ARE WE NATURALLY GOOD OR BAD? by Elena Amézola

ARE WE NATURALLY GOOD OR BAD?

 

 

 

It's a question humanity has repeatedly asked itself, and one way to find out is to take a closer look at the behaviour of babies.… and use puppets.

Are leaders losing touch with reality when they act in a power-hungry way?

Fundamentally speaking, are humans good or bad? It's a question that has repeatedly been asked throughout humanity. For thousands of years, philosophers have debated whether we have a basically good nature that is corrupted by society, or a basically bad nature that is kept in check by society. Psychology has uncovered some evidence which might give the old debate a twist.
One way of asking about our most fundamental characteristics is to look at babies. Babies' minds are a wonderful showcase for human nature. Babies are humans with the absolute minimum of cultural influence – they don't have many friends, have never been to school and haven't read any books. They can't even control their own bowels, let alone speak the language, so their minds are as close to innocent as a human mind can get.
The only problem is that the lack of language makes it tricky to gauge their opinions. Normally we ask people to take part in experiments, giving them instructions or asking them to answer questions, both of which require language. Babies may be cuter to work with, but they are not known for their obedience. What's a curious psychologist to do?
Fortunately, you don't necessarily have to speak to reveal your opinions. Babies will reach for things they want or like, and they will tend to look longer at things that surprise them. Ingenious experiments carried out at Yale University in the US used these measures to look at babies' minds. Their results suggest that even the youngest humans have a sense of right and wrong, and, furthermore, an instinct to prefer good over evil.
How could the experiments tell this? Imagine you are a baby. Since you have a short attention span, the experiment will be shorter and loads more fun than most psychology experiments. It was basically a kind of puppet show; the stage a scene featuring a bright green hill, and the puppets were cut-out shapes with stick on wobbly eyes; a triangle, a square and a circle, each in their own bright colours. What happened next was a short play, as one of the shapes tried to climb the hill, struggling up and falling back down again. Next, the other two shapes got involved, with either one helping the climber up the hill, by pushing up from behind, or the other hindering the climber, by pushing back from above.
Already something amazing, psychologically, is going on here. All humans are able to interpret the events in the play in terms of the story I’ve described. The puppets are just shapes. They don't make human sounds or display human emotions. They just move about, and yet everyone reads these movements as purposeful, and revealing of their characters. You can argue that this “mind reading”, even in infants, shows that it is part of our human nature to believe in other minds.
Great expectations
What happened next tells us even more about human nature. After the show, infants were given the choice of reaching for either the helping or the hindering shape, and it turned out they were much more likely to reach for the helper. This can be explained if they are reading the events of the show in terms of motivations – the shapes aren't just moving at random, but they showed to the infant that the shape pushing uphill "wants" to help out (and so is nice) and the shape pushing downhill "wants" to cause problems (and so is nasty).
The researchers used an encore to confirm these results. Infants saw a second scene in which the climber shape made a choice to move towards either the helper shape or the hinderer shape. The time infants spent looking in each of the two cases revealed what they thought of the outcome. If the climber moved towards the hinderer the infants looked significantly longer than if the climber moved towards the helper. This makes sense if the infants were surprised when the climber approached the hinderer. Moving towards the helper shape would be the happy ending, and obviously it was what the infant expected. If the climber moved towards the hinderer it was a surprise, as much as you or I would be surprised if we saw someone give a hug to a man who had just knocked him over.
The way to make sense of this result is if infants, with their pre-cultural brains had expectations about how people should act. Not only do they interpret the movement of the shapes as resulting from motivations, but they prefer helping motivations over hindering ones.
This doesn't settle the debate over human nature. A cynic would say that it just shows that infants are self-interested and expect others to be the same way. At a minimum though, it shows that tightly bound into the nature of our developing minds is the ability to make sense of the world in terms of motivations, and a basic instinct to prefer friendly intentions over malicious ones. It is on this foundation that adult morality is built.

WHY YOUR BODY JERKS BEFORE YOU FALL ASLEEP - Posted by Angela Blasi

If you have ever wondered why people’s arms and legs twitch suddenly as they are drifting off to sleep, our resident psychologist Tom Stafford has the answer.

As we give up our bodies to sleep, sudden twitches escape our brains, causing our arms and legs to jerk. Some people are startled by them, others are embarrassed. Me, I am fascinated by these twitches, known ashypnic jerks. Nobody knows for sure what causes them, but to me they represent the side effects of a hidden battle for control in the brain that happens each night on the cusp between wakefulness and dreams.

