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Cheerios' Failed Case for Yellow Shows Why It's So Hard for Brands to Trademark Colors
General Mills' defeat illustrates one of branding's trickiest tasks
It turns out a lot of cereal brands use yellow on their boxes. Cheerios
By Robert Klara
It's bad enough for General Mills that Americans have been losing interest in breakfast cereal for the past decade or more, but the brand got more bad news last week when the Trademark Trial and Appeal Board rejected its application to trademark the use of yellow on Cheerios boxes.
The problem for the packaged-foods giant wasn't so much that consumers didn't recognize Cheerios' famous yellow box; it was that too many other cereals were already using yellow on their boxes. Shoppers who are "accustomed to seeing numerous brands from different sources offered in yellow packaging are unlikely to be conditioned to perceive yellow packaging as an indicator of a unique source," wrote Judge Anthony R. Masiello in his decision. "Rather, they are more likely to view yellow packaging simply as eye-catching ornamentation customarily used for the packaging of breakfast cereals generally."
The lack of legal protection for a yellow box probably won't rob Cheerios of sales it was going to make anyway, but the ruling did squash two long years of legal efforts by General Mills' attorneys to secure the trademark. All of this begs some important questions: Why is securing exclusive use of a color so hard to do? And how did brands come to fighting over colors in the first place?
Trademarking a color is legally quite challenging, said John Welch, an intellectual property attorney with the Boston firm of Wolf, Greenfield and Sacks. That's why only a relative handful of brands have succeeded. "It's really difficult," he said. "These nontraditional trademarks like product shape and color are just not seen by consumers as trademarks, so you have to go out and prove that the public has come to recognize these things as marks. It's a high burden, so you start behind the eight ball."
It's not enough to simply argue that a given color is an attribute of a brand. A company applying to the U.S. Patent and Trademark Office must prove that consumers visually equate a specific color with that brand. And trademark protection, when it is granted, doesn't apply to all uses. For example, the 3M corporation has successfully trademarked the color yellow, but only for its Post-it notes. UPS secured trademark No. 2,901,090 for its chocolate-brown color, but the protection is confined to uniforms and, of course, those big brown trucks.
How colors become trademarks
For decades, brands were only permitted to trademark color combinations, and only then when they were used as part of a distinctive design. That changed in 1985, when Owens Corning decided it would try to register the color pink, a recognizable feature of its fiberglass insulation. After the USPTO refused to issue the mark, the company appealed, kicking off a decade-long legal battle that wound up in the U.S. Supreme Court in 1995. The court ruled that a single color could be trademarked so long as it had "distinctiveness" in the marketplace.
Today, the International Trademark Association explains that threshold in this way: "The trademark owner must show that the consumer, upon seeing the color used in connection with the goods or services, views the color not as merely ornamental but, rather, as a means of indicating the origin of those goods or services."
Photo: Nick Ferrari
In other words, if the consumer immediately associates a color with a brand, a case can be made for trademarking. So it's easy to see why Tiffany & Co. was able to secure a trademark for robin's egg blue for its shopping bags and gift boxes. The luxury brand had been using that color since 1845, plenty of time for shoppers to associate color with brand.
Even so, a brand must present a strong argument that goes beyond historical usage. And this, in Welch's view, is where Cheerios faltered. "You have to show what we call acquired distinctiveness, and you have to show exclusive use and extensive use—and they couldn't show exclusive use," he said. "That was the killer for them."
A successful case is more likely to look like the one UPS presented for its color trademark. Even though the brand had used the chocolate-brown color since 1916, that fact alone wasn't enough to secure the mark. UPS's paperwork included examples of media coverage citing the distinctive brown, proof that brown had been part of its advertising to the tune of $100 million a year and no fewer than 109 statements from consumers who associated Pantone 462C with the UPS brand.
Get ready to fight
Even if a brand does secure a trademark for a color, its problems are far from over. Many have had to litigate, often for years, just to fend off challenges to trademarks. In 2015, AstraZeneca, which trademarked the color purple for its heartburn remedy Nexium, went to court to block Indian drugmaker Dr. Reddy's Laboratories from using purple on its generic pills. AstraZeneca prevailed by successfully arguing that "the media and the public associate the color purple with AstraZeneca … and its Nexium products." It probably didn't hurt that Nexium has been famously advertised as "The Little Purple Pill" (also a trademark).
Facebook: Christian Louboutin
Christian Louboutin had a tougher time. Since 1992, the sassy French designer had applied a candy-apple red finish to the soles of his high heels, but not until 2008 did he decide to trademark it. That presented problems for rival design house Yves Saint Laurent, which didn't much care to be told that a color was suddenly off limits. The dispute festered until 2012, when it wound up in a federal appeals court in Manhattan. Judge José A. Cabranes ruled in favor of Louboutin, finding that "the contrast between the sole and the upper … causes the sole to 'pop' and to distinguish its creator." But the decision denied Louboutin in one respect: Its trademark of the red sole did not extend to shoes that were themselves red.
Even Owens Corning, which led the way for color trademarking, has had to defend its claim in court. When U.K. company Kingspan Insulation began selling pink-hued ductwork and roofing products in the U.S., Owens Corning's lawyers essentially had to argue the brand's claim to pink all over again. "As a result of its long usage and extensive sales, advertising and promotion," they argued, "the pink color mark has become distinctive and famous, and Owens Corning Intellectual Capital LLC owns an extremely valuable goodwill which is symbolized by the pink color mark."
For Cheerios, the legal fight has been long, but the recent defeat is apparently still not the end of it. "We are working to protect the iconic yellow color for our Cheerios box," a company spokesperson said in a written statement to Adweek. "We are evaluating our next steps."
Robert Klara
@UpperEastRob robert.klara@adweek.com Robert Klara is a senior editor, brands at Adweek, where he specializes in covering the evolution and impact of brands.


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German police seize thousands of orange 'Trump' ecstasy tablets
German police said they have seized thousands of ecstasy pills in the shape of Donald Trump's head (Police Osnabrueck via AP)
Thousands of ecstasy tablets in the shape of Donald Trump's head have been seized by German police.
https://www.independent.ie/world-news/german-police-seize-thousands-of-orange-trump-ecstasy-tablets-36058605.html
https://www.independent.ie/world-news/8ee77/36058604.ece/AUTOCROP/h342/PANews_P-2071a696-ac5e-48ee-9463-65131d54a634_I1.jpg
The drug haul has an estimated street value of 39,000 euros (£35,700).
Police in Osnabrueck, in north-western Germany, said they found the drugs while checking an Austrian-registered car.
They said the people in the car, a 51-year-old man and his 17-year-old son, told officers they had been in the Netherlands to buy a vehicle but had not succeeded so were returning home.
Officers said they found about 5,000 of the orange, Trump-shaped ecstasy tablets along with a large, but unspecified quantity of cash.
A judge ordered the father and son be kept in custody. The car was seized and towed away.
Nilima Marshall It is not just humans who are left - or right-handed. It turns out some squirrels are also strongly lateralised - that is, they actively favour one side of their body over the other.
The vast chasm between what the Sussexes said they wanted and what they got Britain
Democrats raise stakes in Trump trial as they push for new witnesses President Trump
Billy Keane: 'Dad was right when he made me promise never to go into politics - it's the dirtiest game of them all'
College, job and parenthood key life events that see people pile on the pounds
Going to college, getting a job and...
The vast chasm between what the Sussexes said they wanted and what they got
The Duke and Duchess of Sussex had boldly declared...

redpajama_set_name: RedPajamaCommonCrawl


Apache and Navajo culture, baskets and food [constructed title], 1900.
Title Apache and Navajo culture, baskets and food [constructed title], 1900.
Description Collection includes an article written by K.T. Dodge discussing the construction and decoration of White Mountain Apache Baskets, and a chart on the analysis of typical Navajo food. Items form a part of A.F. Whiting's Navajo and Apache ethnographic notes and papers (volume 1) entitled "Culture"


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2020 Road America Race Results
2020 Road America Race 1 Results
Arie Luyendyk Jr
Sheldon Creed
Robby Gordon
John Holtger
Zane Smith
Jett Noland
Zoey Edenholm
Barry Boes
Bill Hynes
Matt Brabham
2020 Road America Overall Weekend Results
Road America Weekend Schedule
2020 Road America Weekend Schedule
4:40pm-5:10pm – SST Practice/Orientation
9:40am – Practice
2:35pm – Qualifying
Saturday, August 8
10:15am – Race 1 (Prior to Xfinity Race)
3:35pm – Race 2 (After Trans-Am Race)
SST Returns To Action At Road America, August 6-8, 2020
CHARLOTTE, NC., (July 29, 2020) – After a 6 month hiatus due to COVID-19, the Speed SUPER Trucks 2020 season resumes on August 6-8 with the NASCAR XFINITY Series at Road America, located in Elkhart Lake, Wisconsin. This will mark the 3rd consecutive year that the popular SPEED SUPER Trucks Presented By Menards have raced at Road America.
The trucks will take to the track many times throughout the weekend, holding practice and qualifying on Friday, August 7th, and will run 2 high flying action packed races on Saturday, August 8th. The first United States race of the season will take place right before the NASCAR XFINITY Series race. The second SST race will begin upon completion of the Trans-Am race. You will not want to miss this, as both motos will count towards the overall win of the weekend.
As in previous years the Speed SUPER Trucks will run races that utilize the front half of the circuit, crossing between turns 5 and 13, as well as the entire 4-mile track. Some of the drivers expected to compete in this year's races include Matt Brabham, Robby Gordon, Bill Hynes, Sheldon Creed & local driver John Holtger. Stay tuned for other exciting names to be announced later this week.
"I am very excited to get back to racing at the famous Elkhart Lake Road America race track for the first USA race of our season. Road America has provided some awesome races in our SST trucks in the past two years and can not wait to see what we can do this year. The fans at this track have always welcomed us and we hope that we can put on a great show this year."
Fans are welcome at Road America! To purchase tickets, please visit www.roadamerica.com or call 800-365-RACE (7223).
