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Dickerson and Nop

I Cannot Imagine My Life without Music

A college professor of computer science lives another life in music, writing songs, recording albums, exploring mystery and passion

We sat in the engineer’s booth watching through the sound-dampening glass. Over the previous few days of long studio hours we had laid down most of the basic tracks: vocals layered over rhythm guitar or piano chords, with maybe some bass and percussion. Now it was time for our guest studio musicians to add their talents to the project.

The Accordion Player Moment

Our accordion player sat on the other side of the glass, one of his gorgeous handmade Italian accordions in his arms. We could see his expression as he listened to our song through the headphones, entering into the mood and hearing in his head what he might play to serve that song. His hands moved with the melody as though he were conducting an orchestra only he saw. When, after several minutes of listening, he began to pump his instrument and caress the keys—and I heard on my side of the glass the sound of his beautiful playing accompanying the song I had co-written—my eyes filled up with tears. I was overwhelmed.

I knew the pedigree of this musician—the reputation he had as one of the best, not only in Nashville, but in the country, and the long list of famous recording artists he had worked with. A few days earlier I had gone to a well-known music venue and watched him perform in a band whose members were household names and must have had at least fifty major music awards among them. What I didn’t know was what a gracious, humble, and generous human being he was. Indeed, knowing he had worked with many musicians and songwriters dramatically more talented (and famous) than I, I feared he would be disdainful of our music.

Yet he poured his heart into those songs. He didn’t come to the studio to build up his own reputation and fame; in humility he was there to serve the music itself. He talked with us about our vision and what we hoped for, and then he just listened to the music. When he finally began to play, I knew he understood the song. He captured it. He didn’t merely add bits of ornamentation to the edges; he entered the very core of that music and carried it and transformed it into something more full and beautiful than I could have imagined… and yet it still remained my song.

[Editor’s Note: Have a listen to Dickerson and Nop’s “Presence,” featuring Phil Keaggy on guitar and Jeff Taylor on accordion.]

My Life in Music & Otherwise

I cannot imagine life without music.

I am not a professional musician. I make a few dollars here and there performing concerts, and I’ve written a handful of songs that have garnered radio airplay in blues, Americana, and gospel genres. But I don’t put food on my table or pay the rent by writing or performing music, singing, or playing an instrument.

Yet, I cannot imagine life without listening to music, playing music, and writing music.

I am a novelist and an essayist. I teach at a college and write as a profession. I’ve published a dozen or so books, and several dozen magazine and newspaper articles and book chapters. And I do a lot of speaking. To the extent that I am known for anything, these are what I am best known for.

Nonetheless I consider music a vital extension of my creative life. I love the written and spoken word, and yet there is something present in music and songs—whether I am listening, writing, or performing them—that a text by itself is missing. What that something is, I am still trying to put my finger on. Writing this reflection is an effort in that direction.

The Mystery of a Song

I have many poet friends with whom I have had conversations about the difference between song lyrics and poetry. Of course there are similarities: common elements of craft necessary to both forms. Creative art of all forms is rooted in concrete details. It depends on particulars, not generalities. Both the song lyricist and the poet need to work with potent images, or narratives, and not with abstractions or principles. Images reach into our imaginations and grab us; they are able to speak to different people at different times in different ways. Both poems and songs work that way.

But there are also differences between the two. A great song does not necessarily make a great poem, and vice versa. Many of the favorite songs I have written, although I might describe the lyrics as “poetic,” would not work well as poems. Indeed, of the hundreds of songs I have written in my life, I consider only a few to be good poetry apart from the music.

Ironically, the song lyric I think is my best poem is one that began as an instrumental piece without words at all. After I finished writing the instrumental guitar piece, I found it evoked for me a particular mood and image of both the beauty and fragility of life—of something soft and delicate and maybe a little sad yet also joyful. I titled the song accordingly: “Mayfly.”

Almost as soon as I gave the song a title, the lyrics began to arise unbidden in my thoughts. “Rise up and fly on white wings / hear the silent call of the evening sky.” Essentially I wrote an ekphrastic poem—a verbal description of another piece of art, in this case music. That has happened only once. It happened because the mood of the music evoked the imagery so powerfully. And though I almost settled with the song as an instrumental piece, I like it so much better now that it has lyrics.

But back to the difference between writing and song writing—between poems and lyrics.

It goes beyond just the distinction between meter and rhythm (though that is part of it.). In one way, the task of a poet is more difficult than that of a songwriter. I say that as one who holds illusions of being a passably good songwriter, but no illusion of being a poet.

When I write song lyrics, I can trust that some of the emotion or mood will be conveyed by the music—the chord structure, rhythm, and dynamics, the way the melody works, and even the way it is arranged instrumentally. A poet cannot rely on that, and must convey everything through words alone. A poet must accomplish more with a single resource.

Yet in another way, writing a song is a more difficult task. When the poet has written her words, the poem is done. When the songwriter finishes the lyrics, her task has barely begun. She must then struggle to find music that captures those words: melody and harmony and rhythm and instrumentation. Though it is possible to separate them and think of them in isolation—you can look at the lyrics without the music, or listen to the music independent of the words—for the song to work well the lyrics and the music must form a cohesive whole. I have pages and pages of lyrics I have written (and really like) that are languishing; they have never become songs because I have not been able to create music that captures the feeling I sought to evoke with the word-images, or the mood I want to capture in the narrative.

In contrast, for many of the best songwriters I know the lyrics and music come together; they grow simultaneously from the hard work and creative imagination of the songwriter. Or, as happened for me with “Mayfly,” the music comes first and evokes the words.

And then, finally, when I have finished writing a song—when I have a melody and chords to go with my lyrics—still the task is not complete. I then bring that song to my quartet and we work in collaboration to make something out of it, each member pouring into the song his or her own creative ideas.

Or I bring it to the studio, and my producer listens to the song, and we talk about my vision for it, and he imagines how he might arrange it and what other instrumentation might realize the song’s potential. Our two approaches work in collaboration.

[Dickerson and Nop’s “River of Mercy” features Garth Justice on percussion, Peter Wahlers on bass, as well as Keaggy on guitar and Taylor on accordion]

Recording Our Latest with Guitar Virtuosos

The experience I had with the accordion player happened again—in fact, several times—during the recording of our recent album. The drummer on the project did more than just play the beat and reflect the dynamics; he went through his room-sized collection of snares looking for one whose texture would fit the song perfectly. And then he did the same thing with mallets.

Two of my favorite guitarists also contributed to the project, one whose work I have admired since the early 1970s and have seen in concert at least ten times during that period, and another who played in two of my favorite bands of the 1990s and 2000s. They brought to the project more musical talent in their little fingers than I have in my body.

Indeed, they brought more than just talent. They brought passion and a certain type of humility. At one point, one of them was listening to a song, and his own eyes welled for a moment as he made a personal connection between his story and ours. And then when he recorded his part on that song, he brought to it far more than mere technical proficiency or genius (which were certainly considerable in and of themselves); he invested himself. His guitar part carries exactly what we were trying to communicate, even without the words.

