Dear people!
If you want to help our Blind people association, all you need is to
go to this address…
http://www.homer.hr and click the banner in the left column with big
SM letters. This portal donates money to us, for every unique visitor.
Be so kind and participate in this humane act. It costs you nothing
but 2 clicks of your mouse.
Thank you!
With all the hoo-haa about swine flu and every health blog posting
some type of article on this media-hyped topic, I figured I’d take a
different approach. Yes, swine flu is bad, and it has killed many
people but it’s STILL just a flu, and the best way to PREVENT a flu
(or a cold) is by having a strong immune system… Not by having the
right drugs to cure yourself in case you get it. Here are the TOP
Herbs that will give you a strong Immune system… (read more)>>
http://flawlessfitnessbook.com/blog/how-to-boost-strengthen-your-immu…
Forwarded message from Richard Moore <r…@quaylargo.com>
Sunday, May 10, 2009
Swine Flu – Winnipeg lab – Why are Mexicans are being hit the hardest
http://www.thestar.com/article/630370
Flu virus baffles Canadian scientists
Winnipeg lab can’t find reason why Mexicans are being hit the hardest
Joanna Smith
Ottawa Bureau
May 7, 2009
Ottawa – Canadian scientists discovered nothing in the
genetic makeup of the H1N1 virus that would explain why
symptoms are far more severe in Mexico than in all but one
of the 201 confirmed cases here.
A team of researchers at the National Microbiology
Laboratory in Winnipeg worked day and night to finish the
first genetic sequencing of samples of the virus from
Canada and Mexico in less than a week, federal health
officials announced yesterday.
"This does take us a step forward in terms of our
understanding of how the virus works," Chief Public Health
Officer Dr. David Butler-Jones said.
Scientists mapped the building blocks of three samples from
Mexico, Nova Scotia and Ontario and ruled out genetic
mutation as the reason why the virus appears to be far more
virulent in Mexico.
That leaves scientists looking elsewhere for answers. Dr.
Frank Plummer, scientific director at the Winnipeg
laboratory, said they are looking at other factors like the
environment in Mexico, the existence of another infectious
agent spreading through the country at the same time or the
individual genetics of the Mexican patients.
Living conditions in Mexico and how quickly a patient first
went to the hospital are also possible factors, Butler-
Jones said.
The only severe case in Canada remains that of a young girl
from Edmonton.
Last night, a spokesperson at Toronto’s Princess Margaret
Hospital confirmed a hospital worker is at home recovering
after contracting the H1N1 virus, also known as swine flu.
It has been determined the ill worker had no link to
Mexico.
The hospital revealed few details about the employee. All
spokesperson Gillian Howard would say is that she is a
female who was not involved in direct patient care.
The staffer had a nasal swab taken about six days ago.
There is about a five-day turnaround on lab test results,
Howard noted.
Howard said hospital officials were evaluating and
following up with any colleagues who had direct contact
with the ill worker.
Princess Margaret is not advising patients to stay away
from the hospital if they have appointments. It’s business
as usual, Howard said.
Public health authorities across Canada yesterday announced
36 newly confirmed cases of the H1N1 virus to bring the
total to 201.
There are eight new cases in British Columbia, four in
Alberta, six in Quebec, five in Nova Scotia and 13 in
Ontario.
With files from Theresa Boyle
Canadian pork safe despite warning, minister says
The Canadian government says pork is safe to eat despite a
warning by the World Health Organization that the swine flu
virus could survive in slaughtered pigs.
"Canadian pork is safe. There is no danger," Agriculture
Minister Gerry Ritz insisted yesterday after serving up
pork sandwiches to MPs and government workers on Parliament
Hill.
Earlier in the day, a WHO official said the pig strain of
the H1N1 virus may withstand freezing and persist in the
thawed meat and blood of infected animals.
But Dr. Brian Evans of the Canadian Food Inspection Agency
said Canada has safeguards to keep diseased pigs from
making it to market. He said pigs are screened on farms for
illnesses and assessed at slaughterhouses.
