[Editorial] Disappointing decision on U.S. beef petition
The Constitutional Court has ruled against a constitutional petition by 96,000 citizens claiming that the “process by which the Lee Myung-bak administration resumed imports of American beef by formalizing the move with an official announcement (gosi) in the daily government gazette (Gwanbo) was unconstitutional.” The Gwanbo is equivalent to the Federal Register in the United States. Its decision is a big disappointment for the Koreans who had hoped the court would stand in defense of the people’s safety and quarantine inspection sovereignty, because if the gosi was declared unconstitutional in accordance with the petition, which had more signatories than any in history, it would have been automatically invalidated and the Korean government would then have had the justification to renegotiate the beef deal with the United States.
The constitutional petition put before the Constitutional Court asserted that the administration’s move “significantly increases the possibility of bovine spongiform encephalopathy in humans and therefore infringes on constitutionally-guaranteed dignity and worth as humans, the right to pursue happiness, the right to life, and the right to health.” Negotiations with the United States on beef made it so that Korea accepts American beef without limits to age or parts, and that Korea cannot halt beef imports even if there is an outbreak of mad cow disease in the United States. Additional negotiations allowed for restrictions on beef from cows older than 30 months of age and on specified risk material, or SRM, but that was not a fundamental solution. It wrongly assumed that the United States had strengthened prohibitions on animal-based feed that had been relaxed, and another mistake was permitting the importation of some SRM, believing it to be parts that are safe.
Even the current head of the Ministry of Government Legislation said that the process was constitutionally flawed and that he, too, would have taken the issue to the Constitutional Court had he been in the opposition. He said that it is highly problematic, in a constitutional way, to implement something with a directive announcement (gosi) from the relevant Cabinet minister without legislation-drafting procedures, when the issue directly relates to the country’s health.
“While the gosi’s protection measures may not be perfect,” the court said it its decision, “one cannot conclude that this was wholly, or very much, an action that violated the state's constitutional duty to protect the safety of lives and bodies.” It is hard to understand how surrendering quarantine inspection sovereignty and exposing the country to the risk of mad cow disease cannot be concluded to be in inconsistent with or inadequate as far as the duty to the state. It is also disappointing that the court never even had an open oral debate that included expert testimony about a case that was the subject of intense national interest.
The mission of the Constitutional Court is to defend the basic rights of the people and weed out laws that are unconstitutional for violating those rights. The minority opinion was right in stating that the gosi “violates the petitioners’ basic rights because it inadequately carries out the state’s duty to protect basic rights regarding (the safety) of life and body.”
Please direct questions or comments to [englishhani@hani.co.kr]
http://english.hani.co.kr/arti/english_edition/e_editorial/329968.htmlTuesday, May 13, 2008 Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008
snip...
Re..Korea vs USDA beef (the truth)
Greetings KIWA et al and all Koreans,
A kind greetings from Bacliff, Texas.
I submit this data with great concern, sincerity, and in peace.
President Lee Myung-bak states ;
Greetings KIWA et al and all Koreans,
A kind greetings from Bacliff, Texas.
I submit this data with great concern, sincerity, and in peace.
President Lee Myung-bak states ;
"halt imports if another case of bovine spongiform encephalopathy turned up in the United States." now that is funny. a mad cow with BSE would have to drop from the sky onto the white house lawn and run around jerking, trembling, stumbling and staggering uncontrollably for months before anyone would every confirm a mad cow case with BSE, and then it would take an act of congress to confirm it, and President Lee Myung-bak knows this. it's all about commodities and futures $$$
Monday, May 5, 2008
STATEMENT OF DR. RICHARD RAYMOND USDA UNDERSECRETARY FOR FOOD SAFETY Regarding the Safety of the U.S. Food Supply please see full text with some additional information the good Dr. Raymond seems to have forgotten about ;
http://usdameatexport.blogspot.com/2008/05/statement-of-dr-richard-raymond-usda.htmlUSDA BEEF DEAL WITH KOREA AND the truth, what the usda et al are not telling you...
http://flounder068.vox.com/library/post/usda-beef-deal-with-korea-and-the-truth-what-the-usda-et-al-are-not-telling-you.htmlDOWNER CATTLE SCHOOL LUNCH PROGRAM
http://downercattle.blogspot.com/http://downercattle.blogspot.com/2008/05/humane-society-releases-new-video-of.html"Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD."
