably know, some think it is caused by the chronic effect of
exposure to toxic proteins from BSE affected cows.


News to me. Sounds like a torsten fishing expedition.

Quite a bit like
that Minamata disease in Japan caused by exposure to methylmercury,
just slower. But that can't be right, since


there isn't a scrap of evidence for it.

If there were to be toxic protein in the brains of BSE cows,
there should be at least sproadic reports of acute cases of dementia
in humans caused by the sunday dinner,


Why?
Torsten, are you practising your irony again?
You haven't quite got it yet.

IOW, we do not have
a clue what vCJD is caused by,


You ought to look up 'prions'.

and to be worse very many people think
it is caused by something that the EPA has determined that it cannot
be caused by.


Ahhh.
Having lost the 'millions die of vCJD' argument you are now either:

1) Practising irony. Badly.
2) Grasping at straws to 'support' your anti-GM stance.

You never learn, do you.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

  #8   Report Post  
Old 26-04-2003, 01:23 PM
Gordon Couger
 
Posts: n/a
Default UK vCJD October 2002


"Torsten Brinch" wrote in message
...
On Thu, 7 Nov 2002 16:38:18 -0600, "Gordon Couger"
wrote:


"Torsten Brinch" wrote in message
.. .
On Thu, 7 Nov 2002 03:48:45 -0600, "Gordon Couger"
wrote:

Torsten,

Has a trend devolved yet that would indicate that a peak is nearing

..

You are making reference to some thought imagine of a 'normal'
epidemic curve, I think, more or less bell-shaped with a tail. I don't
think our knowledge of the disease gives us basis for assuming such a
model.

Anyhow, if it is assumed, there is no clear indication in data where
we are in this assumed progressive development in relation to a peak.
Said otherwise, one can find support in data for us being as well
past, on, or nearing a peak. Past-peakers might note the decreasing
trend in vCJD deaths since about autumn 2000; on-peakers and
nearing-peakers, that the current incidence does not stand out
as particularly high or particularly low compared to the incidence
the previous 3-4 years.

It wouldn't be bell shaped. I am exactly sure what the curve of an

emerging
diseases looks like it would be different for each one snip


Yes,exactly and the shape is not known a priori unless one has a
reasoned model -- which in this case we most certainly do not have.

As you probably know, some think it is caused by the chronic effect of
exposure to toxic proteins from BSE affected cows. Quite a bit like
that Minamata disease in Japan caused by exposure to methylmercury,
just slower. But that can't be right, since the US EPA has determined
in connection with their approvals of genetically modified crops, that
when proteins are toxic they act by acute toxicity mechanisms and in
very small doses.

If there were to be toxic protein in the brains of BSE cows,
there should be at least sproadic reports of acute cases of dementia
in humans caused by the sunday dinner, and there should be huge
masses of supporting animal evidence for the acute toxic effects of
BSE brain muck. But quite on the contrary, there is a vast body of
evidence proving beyond any doubt, that experimental animals tolerate
large acute doses of BSE muck with no ill effect. IOW, we do not have
a clue what vCJD is caused by, and to be worse very many people think
it is caused by something that the EPA has determined that it cannot
be caused by.

The fantasicly intestisting thing about the TSE diseses is they are an
entirely new class of diseases. The incubation peroiod are so slow and the
method of transmision counter to what we think we know about he digestion of
protiens it will be a long time getting the research done. When you look at
the economic return on investment of reserch in TSE's the return is very
poor. It is simple not worth the opertunity cost spent on it when there are
more important things to spend money on.

Had the press not sensationalized it Mad Cow would be a foot note in
journals. Getting vCJD appears to be two to 3 times as likely as being
killed by lighiningin the UK. I must confess I would prefer lightineing. I
can't find the number on cattle killed by ligthing but the Mad Cow numers
range from 300,000 to 3,000,000. I the lower number is the ones diagnosed
and ones reasonable expected to have died from BSE and I know that the UK
has much better reporting than the US but I am sure that in the early part
of the out break it was low and probalbly to some extent all throug the out
break.

How every even if you take the high figure it was not an economicly
disatorus disease until the panic took over reducing the UK beef industry to
a side line of the dairy business.