Normally we are paralysed while we sleep. Even during the most vivid dreams our muscles stay relaxed and still, showing little sign of our internal excitement. Events in the outside world usually get ignored: not that I’d recommend doing this but experiments have shown that even if you sleep with your eyes taped open and someone flashes a light at you it is unlikely that it will affect your dreams.

But the door between the dreamer and the outside world is not completely closed. Two kinds of movements escape the dreaming brain, and they each have a different story to tell.

Brain battle

The most common movements we make while asleep are rapid eye-movements. When we dream, our eyes move according to what we are dreaming about. If, for example, we dream we are watching a game of tennis our eyes will move from left to right with each volley. These movements generated in the dream world escape from normal sleep paralysis and leak into the real world. Seeing a sleeping persons' eyes move is the strongest sign that they are dreaming.

Hypnic jerks aren't like this. They are most common in children, when our dreams are most simple and they do not reflect what is happening in the dream world - if you dream of riding a bike you do not move your legs in circles. Instead, hypnic jerks seem to be a sign that the motor system can still exert some control over the body as sleep paralysis begins to take over. Rather than having a single “sleep-wake” switch in the brain for controlling our sleep (i.e. ON at night, OFF during the day), we have two opposing systems balanced against each other that go through a daily dance, where each has to wrest control from the other.

Deep in the brain, below the cortex (the most evolved part of the human brain) lies one of them: a network of nerve cells called the reticular activating system. This is nestled among the parts of the brain that govern basic physiological processes, such as breathing. When the reticular activating system is in full force we feel alert and restless - that is, we are awake.

Opposing this system is the ventrolateral preoptic nucleus: 'ventrolateral' means it is on the underside and towards the edge in the brain, 'preoptic' means it is just before the point where the nerves from the eyes cross. We call it the VLPO. The VLPO drives sleepiness, and its location near the optic nerve is presumably so that it can collect information about the beginning and end of daylight hours, and so influence our sleep cycles.

As the mind gives in to its normal task of interpreting the external world, and starts to generate its own entertainment, the struggle between the reticular activating system and VLPO tilts in favour of the latter. Sleep paralysis sets in. What happens next is not fully clear, but it seems that part of the story is that the struggle for control of the motor system is not quite over yet. Few battles are won completely in a single moment. As sleep paralysis sets in remaining daytime energy kindles and bursts out in seemingly random movements. In other words, hypnic jerks are the last gasps of normal daytime motor control.

Some people report that hypnic jerks happen as they dream they are falling or tripping up. This is an example of the rare phenomenon known as dream incorporation, where something external, such as an alarm clock, is built into your dreams. When this does happen, it illustrates our mind's amazing capacity to generate plausible stories. In dreams, the planning and foresight areas of the brain are suppressed, allowing the mind to react creatively to wherever it wanders - much like a jazz improviser responds to fellow musicians to inspire what they play.

As hypnic jerks escape during the struggle between wake and sleep, the mind is undergoing its own transition. In the waking world we must make sense of external events. In dreams the mind tries to make sense of its own activity, resulting in dreams. Whilst a veil is drawn over most of the external world as we fall asleep, hypnic jerks are obviously close enough to home - being movements of our own bodies - to attract the attention of sleeping consciousness. Along with the hallucinated night-time world they get incorporated into our dreams.

So there is a pleasing symmetry between the two kinds of movements we make when asleep. Rapid eye movements are the traces of dreams that can be seen in the waking world. Hypnic jerks seem to be the traces of waking life that intrude on the dream world.

Why the Flu Is So Relentless, and How Technology Might Help

POSTED BY: YOUR TEACHER

FROM: MIT Technology review

http://www.technologyreview.com/news/510316/why-the-flu-is-so-relentless-and-how-technology-might-help/

Why the Flu Is So Relentless, and How Technology Might Help

Researchers are developing quick-brew vaccines and ones that catch multiple strains of flu.

·          By Susan Young on January 28, 2013

Why It Matters

Current seasonal flu vaccines are not always effective, and new ones are needed every year.

Every year, starting in September, public health officials in the U.S. start prodding you to get this year’s flu shot. But even if you do get one, it is not a guarantee against getting sick.

Why is the common illness so difficult to prevent, and what technologies might change this yearly struggle?  

Seasonal flu is caused by influenza viruses, which can mutate as they spread from person to person, meaning every year brings a new strain of virus. Any antibodies your body produced after getting sick or in response to a flu shot may not work a year later.