Sincerely, Pierluigi Gambetti, MD Director, National Prion Disease Pathology Surveillance Center Stephen M. Sergay, MB, BCh President, American Academy of Neurology
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45THE LAST TWO MAD COWS documentED IN TEXAS AND ALABAMA WERE ATYPICAL BSE. then GW, USDA et al shut the testing down $$$ (new they would find more. ...tss)
please see full text with additional comments and links @ ;
http://prionunitusaupdate2008.blogspot.com/Sunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html==============================
THE only fool is one who fools himself, and GW and his administration and their junk science will fool humans for just so long, then the incubation will catch up. none of this was about science, it was all about commodities and futures and the exporting of beef. nothing else mattered, literally, just ask old stanley prusiner the nobel prize winner for the PRION, what did old stan say ;
STANLEY PRUSINER NOBEL PEACE PRIZE WINNER ON THE PRION
US AG SEC AND LAYCRAFT
"nothing matters, except beef from Canada under 30 months bone in beef product, that's ALL THAT MATTERS!" US SENATOR AND STAN THE MAN SLAM USDA "DAMNING TESTIMONY"
Senator Michael Machado from California
"USDA does not know what's going on". "USDA is protecting the industry". " SHOULD the state of California step in"
Stanley Prusiner
"nobody has ever ask us to comment"
"they don't want us to comment"
"they never ask"
i tried to see Venemon, after Canadian cow was discovered with BSE. went to see lyle. after talking with him.
absolute ignorance.
then thought i should see Venemon.
it was clear his entire policy was to get cattle boneless beef prods across the border.
nothing else mattered.
his aids confirmed this.
5 times i tried to see Venemon, never worked.
eventually met with carl rove the political.
he is the one that arranged meeting with Venemon.
just trying to give you a sense of the distance.
threat to health public safety.
was never contacted.
yes i believe that prions are bad to eat and you can die from them.END
Dr. Stan bashing Ann Veneman - 3 minutes - Damning testimony
http://maddeer.org/video/embedded/08snip.ramFile Name: USDA DON'T ASK DON'T TELL POLICY 02snip.rpm DAMNING testimony of consumer consumption of Washington mad cow in California
http://www.maddeer.org/video/embedded/02snip.rmIn this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htmsee full text ;
http://sciencebushwhacked.blogspot.com/10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST REASON Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.htmlSubject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
snip...
see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ; Friday, April 25, 2008
Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46
http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html2006 was a banner year too for mad cow protein fed out into commerce. those were just one of many ; Specified Risk Materials
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.htmlNOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
http://nor-98.blogspot.com/http://www.yacomitservice.com/php/eng/board.php?board=kkkqna&command=body&no=84snip...
http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.htmlUSDA VS KOREA typical or atypical BSe
http://usdavskorea.blogspot.com/Friday, May 9, 2008 USDA VS KOREA typical or atypical BSe Honorable people of Korea,
a kind and warm greetings from Texas.
snip...
http://usdavskorea.blogspot.com/2008/05/usda-vs-korea-typical-or-atypical-bse.htmlWhy Americans, As Well as Koreans, Should Be Worried About Mad Cow Tainted USA Beef
By Terry S. Singeltary Sr. May 15, 2008
Straight to the Source
Web Note: This is an important commentary by Terry S. Singeltary Sr., on a recent Business Week story on the controversy in South Korea over their government's lifting on the ban on conventional (non-organic) beef, despite the fact that the USDA is still allowing slaughterhouse waste and blood and manure to be fed to cows, and refusing to test all cows at slaughter. See the Mad Cow section of the OCA website for in-depth information. Terry is a regular blogger on the OCA website on Mad Cow issues.