Robby Gordon will appear on the Dale Earnhardt Jr Download on Thursday, July 30 on the NBC Sports Network at 6pm/et (3pm/pt)
2018 Road America SST Replay https://youtu.be/nyb3w69sHO4
2019 Road America SST Replay https://youtu.be/jTOyOOjOzVI
For more information, please visit us at www.stadiumsupertrucks.com
CBS Sports Network – Road America – September 26
CHARLOTTE, N.C. (September 25, 2018) – CBS Sports Network will broadcast the MENARDS Stadium SUPER Trucks at Road America, Rounds 13 and 14 of the 2018 Stadium SUPER Trucks World Championship from Elkhart Lake, Wisconsin, Wednesday evening, September 26 at 10 P.M. ET (7 P.M. PT).
Join Sean Sermini, and Australian Matt Naulty as they call all the high-flying action that took place during the SPEED Energy Stadium SUPER Trucks inaugural visit to the famed Road America back on August 24 & 25.
Both races contested at the picturesque permanent road course known as America's national park of SPEED, will be shown in their complete entirety.
Will Robby Gordon use his past experience at the track to his full advantage? Can current SST World Championship Points Leader Matt Brabham continue his points lead?
TEAM UFD enters the weekend with a different lineup of drivers looking to capture the podium in the MENARDS Stadium SUPER Trucks at Road America with first time SST competitor and NASCAR veteran Greg Biffle filling in for Bill 'The Thrill' Hynes, former open-wheel and NASCAR driver Casey Mears replacing Arie Luyendyk Jr., and open-wheel and Trans Am veteran Adam Andretti subbing for 2017 SST World Champion Paul Morris. With not much SST seat time between the three, action on track will surely be interesting. Rounding out the five-truck team will be Championship contender Gavin Harlien and Jeff Hoffman.
Australian import Tommy Dawson of the United Kingdom makes his first SST start on the ultra fast road course, while SST welcomes back Gold Coast, Australia native Matt Nolan to the series for the second time in 2018 joining SST regulars Cole Potts, Blade Hildebrand and Aaron Bambach for an extreme shootout in the Dairy Land.
Tune into CBS Sports Network Wednesday, September 26th at 10 P.M. ET (7 P.M. PT) to find out whom comes out on top in the MENARDS Stadium SUPER Trucks at Road America.
The Newly announced Robby Gordon Off-Road World Championships are to take place November 30, December 1 & 2 at the Glen Helen National MX Track in San Bernardino California.
Featuring a full field of Stadium SUPER Trucks, UTV's, two divisions of Motocross, Freestyle MX, and an amateur jump contest. Tickets are on sale now at https://stadiumsupertrucks.com.
Suites to enjoy the race in luxury are also available, along with vendor locations for the Off-Road Vender Village. Please email info@stadiumsupertrucks.com for additional information and pricing.
STADIUM SUPER TRUCKS COME TO ROAD AMERICA AUGUST 23-25
ELKHART LAKE, Wis., (October 17, 2017) – Road America announced today the addition of the SPEED Energy Stadium SUPER Trucks (SST) to the racing lineup for the NASCAR XFINITY weekend of August 23-25.
Led by the NASCAR XFINITY Series, the weekend also features SCCA Pro Trans Am providing non-stop, on-track action from three separate series' throughout the weekend.
The Stadium SUPER Trucks will take to the track many times throughout the weekend, holding practice and qualifying on Friday prior to the first SST race. The second SST race will take place in advance of the NASCAR XFINITY Series race on Saturday.
"We always enjoy adding more for our fans to experience and the Stadium SUPER Truck Series is the perfect combination for our fans and our facility," said Road America President and General Manager George Bruggenthies. "Wisconsin is truck country and this is going to be a new and incredible experience for our fans. We encourage everyone to stake out a good viewing spot because it's going to be wild watching these racers race, jump and fly through the air around our legendary racecourse."
The widely popular Stadium SUPER Truck Series features identically prepared 650-horsepower trucks that are built to take flight. Being able to race on virtually any surface thrown at them, the Stadium SUPER Trucks will race the front half of Road America, crossing between turns 5 and 13 as compared to the entire 4-mile circuit utilized by NASCAR XFINITY Series and the SCCA Pro Trans Am Series.
The Stadium SUPER Truck races will feature four 36-inch tall aluminum ramps placed in strategic locations on the racecourse, allowing the trucks to fly 20 feet off the ground and hundreds of feet down the racecourse.
"For Stadium SUPER Trucks to visit Wisconsin and America's National Park of Speed, I cannot be more excited," Stadium SUPER Trucks President Robby Gordon said. "Along with other racers, I've been fond of Road America for many years. To bring the door-to-door action and the big air of Stadium SUPER Trucks to Road America for the first time, the fans are going to be ecstatic for Stadium SUPER Truck racing."
The NASCAR XFINITY Series rolls into Road America August 23-25, bringing intense door-to-door stock car, sports car and now truck racing action to the nation's most intimidating road course. The NASCAR XFINITY Series schedule and the event could prove to be a pivotal race for drivers looking to improve their standing in the championship points. The event weekend will feature practice, qualifying and racing from the SCCA Pro Trans Am and the SPEED Energy Stadium SUPER Trucks.
Advance pricing for Road America season passes is available from October through December and 2018 event tickets and camping are now available. To purchase season passes, tickets or learn more about upcoming events at Road America, please visit Road America online at www.roadamerica.com or call 800-365-RACE (7223).
About Road America: Established in 1955, Road America is located midway between Milwaukee and Green Bay in Elkhart Lake, Wisconsin. The world's best racers have competed at this legendary 4-mile, 14-turn road circuit for over 60 years. The 640-acre, park-like grounds offer amazing viewing opportunities, fantastic concessions and high-speed excitement to hundreds of thousands of spectators each year. In addition to public race weekends, Road America offers a variety of group event programs, a new 1,200 foot Zip Line, the CTECH Manufacturing Motorplex for karting and supermoto, and the Road America Motorcycle and Advanced Driving Schools. For more information, visit www.roadamerica.com Follow Road America on www.facebook.com/RoadAmerica and on Twitter: @roadamerica or call 800-365-7223.


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Archives for the month of: May, 2014
Printing history podcast
Elizabeth Eisenstein
One of the most significant books I got to work on in my time was Elizabeth Eisenstein's The Printing Press as an Agent of Change. This 2-volume work was typeset in Cambridge, at the University Press, and printed and bound in in 1979 in America, at Halliday Lithograph Corporation. In those days the U.S. copyright laws mandated that, in order to retain copyright, books by American authors had to be printed in America. When a one-volume abridgment was published, The Printing Revolution in Early Modern Europe, in 1983, I was lucky enough to be the designer, as well as to shepherd it through the press. I confess the design doesn't hold up anywhere near as well as the U.K. design of the 2-volume work. This one we typeset in America as well as printing it here. Both books are still available, though in paperback only: the big book as a 1-volume tome, and the second in a revised (redesigned) 2nd edition. Sentimentalist that I am I rather think that books of this nature, about the history of making books, should be published in hardback. Paperback (or Kindle, and both works are available both ways) just seem to casual. I do recommend reading the book (one or other, or both), though.
Elizabeth Eisenstein, now in her nineties, is interviewed here — click on the Listen button below the copy — on the 24 May, 2014 broadcast of Library Café, a Vassar College radio program hosted by Thomas Hill. She sounds great, and has a detailed discussion focussed on her most recent book Divine Art, Infernal Machine: The Reception of Printing in the West (UPenn, 2011).
Check out the older podcasts: there are some interesting interviewees.
Categories Book manufacturing, Book printing, Book publishing, Letterpress
Reading the tea leaves at CUP
The Bookseller reproduced this address by the CEO of Cambridge University Press on 14 May, under the headline "Different strokes".
Far too much discussion of scholarly communication is bedevilled by generalised assertions about "what students want", "what researchers need", "what librarians require'", "what governments determine", when in practice the world is pretty diverse.
For librarians, the latest Ithaka Library Survey has rammed home that what they want is not at all uniform: what drives young and committed life scientists studying at Stanford or Cambridge isn't necessarily what drives all researchers under all circumstances.
One obvious area of divergence is take-up of digital. Print has remained important for longer than many had expected, and not just in territories such as Japan, where both institutional and cultural frameworks have slowed digital adoption. It's striking that most academics find journal articles digitally but tend to read hard copies of those longer than half a dozen pages. It is commonplace that the more influence a university's faculty has over acquisition policy, the slower the take-up of digital books in the university's library.
I'm sure generational shift has started to change that, and that lack of digital availability means invisibility to the consumer. But at Cambridge University Press we aren't at all unusual in still having the majority of our global academic book sales in hard-copy form, despite the rapid growth of digital. There was a big feature in the Times Higher Education Supplement in March on "Publishing Your First Book", in which various senior academics were canvassed for their dos and don'ts: what struck me was the resolute assumption by everyone that this "first book" would be a printed artefact first and foremost. Digital availability wasn't mentioned by a single respondent. That's changing, but there's some way to go.
That flags another divergence between humanities and sciences and the differing fortunes of long-form research books. For many arts and social science scholars, it is the research article or book itself where the value lies, as opposed to the applications or replications to which that research might be put (which lies behind the dominant science perspective).
Schizophrenic views
Incidentally, no fewer than half of the members of the History faculty of Cambridge University enjoy the services of a literary agent, primarily engaged in selling the fruits of their research and their content (the two being one and the same). This divide has been at the heart of much of the recent debate between historians and life scientists. It also informs the frankly schizophrenic views of many universities about Patent Law (of which universities are generally warm and protective supporters) and Copyright Law (against which some universities rail, as restrictive, expensive and protectionist).
