USDA Chief Veterinary 
Officer On Surveillance And Milk 
Safety
A 
new actuality is available on the USDA FTP site. The 
actuality can also be seen on USDA's YouTube channel. 
Note for broadcasters: 
B-roll of cows follows Dr. Clifford’s actuality on the file available on the FTP 
site. 
FTP Download instructions: 
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Password: Newscontent1 
Filename for 
TV Actuality: Clifford 
safeguards
The new file is in QuickTime 
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YouTube:Clifford Safeguards
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ACTUALITY – USDA Chief Veterinary 
Officer On Surveillance And Milk Safety
INFO: USDA Chief Veterinary Officer Dr. John Clifford explains the 
system of strong interlocking safeguards designed to protect human and animal 
health.
Dr. John Clifford, Chief Veterinary 
Officer For the United States of America: 
Hello, I’m Dr. John 
Clifford, chief veterinary officer for the United States of America. At USDA, we 
oversee a system of strong interlocking safeguards that protect human and animal 
health, as well as food safety in the United States. Those safeguards include 
targeted surveillance activities. Through that surveillance program, on April 
24th we confirmed the nation’s 4th case of bovine spongiform 
encephalopathy, or BSE, in a dairy cow on the west coast. BSE is a fatal disease 
affecting the central nervous system of adult cattle. We proactively test for 
BSE in order to detect the disease at the very low level of less than 1 case per 
million adult cattle, to assess any change in the BSE status of U.S. cattle, 
and to identify any rise in BSE 
prevalence in the country. Our 
targeted surveillance program has been in place since 1990. We currently test 
for BSE at levels 10 times greater than World Animal Health Organization 
standards. We test approximately 40,000 animals per year, taking those samples from cattle 
where the disease is most likely to be found. This includes animals that have clinical 
signs consistent with BSE, have other central nervous system abnormalities, die 
for unknown reasons, or cannot walk or move well. We collect samples from a variety of 
locations where the targeted groups of animals are found. The samples from the animal in 
question were taken at a rendering facility in California. Our surveillance works. We found this 
case of BSE. The carcass of the 
animal was held at the rendering facility and then will be destroyed. It was 
never presented for processing for human consumption. At no time did it present a risk to 
the food supply. Our food supply remains safe. With California being a large dairy 
state, there have been some concerns raised about milk. Let me assure you, our 
milk is safe to drink. Scientific 
research demonstrates that BSE cannot be transmitted in cow’s milk, even if that 
milk comes from a cow with BSE. The World Health Organization has stated that 
tests on milk from BSE-infected animals have not shown any BSE infectivity. Milk 
and milk products, are, therefore considered safe to consume. Let me assure consumers and our 
trading partners that ongoing BSE surveillance allows the USDA to detect BSE at very low 
levels in the U.S. cattle population. The safeguarding system is working. For 
updates on our ongoing investigation and more information about BSE in general, 
visit our website at www.usda.gov. 
these folks should no now to 
never say never $$$
BOTTOM LINE, milk and atypical 
L-type BASE BSE, they have no clue yet. they must do transmission studies. with 
atypical L-type BASE BSE, this type is much more virulent. ...tss
MILK and Transmissible 
Spongiform Encephalopathy TSE PRION
Terry S. Singeltary Sr.
11/18/2011 
TO date, and i imphasize 'to date', there has been no documented evidence 
of transmission of BSE via milk of BSE infected cow to another cow. however, 
with the limited testing done to date, on just the c-BSE, you cannot rule this 
out, especially with the atypical BSE L-type i.e. BASE, being much more 
virulent. Concern has been increasing due to fluids from TSE species i.e. blood, 
urine, and milk, and the fact that infectivity has been detected. 
Prion infectivity has now been detected in blood, urine and milk.
please see ;
Seven main threats for the future linked to prions
The NeuroPrion network has identified seven main threats for the future 
linked to prions.