Furthermore, each flu season is dominated by several different strains of the virus, and health officials must try to predict which ones to combat because it takes months to produce the vaccine. Every February, the World Health Organizationrecommends which three viruses should be included in the next season’s vaccines for the Northern Hemisphere (the WHO makes a similar recommendation for the Southern Hemisphere each September), and in the U.S., the Food and Drug Administration typically recommends that those three strains be included in the coming season’s vaccine. While this process carries the risk that the vaccine will not match the dominant strains in the next season, it is necessary.

A new way of making flu vaccines could reduce this long timeline and make it possible to react to unexpected outbreaks. Currently, flu vaccine production starts with chicken eggs. A live virus is injected into eggs, where it replicates. Manufacturers then crack open the eggs, harvest and purify the viruses, and kill the pathogens and chop them into smaller pieces. The inactivated pieces from the three chosen strains are then mixed into a flu vaccine, which trains the body’s immune system to respond to the actual virus.

Next year’s vaccine production could be different, as some manufacturers may replace this time-consuming process with a new approach. In November, the FDA approved a new vaccine from Novartis, which is produced in cultured dog kidney cells. And earlier this month, the agency approved a vaccine made by ProteinsSciences in cultured insect cells. The methods “offer the potential for faster start-up of the manufacturing process than traditional egg-based vaccine methods,” says a spokesperson for the FDA. Additionally, they may help people with egg allergies safely get flu vaccines.

Public and private researchers are also working to develop so-called universal flu vaccines that would preclude the need to get a new vaccine every year. When you get the flu or a typical flu shot, your body responds by making antibodies that glom onto a protein in the virus called hemagglutinin. This protein allows the virus to enter cells, and antibodies against it will prevent that entry. However, this protein also mutates quickly, so that the antibodies your body produces this year may not recognize the protein next year.

Ian Wilson’s group at the Scripps Research Institute in La Jolla, California, has been studying the rare antibodies produced in some people that bind to other parts of the virus. Because they bind to regions of the protein that do not change as quickly as the typical targets, the hope is that these antibodies will be able to recognize many different strains of the virus. Over the last few years, different research groups have shown that such antibodies can recognize multiple flu strains, and a study from Wilson’s group and the Crucell Vaccine Institute in September 2012 showed that one antibody can recognize strains from both major subtypes of seasonal influenza, more than had been previously shown.

“A universal vaccine was something that people always talked about, but until recently, there was no evidence for much hope of that,” says Wilson. “But now, it has been demonstrated that gives the desired type of immune response,” he says.   

The challenge now is to develop a vaccine that will elicit such a powerful and effective response and to find a way to test it. “A lot of these more universal antibodies don’t work in the standard tests for antibody efficacy,” says Wilson. This means that manufacturers and regulators like the FDA will have to develop new assay systems. “Even if we had the perfect vaccine in hand today, we wouldn’t have a good and approved way to test it,” says Wilson.

Pennsylvania-based biotech Inovio is taking a different approach to developing a universal vaccine. Instead of inoculating people with an inactivated virus fragment or protein, the company is developing a DNA-based vaccine. To make it protective against multiple flu strains, the company combines DNA sequences from existing virus strains into a single dose. The DNA pieces are delivered by a shot combined with the company’s proprietary delivery system. A handheld device that looks like a pen delivers a small electric field which temporarily opens up cell membranes to allow the DNA vaccine to enter cells, says Inovio CEO Joseph Kim. Once inside cells, the DNA is read by the cell’s own machinery to build viral proteins which will activate the body’ immune system. The result is that the body creates antibodies against a diversity of flu strains.

The company is currently testing the vaccine in people 65 and older as a combination treatment along with existing flu vaccines. The elderly are the most at risk when it comes to flu and are the least protected by current immunizations. Every year, some 35,000 people die because of the flu and “90 percent of the deaths are in people who are 65 and older,” says Kim. “But the seasonal flu vaccine only protects about 10 to 20 percent of the elderly.”

Inovio’s clinical trial has shown that combining the seasonal flu vaccine with the company’s experimental universal vaccine has doubled the number of elderly protected from the flu.   

“It is hard to predict the future, but if we can have a universal vaccine that can protect against all known dominant strains, the likelihood of protecting against future unknown is much higher,” says Kim. “If we are correct, we can change the flu paradigm into one more like what we do with other vaccinations.”

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Susan Young Biomedicine Editor

I’m the biomedicine editor for MIT Technology Review. I look for stories where technology stands to improve human health or advance our understanding of the human condition.  

A monkey into space By: Germán Ramón-Cortés

 

Press TV, the state-run satellite broadcaster, said the animal was launched in a space capsule code named Pishgam, or Pioneer. 

The development coincided with continued stalemate in the unrelated Western effort to persuade Iran to abandon its nuclear enrichment program, which Western powers maintain is designed to create nuclear weapons technology — an assertion Iran denies.