What's clearly endangered is the long-form scientific research book, whether in print or online. The incentives for scientists to write long-form content are clearly in decline. Pressure on scientists to produce more frequent outputs is one cause. Another is the need to get work out rapidly because of global competition. The English language is now pretty dominant in advanced scientific communication (though not at all in arts and social sciences). That may also discourage some non-native Anglophone scientists from writing 300-page monographs. It is quite possible that within the next five to 10 years, long-form science research publication—outside the arenas of textbooks and popular science—may be a tiny fraction of what it is today.
There are more general questions about the future of academic books. We're taking part in several Open Access (OA) experiments, but I don't yet see signs of culture and practice changing much.
The final area of divergence to highlight is around OA journals. Rick Anderson, a librarian at the University of Utah, gave a recent thoughtful address to the Smithsonian on OA. He was trying to bring some cool and dispassionate sanity to what remains all too often an area of messianic claim and counter-claim. One thing Rick is surely right to emphasise is that OA publication is at present a minority activity. One abiding reason is that for many tenured faculty in established institutions, the current system isn't broken sufficiently to provoke them to the personal inconvenience of changing their own publication practices. It is very striking—and entirely understandable—how much of the advocacy pressure for OA has come from those who feel themselves disenfranchised by the current system, and from those who feel that the current system only speaks to, is only accessible to, those within the ranks of the resource-privileged. The latter perception matters a lot more, it's self-evident, to some faculty members than to others.
There is also marked variation in the take up of OA by subject. Within science journals, life sciences are clearly leading the way, driven by funders' requirements, but certain areas have barely moved—chemistry, for example. And in subjects driven by individual endeavour rather than large grant-funded teams—such as humanities, history and my own field of mathematics—peer-reviewed OA remains a very small proportion of published articles.
Finally, it's striking who OA payments are going to. One of the first major analyses of OA funding was published by the Wellcome Trust a few weeks ago. Four publishers accounted for more than half of Wellcome's total funding for article processing charges in 2012/13. It's possible gold OA will lead more to market consolidation rather than disruption. Nonetheless, the tide of governmental and funder sentiment—particularly in the UK—is flowing in one direction only. The challenges this poses are considerable, especially in book-based disciplines in the arts and social sciences.
Peter Phillips is chief executive of CUP. This is an edited extract of his address to the 16th Fiesole Collection Development Retreat
Categories Book publishing
Anyone who is an editor for long enough will accumulate a list of books they rejected which went on to success elsewhere. Sometimes you are just wrong; sometimes the book doesn't fit; sometimes the timing is wrong. At Cambridge we used quietly to acknowledge the rejection in the late 1870s of The Philological Society's proposal for a new comprehensive English Dictionary. This was quite possibly the right decision, at least in the short and medium term. The Syndics saved their money; the Delegates hazarded theirs — and the return was a long time coming. The Oxford English Dictionary may not have made Oxford University Press much if any money till the invention of the internet and the need for on-line dictionaries. Prestige of course is a different matter.
Here's a list from io9 of fairly famous sci-fi books which suffered rejection by publishers. These books, from io9 too, were rejected by their authors (disowned) after publication. Stephen King is on both lists.
One example: a rather parodic effort by Arthur Fifield, addressed to Gertrude Stein in 1912, turning down The Making of Americans. I wonder how she took it.
Paper over those cracks
If we are really living through a long-term (if perhaps slower than feared) decline in print as against e-books, we are also going to see effects in the supply chain for books. Here's Bob Sacks' comment on a Dead Tree Edition piece about proposed price increases in the struggling graphic paper market.
"I have been predicting the survival of print, and my steady position for the past decade has been that printing will be/must be a luxury item and that means paper will be, too. For everyone's survival both print and paper need to cost more. That is the brutal honesty of the situation. Print is no longer the commodity that it once was, and as the numbers continue to decrease, the scarcity of the product is on the increase.
There was a time when newsstands were plentiful and all participants in the process – retailer, publisher, printer and paper maker – were rolling in success. It was almost like printing money. Those days are gone, and each component of the supply chain is striving to understand what happened and how they could have gone from riches to rags in a decade."
This seems dead-on to me. I've been moaning on for some time about the long-term effects of the rise of digital on the book manufacturing industry, and obviously paper is a big part of that picture. It's not so much that we will decide to stop printing books, it's more that by printing fewer and fewer as e-books take a larger share of the market, the sources of cheap printing will disappear — so we'll no longer be able to afford to print the short runs we have become used to. "Printing" will remain, but either as POD or de-luxe editions, with similar unit cost implications in both cases. While printed books will still be available, their prices will be sharply higher than they are today. It's tough to see a large sustainable business built on this model.
Categories Book manufacturing, Book publishing, Paper
Edible books
We had drinkable books, so inevitably we now have edible ones too. Here, courtesy of Book Patrol, is La Bibla de Churrasco.
They also posted about a lasagna book.
The trouble with these books is of course that you end up consuming them, so you can't really, as Tramontina claims, put them on your shelves. One might think the e-book applications may be tough to implement, though a Cambridge (UK) company called Dovetailed has just announced 3-D printed fruit — so we may live in hope. This story from 3-D Print was delivered by Slashdot. The Dovetailed website has a video showing a rasp being printed, and consumed with apparent gusto.
Categories Book printing
My step-father used to read Mickiewicz's Pan Tadeusz over and over again (it's apparently a required activity for all Poles). He'd often read in the bath, like 7% of the respondents to this survey by Love Reading sent by Book Patrol. Occasionally he'd fall asleep while reading so we'd end up with a book, swollen and deformed, which was constantly having to be dried out.
Book Patrol has lots of odd stuff. This alphabet by Vladimir Klitschko is right up there. Love Reading, a book recommendation site, can be found here.
Format agnosticism
I can remember writing a memo sometime in the dying years of the last century (well before the Y2K worries — how many colleagues now even know what that means?) about format agnosticism. It was addressed to all departments and had the cutesy title "Pray tell, pray tell, what's SGML?". At its heart was a diagram a bit like this (conceptually if not in fact — I can't remember exactly):
We (primarily, but not exclusively, in academic and reference publishing) are really engaged in creating an ever-growing archive of content divided into chunks each of which started off as a "book" in the mind of an author, but along the road became another entry into the ever growing "Publisher X Archive". If we create it as such we will be able to exploit it in a variety of formats, one of which for the foreseeable future remains a printed book. This is all pretty commonplace now, but it did take more than exhortation to change the thinking of a lot of people, and not just the old lags. We can still find corners of our business which harbor the belief that what we are engaged in is producing books (printed of course) with other applications recognized as valid and valuable of course, but nevertheless seen as secondary. Anyone in academic publishing who still really thinks that this is what we are doing every day should probably be thinking about an alternative career.
In general I do think that book publishing is making a better go of the digital transition than many other businesses. The music business made a fine job of the transfer from anaolg to digital (all those CDs) but came a bit unstuck on the on-line transition. Newspapers are struggling, and it was received wisdom that The New York Times was doing a better job than others. That may still be true — they do have a pretty good website, and have managed the paywall question successfully, but this recently leaked report, commented on by NPR's On the Media shows that digital thinking is proving as hard to inculcate as it is in those corners of the book business alluded to above. The most telling problem is the adherence to the daily news cycle, with all content being readied for the evening, rather than for constant release during the day. Now I do know that content is released to the on-line paper during the day — so I guess this attitude of mind is not quite as universal as the radio story suggests. Listen to the On the Media story here. The Scribd version of the report, linked to above, omits a few pages. If you want the full report this link to Mashable will take you to it. These references were brought to me via SHARP.
We have of course no guarantee that book publishers will continue to negotiate the transition so well (or so fortunately). The current price negotiations between Amazon and Hachette hint at more bits of our lunch being grabbed by our major supplier. This Let's Get Visible post by contrarian indie author David Gaughran gives a good, if partisan, picture of the situation. What will be the outcome of this struggle? I can't believe that we have any choice but to meet the threat head-on — i.e. to start selling on-line ourselves.
Diversity in children's books
NPR's Weekend Edition Sunday did a piece the other day on the lack of diversity in the characters in children's books. You can listen to it here.
Apparently only 1.3% of the characters in today's kids' books are African American. We have obviously come a long way from my childhood when unrepentantly racist characters abounded in the colonial-era books then current in Britain. I recall in particular Epaminondas ("You ain't got the sense you was born with") and Little Black Sambo. We are no doubt better off without these folks (though I'm slightly surprised to find them both featured at Amazon) — but it seems we omitted the other part of the correction, having failed to replace these caricatures with other, better role-models. First Book seems to be determined to do something about it, pledging to buy 10,000 copies of books by and about underrepresented groups.
Drinkable Book
This seems like a really good idea, even though many of the people who need it may not be able to read the text printed on the pages made from specially treated "filter-paper".
The Huffington Post has the account. NPR did a story on it.
Categories Book printing, Book publishing
Secure e-book reading
"The U.S. Navy will soon supply its submariners with a new e-reader — the Navy eReader Device, or NeRD. The NeRD, by Findaway, comes with a library of 300 titles, including fiction from Tom Clancy and James Patterson, as well as classics and naval history. The NeRD is designed to thwart security concerns raised by cameras, network connectivity and data transferability on regular e-readers and tablets."
Story from Shelf Awareness, 9 May, 2014
Apparently Findaway World has supplied audiobooks to the military since 2007. Makes me think of Len Edgerly's Ebooks for troops organization.


Johnson & Johnson and its subsidiary company Ethicon were hit with a $41 million vaginal mesh verdict last month. Of that amount, some $25 million was awarded in punitive damages against the company.
While Johnson & Johnson might be a household name, the names of its subsidiary units are a bit less well known. Names like Ethicon and DePuy fly under the radar for all but those that have been negatively affected by their products' defects while Johnson & Johnson remains known as the makers of the "no more tears" baby shampoo.
Johnson & Johnson's Ethicon manufacturing unit suffered a staggering loss in a Philadelphia courtroom recently when a jury awarded Ella Ebaugh $57 million for the pain and injury she suffered as the result of a pelvic mesh implant.
Ethicon's decision to pull its Physiomesh surgical mesh off the market earlier this year is just one more in a string of failures for the medical device unit of Johnson & Johnson. The decision comes from mounting evidence of a higher number of revision surgeries associated with Physiomesh than with other similar surgical mesh devices.