First threat
The TSE road map defining the evolution of European policy for protection 
against prion diseases is based on a certain numbers of hypotheses some of which 
may turn out to be erroneous. In particular, a form of BSE (called atypical 
Bovine Spongiform Encephalopathy), recently identified by systematic testing in 
aged cattle without clinical signs, may be the origin of classical BSE and thus 
potentially constitute a reservoir, which may be impossible to eradicate if a 
sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently 
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases 
constitute an unforeseen first threat that could sharply modify the European 
approach to prion diseases.
Second threat
In small ruminants, a new atypical form of scrapie currently represents up 
to 50% of detected cases and even involves sheep selected for resistance to 
classical scrapie. The consequences for animal and human health are still 
unknown and there may be a potential connection with atypical BSE. These 
atypical scrapie cases constitute a second threat not envisioned previously 
which could deeply modify the European approach to prion diseases.
Third threat
The species barrier between human and cattle might be weaker than 
previously expected and the risk of transmission of prion diseases between 
different species has been notoriously unpredictable. The emergence of new 
atypical strains in cattle and sheep together with the spread of chronic wasting 
disease in cervids renders the understanding of the species barrier critical. 
This constitutes a third threat not properly envisioned previously that could 
deeply modify the European approach to prion diseases.
Fourth threat
Prion infectivity has now been detected in blood, urine and milk and this 
has potential consequences on risk assessments for the environment and food as 
well as for contamination of surfaces including medical instruments. Furthermore 
the procedures recommended for decontamination of MBM (Meat and Bone Meal), 
which are based on older methodologies not designed for this purpose, have 
turned out to be of very limited efficacy and compromise current policies 
concerning the reuse of these high value protein supplements 
(cross-contamination of feed circuits are difficult to control). It should be 
noted that the destruction or very limited use of MBM is estimated to still cost 
1 billion euros per year to the European economy,
whereas other countries, including the US,
Brazil, and Argentine do not have these constraints.
However, many uncertainties remain concerning the guarantees that can be 
reasonably provided for food and feed safety and scientific knowledge about the 
causative agents (prions) will continue to evolve. This decontamination and 
environmental issue is a fourth threat that could modify deeply the European 
approach to prion diseases.
Fifth threat The precise nature of prions remains elusive. Very recent data 
indicate that abnormal prion protein (PrPTSE) can be generated from the brains 
of normal animals, and under some conditions (including contaminated waste 
water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost 
unchanged, a finding that underlines the possibility of having BSE without any 
detectable diagnostic marker. These are just two areas of our incomplete 
knowledge of the fundamental biology of prions which constitute a fifth threat 
to the European approach to prion diseases.
Sixth threat The absence of common methods and standardisation in the 
evaluation of multiple in vivo models with different prion strains and different 
transgenic mice expressing PrP from different species (different genotypes of 
cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of 
all the data generated by the different scientific groups almost impossible. 
This deeply impairs risk assessment. Moreover, the possibility of generating 
PrPTSE de novo with new powerful techniques has raised serious questions about 
their appropriateness for use as blood screening tests. The confusion about an 
incorrect interpretation of positive results obtained by these methods 
constitutes a sixth threat to European approach to prion diseases.
Seventh Threat The detection of new or re-emerging prion diseases in 
animals or humans which could lead to a new crisis in consumer confidence over 
the relaxation of precautionary measures and surveillance programmes constitutes 
a seventh threat that could modify the European approach to prion 
diseases.
Goat BSE: Proposal for Improvement of Goat TSE Discriminative Diagnosis and 
Susceptibility based Assessment of BSE Infectivity in Goat Milk and Meat
Funded by EU, DEFRA This project is run by a consortium of ten research 
teams in seven EU countries.