I rarely like to listen to my own songs after I record them. But I now listen to several songs on that album repeatedly, not because I am listening to my own songwriting—though I suppose I am—but because I am listening to something more.

The Passion of a Song

Which brings me back to where I started and why music does something for me that no other form of art does. A song has so many components—lyrics, melody, chords, rhythm, instrumentation and arrangement—but though we can study each in isolation, the song is much more than simply the sum of its parts. A good song works powerfully as a whole. It has all that a great poem has. And all that a piece of music has. Combined.

Attempts to express this in words—a good song transports me?—sound cliché. But they are true. The one word that comes to mind that conveys this most clearly is passion. I think a great song—meaning not just a great bit of songwriting, but a great recording and performance of that song, is powerful—because it is full of passion; one conveyed by the entire person. The fullness of song is better able to carry the fullness of that person than any one component alone.

The late Mark Heard (1951-1992) is perhaps the best example of this I know. He is the songwriter I most aspire to be like—the one whose music has most consistently moved me, informed me, challenged me, enlightened me. There is a quality to his songs, and the way he recorded and performed them that was hard to categorize.

His music was never a great commercial success. (“He says ‘Damn the cool-headed and the setters of goals / Who feel no evil, no heat, no cold / Who wouldn’t know passion if it swallowed them whole’” – Mark Heard, “Big Wheels Roll”) But twenty-five years after his death I keep meeting people whose lives were impacted by his music. And those with the best vocabulary for describing it often come back to that word “passion.” The fullness of a song—that combination of lyrics, music, and performance—seems best able to convey it.

If my songwriting ever comes within a stone’s throw of Mark Heard’s, I’ll be content. But whether I ever reach that goal, I will continue to write and play songs, and make music a part of my life, as long as I am able.

Written By
Matthew Dickerson, Professor of Computer Science at Middlebury College, writes, performs, and records roots Gospel with the duet Dickerson and Nop (www.dickersonandnop.net). Dickerson...
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Lincoln Street Enhancements

Project Description

Lincoln Street, in downtown Wamego, is a popular shopping place for residents living between Manhattan and Topeka. Schwab Eaton developed a streetscape master plan encompassing three city blocks of the city’s central business district. Schwab Eaton worked closely with City officials, the Chamber of Commerce, and local businesspeople to secure funding through the popular TEA-21 Program administered by the Kansas Department of Transportation. Hardscape improvements included sidewalk replacements, construction of bulb-outs at the intersections, and raised landscape planters. Pavers were incorporated which included a motif of the historic Dutch windmill located in the nearby City Park. Improvements were also made to the storm drainage, public water, and street lighting systems. Signage, bollards, urns, irrigated planting areas, and street furniture added the finishing touches. The community is very proud of the streetscape enhancements, and some of the design elements have been extended to other parts of town. This project has received commendation from DOT representatives who visited from other states. Lincoln Street has become a benchmark for other small communities who aspire to improve or revitalize their business districts.

Schwab Eaton is a full-service professional engineering and design firm. We offer civil engineering, surveying, landscape architecture, and construction support services.


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Monday, January 26, 2009

Drugs from genetically engineered animals poised to debut in US

Genetically engineered animals and the FDA Are genetically engineered fish and meat coming soon? We examine the Food and Drug Administration's regulations.

By Jill U. Adams January 26, 2009

Fast-growing salmon. Pork containing heart-healthy omega-3 fatty acids. These are two examples of products you might see in your local supermarket soon -- animals developed not through conventional breeding but through genetic engineering.

On Jan. 15, the U.S. Food and Drug Administration decided how it will regulate genetically engineered animals, for the first time paving the way for such animals or their products to be sold as food and medicine. The agency has decided to categorize genetically engineered farm animals, also called transgenic animals, as an "animal drug." They will be held to the same requirements already existing for conventionally bred animals treated with hormones or antibiotics. (In the case of transgenic animals, the "drug" is a snippet of DNA.) Products derived from them or containing them as an ingredient will not necessarily require labeling.

A wide range of interested parties, including companies developing genetically engineered animals and consumer protection groups, are generally comfortable with the FDA decision. And yet, consumer acceptance of transgenic animals, particularly as food products, is still an unknown.

American consumers have been eating food from genetically engineered crops, such as corn, soybeans and canola, for a decade. However, transgenic animals have not been sold, pending the FDA deliberations on how to regulate them.

Why would someone want to genetically engineer animals?

Genetic engineering is a high-tech way to "breed" desirable traits into livestock. The benefits might be for the producer, such as a disease-resistant cow or an easy-to-raise salmon. It might be for the environment -- pigs that produce milder manure, for example -- or for the consumer, say, more nutritious meat.

The old-fashioned way of breeding farmed animals requires selecting offspring with desired traits over successive generations. Ron Stotish, chief executive of Aqua Bounty Technologies in Waltham, Mass., says the power of genetic engineering is that the same end is achieved in "one fell swoop." Transgenic animals also can be fitted with traits they probably would never develop naturally, as in the case of omega-3-producing pigs.

How is an animal genetically engineered?

An extra piece of genetic material (DNA) is inserted into the animal's genome at the earliest stages of development. Sometimes the method involves manipulating a fertilized egg that is then implanted into a surrogate mother; other times, it alters a cell from which an animal will be cloned. As the embryo grows, the DNA splice is replicated with the rest of the genetic material so that it ends up in every cell of the individual.

In fast-growing salmon developed by Aqua Bounty, the inserted gene is a salmon growth hormone, identical to the one the fish have naturally. The benefit comes from the precise placement of the added gene, which makes it active at times that the natural gene is not. "Normal salmon grow very, very slowly, and when it is cold they don't grow at all," Stotish says. "Our gene is active under a broader range of conditions and it allows the animals to grow." At 1 year old, a normal salmon might weigh 30 grams, but the transgenic fish weigh a kilogram, he says.

In pigs developed to contain omega-3 fatty acids, the added gene directs formation of an enzyme that converts naturally occurring omega-6 fatty acids to omega-3s. The gene is derived from tiny roundworms but is modified to make it more mammalian, says Randall Prather, co-director of the National Swine Resource and Research Center at the University of Missouri in Columbia, who developed these pigs.

Why did the FDA opt to regulate genetically engineered animals in this manner and what criteria are used to assess safety?

The FDA is responsible for food safety and already regulates genetically modified crops. By considering a DNA segment a drug, the agency will regulate transgenic animals in the same way it oversees dairy cows that receive growth hormone or beef cattle that get antibiotics, says FDA spokeswoman Siobhan DeLancey.

By using existing guidelines for so-called animal drugs, the FDA can put those products seeking approval into a process that is already up and running. "They have the staff and the process that allows them to look at this. They do it every day," says Stotish of Aqua Bounty, which has been seeking FDA approval for its fast-growing salmon for years.

