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"My word, I thought, a ten- or eleven-year-old having that bright red polish put on, and suddenly the hood of the dryer went back and the child stood up and it was Jean. She was probably twenty-three at the time, but without any makeup and no eyebrows, she looked exactly like a little kid," Rosalind Russell wrote of her Reckless co-star, Jean Harlow. Russell and Harlow became friends in the short time they knew each other, but Rosalind was often called upon to get Jean out of jams, such as dragging her out of bars before she got herself into real trouble. Rosalind described Jean as a very sad girl, and it was certainly devastating to all when her life was suddenly taken from her at the tender age of 26.
When Roz made Reckless with Jean Harlow, it was the year 1935 and she was still stuck in rather limited supporting roles. However, she got to work with two great stars in this one—Jean Harlow and William Powell. These two were in love with each other at the time and Jean was very excited to finally make a film with her beloved. Unfortunately, this film is a bit of a clunker and wasn't the success they wanted it to be. Also along for the ride is Franchot Tone, who, unlike his usual characters, is a boozing jerk in this one. The actor was not very charismatic, but he got the job done.
The true star of Reckless is clearly Jean Harlow. She plays Mona, a singer and dancer who was a thorough professional, but sometimes got herself into trouble. Ned, played by William Powell, is an old friend of the family's and is often called upon to help Mona out.
He is a sports promoter and as Mona's grandmother (May Robson) says, Ned is "like a great big brother to Mona." After Mona is jailed for reckless (just like the title) driving, he gets her out in time for a benefit performance, but he fixes it so she has to return to jail after she is done. The benefit is for a faux group called SAML (Society for the Admiration of Mona Leslie). Bob Harrison (Franchot Tone), drunk as all get out, has rented the entire theater just so Mona can perform for him. This movie gets its name from the song sung by Mona called "Reckless," which is the first song she sings, and then reprises in the final scene. Jean Harlow's singing is dubbed and she clearly does not do her own dancing, either. This is apparent because when Jean dances, you can only see the top half of her body, and then when the dancing legs are shown, it is filmed from such a distance, it could be anyone's uncle in a platinum blonde wig.
Next we get to the story of how Ned has been in love with Mona for a while, but she never takes him seriously as anyone but a "great big brother," so he does not know how to tell her.
At one point, he gets up the nerve to finally tell her that he loves her and wants to marry her, but feels foolish when he sees that Mona has fallen asleep during his heartfelt speech. He decides to forget the whole thing, thinking he dodged a bullet. However, even with this in mind, he buys a ring for Mona and plans to give it to her, but changes his mind when he realizes Mona has fallen in love with Bob. Soon after this, Mona and Bob suddenly elope while quite tipsy. Ned becomes so distraught by the news that he goes into a downward drunken spiral that night. Even Bob, who was there at the wedding, does not seem to realize what he has done and seems to regret it immediately. Mona has no regrets because she loves Bob very much. They are overwhelmed with telegrams that morning, two of them standing out. One is from Jo Mercer, his former fiancée, who says it's all right with her. The other is a very disapproving one from his father who wants to talk to him right away. And so they go to Harrison, the town named after Bob's father and where he grew up. His father, played by Henry Stephenson, is very ashamed of his son for marrying a "showgirl" when he has the family name and reputation to think of. Meanwhile, Mona ends up by a river and meets a girl who is fishing there. The girl teaches her how to cast, but Mona laments that she is better at "fishing for jobs."
The girl says her name is Jo Mercer (Rosalind Russell) and Mona immediately realizes who she is. Jo does not seem to blame Mona at all for breaking her engagement, but Bob instead. After all, Mona didn't know Jo existed before they got married. Soon after, everyone (Ned, Mona, Bob, Jo, and some other friends) are at the horse races and Jo announces that she is getting married. She also makes sure to glance over at Bob to gauge his reaction. Naturally, he looks rather upset. At Jo's wedding, Bob proceeds to get smashing drunk and Jo confronts him about his behavior. At first, she jokes about how she felt she was "getting on in years" and decided to marry the first man who came along. This joking manner quickly turns to anger when she feels he is insulting his wife, Mona. Mona happens to be walking by when he tells Jo that Mona "trapped" him into marriage, keeping him away from the girl he really loves (Jo).
This is heartbreaking for Mona and although she is coerced into putting on a show for everyone, she has tears in her eyes as she sings and dances.
What happens next is tragic. Bob doesn't feel he can live with himself any longer and shoots himself in his bedroom. This opens up a horrific scandal for Mona, as she is pregnant and subsequently gives birth to an adorable baby boy. Mr. Harrison, Bob's father, tries to gain custody of the child by alleging that it is Mona's fault that his son is dead and that Mona is an unfit mother, being a "show person." He does not get her child, but in the end, she gives a performance to revive her sagging career caused by the bad publicity. Although Jo is there fully supporting her like a friend would do, once Mona starts singing, people in the audience start hissing, booing, and trying to disrupt her performance.
No longer able to stand it, Mona shouts at them, "How dare you! How do you dare?" In a moving speech, she tells them that what happened is no more her fault than anyone else's, that Bob was a sad man always drowning himself in sorrow, and that the audience should not be rude and interrupt her performance. As she sings her signature song, Ned proposes to her again. As everyone applauds, she takes his hand, signifying "yes" to him.
Rosalind does not even appear in the film until almost 50 minutes after it starts. And since the movie is a bit bland, it is a long wait for any Roz fan. I try to console myself with the fact that I am watching two great stars in their prime—Jean Harlow and William Powell—but the movie falls flat. However, there is something that makes Roz stand out in this film, and that is her costumes, particularly her wedding dress.
It is a beautiful creation by Adrian and it flows gorgeously behind her as she walks down the aisle. It is nice to see a real life couple in a movie in which they end up together, but it is a shame that it wasn't very well executed and has a mediocre script. I give the film 3 stars out of 5.
Here is the trailer for Reckless for your viewing pleasure…


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Fox Shields Austerity Push From Economic Realities Even Republican Leaders Recognize
Written by Alan Pyke
Fox News covered Democratic criticism of harmful and unnecessary spending cuts as a purely political maneuver, without acknowledging that those criticisms are reflected in actual economic data, and echoed by economists and even by House GOP leadership.
On the April 29 edition of America's Newsroom, host Bill Hemmer set up an interview with Wall Street Journal editorial board member Stephen Moore by suggesting that only Democrats argue that America is not in a "debt crisis," and hinted that the raw total of U.S. debt belies that claim. Moore proceeded to divert the conversation far away from economic reality, first citing a Fox News poll on public concerns about the debt, then accusing anti-austerity Democrats of merely seeking to protect "the favored programs that they care about," before finally misleading viewers on the relationship between economic growth and spending cuts. From America's Newsroom:
There are a few layers of deception to unpack here:
- Speaker John Boehner (R-OH) and Budget Chairman Paul Ryan (R-WI) acknowledged we don't have a "debt crisis." "We do not have an immediate debt crisis," Boehner said on ABC's This Week on March 17, acknowledging that he agrees with the President about the non-immediacy of the debt problem. "We do not have a debt crisis right now," Ryan said on CBS' Face the Nation on March 17, an acknowledgment Media Matters previously caught Fox concealing. This isn't, as Moore called it, "the new Democrat spin on the budget." It's an aisle-crossing reality.
- The primary research pillar of the austerity argument crumbled in mid-April. Insofar as austerity-pushing deficit hawks appeal to economic research at all, they primarily hitch their argument to research by Harvard economists Caroline Reinhart and Kenneth Rogoff. Reinhart and Rogoff argued that there is a tipping point, at a 90 percent debt-to-GDP ratio, past which economic growth is permanently stifled. Their research was thoroughly undermined by economists at University of Massachusetts Amherst, who found not only basic spreadsheet errors but unsupportable statistical weighting choices that render the Reinhart-Rogoff paper flatly wrong. This development might explain the uptick in anti-austerity rhetoric that Hemmer and Moore attribute to Democratic politicking.
- It's not just Democratic politicians arguing rapid austerity is harmful and unnecessary -- it's a broad range of economists. Richard Koo. Mark Thoma. Brad DeLong. Jared Bernstein. Dean Baker. Henry Aaron. Alan Blinder. Larry Summers. Even the American Enterprise Institute's John Makin (to say nothing of Nobel Prize winner Paul Krugman). Observing that austerity is premature and harmful isn't a "new line" from one political party, as Moore claimed, but rather the consensus position of numerous and ideologically disparate economists.
- GDP data actually do show that spending cuts put a drag on the economy. While Moore mentioned the topline data on GDP growth for the first quarter of 2013, and then attributed that "healthy" number to "Washington get[ting] at least semi-serious about cutting wasteful spending," the actual data undermines his entire pro-austerity argument. "The U.S. government is in pullback mode, and whatever one thinks about reducing the size government in the long run, for now it is unequivocally the villain in slowing growth. If there'd been no change in government spending over the last six months, GDP growth would have averaged a respectable 2.55 percent, not the current soft 1.45 percent," The Washington Post WonkBlog's Neil Irwin wrote in his examination of the GDP report. The chart below shows just how slowed government spending has placed a drag on overall GDP growth in the age of austerity:
These sorts of facts in the U.S., and related ones from other economies, are threatening to upend the entire austerity movement, as Irwin observes. But while that debate proceeds and evolves elsewhere, Fox News continues to offer conservatives a venue to avoid reconciling ideology and fact.