Ronnie Cummins
One Korean official says the probability of a human being catching a mad cow disease by eating U.S. beef is like the one of a golf player scoring a hole-in-one and then being killed by lightning.
this is typical BSe. you here industry groups comment 'your more likely to get hit by a car than die from CJD'. well, maybe so, but my mother and many more did not die from getting hit by a car, they died from CJD, my mothers being the hvCJD (confirmed), and my neighbors mother died from CJD (confirmed). the UKBSEnvCJD _only_ theory is incorrect. there are more strains of mad cow than the UK BSE in beef to nvCJD in humans in the UK. The deception by the USDA, FDA, and the Bush administration about mad cow disease, CJD, and all Transmissible Spongiform Encephalopathy over the past 8 years have been outrageous, to a point of being criminal. I am vested in nothing, but the truth.
snip...see full text ;
http://www.grassrootsnetroots.org/articles/article_12387.cfmTuesday, May 13, 2008
Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008
http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.htmlhttp://flounder068.vox.com/library/post/concerned-americans-against-mad-cow-disease-statement-of-solidarity-with-koreans-may-13-2008.htmlhttp://www.koreantopnews.com/story.php?title=USDA_VS_KOREA_typical_or_atypical_BSe_Concerned_Americans_against_Mad_Cow_Disease_STATEMENT_OF_SOLIDARITY_with_Koreans_May_13_2008BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/http://flounder068.vox.com/library/post/bse-youngest-age-statistics-under-30-months.htmlFriday, June 20, 2008
USDA TO KOREA AND THE WORLD, EAT THAT AND LIKE IT
http://usdavskorea.blogspot.com/2008/06/usda-to-korea-and-world-eat-that-and.htmlWednesday, June 11, 2008
OIE Recognition of the BSE Status of Members RESOLUTION No. XXI (Adopted by the International Committee of the OIE on 27 May 2008)
snip...
http://usdavskorea.blogspot.com/2008/06/oie-recognition-of-bse-status-of.htmlhttp://organicconsumers.org/forum/index.php?showtopic=1566U.S. slams door on revising S. Korea beef import pact
June 11, 2008, 10:14PM
http://usdavskorea.blogspot.com/2008/06/us-slams-door-on-revising-s-korea-beef.htmlSaturday, June 7, 2008
Export Requirements for the Republic of Korea IMPORT HEALTH REQUIREMENTS FOR U.S. BEEF AND BEEF PRODUCTS
http://usdavskorea.blogspot.com/2008/06/export-requirements-for-republic-of.htmlWednesday, July 23, 2008
Audit says USDA lost track of imported cattle Report No. 50601-0012-Ch March 2008 Audit says USDA lost track of imported cattle Canada has reported 13 cases of mad cow
http://usdameatexport.blogspot.com/UPDATE DECEMBER 2008
Monday, December 22, 2008
[Docket No. FDA–2008–D–0597] Draft Guidance for Industry: Small Entities Compliance Guide for Renderers—Substances Prohibited From Use in Animal Food
Greetings,
I kindly wish to submit the following to [Docket No. FDA–2008–D–0597] ;
I would kindly like to once again comment on the failed attempts of the FDA et al to stop the spread of animal TSEs, including BSE, through the legal, and illegal feeding practices, of feeding animal protein to livestock for human and animal consumption. Since the terribly flawed, partial, and voluntary August 4, 1997 ruminant to ruminant feed ban was put into place, literally 100s of thousands of tons of banned animal protein has been fed out into commerce, even as late as 2007, when some 10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. NOW, how much of that product that went out into commerce was fed out to cattle, and how much was ever recovered ? AND to think that feeding blood to livestock producing animals is still legal, when scientific study after study shows that TSEs are easily transmitted via blood. IT is absolutely unacceptable that still in 2008, the USA is still feeding highly suspect mad cow feed to USA cattle, and other livestock producing animals. Especially when the last two cases of BSE that were allowed to be tested and reported were of the atypical BSE category, of which we now know the atypical BSE is more virulent than that of the typical BSE, and when ARS research on the atypical BSE said long ago the SRM rules may need to be changed, IF the atypical BSE were to be proven to be more virulent. Why do we continue to flounder? I have submitted to these BSE feed dockets until I am blue in the face, and still to date, they still debate an issue that should have been settled long ago. IT's a fine example of how big ag, big industry, have a stranglehold on sound science and policy making thereof. How many millions of animals and humans have been needlessly exposed to this TSE agent, due to nothing more than ignorance and greed, simply because of a disease that is 100% fatal, but one that has such a long incubation period. For the government and industry as a whole, to continue to flagrantly violate said rules and regulations, in my opinion, should be regarded as criminal, and treated as such. People are dying. ...