Companies must show that their genetic manipulation is safe to the animal and that any food or animal-feed products derived from the animal are safe for the consumer and safe for the environment. Companies must also demonstrate that their claims about the gene-carried traits do occur.

Are there concerns beyond what the FDA can regulate?

Gregory Jaffe, who follows biotechnology for the consumer advocacy group Center for Science in the Public Interest, says the adopted guidelines are a good start "in the sense that the federal government has acknowledged that these animals are on the horizon and there needs to be oversight to ensure their safety."

But, he adds, genes are not the same as drugs. Drugs may have long-lasting effects on an individual, but they wouldn't get passed on to future generations. In the case of biotech animals, however, "you're altering the DNA of that animal, which gets carried on to its offspring." (Aqua Bounty says all the fish it markets will be sterile.)

Such lasting effects may have implications for preventing escape of the genes to natural populations, Jaffe says -- an issue that is beyond the FDA's expertise or authority.

Jaffe thinks the safety review should be more open and transparent. "Our regulatory processes for drugs" -- including animal drugs -- "are, on the whole, secret and done behind closed doors," he says. By law, the company controls what information is made public.

Other regulatory processes, such as those for pesticides at the Environmental Protection Agency, have been opened in past decades to invite public participation.

"Genetically engineered animals are highly controversial," Jaffe says. "I think that they [the FDA] need to have a transparent and participatory regulatory system -- where the public can review safety data and . . . expert scientists can provide comments to the agency."

Why did the FDA decide that food from genetically engineered animals doesn't have to be labeled?

The FDA labels food based on nutritional content, not manufacturing process, says the agency's DeLancey.

"So, if the food product is 'materially different' from a conventional product, then FDA can require that it be labeled. But the FDA doesn't require that a pork chop label specify whether it came from a pig produced through artificial insemination versus conventional breeding."

And similarly, now, if it came from genetically engineered animals. "We understand that consumers want transparency and labeling, but we are constrained by the regulations put in place by Congress," DeLancey says.

How will I know if the food I buy is from genetically engineered animals?

Pork from an omega-3 pig, should it gain approval, will be labeled because nutritional enhancement is a selling point -- and because the product is different from regular pork.

In other cases you may not know, although producers can voluntarily label their products. Researchers at the University of Guelph in Canada, who developed the so-called Enviropig with "greener" manure, say they intend to do so.

The U.S. Department of Agriculture has guidelines for labeling "natural meats," which would allow meat from non-transgenic animals to call attention to that fact.

Tuesday, July 29, 2008

Docket No. 2005N-0373 RIN number 0910-AF54 Use of Materials Derived From Cattle in Medical Products REOPENING COMMENT PERIOD Date: March 30, 2007 at 11:37 am PST

Docket No. 2005N-0373 and RIN number 0910-AF54

Greetings FDA et al, ONCE again I would kindly like to comment on the continuous failed attempts by the FDA to regulate the use of certain cattle material in, or in the manufacture including processing) of, drugs, biologics, and medical devices intended for use in humans and human cells, tissues, and cellular and tissue-based products (HCT/Ps) (collectively, medical products for humans), and in drugs intended for use in ruminant animals (drugs for ruminants) from the proven risk factors of Transmissible Spongiform Encephalopahy i.e. TSE's in all species. I have continued to warn the FDA et al about these risk factors via the surgical and medical arena (vaccines, nutritional supplements, bovine heart valves, and other animal donor tissue), and I have continued to point out the risk factor of the UKBSENVCJD only theory, and the ramifications there from, i.e. BASE (bovine amyloidotic spongiform encephalopathy), and my greatest fears, one I have warned you about time and time again, seems to be coming true ;

64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a mouse model it was possible to alleviate the pathological changes of prion disease by suppressing expression of the prion protein gene after infection.

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Tuesday, April 29, 2008

Interference at the EPA - Science and Politics at the U.S. Environmental Protection Agency

----- Original Message -----

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Sent: Monday, April 28, 2008 9:48 PM

Subject: Interference at the EPA Science and Politics at the U.S. Environmental Protection Agency

Reports and Research

Interference at the EPA

Science and Politics at the U.S. Environmental Protection Agency

The U.S. Environmental Protection Agency (EPA) has the simple yet profound charge "to protect human health and the environment." EPA scientists apply their expertise to protect the public from air and water pollution, clean up hazardous waste, and study emerging threats such as global warming. Because each year brings new and potentially toxic chemicals into our homes and workplaces, because air pollution still threatens our public health, and because environmental challenges are becoming more complex and global, a strong and capable EPA is more important than ever.

Yet challenges from industry lobbyists and some political leaders to the agency's decisions have too often led to the suppression and distortion of the scientific findings underlying those decisions—to the detriment of both science and the health of our nation. While every regulatory agency must balance scientific findings with other considerations, policy makers need access to the highest-quality scientific information to make fully informed decisions.

Concern over this problem led the Union of Concerned Scientists (UCS) to investigate political interference in science at the EPA. The investigation combines dozens of interviews with current and former EPA staff, analysis of government documents, more than 1,600 responses to a survey sent to current EPA scientists, and written comments from EPA scientists.

The results of these investigations show an agency under siege from political pressures. On numerous issues—ranging from mercury pollution to groundwater contamination to climate change—political appointees have edited scientific documents, manipulated scientific assessments, and generally sought to undermine the science behind dozens of EPA regulations. ...

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Interference at the EPA Science

Thu Dec 6, 2007 11:38

Monday, January 12, 2009

FDA scientists complain to Obama of 'corruption'

January 26, 2009

A kind greetings from Bacliff, Texas !

O.K., let us suppose the impossible, that indeed spontaneous Transmissible Spongiform Encephalopathy _does_ exists (to date, this has never been proven in the field, under natural conditions), at whatever rate they choose (i do not believe in the spontaneous TSE as the cause for 85%+ of all CJD i.e. the sporadic CJD's, i.e. that all these poor victims died from a 'happenstance of bad luck', or 'that a twisted funked out protein just chose this group on it's own, with no route and source of nothing involved'), BUT for now, lets say they exist.

PLEASE tell me then how a GM cow will be free from the spontaenous TSE ???

Spontaneous occurrence (14-16)

The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very few of them did so. The possibility of a very low frequency of spontaneous occurrence of BSE may be monitored from the output of surveillance in cattle populations elsewhere. R: A watching brief is kept on surveillance efforts world-wide.

Perspectives BIOMEDICINE: A Fresh Look at BSE Bruce Chesebro*

Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either "prion diseases" because of the association of a misfolded cellular prion protein in pathogenesis or "transmissible spongiform encephalopathies" (TSEs) because of the spongelike nature of the damaged brain tissue (1).

The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).

Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by "spontaneous" misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or "prion."

Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven. CREDIT: KATHARINE SUTLIFF/SCIENCE

Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent--unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.

Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD--which is considered by some researchers to begin by spontaneous misfolding of the prion protein--usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.