The Canadian Press
Web sites:
http://www.governourselves.org/
http://escapingthematrix.org/
http://cyberjournal.org
Recent archives:
http://groups.yahoo.com/group/newslog/messages
http://groups.yahoo.com/group/cyberjournal/messages
Old archives:
http://cyberjournal.org/show_archives/?lists=newslog
http://cyberjournal.org/show_archives/
End of forwarded message from Richard Moore <r…@quaylargo.com>
Jai Maharaj
http://tinyurl.com/24fq83
http://www.mantra.com/jai
http://www.mantra.com/jyotish
Om Shanti
Hindu Holocaust Museum
http://www.mantra.com/holocaust
Hindu life, principles, spirituality and philosophy
http://www.hindu.org
http://www.hindunet.org
The truth about Islam and Muslims
http://www.flex.com/~jai/satyamevajayate
DISCLAIMER AND CONDITIONS
o Not for commercial use. Solely to be fairly used for the educational
purposes of research and open discussion. The contents of this post may not
have been authored by, and do not necessarily represent the opinion of the
poster. The contents are protected by copyright law and the exemption for
fair use of copyrighted works.
o If you send private e-mail to me, it will likely not be read,
considered or answered if it does not contain your full legal name, current
e-mail and postal addresses, and live-voice telephone number.
o Posted for information and discussion. Views expressed by others are
not necessarily those of the poster who may or may not have read the article.
FAIR USE NOTICE: This article may contain copyrighted material the use of
which may or may not have been specifically authorized by the copyright
owner. This material is being made available in efforts to advance the
understanding of environmental, political, human rights, economic,
democratic, scientific, social, and cultural, etc., issues. It is believed
that this constitutes a ‘fair use’ of any such copyrighted material as
provided for in section 107 of the US Copyright Law. In accordance with Title
17 U.S.C. Section 107, the material on this site is distributed without
profit to those who have expressed a prior interest in receiving the included
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subscribing to USENET newsgroups or visiting web sites. For more information
go to: http://www.law.cornell.edu/uscode/17/107.shtml
If you wish to use copyrighted material from this article for purposes of
your own that go beyond ‘fair use’, you must obtain permission from the
copyright owner.
Forwarded message from Ted:
WHAT MIGHT BE THE GREATER LIFESPAN OF VEGETARIANS?
Scharffenberg [John Scharffenberg PROBLEMS WITH MEAT, 1989]
drawing upon epidemiological data provided by Lemon &
Walden (JAMA, 1969, 18:950) reported that the best diet for
human beings in terms of health and longevity is
vegetarian. In general, vegetarians live about 6 years
longer than their meat eating counterparts (i.e., meat-
eating Seventh Day Adventists).
If we select as our comparison group only those Seventh Day
Adventists who still eat meat AND who do not smoke, it
turns out that their total vegetarian counterparts still
out live them by 3 years. Hence, even when we use a
somewhat CONSERVATIVE comparison group (remember, even
though not all SDA’s are vegetarian but on the whole they
would still eat less meat then the average North American)
and thereby control for known life style hazards like
smoking, VEGETARIANS STILL LIVE LONGER (ABOUT 3 YEARS) THAN
EVEN MODERATE MEAT EATERS, and here we are talking a
comparable comparison group of meat eaters who otherwise
share essentially the same life style. This is still a
substantial difference and it would appear that the hazards
of meat eating are on the same level as that of smoking
(which as we have seen shortens this comparison group’s
life-span by about 3 years).
Also, keep in mind that the observed-to-expected coronary
heart disease mortality among total vegetarians is only
14%. Vegetarians, of course, do have heart attacks but they
occur approximately 20 years later in life than for meat
eaters. Thus, not only is longevity increased but so is the
quality of health for the life span that one does live out.
This is important, especially if we hope to live a robust
and vital life and not end up being a valetudinarian or
invalid during our "golden" years, which indeed should be
golden.
Now, it is the case that the 3 year figure I cited for
greater longevity of vegetarian SDAs over their meat-eating
SDA counterparts (after activity levels, smoking, etc. had
been controlled) would LIKELY BE GREATER between
vegetarians and non-vegetarians in the population at large.
There is a greater heterogeneity (or heteroscadasticity, if
you wish) of dietary practices in the larger population.
That is, North Americans as a whole eat about twice as much
meat as even our SDA omnivores. Hence, our "with-in"
population comparison of SDA vegetarians with SDA non-
vegetarians is more homogeneous with respect to meat
consumption and would therefore likely manifest a smaller
magnitude of difference.
Also, when attempting a proper longitudinal follow-up study
there are real-world constraints that WORK AGAINST the
comparison. That is, many omnivores in our SDA population
during the interim of a longitudinal study actually reduce
their meat consumption or even become vegetarians. For
instance, Snowdon and Phillips (AMER. JOURNAL OF PUBLIC
HEALTH, 75(5): 507-12) found in their 21 year long follow-
up study that meat consumption patterns changed as follows
in a sample of 7,012 SDA’s:
1960 1976
<1 day/wk (vegetarian) 12% ate meat at least >1 day/wk
1-2 days/wk 49% " " " " " "
3-5 days/wk 72% " " " " " "
6+ days/wk 83% " " " " " "
Hence, some vegetarians during the interim became meat-
eaters and many meat-eaters became vegetarians. This change
of dietary habits does NOT explain the finding of why
vegetarians live 3 years longer but works AGAINST it.