I have blamed the greens for the fools debate on food safety but my side
shares the blame in not coming out a standing up in the harsh public light
and standing their ground. We have a 89 year old Noble prize winner we
shamed in to reentering the fray funded a few institutes to put out our
propaganda based on better science than the other side but still it is plain
that their job is to run interference for the scientist that should be
standing up and explaining to people why what they do is needed and safe but
most still hide in their holes (offices) afraid controversy will hurt their
funding. They need the balls to come out and tell their side of the story
and get pie in the face and earn the respect of the people because a few
voice in the wilderness will not over come the well oiled green machine.

No government is funding ag or another kind or research at the same rate
they were 20 years ago. So it is either commercial or very damn little when
it comes to research. A lot of the US research in the USDA and USGS is
being done by retired civil servants that have invested their lives in those
projects and when no one was there to take them up they just kept on working
with out pay. People don't go into science for money if they have all their
marbles. A few make it big but my son's starting salary fresh out of college
was higher than some full professors salary that taught him.

Torsten, we have been at this discussion a very long time. What I want for
the future is not much different than what you want. I want a world that is
capable of feeding it's self with each country being self sustaining as
possible using methods that at worst leave the ground as good as it was when
they pass it on to the next generation as it was when they got it. I want a
world that as people are needed in other areas of the economy they can be
freed from the back breaking labor of hand farming. I don't want to preserve
our soils I want to improve them. I see the only successful future of the
world as one where education, health care, and opportunity are available to
all. Feeding them is number one on the list and health is number two. They
have to be met before you can educate anyone. I expect that health care will
be the easiest in the coming century. Food next and education impossible in
large parts of the world.


In the years I farmed I tried to do that. I was not as succubus as I would
have like to have been But out of over 10,000 acres I worked at one time or
another on 20 acres is worse than when I took it on. A heavy rainfall event
caught it in cotton that I had not had time to put to wheat because I got it
too late in the year. I should have planted to a close rooted summer crop
but the land lord wanted another year of cotton. I could of probably changed
his mined if I had tried harder. I maintained the terraces and flood control
structures and added some of my own and planted a good many spots that
washed to grass it only cost an acre or two usualy and stopped a lot of
problems.

I left them every one with better more balanced fertility than when I got
them.

We are still working to put in the best practices on the land we own.
Spending nearly twice what a center pivot would cost to put in drip partly
because it pays better but it also uses less water a very precious commodity
in west Texas and by using drip we could use the shallow local recharge
aquiver that has only dropped 1 foot in 50 years and drilling 6 wells
instead drilling one well thorough to the Olagalla fossil water that would
probably have given us all the water we needed all our lives but it is
dropping a foot a year. Had I don't that the government would have let me
deduct the decrease in value of my land from the falling water table. This
way they don't But this way my son and his kids will still have water.

I am looking a doing something similar on my dad's place. The circumstances
are different and the whole thing hinges on the water quality. If it is good
enough for use forever we go if not we don't use.

I spent 5 years working on spray technology to reduce the amount of
fertilzer and herbicide by half with out reducing their effect.

In my 45 year of hands on work with agriculture I am convinced that
technology has steadily improved yields and reduced the impact of farming on
the environment. In the years after the war we got carried away with
pesticides and over did them but we are using every resource at our disposal
to do more with less. In my life grain yields have doubled and we need to do
it again before I die if I live as long as many in my family. I am satisfied
that the best affronts of science are the only way we have a chance to
improve the output of agriculture.

If you have a way to meet the needs of the coming century with out the every
effort of science I would be interested in hearing how we double the world
out put of food and do it where it is needed and not have situation like
Africa where food is being with held from starving people over some lame
excuse or another. If it wasn't GM it would be something. This is not the
first problem like this nor will it be the last. The only sure way to feed a
man is to give him a plant he can raise in his back yard. Preferable a
native one that deals with the climate. Corn is not a drought or heat
tolerant plant.

I know you are a protester at heart and protests shine the light of day on
situation that need correction but they aren't the way to correct them.
That's the job for people like me that fully understand the ramification or
a least have some idea what to look for when you change a faming system.