In light of the known ability of the BSE agent to cross the animal/human 
species barrier, recent evidence establishing the presence of BSE in goat is 
especially alarming, as it represents a new potential risk of food-born 
contamination to human consumers of goat milk and meat products. The main 
objective is to determine the tissue distribution of BSE after oral exposure of 
goats and to do this while simultaneously generating data on genetic 
susceptibility in the most common used production breeds. This proposal aims at 
(i) providing data for the evaluation of human risk associated with goat BSE, 
(ii) providing pathogenesis data and biological material from first and second 
passage BSE in goats, (iii) evaluating the possibility of BSE self-maintenance 
in goat herds through maternal or horizontal transmission, (iv) validating and 
improving our ability to detect caprine BSE and discriminate it from scrapie in 
goats. Our approach will establish the influence of PrP gene polymorphisms on 
scrapie and BSE susceptibility so that genetics could potentially be used for 
the control of field TSE outbreaks in goats. We will also document European 
field TSE strain variability in goats by recruiting a large number of TSE goat 
isolates from affected European countries. Already established or specifically 
created animal models (strain typing) and biochemical tools (PrPSc typing), will 
be tested for their ability to efficiently discriminate goat BSE/scrapie. 
Finally, by measuring infectivity in various tissues collected from goats at 
different stages of BSE infection, we will provide essential data for 
quantitative risk assessment.
Vet. Res. (2010) 41:48 Original article
Pathogenesis of natural goat scrapie: modulation by host PRNP genotype and 
effect of co-existent conditions
Lorenzo González1*, Stuart Martin1, Stephen A.C. Hawkins2, Wilfred 
Goldmann3, Martin Jeffrey1 and Sílvia Sisó1
1 Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science Park, 
Penicuik, Midlothian EH26 0PZ, United Kingdom 2 VLA-Weybridge, Addlestone, 
Surrey KT15 3NB, United Kingdom 3 The Roslin Institute and R(D)SVS University of 
Edinburgh, Roslin, Midlothian EH25 9PS, United Kingdom
* Corresponding author: l.gonzalez@vla.defra.gsi.gov.uk
Received: 13 January 2010 Accepted: 7 April 2010
Abstract
After detection of a high prevalence of scrapie in a large dairy goat herd, 
72 infected animals were examined by immunohistochemistry with prion protein 
(PrP) antibody Bar224 to study the pathogenesis of the infection. Tissues 
examined included the brain and thoracic spinal cord (TSC), a wide selection of 
lymphoreticular system (LRS) tissues, the distal ileum and its enteric nervous 
system (ENS), and other organs, including the mammary gland. The whole open 
reading frame of the PRNP gene was sequenced and antibodies to caprine 
arthritis-encephalitis virus (CAEV) infection were determined. Unexpectedly, 
accumulation of disease-associated PrP (PrPd) in the brain was more frequent in 
methionine carriers at codon 142 (24/32, 75.0%) than amongst isoleucine 
homozygotes (14/40, 35.0%). The latter, however, showed significantly greater 
amounts of brain PrPd than the former (average scores of 9.3 and 3.0, 
respectively). A significant proportion of the 38 goats that were positive in 
brain were negative in the ENS (44.7%) or in the TSC (39.5%). These results, 
together with the early and consistent involvement of the circumventricular 
organs and the hypothalamus, point towards a significant contribution of the 
haematogenous route in the process of neuroinvasion. Chronic enteritis was 
observed in 98 of the 200 goats examined, with no association with either 
scrapie infection or presence of PrPd in the gut. Lymphoproliferative 
interstitial mastitis was observed in 13/31 CAEV-positive and scrapie-infected 
goats; PrPd in the mammary gland was detected in five of those 13 goats, 
suggesting a possible contribution of CAEV infection in scrapie transmission via 
milk.
Key words: scrapie / goat / prion neuroinvasion / transmissible spongiform 
encephalopathy / CAEV
© The British Crown, published by INRA/EDP Sciences, 2010
6 January 2010 - 
The public “TSEs in goats” website Link: 
Since December 2006 a new EU funded project has started that has been 
essentially developed from NeuroPrion TSEgoat task group members and their 
progress: “GoatBSE: Proposal for improvement of goat TSE discriminative 
diagnosis and susceptibility based assessment of BSE infectivity in goat milk 
and meat.” (European STREP project FOOD-CT-2006-36353, frame work 6, area 
Thematic priority: Food quality and safety). In this project the focus of study 
is about consequences of an infection with BSE in goats for disease transmission 
and product safety.
Sheep with Scrapie and Mastitis Transmit Infectious Prions through the 
Milk?