Hence, this 3 year figure is a very conservative
underestimation of the even the actual difference, let
alone the potential difference of how vegans and meat-
eaters in the population at large would compare..
This figure of three years is therefore a CONSERVATIVE
figure and one can say, therefore, that vegetarians live AT
LEAST 3 years longer than omnivores. And this is not even
taking into account the greater difference that likely
would further occur if vegans rather than just lacto-ovo-
vegetarians were instead used as our comparison group. It
is this figure, conservative as it is, that ought to be the
figure you cite since at least we here a figure that is
empirically justified and applicable to the North American
situation. Incidentally, I’ve seen higher estimates but I
can’t find them right now.
One last note. The biologic cost of a North American
omnivorous diet is only partly given by life expectancy
estimates. Certainly, the quality of life is reduced when
one has to suffer from, say, non-lethal but debilitating
strokes and heart attacks. Problems of obesity, reduced
endurance, crapulence, and so on are not to be ignored.
Even the cognitive contradiction of being one who loves
animals but who would still sit down at dinner to eat dead
animals might also be something that detracts from enjoying
a quality life, a life in which one can say
"I lived a good life and in my small way helped to
mitigate some of the suffering in the world instead of
helping to increase it".
Ted
End of forwarded message
Jai Maharaj
http://tinyurl.com/24fq83
http://www.mantra.com/jai
http://www.mantra.com/jyotish
Om Shanti
Hindu Holocaust Museum
http://www.mantra.com/holocaust
Hindu life, principles, spirituality and philosophy
http://www.hindu.org
http://www.hindunet.org
The truth about Islam and Muslims
http://www.flex.com/~jai/satyamevajayate
DISCLAIMER AND CONDITIONS
o Not for commercial use. Solely to be fairly used for the educational
purposes of research and open discussion. The contents of this post may not
have been authored by, and do not necessarily represent the opinion of the
poster. The contents are protected by copyright law and the exemption for
fair use of copyrighted works.
o If you send private e-mail to me, it will likely not be read,
considered or answered if it does not contain your full legal name, current
e-mail and postal addresses, and live-voice telephone number.
o Posted for information and discussion. Views expressed by others are
not necessarily those of the poster who may or may not have read the article.
FAIR USE NOTICE: This article may contain copyrighted material the use of
which may or may not have been specifically authorized by the copyright
owner. This material is being made available in efforts to advance the
understanding of environmental, political, human rights, economic,
democratic, scientific, social, and cultural, etc., issues. It is believed
that this constitutes a ‘fair use’ of any such copyrighted material as
provided for in section 107 of the US Copyright Law. In accordance with Title
17 U.S.C. Section 107, the material on this site is distributed without
profit to those who have expressed a prior interest in receiving the included
information for research, comment, discussion and educational purposes by
subscribing to USENET newsgroups or visiting web sites. For more information
go to: http://www.law.cornell.edu/uscode/17/107.shtml
If you wish to use copyrighted material from this article for purposes of
your own that go beyond ‘fair use’, you must obtain permission from the
copyright owner.
"Maltol more effective"
An Efficient Synthesis of 5-Amido-3-Hydroxy-4-Pyrones as
Inhibitors of Matrix Metalloproteinases
Yi-Long Yan and Seth M. Cohen*
Department of Chemistry and Biochemistry, University of California,
San Diego, La Jolla, California 92093-0358
E-mail: Email: sco…@ucsd.edu
Abstract
3-Hydroxy-4-pyrones are a class of important metal chelators with
versatile medicinal applications.
An efficient pathway for the preparation of new 5-amido-3-hydroxy-4-
pyrone
derivatives has been developed.
The synthesized 5-amido-3-hydroxy-4-pyrones have been evaluated as
inhibitors of matrix metalloproteinases.
PMID: 17521196
————–
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2531216
We have found that maltol and thiomaltol are more effective chelating
inhibitors
for MMP-3 (stromelysin) than the widely reported hydroxamate ligands.
————
http://books.google.com/books?isbn=9067643084
"On the basis of the data obtained in this investigation , the
mechanism of the maltol action was stated.