Best regards
Gordon


  #9   Report Post  
Old 26-04-2003, 01:23 PM
Torsten Brinch
 
Posts: n/a
Default UK vCJD October 2002

On Fri, 8 Nov 2002 02:54:29 -0600, "Gordon Couger"
wrote:


"Torsten Brinch" wrote in message
.. .


If there were to be toxic protein in the brains of BSE cows,
there should be at least sproadic reports of acute cases of dementia
in humans caused by the sunday dinner, and there should be huge
masses of supporting animal evidence for the acute toxic effects of
BSE brain muck. But quite on the contrary, there is a vast body of
evidence proving beyond any doubt, that experimental animals tolerate
large acute doses of BSE muck with no ill effect. IOW, we do not have
a clue what vCJD is caused by, and to be worse very many people think
it is caused by something that the EPA has determined that it cannot
be caused by.


The fantasicly intestisting thing about the TSE diseses is they are an
entirely new class of diseases. The incubation peroiod are so slow and the
method of transmision counter to what we think we know about he digestion of
protiens it will be a long time getting the research done.


Again, compare with the time delayed effect of methyl mercury.
We would not say that a person who has just ingested a dose
of methyl mercury which will in time make him go down with
neurological disease, has had a disease transmitted to him, nor
would we say that the time passing until his symptoms appear
is an incubation time. We would say that he has been exposed
to a toxic dose of methylmercury, sufficient to cause chronic
effects.

When you look at
the economic return on investment of reserch in TSE's the return is very
poor. It is simple not worth the opertunity cost spent on it when there are
more important things to spend money on.


Well, in practice it apparently has been worth a Nobel prize, and a
whole lot of research besides, and the knowledge gathered so far has
made pretty much everyone adopt the view that proteins may well exist
which act by chronic toxicity mechanism while causing effects which
can not be provoked by short term feeding experiments using large
doses.

The US EPA, in the context of GM approvals, is a notable exception.
In that context the EPA has determined, that it is 'known' that when
proteins are toxic they act invariably by acute mechanism and in very
small doses. That is quite expedient, because that means one can just
feed large doses of the protein to the calf for a few days to prove
that no ill effect can come from the ingestion of the protein in the
feed in the long term.

Getting vCJD appears to be two to 3 times as likely as being
killed by lighiningin the UK. I must confess I would prefer lightineing.


That's an idiotic comparison, don't try to get a job in risk
communication.

I can't find the number on cattle killed by ligthing


Oh well. Putting up that number here would be idiotic and it's hard to
see how you can find use for on this avenue anyway.

but the Mad Cow numers
range from 300,000 to 3,000,000. I the lower number is the ones diagnosed
and ones reasonable expected to have died from BSE and I know that the UK
has much better reporting than the US but I am sure that in the early part
of the out break it was low and probalbly to some extent all throug the out
break.How every even if you take the high figure it was not an economicly
disatorus disease


considerably more disastrous than lightning, tho' :-)

snip load of completely unrelated stuff
  #10   Report Post  
Old 26-04-2003, 01:23 PM
Gordon Couger
 
Posts: n/a
Default UK vCJD October 2002


"Torsten Brinch" wrote in message
...
On Fri, 8 Nov 2002 02:54:29 -0600, "Gordon Couger"
wrote:


"Torsten Brinch" wrote in message
.. .


If there were to be toxic protein in the brains of BSE cows,
there should be at least sproadic reports of acute cases of dementia
in humans caused by the sunday dinner, and there should be huge
masses of supporting animal evidence for the acute toxic effects of
BSE brain muck. But quite on the contrary, there is a vast body of
evidence proving beyond any doubt, that experimental animals tolerate
large acute doses of BSE muck with no ill effect. IOW, we do not have
a clue what vCJD is caused by, and to be worse very many people think
it is caused by something that the EPA has determined that it cannot
be caused by.


The fantasicly intestisting thing about the TSE diseses is they are an
entirely new class of diseases. The incubation peroiod are so slow and

the
method of transmision counter to what we think we know about he digestion

of
protiens it will be a long time getting the research done.


Again, compare with the time delayed effect of methyl mercury.
We would not say that a person who has just ingested a dose
of methyl mercury which will in time make him go down with
neurological disease, has had a disease transmitted to him, nor
would we say that the time passing until his symptoms appear
is an incubation time. We would say that he has been exposed
to a toxic dose of methylmercury, sufficient to cause chronic
effects.