What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? "Sporadic" pertains to the rarity of disease occurrence. "Spontaneous" pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE of unknown etiology--might be a better term to describe the origin of this malady. ...

snip...full text ;;305/5692/1918

Release No. 0106.04

Contact: Office of Communications (202) 720-4623

Transcript of Remarks From Technical Briefing on BSE and Related Issues With Agriculture Secretary Ann M. Veneman and USDA Chief Veterinary Officer Dr. Ron DeHaven Washington D.C. - March 15, 2004

OPERATOR : “Yes. Our next one is coming from Elizabeth Weiss. Please state your company.”

ELIZABETH WEISS: “This is Elizabeth Weiss with USA Today.”

“I actually had two questions. First off, when you say you're looking for 1 in 10,000 cases, is USDA doing any work to find out the possibility of whether or not BSE exists in a spontaneous form in the way that it does in humans and elk populations?

“And secondly, how will any of this fit into some of the consternation that's been raised in California and with the Midwest packer that wanted to test all of its cattle?

DR. DEHAVEN: “All right. I think we've got three different questions in there, and I'll try to touch on each one of them.

“First of all, let me correct just a technical issue, and that is you mentioned 1 in 10,000. And actually our surveillance system currently is designed, the one that we have in place now is designed to detect 1 positive in 1 million cattle, and I gave some numbers between 200,000 and 268,000 that would allow us to detect 1 in 10 million as opposed to 1 in 10,000.

“So we would, if we were able to collect in the ballpark of those numbers of samples then we with increasing numbers of samples have an increasingly statistically valid sample from which to determine, one, whether or not the disease exists and, if so, at what prevalence level.

“So our real emphasis is to test as many of those animals as we can, ensure that we get an appropriate geographical distribution, but not setting a specific number as far as a target. Again, consistent with the recommendation from the International Review Team, their recommendation was to test all of them.

“So that's consistent with where we're going is to test as many as we possibly can.

“As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.

“Again, it's a very difficult situation to prove a negative.

“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.

Matthews confirmed that the brain tissue samples from the US animal had arrived at Weybridge. Test results were likely to be ready by the end of next week, he said.

The suspect animal has already undergone a series of tests. A rapid screening test on Nov. 15 returned inconclusive results. Sophisticated immunohistochemistry (IHC) tests cleared the animal of any infection, but a third round of testing using a Western blot procedure showed a "weak positive".

Weybridge will do an IHC test plus three kinds of Western Blot tests on the samples. They will use "methods of slightly different analytical sensitivity that give us the greatest number of opportunities to interpret what we see," he said.

US beef industry leaders say scientists should not speculate about the unusual case.

"There's no evidence that it's atypical ... and there's absolutely no evidence that it's spontaneous," said Gary Weber, head of regulatory affairs at the National Cattlemen's Beef Association.

Matthews noted scientists are still grappling with what is typical and atypical BSE.

"Far too few people have looked at BSE in depth using all of the tests to be able to define 'this is normal and that one isn't'," he said.

Weber noted Japan used the term to describe two very young infected cattle because BSE is usually found in older animals. Italy labeled a case "atypical" because the misshaped prions were found in unexpected parts of the animal's brain. ...snip...end

Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease

Spontaneous occurrence

14. Spontaneous cases of classical CJD in humans are found at a rate of about 1/million around the world (Will, 1993), without appreciable racial or geographical variation except in a few specific cases, notably Jews of Libyan origin that have a mutation in the open reading frame of the PRNP gene (Chapman and Korczyn, 1991). Thus it is theoretically possible that spontaneous cases of BSE could occur as a consequence of a germ line mutation, in which case relatives would also have a certain or increased incidence of the disease, or a somatic mutation, which would be unlikely to be detectable unless the appropriate tissue were identified, or after some transformation in the PrP protein in the animal concerned. BSE was unknown prior to its detection in Britain in the mid 1980s, and Index cases found around the world since then can all be explained in terms of export from the UK directly or indirectly of cattle or of feed components. No BSE affected animals have been reported in many developed countries with large cattle populations, including Australia, New Zealand, Norway and Sweden, which have mixed cattle populations; and the only infected animal detected in the US was of Canadian origin. The disease seems to have a highly homogeneous aetiology (e.g. Bruce, 2003).

15. Data from the USA, where the dairy population in particular is highly related to that in GB provide an upper limit to the spontaneous rate. A programme of testing is in place of a target population of adult cattle exhibiting some clinical sign that might be consistent with BSE (animals reported as having CNS or clinical signs of BSE or were non-ambulatory). In the intensive programme from June 2004 over 375000 animals were tested in the following 12 months. No positive results have yet been obtained in these or previous tests (USDA BSE Testing). This implies a putative upper limit of under 10 per million in this target group. Assuming, as analysis has shown, the relative risk in this group is about 30 times higher than in the population as a whole (European Commission, 2002c), then the incidence in the population as a whole is under 3 per 10 million. This figure could possibly be biased downwards if affected animals are diagnosed and disposed of without being tested. Taking account of testing done and the lack of clinical cases seen in many other countries also, it seems highly unlikely that the spontaneous rate can be as much as 3 per 10 million head. Nor can spontaneous occurrence explain incidences of ca. 30 cases of BARBs per year in 2002/4 in the UK adult cattle population of ca. 4 million. [NOTE ADDED 30 JUNE: The recent confirmation of a previously inconclusive case in the USA affects these calculations. If the animal did not have access to infected feed, the calculations have to be revised: they suggest a sporadic incidence in the population of 1/(375000 x 30) or almost 1 per 10 million, with the upper limit under 5 per 10 million.]

16. Calculation of a maximum rate of possible transformation from scrapie to BSE is less feasible. Nevertheless, BSE appears not to have arisen in the UK until around the early 1980s, despite the presence of scrapie in sheep here for at least 200 years. Although a change in the scrapie prion may have been the cause of the initial cases of BSE, the difference between their properties in mice and the uniformity of the BSE brain lesions suggest it is unlikely that more than one such mutation was the source of BSE. It is most unlikely that the same mutation could be occurring often enough to contribute significantly to BARBs cases. Furthermore BARBs cases do not match the geographical distribution of the sheep population. The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very ...

242 Atypical and classical BSE are different strains based upon Western blot profiles 243 (Hill, 2004; Normile, 2004; Baron et al., 2006), and this study indicates that disease Page 11 of 23 Journal of Animal Science Downloaded from by on November 12, 2008. 12 progresses via different routes for these strains. The disparate 244 routes of pathogenesis in 245 atypical BSE can occur by 1 of 2 means. One possibility is that the source of infectivity 246 in atypical BSE is exposure to contaminated feedstuffs, as is the case for classical BSE, 247 but progression occurs in a disparate manner that bypasses the influence of the indel 248 polymorphisms. The other possibility is that atypical BSE is occurring spontaneously in 249 the host. Support for atypical BSE occurring spontaneously are the parallels to sporadic 250 TSE in humans, specifically, occurrence in older hosts and a comparable low incidence 251 rate (Baron and Biacabe, 2006). Furthermore, atypical BSE occurs as isolated, sporadic 252 cases in contrast to the clustering of cases observed for feed borne classical BSE 253 (Donnelly et al., 1997). Interestingly, the only native born cases of BSE in the United 254 States identified to date have been classified as atypical BSE.