It includes the chelating of Fe(II) and Fe(III) ions by maltol
in the system of iron /NADPH-dependent LPO.
Chelating properties of 3-hydroxy-4-pyrones suggested a
role as regulators of absorption and metabolism of iron in
animals.
The antioxidant properties of hydroxypyrones allow us to
explain and apply their chemoprotective activity and
anticarcinogenic effects.
Besides their ability to inhibit formation of N-nitrosoamines,
the ability of maltol and ethylmaltol to suppress oxidative stress,
which accompanies consumption of alcohol and smoking , is to
be considered as a most valuable property.
Maltol and ethylmaltol as tobacco smoking inhibitors are introduced
in a 500 mg/day dose into the compositions of chewing gums,
caramels or other food agents, which should be present in the mouth
over 10 minutes.
The administration of these peroaral medicinal forms of maltol
displays an additional advantage, since a chewing gum with maltol is
patented as a dental caries inhibitor."
———————
Matrix metalloproteinase inhibitors as therapy for inflammatory and
vascular diseases
Nature Reviews Drug Discovery 6, 480-498 (June 2007)
Jialiang Hu1,3, Philippe E. Van den Steen1,3, Qing-Xiang A. Sang2 &
Ghislain Opdenakker1 About the authors
Top of page
Abstract
Matrix metalloproteinases (MMPs) have outgrown the field
of extracellular-matrix biology and have progressed towards
being important regulatory molecules in cancer and inflammation.
This rise in status was accompanied by the development of various
classes of inhibitors.
Although clinical trials with synthetic inhibitors for the treatment
of cancer were disappointing, recent data indicate that the use of
selective inhibitors might lead to new therapies for acute and
chronic
inflammatory and vascular diseases.
In this Review, we compare the major classes of MMP inhibitors
and advocate that future drug discovery should be based on crucial
insights into the differential roles of specific MMPs in
pathophysiology
obtained with animal models, including knockout studies.
doi:10.1038/nrd2308
———-
http://theoncologist.alphamedpress.org/cgi/content/full/3/4/271
New Drugs on the Horizon: Matrix Metalloproteinase Inhibitors
Mace L. Rothenberg, Amy R. Nelson, Kenneth R. Hande
The Oncologist, Vol. 3, No. 4, 271-274, August 1998
© 1998 AlphaMed Press
——————–
Structure-based design of HIV protease inhibitors:
5,6-dihydro-4-hydroxy-2-pyrones as effective, nonpeptidic
inhibitors.
J Med Chem. 1996 Nov 8;39(23):4630-42.
Thaisrivongs S, Romero DL, Tommasi RA,
Janakiraman MN, Strohbach JW, Turner SR,
Biles C, Morge RR, Johnson PD, Aristoff PA,
Tomich PK, Lynn JC, Horng MM, Chong KT,
Hinshaw RR, Howe WJ, Finzel BC, Watenpaugh KD.
Medicinal Chemistry Research, Pharmacia & Upjohn, Inc.,
Kalamazoo, Michigan 49001, USA.
From a broad screening program, the 4-hydroxycoumarin
phenprocoumon (I) was previously identified as a lead
template with HIV protease inhibitory activity.
The crystal structure of phenprocoumon/HIV protease complex
initiated a structure-based design effort that initially identified
the
4-hydroxy-2-pyrone U-96988 (II) as a first-generation clinical
candidate for the potential treatment of HIV infection.
Based upon the crystal structure of the 4-hydroxy-2-pyrone III/HIV
protease complex, a series of analogues incorporating a
5,6-dihydro-4-hydroxy-2-pyrone template were studied.
It was recognized that in addition to having the required
pharmacophore (the 4-hydroxy group with hydrogen-bonding
interaction with the two catalytic aspartic acid residues and the
lactone moiety replacing the ubiquitous water molecule in the
active site), these 5,6-dihydro-4-hydroxy-2-pyrones incorporated
side chains at the C-6 position that appropriately extended into
the S1′ and S2′ subsites of the enzyme active site.
The crystal structures of a number of representative
5,6-dihydro-4-hydroxy-2-pyrones complexed with the HIV
protease were also determined to provide better understanding
of the interaction between the enzyme and these inhibitors to
aid the structure-based drug design effort.
The crystal structures of the ligands in the enzyme active site
did not always agree with the conformations expected from
experience with previous pyrone inhibitors.
This is likely due to the increased flexibility of the dihydropyrone
ring.
From this study, compound XIX exhibited reasonably high enzyme
inhibitory activity (Ki = 15 nM) and showed antiviral activity
(IC50 = 5 microM) in the cell-culture assay.