--------------------------------
It would be facinting to find out how and why man contacts vCJD with so few
pateints I expect a guess will be best they can do with spieces that catch
TSE diseases not developed in their species.

Probably our best bet scrapie or CWD. If I were to guess and it is a guess
only if come from sniffing another animal wiht and getting the protien on
the nerve endings of the nerves that do the smelling. The ony reason for the
guess is it is the shortest path to the brain. It may well be licking and a
oral route.


When you look at
the economic return on investment of reserch in TSE's the return is very
poor. It is simple not worth the opertunity cost spent on it when there

are
more important things to spend money on.


Well, in practice it apparently has been worth a Nobel prize, and a
whole lot of research besides, and the knowledge gathered so far has
made pretty much everyone adopt the view that proteins may well exist
which act by chronic toxicity mechanism while causing effects which
can not be provoked by short term feeding experiments using large
doses.

==================
Discovering a completly new mode of disease tramission is the stuff Nobe
prizes are made their econimic revalace is not a consideration.

The US EPA, in the context of GM approvals, is a notable exception.
In that context the EPA has determined, that it is 'known' that when
proteins are toxic they act invariably by acute mechanism and in very
small doses. That is quite expedient, because that means one can just
feed large doses of the protein to the calf for a few days to prove
that no ill effect can come from the ingestion of the protein in the
feed in the long term.

===========
Prions are not toxic in the usual sense that cause the body to make more of
them clogging up the works. The EPA head has been replaced wih a science guy
insted of a political guy I expect things will start to get streightined out
there.

Getting vCJD appears to be two to 3 times as likely as being
killed by lighiningin the UK. I must confess I would prefer lightineing.


That's an idiotic comparison, don't try to get a job in risk
communication.


Give a better example of you chancge of getting vCJD.

I can't find the number on cattle killed by ligthing


Oh well. Putting up that number here would be idiotic and it's hard to
see how you can find use for on this avenue anyway.

but the Mad Cow numers
range from 300,000 to 3,000,000. I the lower number is the ones diagnosed
and ones reasonable expected to have died from BSE and I know that the

UK
has much better reporting than the US but I am sure that in the early

part
of the out break it was low and probalbly to some extent all throug the

out
break.How every even if you take the high figure it was not an economicly
disatorus disease


considerably more disastrous than lightning, tho' :-)

Regardless the only thing that mad a economic problem of Mad Cow Disease is
caused by the press and the governments bungling. Higher risks like
Ecoli:157, listeria, salmonella, that we have real solutions for we are not
interested enough to get around to irradiating the food after it is
packaged. In fact the greens are against it. Again with no proof against 50
year of proof that it has caused no harm. We also have the solution to BSE
don't feed cows MBM.

Gordon






  #11   Report Post  
Old 26-04-2003, 01:23 PM
Torsten Brinch
 
Posts: n/a
Default UK vCJD October 2002

On Fri, 8 Nov 2002 12:26:14 -0600, "Gordon Couger"
wrote:
"Torsten Brinch" wrote in message
.. .
Again, compare with the time delayed effect of methyl mercury.
We would not say that a person who has just ingested a dose
of methyl mercury which will in time make him go down with
neurological disease, has had a disease transmitted to him, nor
would we say that the time passing until his symptoms appear
is an incubation time. We would say that he has been exposed
to a toxic dose of methylmercury, sufficient to cause chronic
effects.

--------------------------------
It would be facinting to find out how and why man contacts vCJD with so few
pateints I expect a guess will be best they can do with spieces that catch
TSE diseases not developed in their species.


With the number of species involved in the sudden UK upsurge of TSE in
the last few decades of the 20th century and in all sorts of species
the simplest hypothesis is that they all got it from the same source
directly and/or via consumption of meat or dairy products.

Probably our best bet scrapie or CWD. If I were to guess and it is a guess
only if come from sniffing another animal wiht and getting the protien on
the nerve endings of the nerves that do the smelling. The ony reason for the
guess is it is the shortest path to the brain. It may well be licking and a
oral route.


Yes. Come to think of it, kissing as a risk actor for these relatively
young people dying of vCJD is territory relatively uncharted by
science, afaik.
..