Ciriaco Ligios1,†, Maria Giovanna Cancedda1, Antonello Carta2, Cinzia 
Santucciu1, Caterina Maestrale1, Francesca Demontis1, Mariangela Saba1, 
Cristiana Patta1, James C. DeMartini3, Adriano Aguzzi4,†,* and Christina J. 
Sigurdson4,5,6,†,*
+ Author Affiliations
1Istituto Zooprofilattico Sperimentale della Sardegna, Sassari, Italy
2Research Unit of Genetics and Biotechnology, DIRPA, AGRIS Sardinia, 
Olmedo, Italy
3Department of Microbiology, Immunology, and Pathology, Colorado State 
University, Fort Collins, Colorado
4Institute of Neuropathology, UniversitätsSpital Zürich, Zürich, 
Switzerland
5 Department of Pathology, School of Medicine, University of California, 
San Diego, California
6Department of Pathology, Microbiology, and Immunology, University of 
California, Davis, California
Next Section ABSTRACT
Prions are misfolded proteins that are infectious and naturally 
transmitted, causing a fatal neurological disease in humans and animals. Prion 
shedding routes have been shown to be modified by inflammation in excretory 
organs, such as the kidney. Here, we show that sheep with scrapie and lentiviral 
mastitis secrete prions into the milk and infect nearly 90% of naïve suckling 
lambs. Thus, lentiviruses may enhance prion transmission, conceivably sustaining 
prion infections in flocks for generations. This study also indicates a risk of 
prion spread to sheep and potentially to other animals through dietary exposure 
to pooled sheep milk or milk products.
EFSA Journal 2011; 9(1):1945 Suggested citation: 
EFSA Panel on Biological Hazards (BIOHAZ); 
Joint Scientific Opinion on any possible epidemiological or molecular 
association between TSEs in animals and humans. 
EFSA Journal 2011;9(1):1945. [111 pp.] doi:10.2903/j.efsa.2011.1945. 
Available online: www.efsa.europa.eu/efsajournal © European Food Safety 
Authority, 2011 SCIENTIFIC OPINION Joint Scientific Opinion on any possible 
epidemiological or molecular association between TSEs in animals and humans1 
EFSA Panel on Biological Hazards (BIOHAZ)2, 3 European Food Safety Authority 
(EFSA), Parma, Italy European Centre for Disease Prevention and Control (ECDC)4, 
5 Stockholm, Sweden 
More recent EFSA opinions focused on the human exposure risk to TSEs 
through consumption of products deriving from small ruminants (ovine and caprine 
carcasses below six months, milk and milk products), but only focused on human 
exposure, without discussing the zoonotic potential of small ruminants TSEs 
(EFSA, 2008a, 2008c). A recent EFSA opinion (EFSA Panel on Biological Hazards 
(BIOHAZ), 2010a) provided updated data on the TSE infectivity distribution in 
small ruminant tissues. It also estimated the relative reduction of BSE 
infectivity load that can be achieved in the carcass of a small ruminant through 
the implementation of the current or alternative policies in terms of removal of 
Specified Risk Material (SRM). The zoonotic potential of TSE agents in small 
ruminants is, however, not discussed in the opinion. 
The TSE agent disseminates to the CNS (brain and spinal cord) apparently 
via the Enteric Nervous System and its nerves fibers (Andreoletti et al., 2000; 
Jeffrey et al., 2001; van Keulen et al., 2002), which is considered to 
accumulate TSE agents until around half of the incubation period. From there the 
agent could redistribute (centrifugally) to the peripheral nervous system and 
skeletal muscle (Andreoletti et al., 2004). Additionally, infectivity was also 
reported to be present in blood (Hunter et al., 2002), and in blood and in milk 
and colostrum (from the first lactation) from animals during incubation (Konold 
et al., 2008; Lacroux et al., 2008). In blood, the infectious agent can be 
detected as early as at 3 months of age and persists throughout the incubation 
period (Andreoletti et al., 2007). 
Finally, protection measures applied all along the food chain against small 
ruminants TSEs in the EU mainly rely at operational level on specified risk 
material (SRM) removal, i.e exclusion from food chain of tissues that can 
contain a high infectious load. However, for practical reasons, the SRM measures 
do not imply discarding from the food chain of all the infectious tissues and 
animal products that could contain infectivity (EFSA, 2008c). Moreover, 
infectivity was recently identified in tissues like skeletal muscles or in 
products like milk from small ruminants incubating scrapie, tissues that were 
previously considered to be non infectious. 
Commentary
In vitro amplification of prions from milk in the detection of subclinical 
infections
Volume 3, Issue 4   October/November/December 2009 Pages 236 - 239 http://dx.doi.org/10.4161/pri.3.4.10425
Kevin C. Gough, Claire A. Baker, Maged Taema and Ben C. Maddison
View affiliations
Prions can be amplified by serial protein misfolding cyclic amplification 
(sPMCA) from the milk of a high proportion of apparently healthy, scrapie 
exposed sheep with PRNP genotypes not previously associated with high disease 
penetrance1. These data strongly suggest the widespread presence of subclinical 
scrapie infections within scrapie-exposed flocks containing sheep with a range 
of susceptible PRNP genotypes. These data also lead to the hypothesis that 
similar subclinical disease states may be common for other animal and human 
prion diseases. Furthermore, the application of sPMCA to milk provides a method 
to detect such subclinical disease. Here, we describe the high level 
amplification of bovine spongiform encephalopathy (BSE) prions from both ovine 
and bovine origin, a methodology that will facilitate the detection of any 
prions secreted within bovine and ovine milk during subclinical and clinical BSE 
disease.
Prion Protein in Milk
Nicola Franscini,1 Ahmed El Gedaily,1 Ulrich Matthey,1 Susanne Franitza,1 
Man-Sun Sy,2 Alexander Bürkle,3 Martin Groschup,4 Ueli Braun,5 and Ralph 
Zahn1
Conclusions/Significance
In view of a recent study showing evidence of prion replication occurring 
in the mammary gland of scrapie infected sheep suffering from mastitis, the 
appearance of PrPC in milk implies the possibility that milk of TSE-infected 
animals serves as source for PrPSc.
WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform 
Encephalopathies Updated 2010
snip...
Since the publication in 2006 
of Annex 1 (Major Categories of Infectivity) in the ‘‘WHO Guidelines on Tissue 
Infectivity Distribution in Transmissible Spongiform Encephalopathies’’, some 
tissues (ovary, uterus, mammary glands/udder, skin, adipose tissue, and 
heart/pericardium) and body fluids (saliva, milk, urine, and feces) in which 
infectivity had not been detected, have since been found to contain infectivity 
or PrPTSE and therefore have there been moved from the category of ‘‘tissues 
with no detectable infectivity’’ ’’ to the category of ‘‘lower-infectivity 
tissues.’’
When 
L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the 
resulting molecular fingerprint had changed, either in the first or a subsequent 
passage, from L-type into C-type BSE. In addition, non-human primates are 
specifically susceptible for atypical BSE as demonstrated by an approximately 
50% shortened incubation time for L-type BSE as compared to C-type. Considering 
the current scientific information available, it cannot be assumed that these 
different BSE types pose the same human health risks as C-type BSE or that these 
risks are mitigated by the same protective measures. 
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2 
Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1 http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
PLoS One. 2012; 7(2): e31449.
Published online 2012 February 21. doi: 10.1371/journal.pone.0031449
PMCID: PMC3283643
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy
The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.
PINK SLIME LFTB MSM MRM BSE TSE PRION
Saturday, April 21, 2012 
HISD seeks refund on burgers with 'pink slime' 
Wednesday, March 14, 2012
PINK SLIME, MRM’s, BSE AKA MAD COW 
DISEASE, AND THE USDA NSLP
Sunday, August 28, 2011
Tuesday, April 24, 2012
MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA 
Wednesday, April 25, 2012
4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/4th-mad-cow-disease-usa-california.html
Wednesday, April 25, 2012
USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012
http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/usa-mad-cow-disease-and-cjd-there-from.html
America's Mad Cow crisis by John Stauber
http://www.commondreams.org/view/2012/04/26-1
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