This result provided a research direction which led to the discovery
of active 5,6-dihydro-4-hydroxy-2-pyrones as potential agents for the
treatment of HIV infection.
PMID: 8917652
———–
Matrix metalloproteinase inhibitors: new challenges
in the era of post broad-spectrum inhibitors.Nuti E,
Tuccinardi T, Rossello A.
Curr Pharm Des. 2007;13(20):2087-100.
Dipartimento di Scienze Farmaceutiche,
Università di Pisa, Pisa, Italy.
More than two decades have been spent to develop
many families of synthetic matrix metalloproteinases
inhibitors (MMPI) as therapeutical agents for serious
pathologies.
Unfortunately, clinical trials conducted on broad-spectrum
inhibitors have yielded disappointing results, especially in
the cancer pathology area.
Despite these outcomes, some small synthetic MMPI are
in advanced trials or launched in clinical ones for cancer,
arthritis, periodontal diseases.
Today many groups are developing intensive efforts to find
new classes of inhibitors characterized by improved potency
and, above all, high selectivity against the specific MMP
involved in each targeted pathology.
The new challenges include the development of new MMPI
bearing more effective ZBGs and the development of new
allosteric non-zinc binding inhibitors, devoid of ZBGs.
An analysis of more recent results in this field reported on
journals and patents will be developed, to consider some of
the more interesting new highly selective synthetic MMPI,
their SARs, the new theoretical approaches used for modelling
and the results of their biological evaluations.
PMID: 17627541
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
You Alties just love to claim that a strong immune system is important
for health. Make sure it is working at peak performance.
http://www.globalhealth.org/sources/view.php3?id=1185
http://www.cdc.gov/eid/content/14/8/pdfs/07-1313.pdf
http://www3.niaid.nih.gov/news/newsreleases/2006/1918mouse.htm
http://www.nature.com/nature/journal/vaop/ncurrent/abs/nature05181.html
Excerpts: “Influenza [in pigs] is closely correlated with pig
density,” said a European Commission-funded researcher studying the
situation in Europe.[17] As such, Europe’s rapidly intensifying pig
industry has been described in Science as “a recipe for
disaster.”[18] Some researchers have speculated that the next
pandemic could arise out of “Europe’s crowded pig barns.”[19] Concern
over epidemic disease is so great that Danish laws have capped the
number of pigs per farm and put a ceiling on the total number of pigs
allowed to be raised in the country.[21] No such limit exists in the
United States.
With massive concentrations of farm animals within which to mutate,
these new swine flu viruses in North America seem to be on an
evolutionary fast track, jumping and reassorting between species at an
unprecedented rate.[22] This reassorting, Webster’s team concludes,
makes the 60 million strong U.S. pig population an “increasingly
important reservoir of viruses with human pandemic potential.”[23]
In the 1980s, more than 85 percent of all North Carolina pig farms had
fewer than 100 animals. By the end of the 1990s, operations confining
more than 1,000 animals controlled about 99 percent of the state’s
inventory.[12] Given that the primary route of swine flu transmission
is thought to be the same as human flu—via droplets or aerosols of
infected nasal secretions[13]—it’s no wonder experts blame
overcrowding for the emergence of new flu virus mutants.
========= Full:
Swine Flu and Factory Farms: Fast Track to Disaster
by Michael Greger, M.D.
The H1N1 swine flu virus in North America currently concerning global
public health officials is not the first triple hybrid human/bird/pig
flu virus to be discovered.
First Found on a Factory Farm
The first was discovered in a North Carolina factory farm in 1998.
Since the 1918 pandemic, an H1N1 flu virus has circulated in pig
populations, becoming one of the most common causes of respiratory
disease on North American pig farms.[1]
In August 1998, however, a barking cough resounded throughout a North
Carolina pig farm in which all the thousands of breeding sows fell
ill. An aggressive H3N2 virus was discovered, the type of influenza
that had been circulating in humans since 1968.
Not only was this highly unusual—only a single strain of human virus
had ever previously been isolated from an American pig population—but
upon sequencing of the viral genome, researchers found that it was not
just a double reassortment (a hybrid of human and pig virus, for
example), but a never-before-described triple reassortment, a hybrid
of three viruses—a human virus, a pig virus, and a bird virus.[2]
Intensive Farming is the Problem
Dr. Robert Webster, one of the world’s leading experts of flu virus
evolution, blames the emergence of the 1998 virus on the “recently
evolving intensive farming practice in the USA, of raising pigs and
poultry in adjacent sheds with the same staff,” a practice he calls
“unsound.”[3] “Within the swine population, we now have a mammalian-
adapted virus that is extremely promiscuous,” explained another
molecular virologist at the time, referring to the virus’s proclivity
to continue to snatch up genes from human flu viruses. “We could end
up with a dangerous virus.”[4] This may indeed be what we are now
facing.