subset: commoncrawl


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Well, we too weren't expecting the Bentley to be doing this sort of activity, but finally we learnt that it is the Bentley Home, a section of British carmaker, which has launched the 'latest range of Furniture'.
Hopefully, the new collection of Bentley Home is inspired by the renowned craftsmanship and exquisite materials that characterise the interiors of all 'Bentley models'. Designed to furnish luxury homes and offices, the collection combines Bentley's inherent qualities of craftsmanship, heritage and tradition, exclusivity and style, with the exacting design of one of Europe's leading furniture makers.
This exclusive collection blends the finest elements of traditional and modern design, an exercise in subtlety rather than showmanship, incorporating functional performance with comfort and luxurious, sensuous quality. It captures the elan of the Bentley driver, through items that mirror the impeccable quality and attention to detail which is a landmark of the Bentley brand.
The bodies of the new Richmond pieces are created with an embracing double shell and can be covered in either leather or a fine veneer of burr walnut. The same wide selection of veneers which is available for Bentley car customers is also available for most pieces in the collection. The wood is then carefully matched to a padded structure covered in a sophisticated light cashmere. The seating reflects the level of comfort and luxury found in the Crewe-based marquee, which makes it unique in its class.
The colour palette is composed of varying neutral tones of ivory and taupe matched with shades of beige and cream. Intricate details such as the leather braid around the contours highlight the soft and sinuous lines. The iconic quilted diamond pattern embossed in the leather interiors of a Bentley has also been interpreted into the unique designs of the furniture.
The new collection consists of the following new pieces:
An elegant and sophisticated line of seating which includes sofas, chaise longues and armchairs. The enveloping external structure can have a veneer finish or leather cover. In contrast, the inner structure is covered in leather or linen or in fine cashmere velvet. The profile is embellished by a leather braid.
Madeley & Kendal
A large oval or round meeting table with refined Kendal chairs embellished with leather and the Bentley logo which can be embroidered on the back, on request. A trapezoidal structured table made of curved wood panels with edges embellished in hand-made leather coating. The feet are made of steel with a gun-metal finish.
Sherbourne & Kingsbridge
Tall and short leather-coated cabinets with veneered fronts; these are also available in smooth or quilted leather. Tone-on-tone lacquered interiors with external coatings and shelves of crystal represent the luxury and quality of both Bentley and Club House Italia, part of the Luxury Living Group. The handles and feet are also made from steel with a complementing gun-metal grey finish.
A modern coffee table with metal steel structure and a complimentary gun-metal grey finish. The surface is made from onyx or leather coated.
The bed is characterised by an imposing headboard, embracing coated structure available in leather or fabric. The shapes are soft and convoluted, working in harmony with the contemporary and informal line. An innovative duvet cover, Fibra di Legno®, is a high-quality fabric made from wood pulp that gives the yarn softness and smoothness, adding to the luxurious feel of this piece.


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Those that have been hoping for some sort of a "V-shaped recovery" have had their hopes completely dashed. U.S. workers continue to lose jobs at a staggering rate, and economic activity continues to remain at deeply suppressed levels all over the nation. Of course this wasn't supposed to happen now that states have been "reopening" their economies. We were told that things would soon be getting back to normal and that the economic numbers would rebound dramatically. But that is not happening. In fact, the number of Americans that filed new claims for unemployment benefits last week was much higher than expected…
Weekly jobless claims stayed above 1 million for the 13th consecutive week as the coronavirus pandemic continued to hammer the U.S. economy.
First-time claims totaled 1.5 million last week, higher than the 1.3 million that economists surveyed by Dow Jones had been expecting. The government report's total was 58,000 lower than the previous week's 1.566 million, which was revised up by 24,000.
To put this in perspective, let me once again remind my readers that prior to this year the all-time record for a single week was just 695,000. So even though more than 44 million Americans had already filed initial claims for unemployment benefits before this latest report, there were still enough new people losing jobs to more than double that old record from 1982.
That is just astounding. We were told that the economy would be regaining huge amounts of jobs by now, but instead job losses remain at a catastrophic level that is unlike anything that we have ever seen before in all of U.S. history.
With the addition of this latest number, a grand total of nearly 46 million Americans have now filed initial claims for unemployment benefits since the COVID-19 pandemic began.
If you can read that statement and still believe that the U.S. economy is not imploding, I would like to know what you are smoking, because it must be pretty powerful.
Some of the things that we are seeing happen around the country right now are absolutely nuts. For example, earlier this week in Kentucky it was being reported that people were waiting in line for up to 8 hours to talk with a state official face to face about their unprocessed unemployment claims…
The state police said it will be an 8 hour wait from the back of the line to speak to a state employee about unemployment. pic.twitter.com/plGONcpS6n
— Daniel Desrochers (@drdesrochers) June 17, 2020
This wasn't supposed to happen.
By now, the U.S. economy was supposed to be roaring back to life and we were supposed to be entering a new golden age of American prosperity.
Unfortunately, the truth is that more bad economic news is hitting us on a continual basis, and that isn't going to change any time soon.
Over the past few days, we have learned that Hilton is laying off 22 percent of its corporate staff, and AT&T has announced that it will be eliminating 3,400 jobs and closing 250 stores…
The wireless carrier AT&T is cutting 3,400 jobs and shutting down 250 stores over the next few weeks, according to a statement from the Communications Workers of America, a union representing AT&T workers.
The AT&T Mobility and Cricket Wireless retail closures will affect 1,300 jobs, while the other layoffs are said to be affecting technical and clerical workers.
Needless to say, all of these job losses are having a tremendous ripple effect throughout the economy.
Without paychecks coming in, a lot of Americans are having a really tough time paying their bills, and the Wall Street Journal is reporting that payments have already been skipped on more than 100 million loans…
Americans have skipped payments on more than 100 million student loans, auto loans and other forms of debt since the coronavirus hit the U.S., the latest sign of the toll the pandemic is taking on people's finances.
The number of accounts that enrolled in deferment, forbearance or some other type of relief since March 1 and remain in such a state rose to 106 million at the end of May, triple the number at the end of April, according to credit-reporting firm TransUnion.
To me, that is an almost unimaginable number, and it has become clear that a tremendous amount of pain is ahead for the financial institutions that are holding these loans.
A lot of people out there are going to keep hoping that there will be some sort of an economic rebound, but the cold, hard reality of the matter is that fear of COVID-19 is going to keep a large segment of the population from resuming normal economic activities for the foreseeable future. And it certainly doesn't help that the number of confirmed cases in the U.S. has been steadily rising over the past couple of weeks and that the mainstream media has been endlessly warning that a "second wave" is coming.
If you doubt what I am saying, just look at what is happening to the restaurant industry. We had started to see a small bit of improvement in the numbers, but now fear of a "second wave" has caused restaurant traffic to start cratering again…
After three months of slow but consistent improvement in restaurant dining data in the US and across the globe, in its latest update on "the state of the restaurant industry", OpenTable today reported the biggest drop in seated restaurant diners (from online, phone and walk-in reservations) since the depth of the global shutdown in March.
As shown in the OpenTable graphic below, on Sunday, June 14, restaurant traffic suddenly tumbled, sliding from a -66.5% y/y decline as of June 13 to -78.8% globally.
This was mostly due to a sharp drop in US restaurant diners, which plunged by 13% – from -65% to -78% – the biggest one day drop since the start of the shutdown in the US, and the second biggest one day drop on record.
Business travel is another area where we are seeing signs of big trouble ahead. The following comes from Yves Smith…
Business travel is not coming back any time soon. People are getting accustomed to Zoom. And word may also get out that domestic flying is much worse than it used to be, which will be a deterrent to those who might be so bold as to want to get on a plane. That is a fundamental blow to airlines, airport vendors, hotels, restaurants, and convention centers. Hotel occupancy in April was 24.5% which if anything seems high based on my personal datapoints. The pricings I see say that hotel operators are not expecting much if any improvement through the summer.
Like many of you, I wish that economic conditions would go back to the way they used to be, but that simply is not going to happen.
Yes, we will see economic numbers go up and down over the coming months, but a return to "the good times" is not in the cards.
And what hardly anyone realizes is that this is just the beginning of our problems, and I am working on a new project right now which will explain why this is true in great detail.
So stay tuned, because things are about to get really, really "interesting".
About the Author: I am a voice crying out for change in a society that generally seems content to stay asleep. My name is Michael Snyder and I am the publisher of The Economic Collapse Blog, End Of The American Dream and The Most Important News, and the articles that I publish on those sites are republished on dozens of other prominent websites all over the globe. I have written four books that are available on Amazon.com including The Beginning Of The End, Get Prepared Now, and Living A Life That Really Matters. (#CommissionsEarned) By purchasing those books you help to support my work. I always freely and happily allow others to republish my articles on their own websites, but due to government regulations I need those that republish my articles to include this "About the Author" section with each article. In order to comply with those government regulations, I need to tell you that the controversial opinions in this article are mine alone and do not necessarily reflect the views of the websites where my work is republished. The material contained in this article is for general information purposes only, and readers should consult licensed professionals before making any legal, business, financial or health decisions. Those responding to this article by making comments are solely responsible for their viewpoints, and those viewpoints do not necessarily represent the viewpoints of Michael Snyder or the operators of the websites where my work is republished. I encourage you to follow me on social media on Facebook and Twitter, and any way that you can share these articles with others is a great help. During these very challenging times, people will need hope more than ever before, and it is our goal to share the gospel of Jesus Christ with as many people as we possibly can.