Kentucky has followed California and Washington and filed a multimillion dollar lawsuit against pharmaceutical giant Johnson & Johnson and its Ethicon unit. Ethicon is the branch of Johnson & Johnson that handles medical device manufacturing.
The FDA previously advised doctors to stop all use of power morcellators while the devices' propensity to spread cancer was reviewed. Now J&J is pursuing a global, voluntary return of its power morcellator devices. An article in Reuters reports that this move comes as a result of concerns that the surgical device potentially spreads cancerous uterine growths in women.


text:
Occupational hazards of war depleted uranium: all the questions about du and gulf war syndrome are not yet answered rosalie be
International Journal of Health Services, Volume 36, Number 3, Pages 503–
520, 2006 2006, Baywood Publishing Co., Inc.
Occupational Hazards of War
DEPLETED URANIUM: ALL THE QUESTIONS ABOUT DU AND
GULF WAR SYNDROME ARE NOT YET ANSWERED
Rosalie Bertell
For 15 years, the debate about depleted uranium (DU) and its detrimental effects on the
health of veterans of the Gulf War of 1991, on the Iraqi people and military (and
subsequently on the people of Kosovo, Afghanistan, and Iraq during the second war) has
remained unresolved. Meanwhile, the number of Gulf War veterans who have
developed the so-called Gulf War syndrome has risen to about one-third of the 800,000
U.S. forces deployed, and unknown proportions of those involved in the subsequent wars.
Uncounted civilians and personnel of other nations that fought in Iraq and other wars
since 1991 have also been afflicted. The veterans have suffered from multiple serious
physiological disorders and have received little or no official recognition, medical relief,
or compensation. We need to take another look at this issue, using a holistic and
interactive model for the toxic matrix of exposures, identifying the major roadblocks
to resolving the scientific questions, and finding appropriate medical and political
responses. This commentary is such an attempt.
One of the novel exposures of the Gulf War of 1991 was the depleted uranium (DU)
missiles, rockets, and armament. Uranium is a radioactive heavy metal, one that has no
positive biological use. Exposure to DU during the Gulf War occurred along with
exposure to other heavy metals well known to cause havoc with the cellular immune
system . ―D epleted uranium ‖ is an industry term for uranium w aste from the
enrichment of uranium ore, which concentrates the isotope uranium-235 for use in
nuclear bombs or nuclear power reactors. It makes up the largest amount of radioactive
waste globally, related to the nuclear industry (excluding mining waste). In the United
States, DU must be handled by persons trained in radiation safety and must be isolated
from the biosphere according to strict regulations
Uranium-238 (U-238) is an alpha emitter with rare spontaneous fission. The alpha half-
life of U-238 is 4.5 billion (4.5 x109) years. It decays to thorium-234 (Th-234), which has
a half-life of 24.1 days and is a beta and gamma emitter. Thorium-234 decays to
protactinium-234m (Pa-234m), an isomer of Pa-234, which has a half-life of 1.17
minutes and is a beta emitter. Protactinium-234m decays to Pa-234, which has a half-life
of 6.7 hours and is an alpha emitter. Effectively, in four to six months after it is discarded
from the enrichment facility, freshly produced DU, composed mostly of U-238, through
these continuous radioactive transformations becomes a mixture of U-238, Th-234, Pa-
234m, Pa-234, and U-234 in equilibrium proportions. The first two decay products, Th
and Pa, along with U-238 account for most of the alpha, beta, and small amount of gamma radioactivity of the mixture (1, p. 11). With air friction or impact on a hardened target, uranium bursts into flame. The temperature of this spontaneous metal fume produced by DU is between 3000°C and 6000°C. This is in contrast to an Iraqi ambient temperature of 22°C to 45°C or the 575°C fire produced by TNT in other wars. At this high temperature the uranium oxide becomes ceramic-like, and insoluble in body fluids (2). For this reason, once inhaled, it provides a chronic source of uranium heavy metal and contact radiation poisoning within the body. Other heavy metals, in addition to DU, especially mercury, lead, arsenic, and cadmium, were used extensively in the Gulf War. They were contained in pesticides and herbicides; in vaccines, including anthrax and botulinum toxin; in nerve agents: sarin, cyclosarin, tabun, soman, VX, multiple seven, and novachuks (novichoks); and in chemicals released from the Kamasiyah toxic chemical depot, which was destroyed by bombing. Many veterans were also subjected to petroleum products and the horrendous oil well fires (3). Most had very little training for handling these hazardous materials, and no protective clothing or respirators. One focus of the dispute about Gulf War syndrome (GWS) has been whether or not the use in battle of DU weaponry could be one of the principal causes of the disabling syndrome. The first roadblock to clarifying this scientific hypothesis results from focusing on only one item at a time to which veterans were exposed in battle and attem pting to ―prove‖ that it w as or w as not one of the m ain causes of their serious illness. One could attempt to do this for each pesticide, vaccine, toxic chemical, and heav y m etal sep arately, p reten d in g to ―p ro v e‖ fo r each th at it w as not the cause. Such reductionist discourse confuses the true issues and delays research into treatment and legal recognition of harm caused. It leads one to the absurd conclusion that the veterans are not really sick— that the problems are all in their imagination. Influential papers by physicists and several semi-official governmental organizations have attempted to eliminate DU from consideration by just such analyses (4– 8). These studies are not really independent, since each follows the guidelines, methodology, and risk estimates recommended by the International Commission on Radiological Protection (ICRP) (9). Since the U.S. Research Advisory C o m m ittee o n G u lf W ar V eteran s' Illn esses has ruled out psychiatric illness as a cause of GWS (3), it is important to look again. at all the circum stances associated w ith the use of D U , including uranium 's heav y m etal as w ell as radiological properties, and their combined effects on the immune, neurological, hormonal, and reproductive systems of exposed veterans and civilians. A damaged immune system leaves one vulnerable to all sorts of viral, bacterial, electromagnetic, radiological, and toxic metal exposures. The hormonal system regulates homeostasis, the nocturnal resting cycle (for repair), and kidney clearance rates of heavy metals. When evaluating DU use in war, we must do so within this total toxic matrix. ANALYZING THE RADIOLOGICAL HAZARD Uranium-238 is radioactive, an alpha emitter with rare spontaneous fission. As noted above, freshly produced DU, composed mostly of U-238, becomes a mixture of U-238, Th-234, Pa-234m, Pa-234 and U-234 in equilibrium proportions within about six months. The first two decay products, Th and Pa, along with U-238 account for most of the alpha, beta, and small amount of gamma radioactivity of the mixture. One microgram (1 x10-6 gram) of pure U-238 undergoes 12.4 atomic transformations (submicroscopic explosions) every second, each giving off one alpha particle with energy between 4.15 and 4.2 MeV (million electron volts) in random directions. It only requires 6 to 10 eV (electron volts) to break the nuclear DNA strand in a cell. In one day, 1 microgram of pure U-238 would release 1,071,000 alpha particles, each with more than 4 MeV of energy, into the organ or tissue where it was lodged. The spherical range of these alpha particles is about six cells. The radioactivity emitted by the mixture of uranium and its decay products is even greater. The spontaneous fission half-life for U-238 is estimated to be 8.5 x1017 years, which, although much longer than its alpha decay half-life, results in approximately two atoms of U-238 in every milligram of uranium decaying by this process each year. When it decays by spontaneous fission, U-238 releases approximately 40 times more energy than in nuclear decay (1, p. 6). The widely accepted scientific causality methodology for analyzing radiation dose-response includes a mathematical model predicting damage to the cellular DNA resulting from a homogeneous spread of ionizing radiation over the critical organ(s), weighting the organ dose to approximate whole-body exposure, and using a risk formula to estimate the expected number of fatal cancers due to that dose. If the calculation yields only a small expected number of cancer deaths, the radiological hazard is declared to be trivial. This ICRP methodology assumes that the affected persons care only about cancer death, that they have normal physiological health and intact cellular repair systems, and that no other life-threatening exposures confound the radiation experience. The methodology assumes that radiation effects are independent of the effects of the toxic matrix and can be separately ruled out using a radiation-exposure-specific mathematical formula recommended by physicists on the main committee of the ICRP. Whether an assumption of homogeneous spread of the energy over the organ in question is reasonable under the circumstances, whether the estimates of the amount of radiation inhaled are accurate in the confusion of the battlefield, whether the cellular repair system is working, whether the clearance rate for heavy metals by the kidneys is normal, or even whether cancer is meaningful as the biological endpoint of concern for veterans— all makes no difference. These details seem to be irrelevant when applying this ―objective‖ m ethodology. In this report I will show that this trusted methodology is especially inappropriate and misleading in the case of Gulf War syndrome. The mathematical equation contains no terms for dealing with cellular repair dysfunction, damage to mitochondrial DNA, and synergistic effects with a variety of toxic metals, halogens, and complex nano-debris. Inhalation of airborne nano-debris is especially difficult to measure, since this debris can theoretically remain in the air forever by Brownian motion, or can suffer multiple resuspension events if it does fall to the ground. In war, the build-up of this airborne debris is cumulative. ORIGIN AND LIMITATIONS OF THE PHYSICS METHODOLOGY In 1945, the physicist Erwin Schrödinger published what became one of the most influential monographs of the incipient atomic age. In What Is Life (10) Schrödinger gave the central and primary informational role in life to the nuclear DNA. He found it to be the basis of all organic existence, and he explained it well in terms of fundamental physical and quantum principles. This was a brilliant thesis, and it was followed in 1953 by W atson and C rick's discovery of the m ethod of DNA replication. DNA was spectacular news in the scientific world at this time. However, nuclear DNA, while central to protein production and human reproduction, failed to describe the many seemingly unrelated life-support mechanisms, including the tasks of mitochondrial DNA, which also go into making the cell functional. The developing science of radiobiology accepted the thesis that nuclear DNA was the essential