255 No experiment can conclusively confirm a spontaneous nature for atypical BSE.

Monday, February 11, 2008 7:00 am Registration and Morning Coffee

Emerging Concerns: De novo Formation of Prions

9:05 De novo Generation of Prion Infectivity in a Cell-Free System Joaquin Castilla, Ph.D., Assistant Professor, Department of Infectology, Scripps Research Institute-Florida Transmissible spongiform encephalopathies (TSEs) are a group of neurodegenerative disorders affecting both humans and animals. There is no available treatment or therapy for these fatal diseases. The infectious agent associated with TSEs (termed prion) appears to be composed uniquely of a protein, which is a conformationally-modified version (PrPSc) of the cellular prion protein (PrPC). The disease is propagated by the conversion of host PrPC into PrPSc induced by small quantities of PrPSc. Interestingly, prions occur in the form of different strains that show distinct biological and physicochemical properties. TSEs can have diverse origins, including genetic, sporadic (putatively spontaneous) and infectious. The occurrence of sporadic cases of prion diseases in humans and maybe in other species, i.e. atypical bovine spongiform encephalopathy (BSE) in European and USA cattle and atypical scrapie cases in sheep suggest that spontaneous prion diseases may happen infrequently but ubiquitously. However, there are no reported cases of spontaneously-occurring prion disease in experimental wild-type rodent models. We have used a novel technique, Protein Misfolding Cyclic Amplification (PMCA) to rapidly propagate prions in the test tube, using normal brain homogenate as substrate. Prions propagated in vitro are infectious in vivo and maintain their prion strain specificity. PMCA has been used to efficiently amplify a variety of prion strains from mouse, hamster, bank vole, deer, cattle, sheep and human. Therefore, to mimic spontaneous generation of infectivity in vitro becomes one of the most important challenges in the prion field. We show here, for the first time, the de novo generation of infectious prions from bank voles (Clethrionomys glareolus) starting with non-infectious brain homogenates. Several biochemically different prion strains were generated using two different wild-type vole genotypes. The de novo in vitro generated PrPSc was highly infectious after its inoculation in bank voles. We show an extensive characterization of this "spontaneous" phenomenon.

Pathogenesis Chairperson: Suzette Priola, Ph.D.

11:10 Accumulation of Prion Protein in the Brain That is Not Associated with Transmissible Disease Pedro Piccardo, M.D., Senior Investigator, OBRR / DETTD / LBPUA, FDA (Invited)

11:35 High Levels of TSE Infectivity Can Be Associated with Little or No Detectable PrPSc in Vivo Rona Barron, Ph.D., Neuropathogenesis Unit, Roslin Institute and Royal (Dick) School of Veterinary Studies This work examines the relationship between TSE infectivity and the abnormal prion protein, PrPSc. In a mouse model of disease we have shown high titres of TSE infectivity in brain tissue which contains little or no PrP-res. We also found no evidence of other abnormal PrP isofoms such as PK-sen PrPSc. These data question the true relationship between PrPSc and TSE infectivity, and the current reliance on PrPSc as the sole diagnostic marker for TSE disease.

12:00 Conversion of the BASE Prion into the BSE Prion: The Origin of BSE? Fabrizio Tagliavini, Ph.D., Director, Division of Neurology 5 & Neuropathology, Neurological Institute "Carlo Besta" Twenty years after the identification of bovine spongiform encephalopathy (BSE), the origin of the causal agent is still unknown. This issue is of fundamental importance, since knowledge of the origin of the BSE agent is essential for prevention of future outbreak of the disease or variants thereof in cattle and other mammals. We carried out transmission studies with transgenic mice expressing bovine PrP and four lines of non-transgenic mice and found that an atypical form of spongiform encephalopathy of cattle, termed BASE or BSE-L, is caused by a prion strain distinct from that of classical BSE. Noteworthy, this newly characterized prion strain has the ability to convert into the classical BSE strain upon serial transmission to inbred mouse lines. According to these results, BASE--which is regarded as a sporadic form of prion disease in cattle--may be the origin of BSE, following conversion of the causal agent in an intermediate host.

12:45 Luncheon Technology Workshop (Sponsorship Available) or Lunch on Your Own

2:00 Sporadic CJD and Atypical BSE: Two Children of One Protein Maurizio Pocchiari, Ph.D., Director of Research, Virology, Istituto Superiore Di Sanita The identification of forms of TSE diseases in cattle caused by prion strains different from BSE has raised new concerns on the possibility that these novel agents might induce disease in humans with a phenotype resembling sporadic CJD. The analysis of the distribution of the different molecular subtypes of sporadic CJD might give some answers.

let's see, a few examples of our extensive BSE surveillance plan ;

On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of the first known case of BSE in the United States. It was in an adult Holstein cow from Washington State. This diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Trace-back based on an ear-tag identification number and subsequent genetic testing confirmed that the BSE-infected cow was imported into the United States from Canada in August 2001. Because the animal was non-ambulatory (a “downer cow”) at slaughter, brain tissue samples were taken by USDA’s Animal and Plant Health Inspection Service as part of its targeted surveillance for BSE. However the animal’s condition was attributed to complications from calving. After the animal was examined by a USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both before and after slaughter, the carcass was released for use as food for human consumption. During slaughter, the tissues considered to be at high risk for the transmission of the BSE agent were removed. On December 24, 2003, FSIS recalled beef from cattle slaughtered in the same plant on the same day as the BSE positive cow. (see Bovine Spongiform Encephalopathy in a Dairy Cow - Washington State, 2003.)

On June 24, 2005, the USDA announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas, died at approximately 12 years of age, and represented the first endemic case of BSE in the United States. (see Texas BSE Investigation, Final Epidemiology Report, August 2005 (PDF – 83 KB))

On March 15, 2006, the USDA announced the confirmation of BSE in a cow in Alabama. The newly confirmed case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10-years-old. It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation (see second featured item above and Alabama BSE Investigation, Final Epidemiology Report, May 2006).

Strains of BSE There is increasing evidence that there are different strains of BSE: the typical BSE strain responsible for the outbreak in the United Kingdom and two atypical strains (H and L strains).

Typical BSE strain -- The BSE strain responsible for most of the BSE cases in Canada is the same classic or typical strain linked to the outbreak in the United Kingdom. It is known to be preventable through elimination of BSE contaminated feed and has been causally linked to vCJD in humans. This typical strain has not yet been identified in any U.S.-born cattle.

Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease

Both of the U.S.-born BSE cases and two of the 15 Canadian-born BSE cases were 10 years of age or older and three of these older North American cases for whom the strain type is presently known were linked to an atypical BSE strain known as the H-strain. Publication of the strain testing results on the 13 year-old BSE-infected Canadian cow identified in December 2007 is pending.