Please see references ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
REASON
Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.htmlNEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm2006 WAS A BANNER YEAR ALSO FOR MAD COW FEED BAN VIOLATIONS ''IN COMMERCE''
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
snip...
see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ;
see full text ;
Friday, April 25, 2008
Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46
http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.htmlSPECIFIED RISK MATERIALS
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html0C3.01
Transmission of atypical BSE to Microcebus murinus, a non-human primate: Development of clinical symptoms and tissue distribution of PrPres
Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L -type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).
Objectives and Methods: In order to see if the atypical BSE cases were transmissible to primates, either animals (were intracerebrally inoculated with 50 ul of a 10% brain homogenates of two atypical French BSE case, a H-type (2 males and 2 females) and a L-type (2 males and 2 females).
Results: Only one of the four lemurs challenged with H-type BSE died without clinical signs after 19 months post inoculation (mpi), whereas all the 4 animals inoculated with L -type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms got worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-type, spongiform changes without PrPres accumulation were observed in the brainstem. However Western blot analysis did not allow to detect PrPres into the brain. For the L-type, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem. whereas into the cortex the spongiosis was evidenced, but the Vacuolisation was weaker. Strong deposits of PrPres were detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis also readily confirmed the presence of protease-resistant prion protein.
Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain in a model of non human primate.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdflook 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.isaP04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdfCalves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........
http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#doseIt 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.pdf6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also 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/s147f.pdfsnip... full text ;
http://madcowfeed.blogspot.com/2008/12/docket-no-fda2008d0597-draft-guidance.htmlEvaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain
Qingzhong Kong,1* Mengjie Zheng,1 Cristina Casalone,2 Liuting Qing,1 Shenghai Huang,1? Bikram Chakraborty,1 Ping Wang,1 Fusong Chen,1 Ignazio Cali,1 Cristiano Corona,2 Francesca Martucci,2 Barbara Iulini,2 Pierluigi Acutis,2 Lan Wang,1 Jingjing Liang,1 Meiling Wang,1 Xinyi Li,1 Salvatore Monaco,3 Gianluigi Zanusso,3 Wen-Quan Zou,1 Maria Caramelli,2 and Pierluigi Gambetti1* Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106,1 CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy,2 Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy3 *Corresponding author. Mailing address: Department of Pathology, Case Western Reserve University, Cleveland, OH 44106. Phone for Pierluigi Gambetti: (216) 368-0586. Fax: (216) 368-2546. E-mail:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000025/!x-usc:mailto:pxg13@case.edu . Phone for Qingzhong Kong: (216) 368-1756. Fax: (216) 368-2546. E-mail:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000025/!x-usc:mailto:qxk2@case.edu ?Present address: Department of Patient Education and Health Information, Cleveland Clinic Foundation, Cleveland, OH 44195. Received November 30, 2007; Accepted January 16, 2008.
Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to be caused by only one strain, BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE strains by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE strain-infected cattle. Sixty percent of the inoculated Tg mice became infected after 20 to 22 months of incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE strain-infected Tg mice, but none of the Tg mice infected with prions causing a sporadic human prion disease, showed the presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE strain-infected humanized Tg mouse brains are different from those from the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation times are observed for the BASE strain-infected Tg mice. These results suggest that in humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2268471Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." ... interesting. ... TSS
Thursday, June 05, 2008
Review on the epidemiology and dynamics of BSE epidemics
Vet. Res. (2008) 39:15
www.vetres.org DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article
snip...
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
snip...
Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
full text 18 pages ;
http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdfplease see full text ;
http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***
Progress Report from the National Prion Disease Pathology Surveillance Center
An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD
April 3, 2008
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htmWednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.htmlA New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.htmlCommunicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.htmlhttp://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htmhttp://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdfsporadic Fatal Familial Insomnia
http://sporadicffi.blogspot.com/JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
mailto:flounder9@verizon.netI lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIThttp://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT2 January 2000 British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#611715 November 1999 British Medical Journal vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406Creutzfeldt Jakob Disease
http://creutzfeldt-jakob-disease.blogspot.com/USA PRION UNIT BLOG
http://prionunitusaupdate2008.blogspot.com/Sunday, April 20, 2008 Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008
Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.
see full text ;
http://prionunitusaupdate2008.blogspot.com/2008/04/progress-report-from-national-prion.htmlCJD TEXAS (cjd clusters)
http://cjdtexas.blogspot.com/USA WRITTEN CJD QUESTIONNAIRE ???
http://cjdquestionnaire.blogspot.com/Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html2007
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.htmlFriday, August 29, 2008
CREEKSTONE VS USDA COURT OF APPEALS, BUSH SAYS, NO WAY, NO HOW
http://madcowtesting.blogspot.com/2008/08/creekstone-vs-usda-court-of-appeals.htmlSunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.htmlHUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html0C3.01
Transmission of atypical BSE to Microcebus murinus, a non-human primate: Development of clinical symptoms and tissue distribution of PrPres
Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L -type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).
Objectives and Methods: In order to see if the atypical BSE cases were transmissible to primates, either animals (were intracerebrally inoculated with 50 ul of a 10% brain homogenates of two atypical French BSE case, a H-type (2 males and 2 females) and a L-type (2 males and 2 females).
Results: Only one of the four lemurs challenged with H-type BSE died without clinical signs after 19 months post inoculation (mpi), whereas all the 4 animals inoculated with L -type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms got worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-type, spongiform changes without PrPres accumulation were observed in the brainstem. However Western blot analysis did not allow to detect PrPres into the brain. For the L-type, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem. whereas into the cortex the spongiosis was evidenced, but the Vacuolisation was weaker. Strong deposits of PrPres were detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis also readily confirmed the presence of protease-resistant prion protein.
Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain in a model of non human primate.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdfP7.09
Biochemical screening for identification of atypical bse in belgium, 1999-present
Authors
Alexandre DobIy: Caroline Rodeghiero, Riet Geeroms; Stephanie Durand, Jessica De Sloovere, Emanuel Yanopdenbosch, Stefan Roels,
Content
Background: Recently atypical forms of BSE have been described. Western blot analyses showed that, in comparison to the classic BSE (C-type), they are demonstrable by a higher or lower molecular weight of the unglycosylated PrPres. They Viere thus named H-type and L-type BSE (L-type is also called BASE). In addition they show a lower proportion of diglycosylated PrPres than C-type. These emerging types represent different strains of BSE. They show unique incubation periods and histological lesions. Such types have been described on different continents. Indeed they might correspond to "sporadic" forms of BSE. In 2004 we already described one L-type in Belgium.
Objective: We retrospectively analysed the bovines at least 7-year-old in the Belgian archive of BSE diagnosed cattle in order to determine the prevalence of the two types of atypical BSE in Belgium.
Methods: We analysed homogenates from 39 bovines of 93 months old in median (min: 84, max: 181 months). The most recent one was diagnosed in 2006. We used Western blot with a panel of anti-PrP antibodies (Ab). They detect different regions of the PrP protein, from N-terminal to C-terminal: 12B2, 9A2, Sha31. SAFB4, 94B4. Their combination is aimed at an efficient typing diagnostic. We detected bound Ab with SuperSignal West Dura (Pierce) and analysed PrPres, signals with an image-analysis software (Quantity One, Bio-Rad).
Results: The results are still under analysis. We will detail the most crucial characteristics for typing PrPres. These include 1) the apparent molecular mass of the an-, mono- and diglycosylated bands, 2) the binding affinity to the five Ab (e.g.12B2 for H-type), 3) the presence of a fourth (unglycosylated) band and 4) the glycoprofile based on the relative proportions of the visible bands.