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A Website That Doesn't Market— and Sell —Your Business is Only Doing Half Its Job
If You're Looking for a Website That Makes It Easy to Attract New Clients, You're in the Right Place
You're a very successful consultant, speaker, trainer, or professional who charges high fees and has a busy practice. In fact, you're so busy running your business and working with clients, that you don't have time to wrangle with marketing. You're enthusiastic and passionate about your work, and are committed to making a positive difference. Now, you need an effective way to spread that passion—without taking time away from your business.
You know you need content marketing and social media to get—and keep—your message in front of your target market, but you don't need more stress or headaches. You want to get it done without it consuming your valuable time, energy and resources.
Do You Occasionally Have the Marketing Problem of a "Dry" Pipeline?
You make a high hourly rate and sell programs for big money, and you have a steady stream of business…except when you have lulls. Darn, you've let your marketing lapse again and the pipeline's run dry! What if you had the web infrastructure to market automatically for your business? What if you could spend more of your time doing the highly paid work you LOVE—and you could count on your website doing the marketing for you 24/7?
The Websites We Create Are Not Just Websites…
…They Are Designed To Be Automatic Marketing Machines
You get that you need a system to consistently present your message to your target market. You understand that the best internet marketers use blog posts, newsletters, Facebook, and other social media to get that done. Where you're having trouble is fitting that into your already packed schedule. How can you figure out everything and stay on top of the changes? It's exhausting!
Our Website Designs Have Every Marketing Feature You Need—Built Into the Basic Structure of the Site
If you are going to succeed at internet marketing, your website must be built to support promoting your brand. Let's look at a summary of the features we build into our websites that make it easy for you to market your services.
- Our sites are designed to help you organically drive traffic to your site and improve your search engine rankings. Using the blog and newsletter, you can consistently put new content in front of your audience. Your site is designed to make it easier to position your brand at the top of the competition.
- We incorporate blogs into all our sites. Even if you're not ready for the commitment of blogging, you've got the capability to start at any time, without any additions to your site, and only a minor tweak to get started.
- We give you the ability to capture contacts and build an email list, so that you can create ongoing relationships with your prospects. You have the means to establish yourself as an expert in your field, and develop the trust and loyalty of your target market.
- We make it easy for your site visitors to contact you, and inquire about hiring your services. Once you've got a prospect ready to talk to you, we want them to be able to connect with you quickly and easily.
- We also give you the tools to know, understand and use the statistics about your site visitors. This gives you a competitive advantage over similar service providers. You can know what is working and not working on your site, and what to do about it.
We Don't Just Build Great Websites…
…We Also Help You Manage Your Ongoing Strategic Site Promotion
We don't just give you the finished site and say, "Good luck with that." We can also provide ongoing web strategy for you. You might feel mystified about what you need to do to market your site. Maybe you know what you need to do, but wonder why your website strategy isn't working. Perhaps you simply can't or don't want to spend the time away from your business to keep it all going.
We offer several options to solve your post-launch website marketing challenges:
- As part of an ongoing web promotion relationship, we perform a wide range of web marketing services for you. We consult with you to plan out a web marketing strategy and specific action items that we implement for you. We help you accomplish your marketing objectives while you stay focused on serving your clients.
- Beyond the creation of your new site, we can make sure your new site brings you the targeted business you want. We provide the means for you to automatically keep in touch with your market—with the absolute minimal work for you.
- If you have concerns about your existing site, we can analyze your website to identify what is working and what is not working. You get a detailed report of your current site results and what can be done to optimize your site. From there, you decide what needs to be done and when.
This Is Our Promise to You
We consistently work to minimize your time away from earning—while you get a new website, and enjoy the fruits of ongoing web marketing. Our objective is that you maximize your billable hours during all phases of the website process.
I've been involved in many aspects of the Web and websites for 15 years. A lot of what I have learned has been driven purely by the needs of my clients' businesses. I understand what consultants and professionals need in their websites to build a brand and promote unique services. Look at me as a partner in building and growing your service business.
Where to Next?
Now that you have an overview of our business and what we provide, learn more about Who We Work With and the web strategy problems we solve.


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Quick Overview
Straight stylus with M2 thread, ruby ball Ø3 mm, tungsten carbide stem, length 20 mm. For use on machine tools. Previous part number: 91.00-T21.5/3-HM-M2
Hexagon original accessories for measurement systems on machine tools ensure highest precision and reliability in the production.
The stylus is an important part of the measuring system. During the measurement, the stylus is in direct contact with the part. Straight styli are the most common type used in the metrology industry. Depending on the application, different connections, materials for stems and tips are available.
Ruby is the most widely-used material for stylus tips. Thanks to its inexpensive price and high quality, it is the standard choice for most applications. It is an extremely hard material.
A tungsten carbide stem has high stiffness and less thermal expansion, compared to stainless steel.
All images are for illustration purposes only and may differ from the actual product.
Previous Part Number | 91.00-T21.5/3-HM-M2 |
Related Device | Machine Tool |
Thread | M2 |
Tip Material | Ruby |
Tip Diameter (D) | 3 mm |
Length (L) | 20 mm |
Stem Material | Tungsten Carbide |
Stem Diameter (S) | 1.5 mm |
Weight | 0.8 g |


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A perfect addition to your favorite stack - our signature nameplates are a quirky spin on an old school favorite. Guacamole? Winetime? Sweatpants? Whatever your passion... we GET you.
These items are handmade! Please allow 5-10 business days for rings to be sized and shipped. Rush shipping is available upon checkout.


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Is Iraq another Vietnam?
Published 10:37 pm Tuesday, January 23, 2007
Nothing is easier than to second-guess decisions made in wartime. Anyone who has bothered to read the history of wars knows that very few wars have been without disastrous surprises, often on both sides.
It is not that the people in charge are stupid. Too many things are unpredictable in war, despite politicians who demand timetables, as if running a war is like running a train.
We can now look at the Iraq war with hindsight, as no President or Secretary of Defense could when making decisions that had to be made. Still, it can be useful to determine with hindsight what went wrong, if only to avoid similar mistakes in the future and to see what needs to be changed in the present.
Despite all the politicians who were demanding more troops a year ago, and who have turned around and are now demanding that no more troops be sent to Iraq, the purely military aspects of the war have gone better than in most wars.
We have learned the hard way, notably in the Vietnam war, that military victories are not enough. American troops scored a big victory on the battlefield in 1968 that was presented in the American media as a big defeat — and that began the political unravelling of the Vietnam war.
Many in the media seem to think that they did something noble, to get us out of an "unwinnable" war. But the war was unwinnable only because they made it so politically. Even after American troops were withdrawn from Vietnam, South Vietnam was able to hold off the invaders from North Vietnam.
Only after Congress cut off financial support for South Vietnam, while the North Vietnamese continued to get support from the Communist bloc, did South Vietnam fall.
Since then, even the Communist conquerors have admitted that they did not win on the battlefield, but in the American media and in the American political arena, surrounded by an atmosphere created by a defeatist media.
Most of the today's media, led by the New York Times, has been even more blatantly one-sided in their reporting. Everyone I have heard from in person who has actually been in Iraq paints a far different picture from that of the gloom and doom of the media.
Make no mistake about it, we can still lose this war, but it will have to be lost politically. Most of the tragic chaos in Iraq today has its origins in politics.
American and other coalition troops in Iraq have had their hands tied with "rules of engagement" based on political, rather than military, considerations.
You cannot have law and order in any country where armed bands of competing militias can terrorize the population. Instead of confronting these militias at the outset with an ultimatum to disarm or be killed, we let the Iraqi government veto what our military forces could do, leaving Shi'ite militias intact in Baghdad's "Sadr City" neighborhood and elsewhere.
Having pushed the "democracy" vision for Iraq, we could not simply disregard the country's elected government. But democracy arose in western civilization centuries after law and order had been established. We tried to do it in the reverse order in Iraq.
When push comes to shove, people will support tyranny rather than suffer lethal chaos that makes normal everyday life impossible for themselves and their children.
The success or failure of the troop surge in Iraq may depend far more on whether those troops can again be hamstrung by politically restrictive "rules of engagement" than on how many troops there are.
The Maliki government is politically dependent on one of the very Baghdad militias that needs to be disarmed. We can pressure and warn Maliki all we want, but his real choice will be whether he can survive — either politically or personally — without militia support.
Our choice may become whether we are prepared to sacrifice more American lives in order to prop up the Maliki government or whether we are prepared to sacrifice the Maliki government in order to restore law and order in Iraq.
That government is a product of our "nation-building" under the banner of a "democracy" for which Iraq may not have been ready.
(To find out more about Thomas Sowell and read features by other Creators Syndicate columnists and cartoonists, visit the Creators Syndicate web page at www.creators.com. Thomas Sowell is a senior fellow at the Hoover Institution, Stanford University, Stanford, CA 94305. His Web site is www.tsowell.com.)