Press TV quoted the director of the Iran Space Agency, Hamid Fazeli, as saying earlier this month that “because of biological similarities between humans and monkeys, the latter were selected for the space mission.” 

He also forecast that Iran would send a human into space within the “next five to eight years,” and said Iran would send its Sharifsat satellite into orbit before the end of March.

There was no independent corroboration of the report, which Press TV called evidence of “yet another” scientific achievement following earlier claims that satellites and living creatures had been launched into space. 

Western monitors have not announced any missiles launchings by Iran in recent days.

The state news agency, IRNA, said the monkey was sent into space on a Kavoshgar rocket that reached a height of 75 miles and “returned its shipment intact,” Reuters reported. The monkey survived, according to Press TV. 

The timing of the reported launching was unclear — either on Monday or within the past few days. An earlier attempt to launch a monkey into space in 2011 was reported to have failed.

A year earlier, Iran said it sent a mouse, a turtle and worms into space.

Western powers are sometimes skeptical of Iranian claims of technical advance, but they also fret that ballistic missiles could be used with nuclear warheads — a concern Iran has dismissed.

The news emerged as Western officials in Brussels said they had offered Iran new dates in February to resume the long-running and inconclusive nuclear talks after Iranian officials turned down a request for a meeting in Istanbul at the end of January, Reuters reported. 

The idea of using animals as a precursor to human spaceflight dates to the 1940s and 1950s and became part of the space race between the United States and the Soviet Union during the cold war.

United States scientists sent a rhesus monkey into space in 1949 but the animal died when a parachute malfunctioned. The Soviet Union lofted dogs into space in 1951 and they returned to earth.

In 1957, Moscow’s scientists were the first to launch an animal — a dog called Laika — into orbit. The Soviet Union also won the race to send a human aloft when Yuri A. Gagarin became the first man to orbit the globe in 1961. 

Spurred to respond, the United States embarked on a space program that led to the moon landing of 1969.

We still have hope- by Andrea Carmona

Mutations Found in Melanomas May Shed Light on How Cancers Grow

By GINA KOLATA

Published: January 24, 2013

http://www.nytimes.com/2013/01/25/science/new-mutations-discovered-in-melanomas.html?ref=science

In a leap forward in understanding the basic science of one of the most lethal cancers, two groups of researchers have found mutations in most melanomas that are unlike any they have seen before in cancer. The changes are in regions that control genes, not in the genes themselves. The mutations are exactly the type caused by exposure to ultraviolet light, indicating they might be among the first DNA changes in a cell’s path to melanoma.

The discoveries, published online Thursday in two papers in the journal Science Express, do not immediately suggest new treatments or ways to prevent melanoma, researchers said. But the findings help explain how melanomas — and, possibly, other cancers — develop and what drives their growth, insights that may be critical to long-term efforts to develop ways to prevent or stop the cancer.

For years, cancer researchers have searched for mutations in genes, but this time, they looked for — and found — mutations in a region that regulates genes. They did it by examining the entire DNA of multiple tumors, studying not just genes but also what has been called the dark matter, the 99 percent of the DNA that includes regions that control genes.

“You could think of this as one glimmer in what has been called cancer’s dark matter,” said Dr. Levi A. Garraway of the Dana-Farber Cancer Institute and the Broad Instituteof Harvard and M.I.T.

The DNA sequences of 70 malignant melanomas led to the new discovery. A small control region was mutated in 7 out of 10 of the tumors, and also, the investigators found, in liver and bladder cancers. The cancer cells had one of two tiny changes that together were more common than any mutation ever found in the genes of melanoma.

A team led by Rajiv Kumar of the German Cancer Research Center in Heidelberg and Dirk Schadendorf of the University of Essen looked for the mutations in a family whose members tended to get melanoma. Four relatives who developed melanoma had inherited one of them, while four who remained melanoma-free did not have it. They also found the mutation in a 36-year-old member of the family who had not developed melanoma but had had many moles, often a sign of risk in families prone to melanoma.

Their findings indicate that those who inherit the mutations might be born with cells that have taken a first step toward cancer.

The mutations spur cells to make an enzyme, telomerase, that keeps cells immortal by preventing them from gradually losing the ends of their chromosome, the telomeres. When telomeres erode, a cell dies. But the enzyme also has other, poorly understood functions that are thought to keep cancer cells alive, said Robert Weinberg, an M.I.T. researcher who studies telomerase and cancer and was not involved with the research. “The paradigm that it does nothing but extend telomeres is a gross oversimplification,” he said.