Discussion: The emergence of atypical types of BSE is partially due to a better knowledge of prion strains and more efficient diagnostic techniques. As the area in the brain where the PrPres is deposited can differ drastically between the types, it is essential to ascertain that the sampling techniques and analyses are adapted to these new types. As these new strains seem more virulent than classic types, they represent one of the next challenges in the field of prions.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdfhttp://www.prion2008.com/Tuesday, November 11, 2008
Transmission of atypical bovine prions to mice transgenic for human prion protein
DOI: 10.3201/eid1412.080941
http://bse-atypical.blogspot.com/2008/11/transmission-of-atypical-bovine-prions.htmlWednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.htmlTuesday, June 3, 2008
SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.htmlSCRAPIE USA
http://scrapie-usa.blogspot.com/Sunday, September 07, 2008
CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA
http://chronic-wasting-disease.blogspot.com/2008/09/cwd-live-test-and-political-aspects-or.htmlSaturday, October 18, 2008
WYOMING STAR VALLEY MOOSE TESTS POSITIVE FOR CWD
http://chronic-wasting-disease.blogspot.com/2008/10/wyoming-star-valley-moose-tests.htmlhttp://chronic-wasting-disease.blogspot.com/Friday, December 12, 2008
The prion strain phenomenon: Molecular basis and unprecedented features
http://bse-atypical.blogspot.com/2008/12/prion-strain-phenomenon-molecular-basis.htmlDocket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC -254 Accepted - Volume 11
http://www.fda.gov/OHRMS/DOCKETS/DOCKETS/02n0276/02N-0276-EC-254.htmhttp://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htmDocket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.htmlPART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.htmlMonday, December 08, 2008
vCJD & dental treatment
http://creutzfeldt-jakob-disease.blogspot.com/2008/12/vcjd-dental-treatment.htmlFriday, December 12, 2008
Prions in Milk from Ewes Incubating Natural Scrapie
http://scrapie-usa.blogspot.com/2008/12/prions-in-milk-from-ewes-incubating.htmlFriday, December 05, 2008
Detection of Prion Infectivity in Fat Tissues of Scrapie-Infected Mice
http://scrapie-usa.blogspot.com/2008/12/detection-of-prion-infectivity-in-fat.htmlREPORT ON CURRENT & FUTURE SURVEILLANCE FOR BOVINE SPONGIFORM ENCEPHALOPATHY
http://madcowtesting.blogspot.com/2008/11/report-on-current-future-surveillance.htmlNovember 25, 2008
Update On Feed Enforcement Activities To Limit The Spread Of BSE
http://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.htmlPlasma & Serum Proteins Receive Continued FDA Approval
4/25/2008 APC, Inc. is pleased to advise our customers and industry partners that as anticipated, the Food and Drug Administration (FDA) will continue to allow the use of bovine blood, plasma and serum proteins in ruminant feeds.
In April 2008 FDA announced the publication of its Final Rule for 21 CFR Part 589.2001 - Substances Prohibited From Use in Animal Food or Feed. FDA specifically stated in their opinion that, "FDA is not prohibiting the use of blood and blood products in animal feed because we believe such a prohibition would do very little to reduce the risk of BSE transmission."
Known as a leader in developing nutritional products for the swine industry, where 95% of pig starter diets in the United States contain functional proteins, APC has more recently developed their line of colostrum replacers, supplements, feed additives and milk replacer ingredients for calves. Products include plasma, serum and immunoglobulin concentrate based Acquire®, Lifeline®, Gammulin® and Nutrapro® used to optimize the health and performance of calves.
To view the full report for Final Rule 21 CFR Part 589.2001 visit:
http://www.fda.gov/OHRMS/DOCKETS/98fr/FDA-2002-N-0031-nfr.pdfTo view the complete Feed Rule 21 CFR Part 589 visit:
http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=589&showFR=1Friday, November 21, 2008
Plasma & Serum Proteins Receive Continued FDA Approval
http://madcowfeed.blogspot.com/2008/11/plasma-serum-proteins-receive-continued.htmlhttp://madcowfeed.blogspot.com/Thursday, November 27, 2008
Prion diseases are efficiently transmitted by blood transfusion in sheep
http://vcjdblood.blogspot.com/2008/11/prion-diseases-are-efficiently.htmlstupid is, as stupid does. (forest gump)
Thank You,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