molecule of radiosensitivity, and this focus continues to strongly influence decisions about the potential hazard of exposures to ionizing radiation, even in 2006, as nations are called upon to deal with the complex Gulf War syndrome. We now know that cellular organelles, cell membranes, and biochemical reactions within the cell are crucial when assessing the simultaneous damage caused by internal radiation, heavy metal contamination, and nano-particles. The radiation dose-response methodology, developed from studies of high-level radiation, seems to work by masking the low-dose effects. It is not appropriate for understanding low-dose DU exposures, because radiation, heavy metals, and other toxic chemicals can destroy the functionality of the cellular respiratory system (the mitochondria), disrupt the chemistry of enzymes and hormones, frustrate normal cellular detoxification and repair, and leave the person alive but chronically ill. Also at low doses, many other toxic agents become potentially synergistic or significant confounding variables for any radiation toxic effect. As I will show, a system approach is more fruitful, and for the individual, the two most important systems to examine are the cellular immune system and hormonal system. Critical for civilization and survival is human reproductive health. The ionizing radiation exposure in the first Gulf War included, in addition to DU, exposure to nuclear debris caused by the bombing of the Iraqi experimental nuclear reactors and spent fuel pools, and radiation from the Doha explosions and six-day fire that consumed DU ordnance stored at the U.S. military depot near the border with Kuwait. No one single radiation dose would comprise all these many levels of radiation exposure experienced by military and civilian personnel. These various exposures would be cumulative. TOXIC CHEMICAL AND RADIOLOGICAL DAMAGE TO CELLS Depleted uranium powder is pyrophoric, and spontaneously creates an invisible metal fume (often called an aerosol) when exposed to air friction or impact on a hardened target. The nano-particles created in the metal fume, when inhaled, can cross the lung-blood barrier, penetrate cells, and provide the maximum dose to tissue (contact dose from a maximized surface area-to-volume particle, with little self-shielding), creating free radicals and oxidative stress within cells. Some scientists believe that the oxidative stress caused by u ran iu m 's heavy metal properties is even more damaging than its radiological properties. Total oxidative stress causes failure of protective enzymes, leaving cells vulnerable to viruses and mycoplasmas. Damage to the cellular communication system and the mitochondria; heavy metal replacement of magnesium in molecules that normally function as antioxidants; an d d estru ctio n o f th e b o d y's rep air m ech an ism s, have serious consequences including chronic disease and tumorogenesis. Some cellular mechanisms are of special interest here. For example, after a protein, sequenced by the DNA, is properly synthesized by the RNA, it has to undergo a process of folding. This gives it the proper three-dimensional shape to carry out its functions and chemical reactions. Biochemists now believe that proteins do not fold spontaneously into their final, active conformation (11). Proteins destined to be embedded in the cell membrane or to be secreted from the cell are synthesized in the endoplasmic reticulum, where templates, enzymes, and sugars promote some protein conformations and inhibit others. This is delicate work with sequential rounds of intricate modifications, overseen by the cell's quality-control system. Free radicals can totally disrupt this process, forming unusual molecules; and in the presence of heavy metals, the process may use trace amounts of toxic metals to replace the normally used zinc and manganese. Improperly folded proteins can fail to be routed to the cell membrane or to a gland where, as hormones, they are needed to release biochemical signal molecules. Some diseases caused by misrouted proteins include cystic fibrosis, diabetes insipidus, and cancer (12). Widespread misfolding of proteins can lead to cellular stress, clogging of the system, and an accumulation of imperfect proteins. Many scientists now believe that accumulation and aggregation of misfolded proteins is responsible for neurodegenerative diseases, as well as early-onset A lzh eim er's d isease, P ark in so n 's disease, and diabetes mellitus. In these diseases, proteins or protein fragments convert from normal, soluble conformations to insoluble, sticky fibers called amyloids. Amyloids coalesce into fibrillar aggregates that have a characteristic structure. The insoluble clumps can form either inside or outside cells. Misfolded proteins are a central pathogenic mechanism, and Gulf War veterans have manifested many of the symptoms of these neurodegenerative diseases. THE PROBLEM OF AMYOTROPHIC LATERAL SCLEROSIS Amyotrophic lateral sclerosis (ALS; commonly kno w n as L o u G eh rig's d isease) is being diagnosed at about twice the expected rate in young Gulf War veterans relative to veterans who did not serve in the first Gulf War (confirmed in September 2004 by the U.S. Research Advisory C o m m ittee o n G u lf W ar V eteran s' Illn esses). Normally, ALS is diagnosed after the age of 55 years, but most of these Gulf War veteran patients are younger. In two-thirds of the 40 cases, the patients are between 20 and 54 years old. ALS is officially listed as ―of unknow n cause.‖ H ow ever, it seems clearly related to the failure of anti-inflammatory and antioxidant enzymes, together with mitochondrial dysfunction. ALS was thought to be caused by the death of motor neurons. Recent data suggest, however, that neurons do not so much die as they are killed by surrounding cells called glia. The glia usually support and nourish neurons, but they can become dysfunctional and toxic in certain diseases. This p ro cess is called ―n eu ro -in flam m atio n .‖ Cytokines are small proteins that communicate between neurons and glia cell types (13). The cytokine signaling is, in turn, regulated by major lipid metabolic pathways. Recent data suggest that neuro-inflammation in a mouse model of ALS is caused by dysregulated cytokine signaling. Michael Vickers (14) has documented that even microgray doses of ionizing radiation cause inflammation of the blood vessels and can initiate the arachidonic cascade, with its well-known sequel of damaging effects on the body. Arachidonic acid is the lipid produced when fatty acids in various states of oxidation mediate inflammatory reactions in the blood and other cells. This certainly merits further study, since ALS is a very serious and unexpected outcome for these Gulf War veterans. An unusually high incidence of A L S an d P ark in so n 's d isease in in d ig en o u s populations in Guam and Papua New Guinea suggests a possible correlation between the diseases and local environmental conditions, including high levels of aluminum and low levels of calcium and magnesium in soil and food. As in A lzh eim er's, h u m an s w ith th ese disorders tend to have high levels of aluminum in some areas of the brain, although it has not been demonstrated that the presence of aluminum in the brain initiates the onset of the diseases. It has been suggested that other possible contributing factors need to be examined more closely, including the diet of the Guam population— in particular, the seeds of the false sago palm, which contain a toxic amino acid that causes a condition similar to ALS in monkeys— as well as the possibility that the dementia is caused by genetic rather than environmental factors (15). Both potential factors— the false sago palm and genetic factors— seem to be absent in the Gulf War cases, but exposure to aluminum and depletion of calcium and magnesium were present. Guam and Papua New Guinea likely received some fallout from U.S. and U.K. nuclear bomb tests in the Australian and Pacific areas, which may have introduced unexamined internal radiation exposure factors that would clarify this mystery. IMMUNE AND HORMONAL SYSTEMS DAMAGED IN THE GULF WAR The DNA of mitochondria is 16 times more sensitive to radiation than is nuclear DNA. This is because mitochondrial DNA has no protective histone proteins, like those within the cell nucleus (16). It is well known and well accepted in the scientific community that ionizing radiation produces free radicals (molecules with one or more unpaired electrons) in living cells, which are composed mostly of water. It does this because of its ionizing energy deposit, which knocks an electron out of orbit, creating a positively charged atom or molecule with at least one unpaired electron (a positive ion) and a free electron (a negative ion). Because another molecule can easily pick up the free electron, causing a chemical reaction, free radicals can effect dramatic and destructive changes in the cell and in the intercellular fluid. Karl Z. Morgan, the renowned health physicist, described this effect as ―a m ad m an in a library.‖ All cells contain an endogenous antioxidant in the water-soluble part of the cellular fluid, which normally deals with free radicals. This antioxidant, called glutathione (GSH), repairs most cellular structures that are damaged and oxidized by free radicals. It can also detoxify many electrophilic mutagenic threats to the cell. This antioxidant function of GSH is normally credited as having cancer-protective properties, since it neutralizes free radicals. Cellular repair mechanisms depend heavily on the presence of GSH in cells. Another function of GSH is to rid cells of toxic heavy metals. Heavy metals bind with the GSH and are carried out of the cell and to the gallbladder, for excretion in bile. This process is a mechanism for depleting the GSH, as well as for ridding the cells of heavy metals. Hence heavy metals, such as DU, deplete GSH at the time when it is most needed for its protective cell-repair and antioxidant work. Individuals may have more or less GSH by nature or through exposure history. Yet this is one of the main biochemicals needed for the repair mechanisms on which the physics methodology for calculating radiation dose-response depends for its applicability. Superoxide dismutase (SOD) is another chemical, an enzyme produced both by the liver and in the mitochondria of all cells, which acts as an anti-inflammatory and antioxidant. The body needs zinc, copper, and manganese to produce sufficient functional SOD. Toxic metals can replace the manganese, making the SOD dysfunctional, or the cell can merely run out of SOD because of overdemand for antioxidants in the mitochondria. This overdemand can also deplete the manganese needed for protective enzymes in the cell, leaving it open to viral or bacterial invasion. SOD also varies in abundance and can be damaged by a variety of chemicals. Mercury and arsenic are found in pesticides and fungicides, and in vaccines. Nickel is a component of steel, which can be vaporized in a DU metal fume. Nickel can deplete the b o d y's zinc stores, compromising the SOD cellular immune system. These other metals also play parts in the breakdown of cellular functions. Thus heavy metal exposure causes oxidative stress that weakens the cellular repair mechanism, which would normally provide some protection against low-dose radiation exposure from DU. Disturbance of Thyroid Function Trace