Saturday, January 24, 2009

Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report

Research Project: Study of Atypical Bse

Location: Virus and Prion Diseases of Livestock

2008 Annual Report

Thursday, December 04, 2008 2:37 PM

"we have found that H-BSE can infect humans."

personal communication with Professor Kong. ...TSS

Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy

I thought a quick review of the Bush's terribly flawed and failed mad cow disease policy, from the illegal feeding of literally millions and millions of pounds of highly suspect, and banned mad feed, to the failed BSE surveillance program, all of which exposed, needlessly, millions of people to the mad cow agent i.e. Transmissible Spongiform Encephalopathy. ...

Parentage-based DNA traceback in beef and dairy cattle 2008

48 hour traceback for BSE mad cow disease in the USA ???

NOT in your lifetime !

FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms

snip...full text ;

Friday, August 29, 2008

Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008

Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

November 25, 2008

Update On Feed Enforcement Activities To Limit The Spread Of BSE

"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." ... interesting. ... TSS

Thursday, June 05, 2008

Review on the epidemiology and dynamics of BSE epidemics

Vet. Res. (2008) 39:15 DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;

please see full text ;

***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***

Progress Report from the National Prion Disease Pathology Surveillance Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008

In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.

In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.

Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

A New Prionopathy OR more of the same old BSe and sporadic CJD

Communicated by: Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP],F2400_P1001_PUB_MAIL_ID:1010,39963

There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

sporadic Fatal Familial Insomnia

MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT

2 January 2000

British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

15 November 1999

British Medical Journal vCJD in the USA * BSE in U.S.

Creutzfeldt Jakob Disease

Sunday, April 20, 2008

Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

see full text ;

CJD TEXAS (cjd clusters)

Attending Dr.: Date / Time Admitted : 12/14/97 1228

UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report

FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858

I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

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Irma inundates Naples area with storm surge after second Florida landfall

Storm surges are expected in Naples and other areas of Florida after Hurricane Irma made landfall on Marco Island Sunday afternoon — its second landfall in Florida as the state continues to brace for the now-Category 2 storm’s strong, 115-mph winds and flooding.

Full Story Via FOX News

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Thursday, 7 June 2012

It's a starling, darling...

Here's my blipfoto post's photo from last night. You can read the story here.

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New Memory Box 2011!

We've got the newest release from Memory Box and let me tell you, it is amazing!  There is brand new 8 1/2 x 11 paper, new 6x6 paper packs and 12 x 12 papers, plus the stamps we've all come to love!  You can check it all out here.  But, you really should come in and see the samples Dave sent with the newest release!  They are to die for!!!  Hope to see you all soon!

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Sunday, May 31, 2015

Teacher Gifts Inspired by Taste of Summer

 I wanted to do something special for the boys' teachers this year, and I found the idea for "Orange you glad it's summer" on Pinterest.  It worked perfectly with CTMH's June special, Taste of Summer. I found the gift buckets and a few items at Dollar Tree.  The rest I made or purchased at various stores.

For each basket, I made a set of 5 cards and the big card using Taste of Summer papers and stamps.

Here's an up close shot of some of the goodies. Each one had a cup, orange slices, Trident, bubbles, a popsicle notepad, a Reese's, cards, a gift card, and beverages. Of course, I added an orange lei for fun.

A picture of all five completed baskets.

Thursday, May 21, 2015

If You Stamp It Use Your Stash Blog Hop

If you are joining us for the "Use Your Stash Blog Hop," you are right on track. WELCOME!

You should be coming from Cassandra's blog

If you get lost along the way you can see the entire list of hoppers on Shirley's blog

This month we are showcasing stamp sets we haven't used.  I have a few projects with a combination of old and new stamps. The first card uses the new Blossom papers.  It was inspired by a card I saw from Patricia

I used a brand new stamp set I just bought, the new Operation Smile stamp set, Happy Everything.  When you purchase this set, Close To My Heart will donate $3 to Operation Smile. I have a feeling this is going to be one of my go-to sets!

I also used a really old stamp set, A Posey. I've had this stamp set forever and never used it.  I thought it worked perfectly with the Blossom paper.

For my second project I wanted to do some random stamping for background paper.  I started with one sheet, and cut it up.

I made the cards using the Chalk It Up Picture My Life cards.

The stamp sets I used were Geek is Chic and LOL.  I bought these stamps when the Annual Inspirations book came out, but hadn't used them.  As a teacher, I thought I'd get a lot of use out of them, but they've sat there collecting dust.  The "Happy Birthday" is from the Operation Smile set.

Thanks for visiting!  Now hop on over to Heather's Blog for more ideas of using up your stash.


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All the way from Brooklyn! Photo: Eric Zelermyer

On the dock in New York, we imagined we’d be overrun by visiting friends and family right about now. Who wouldn’t want to escape icy winter and come hang with us in tropical paradise? Sadly, it turns out that planning a rendezvous in the Exhumas (outside of George Town, that is) is tricky and pricy. Not wishing to put anyone out, we suspended our campaign for visitors this season.

Then, we got an email from our friend Eric. I’d just posted photos of the swimming pigs on Facebook, and his partner Thea was completely obsessed. Eric found mid-week seats on a tiny flight bound for Staniel Cay, and we carved out a nine day weather window to sail back up north from George Town in time to receive them.

I was a tad anxious about bringing additional bodies into our tiny ecosystem. But, thanks to the House Rules and Visitor Information document that I’d emailed in advance, Eric and Thea arrived game and ready to embrace the good, bad, and ugly of boat life.  If they were phased by the complete lack of privacy, our water-saving strategies, using a marine toilet, or our 9PM bedtime (known as “cruisers’ midnight”), they didn’t let on.

We had such a great time together. Brian and I enjoyed revisiting favorite anchorages from our first months in the Bahamas, as well as checking out a few places we’d missed the first time around. A couple of freakishly calm days gave us perfect conditions for snorkeling early in the week, then the wind picked up just the right amount for some easy sailing. In the evenings we enjoyed some fabulous sunsets and plenty of good meals, fortified with special wine and foodstuffs from home that Eric brought along in his duffel bag.

Frozen arrival cocktails at the Staniel Cay Yacht Club

Eric and Thea very generously agreed to bring us stuff that we haven’t been able to get in the Bahamas. They received dozens of packages at their apartment and amassed a strange collection of boat parts, baking supplies, snacks, towels, snorkel gear, guitar strings, and so much more.

Getting the hang of four in the dinghy

When we arrived at the pig beach, most of the pigs were missing. We walked around a bit and discovered piles of pigs asleep in the bushes. Perhaps they were taking the day off from entertaining tourists?

(Photo: Eric Zelermyer)

Perfect calm (Photo: Eric Zelermyer)

Thea, posing with the breakfast inspired by this catchy tune  (Photo: Eric Zelermyer)

Running with Laura and Stan in Pipe Cay. It was a million degrees with no wind.