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Dinosaur wind tunnel test provides new insight into the evolution of bird flight
A study into the aerodynamic performance of feathered dinosaurs, by scientists from the University of Southampton, has provided new insight into the evolution of bird flight.
In recent years, new fossil discoveries have changed our view of the early evolution of birds and, more critically, their powers of flight. We now know about a number of small-bodied dinosaurs that had feathers on their wings as well as on their legs and tails: completely unique in the fossil record.
However, even in light of new fossil discoveries, there has been a huge debate about how these dinosaurs were able to fly.
Scientists from the University of Southampton hope to have ended this debate by examining the flight performance of one feathered dinosaur pivotal to this debate — the early Cretaceous five-winged paravian
The first theropod described with feathers on its arms, legs and tail (five potential lifting surfaces),
implies that forelimb-dominated bird flight passed through a four-wing ('tetrapteryx') phase and represents an important stage in the evolution of gliding and flapping.
The Southampton researchers performed a series of wind tunnel experiments and flight simulations on a full-scale, anatomically accurate model of
Results of the team's wind tunnel tests show that
would have been most stable gliding when generating large amounts of lift with its wings. Flight simulations demonstrate that this behaviour had advantages since this high lift coefficient allows for slow glides, which can be achieved with less height loss. For gliding down from low elevations, such as trees, this slow, and aerodynamically less efficient flight was the gliding strategy that results in minimal height loss and longest glide distance.
Much debate, centred on the position and orientation of
legs and wing shape turns out to be irrelevant – tests show that changes in these variables make little difference to the dinosaur's flight.
Dr Gareth Dyke
, Senior Lecturer in Vertebrate Palaeontology at the University of Southampton and co-author of the study, says: "Significant to the evolution of flight, we show that
did not require a sophisticated, 'modern' wing morphology to undertake effective glides, as the high-lift coefficient regime is less dependent upon detail of wing morphology."
"This is consistent with the fossil record, and also with the hypothesis that symmetric 'flight' feathers first evolved in dinosaurs for non-aerodynamic functions, later being adapted to form aerodynamically capable surfaces."
Dr Roeland de Kat
, Research Fellow in the Aerodynamics and Flight Mechanics Research Group at the University of Southampton and co-author of the study, says: "What interests me is that aerodynamic efficiency is not the dominant factor in determining
glide efficiency. However, it needs a combination of a high lift coefficient and aerodynamic efficiency to perform at its best."
The paper 'Aerodynamic performance of the feathered dinosaur
and the evolution of feathered flight' is published in the latest issue of
Nature Communications
Dr Dyke and fellow Southampton palaeontologists will showcase their ground-breaking research at the
Celebrating Dinosaur Island
: Jehol-Wealden International Conference on 21 and 22 September.
The Isle of Wight (Dinosaur Island) and China are key areas for Cretaceous fossils, especially dinosaurs. To celebrate this connection, Chinese and UK dinosaur palaeontologists will discuss their research at the National Oceanography Centre, Southampton and visit key dinosaur sites on the Isle of Wight and network with tourism and business leaders to build connections for future palaentological research.
Notes for editors
For further information contact: Glenn Harris, Media Relations, University of Southampton, Tel: 023 8059 3212, email: firstname.lastname@example.com


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2009 Mercedes-Benz SLR McLaren Stirling Moss
Stuttgart– Mercedes-Benz and McLaren are adding the crowning glory to the model family of their highly successful SLR super sports car with a new, uncompromisingly spectacular car. There is neither a roof nor a windscreen to separate the driver and passenger from the outside world; they enjoy unadulterated high-speed excitement with all the attributes of a speedster.
The new SLR Stirling Moss is also characterised by the most sophisticated technology and a breathtaking design which reinterprets the SLR legend. With 478 kW/650 hp the SLR Stirling Moss accelerates its V8 supercharged engine from standstill to 100 km/h in less than 3.5 seconds, and has a top speed of 350 km/h – no other series-production car is at the same time so open and so fast. This extreme concept makes the new high-performance sports car a legitimate bearer of the name of the British motor racing legend and Mille Miglia record-holder Stirling Moss, who drove the legendary Mercedes-Benz SLR racing cars from victory to victory during the 1950s.
The exclusive SLR Stirling Moss rounds off the current SLR family and is limited to 75 units. It is priced at 750,000 euros. The SLR Roadster will cease to be manufactured at the end of May 2009 as planned, and production of the SLR Stirling Moss will commence in June 2009.
Three letters are all it takes to make car fans' hearts beat faster: SLR. In the 1950s the Mercedes-Benz SLR 300 celebrated victory after victory. It won the Mille Miglia and the Targa Florio as well as the Tourist Trophy. It was driven by the stars of the time: Juan Manual Fangio and Karl Kling – and, first and foremost, by the British racing driver Stirling Moss. At ten hours, seven minutes and 48 seconds he still holds the Mille Miglia record.
This is why the modern-day version of the legendary SLR carries the additional words "Stirling Moss" in its name. As the new SLR Stirling Moss unites the character of the current SLR models with the fascination of the SLR of 1955. The core values of both the historical and the present-day SLR models include an exciting new design, innovative technology, high-class materials displaying perfect craftsmanship, and, above all: a unique driving experience for all the senses.
Whilst the 300 SLR earned its spurs on racing circuits the world over, the new member of the SLR family is not designed for the racetrack. Although it sets new standards in terms of technology, performance and excitement – just like its forebears – it is aimed at individuals who have exquisite requirements and nurture very special dreams.
Highly puristic concept without a roof or a windscreen
Remaining totally true to the specifications of the 300 SLR, the new Silver Arrow's equipment is extremely sophisticated and yet at the same time decidedly spartan, doing without both a roof and side windows. There are just two wind deflectors a couple of centimetres in height to protect the driver and passenger from the airflow. Two air scoops integrated into the bodywork serve as roll-over bars. With this extreme concept the new SLR Stirling Moss is visually very different from all the other vehicles which belong to the elite sports car class.
Just like the legendary racing vehicles of yesteryear, the SLR Stirling Moss dazzles with its superlative performance. Accelerating from zero to 100 km/h in less than 3.5 seconds and with a top speed of 350 km/h this puristic high-performance sports car denotes completely new dimensions in open-top driving. And not just because of the impressive performance figures; every time drivers take to the wheel of the SLR Stirling Moss their senses are addressed with a previously unheard of intensity, conveying a driving experience in its purest and most sensual form. This automotive thoroughbred thus facilitates the kind of open-air feeling that is utterly unique for a road-going vehicle.
Exciting design reminiscent of the SLR racing cars
The SLR Stirling Moss, its entire bodywork made of fine lightweight carbon fibre, represents a stand-alone design concept. Whilst the Mercedes-Benz designers were working on the body of the new SLR Stirling Moss, they were fully aware every single moment that they were creating a vehicle with a top speed of 350 km/h. At the same time this supreme athlete is highly reminiscent of the SLR racing cars from the 1950s, whose design idiom still never fails to impress to this day.
The SLR Stirling Moss sports an exciting, pronounced arrow-shaped form and is characterised by an elongated bonnet and a compact, muscular rear. As there is no windscreen, the exterior and interior flow smoothly into one. The bonnet also stretches from its striking tip right down into the interior, giving the vehicle body a distinctly sleek air. Even when standing still, the sports car radiates such dynamism that the observer immediately falls under its spell.
Further eye-catching features include two air scoops behind the driver and passenger. They carry additional roll-over bars, also uniting the traditional and the modern. The wings are powerfully contoured. Black-painted ventilation "gills" sitting facet-like on the sides and on the bonnet also cite the legend. A thrilling interplay of light and shadow ensues through the expressive lines, underlining the dynamic overall impression. Exactly as they were on the shining historical example, the side skirts on the new SLR Stirling Moss are also very high. This prompted the designers' decision in favour of folding swing-wing doors which open forwards.
The vehicle can be closed by two tonneau covers which are carried in the boot. When both tonneau covers and the doors are closed the SLR Stirling Moss resembles a sculpture.
In keeping with the puristic exterior of the vehicle, the interior is also reduced to the bare essentials. Surfaces penetrating each other in the instrument panel and doors make for an exciting atmosphere and resonate perfectionism. A mixture of high-class authentic materials such as carbon fibre, aluminium and fine-quality leather sets the style here. An aluminium plate carries the engraved signature of Stirling Moss and covers the area around the shift lever.
Innovative technology and polished aerodynamic concept
Developers working on the Stirling Moss were able to fall back on a wealth of experience gathered when producing the SLR Coupé and Roadster, in particular where the technical base was concerned, with its extravagant carbon-fibre design, high-performance suspension and throaty V8 engine. The common denominator uniting the Stirling Moss with the other members of the SLR family is the aerodynamic concept with a closed underbody and a diffuser in the rear bumper for maximum possible downforce at the rear axle – with one difference: the diffuser here is considerably larger than that on the coupé and roadster.
Thanks to the high-precision work carried out in the wind tunnel, the SLR Stirling Moss always generates sufficient downforce for extremely safe handling. But the driver can also manually operate the AIRBRAKE in order to increase the contact pressure further, during particularly sporty driving, for example. The AIRBRAKE is also raised during powerful braking at speeds above 120 km/h, so as to stabilise the vehicle even more in such situations, thus facilitating maximum possible deceleration.
Limited to 75 units – the SLR models' crowning glory
The new SLR Stirling Moss is the kind of high-calibre speedster coveted by the sporting gentry and enthusiasts alike. At the same time it is a collector's item which marks the pinnacle of an era and, for the foreseeable future, at least, the final curtain for the SLR. In May 2009 production of the SLR models will cease; only a total of 75 units of the Stirling Moss will be manufactured between June and December 2009, bearing chassis numbers from 1 to 75. Not only does this exclusive vehicle represent the conclusion of the current SLR family; it also serves as a very special thank you to the most loyal of SLR customers, for they are the only ones able to acquire a Stirling Moss.
Story by Daimler AG
In Detail
submitted by | admin |
type | Series Production Car |
released at | 2009 Detroit Motor Show |
built at | Woking, England |
production | 75 |
price €/td> | €750,000 |
price £/td> | £687,000 |
predeccesor | 2007 Mercedes-Benz SLR McLaren Roadster |
engine | 90 Degree AMG V8 w/Dry Sump Lubrication |
position | Front-Mid, Longitudinal |
aspiration | Screw-Type Compressor w/Two Charge-Air Coolers |
valvetrain | SOHC, 3 Valves per Cyl |
displacement | 5439 cc / 331.91 in³ |
bore | 97 mm / 3.8 in |
stroke | 92 mm / 3.6 in |
compression | 8.8:1 |
power | 478.0 kw / 641 bhp @ 6500 rpm |
specific output | 117.85 bhp per litre |
torque | 820.3 nm / 605 ft lbs @ 4000 rpm |
body / frame | Cabon Fibre & Aluminum Monocoque |
driven wheels | RWD |
front brakes | Internally Vented Carbon Discs w/8-Piston Calipers, ESP, SBC |
rear brakes | Solid Carbon Discs w/4-Piston Calipers, ESP, SBC |
steering | Rack & Pinion w/Speed Sensitive Assis |
f suspension | Double Wishbones w/Anti-Roll Bar |
r suspension | Doube wishbones |
transmission | 5-Speed Auto w/Speedshift System |
top speed | ~350 kph / 217.35 mph |
0 – 100 kph | ~3.5 seconds |