Within months of the 1998 emergence, the virus showed up in Texas,
Minnesota, and Iowa.[5] Within a year, it had spread across the
United States.[6] This rapid dissemination across the country has
been blamed on long-distance live animal transport.[7]
Long Way to Go
In the United States, pigs travel coast to coast. They can be bred in
North Carolina, fattened in the corn belt of Iowa, and slaughtered in
California.[8] While this may reduce short-term costs for the pork
industry, the highly contagious nature of diseases like influenza
(perhaps made further infectious by the stresses of transport) needs
to be considered when calculating the true cost of long-distance live
animal transport.
What led to the emergence of the North Carolina strain in the first
place? What changed in the years leading up to 1998 that facilitated
the surfacing of such a unique strain? It is likely no coincidence
that the virus emerged in North Carolina, the home of the nation’s
largest pig farm. North Carolina has the densest pig population in
North America and reportedly boasts more than twice as many corporate
swine mega-factories as any other state.[9]
Agricultural Intensification
The year of emergence, 1998, was the year North Carolina’s pig
population hit ten million, up from two million just six years before.
[10] At the same time, the number of hog farms was decreasing, from
15,000 in 1986 to 3,600 in 2000.[11] How do five times more animals
fit on almost five times fewer farms? By crowding about 25 times more
pigs into each operation.
In the 1980s, more than 85 percent of all North Carolina pig farms had
fewer than 100 animals. By the end of the 1990s, operations confining
more than 1,000 animals controlled about 99 percent of the state’s
inventory.[12] Given that the primary route of swine flu transmission
is thought to be the same as human flu—via droplets or aerosols of
infected nasal secretions[13]—it’s no wonder experts blame
overcrowding for the emergence of new flu virus mutants.
Starting in the early 1990s, the U.S. pig industry restructured itself
after Tyson’s profitable poultry model of massive industrial-sized
units. As a headline in the trade journal National Hog Farmer
announced, “Overcrowding Pigs Pays—If It’s Managed Properly.”[14]
Crowding Breeds Disease
The majority of U.S. pig farms now confine more than 5,000 animals
each. A veterinary pathologist from the University of Minnesota stated
the obvious in Science: “With a group of 5,000 animals, if a novel
virus shows up it will have more opportunity to replicate and
potentially spread than in a group of 100 pigs on a small farm.”[15]
Recent Outbreak
The swine flu virus discovered this week in California and Mexico
appears to be a quadruple reassortment virus incorporating genes from
human and avian flu viruses as well as North American and European
strains of swine flu. In Europe in 1993, a bird flu virus had adapted
to pigs, acquiring a few human flu virus genes, and infected two young
Dutch children, even displaying evidence of limited human-to-human
transmission.[16]
Recipe for Disaster
“Influenza [in pigs] is closely correlated with pig density,” said a
European Commission-funded researcher studying the situation in
Europe.
[17] As such, Europe’s rapidly intensifying pig industry has been
described in Science as “a recipe for disaster.”[18] Some researchers
have speculated that the next pandemic could arise out of “Europe’s
crowded pig barns.”[19]
The European Commission’s agricultural directorate warns that the
“concentration of production is giving rise to an increasing risk of
disease epidemics.”[20] Concern over epidemic disease is so great
that Danish laws have capped the number of pigs per farm and put a
ceiling on the total number of pigs allowed to be raised in the
country.[21] No such limit exists in the United States.
With massive concentrations of farm animals within which to mutate,
these new swine flu viruses in North America seem to be on an
evolutionary fast track, jumping and reassorting between species at an
unprecedented rate.[22] This reassorting, Webster’s team concludes,
makes the 60 million strong U.S. pig population an “increasingly
important reservoir of viruses with human pandemic potential.”[23]
“We used to think that the only important source of genetic change in
swine influenza was in Southeast Asia,” said Christopher Olsen, a
molecular virologist at the University of Wisconsin, Madison. Now, “we
need to look in our own backyard for where the next pandemic may
appear.”[24]
Dr. Michael Greger is director of Public Health and Animal Agriculture
in the farm animal welfare division of The Humane Society of the
United States. A physician specializing in clinical nutrition, Greger
focuses his work on the human health implications of intensive animal
agriculture, including the routine use of non-therapeutic antibiotics
and growth hormones in animals raised for food, and the public health
threats of industrial factory farms.