Brian, me, Laura, Stan, post run (Photo: Eric Zelermyer)

At the top of the lookout tower that Laura and Stan built

Laura and Stan hosted a really nice cocktail hour aboard the 60 foot fishing boat that they gut-renovated and converted into their floating dream home.

Thea and Enzo

Me, blowing the traditional conch horn at sunset aboard Laura D (Photo: Eric Zelermyer)

Snorkeling Pipe Cay

Eric, holding the conch that Thea found just before it became fritters.

Brian insisted that Eric eat the translucent, slimy conch penis. The locals call it Bahamian Viagra.(Photo: Eric Zelermyer)

Thea, taking morning tea and wearing her snazzy cats in space leggings

Revisiting Rachel’s Bubble Bath

Eric and Brian added a new cairon to the collection at the top of the cliff

Sunset on the deck of m/v Laura D

Eric and Thea, thank you for being your chill and flexible selves, you were the best boat guests we could ever hope to have. We miss you already!

Nightingale Tune has returned to George Town, where we’ve been enduring some uncomfortable days at anchor in extremely high winds. I’ve got a to-do list a mile long, preparations for a month of touring in places where we expect resources to be scarce, but right now the harbor is so choppy, we don’t feel safe hauling jerry cans and propane tanks in the dinghy. Last night we enjoyed a beautiful dinner with our friends Deb and Pete aboard s/v Delancey, anchored just off our bow. That 100 yard ride soaked us through coming home, so we’ll be waiting patiently for calmer seas before we venture any further. For now, I’ve got a pile of insurance forms to complete, a guitar (thanks to Bo!) to practice, and more meals to prepare and stow for the month ahead. Brian is pouring over charts and doing odd jobs around the boat. We’re both excited and anxious to get going with the next leg of our trip.


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Collecting Sea Glass in the C-C-C-old

So, there I was vaccuuming the house  today and daydreaming about the beach. Sure it’s November and the sky is battleship grey and the temperature makes my fingertips feel like icicles and the wind is raw and stinging. Sure, I have more sea glass than I know what to do with. Just get me to the damn beach.

I went yesterday with my mother and my four year old. My mom was getting over a cold and my little one’s hands were frozen, so we only stayed for half an hour. I felt like I was being pulled away from really great book – just at the part where it gets extra good. But sometimes selfish wants are trumped my more important things … like keeping the peace (not the piece…hahaha).

As the weather gets increasingly cold, I’m wondering if my kids will find our little outings miserable. If so, should I abandon the outings until spring, or do I help them overcome the cold and find joy in our winter adventures? I shall take the latter approach and see where it takes us. Really, it’s all about having fun. I want my kids to have pleasant memories of our trips to the beach. To me, that’s the most important thing of all.

Photo: Christina Friedrichsen (that’s the fam!)

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On 20/11/2017 15:22, [EMAIL PROTECTED] wrote:
> Yes, that will work, but note that you do still continue to skip constants, which are callable as methods.  I don’t know whether that matters to you.

I think it doesn't matter much and it's OK to stick to the current behavior
for now.

It seems that constants are initially stored as refs in a stash (for example
as scalarrefs, arrayrefs, refs-to-refs), but if they're evaluated using method
syntax for the first time, they get converted to globs. So we treat constants
inconsistently which is a bug, although a really minor one.

If there is a way to detect constants reliably, maybe via %constant::declared,
we could make sure that they are ignored or throw an error if a constant
shadows a method name. OTOH, constants can be called with method syntax, so we
could also allow them as methods.

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Unified Compliance Framework unties overlapping compliance standards

Compliance professionals and vendors are turning to the Unified Compliance Framework as a common language for overlapping compliance standards.

Compliance regulations and standards, like other bodies of laws, are straightforward in theory -- but they're maddeningly...

opaque and complex in practice.

If you have any doubt, just Google a term like Payment Card Industry Data Security Standard and look at the great variety of links that come back promising to help you sort it all out. Now multiply PCI by three or four or 50 to account for the multiple and overlapping sets of regulations and statutes that government entities and public companies in the U.S., Europe and elsewhere are being asked to comply with, and you get a sense of the challenges facing chief information security officers and IT staffs in ensuring compliance.

One constant need is harmonizing the requirements of different sets of regulations and compliance standards. Presumably, if companies can identify which regulations they're bound by and then areas that overlap, they can reduce their compliance costs by taking a "fix once, comply many" approach that will streamline internal audits and reduce capital expenditures.

Such an approach also allows organizations to focus more time and energy on their areas of greatest risk and exposure and requirements with the sharpest teeth. But making sense of hugely complex regulatory frameworks is no mean task, which is why many have found it easier to rush into the arms of (expensive) consultants and managed services firms that can do the heavy lifting for them.

Connecting the compliance dots

What's needed, of course, is an easy way to make sense of the various regulations that bear upon your business -- to connect the dots between similar sets of requirements and identify areas that are unique to each.

This isn't exactly a new problem in the history of human thought. In fact, Jewish scholars living in the Middle Ages had a very similar problem. They had a defined body of Jewish law rooted in three texts: the Bible (or Torah); the Mishnah, a codification of Biblical law dating to the third century; and the Talmud, a kind of extended Rabbinic commentary on those laws. The problem was the source documents were unwieldy: loosely coupled collections of stories, laws and then reflections on those laws from which it was difficult to extract clear guidance. There might be dozens of direct or indirect discussions of dietary laws, for example, but those discussions were sprinkled through numerous texts in different places. Some prescriptions might contradict others. Lots of gray area. Starting to sound familiar?

A solution came in the 12th century in the form of the Mishneh Torah, a work of the famous medieval scholar Maimonides. Working for more than a decade, he consolidated the sum of those three source texts and other important works of Jewish thought at the time into 14 volumes, organized by topic (knowledge, law, observance, etc.) and subdivided those into sections, chapters and paragraphs that could be easily referenced.

With the Mishneh Torah (which translates, literally, as "repetition of the Torah"), a scholar who wanted a question answered about dietary laws or a civil dispute could go to the appropriate section and find a clearly worded compendium of laws and rulings culled from all the relevant source documents that spoke -- directly or indirectly -- to the issue at hand.

My mind turned to Maimonides and his massive project the other day when I was speaking with a company, Network Frontiers LLC. It has undertaken a very similar project with the Web of laws, industry and government regulations that, increasingly, resemble a kind of secular religion for the enterprise.

Untying the compliance knot

Working over the past couple of years with a team of linguists, lawyers, compliance experts and practitioners, Network Frontiers created the Unified Compliance Framework (UCF), a database that distills 450 regulatory and legal authority documents (U.S. and international) into a set of 30,000 unique citations and 2,500 distinct controls, each with a unique and persistent ID.

What's needed is an easy way to make sense of the various regulations that bear upon your business -- to connect the dots between similar sets of requirements and identify areas unique
to each.

 Controls are grouped into 13 high-level "impact zones" -- records management, technology acquisition, human resources management, systems continuity, physical security and so on. The controls are published in a series of spreadsheets with pivot tables and links back to the original source material, allowing practitioners to ground controls in chapter and verse.