amounts of inhaled or ingested aluminum from inoculations, aluminum food wrappings, cooking utensils, salt, baking powder, beer, soft drink cans, or other sources could combine with fluorides from hydrogen fluoride released from oil well fires, fluoridated drinking water, soft drinks, toothpaste, or foods (made with fluoridated U.S. water) to form a pseudo-hormone that mimics the thyroid-stimulating hormone (TSH)— even confusing medical tests for thyroid dysfunction. Hormonal damage to the thyroid and pituitary glands, which regulate metabolism, has severe repercussions for every organ system in the body, including the brain. Aluminum fluoride compounds act like TSH, which regulates the thyroid hormones T-3 and T-4. When persons are subject to trace aluminum and fluoride, they exhibit the same symptoms as in hyperthyroidism. This pseudo-TSH bypasses the pituitary control of cell metabolism, drives up mitochondrial activity, and depletes the selenium-GSH in all cells (17). Aluminum fluoride compounds provide another mechanism that interferes with cellular repair of radiation damage due to DU. The aluminum fluoride compounds do not clear from the body as does TSH. The highly electronegative effects of the fluorides cause long-term (almost permanent) bonding to the TSH receptor sites of cells. This process greatly disturbs the normal pulse and amplitude processes of pituitary control by TSH and damages the cellular nocturnal repair processes, overworking the GSH in cells. Authentic TSH provides for the normal sleep cycle, which helps the body recover from toxic shock. Sleep deprivation can lead to many functional problems. Aluminum fluoride complexes have been widely used in laboratory investigations for stimulation of various guanine nucleotide– binding proteins (called G-proteins). These complexes can simulate phosphate groups in many biochemical reactions. It is evident that an aluminum fluoride complex gives false information, which is then amplified by cellular processes of signal transmission, influencing the G-proteins that carry signals from numerous receptors to the cell interior (18). Serious aluminum fluoride problems have been reported at the St. Regis Akwesasne Indian Reserve on Cornwall Island, New York State, downwind from the Reynolds Metal Company aluminum smelter. At Oak Ridge, the U.S. Department of Energy nuclear weapons facility, illnesses similar to GWS are increasingly encountered. These illnesses have not been diagnosed and many go untreated. Aluminum and hydrofluoric acid, as well as DU waste, are part of the pollution of this and other Department of Energy facilities. Victims of the environmental disasters at the weapons facilities report muscular and skeletal problems, nervous system disorders, anemia, rashes, irritability, high blood pressure, and thyroid problems (19, 20). Heavy metal exposure (including uranium) can cause loss of cellular immunity, autoimmune diseases, joint diseases such as rheumatoid arthritis, and diseases of the kidneys, circulatory system, and nervous system. Heavy metals supplant the normal calcium and other minerals in enzymes, and cause these molecules to lose their important functions in the body. Peroxynitrite, a toxic product of the free radicals nitric oxide and superoxide, can also degrade the functions of respiratory enzymes (21) and inactivate the manganese-SOD enzyme (22). Decline in functional mitochondria is most damaging to those organs that have the highest energy demands per gram of tissue—namely, the heart, kidney, brain, liver, and skeletal muscle, in that order (16, 23). These organs become poorly protected against irradiation from circulating uranium particles, as well as various other pathogens. Mycoplasmal Invasion Related to Depleted Uranium Exposure Failure of cellular immunity leaves an organism vulnerable to viral, bacterial, and mycoplasmal invasion. Mycoplasmas are small bacterial organisms. Lacking cell walls, they are capable of invading several types of human cells and are associated with a wide variety of human diseases. Several separate laboratories in the United States (e.g., Dr. See at the University of California, Irvine, and Dr. Lesko of Del Mar, California) have identified mycoplasmal organisms in patients with chronic fatigue syndrome and Gulf War syndrome. The percentage of positive findings for mycoplasma ranged from 60 to 80 percent of patients examined. Research by Drs. Garth and Nancy Nicolson of the University of Texas M.D. Anderson Cancer Center resulted in the discovery of Mycoplasma incognitus as one cause of the symptoms of GWS. Their daughter had returned from the Gulf with the syndrome. Normal laboratory blood tests do not detect M. incognitus. The only way to detect this mycoplasma is to use a sensitive genetic marker analysis. Even with this method it is difficult to detect, because unlike conventional bacteria, the mycoplasma is found mainly inside cells and not in body fluids (24). Mycoplasma incognitus causes chronic fatigue, recurring fever, night sweats, joint pain, stomach upsets, stomach cramps, headaches, skin rashes, heart pain, kidney pain, thyroid problems, and, in extreme cases, autoimmune-like disorders. Certainly there was nothing normal about the metabolic responses of Gulf War veterans to the radiation injuries from DU. While it is credible that uranium was not responsible for all the sickness experienced by the veterans, it clearly was not as minimal a component as would be indicated by the mathematical approach used in physics. The mathematical approach cannot predict what DU exposure would cause in this situation, since the chemical and biological reactions are interdependent and find no accommodation in the mathematical formula. DEPLETED URANIUM IN BATTLE VERSUS URANIUM OXIDE IN MINES OR MILLS Uranium oxide, as found in uranium mining and milling, has provided much of the information used for the official understanding and evaluation of exposures to DU in the first Gulf War (5). DU exposure in war differs, however, in that uranium oxide in the mining and milling situation is dust— visible particles of, on average, 5 microns aerodynamic diameter. Some of the inhaled uranium in war will be similar to this mine dust, but the aerosolized uranium oxide from a metal fume, produced through air friction or impact on a hardened target, is invisible, with an aerodynamic diameter between 1 nanometer and 2.5 microns. Size is an important factor for inhalation. Particles with an aerodynamic diameter less than 2.5 microns can penetrate into the deep lung alveoli. When the aerodynamic diameters are in the nanometer range, particles easily penetrate the lung-blood barrier and are carried throughout the body. The aerosolized molecule may well be a crystal with a different number of oxygen atoms than the uranium oxide in mines. Another difference between the two situations is that mine uranium is contaminated with radium and radon, whereas these have been virtually eliminated in DU. Mine dust is produced at ambient temperatures, while the metal fume is produced at temperatures between 3000°C and 6000°C. Subjecting uranium oxide to more than 3000°C produces what the U.K. National Radiation Protection Board (NRPB) refers to as ceramic uranium oxide, which is highly insoluble in body fluids (2). These high temperatures also sublimate all other metals and materials that happen to be nearby, caught in the powdered uranium fire: steel, nickel, aluminum, iron, and so forth. This other debris will also aerosolize and produce nanometer-size debris, which can be inhaled (25). The small size of these particles facilitates uptake into cells and transit across epithelial and endothelial cells into the blood and lymph circulation, thus reaching potentially sensitive targets. These targets include lymph nodes, spleen, and heart. Access to the central nervous system and ganglia via translocation among axons and dendrites of neurons has also been observed. The greater surface area per volume, compared with larger particles, renders nano-particles more biologically active. Uranium miners must assume simultaneous exposure to radium and radon, while DU used in battle eliminates these exposures but involves a complex toxic matrix of other exposures. The differences in health effects in the receptor or host in the mining versus the battlefield environment are major. HUMAN ABILITY TO SCREEN OUT URANIUM The human body is normally exposed to uranium in food and water at a rate of about 1.9 micrograms a day, but only about 1 to 2 percent— between 0.019 and 0.038 micrograms (19 to 38 nanograms)— is absorbed through the intestines. The output of natural uranium in feces is 1.862 to 1.881 micrograms daily. Physiologists consider the entire gastrointestinal tract to be external to the body (like the hole in a donut), so this fraction of ingested uranium in water and food is not considered internal contamination. The 19 to 38 nanograms of natural uranium that is absorbed through the intestinal wall is considered to be internal to the body. It passes through the hepatic portal system and is screened by the liver, then either sent directly to the kidneys to be excreted in urine or circulated in the blood. Circulating uranium is usually stored in bone, to be excreted at a later time. These outcomes vary according to the solubility of the uranium compounds in food and water. However, these estimates are typical for natural uranium The human body has an excellent screening system for natural uranium reducing the ambient average environmental concentration of 1 part per million to less than 38 parts per billion internally. However, this gastrointestinal and liver screening system does not operate to screen out the uranium or other metals that enter the body through the lungs, are ceramic, and have an aerodynamic diameter in the nanometer range. Gulf War exposures to inhaled DU were likely well above the normal 19 to 38 nanograms per day and added considerable stress to the body, regardless of the other stresses present in this toxic war. Nano-particles (whether uranium, steel, iron, or aluminum) pose an especially difficult problem for the body's screening and filtering ability. T hey pass through the lung-blood barrier, the blood-brain barrier, and the placenta, and they are too small to be filtered out by the kidneys and excreted from the body (26). They take a long time to dissolve in the body fluid, and only the dissolved portion can be chemically active or eliminated in urine. Because of the variable times needed for dissolving the ceramic forms, the negative effect of the radioactive heavy metal is ongoing. Ceramic uranium may never dissolve, and it does not lose its radioactive properties. CARCINOGENIC PROPERTIES OF URANIUM While the neurological, immunological, and reproductive damage are the first problems to surface for veterans and civilians exposed to DU, the long-term effect of greatest concern, other than intergenerational genetic deterioration, is likely to be cancer. Note also that early cancers, which have at times been attributed to DU, are most likely secondary to the immunological effect. A depressed immune system often changes the status of a subclinical cancer, with which the individual is coping, into a clinically diagnosable cancer. There is no doubt about the ability of radiation to initiate cancer and also to promote cancers initiated by other carcinogens. The work of Peter Nowell (27) has recently been