The US EPA, in the context of GM approvals, is a notable exception.
In that context the EPA has determined, that it is 'known' that when
proteins are toxic they act invariably by acute mechanism and in very
small doses. That is quite expedient, because that means one can just
feed large doses of the protein to the calf for a few days to prove
that no ill effect can come from the ingestion of the protein in the
feed in the long term.

===========
Prions are not toxic in the usual sense


What do you mean not toxic in the usual sense. We say that a substance
is toxic when it through its chemical action kills, injures, or
impairs an organism, and that is exactly what this prion-substance
seems to be doing.

that cause the body to make more of them clogging up the works.


Well, we are not sure if -that- is what they are doing, but even if
it was, so what. It is not disallowed for a toxic substance to work
in its own peculiar ways.


  #12   Report Post  
Old 26-04-2003, 01:23 PM
Gordon Couger
 
Posts: n/a
Default UK vCJD October 2002


"Torsten Brinch" wrote in message
...
On Fri, 8 Nov 2002 12:26:14 -0600, "Gordon Couger"
wrote:
"Torsten Brinch" wrote in message
.. .
Again, compare with the time delayed effect of methyl mercury.
We would not say that a person who has just ingested a dose
of methyl mercury which will in time make him go down with
neurological disease, has had a disease transmitted to him, nor
would we say that the time passing until his symptoms appear
is an incubation time. We would say that he has been exposed
to a toxic dose of methylmercury, sufficient to cause chronic
effects.

--------------------------------
It would be facinting to find out how and why man contacts vCJD with so

few
pateints I expect a guess will be best they can do with spieces that

catch
TSE diseases not developed in their species.


With the number of species involved in the sudden UK upsurge of TSE in
the last few decades of the 20th century and in all sorts of species
the simplest hypothesis is that they all got it from the same source
directly and/or via consumption of meat or dairy products.

===============\
The upsurge in TSE is usualy connected with feeding meat from the same
spices. I believe mink were the first well stuided case in the 50's or so.
In the UK an EU with your high population density forcing nearly anything
larger than a sparrow to go to the renering pland and manageries of many
kinds of animals scattered over the country coupled with the a shortage of
vegtable protien there is not telling what got chopped up and fed to what.
Giving every TSE a chance at nearly every animal in the country by the oral
route.

Probably our best bet scrapie or CWD. If I were to guess and it is a

guess
only if come from sniffing another animal wiht and getting the protien on
the nerve endings of the nerves that do the smelling. The ony reason for

the
guess is it is the shortest path to the brain. It may well be licking and

a
oral route.


Yes. Come to think of it, kissing as a risk actor for these relatively
young people dying of vCJD is territory relatively uncharted by
science, afaik.
..

The US EPA, in the context of GM approvals, is a notable exception.
In that context the EPA has determined, that it is 'known' that when
proteins are toxic they act invariably by acute mechanism and in very
small doses. That is quite expedient, because that means one can just
feed large doses of the protein to the calf for a few days to prove
that no ill effect can come from the ingestion of the protein in the
feed in the long term.

===========
Prions are not toxic in the usual sense


What do you mean not toxic in the usual sense. We say that a substance
is toxic when it through its chemical action kills, injures, or
impairs an organism, and that is exactly what this prion-substance
seems to be doing.

============
I will thing more on toxic in the usasl senses.
It appers that only certian geontype are suscptable to them. There are not
known to be dose dependent and spoke of as a disease not a posining. Of
course with a new disease we might as well usign gerogre, soe and thumb tack
as terms. Using familure terms could lead to mistakes.

In the case of cronic wasting disease if 20 to 30% the deer were resistant
to CWD it would get us back to decent dear herds.

that cause the body to make more of them clogging up the works.


Well, we are not sure if -that- is what they are doing, but even if
it was, so what. It is not disallowed for a toxic substance to work
in its own peculiar ways.


There is prion that grows in yeasts. I haven't looked into it much. It seem
to be more tractable in its culture. I thnke they are class 1 bugs you can
grow them any place but your kitchen.
--
Gordon

Gordon Couger
Stillwater, OK
www.couger.com/gcouger

Gordon




 
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