For example, you know that changing vendor default settings is a requirement of PCI, but did you know that it's also called for by NERC, the Federal Financial Institutions Examination Council and in guidance from the National Institute of Standards and Technology and the IRS? Probably not, but UCF connects the dots. Moreover, because each control is assigned a unique ID (UCF ID 00877, in the case of "always changing vendor defaults"), suddenly practitioners have a common language to talk about a requirement that may be framed differently in different compliance frameworks.

Finally, Network Frontiers offloads the task of keeping current with changes to existing regulations as well as pulling in and correlating new regulations and laws. (Consider the job of parsing multiple state data privacy laws and the federal data privacy laws working their way through Congress.)

In short, UCF is an incredibly useful tool that security vendors, especially those targeting governance, risk and compliance, have started to seize on. Vendors such as CA Inc., Archer Technologies LLC, McAfee Inc., Lumension Security Inc. and OpenPages Inc. have all licensed UCF content for use in their risk management products in recent months, and we expect more to sign on in 2010, as customers look for help cutting through the Gordian Knot of compliance mandates. Network Frontier makes money by licensing its spreadsheet on an annual subscription model, and also provides various compliance toolkits for a fee. But its UCF spreadsheets are available for viewing free through its website. Check them out.

Paul Roberts is a senior analyst at The 451 Group. Let us know what you think about the story; email

This was last published in December 2009

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Mobile endpoints require new look at cybersecurity awareness training

During a recent SearchCompliance webcast, Georgia Weidman, founder and CTO of Shevirah, Inc. and Bulb Security LLC,  discussed how modern mobile technology is creating cybersecurity gaps for enterprises. Here in part three of this four-part webcast, Weidman discusses how changing mobile endpoints should make organizations reconsider their data protection strategies such as cybersecurity awareness training.

Editor's note: The following is a transcript of the third of four excerpts of Weidman's webcast presentation about how enterprise cybersecurity is being influenced by mobile, IoT and non-traditional endpoints. It has been edited for clarity and length.

Georgia Weidman: Employees are typically selecting their own devices, and organizations are just dealing with it. There's a varying degree of how much we're dealing with that being a risk. I've worked at places or I worked with places where, basically, there was the Wi-Fi password in the breakroom and whatever you wanted to put on the network was what you were going to put on the network. We're seeing less and less of that, but, unfortunately, in my experience, not always.

We've got employees using whatever devices they want. In IT, you're not going to be able to keep up with everything that's in the network. Did you ever think when you signed on to be in the IT Department that you were going to be in charge of seeing whether somebody's home television was a security risk? But that's what you need to be doing, right? Somebody just got the TV, it hooks up to the phone via Bluetooth -- if either one of those is compromised and then it comes to work or logs into work, then you've got a problem.

As I said in the beginning, the perimeters don't exist anymore, it's all about these devices. But with all these networks running around that you don't control and all these devices running around that you don't control, how can you possibly expect something like PCI compliance to solve all your problems? The main problem with compliance is that it's so limited. There's a specific set of checks that you do, and if you pass those checks and nothing more than those checks, you are compliant. It gets a lot of flak for that reason, I guess, but having a set of checks to get you started with something like PCI or HIPAA is, certainly, a step in the right direction. But when was the last time you saw anything about near-field communication, or Bluetooth, or anything like that in your compliance?

Everybody tries to shut me down at this point and say, "But Georgia, this mobile thing has been going on for a really, really long time, right? You've been up there on these stages talking about how this mobile apocalypse is coming for several years now, and it never seems to come. How is it that you can still continue to say that mobile is such a risk?"

At which point, I like to say, "Well, how many like intrusion detection systems are checking for things around mobile devices?" Are you able, with your current infrastructure right now, to be able to say what data someone has on their corporate email and it is not being sent out like via the cell carrier?" Of course not. There's no like technology being sold on the market that can do that. With things like this, the controls just aren't there yet so really only the thing we can do is test.

Endpoint security awareness

I do a fair amount of phishing engagements and I really do see the places that have the secure culture -- they think about the security stuff, they talk about it. They know that these are threats. Social engineering still definitely works, but then you start bringing in these mobile devices. You start bringing in all these other devices and they don't really fit the picture of our cybersecurity awareness training. One of the things I'm trying to fix is getting security awareness training to where it does cover these kinds of new endpoints.

See other excerpts from this webcast presentation on cybersecurity

Part 1: Enterprise cybersecurity further complicated by mobility, IoT

Part 2: Corporate network: Assumptions vs. Reality

Part 4: Mitigating enterprise security threats

I think that people have shown that the cybersecurity awareness training does, to an extent, work. Now, we need to bring security awareness training up to speed in order to get to the rest of these end-points. This brings us back to compliance, because I've never seen any compliance that does anything around requirements for things like security awareness training and phishing.

Think about your internal network -- it's probably a rich place to hang out as an attacker. We don't have a perimeter anymore, so using the mobile device that's been compromised to attack other devices goes a lot of places, it sees a lot of things. It's a really good place to hang out, if you're an attacker and, again, it allows you to bypass all those perimeter controls. If I attack another machine in the network, it's caught at the perimeter, by the firewall, by intrusion detection -- all that catches it and it cuts that off. Your data loss prevention gets rid of it.

Well, if I'm using the phone, then I can send it out, again, through that cell tower and your perimeter never saw it. There was no way it could see it because it's, again, sitting at the perimeter. And I'm not on the Wi-Fi, I'm on the cellular network so you didn't see that data leave, you never knew it left.

Some of the larger enterprises are using things like enterprise mobility management and things like that, which still have a long way to go, as well. A lot of people also want to only allow, "Corporate-owned devices only that only do corporate things," and we don't see that working very well. People don't like that and just end up, breaking the policy and using their own things anyways.

So what should you do? The only way, really, to do this around these new devices is, one, we've got to figure out what our risks are through testing. How well do the security controls you have in place protect you, and what do we need to do to fill in that gap?

If we're going to stay able to do business, we are going to have to have every device that comes into the network be subject to security testing. That's just how it's going to be. Again we're going to figure out what our current risk is, figure out how well our mobility program is working, see how far like a malicious actor could get using a mobile device. We have the problem that when we do security testing, particularly around compliance, we limit it so much. We say, "This is what compliance requires, so this is what we're going to test." And the malicious actors are not following the compliance script.

What's weird about mobile is that it's really not static, so you're going to have to keep changing this and updating these policies for new devices that come out and new ways of communicating. Near-field communication, and Bluetooth, and all these things weren't necessarily things we had to think about in the enterprise not so many years ago so.

I think we're still kind of in the Dark Ages about what corporate security is and what kind of testing we need to do to be compliant. I get that if you check the box, you're compliant, but I really think we need to take this a lot farther in order to actually provide security.

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What cybersecurity awareness training techniques are most effective to protect corporate data transferred on mobile devices?