extended by research into radiation-induced genomic instability. A cco rd in g to W . F . M o rgan an d co lleagu es, ―T h e lo ss o f stab ility o f th e genome is b eco m in g accep ted as o n e o f th e m o st im p o rtan t asp ects o f carcin o gen esis‖ (28). The Armed Forces Radiobiological Research Institute has now admitted that DU can cause cancer (29). Miller and colleagues have also found that tiny amounts of DU, too small to be toxic and only mildly radioactive, cause more cytogenetic damage in cells than either the toxicity or radiation alone could explain. Their latest results (30) corroborate a tentative report by the Royal Society (7), which suggests that the toxicity and radioactivity of DU reinforce one another in an unknown way, to the extent that more than eight times as many cells suffer cytogenetic damage than predicted. Thus the carcinogenic and genotoxic health risk of DU could be grossly underestimated by current theories. There is also serious discussion among radiobiologists about the inadequacy of the ICRP model for dose and dose-response, based on the physics model. There is growing agreement that this model is inappropriate for application to internal alpha emitters (31). Both NATO (32) and the Institut de Radioprotection et de Sûreté Nucléaire (33), the official French radiation protection organization, have found the ICRP methodology to be faulty. The question of DU carcinogenicity is actually much larger than the questions raised by Gulf War syndrome; it involves the actual cause of the excess cancers at Hiroshima, Nagasaki, and Chernobyl, where burning uranium fuel particulates may have played a much larger part in the observed cancers than atomic bomb or International Atom Energy Agency research has projected. Since no internal dose estimates were ever attempted at Hiroshima and Nagasaki (34), and the dose estimates around Chernobyl were focused on cesium-137 and iodine-131 (35), the effect of uranium and plutonium fuel aerosol was neglected. By assuming that the DU in war would act like uranium dust in mines, the experts made the mistake of assuming that the signature of this exposure would be uranium storage in bone and damage to the kidney tubules. Because these effects were not dominant— though they did occur— DU was dismissed as a cause of GWS. With what is now known about the physical form of the DU, with the complication of ceramic nanoparticle formation, this was not a realistic assumption. The cancers may be expected to appear over the next 20 to 50 years. The latency period will probably be longer than expected for these cancers because of the chronic low-dose effect. Moreover, many Gulf War veterans will die before expression of the cancers, because of competing causes of death. TERATOGENIC TOXICITY Soluble uranium oxide and all nano-particles can cross the placenta, and these are particularly toxic to the rapidly developing embryo or fetus. At low doses, they damage the fetal brain, causing behavioral problems, such as aggressiveness and hyperactivity, and mental retardation. Other teratogenic effects are congenital malformations and diseases. The underdeveloped immune and hormonal systems of the fetus are more easily compromised than in a fully mature adult. One official epidemiological study did look at the health of the offspring of Gulf War veterans. This was a study of veterans in general and was not limited to those either with GWS or with known exposure to DU. This study of birth defects in the children of veterans in the United States, undertaken by Han Kang of the U.S. Department of Veterans Affairs (36), focused on the first pregnancy after returning home from the Gulf War. Slightly less than 21,000 veterans, from all four branches, active and retired, were included in the study (about 70% of those to whom questionnaires were sent). Male Gulf War veterans were twice as likely, and female veterans almost three times as likely, to report children with birth defects than their counterparts who did not serve in the first Gulf War. Birth defects included webbed fingers and toes, heart murmurs, chromosomal abnormalities, and brain tumors. The researchers excluded developmental disorders, perinatal complications, and pediatric disorders from the study. Male veterans reported miscarriages more often, and the increase, 1.62 times, was statistically significant. Female veterans also reported more miscarriages, but the sample size of female veterans was too small to reach statistical significance. No attempt was made to relate these findings to DU or any other Gulf War exposure (36). The studies of veterans with embedded shrapnel, done at the Baltimore, Maryland, V eterans' Hospital, reported finding DU in seminal fluid, indicating expected reproductive problems related to the genotoxic agent (37). This information should have led the Gulf War veteran reproductive research to zero in on those veterans known to have been exposed to DU. Unfortunately, this opportunity to clarify the science in the large Gulf War study of reproduction has been lost. EMPIRICAL FINDINGS Hari Sharma (38), professor emeritus from the University of Waterloo, tested some U.S., Canadian, and U.K. veterans, and Iraqi civilians from Basra and Baghdad, for urine DU about eight to ten years after the 1991 war. His findings, when DU was estimated from an isotopic analysis of the uranium present in a 24-hour urine sample, ranged from 81 to 1,340 nanograms of DU. This was surprising to those who trust the ICRP guidelines predicting a three-year biological half-life for insoluble uranium oxide. It was eight to nine years since the v eteran s' exposure to DU had terminated— approximately three biological half-lives of uranium oxide. Either the biological half-life estimate was wrong or the initial contamination exceeded any known credible estimate. Of the three Iraqi residents of Basra included in the study, the first had urine with 147 nanograms of DU, the second had no DU, and the third had 426 nanograms of DU. Of the five residents of Baghdad, the first had urine with uranium that was 20 percent DU; the second, 64 percent DU. The other three had all natural uranium in the urine (38). Microgram content could not be calculated for some samples. However, it is clear that the DU aerosol from the battlefield was transported to Basra and Baghdad, although there was no fighting there. SUMMARY In this prolonged and complex exposure picture, one cannot assume that cellular repair systems and hormonal systems will remain intact and function satisfactorily. Failing repair, radiation damage will increase, and cancer may well follow. When the biological half-life for a radioactive compound is wrong by such a large factor, as detailed here, the dose and cancer death risk calculations, based on old science, are unreliable. Much of the uranium oxide was in the nanoparticle size range and ceramic oxide form. The ceramic form would be expected to resist dissolution in body fluid, prolonging the biological half-time. Moreover, the dose from nano-particles cannot be estimated using the physics methodology described above. For one thing, these ceramic nano-particles cannot spread homogeneously in an organ, and for another, the contact dose is increased because of maximized surface area (for volume) and reduced self-screening. These particles remain point sources of internal (contact) dose until (if ever) they dissolve in body fluid. Ceramic nano-particles may well stay in the body for a lifetime. The portion of DU excreted in urine may not correctly predict either the original internal contamination or the residual amount still stored in the body, as based on outdated formulas. Ceramic particles most likely do not bind to bone but continue to circulate in blood and lymph fluid, irradiating blood and lymph vessels and surrounding tissues. Nano-p articles can ev en ―h id e‖ w ith in cells, d isru p tin g b io ch em ical activities. If the ceramic DU does dissolve, it can bind to the phosphate in DNA or can be stored in bone, irradiating the stem cells involved in blood formation. DU can easily penetrate the blood-brain and reproductive barriers, contaminating brain tissue, seminal fluid, or the uterus, damaging the developing embryo or fetus. Because of their small size, DU particles resist filtering out by the kidneys. The observed DU in urine eight or nine years after exposure may well be only the tip of the iceberg. Damage to the individual will occur not only from the inhaled DU aerosol but also from all the other toxic debris generated by the DU metal fume. Metal debris in the body, like debris from deteriorating hip implants, dental amalgams, or breast implants, has been shown to be detrimental. Hence the variety of symptoms reported by Gulf War veterans derives partially from the complexity, variety, and persistence of the foreign body invasions from their battlefield environment, not least of which was the DU-caused metal fume. Use of DU in battle is certainly a major contributor to this medical disaster that has affected at least one-third of U.S. Gulf War veterans. CONCLUSION The problems of Gulf War syndrome are too complex for a reductionist methodology that extracts the toxic effect of a single component, even depleted uranium. Increased free radicals, heavy metal toxicity, the complexity and sensitivity of disrupted cellular reactions, damaged organelles, dysfunctional enzymes and hormones, and mycoplasmal invasion— all occurring simultaneously within vital organs— pose monumental problems for function and survival. The mathematical methodology used by physicists is inappropriate for an insoluble nano-particle such as the ceramic DU internally deposited along with this toxic soup. The standard mathematical calculation of the radiation risk of cancer death is likely misleading, because of the many other carcinogenic mechanisms, cellular repair dysfunction, and complex biochemical reactions not incorporated into the mathematics. For those veterans with illnesses resulting from internal radioactive contamination and multiple cellular dysfunction problems, who are trying to live normally and work to support their families, the radiation physics prediction of low radiation-related cancer death risk is likely both wrong and irrelevant. However, regulators will take the mathematical prediction very seriously when awarding compensation. Veterans, and the medical personnel helping them, need to understand what happened in this war and what can be done to im p ro v e v eteran s' situ atio n s. T h ey n eed m ed ical, financial, and political help. I hope that some remedies will soon be found but, while waiting, I would su g gest n atu re's o w n d eto x ifyin g m eth o d . N atu re clean ses th e so il w ith distilled water, evaporated by the sun and condensed in the clouds, falling as rain. Using distilled water for drinking could provide some relief to Gulf War veterans, as it did for many atomic veterans in the 1950s and 1960s. (See 39 for the successful use of distilled drinking and cooking water for children with iron-deficiency anemia caused by a uranium-contaminated environment.) Re-su p p lyin g th e b o d y's protein and mineral loss would also be helpful. Undenatured (organic) whey products can be taken to replace proteins, and stressing zinc, calcium, and magnesium products in the diet would also help. Serious questions about the legality of DU, as used in war, also need answers. These cannot