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What is Lateral Impingement of the Elbow?
Lateral elbow impingement is a medical condition characterized by compression and injury of the soft tissue structures, such as cartilage located at the outer aspect of the elbow joint. The impingement is caused by repetitive forced extensions and overuse of the elbow.
When the elbow is extended fully, the soft tissue structures at the back of the joint become compressed. When these compressive forces become too much or too frequent and more than what the elbow joint can tolerate, it may result in inflammation and damage to the soft tissue and/or cartilage at the back of the joint causing impingement of the elbow. Sometimes, bony spurs may also develop inside the joint contributing to further worsening of the impingement. Other factors that could contribute to impingement include congenital ligamentous laxity or ulnar collateral ligament insufficiency.
Lateral impingement of the elbow is mostly seen in athletes involved in overhead sports, such as baseball, American football, volleyball, tennis, gymnastics, weight lifting, and people involved in vigorous workouts such as heavy bench pressing.
Anatomy of the Elbow
The elbow is a complex hinge joint formed by the articulation of three bones - humerus, radius and ulna. The upper arm bone or humerus connects the shoulder to the elbow, forming the upper portion of the hinge joint. The lower arm consists of two bones, the radius and the ulna. These connect the elbow to the wrist to form the lower portion of the hinge joint. A joint capsule surrounds the elbow joint, which contains a lubricating fluid called synovial fluid. The elbow is held in place with the support of various soft tissues including cartilage, tendons, ligaments, muscles, nerves, blood vessels, and bursae.
Causes of Lateral Impingement of the Elbow
Some of the conditions that can trigger lateral elbow impingement include:
- Synovitis or inflammation of the synovium, a membrane that lines the joints
- Bursitis or inflammation of the bursae, fluid-filled sacs that cushion the joints
- Bone spurs or abnormal bony projections along the ends of bones
- Inflammation of the joints
- Rupture of cartilage or other soft tissues
- Stiffening of the ligaments, muscles, and tendons
Signs and Symptoms of Lateral Impingement of the Elbow
Some of the sign and symptoms of lateral elbow impingement include:
- Pain and tenderness at the elbow
- Joint stiffness
- Locking and catching of the elbow
- Abnormal popping or crackling sound
- Joint effusion
- Decreased range of motion
- Swelling and bruising of the elbow
- Inability or difficulty to extend or straighten the elbow
Diagnosis of Lateral Impingement of the Elbow
Your doctor will review your symptoms and medical history and perform a physical examination to check for range of motion, stability, and strength of your elbow. If necessary, your doctor will order certain imaging tests such as X-rays, MRI, CT scan, or ultrasound to confirm the diagnosis and narrow down any associated problems.
Treatment for Lateral Impingement of the Elbow
Treatment for lateral elbow impingement includes both surgical as well as non-surgical options. Your doctor will decide the best option based on the condition of your elbow.
Nonsurgical treatment options may include:
- Ice: Application of ice packs on the elbow to decrease swelling and pain
- Activity Modification: Avoiding activities that trigger symptoms and changing lifestyle
- Physical Therapy: Regular exercise regimen to improve range of motion and strengthen elbow muscles
- Anti-inflammatory Medication: Meds like naproxen and ibuprofen can relieve inflammation and pain.
- Cortisone Injection: If physical therapy, medications, rest, and activity modification do not yield the desired results, then a cortisone injection may be helpful. Cortisone is a very effective anti-inflammatory medicine for bursitis and long-term pain reliever for tears and structural damage.
Surgical treatment options may include:
- Arthroscopy: Your doctor will be able to repair damage to soft tissues of the elbow by using this technique. Arthroscopy is a minimally invasive surgical procedure that involves making small keyhole incisions to pass a fiber-optic tube with a tiny camera called an arthroscope and miniature instruments into the elbow joint. The camera displays pictures of the affected region on a television screen and the doctor uses these images to carry out the necessary repair.
- Open Surgery: A traditional open surgery approach would require a large surgical incision to be made to repair the affected region if the injury is large and complex. Open surgery has been utilized for joint debridement (removal of damaged cartilage or bone) or removal of osteophytes (bone spurs).


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All photos by James D. Schwartz / The Urban Country
Seven years ago, I regularly consulted the weather forecast (almost obsessively), making sure there was no rain on the way. I didn't like to show up soaking wet at the office, nor did I enjoy skunk streaks up my back.
Much has changed since then. I actually enjoy riding in the rain these days. It can partially be attributed to wisdom that comes with age; plus a lot of trial and error. Seven years later, I rarely ever look at the weather forecast – except on the odd winter day, or if I'm traveling.
Other bicycling blogs will give you long lists of gear that you need to endure the rain. Over here on The Urban Country, we are more pragmatic and try to find the minimum required gear to make that ride in the rain comfortable and not too overwhelming.
Just like bicycles, rain and weather come in a variety of forms. So I have broken this post down to provide other bicyclists with some tips that I've learned from my experience over the years.
This is by no means an exhaustive list, and just because these simple ideas work well for me, it doesn't mean my way is the only way to go. I'd love to hear tips from readers on what makes your ride in the rain comfortable and pleasurable.
First, the basics:
I rode for years without fenders (mud guards). They just aren't common on North American bikes. There is a store here in Toronto that promotes chic urban bicycles with fenders and chain guards on posters on the wall, but not a single bike they sell comes equipped with these components.
I gradually worked my way up from no fenders, to a rear basket (which protected my back), to finally installing fenders on my old Trek, to finally buying a Dutch bike last year that came equipped with fenders, a full chain cover, and internal maintenance-free components.
The fenders make a world of difference when riding in the rain. And I'm not talking about those fenders that sit 20 centimeters above the rear wheel. I'm talking about the fenders that come standard on most Dutch, British and Chinese style bicycles.
Once your bike is equipped with the fenders, we can talk about the "carry-ons".
The carry-on gear
I never leave home without my "rain gear". Carrying this "gear" with me all the time is one of the reasons I never need to check the forecast. Ignorance truly is bliss in a society where we stress over the most trivial of matters. And proper preparation makes it easy to discard the weather forecasts.
My carry-on rain gear consists of but three core items. First is my hat. I picked up this fisherman-style hat in China last year for $3. It keeps my head completely dry even in the worst of downpours.
Secondly, I bring a pair of splash pants that I throw on top of my regular clothes in hard downpours. I paid $40 for these pants from a local outdoor outfitters store. They are lightweight and fold up nicely in my pannier bag.
Third is my thin water-resistant hooded jacket that I either wear under my winter coat in colder weather, or above my regular clothes in warmer weather. The hooded jacket is nice especially in the winter because it adds an extra layer of warmth and allows me to zip up and cover my face when it's really cold or while it's hailing.
That's it. Those are the three items that keep me dry whether I'm in shorts, jeans or a suit.
This is a photo of me in "business casual" attire with my rain hat and jacket underneath my winter coat after riding in a light rainfall.
The "Extras"
There are very rare days where the 3 "carry on" items aren't enough to keep me completely dry, so I will sometimes decide to wear my waterproof boots through torrential rain while transporting my dress shoes in a dry sack on my rear rack. I also generally wear these boots to keep my feet warm on cold winter days.
In China, it is very common for people on bicycles to carry umbrellas – both to protect from the rain, and from the sun. Similarly in the Netherlands, people use umbrellas on their bicycles. (Unfortunately, this is an illegal act here in Toronto):
Photo courtesy of Brian Underwood
Being prepared and staying dry helps to make riding in the rain more enjoyable. With very little effort you can show up at your destination dry, and you don't need to carry a large backpack with a change of clothes or heavy rain gear.
You might even find yourself singing in the rain one day.
James D. Schwartz is the editor of The Urban Country. You can contact James at firstname.lastname@example.com.
Related Articles:
- Bicycling in the Winter (Nov 2010)
- Barriers to Cycling: Debunking the Myths (Nov 2009)
- Rush Hour in Toronto At –11 Celsius (March 2011)
- Anatomy of a Dutch Bicycle (Jan 2011)


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BAIR Lab forms research partnership with China's Huawei Noah's Ark Lab
The BAIR Lab (Berkeley Artificial Intelligence Research Lab) will be forming a research partnership with China's Huawei Noah's Ark Laboratory to the initial tune of $1M covering areas like deep learning, reinforcement learning, machine learning, natural language processing and computer vision. Machine learning has become a central part of a lot of basic large-scale computing projects, from bots to search engines and more. Computer vision is being applied in areas like facial recognition tech, AR, VR and self-driving applications. NLP is what makes services like Amazon's Alexa, Apple's Siri, and Microsoft's Cortana work.