1 Zhou NN, Senne DA, Landgraf JS, et al. 1999. Genetic reassortment of
avian, swine, and human influenza A viruses in American pigs. Journal
of Virology 73:8851-6. http://birdflubook.org/resources/ZHOU8851.pdf.
2 Zhou NN, Senne DA, Landgraf JS, et al. 2000. Emergence of H3N2
reassortant influenza A viruses in North American pigs. Veterinary
Microbiology 74:47-58. http://birdflubook.org/resources/Zhou47.pdf.
3 Webster RG and Hulse DJ. 2004. Microbial adaptation and change:
avian influenza. Revue Scientifique et Technique 23(2):453-65.
4 Wuethrich B. 2003. Chasing the fickle swine flu. Science 299:1502-5.
http://birdflubook.org/resources/WUETHRICH1502.pdf.
5 Zhou NN, Senne DA, Landgraf JS, et al. 1999. Genetic reassortment of
avian, swine, and human influenza A viruses in American pigs. Journal
of Virology 73:8851-6. http://birdflubook.org/resources/ZHOU8851.pdf.
6 Webby RJ, Swenson SL, Krauss SL, Gerrish PJ, Goyal SM, and Webster
RG. 2000. Evolution of swine H3N2 influenza viruses in the United
States. Journal of Virology 74:8243-51.
7 Wuethrich B. 2003. Chasing the fickle swine flu. Science 299:1502-5.
http://birdflubook.org/resources/WUETHRICH1502.pdf.
8 Shields DA and Mathews KH Jr. 2003. Interstate livestock movements.
USDA Economic Research Service: Electronic Outlook Report from the
Economic Research Service, June. usda.mannlib.cornell.edu/reports/
erssor/livestock/ldp-mbb/2003/ldp-m108-01.pdf.
9 Environmental Defense. 2000. Factory hog farming: the big picture.
November.http://environmentaldefense.org/
document…armingBigPicture.pdf.
10 Duke University Center on Globalization, Governance and
Competitiveness. 2006. Hog farming overview. February 23.
http://www.soc.duke.edu/NC_GlobalEconomy/hog/overview.php.
11 North Carolina Department of Agriculture and Consumer Services.
2001. North Carolina agriculture overview. February 23.
http://ncagr.com/stats/general/livestoc.htm.
12 Wuethrich B. 2003. Chasing the fickle swine flu. Science
299:1502-5. http://BirdFluBook.org/resources/WUETHRICH1502.pdf.
13 Brown IH. 2000. The epidemiology and evolution of influenza viruses
in pigs. Veterinary Medicine 74:29-46. http://BirdFluBook.org/resources/Brown29.pdf.
14 1993. Overcrowding pigs pays-if it’s managed properly. National Hog
Farmer, November 15.
15 Wuethrich B. 2003. Chasing the fickle swine flu. Science
299:1502-5. http://BirdFluBook.org/resources/WUETHRICH1502.pdf.
16 Webster RG, Sharp GB, and Claas CJ. 1995. Interspecies transmission
of influenza viruses. Americal Journal of Respiratory and Critical
Care Medicine 152:525-30.
17 MacKenzie D. 1998. This little piggy fell ill. New Scientist,
September 12.
18 Ibid.
19 Delgado C, Rosegrant M, Steinfeld H, Ehui S, and Courbois C. 1999.
Livestock to 2020: the next food revolution. Food, Agriculture, and
the Environment Discussion Paper 28. For the International Food Policy
Research Institute, the Food and Agriculture Organization of the
United Nations and the International Livestock Research Institute.
http://ifpri.org/2020/dp/dp28.pdf.
20 MacKenzie D. 1998. This little piggy fell ill. New Scientist,
September 12, p. 1818.
21 Ibid.
22 Wuethrich B. 2003. Chasing the fickle swine flu. Science
299:1502-5. http://birdflubook.org/resources/WUETHRICH1502.pdf.
23 Webby RJ, Rossow K, Erickson G, Sims Y, and Webster R. 2004.
Multiple lineages of antigenically and genetically diverse influenza A
virus co-circulate in the United States swine population. Virus
Research 103:67-73. http://BirdFluBook.org/resources/webby67.pdf.
24 Wuethrich B. 2003. Chasing the fickle swine flu. Science
299:1502-5. http://BirdFluBook.org/resources/WUETHRICH1502.pdf.