be provided by an isolated mathematical calculation of the DU exposure risk of radiation-related can cer d eath . In o th er w o rd s, th e ―triv ial‖ n u m b er of calculated cancer deaths thought to have been caused will not make this weapon acceptable to the Geneva Protocols, or to ordinary people using common sense. Individuals from many countries have joined their efforts to bring this issue to the Human Rights Tribunal of the United Nations (which consists of the U.N. Commission on Human Rights, and the U.N. Sub-Committee on the Promotion and Protection of Human Rights) and have formed global organizations to support victims of DU and work toward a ban on its use. The special investigator of the Sub-Committee on the Promotion and Protection of Human Rights has found that the use of DU is illegal under existing Humanitarian Law. Yet millions of dollars have been spent on sending out fact-finding teams of experts from respected international agencies, all using the same ICRP outmoded guidelines and methodology, and all coming to similar irrelevant conclusions. It is not disputable that DU powder produces an invisible metal fume. This alone is a violation of the Geneva Protocol on the Use of Gas (metal fumes constitute a gas) in War (Geneva, 1925), which was ultimately signed, with reservation (i.e., use for crowd control), by President Ford for the United States on January 22, 1975, and was proclaimed in the United States on April 29, 1975. The United Kingdom signed the protocol on April 9, 1930. The commitment to this Geneva Protocol was clearly known by the United States and United Kingdom before the 1991 war against Iraq (40). The illegality arguments can be left to lawyers. However, disruption of biochemical processes, not an isolated mathematical estimate of DU radiation-related cancer deaths, must be the foundation of the legal claim of harm. Clearly, depleted uranium is at least partially responsible for a series of biochemical events that are significantly harmful to human beings. The damage is indiscriminate, caring not for national affiliation, age, gender, or status as com batant or civilian. In other w ords, D U is a w eapon that destro ys one's ow n m ilitary and the generally exposed civilian population, as well as enemy combatants. It renders the postwar civilian environment hazardous for many years to come— much like land mines, which are now banned. Acknowledgment — Personal financial support was given by the Grey Nuns of the Sacred Heart of Yardley, Pennsylvania. Note — Portions of this article were posted on the website of the International Institute of Concern for Public Health, www.iicph.org. The author is the retired president of this organization. REFERENCES 1. Department of Protection of the Human Environment, World Health Organization. Depleted Uranium: Sources, Exposure and Health Effects. WHO/SDE/PHE/01.1. Geneva, April 2001. 2. Stradling, G. N., et al. The metabolism of ceramic and non-ceramic forms of uranium dioxide after deposition in the rat lung. Hum. Toxicol. 7(2):133– 139, 1988. 3. U .S . R esearch A d visory C o m m ittee on G u lf W ar V eteran s' Illn esses. Scientific Progress in Understanding G ulf W ar V eterans' Illnesses: R eport and R ecom m endations. Washington, DC, September 2004. 4. Fetter, S., and Von Hipple, F. The hazard posed by depleted uranium munitions. Science and Global Security 8:125–161, 2000. 5. Harley, N. H., et al. A Review of the Scientific Literature as It Pertains to Gulf War Illness, Depleted Uranium, vol. 7. RAND, Santa Monica, CA, 1999. 6. U.S. National Academy of Science. Gulf War and Health: Depleted Uranium, Sarin, Pyridostigmine, Bromide, Vaccines, vol. 1. Washington, DC, September 2000. 7. Royal Society (U.K.). The Health Effects of Depleted Uranium Munitions, Parts I and II. London, May 2001 and March 2002. 8. United Nations Environment Program. The Potential Effects on Human Health and the Environment Arising from Possible Use of Depleted Uranium during the 1999 Kosovo Conflict. Geneva, October 1999. 9. Bertell, R. Avoidable tragedy post-Chernobyl. Humanitarian Med. 2(3):21–28, 2002. 10. Schrödinger, E. What Is Life? Cambridge University Press, Cambridge, 1945. 11. Conn, P. M., and Janovick, J. A. A new understanding of protein mutation folds. Am. Sci. 93:314– 321, 2005. 12. Castro-Fernandez, C., Maya-Nunez, G., and Conn, P. M. Beyond the signaling sequence: Protein routing in health and disease. Endocr. Rev. 26(3), 2005. 13. Hensley, K. Neuroinflammatory aberrations of arachidonate pathway in ALS. Neuroscience, 2004. 14. Vickers, M. G. Radiosensitivity mechanisms at low doses: Inflammatory responses to microgray radiation levels in human blood. Int. Perspect. Public Health 9:4–20, 1993. 15. Health Canada. Health Canada Fact Sheet: Aluminum. Ottawa, 2003. 16. Best, B. Mechanisms of Aging 17. Luft, R., and Landau, B. R. Mitochondrial medicine. J. Intern. Med. 238:405– 421, 1995. 18. Somlyo, A. P., and Somlyo, A. V. Signal transduction by G-proteins, Rho-kinase and protein phosphatase to smooth muscle and non-muscle myosin II. J. Physiol. 522(2):177– 185, 2000. 19. Slavin, E. A., Jr. Persistence may pay off for sick workers. Tennessean Online, May 29, 2000. 20. A n in vestigatio n into illn ess aro u n d the n atio n 's nu clear w eap o n sites, th ird of a series o n the Nuclear Weapon Site Workers and citizens from the surrounding communities. Tennessean Online, August 199 21. Hooper, D. C. et al. Uric acid, a peroxynitrite scavenger, inhibits CNS inflammation, blood-CNS barrier permeability changes, and tissue damage in a mouse model of multiple sclerosis. FASEB J. 14:691– 698, 2000. 22. MacMillan-Crow, L. A. Nitration and inactivation of manganese superoxide dismutase in chronic rejection of human renal allografts. Proc. Natl. Acad. Sci. USA 93(21):11853–11858, 1996. 23. Best, B. Mechanisms of aging. J. Intern. Med. 238:405– 421, 1995. 24. Nicolson, G. L., et al. Progress on Persian Gulf War illness— Reality and hypothesis. Int. J. Occup. Med. Toxicol. 4(3): 365–370, 1995. 25. Gatti, A. M., and Montanari, S. So-called Balkan syndrome: A Bioengineering Approach. Laboratory of Biomaterials of the University of Modena and Reggio Emilia, Italy, February 11, 2004. 26. Oberdorster, G., Oberdorster, E., and Oberdorster, J. Nanotoxicology: An emerging discipline evolving from studies of ultrafine particles. Environ. Health Perspect. 113(7), 2005. 27. Nowell, P. The clonal evolution of tumor cell populations. Science, October 1976. 28. Morgan, W. F., et al. Genome instability and ionizing radiation. Radiat. Res. 146: 247–254, 1996. 29. Miller, A. C., et al. Observation of radiation-specific damage in human cells exposed to depleted uranium: Dicentric frequency and neoplastic transformation as endpoints. Radiol. Protection Dosimetry 99(1–4):275–278, 2002. 30. Miller, A. C., et al. Potential late health effects of depleted uranium and tungsten used in armor-piercing munitions: Comparison of neoplastic transformation and genotoxicity with the known carcinogen nickel. In Proceedings of the International Conference on Low-Level Radiation Injury and Medical Countermeasures, ed. T. M. Blakely et al. Bethesda, MD, November 8– 10, 1999; reported in Military Med. 167(2): 120– 122, 2002. 31. European committee on Radiation Risk. 2003 Recommendations of the European Committee on Radiation Risk, ed. C . B usby. R egulator's E ditione, Brussels, 2003. 32. NATO Report, August 1992, submitted to Defense Ministry, Paris, June 29, 2005; made public by France, July 1, 2005. 33. Institute de Radioprotection et de Sûreté Nucléaire. Response to ECCR: Health Consequences of Chronic Internal Contamination by Radionuclides. DRPH/2005-20. Paris, 2005. 34. Roesch, W. C. (ed.). US-Japan Joint Reassessment of Atomic Bomb Radiation Dosimetry. Radiation Effects Research Foundation, Hiroshima, 1987. 35. Exposures and Effects of the Chernobyl Accident, vol. II: Effects, Annex J, pp. 451–566. UNSCEAR, 2000. 36. Kang, H. Questionnaire study of about 21,000 veterans, conducted by the Department of Veterans Affairs. Ann. Epidemiol., October 2001. 37. McDiarmid, M., et al. Biological monitoring and medical surveillance results of depleted uranium exposed Gulf War veterans. In Program and Abstract Block, Conference on Federally Sponsored G ulf W ar V eterans' Illness R esearch , June 17–19, 1998. 38. Sharma, H. D. Investigations of Environmental Impacts from the Deployment of Depleted Uranium-Based Munitions, Part I: Report and Tables. Military Toxics Project, Lewiston, ME, December 2003. 39. Bertell, R. Internal bone seeking radionuclides and monocyte counts. Int. Perspect. Public Health 9:21–27, 1993. 40. Prohibition of the Use of Asphyxiating, Poisonous or Other Gases and Bacteriological Methods of Warfare. Geneva Protocol. Geneva, June 17, 1925. Direct reprint requests to: Dr. Rosalie Bertell 1750 Quarry Road Yardley, PA 19067-3910 e-mail: rosaliebertell@greynun.org
Source: http://www.holoninstitut.de/dateien/Bertell-Rosalie-DepletedUranium.pdf
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Syllabus for Bio200B Winter 2005: Biomolecules and energetics John Wagner Kate Heston The textbook we will use in this class is Principles of Biochemistry with a Human Focus by Garret and Grisham. 2002, Harcourt Publishers. Some reading will also be assigned in the book that you used in the first quarter, The Cell a Molecular Approach (Third ed.) by Cooper and Hausman. 2004, ASM Press.
Microsoft word - pillconsentform.doc
POTOMAC FAMILY PLANNING CENTER Voluntary Informed Consent for Medical Abortion with Mifepristone and Misoprostol I, _____________________, age _____, hereby give my consent to and request and authorize Earl N. McLeod, M.D., or a physician designated by he/she, together with any necessary assistants, to perform upon me, a MEDICAL ABORTION by use of Mifeprex 200mg and Misoprostol 800mcg. I have


My Name_> does that mean that none of the VAIO computers will support Virtualization?
Sony Agent_>Yes, My Name_. That's correct.
That means that although Intel processors supports Virtualization by default Sony disables it. I have heard that before and Sony does not provide an option to enable it. Everyone knows that Virtualization (and Open Source) is the future not only for businessess but for students as well. Nowadays, everybody virtualizes. It is a shame Sony does that. You should be able to use your laptop the way you want to. So, If you want to be up to speed with techonology look somewhere else. H-P, A-s-u-s, or D-e-l-l are good alternatives.
I have a nice idea !!


The European Pellet Council (EPC) is an umbrella organisation representing the interests of the European wood pellet sector. Its members are national pellet associations or related organisations from 16 countries.
The IWPB was launched by GDF SUEZ and unites utility firms that fire large quantities of wood pellets. The goal is to enable the trading of industrial wood pellets among the partnering companies.
A website set up by the Renewable Energy Association (on behalf of the biomass industry) to help deliver a clear message on the benefits of biomass.
Find information on the pellet-specific safety audit and certification program.
The European Biomass Association is the common voice of the European bioenergy sector with the aim to develop the market for sustainable bioenergy, and ensure favorable business conditions for its members.


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