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Previous Lesson
Complete and Continue
Christmas Carols Made Easy ~ a Singing Made Easy course
Introduction & FAQ
How to Use (3:02)
Certificate of Completion
All Christmas Carols Made Easy Lessons, Song Sheets, & Coloring Pages
Free sample: Lesson #6 "The Holly and the Ivy" (for those thinking about buying) (1:10)
Course Tour Video (3:38)
Refer a Friend Program
Christmas Carols Made Easy Lessons
#1: Kling, Glöckchen (Ring, Little Bells), Germany (1:43)
#2: King Jesus Hath a Garden, Holland (4:55)
#3: The Son of Mary (El Noi de la Mare), Catalonian Carol, Spain (1:32)
#4: Campana Sobre Campana (Bells over Bethlehem) Andalucian Carol, Spain (3:58)
#5: Song of the Wise Men, Puerto Rico (1:22)
#6: The Holly and the Ivy, England (1:10)
#7: Rise Up, Shepherd, and Follow, America (2:22)
#8: Il est né, le divin Enfant (He is Born, the Holy Child), France (2:22)
#9: Un Flambeau, Jeanette, Isabelle (Bring a Torch, Jeannette, Isabella), France (1:32)
#10: What Child is This? England (1:38)
#11: Ding Dong! Merrily on High, France (1:42)
Bonus Songs from "Singing Made Easy" Levels 1-5
Level 1: I Saw Three Ships (0:54)
Level 2: O Come, Little Children (1:51)
Level 3: Sleep, O Holy Child of Mine (Italian) (2:48)
Level 4: Fum, Fum, Fum (Catalonian, in Spanish) (3:03)
Level 5: Virgin's Slumber Song (1:42)
Bonus Christmas Lyric Song Sheets & Twelve Days of Christmas Printable Set
Song Sheets, Twelve Days Set, & Sing-Along Video
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Vocal Warm-up #1 (audio and video) (8:41)
Vocal Warm-up #2 (audio and video) (11:12)
Vocal Warm-up #3 (video) (7:13)
Vocal Warm-up #4 (video) (7:28)
Vocal Warm-up #5 (video) (9:48)
Vocal Warm-up #6 (video) (6:58)
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All Available Courses & Coupon Code
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Sitting in a refrigerator in a Swedish laboratory is what promises to be a cheap and effective cancer treatment. So why are the trials to bring it to market not going ahead?
On the snow-clotted plains of central Sweden where Wotan and Thor, the clamorous gods of magic and death, once held sway, a young, self-deprecating gene therapist has invented a virus that eliminates the type of cancer that killed Steve Jobs.
'Not "eliminates"! Not "invented", no!' interrupts Professor Magnus Essand, panicked, when I Skype him to ask about this explosive achievement.
'Our results are only in the lab so far, not in humans, and many treatments that work in the lab can turn out to be not so effective in humans. However, adenovirus serotype 5 is a common virus in which we have achieved transcriptional targeting by replacing an endogenous viral promoter sequence by…'
It sounds too kindly of the gods to be true: a virus that eats cancer.
'I sometimes use the phrase "an assassin who kills all the bad guys",' Prof Essand agrees contentedly.
Cheap to produce, the virus is exquisitely precise, with only mild, flu-like side-effects in humans. Photographs in research reports show tumours in test mice melting away.
'It is amazing,' Prof Essand gleams in wonder. 'It's better than anything else. Tumour cell lines that are resistant to every other drug, it kills them in these animals.'
Yet as things stand, Ad5[CgA-E1A-miR122]PTD – to give it the full gush of its most up-to-date scientific name – is never going to be tested to see if it might also save humans. Since 2010 it has been kept in a bedsit-sized mini freezer in a busy lobby outside Prof Essand's office, gathering frost. ('Would you like to see?' He raises his laptop computer and turns, so its camera picks out a table-top Electrolux next to the lab's main corridor.)
Two hundred metres away is the Uppsala University Hospital, a European Centre of Excellence in Neuroendocrine Tumours. Patients fly in from all over the world to be seen here, especially from America, where treatment for certain types of cancer lags five years behind Europe. Yet even when these sufferers have nothing else to hope for, have only months left to live, wave platinum credit cards and are prepared to sign papers agreeing to try anything, to hell with the side-effects, the oncologists are not permitted – would find themselves behind bars if they tried – to race down the corridors and snatch the solution out of Prof Essand's freezer.
I found out about Prof Magnus Essand by stalking him. Two and a half years ago the friend who edits all my work – the biographer and genius transformer of rotten sentences and misdirected ideas, Dido Davies – was diagnosed with neuroendocrine tumours, the exact type of cancer that Steve Jobs had. Every three weeks she would emerge from the hospital after eight hours of chemotherapy infusion, as pale as ice but nevertheless chortling and optimistic, whereas I (having spent the day battling Dido's brutal edits to my work, among drip tubes) would stumble back home, crack open whisky and cigarettes, and slump by the computer. Although chemotherapy shrank the tumour, it did not cure it. There had to be something better.
It was on one of those evenings that I came across a blog about a quack in Mexico who had an idea about using sub-molecular particles – nanotechnology. Quacks provide a very useful service to medical tyros such as myself, because they read all the best journals the day they appear and by the end of the week have turned the results into potions and tinctures. It's like Tommy Lee Jones in Men in Black reading the National Enquirer to find out what aliens are up to, because that's the only paper trashy enough to print the truth. Keep an eye on what the quacks are saying, and you have an idea of what might be promising at the Wild West frontier of medicine. This particular quack was in prison awaiting trial for the manslaughter (by quackery) of one of his patients, but his nanotechnology website led, via a chain of links, to a YouTube lecture about an astounding new therapy for neuroendocrine cancer based on pig microbes, which is currently being put through a variety of clinical trials in America.
I stopped the video and took a snapshot of the poster behind the lecturer's podium listing useful research company addresses; on the website of one of these organisations was a reference to a scholarly article that, when I checked through the footnotes, led, via a doctoral thesis, to a Skype address – which I dialled.
'Hey! Hey!' Prof Magnus Essand answered.
To geneticists, the science makes perfect sense. It is a fact of human biology that healthy cells are programmed to die when they become infected by a virus, because this prevents the virus spreading to other parts of the body. But a cancerous cell is immortal; through its mutations it has somehow managed to turn off the bits of its genetic programme that enforce cell suicide. This means that, if a suitable virus infects a cancer cell, it could continue to replicate inside it uncontrollably, and causes the cell to 'lyse' – or, in non-technical language, tear apart. The progeny viruses then spread to cancer cells nearby and repeat the process. A virus becomes, in effect, a cancer of cancer. In Prof Essand's laboratory studies his virus surges through the bloodstreams of test animals, rupturing cancerous cells with Viking rapacity.
The Uppsala virus isn't unique. Since the 1880s, doctors have known that viral infections can cause dramatic reductions in tumours. In 1890 an Italian clinician discovered that prostitutes with cervical cancer went into remission when they were vaccinated against rabies, and for several years he wandered the Tuscan countryside injecting women with dog saliva. In another, 20th-century, case, a 14-year-old boy with lymphatic leukaemia caught chickenpox: within a few days his grotesquely enlarged liver and spleen had returned to ordinary size; his explosive white blood cell count had shrunk nearly 50-fold, back to normal.
But it wasn't until the 1990s, and the boom in understanding of genetics, that scientists finally learnt how to harness and enhance this effect. Two decades later, the first results are starting to be discussed in cancer journals.
So why is Magnus – did he mind if I called him 'Magnus'? – about to stop his work?
A reticent, gently doleful-looking man, he has a Swedish chirrup that makes him sound jolly whatever his actual mood. On the web, the first links to him proclaim the Essand Band, his rock group. 'Money,' he said. 'Lack of.'
'Lack of how much money? Give me a figure,' I pressed. 'What sort of price are we talking about to get this virus out of your freezer and give these people a chance of life?'
Magnus has light brown hair that, like his voice, refuses to cooperate. No matter how much he ruffles it, it looks politely combed. He wriggled his fingers through it now, raised his eyes and squinted in calculation, then looked back into his laptop camera. 'About a million pounds?'
More people have full-blown neuroendocrine tumours (known as NETs or carcinoids) than stomach, pancreas, oesophagus or liver cancer. And the incidence is growing: there has been a five-fold increase in the number of people diagnosed in the last 30 years.
In medical school, students are taught 'when you hear hoof beats, think horses not zebras' – don't diagnose a rare disease when there's a more prob-able explanation. It leads to frequent misdiagnoses: until the death of Steve Jobs, NETs were considered the zebras of cancer, and dismissed as irritable bowel syndrome, flu or the patient getting in a tizz. But doctors are now realising that NETs are much more prevalent than previously thought. In a recent set of post-mortem investigations, scientists cut open more than 30,000 bodies, and ran their hands down the intestines of the dead as if they were squeezing out sausage skins. One in every 100 of them had the distinctive gritty bumps of NETs. That's two people in every rush-hour tube carriage on your way home from work, or scaled up, 700,000 people in Britain, or roughly twice the population of the city of Manchester. The majority of these tumours are benign; but a small percentage of them, for reasons that no one understands, burst into malignancy.
Many other cancers, if they spread, acquire certain features of neuroendocrine tumours. The first person to own a successful anti-neuroendocrine cancer drug – it doesn't even have to cure the disease, just slow its progress as anti-retrovirals have done with Aids – will be not only healthy but also Steve Jobs-rich. Last year the pharmaceuticals giant Amgen bought a cancer-assassinating version of the herpes virus for $1 billion. That Magnus's virus could be held up by a minuscule £1 million dumbfounded me.
'That's a banker's bonus,' I said. 'Less than a rock star's gold toilet seat. It's the best bargain going. If I found someone to give you this money, would you start the clinical trials?'
'Of course,' replied Magnus. 'Shall I ask the Swedish Cancer Board how soon we can begin?'
I do not have a million pounds. But for £68 I flew to Uppsala. I wanted to pester Prof Essand about his work, face to face, and see this virus, face to petri dish. I wanted to slip some into my mittens, smuggle it back to England in an ice pack and jab it into Dido.
Magnus's work is already funded by the Swedish Cancer Society and the Swedish Children Cancer Society (neuroblastoma, the most common cancer in infants, is a type of neuroendocrine tumour). A virus that he previously developed (against prostate cancer) is about to enter human trials in Rotterdam, supported by a European Union grant.
The difficulty with Magnus's virus is not that it is outré, but that it is not outré enough. It is a modified version of an adenovirus, which is known to be safe in humans. It originates from humans, occurring naturally in the adenoids. The disadvantage is that it is too safe: the immune system has had thousands of years to learn how to dispatch such viruses the moment they stray out of the adenoids. It is not the fact that Magnus is using a virus to deal with cancer that makes his investigation potentially so valuable, but the novel way he has devised to get round this problem of instant elimination by the immune system, and enable the virus to spread through tumours in other parts of the body.
The closer you get to manipulating the cellular forces of human existence, the more you sound like a schoolboy babbling about his model aeroplane. Everything in the modern genetics lab is done with kits. There are no fizzing computer lights or fractionating columns dribbling out coagulations of genetic soup in Magnus's lab; not a single Bunsen burner. Each narrow laboratory room has pale, uncluttered melamine worktops running down both sides, wall units above and small blue cardboard cartons dotted everywhere. Even in their genetics labs, Swedes enjoy an air of flatpack-ness. The most advanced medical lab in the world, and it looks like a half-fitted kitchen.
To make and test their virus, Magnus buys cell lines pre-fab (including 'human foreskin fibro-blast') for $50-100 from a company in California; DNA and 'enzyme mix' arrive in $179 packets from Indiana; protein concentrations are tested 'according to the manufacturer's instructions' with a DIY kit ($117) from Illinois; and for $79, a parcel from Santa Cruz contains (I haven't made this up) 'horseradish peroxidase conjugated donkey anti-goat antibody'.
In a room next to Magnus's office, a chatty woman with a ponytail is putting DNA inside bacteria. This God-like operation of primal delicacy involves taking a test tube with a yellow top from a $146 Qiagen kit, squirting in a bit of liquid with a pipette and putting the result in a box similar to a microwave: 'turn the dial to 25 kilovolts and oophlah! The bacteria, they get scared, they let the DNA in. All done,' the woman says. As the bacteria divide, the desirable viral fragments increase.
What costs the £1 million (less than two per cent of the price of Francis Bacon's Triptych 1976) that Magnus needs to bring this medicine to patients is not the production, but the health-and-safety paperwork to get the trials started. Trials come in three phases. What Magnus was suggesting for his trifling £1 million (two Mont Blanc diamond-encrusted pens) was not just a phase I trial, but also a phase II, which, all being well, would bring the virus right to the point where a big pharmaceuticals company would pay 10 or 100 times as much to take it over and organise the phase III trial required by law to presage full-scale drug development.
'So, if Calvin Klein or Elton John or… Paris Hilton stumped up a million, could they have the virus named after them?'
'Why not?' Magnus nodded, showing me the bacteria incubator, which looks like an industrial clothes washer, only less complicated. 'We can make an even better one for two million.'
There are reasons to be cautious. A recent investigation by Amgen found that 47 of 53 papers (on all medical subjects, not just viruses) by academics in top peer-reviewed science journals contained results that couldn't be reproduced, even though company scientists repeated the experiments up to 50 times. 'That's why we have to have such a careful peer-review process,' Dr Tim Meyer, Dido's energetic, soft-spoken oncologist, warns. 'Everybody thinks that their new treatment for cancer is worth funding, but everybody is also keen that only good-quality research is funded.' Similar to Prof Essand in youth but less polite of hair, Dr Meyer is the co-director of the Experimental Cancer Medicine Centre at University College London. Beside his office, banks of white-coated researchers are bent over desks, busy with pipettes and microscopes. His team pursues an exciting brew of new anti-cancer ideas: antibody-targeted therapy, vascular therapy, DNA binding agents and photodynamic therapy. Each of these shows remarkable promise. But even for such a brilliant and innovative team as this, money is not flowing.
Everyone in cancer science is fighting for ever-decreasing small pools of cash, especially now the government has started tiptoeing into charities at night and rifling the collection boxes. It is big news that Dr Meyer and the UCL team won a grant of £2.5 million, spread out over the next five years, to continue his institute's cutting-edge investigations into cancers that kill off thousands of us every week: leukaemia; melanoma; gynaecological, gastrointestinal and prostate cancers. Without this money, he would have had to sack 13 members of staff. The sum of £2.5 million is roughly what Madonna earns in 10 days.
He peers at Magnus's pairs of photographs of splayed rodents with glowing tumours in one shot that have vanished in the next. He knows the Uppsala neuroendocrine team well and has great respect for them. 'It may be good,' he agrees. But until Magnus's findings are tested in a clinical trial, nobody knows how good the work is. Astonishing results in animals are often disappointing in humans. 'We all need to be subject to the same rules of competitive grant funding and peer review in order to use scarce resources in the most effective manner.'
Back at home with whisky and fags, I nursed my entrepreneurialism. There are currently about half a dozen cancer research institutes in Europe developing adenoviruses to treat cancer – all of them pathetically short of cash. Enter the Vanity Virus Initiative. Pop a couple of million over to Uppsala University, and you will go down in medical books as the kind heart who relieved Ad5[CgA-E1A-miR122]PTD of its hideous hump of a moniker, and gave it the glamour of your own name. What's the worst that can happen? Even if Magnus's innovations don't work in clinical trials the negative results will be invaluable for the next generation of viruses. For the rest of time, your name will pop up in the reference sections of medical papers as the (insert your name here) virus that enabled researchers to find the cure for cancer by avoiding Magnus's error.
On my third glass of whisky, I wrote an email to Dr Meyer suggesting that he issue a shopping list each year at the time that bankers receive their bonuses, which could be circulated in the City. The list would itemise the therapies that his Experimental Cancer Medicine Centre have selected for support, and quantify how much would be needed in each case to cover all outstanding funds and ensure that the work is branded with your name.
The corridors connecting the different research departments of the Uppsala medical campus are built underground, in order to protect the staff from death during the Swedish winters. Professors and lab technicians zip back and forth along these enormous rectangular tunnels on scooters, occasionally scratching their heads at the tangled intersections where three or four passageways meet at once, then pushing off again, gowns flying, one leg pounding the concrete floor like a piston, until they find the right door, drop the scooter and rise back upstairs by lift. Suspended from the ceiling of these corridors is a vacuum tube that schluuuuups up tissue samples at top speed, and delivers them to the appropriate investigative team. Magnus led me along these tunnels to the Uppsala University Hospital, to visit the chief oncologist, Kjell (pronounced 'Shell') Oberg – the man who will run the trial once the money is in place.
'The trouble with Magnus's virus is Magnus is Swedish,' he says, wincing and clutching the air with frustration.
'It is so,' Magnus agrees sorrowfully. Swedishly uninterested in profiteering, devoted only to the purity of science, Magnus and his co-workers on this virus have already published the details of their experiments in leading journals around the world, which means that the modified virus as it stands can no longer be patented. And without a patent to make the virus commercial, no one will invest. Even if I could raise the £2 million (I want only the best version) to get the therapy to the end of phase II trials, no organisation is going to step forward to run the phase III trial that is necessary to make the therapy public.
'Is that because pharmaceuticals companies are run by ruthless plutocrats who tuck into roast baby with cranberry sauce for lunch and laugh at the sick?' I ask sneerily.
'It is because,' Kjell corrects me, 'only if there's a big profit can such companies ensure that everyone involved earns enough to pay their mortgage.'
There is no ready source of public funds, either. For reasons understood only by Wotan and Thor, the Swedish government refuses to finance clinical trials in humans, even when the results could potentially slash the country's health bill by billions of kronor.
All is not lost, however. Kjell does not have to wait until the end of the trials – which could take as much as 10 years – for the full, three-phase process before being able to inject Magnus's virus into his patients, because as soon as the test samples are approved and ready for use, he can by European law start offering the medicine, on an individual basis, to patients who sign a waiver confirming that they're prepared to risk experimental treatments. Within 18 months he could be starting his human case-studies.
At several moments during my research into this cancer-delaying virus from the forests of Scandinavia I have felt as though there were someone schlocky from Hollywood operating behind the scenes. The serendipitous discovery of it on the internet; the appalling frustration of being able to see the new therapy, to stand with my hand against the freezer door knowing that it is three inches away, not well-guarded, and that it might work even in its crude current state, but that I may not use it; the thrill of Kjell Oberg's powerful
support; the despair over the lack of such a silly, artificial thing as a patent. Now, Dr Leja steps into the narrative: she is the virologist whose brilliant doctoral thesis first put me on to the cancer-eating-virus-left-in-a-freezer, and whose name heads all the subsequent breakthrough research papers about this therapy. She turns out to be 29, to look like Scarlett Johansson and to wear voluptuous red lipstick.
Justyna Leja slinks up from her chair, shakes my hand and immediately sets off into a baffling technical discussion with Magnus about a good way to get the patent back for the virus, by a subtle manipulation that involves something called a 'new backbone'. She also has in mind a small extra tweak to the new-backboned microbe's outer coat, which will mean that the virus not only bursts the cancer cells it infects, but also provokes the immune system to attack tumours directly. It will be easy to see if it works in animals – but is it worth lumbering the current virus with it for use in humans, who tend to be less responsive? The extra preparatory work could delay the phase I and II trials for a further year.
Back at his lab, Magnus opened up the infamous freezer. I took a step towards the plastic flasks of virus: he nipped the door shut with an appreciative smile.
'What would you do,' I asked bitterly, returning my hand to my pocket, 'if it were your wife who had the disease, or one of your sons whose photograph I saw on your desk?'
He glanced back at the freezer. Although his lab samples are not made to pharmaceutical grade, they would be only marginally less trustworthy than a fully-sanctioned, health-and-safety certified product that is between 1,000 and 10,000 times more expensive.
'I don't know,' he groaned, tugging his hair in despair at the thought. 'I don't know.'
To donate money to Professor Magnus Essand's research on viral treatments for neuroendocrine cancer, send contributions to Uppsala University, The Oncolytic Virus Fund, Box 256, SE-751 05 Uppsala, Sweden, or visit www.uu.se/en/support/oncolytic. Contributions will be acknowledged in scientific publications and in association with the clinical trial. A donation of £1 million will ensure the virus is named in your honour
Bron: telegraph.co.uk
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Lowering the drinking age is unlikely to curb college binge drinking
Although presidents at some U.S. colleges have argued that lowering the minimum legal drinking age could help curb binge drinking on campuses, a new study in the January issue of the Journal of Studies on Alcohol and Drugs suggests such a measure would be ineffective.
In 2008, a group of college presidents and chancellors formed the Amethyst Initiative, a call to rethink the current minimum legal drinking age of 21. They argue that the law encourages underage college students to drink at parties, where binge drinking is common. The main argument states that if students as young as 18 could legally drink in bars and restaurants, they might instead learn more-moderate drinking habits, which could then lead to less binge drinking on college campuses.
So far, 135 college presidents have signed the Initiative's public statement urging lawmakers to reconsider the legal drinking age.
But to simply lower the drinking age without an understanding of its effects would constitute a "radical experiment," said Richard A. Scribner, M.D., M.P.H., of the Louisiana State University School of Public Health, one of the researchers on the new study.
So Scribner and colleagues at BioMedware Corporation in Ann Arbor, MI, and other institutions used a mathematical model to estimate the effects that a lower drinking age would have on college binge drinking.
The model, developed based on survey data from students at 32 U.S. colleges, aimed to evaluate the "misperception effect" emphasized by the Amethyst Initiative -- that is, the idea that underage students widely perceive "normal" drinking levels to be higher than they actually are and that students would adjust their own habits if they were surrounded by social drinkers rather than binge-drinking party-goers.
Overall, the researchers found that the campuses that were most likely to see a decline in binge drinking from a lowered legal drinking age were those that had the poorest enforcement of underage drinking laws -- being surrounded, for instance, by bars that do not check identification -- and a significant level of student misperception of "normal" drinking (that is, students thinking that the average fellow student drinks much more than he or she actually does). If misperception levels were not present or were at the levels shown by the survey data, these campuses would likely see more binge-drinking if the legal age were lowered.
On "drier" campuses, the study found, student misperceptions would have to be even greater.
"The higher the level of enforcement of underage drinking laws, the higher the level of misperception would have to be for the Amethyst Initiative to have any hope of being effective," explained lead researcher Dr. Jawaid W. Rasul, of BioMedware Corporation. "The misperception effect would have to be extremely large."
And without data supporting the existence of such high levels of student misperception, Rasul said, lowering the legal drinking age would be unlikely to curb college binge drinking.
Scribner also pointed out that lowering the drinking age would not only affect college students but all currently underage young adults. And past research has suggested that when alcohol becomes more readily accessible to young people, alcohol-related problems, such as drunk driving, go up.


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Patricia F. Fitzpatrick Dimond Ph.D. Technical Editor of Clinical OMICs President of BioInsight Communications
Do bacteria contribute to human health, and how?
As organizers and participants gear up for the Fourth International Human Microbiome Congress 2013 in Hangzhou, September 13th–15th, research reports continue to document the critical role of bacteria in human health. At the same time, a wealth of probiotic mythology promising that good gut bacteria can cure everything from Crohn's disease and obesity to cancer continues to be misleading.
But there is some truth in advertising, if the power of the biome could be harnessed in a rational way. As Martin J. Blaser, M.D., Muriel G. and George W. Singer professor of translational medicine and director of Human Microbiome Program at the New York University School of Medicine, put it in an interview for a New Yorker article, "Germs make us sick. But everyone focuses on the harm. And it's not that simple, because without most of these organisms we could never survive."
The almost ten thousand bacterial species we share our bodies with, scientists say, outnumber our own by ten to one, and weigh about three pounds—the same as our brain. This "microbiome" plays such a crucial role in our lives that scientists like Blaser have begun to reconsider "what it means to be human."
The Human Microbiome Project
In Nature last January, David A. Relman, M.D., and his colleagues commented that "the shared evolutionary fate of humans and their symbiotic bacteria has selected for mutualistic interactions that are essential for human health, and ecological or genetic changes that uncouple this shared fate can result in disease. In this way, looking to ecological and evolutionary principles might provide new strategies for restoring and maintaining human health."
But while knowledge continues to accumulate detailing how bacteria interact among themselves, with human cells, and how their metabolism affects their human habitats, "there are relatively few circumstances where you can meet a patient who is benefitting from this," says Dr. Relman, adding that our biome is "a complex and dynamic network." Dr. Relman is a professor of medicine and of microbiology & immunology at Stanford University, and his research program focuses on the human microbiome.
And an individual's microbiome is as unique as the DNA in their cells, investigators are discovering. In June 2012, in an article in Nature entitled "Structure, function, and diversity of the healthy human microbiome," results of studies conducted by the Human Microbiome Project reported, "We found the diversity and abundance of each habitat's signature microbes to vary widely even among healthy subjects, with strong niche specialization both within and among individuals," niche meaning the intestinal tract and other body mucosa that microbes habitually inhabit.
The five-year NIH-funded $157 million project sequenced and classified 900 microbes believed to play a role in human health. Goals of the project included development of microbiome taxonomic, metagenomic, and functional data from clinical biospecimens obtained from a cohort(s) of carefully phenotyped subjects with a specific disease or health state, and the combination of the microbiome and host data to produce a community resource.
But Dr. Relman noted with regard to expectations generated around the information produced from the microbiome project, "There's sensitivity about the expected returns. We need to be grounded about what it is we'll be able to gain at what point in time. I think the shorter-term gains may be around diagnostics, and novel ways of classifying both health and disease."
The long-term objective of the initiative is to develop a dataset that the community can utilize to explore whether study of the human microbiome beyond sequenced-based analyses will yield important new insights in understanding human health and disease.
The consortium of scientists have already found the diversity and abundance of each habitat's (gut, skin, and vagina) signature microbes varied widely even among healthy subjects, with strong niche specialization both within and among individuals.
The project encountered an estimated 81–99% of the genera, enzyme families, and community configurations occupied by the healthy Western microbiome. Metagenomic carriage of metabolic pathways was stable among individuals despite variation in community structure, and ethnic/racial background proved to be one of the strongest associations of both pathways and microbes with clinical metadata.
Analysis of the sequences of the first 178 microbes, which was published in the May 21, 2010, issue of Science, "held some surprises" particularly with regard to the extent and complexity of microbial diversity. About 90% of their DNA was previously unknown. The study also identified novel genes and proteins that contribute to human health and disease.
Data emerging from this project, consortium investigators hope, could lead to development of new diagnostic tests because individual biomes are as unique, some scientists say, as an individual's DNA.
Quantitative Metagenomics
And this data is already enabling new research. Earlier this year, Danish research, citing the obesity epidemic in developed nations, reported the human gut microbial composition in a population sample of 123 nonobese and 169 obese Danish individuals. Establishment of a catalog of bacterial genes from the human gut, the researchers said, encouraged them to ask whether variation in the gut microbiome at gene and species levels defines subsets of individuals in the adult population who are at increased risk of obesity-related metabolic disorders.
The abundance of known intestinal bacteria can be assessed, the authors said, by the mapping of a large number of sequencing reads from total fecal DNA onto a reference set of their genomes. This "quantitative metagenomics" approach was extended by the authors to assess the abundance of genes from the reference catalog in a cohort of 292 nonobese and obese individuals.
They found that two groups of individuals differed by the number of gut microbial genes and therefore, gut bacterial richness. Individuals with a low bacterial richness (23% of the population) were characterized by more marked overall adiposity, insulin resistance, and dyslipidemia and a more pronounced inflammatory phenotype when compared with high bacterial richness individuals.
The obese individuals among the lower bacterial richness group also gain more weight over time. Only a few bacterial species are sufficient to distinguish between individuals with high and low bacterial richness, and even between lean and obese participants. Our classifications based on variation in the gut microbiome identify subsets of individuals in the general white adult population who may be at increased risk of progressing to adiposity-associated comorbidities.
The implications individual microbiomes has, investigators discovered, clear implications for health and disease. Jeffrey Gordon, M.D., director of the Center for Genome Sciences and Systems Biology, Washington University School of Medicine, and his researchers in his laboratory at Washington University, who this August reported experiments introducing gut microbiomes from lean and obese humans into mice with some unexpected results, showed the bacteria could transfer characteristic of lean animals into obese animal, or prevent the development of obesity.
Several years ago, in another study, Dr. Gordon described two groups of beneficial bacteria that are dominant in the human gut, the Bacteroidetes and the Firmicutes. When Gordon's team had 12 obese people follow either a low-fat or a low-carb diet to lose weight, the result was more Bacteroidetes and fewer Firmicutes—the profile of slim people. The more Bacteroidetes, the more weight the volunteers lost.
The scientists showed that the relative proportion of Bacteroidetes is decreased in obese people by comparison with lean people, and that this proportion increases with weight loss on two types of low-calorie diet. Their findings indicate that obesity has a microbial component, which might have potential therapeutic implications. But these findings, and relatively simplistic interpretations, helped fuel the frenzy to sell probiotics, rationally or not, despite Dr. Gordon's clear statements about the importance of how the microbiome operates in relation to diet.
But according to Dr. Gordon, at the moment, a far more complicated picture has emerged than just ingesting the right bacteria. He says, "There's an intricate relationship between our diet and how our gut bugs alternately affect us."
"Cocktails of classic probiotics, which people have been trying for years, may have some benefit but the effect seems to be quite small," says Dr. Relman. A targeted approach that manipulates specific species could be more effective, but, Relman adds, "I don't think we're there yet".
Patricia Fitzpatrick Dimond, Ph.D. ([email protected]), is technical editor at Genetic Engineering & Biotechnology News.