Article Source:
http://www.humanesociety.org/farm/news/ournews/swine_flu.html
= = = =
STILL FEELING LIKE THE MAINSTREAM U.S. CORPORATE MEDIA
IS GIVING A FULL HONEST PICTURE OF WHAT’S GOING ON?
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On usenet (groups.google.com) see misc.activism.progressive
= = = =
Sorry, we cannot read/reply to most usenet posts but welcome email
FOR MORE INFORMATION: http://EconomicDemocracy.org/wtc/ (peace)
http://economicdemocracy.org/eco/climate-summary.html (Climate)
And http://EconomicDemocracy.org/ (general)
** New email: econdemocracy[at]gmail[dot]com
If you have experienced Acne or currently experience problems with Acne,
please help us with our research. We are conducting
research for an upcoming e-book. The following link will take you
to a zoomerang survey. We would appreciate your participation and input.
http://tiny.cc/9AYqp
–Bill Buck, http://improvementguru.com
Mike, who lives in England went in for a 6 month check up on his
prostate cancer.
He’s been following my recipe off and on for a few months. Most
recently he did it for 28 days.
He reported two stats. The tumor had shrunk from 5×7 to 4×4. I’m
pretty sure those are centimeters.
5 times 7 = 35, whereas 4 times 4 = 16, so the overall area has been
reduced to less than half.
The other stat he provided is that his entire prostate has shrunk from
109cc to 93cc.
One aspect that might be limiting his recovery is that he is a dietary
Vegan. I think he has avoided the emulsified cod liver oil at least
part of the time.
I guess because he is under the UK medical system, he won’t be tested
again for another six months.
"Maltol and thiomaltol are more effective chelating inhibitors
for MMP-3 (stromelysin) than the widely reported hydroxamate
ligands. "
Matrix metalloproteinase inhibitors reduce collagen gel
contraction and alpha-smooth muscle actin expression
by periodontal ligament cells.
Bildt MM, Bloemen M,
Kuijpers-Jagtman AM, Von den Hoff JW.
Orthodontics & Oral Biology,
Radboud University Nijmegen Medical Centre,
Philips van Leydenlaan 25, Nijmegen, The Netherlands.
BACKGROUND AND OBJECTIVE:
Orthodontic tooth movement requires remodeling of the periodontal
tissues.
The matrix metalloproteinases (MMPs) degrade the extracellular matrix
components of the periodontal ligament, while the tissue inhibitors
of
metalloproteinases (TIMPs) control their activity.
Synthetic MMP inhibitors have been developed to inhibit MMP activity.
In this study, periodontal ligament cells in contracting collagen gels
served
as a model for enhanced periodontal remodeling.
The effect of MMP inhibitors on gel contraction and on MMP and TIMP
expression was analyzed.
MATERIAL AND METHODS:
Human periodontal ligament cells were cultured in three-dimensional
collagen gels and incubated with the MMP inhibitors BB94, CMT-3,
doxycycline and Ilomastat.
Gel contraction was determined using consecutive photographs.
The relative amounts of MMPs and TIMPs were analyzed using substrate
zymography and mRNA expression using quantitative polyermase chain
reaction.
RESULTS:
All MMP inhibitors reduced MMP activity to about 20% of the control
activity.
They all reduced contraction, but CMT-3 and doxycycline had the
strongest effect.
These inhibitors also reduced MMP-2, MMP-3 and alpha-smooth muscle
actin
mRNA expression.
The expression of MMP-1 mRNA seemed to be increased by CMT-3.
No effects were found on the amounts of MMPs and TIMPs.
CONCLUSION:
Synthetic MMP inhibitors strongly reduced gel contraction by
periodontal
ligament cells.
This was primarily caused by an inhibitory effect on MMP activity,
which
reduces matrix remodeling.
In addition, alpha-smooth muscle actin expression was reduced by
CMT-3
and doxycycline, which limits the contractile activity of the
fibroblasts.
PMID: 18973523
——————
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2531216
We have found that maltol and thiomaltol are more effective chelating
inhibitors for MMP-3 (stromelysin) than the widely reported
hydroxamate
ligands.
————
http://www.jbc.org/cgi/reprint/184/1/131.pdf
"The formation of maltol upon heating certain aqueous
carbohydrate glycine systems has been investigated.
Carbohydrates used in the experiment included starch,
cellulose, sucrose, lactose, maltose, glucose, galactose,
and methyl a-n-glucopyranoside.
Of these, maltol was obtained from only lactose and maltose.
————————–
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk