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Bovine spongiform encephalopathy
|Bovine spongiform encephalopathy
A cow with BSE: Infected animals lose the ability to stand.
|Classification and external resources
Bovine spongiform encephalopathy (BSE), commonly known as mad cow disease, is a fatal neurodegenerative disease (encephalopathy) in cattle that causes a spongy degeneration of the brain and spinal cord. BSE has a long incubation period, of 2.5 to 5 years, usually affecting adult cattle at a peak age onset of four to five years. BSE is caused by a misfolded protein—a prion.[1] In the United Kingdom, the country worst affected by an epidemic in 1986–1998, more than 180,000 cattle were infected and 4.4 million slaughtered during the eradication program.[2]
The disease may be most easily transmitted to humans by eating food contaminated with the brain, spinal cord or digestive tract of infected carcasses.[3] However, the infectious agent, although most highly concentrated in nervous tissue, can be found in virtually all tissues throughout the body, including blood.[4] In humans, it is known as new variant Creutzfeldt–Jakob disease (vCJD or nvCJD), and by June 2014 it had killed 177 people in the United Kingdom, and 52 elsewhere, primarily in western Europe in countries supplied with beef or beef products from the UK. [5] Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989.[6][7]
A British and Irish inquiry into BSE concluded the epizootic was caused by cattle, which are normally herbivores, being fed the remains of other cattle in the form of meat and bone meal (MBM), a protein supplement in concentrated feeds.[8] [9][10] Since dairy calves are generally fed concentrated feed after they are weaned, they usually develop this disease more often then beef cattle[11]
The cause of BSE may be from the contamination of MBM from sheep with scrapie that were processed in the same slaughterhouse. The epidemic was probably accelerated by the recycling of infected bovine tissues prior to the recognition of BSE.[12] The origin of the disease itself remains unknown. The infectious agent is distinctive for the high temperatures at which it remains viable, over 600 °C (about 1100 °F).[13] This contributed to the spread of the disease in the United Kingdom, which had reduced the temperatures used during its rendering process.[9] Another contributory factor was the feeding of infected protein supplements to very young calves.[9][14]
The pathogenesis of BSE is not well understood or documented like other diseases of this nature. Even though BSE is disease that results in neurological defects, its pathogenesis occurs in areas that reside outside of the nervous system.[15] There was a strong deposition of PrPSc initially located in the Ileal Peyer's patches of the small intestine.[16] The lymphatic system has been identified in the pathogenesis of scrapies, it has not, however, been determined to be an essential part of the pathogenesis of BSE. The Ileal Peyer's patches have been the only organ from this system that has been found to play a major role in the pathogenesis.[15] Infectivity of the Ileal Peyer's patches has been observed as early as 4 months after inoculation.[16] PrPSc accumulation was found to occur mostly in tangible body macrophages of the Ileal Peyer's patches. Tangible body macrophages involved in PrPSc clearance are thought to play a role in in PrPSc accumulation in the Peyer's patches. Accumulation of PrPSc was also found in follicular dendritic cells; however, it was of a lesser degree.[17] Six months after inoculation, there was no infectivity in any tissues, only that of the ileum. This led researchers to believe that the disease agent replicates here. In naturally confirmed cases, there have been no reports of infectivity in the Ileal Peyer's patches. Generally, in clinical experiments, high doses of the disease are administered. In natural cases, it was hypothesized that low doses of the agent were present, and therefore, infectivity could not be observed.[18]
Signs and symptoms
Symptoms are not seen immediately in cattle due to the diseases' extremely long incubation period.[19] Some cattle have been observed to have an abnormal gait, changes in behavior, tremors and hyperresponsiveness to certain stimuli.[20] Hindlimb ataxia affects the animal's gait and occurs when muscle control is lost. This results in poor balance and coordination.[21] Behavioural changes may include aggression, anxiety relating to certain situations, nervousness, frenzy or an overall change in temperament. Some rare but previously observed symptoms also include persistent pacing, rubbing or licking. Additionally, nonspecific symptoms have also been observed which include weight loss, decreased milk production, lameness, ear infections and teeth grinding due to pain. Some animals may show a combination of these symptoms, while others may only be observed demonstrating one of the many reported. Once clinical symptoms arise, they typically get worse over the upcoming weeks and months, eventually leading to recumbency, coma and death.[20]
The infectious agent in BSE is believed to be a specific type of misfolded protein called a prion. Other theories state that the agent is a virus,[22] virino,[23] Spiroplasma species, or Acinetobacter species.[24] Prions are not destroyed even if the beef or material containing them is cooked or heat-treated. Prion proteins carry the disease between individuals and cause deterioration of the brain. BSE is a type of transmissible spongiform encephalopathy (TSE).[25] TSEs can arise in animals that carry an allele which causes previously normal protein molecules to contort by themselves from an alpha helical arrangement to a beta pleated sheet, which is the disease-causing shape for the particular protein. Transmission can occur when healthy animals come in contact with tainted tissues from others with the disease. In the brain, these proteins cause native cellular prion protein to deform into the infectious state, which then goes on to deform further prion protein in an exponential cascade. This results in protein aggregates, which then form dense plaque fibers leading to the microscopic appearance of "holes" in the brain, degeneration of physical and mental abilities, and ultimately death.
Different hypotheses exist for the origin of prion proteins in cattle. Two leading hypotheses suggest it may have jumped species from the disease scrapie in sheep, or that it evolved from a spontaneous form of "mad cow disease" that has been seen occasionally in cattle for many centuries.[26] In the fifth century BC, Hippocrates described a similar illness in cattle and sheep, which he believed also occurred in man.[27] Publius Flavius Vegetius Renatus recorded cases of a disease with similar characteristics in the fourth and fifth centuries AD.[28] The British Government enquiry took the view the cause was not scrapie, as had originally been postulated, but was some event in the 1970s that was not possible to identify.[29]
Research in 2008 suggested that mad cow disease also is caused by a genetic mutation within the prion protein gene. The research showed, for the first time, that a 10-year-old cow from Alabama with an atypical form of bovine spongiform encephalopathy had the same type of prion protein gene mutation as found in human patients with the genetic form of Creutzfeldt–Jakob disease (genetic CJD). This form of Creutzfeldt–Jakob disease is called variant CJD.[30]
Diagnosis of BSE continues to be a practical problem. It has an incubation period of months to years, during which no symptoms are noticed, though the pathway of converting the normal brain prion protein (PrP) into the toxic, disease-related PrPSc form has started. At present, virtually no way is known to detect PrPSc reliably except by examining post mortem brain tissue using neuropathological and immunohistochemical methods. Accumulation of the abnormally folded PrPSc form of PrP is a characteristic of the disease, but it is present at very low levels in easily accessible body fluids such as blood or urine. Researchers have tried to develop methods to measure PrPSc, but no methods for use in materials such as blood have been accepted fully.
The traditional method of diagnosis relies on histopathological examination of the medulla oblongata of the brain, and other tissues, post mortem. Immunohistochemistry can be used to demonstrate prion protein accumulation.[31]
In 2010, a team from New York described detection of PrPSc even when initially present at only one part in a hundred billion (10−11) in brain tissue. The method combines amplification with a novel technology called surround optical fiber immunoassay and some specific antibodies against PrPSc. After amplifying and then concentrating any PrPSc, the samples are labelled with a fluorescent dye using an antibody for specificity and then finally loaded into a microcapillary tube. This tube is placed in a specially constructed apparatus so it is totally surrounded by optical fibres to capture all light emitted once the dye is excited using a laser. The technique allowed detection of PrPSc after many fewer cycles of conversion than others have achieved, substantially reducing the possibility of artifacts, as well as speeding up the assay. The researchers also tested their method on blood samples from apparently healthy sheep that went on to develop scrapie. The animals' brains were analysed once any symptoms became apparent. The researchers could, therefore, compare results from brain tissue and blood taken once the animals exhibited symptoms of the diseases, with blood obtained earlier in the animals' lives, and from uninfected animals. The results showed very clearly that PrPSc could be detected in the blood of animals long before the symptoms appeared. After further development and testing, this method could be of great value in surveillance as a blood- or urine-based screening test for BSE.[32][33]
A ban on feeding meat and bone meal to cattle has resulted in a strong reduction in cases in countries where the disease was present. In disease-free countries, control relies on import control, feeding regulations, and surveillance measures.[31]
In UK and US slaughterhouses, the brain, spinal cord, trigeminal ganglia, intestines, eyes, and tonsils from cattle are classified as specified risk materials, and must be disposed of appropriately.[31]
An enhanced BSE-related feed ban is in effect in both the United States and Canada to help improve prevention and elimination of BSE.[34]
|BSE cases
|vCJD cases
|Czech Republic[37]
|Falkland Islands
|Hong Kong
|Republic of Ireland[5]
|Saudi Arabia[5]
|United Kingdom[5][45]
|United States[5][36]
The table to the right summarizes reported cases of BSE and of vCJD by country. (The vCJD column is by country of residence of patient at time of diagnosis and not suspected origin of beef.) BSE is the disease in cattle, while vCJD is the disease in people.
The tests used for detecting BSE vary considerably, as do the regulations in various jurisdictions for when, and which cattle, must be tested. For instance in the EU, the cattle tested are older (30 months or older), while many cattle are slaughtered younger than that. At the opposite end of the scale, Japan tests all cattle at the time of slaughter. Tests are also difficult, as the altered prion protein has very low levels in blood or urine, and no other signal has been found. Newer tests are faster, more sensitive, and cheaper, so future figures possibly may be more comprehensive. Even so, currently the only reliable test is examination of tissues during a necropsy.
As for vCJD in humans, autopsy tests are not always done, so those figures, too, are likely to be too low, but probably by a lesser fraction. In the United Kingdom, anyone with possible vCJD symptoms must be reported to the Creutzfeldt–Jakob Disease Surveillance Unit. In the United States, the CDC has refused to impose a national requirement that physicians and hospitals report cases of the disease. Instead, the agency relies on other methods, including death certificates and urging physicians to send suspicious cases to the National Prion Disease Pathology Surveillance Center (NPDPSC) at Case Western Reserve University in Cleveland, which is funded by the CDC.
To control potential transmission of vCJD within the United States, the American Red Cross has established strict restrictions on individuals' eligibility to donate blood. Individuals who have spent a cumulative time of 3 months or more in the United Kingdom between 1980 and 1996, or a cumulative time of 5 years or more from 1980 to present in any combination of countries in Europe, are prohibited from donating blood.[46]
North America
The first reported case in North America was in December 1993 from Alberta, Canada.[47][48] Another Canadian case was reported in May 2003. The first known U.S. occurrence came in December of the same year, though it was later confirmed to be a cow of Canadian origin imported to the U.S.[49] Canada announced two additional cases of BSE from Alberta in early 2005.[50] In June 2005, John R. Clifford, chief veterinary officer for the United States Department of Agriculture animal health inspection service, confirmed a fully domestic case of BSE in Texas.[51]
Practices in the United States relating to BSE
Soybean meal is cheap and plentiful in the United States. Cottonseed meal, 1.5 million tons of which are produced in the U.S. every year, none of which is suitable for humans or any other simple-stomach animals, is even cheaper than soybean meal. Historically, meat and bone meal, blood meal, and meat scraps have almost always commanded a higher price as a feed additive than oilseed meals in the U.S., so not much incentive existed to use animal products to feed ruminants. As a result, the use of animal byproduct feeds was never common, as it was in Europe. However, U.S. regulations only partially prohibited the use of animal byproducts in feed. In 1997, regulations prohibited the feeding of mammalian byproducts to ruminants such as cattle and goats. However, the byproducts of ruminants can still be legally fed to pets or other livestock, including pigs and poultry. In addition, it is legal for ruminants to be fed byproducts from some of these animals.[52] Because of this, some authors have suggested that under certain conditions, it is still possible for BSE incidence to increase in U.S. cattle.[53] A proposal to end the use of cattle blood, restaurant scraps, and poultry litter (fecal matter, feathers, bedding material)[54] in January 2004 has yet to be implemented.[55]
In February 2001, the US Government Accountability Office reported the FDA, which is responsible for regulating feed, had not adequately enforced the various bans.[56] Compliance with the regulations was shown to be extremely poor before the discovery of a cow in Washington infected with BSE in 2003, but industry representatives report that compliance is now total. Even so, critics call the partial prohibitions insufficient. Indeed, US meat producer Creekstone Farms was forcibly prevented from conducting BSE testing by the USDA, which under an obscure 1913 law had the authority to restrict sales of BSE testing kits, allegedly to protect other producers from being forced to conduct the same tests to stay competitive.[57]
The USDA has issued recalls of beef supplies that involved introduction of downer cows into the food supply. Hallmark/Westland Meat Packing Company was found to have used electric shocks to prod downer cows into the slaughtering system in 2007.[58] Possibly due to pressure from large agribusiness, the United States has drastically cut back on the number of cows inspected for BSE.[59]
Effect on the US beef industry
Japan was the top importer of US beef, buying 240,000 tons valued at $1.4 billion in 2003. After the discovery of the first case of BSE in the US on 23 December 2003, Japan halted US beef imports. In December 2005, Japan once again allowed imports of US beef, but reinstated its ban in January 2006 after a violation of the US-Japan beef import agreement: a vertebral column, which should have been removed prior to shipment, was included in a shipment of veal.
Tokyo yielded to US pressure to resume imports, ignoring consumer worries about the safety of US beef, said Japanese consumer groups. Michiko Kamiyama from Food Safety Citizen Watch and Yoko Tomiyama from Consumers Union of Japan[60] said about this: "The government has put priority on the political schedule between the two countries, not on food safety or human health."
Sixty-five nations implemented full or partial restrictions on importing US beef products because of concerns that US testing lacked sufficient rigor. As a result, exports of US beef declined from 1,300,000 metric tons in 2003, (before the first mad cow was detected in the US) to 322,000 metric tons in 2004. This has increased since then to 771,000 metric tons in 2007.[61]
On 31 December 2006, Hematech, Inc, a biotechnology company based in Sioux Falls, South Dakota, announced it had used genetic engineering and cloning technology to produce cattle that lacked a necessary gene for prion production – thus theoretically making them immune to BSE.[62]
In April 2012, some South Korean retailers ceased importing beef from the United States after a case of BSE was reported.[63] Indonesia also suspended imports of beef from the US after a dairy cow with mad cow disease was discovered in California.[64]
With 36 confirmed cases, Japan experienced one of the largest number of cases of BSE outside Europe.[65] It was the only country outside Europe and the Americas to report non-imported cases.[66] Reformation of food safety in the light of the BSE cases resulted in the establishment of a governmental Food Safety Commission in 2003.[67]
Cattle are naturally herbivores, eating grasses. In modern industrial cattle-farming, though, various commercial feeds are used, which may contain ingredients including antibiotics, hormones, pesticides, fertilizers, and protein supplements. The use of meat and bone meal, produced from the ground and cooked leftovers of the slaughtering process, as well as from the carcasses of sick and injured animals such as cattle or sheep, as a protein supplement in cattle feed was widespread in Europe prior to about 1987.[3] Worldwide, soybean meal is the primary plant-based protein supplement fed to cattle. However, soybeans do not grow well in Europe, so cattle raisers throughout Europe turned to the cheaper animal byproduct feeds as an alternative. The British Inquiry dismissed suggestions that changes to processing might have increased the infectious agents in cattle feed, saying, "changes in process could not have been solely responsible for the emergence of BSE, and changes in regulation were not a factor at all."[68] (The prion causing BSE is not destroyed by heat treatment.)
The first confirmed instance in which an animal fell ill with the disease occurred in 1986 in the United Kingdom, and lab tests the following year indicated the presence of BSE; by November 1987, the British Ministry of Agriculture accepted it had a new disease on its hands.[69] Subsequently, 177 people (as of June 2014) contracted and died of a disease with similar neurological symptoms subsequently called (new) variant Creutzfeldt–Jakob disease (vCJD).[5][70] This is a separate disease from 'classical' Creutzfeldt–Jakob disease, which is not related to BSE and has been known about since the early 1900s. Three cases of vCJD occurred in people who had lived in or visited the UK – one each in the Republic of Ireland, Canada, and the United States of America. Also, some concern existed about those who work with (and therefore inhale) cattle meat and bone meal, such as horticulturists, who use it as fertilizer. Up-to-date statistics on all types of CJD are published by the National Creutzfeldt–Jakob Disease Surveillance Unit in Edinburgh, Scotland.
For many of the vCJD patients, direct evidence exists that they had consumed tainted beef, and this is assumed to be the mechanism by which all affected individuals contracted it. Disease incidence also appears to correlate with slaughtering practices that led to the mixture of nervous system tissue with ground meat (mince) and other beef. An estimated 400,000 cattle infected with BSE entered the human food chain in the 1980s. Although the BSE epizootic was eventually brought under control by culling all suspect cattle populations, people are still being diagnosed with vCJD each year (though the number of new cases currently has dropped to fewer than five per year). This is attributed to the long incubation period for prion diseases, which is typically measured in years or decades. As a result, the full extent of the human vCJD outbreak is still not known.
The scientific consensus is that infectious BSE prion material is not destroyed through cooking procedures, meaning that even contaminated beef foodstuffs prepared "well done" may remain infectious.[71][72] In fact the infectious agent remains viable over 600 °C (about 1100 °F).
Alan Colchester, a professor of neurology at the University of Kent, and Nancy Colchester, writing in the 3 September 2005 issue of the medical journal The Lancet, proposed a theory that the most likely initial origin of BSE in the United Kingdom was the importation from the Indian Subcontinent of bone meal which contained CJD-infected human remains.[73] The government of India vehemently responded to the research, calling it "misleading, highly mischievous; a figment of imagination; absurd," further adding that India maintained constant surveillance and had not had a single case of either BSE or vCJD.[74][75] The authors responded in the 22 January 2006 issue of The Lancet that their theory is unprovable only in the same sense as all other BSE origin theories are and that the theory warrants further investigation.[76]
During the course of the investigation into the BSE epizootic, an enquiry was also made into the activities of the Department of Health Medicines Control Agency (MCA). On 7 May 1999, David Osborne Hagger, a retired civil servant who worked in the Medicines Division of the Department of Health between 1984 and 1994, produced a written statement to the BSE Inquiry in which he gave an account of his professional experience of BSE.[77]
In February 1989, the MCA had been asked to "identify relevant manufacturers and obtain information about the bovine material contained in children's vaccines, the stocks of these vaccines and how long it would take to switch to other products." In July, "[the] use of bovine insulin in a small group of mainly elderly patients was noted and it was recognised that alternative products for this group were not considered satisfactory." In September, the BSE Working Party of the Committee on the Safety of Medicines (CSM) recommended that "no licensing action is required at present in regard to products produced from bovine material or using prepared bovine brain in nutrient media and sourced from outside the United Kingdom, the Channel Isles and the Republic of Ireland provided that the country of origin is known to be free of BSE, has competent veterinary advisers and is known to practise good animal husbandry."
In 1990, the British Diabetic Association became concerned regarding the safety of bovine insulin. The CSM assured them "[that] there was no insulin sourced from cattle in the UK or Ireland and that the situation in other countries was being monitored."
In 1991, the European Commission "[expressed] concerns about the possible transmission of the BSE/scrapie agent to man through use of certain cosmetic treatments."
In 1992, sources in France reported to the MCA "that BSE had now been reported in France and there were some licensed surgical sutures derived from French bovine material." Concerns were also raised at a CSM meeting "regarding a possible risk of transmission of the BSE agent in gelatin products."[77]
The ban on British beef
The BSE crisis led to the European Union banning exports of British beef with effect from March 1996; the ban lasted for 10 years before it was finally lifted on 1 May 2006[78] despite attempts in May 1996 by British prime minister John Major to get the ban lifted. The ban resulted in trade controversies between the UK and other EU states, dubbed "beef war" by media.[79] Restrictions remained for beef containing "vertebral material" and for beef sold on the bone.[80]
Russia was proceeding to lift the ban sometime after November 2012 after 16 years; the announcement was made during a visit by the UK's chief veterinary officer Nigel Gibbens.[81]
It was successfully negotiated that beef from Wales was allowed to be exported to the Dutch market, which had formerly been an important market for Northern Irish beef. Of two approved export establishments in the United Kingdom in 1999, one was in Scotland – an establishment to which live beef was supplied from Northern Ireland. As the incidence of BSE was very low in Northern Ireland – only six cases of BSE by 1999 – partly due to the early adoption of an advanced herd tagging and computerization system in the region, calls were made to remove the EU ban on exports with regard to Northern Irish beef.[82]
See also
- Health crisis
- Meat on the bone
- US beef imports in Japan
- US beef imports in Taiwan
- US beef imports in South Korea, 2008 US beef protest in South Korea
- Beef war (disambiguation)
- William Drohan, mad cow disease in the blood supply investigator
- ↑ "A Focus on Bovine Spongiform Encephalopathy". Pathogens and Contaminants. Food Safety Research Information Office. November 2007. Archived from the original on 3 March 2008. Retrieved 7 April 2008.
- ↑ Brown, David (19 June 2001). "The 'recipe for disaster' that killed 80 and left a £5bn bill". The Daily Telegraph. London. Retrieved 7 April 2008.
- 1 2 "Commonly Asked Questions About BSE in Products Regulated by FDA's Center for Food Safety and Applied Nutrition (CFSAN)". Center for Food Safety and Applied Nutrition, Food and Drug Administration. 14 September 2005. Archived from the original on 9 May 2008. Retrieved 8 April 2008.
- ↑ I Ramasamy; M Law; S Collins; F Brook (April 2003). "Organ distribution of prion proteins in variant Creutzfeldt–Jakob disease". The Lancet Infectious Diseases. 3 (4): 214–222. doi:10.1016/S1473-3099(03)00578-4. PMID 12679264.
- 1 2 3 4 5 6 7 8 9 10 11 12 13 "Variant Creutzfeld–Jakob Disease, Current Data (October 2009)". The National Creutzfeldt–Jakob Disease Surveillance Unit (NCJDSU), University of Edinburgh. October 2009. Archived from the original on 21 July 2012. Retrieved 14 October 2009.;
- ↑ Valleron AJ, Boelle PY, Will R, Cesbron JY (November 2001). "Estimation of epidemic size and incubation time based on age characteristics of vCJD in the United Kingdom". Science. 294 (5547): 1726–8. doi:10.1126/science.1066838. PMID 11721058. Lay summary – BBC News (23 November 2001).
- ↑ Kimberlin, Richard H.; Wilesmith, John W. (1994-05-01). "Bovine Spongiform Encephalopathy". Annals of the New York Academy of Sciences. 724 (1): 210–220. doi:10.1111/j.1749-6632.1994.tb38911.x. ISSN 1749-6632.
- 1 2 3 "BSE: Disease control & eradication – Causes of BSE". Department for Environment, Food, and Rural Affairs. March 2007.
- ↑ "The BSE Inquiry Website at The UK National Archives".
- ↑ Nathanson, Neal; Wilesmith, John; Griot, Christian (1997). "Bovine Spongiform Encephalopathy (BSE): Causes and Consequences of a Common Source Epidemic" (PDF). American Journal of Epidemiology. 145: 959–969.
- ↑ Nathanson N, Wilesmith J, Griot C (1997). "Bovine spongiform encephalopathy (BSE): causes and consequences of a common source epidemic". Am. J. Epidemiol. 145 (11): 959–69. doi:10.1093/oxfordjournals.aje.a009064. PMID 9169904.
- ↑ Brown, P; Rau, EH; Johnson, BK; Bacote, AE; Gibbs Jr., CJ; Gajdusek, DC (28 March 2000). "New studies on the heat resistance of hamster-adapted scrapie agent: threshold survival after ashing at 600°C suggests an inorganic template of replication.". Proc. Natl. Acad. Sci. USA. 97 (7): 3418–21. doi:10.1073/pnas.050566797. PMC 16254. PMID 10716712.
- ↑ Harden, Blaine (28 December 2003). "Supplements used in factory farming can spread disease". The Washington Post. Retrieved 8 April 2008.
- 1 2 Espinosa, Juan Carlos; Morales, Mónica; Castilla, Joaquín; Rogers, Mark; Torres, Juan María (2007-01-01). "Progression of prion infectivity in asymptomatic cattle after oral bovine spongiform encephalopathy challenge". Journal of General Virology. 88 (4): 1379–1383. doi:10.1099/vir.0.82647-0.
- 1 2 Balkema-Buschmann, A.; Fast, C.; Kaatz, M.; Eiden, M.; Ziegler, U.; McIntyre, L.; Keller, M.; Hills, B.; Groschup, M. H. (2011-11-01). "Pathogenesis of classical and atypical BSE in cattle". Preventive Veterinary Medicine. Special Issue: Animal Health in the 21st Century - A Global ChallengeAnimal Health in the 21st Century. 102 (2): 112–117. doi:10.1016/j.prevetmed.2011.04.006.
- ↑ Hoffmann, Christine; Ziegler, Ute; Buschmann, Anne; Weber, Artur; Kupfer, Leila; Oelschlegel, Anja; Hammerschmidt, Baerbel; Groschup, Martin H. (2007-01-01). "Prions spread via the autonomic nervous system from the gut to the central nervous system in cattle incubating bovine spongiform encephalopathy". Journal of General Virology. 88 (3): 1048–1055. doi:10.1099/vir.0.82186-0.
- ↑ Wells, G; Hawkins, S; Green, R; Austin, A; Dexter, I; Spencer, Y; Chaplin, M; Stack, M; Dawson, M (1998). "Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update" (PDF). The Veterinary Record. 142: 103–106.
- ↑ Thomson, Gavin. "Bovine Spongiform Encephalopathy (BSE)" (PDF). Retrieved November 21, 2016.
- 1 2 "Bovine Spongiform Encephalopathy" (PDF). The Center for Food Security & Public Health. The Center for Food Security & Public Health. August 2016. Retrieved October 30, 2016.
- ↑ "Ataxias and Cerebellar or Spinocerebellar Degeneration Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". www.ninds.nih.gov. Retrieved 2016-12-01.
- ↑ Miyazawa K, Kipkorir T, Tittman S, Manuelidis L (2012). "Continuous production of prions after infectious particles are eliminated: implications for Alzheimer's disease". PLOS ONE. 7 (4): e35471. doi:10.1371/journal.pone.0035471. PMC 3324552. PMID 22509412.
- ↑ "Genetic aspects of unconventional virus infections: the basis of the virino hypothesis.". Ciba Found Symp. 135: 63–83. 1988. PMID 3044709.
- ↑ Tiwana H, Wilson C, Pirt J, Cartmell W, Ebringer A (1999). "Autoantibodies to brain components and antibodies to Acinetobacter calcoaceticus are present in bovine spongiform encephalopathy". Infect. Immun. 67 (12): 6591–5. PMC 97071. PMID 10569779.
- ↑ "Bovine Spongiform Encephalopaphy: An Overview" (PDF). Animal and Plant Health Inspection Service, United States Department of Agriculture. December 2006. Archived from the original (PDF) on 8 March 2008. Retrieved 8 April 2008.
- ↑ MacKenzie, Debora (17 March 2007). "New twist in tale of BSE's beginnings". New Scientist. 193 (2595): 11. doi:10.1016/S0262-4079(07)60642-3. Retrieved 20 June 2009.
- ↑ McAlister, Vf (June 2005). "Sacred disease of our times: failure of the infectious disease model of spongiform encephalopathy.". Clin Invest Med. 28 (3): 101–4. PMID 16021982. Retrieved 20 June 2011.
- ↑ Digesta Artis Mulomedicinae, Publius Flavius Vegetius Renatus
- ↑ Vol.1 – Executive Summary of the Report of the Inquiry
- ↑ Richt JA, Hall SM (2008). Westaway, David, ed. "BSE case associated with prion protein gene mutation". PLoS Pathogens. 4 (9): e1000156. doi:10.1371/journal.ppat.1000156. PMC 2525843. PMID 18787697. Lay summary – Newswise (12 September 2008).
- 1 2 3 Bovine Spongiform Encephalopathy reviewed and published by WikiVet. Retrieved 11 October 2011.
- ↑ "Detecting Prions in Blood" (PDF). Microbiology Today.: 195. August 2010. Retrieved 21 August 2011.
- ↑ "SOFIA: An Assay Platform for Ultrasensitive Detection of PrPSc in Brain and Blood" (PDF). SUNY Downstate Medical Center. Retrieved 19 August 2011.
- ↑ "Feed Bans BSE (Bovine Spongiform Encephalopathy) | Prion Diseases | CDC". www.cdc.gov. Retrieved 2016-09-30.
- ↑ "BSE in Belgium". 12 November 2006. Retrieved 9 November 2008.
- 1 2 "BSE Cases in North America, by Year and Country of Death, 1993–2008". Centers for Disease Control and Prevention, Department of Health and Human Services. 2008. Retrieved 9 November 2008.
- ↑ "BSE Positive Findings in the Czech Republic" (pdf). State Veterinary Administration, Ministry of Agriculture, Czech Republic. 2007. p. 2. Retrieved 9 November 2008.
- ↑ "The Current Status of BSE and scrapie in Denmark" (PDF). Danish Veterinary and Food Administration. May 2007. Archived from the original (pdf) on 16 December 2008. Retrieved 9 November 2008.
- ↑ France reports more than 900 BSE cases
- ↑ "BSE in Greece". Retrieved 9 November 2008.
- ↑ "Israel: BSE testing according to source of cattle and age groups, 2002–2008". 5 March 2008.
- ↑ "vCJD Cases Worldwide 2011". 2 July 2011.
- ↑ "BSE cases – Italy 2001 – 2006". 2006. Retrieved 10 November 2008.
- ↑ "Overzicht BSE-gevallen" (in Dutch). Ministerie van Landbouw, Natuur en Voedselkwaliteit. 2008. Retrieved 9 November 2008.
- ↑ http://www.cjd.ed.ac.uk/documents/figs.pdf; April 2013
- ↑ Eligibility Criteria for Blood Donation, American Red Cross
- ↑ "Mad Cow in Canada: The science and the story". CBC News. 24 August 2006. Retrieved 20 January 2015.
- ↑ "Mad Cow in Canada – 1993". Parliament of Canada. Retrieved 23 August 2011.
- ↑ "Investigators Trace Diseased Cow to Canada".
- ↑ Becker, Geoffrey S. (11 March 2005). "Bovine Spongiform Encephalopathy and Canadian Beef Imports" (PDF). CRS Report for Congress. RL32627.
- ↑ reported "Case of Mad Cow in Texas Is First to Originate in U.S.", New York Times
- ↑ Rampton, Sheldon; Stauber, John (2004). Mad Cow USA (1st ed.). Monroe, Maine: Common Courage Press. ISBN 978-1-56751-110-9.
- ↑ Barnes, Richard; Lehman, Clarence (June 2013). "Modeling of bovine spongiform encephalopathy in a two-species feedback loop". Epidemics. Elsevier. 5 (2): 85–91. doi:10.1016/j.epidem.2013.04.001.
- ↑ The term "chicken litter" also includes spilled chicken feed, as well as fecal matter and feathers. It is still legal in the United States to use ruminant protein to feed chickens. Thus, ruminant protein can get into the food chain of cattle in this roundabout way.
- ↑ Peck, Clint (5 November 2004). "Reader Questions Poultry Litter And "Downer" Bans". Organic Consumers Association. Retrieved 20 June 2009.
- ↑ Phillips, Kyra; Meserve, Jeanne (26 February 2001). "FDA Not Doing Enough to Prevent Mad Cow Disease?". Organic Consumers Association. Retrieved 20 June 2009.
- ↑ "Creekstone Farms response to USDA appeal of summary judgement" (Press release). 3buddies. 30 May 2007. Archived from the original on 28 September 2007. Retrieved 20 June 2009.
- ↑ Seltzer, Molly (12 July 2008). "Meat Recalls to Name Retailers". The Washington Post. Bloomberg News. Retrieved 20 June 2009.
- ↑ "Mad cow watch goes blind". USA Today. 3 August 2006. Retrieved 20 June 2009.
- ↑ http://www.fswatch.org/newsletter/english/issue05.html
- ↑ "Statistics". Trade Library. U.S. Meat Export Federation. Archived from the original on 14 May 2009. Retrieved 20 June 2009.
- ↑ Weiss, Rick (1 January 2007). "Scientists Announce Mad Cow Breakthrough". The Washington Post. Retrieved 1 January 2007.
- ↑ "UPDATE 1-S.Korea retailers halt US beef sales, govt may act". Reuters. 25 April 2012.
- ↑ citation outdated
- ↑ Ministry of Health, Labour and Welfare: BSE Cases in Japan (accessed 7 May 2013)
- ↑ World Organisation for Animal Health: BSE situation in the world and annual incidence rate (accessed 7 May 2013)
- ↑ Kamisato Tatsuhiro (2005). "BSE crisis in Japan: A chronological overview". Environ Health Prev Med. 10: 295–302. doi:10.1007/BF02897705. PMC 2723414. PMID 21432134.
- ↑ "The BSE Inquiry:Home". Open.gov.uk. October 2000. Retrieved 27 August 2014.
- ↑ Brain disease drives cows wild
- ↑ "Mad cow disease: Still a concern". MayoClinic.com. CNN. 10 February 2006. Archived from the original on 25 April 2005. Retrieved 20 June 2009.
- ↑ "Bovine Spongiform Encephalopathy – "Mad Cow Disease"". Fact Sheets. Food Safety and Inspection Service. March 2005. Retrieved 8 April 2008.
- ↑ Colchester AC, Colchester NT (2005). "The origin of bovine spongiform encephalopathy: the human prion disease hypothesis". Lancet. 366 (9488): 856–61. doi:10.1016/S0140-6736(05)67218-2. PMID 16139661.
- ↑ Mago, Chandrika; Sinha, Kounteya (2 September 2005). "India dismisses Lancet's mad cow". The Times of India. Retrieved 20 June 2009.
- ↑ Thompson, Geoff (5 September 2005). "New theory traces mad cow disease to animal feed exported from India". The World Today. ABC. Retrieved 20 June 2009.
- ↑ Colchester, A; Colchester, N (28 January 2006). "Origin of bovine spongiform encephalopathy – Authors' reply". The Lancet. Elsevier. 367 (9507): 298–299. doi:10.1016/S0140-6736(06)68062-8.
- 1 2 "BSE Inquiry, Statement No. 476" (PDF). BSE Inquiry. 7 May 1999. Retrieved 16 October 2008. Statement of David Osborne Hagger, Head of Abridged Licensing and Coordinator of the Executive support business of the Medicines Division of the Department of Health at Market Towers in London.
- ↑ "End to 10-year British beef ban". BBC News. 3 May 2006.
- ↑ "EU beef war escalates"
- ↑ http://news.bbc.co.uk/2/hi/4967480.stm
- ↑ "Russia to lift 16-year ban on British beef and lamb". bbc.co.uk. 22 November 2012.
- ↑ UK Parliament website Select Committee on Northern Ireland Affairs Second Report
Further reading
- Altman, Lawrence K. "Four States Watching for Brain Disorder." New York Times, 9 April 1996a.
- Altman, Lawrence K. "U.S. Officials Confident That Mad Cow Disease of Britain Has Not Occurred Here." New York Times, 27 March 1996d: 12A.
- "Apocalypse Cow: U.S. Denials Deepen Mad Cow Danger." PR Watch, 3.1 (1996): 1–8
- Berger Joseph R.; et al. (1994). "Creutzfeldt–Jakob Disease: A Ten-Year Experience". Neurology. 44: A260.
- Bleifuss, Joel. "Killer Beef." In These Times, 31 May 1993: 12–15.
- Boller F, Lopez OL, Moossy J (1989). "Diagnosis of Dementia". Neurology. 38 (7 Suppl 2): 76–79. doi:10.1212/WNL.39.1.76. PMID 3290719.
- Boule, Margie. "Despite Anecdotal Evidence, Docs Say No Mad Cow Disease Here." The Oregonian, 16 April 1996: C01.
- "Brain Disease May Be Commoner Than Thought – Expert." Reuters Information Service, 15 May 1996.
- Brayne, C. "How Common are Cognitive Impairment and Dementia?" Dementia and Normal Aging, Cambridge University Press, 1994.
- Brown Paul (1989). "Central Nervous System Amyloidoses". Neurology. 39 (8): 1103–1104. doi:10.1212/WNL.39.8.1103.
- Davanpour Zoreth; et al. (1993). "Rate of Creutzfeldt–Jakob Disease in USA". Neurology. 43: A316.
- Flannery, Mary. "Twelve – Fifteen 'Mad Cow' Victims a Year in Area." Philadelphia Daily News, 26 March 1996: 03.
- Folstein, M. "The Cognitive Pattern of Familial Alzheimer's Disease." Biological Aspects of Alzheimer's Disease. Ed. R. Katzman. Cold Spring Harbor Laboratory, 1983.
- Gruzen, Tara. "Sheep Parts Fail to Cause Mad Cow Disease in U.S. Test." Seattle Times, 29 March 1996: A11.
- Hager, Mary and Mark Hosenball. "'Mad Cow Disease' in the U.S.?" Newsweek, 8 April 1996:58–59.
- Harrison Paul J., Roberts Gareth W.; Roberts (1991). "'Life, Jim, But Not as We Know It'? Transmissible Dementias and the Prion Protein". British Journal of Psychiatry. 158 (4): 457–70. doi:10.1192/bjp.158.4.457. PMID 2054560.
- Holman, RC; Khan, AS; Kent, J; Strine, TW; Schonberger, LB (1995). "Epidemiology of Creutzfeldt–Jakob disease in the United States, 1979-1990: analysis of national mortality data.". Neuroepidemiology. 14 (4): 174–181. doi:10.1159/000109793. PMID 7643951.
- Hoyert, Donna L. "Vital and Health Statistics. Mortality Trends for Alzheimer's Disease, 1979–1991." Washington: U.S. Dept. of Health and Human Services, 1996.
- Little Brian W.; et al. (1993). "The Epidemiology of Creutzfeldt–Jakob Disease in Eastern Pennsylvania". Neurology. 43: A316. doi:10.1212/wnl.43.4_suppl_2.a11.
- Mahendra, B. Dementia, Lancaster: MTP Press Limited, 1987: 174.
- Manuelidis Elias E (1985). "Presidential Address". Journal of Neuropathology and Experimental Neurology. 44 (1): 1–17. doi:10.1097/00005072-198501000-00001. PMID 3880808.
- Manuelidis Elias E., Manuelidis Laura; Manuelidis (1989). "Suggested Links between Different Types of Dementias: Creutzfeldt–Jakob Disease, Alzheimer Disease, and Retroviral CNS Infections". Alzheimer Disease and Associated Disorders. 2: 100–109. doi:10.1097/00002093-198903010-00009.
- McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM (1984). "Clinical Diagnosis of Alzheimer's Disease". Neurology. 34: 939. doi:10.1212/WNL.34.7.939.
- Prusiner S (1984). "Some Speculations about Prions, Amyloid, and Alzheimer's Disease". New England Journal of Medicine. 310 (10): 661–663. doi:10.1056/NEJM198403083101021. PMID 6363926.
- Perry RT, Go RC, Harrell LE, Acton RT (1995). "Human Prion Protein Gene: Two Different 24 BP Deletions in an Atypical Alzheimer's Disease Family". American Journal of Medical Genetics. 60 (1): 12–18. doi:10.1002/ajmg.1320600104. PMID 7485229.
- Scully R. E.; et al. (1993). "Case Records of the Massachusetts General Hospital Case 17: 1993". New England Journal of Medicine. 328: 1259–1263. doi:10.1056/NEJM199304293281709. PMID 8464437.
- Teixeira F.; et al. (1995). "Clinico-Pathological Correlation in Dementias". Journal of Psychiatry and Neuroscience. 20: 276–282.
- United States Department of Commerce. Statistical Abstract of the United States, Washington: Bureau of the Census, 1995.
- Van Duijn C. M. (1996). "Epidemiology of the Dementia: Recent Developments and New Approaches". Neuroepidemiology. 60: 478–488. doi:10.1136/jnnp.60.5.478.
- Wade J. P. H.; et al. (1987). "The Clinical Diagnosis of Alzheimer's Disease". Archives of Neurology. 44 (1): 24–29. doi:10.1001/archneur.1987.00520130016010. PMID 3800717.
- Wlazelek, Ann (23 September 1990). "Fatal Brain Disease Mystifies Experts". The Morning Call. Retrieved 9 November 2013.: B01
- Wlazelek, Ann (27 September 1990). "Scientists Try To Track Fatal Disease International Expert Visits Area To Study Unusual Incidence Rate". The Morning Call. Retrieved 9 November 2013.: B04
- "World Health Organization Consultation on Public Health Issues Related to Bovine Spongiform Encephalopathy and the Emergence of a New Variant of Creutzfeldt–Jakob Disease.", Morbidity and Mortality Weekly Report, 12 April 1996: 295–303.*/
External links
|Look up Bovine spongiform encephalopathy in Wiktionary, the free dictionary.
|Wikinews has news related to:
|Wikimedia Commons has media related to Bovine spongiform encephalopathy.
- Bovine spongiform encephalopathy at DMOZ
- OIE – World Organisation for Animal Health: BSE situation in the world and annual incidence rate
- UK BSE Inquiry Website, Archived at The National Archives


text:
FreshBooks Brings On-The-Go Cloud Accounting To iPad
The FreshBooks invoicing service has been the go-to service for many "one man show" businesses out there who need a quick, but professional way to get paid. in 2012, FreshBooks has expanded to a full-service cloud accounting service, and has also expanded account access via the iOS platform with the release of an iPhone app back in August.
FreshBooks hasn't taken their foot off the gas and released an iPad version of the app today. Similar to the iPhone app, FreshBooks for iPad focuses on small business owners who want quick access and management of expenses, invoicing, and payment management no matter where they are or what device they are using.
The homepage of the iPad app gives FreshBooks users a quick 3-month snapshot of outstanding invoices and company expenses. There is section where you can view additional reports, but that link takes you to the web version of FreshBooks - Would've been nice if the reports were accessible in the app, especially since the app offers offline access where you can work in Freshbooks without internet access and your changes autmatically sync when you gain access.
Additional tabs located at the bottom of the app lets users complete a variety of tasks:
- Create and manage invoices, estimates, expenses, and projects
- Attach images of expense receipts to invoices
- Up-to-date status of invoices (sent, paid, viewed, etc.)
- Work on other tasks in Freshbooks while running the timer and view timesheets according to calendar or specific project
I'm a FreshBooks user and it's nice to know that now I have a choice of devices to manage my "one man show."
For more from Terrance Gaines, follow him on Twitter @BrothaTech

subset: commoncrawl


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ReleasesBack to
Jimmy Smith
This CD reissue of a formerly rare date has a perfectly suitable title for it is the first of four albums that organist Jimmy Smith made within an eight-day period for Blue Note before permanently leaving the label for Verve. Although notable for matching Smith with guitarist Grant Green in what would be their only joint recording (drummer Donald Bailey completes the trio), the music is fairly typical of a Jimmy Smith session with the repertoire including blues, a couple of standards and ballads. The solos are well-played but nothing too surprising occurs (except perhaps for the sappiness of "What Kind of Fool Am I"); the original LP program is expanded by the inclusion of two other selections from the same date. ~ Scott Yanow


text: On Mon, 22 Nov 2004, Roger L. Smith wrote: > > During a conversation at the LECCIBG at SC'04 this year, I openly wondered > where and what the oldest still-functioning cluster system is. > > So, who has the oldest cluster on this list? For my curiousity, I'm not > limiting the submissions to Intel or Linux, so it doesn't have to be a > traditional "Beowulf" system, but it should be a system designed and used > exclusively as a cluster, and it should still be in service of some sort > today. You need a few more rules. Do we count a cluster as being in continuous service even if its hardware has rolled over several times in its existence? If yes, brahma has been running continuously since the fall of '96, although the last of its original systems (200 MHz PPros) have been dead for a year or three now. I have a mini-cluster at home with 400 MHz components -- maybe six years old -- although truthfully only one system is still powered up as part of my current home cluster as I got tired of paying for the power and they were making funny noises and what CAN you do with only 96 MB of memory these days? Otherwise, we tend not to run hardware much past four years or our systems persons get Angry -- that TCO thing as maintenance efforts and the cost of power rise. Besides, one can show pretty easily that one can get more work done with a single system that costs only what the differential POWER to run a cluster of 8 five year old systems costs -- Moore's Law is brutal. So production clusters older than five (really three, but certainly five) are a net loss and make negative sense. Even my home cluster gets painful to pay for out there and it only exists for prototyping and column writing and play. Upgrading the OS eventually is just impossible. rgb Robert G. Brown http://www.phy.duke.edu/~rgb/ Duke University Dept. of Physics, Box 90305 Durham, N.C. 27708-0305 Phone: 1-919-660-2567 Fax: 919-660-2525 email:rgb at phy.duke.edu


text:
March 9, 2010 — An analysis of six tests that are used to measure platelet function and help gauge the effectiveness of antiplatelet drugs for patients undergoing a cardiac procedure such as a coronary stent implantation found that only three of the tests were associated with a modest ability to predict outcomes such as heart attack or death, according to a study in the Feb. 24 issue of the Journal of the American medical Association (JAMA).
Dual antiplatelet therapy with aspirin and clopidogrel (anti-platelet agent used to inhibit blood clots) reduces atherothrombotic (vascular obstruction) complications in patients undergoing percutaneous coronary intervention (PCI; procedures such as balloon angioplasty or stent placement used to open narrowed coronary arteries) with stenting. However, the individual response to dual antiplatelet therapy is not uniform, according to background information in the article. There currently is no consensus regarding the most appropriate method to quantify the magnitude of effect an antiplatelet agent may have on platelet reactivity.
Nicoline J. Breet, M.D., of St. Antonius Hospital and St. Antonius Center for Platelet Function Research, Nieuwegein, the Netherlands, and colleagues conducted a study to evaluate the ability of multiple platelet function tests to predict atherothrombotic events, including stent thrombosis (blood clot within the stent), in 1,069 clopidogrel-pretreated patients undergoing elective coronary stent implantation. Using blood samples, platelet reactivity was measured in parallel with six platelet function tests. The primary outcome measured was a composite of all-cause death, nonfatal heart attack, stent thrombosis and ischemic stroke.
The researchers found that at one-year follow-up, the primary outcome occurred more frequently in patients with high platelet reactivity when assessed by the tests light transmittance aggregometry, VerifyNow and Plateletworks, which also had modest ability to discriminate between patients having and not having a primary event. The three other testing methods (IMPACT-R, Dade PFA collagen/ADP, and Innovance PFA P2Y) were unable to discriminate between patients with and without the primary outcome. None of the tests identified patients at risk for bleeding.
"In conclusion, of the platelet function tests assessed, only light transmittance aggregometry, VerifyNow, and Plateletworks were significantly associated with the primary end point. However, the predictability of these three tests was only modest. None of the tests provided accurate prognostic information to identify patients at higher risk of bleeding. Thus, [this study] does not support the use of platelet function testing to guide clinical practice in a low-risk population of patients undergoing elective PCI," the authors wrote.
For more information: http://pubs.ama-assn.org/media/controlled/jama


text:
> I am curious as to what everyone thinks a font creator should do if they have a family with three or more weights that are heavier than "bold" (which maps to 700). When designers have called those weights extrabold, black, ultra, super, etc. with no naming rule, I think it's not unfair to expect a system to be able to handle inputs above 1000 without breaking. –Bram On Wed, Feb 9, 2011 at 8:41 PM, Thomas Phinney <email@example.com> wrote: > I'll just note that if one wants a system to deal with real-world fonts, it should deal with inputs for usWeightClass that are any integer from 0-1000. > > I am curious as to what everyone thinks a font creator should do if they have a family with three or more weights that are heavier than "bold" (which maps to 700). > > In our collection of about two thousand web fonts, as I recall there are four such cases. > > This is aside from the many other cases where values aren't in hundreds, etc. > > I remain puzzled that CSS 3 will remain deliberately incompatible with real fonts in this area. > > T > > On Feb 9, 2011, at 6:20, Chris Lilley <email@example.com> wrote: > >> Hello www-font, >> >> Open Font Format (OFF [1]) states that OS2.usWeightClass is a 2-byte unsigned short and describes it as >> >> "Indicates the visual weight (degree of blackness or thickness of strokes) of the characters in the >> font." >> >> There is an accompanying table which relates particular values 9100, 200 etc) to textual descriptions (e.g. 'Thin') and C definitions from windows.h (e.g. FW_THIN). >> >> Values which are not multiples of 100 are not specifically allowed and not specifically disallowed; they just don't have a defined mapping to those two string sources. >> >> I have seen fonts with weights like 250 etc so I conclude that in OFF, OS2.usWeightClass is a continuous range of cardinal numbers. >> >> CSS3 Fonts states that the font-weight property [2], used to request styling, is an ordered sequence of tokens: >> >> "100 to 900 >> These values form an ordered sequence, where each number indicates a weight that is at least as dark as its predecessor." >> >> and >> >> "Font formats that use a scale other than a nine step scale should map their scale onto the CSS scale" >> >> and that the font-weight descriptor [3], used to tell CSS about the weight of a particular font, is also a discrete series of tokens: >> >> "Value: normal | bold | 100 | 200 | 300 | 400 | 500 | 600 | 700 | 800 | 900" >> >> so I conclude that values like 250 are explicitly disallowed. >> >> The point of this email is to ask: >> >> a) are the above assumptions correct? >> b) if a value which is not a multiple of 100 is used in the CSS style system, (e.g by script, or by direct specification in a style sheet, or by animation) then it gets mapped to the nearest multiple of 100? >> c) thus, animation of the font-weight property should be discrete, not continuous, despite the fact that fonts with wights that are not a multiple of 100 may be available, as the CSS style shystem does not expose their native weights? >> >> Tracker, this relates to SVG-ACTION-2936 >> >> >> [1] ISO 14496-11:2009(E) >> PDF downloadable at no charge by agreeing to >> http://standards.iso.org/ittf/licence.html >> >> [2] http://dev.w3.org/csswg/css3-fonts/#font-weight-prop >> >> [3] http://dev.w3.org/csswg/css3-fonts/#font-prop-desc >> >> >> -- >> Chris Lilley Technical Director, Interaction Domain >> W3C Graphics Activity Lead, Fonts Activity Lead >> Co-Chair, W3C Hypertext CG >> Member, CSS, WebFonts, SVG Working Groups >> >> > >Received on Wednesday, 9 February 2011 16:25:41 UTC
This archive was generated by hypermail 2.3.1 : Wednesday, 8 March 2017 09:47:24 UTC


text:
Event box
First Institute
The Medical Office Assistance program is designed to prepare you for a career in the healthcare field. You will be trained in 6 courses to prepare for the certification test, qualify for a paid internship, and assistance with employment within your community! Please contact to register at firstname.lastname@example.com and 708-663-0792.
- Date:
- Friday, February 23, 2018
- Time:
- 10:00am - 4:30pm
- Location:
- Adult Literacy Computer Room dedicated in honor of Carlos & Marjorie Hidalgo
- Categories:
- Outside Organization


text:
Model-turned-fashion designer Kimora Lee Simmons has split from her actor boyfriend Djimon Hounsou.
A representative for Hounsou, who has been dating Lee Simmons since 2007, announced the sad news on Wednesday after weeks of speculation suggesting the couple's romance was in trouble.
The rep tells People.com, "Djimon Hounsou and Kimora Lee Simmons have officially separated after five and a half years."
Lee Simmons and the Blood Diamond star never officially wed, but they staged a traditional commitment ceremony in Hounsou's native Benin in 2008.
They are parents to a 3-year-old son, Kenzo. Lee Simmons is also mum to two daughters from her marriage to music mogul Russell Simmons.


text:
'Incredible focal range'
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'16x zoom lens (24 - 384mm).'
'built-in GPS'
'Despite its budget price-tag, the Panasonic Lumix DMC-S3 is a good-looking camera, with a distinctive pebble shape, rounded corners and an attractively glossy finish to the all-plastic body. '
'Despite a minimum focusing distance of 5cm the camera is capable of taking excellent macro pictures.'
'Our exterior daylight tests produced some remarkably strong shots for such a low-cost camera. '
'latest generation Venus Engine VI image processor'
'Video images appear blocky and without sharpness, and the audio is only just passable from the internal microphone.'
'LCD screen struggles in bright conditionsCan't handle highlights properlyNo ISO limiting.'
'small pocket digital camera'
Deliver usable results without having to pore over a manual on the train or plane
'somewhat expensive'
'well-made overall'
Affordable long zoom in an compact package
Good image quality
ReviewGist helps you find the best products to buy by making sense of online reviews.
We are currently aggregating 376,500 reviews
covering over 29,477 products.
© 2019 ReviewGist.com. All Rights Reserved.


text:
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Here's an elegant Ascot ad from 1952. It looks all the world like something you might expect to find Al Parker's signature attached to... but in fact its the work of Dorothy Monet.
Monet worked at the Rahl Art Studio in New York and was apparently quite a woman as well as being an exceptional illustrator. Here's what Anita Virgil, who worked at Rahl during the '50s, once wrote to me about Dorothy Monet:
"I always thought of her as the heroine of a loooooooong and lusty French novel. She was quite gorgeous, like Vivian Leigh with more nose to her. And petite. Intelligent. Literate. Adventuresome. And quite the actress, innately. Donned all kinds of elegant clothing to fit "the role of the moment" . . . and likely did a few Goyaesque Maja Desnuda numbers on her fainting couch -- and anywhere else."
Monet's illustrations for this Ascot campaign garnered some positive mention in a trade magazine of the day. For any illustrator that kind of thing has to be good for your ego (not to mention your profile in the business), but I think especially so because Monet, being a female illustrator in a highly competitive, male dominated industry, was showing the 'old boys club' that they better watch out - anything they could do she could better.
And Dorothy Monet really could do it all. I've been setting aside examples of her work whenever I can find them in anticipation of writing a week-long series on her some time. Here are a couple of funny Old Gold ads Monet did in the mid-'40s.
Notice her style here is quite different. Its more typical of a 'straight' advertising style from that period... but she manages to convey just a slight touch of humour without getting all 'big foot' and 'cartoony'. Not an easy balance to achieve. Based on what I interpret of Old Gold's strategy for these ads I'd say they were trying to appeal to both male and female customers. Monet's approach seems to really hit the mark; broad enough to appeal to guys while still gentle enough to not alienate the ladies.
Here's another ad piece by Dorothy Monet, from a 1954 campaign she did for Ballantine Beer. Its a great example of Monet's straightforward literal realism style - so drastically different from the Ascot ads - but so perfectly professional for the subject matter and client expectations.
And here's the food for thought: according to the AD&SN article above, Dorothy Monet's Ascot ads were appearing all year (1952) in Life magazine. I only have the one, unfortunately, but look at this story art Monet created for the May '52 issue of Woman's Home Companion. Was it the Ascot ads that put her in the frame of mind to design the WHC piece as she did, with a strong emphasis on flat, graphic shapes and a focus on hands and faces? Remember, this was not the way she typically worked (the Ballantine ad is closer to her most familiar style).
And if the Ascot ads lead to the WHC illustration, why was Monet chosen for the Ascot ads? Could it have been this piece Monet did two years earlier, in 1950...?
We will likely never know. But we'll definitely revisit the "gorgeous, literate, adventuresome" - and talented - Dorothy Monet. Some time soon.
* My Dorothy Monet Flickr set.
Celebrating illustration, design, cartoon and comic art of the mid-20th century.
Tuesday, January 26, 2010
Dorothy Monet's Elegant Ascot ads
5 comments:
- Chad Sterling3:32 AM
Anita's recollection of DM is a gloriously nuanced piece of character description...I'm left feeling that what is not being said is as important as what is.ReplyDelete
Still, a talented and versatile artist.
Chad; That's an astute observation. I wish Anita would allow me to say more. ;^)ReplyDelete
- Anonymous11:01 AM
Monet is great, but when tackling the Al Parker look she lacks his sensitivity.ReplyDelete
Waited for years to find out who did the Ascot ads, I've got a great copy in a September 1952 LIFE Magazine. The same mag features Suzy Parker in red sequins. I'll be seeking more Monet illustrations now!ReplyDelete
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The Dodge Circuit EV may not get a full reveal until later, but our quick-shuttered photographers already nabbed photos of the new EV. You can find it unwrapped below.
As we mentioned last night, the Circuit EV is basically a Lotus Europa with some body work and the mysterious Chrysler EV pack. The similarity, especially given the small size, is undeniable up close. We'll get into the "engine bay" if it isn't glued shut.


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The annual Goldsmiths Jewellery Fair showcases bespoke, one-off jewelry handmade by artisan crafts people.
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The Fair runs from Monday Sept. 23rd until Oct. 6th at Goldsmith's Hall in London.


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UNEP, acting as the interim Secretariat of the Intergovernmental Platform on Biodiversity and Ecosystem Services (IPBES), has published all comments received from governments and other stakeholders on the draft elements of the IPBES work programme, the rules of procedure of the plenary and related IPBES procedures. The comments also include contributions from the IUCN network.
IUCN noted that interested parties are increasingly supporting a rapid establishment of IPBES and are eager to endorse it with a robust and effective work programme. Several concrete proposals were made to prioritize activities to be implemented in the first years.
IUCN also recognized the consensus to address the role of observers in the Plenary properly and timely. Additional thinking and lobbying is still necessary to safeguard a constructive place for civil society organizations in IPBES.
The full text of all comments received from governments and other stakeholders, including IUCN, can be accessed on the official IPBES website.
For the summary of all comments received, please see an article on the IISD Biodiversity Policy & Practice knowledgebase.
The comments will be incorporated into preparations for the Second Plenary Session to build IPBES scheduled to take place from 16 - 21 April 2012, in Panama.


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David Mertz
CTO, Open Voting ConsortiumDr. Mertz is a board member and CTO of the Open Voting Consortium and serves on IEEE Standards Committee P1622 on data formats for voting systems. After receiving his doctorate in political philosophy, David became a well-known author in the seemingly little related areas of computer science and programming, and in information security. He feels that procedural democracy requires that the technical instruments of governance be open for public inspection, every bit as much as it requires the legal acts of government remain so open.
- Session: Open Source Voting


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The way the law works now, the Department of Children and Families has no incentive to adopt effective policies because there's no downside to using cheaper ineffective policies that, for example, allow them to select child molesters as foster parents.
The controversy at the Massachusetts Department of Children and Families remains in the headlines despite the best efforts of Gov. Deval Patrick and other public officials to put the story to rest with awkwardly calm comments about outside reviews, blah, blah, blah.Some are calling on Patrick to fire DCF Commissioner Olga Roche, but symbolic head-rolls won't change a thing because another widget bureaucrat will take Roche's place and the sludge-flow will continue.
The problems at DCF emanate from a baseline design flaw in law that allows children in state custody (including foster care) to be abused with impunity. Here's why:
Under state law, even a child who gets raped by a foster parent with a criminal record for child molestation has no hope of winning a lawsuit unless DCF "originally causes" the abuse. In other words, someone who works at DCF would have to be a molester or a pimp.
The Legislature has for decades refused to adjust the "original causation" standard so that DCF could more easily be sued. It isn't that lawmakers hate children, it's that they're controlled by lobbyists and they love money more.
Social workers say lawsuits aren't the answer and that they're under enough pressure. But changing the law won't burden decent social workers, it will force insurance companies and policy-makers to spend a few bucks putting in place the best possible policies to protect children from harm.
The way the law works now, DCF has no incentive to adopt effective policies because there's no downside to using cheaper ineffective policies that, for example, allow them to select child molesters as foster parents.
Some advocates have turned to federal court for help because children can assert a due process right to "reasonable care and safety" when in state custody. Though there's no "original causation" rule there, the federal courts have embraced an immunity of sorts by ruling that there can be no liability unless DCF's actions "shock the conscience."
"Shock the conscience" is as ineffective as "original causation" because it requires proof that DCF officials were "deliberately" indifferent to a child's needs and that such indifference was "egregious" and "outrageous."
The meaning of "shock the conscience" was discussed in a recent federal lawsuit against DCF where the judge described the standard as an "extremely high" burden and a "virtually unscalable peak" that requires "stunning evidence." The lawsuit was rejected because even though DCF violated state law by failing to perform background checks and allowing convicted molesters to live with children in their care, it wasn't "conscious-shocking" enough to find DCF liable for the children's suffering.
The worst thing about these inadequate laws is that they reward DCF officials for turning a blind eye to abuse because the more DCF knows, the greater the chance a judge will find "original causation" and "conscience-shocking" behavior if a child dies or disappears.
Wendy Murphy is adjunct professor of law at New England Law|Boston and a well-known television legal analyst. A former prosecutor, Murphy specializes in the representation of crime victims in civil and criminal litigation. Her first book "And Justice For Some" was published in 2007 and was released in paperback in 2013. Read more of her columns at wendymurphylaw.com.By rewarding official blindness, the law perpetrates the very harm it purports to abhor. Scandal avoidance when kids suffer harm in institutional settings is already the politically preferred path of least resistance.
To better protect kids, the law should be changed so that DCF can be sued under a negligence standard. "Negligence" would mean DCF would be held liable not only for what they "originally cause" or "deliberately" do wrong, but also for what they "could have prevented" and "should have known about." Under a more protective negligence standard, DCF officials can't simply look the other way without increasing their liability exposure.
Good social workers have gut instincts about what's going on behind closed doors. It's time for state lawmakers and federal courts to add rocket fuel to those guts by opening the door wider to the possibility of lawsuits. It won't fix everything but the mere threat of more litigation will improve the quality of children's lives overnight – not because people who don't care about kids will suddenly give a damn, but because the risk of harm to children will, for the first time, affect the bottom lines of people who do care about money.
Wendy Murphy is adjunct professor of law at New England Law|Boston and a well-known television legal analyst. A former prosecutor, Murphy specializes in the representation of crime victims in civil and criminal litigation.
Here's one opinion. What's yours? Click here to write a letter to the editor or leave a comment on the story. Read more columns, editorials and letters


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text: > The new Dell R5400 Rackmount workstation is ideal for this. You can > slip two Xeons, 16GB ram and two chunky graphics cards in there. The slots in R5400 are PCIe gen1 and 300W total for the graphics might be a bit too low. The best I've seen so far are 1U HP DL160G5 servers which offer two PCIe 16x Gen2 slots. Granted, you will not be able to fit in a powerful graphics card in there but a Tesla setup works quite well. There is a very interesting recent report published by HP http://www.hp.com/techservers/hpccn/hpccollaboration/ADCatalyst/download s/accelerating-HPCUsing-GPUs.pdf They benchmarked DL160G5 (with single processor => pretty low cost of the host server) with S870 attached to it. Observed peak performance on SGEMM was about 200 GFLOPS which is much lower than the theoretical peak 512 GFLOPS (even much less than 350 sustained claimed by Nvidia). When they factor in i/o, the performance rapidly approaches that of Intel quad-core. That's not to say GPUs are useless even at single precision; some results are pretty good. The team promised to benchmark FireStream next. > Generally a XEON or Opteron chipset and CPUs will be the choice. > > Also, for most GPU/FPU performance work, the memory bandwidth bottleneck > on the Intel product is too much of a negative factor. Yes, memory bandwidth can be a problem for Intel servers. Now. But we all know this is going to change soon. More surprisingly Opteron based servers do not offer PCIe Gen2 just yet. Perhaps it was long time ago when I checked it last time. The paper cited above indicates very significant impact of PCIe Gen2 on the bandwidth.


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Invisible et Insaisissable // Invisible and ElusiveActivity by Niki Baccile | added on Sep 20, 2011 | France
Sponsor(s): CNRS, Nanosciences Ile-de-France, Centre des Arts
The exhibition "Invisible and Elusive" takes place within the framework of the International Year of Chemistry and is the accomplishment of the OpenLab Project, to which four CNRS (French National Research Council) research laboratories participated. The OpenLab Project consists of a 6-month collaboration between six major in
The OpenLab Project identifies itself in the very general context of nanosciences in society discussion. It focuses, in particular on the contribution, often disregarded by non-specialists, of chemistry to nanoscience. The OpenLab Project aims to involve contemporary art in its widest forms: aid to expression, knowledge transfer and catalyst towards debate. The free access to scientific laboratories, hence the name OpenLab, is a major point and it means a will to communicate and a desire for transparency. This approach will allows a more effective communicate on such a complex and controversial topic. From the perspective of artistic creation, this project offers a significant number of new opportunities for artists in the field of chemistry and in their relationship to nanoscience.
Being organized in the framework of the International Year of Chemistry 2011, OpenLab is an innovative project at the intersection between contemporary art and nanoscience. OpenLab allowed six contemporary artists to access four research laboratories of the CNRS (French National Scientific Research Council), specialized in chemistry and nanoscience. The project is based on the reciprocal exchange of experience and knowledge between scientists and artists.
Developed in 2010 after a unique collaboration between a researcher in chemistry and an art critic, the OpenLab Project, in collaboration with the CNRS, Nanosciences Ile-de-France, Université Pierre et Marie Curie, Collège de France anf the Centre des Arts in Enghien-les-Bains, produced six new artworks / experiences that will be on display from September 23, 2011 until December 16, 2011 at the Centre des Arts d'Enghien-les-Bains.
The opening will take place September 22, 2011 at 19h, Centre des Arts, Enghien-les-Bains.
|nanosciences, art, contemporary art, nanotechnology, chemistry, creation, artistic, centre des arts, cnrs, nanosciences ile-de-france, science society, society, exhibition, paris
see write-up (in french) and video of the expo opening at http://www.cda95.fr/content/invisible-et-insaisissable
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Can you be the first to complete a row of three?
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Using the 8 dominoes make a square where each of the columns and rows adds up to 8


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NEW YORK — The stock market had its best day of the year as technology companies surged.
The Dow Jones industrial average rose 115 points, or 0.7 percent, to close at 16,373 Tuesday. It was only the third gain of the year for the Dow.
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Bond prices fell. The yield on the 10-year Treasury note rose to 2.87 percent.


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When looking for a fun weekend outing, nothing comes close to the unique experience many had at the Orvis Game Fair and Country Sporting Weekend at Sandonona Shooting Grounds in Millbrook, New York. Sandonona Shooting Grounds are a place of extreme natural beauty, especially in the fall with the gorgeous scenery of the Historic Hudson Valley. Not only is it a stunning location, but also it brings traditions of field and hunt to experts and newbies alike.
Around this picturesque site you find artists, craftsmen, exhibitors, vendors, events all dedicated to the country-sporting lifestyle. Everyone had a great time with the fly-fishing and shooting lessons, dog-training seminars, birds of prey exhibitions, learning how to cook wild game, and an adventurous Land Rover driving course. Most of these activities were open to all ages and all experience levels. It was a chance to experiment and try to find a new lifetime hobby, refine your skills, or try out some of the best equipment available.
When looking at the weekend as a whole, it is almost as if you are stepping back in time creating a link from the past passions to the current ones and passing traditions on to future generations.


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Express. Home of the Daily and Sunday Express.
We trust in Almunia - Fabregas
Arsenal captain Cesc Fabregas maintains goalkeeper Manuel Almunia has the complete trust of the team as they look to mount a double challenge for domestic and European honours.
The Gunners have kicked off the Barclays Premier League season with three wins from four games to sit two points behind Chelsea. Almunia's position as first choice was the subject of much speculation over the summer, as Arsenal had bids for Fulham's Australia international Mark Schwarzer turned down.
Fabregas said: "Manuel commanded the defence very well at Blackburn - but it is not just about one game or two or three. He is a well-loved player among everybody here and performs well for this club. We all wish him a super season and have a lot of trust."
Wenger saw Abou Diaby (leg) added to the injury list on Saturday following what looked a bad tackle from Bolton defender Paul Robinson, which went unpunished, and resulted in the midfielder, who had only just come on, having to be substituted.
Winger Samir Nasri - fit again following knee surgery - will return into contention to face Braga in the Gunners' Champions League opener after being an unused substitute.
Wenger chose to rest both full-backs Gael Clichy and Bacary Sagna for the Premier League game. England international Kieran Gibbs, who turns 21 later this month, believes the competition for places can only be positive.
"It is difficult to play the same team through all of the season because players are going to get tired - that is when we start to get injuries," Gibbs told Arsenal TV Online.
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"Not only is the competition going to be good for Gael to play well, it is also going to be good for the club as well because we are both fighting to win help the team win something this year."