Abundant telomerase is so important to cancers that it occurs in 90 percent of them, said Immaculata De Vivo, a Harvard Medical School researcher who studies telomerase and cancer and directs a DNA sequencing program. She, too, was not involved with the research.

The results of the two studies presented in the papers “are like a court of law — it’s the preponderance of the evidence,” she said. “We all knew telomerase was important for cancer, but now we are finding the mechanisms, the machinery.”

Scientists were surprised that the mutations in the dark matter of melanoma tumors were so commonplace. Dr. Garraway and his colleagues had the entire DNA sequences for a collection of melanomas — genes as well as the rest of the DNA, including areas that turn genes on and off.

“We said, ‘Let’s just take a look and see if there are any mutations in a regulatory region,’ ” Dr. Garraway said.

At first, they looked at the DNA sequences of 19 tumors. They were amazed to find one or the other of the two mutations in 17 of them. So the researchers decided to look at 51 additional melanomas and a handful of bladder and liver cancers. The mutations popped up again.

“It was really quite striking,” Dr. Garraway said.

But it is not clear how to reverse the mutations’ cancer-causing effects, Dr. Garraway said. And although people have long wanted to block telomerase production in cancer cells, they have not found a drug to do it.

Still, the findings are highly significant, experts said.

“We have always known that just looking at genes alone would provide a limited number of answers about why cancer develops,” said Elaine Mardis of Washington University, who was not involved with the research. “The brakes or the gas that control the genes that cause cancer are as important as gene mutations,” she said. The new papers, Dr. Mardis added, “show where additional answers may lie.”

THE MUSICAL EVENT OF A LIFETIME

By Cameron Mackintosh

The opening night of Les Misérables at the Barbican Theatre on 8 October 1985 was one of those extraordinary occasions when against all the odds a theatrical alchemy took place that made everyone forget the years of work and months of rehearsal – racing against the clock – that went into adapting Hugo’s sweeping masterpiece for the musical stage.

After only a week of previews the show simply soared, and both the audience and the cast were elevated to a state of powerful emotion rarely seen in the theatre. Back in 1982, when I first heard the French concept album, a dream of what the show could be flashed through my mind – that dream was fulfilled beyond my expectations.

Intoxicated by the events of the evening, I rushed off to Fleet Street to get the papers. One of the first I read said “Les Misérables has, sadly, been reduced to The Glums,” and my heart sank. I couldn’t reconcile the sense of uplift and exhilaration I had witnessed in the theatre with these words.

Many of the other papers were equally dismissive but a few key critics came out fighting in the show’s defense. Later, many more of their colleagues joined in with their appreciation of the show’s qualities. But that bleak day after the opening left me poleaxed.

SWEEPING MASTERPIECE

About midday I thought I would get all the bad news out of the way and ring the box office to find out how badly the reviews had affected ticket sales. I was greeted by an incredulous box office manager who wondered how I had managed to get through as they had been besieged, having already sold a record-breaking 5,000 seats that morning. I was stunned.

The public had just voted with its feet. Without any media hype or any mass marketing the public was able to see in Les Misérables what many a professional scribe could not. For me it was a great lesson in the real power of word of mouth and the often under-appreciated sense of perception of the public. Ironically, the musical’s reception in London almost exactly mirrored that of the original publication in Paris of Hugo’s masterpiece.

Since then many thousands of productions of Les Misérables have been performed and loved all over the world. One of the least likely subject matters for a popular musical of all time. But is it? Hugo wrote one of the most powerful and exciting stories ever published and it has remained a timeless classic for all nations ever since. Alain and Claude-Michel’s brilliant adaptation and collaboration with Herbert Kretzmer caught the essence of Hugo’s work precisely and made it even more accessible to a modern audience. No musical has had greater source material from which to draw its inspiration nor a more brilliant production team under the inspired leadership of Trevor Nunn and John Caird to stage it.

RECORD-BREAKING

Little did I think when the show transferred to the Palace Theatre that it would run there for 18 happy years and then continue its triumphant run at the Queen’s Theatre, where the production has gained in intimacy and power, and still has standing ovations after nearly every performance.

During our 21st year, Les Miz, broke yet more records when in July 2005 the show was acclaimed as the British nation’s favourite musical by the listeners of BBC Radio 2 – Les Misérables receiving almost 50% of the votes of all the shows combined – and the Guinness Book of Records confirmed that Les Miz had had more concurrent productions (15 at one time) than any other musical in history. As well as the show’s professional success, to celebrate Victor Hugo’s bicentenary in 2002 it was made available to students under 19 to perform in the remarkably successful Les Misérables School Edition. In almost ten years, more than 145,000 students in over 2,900 productions worldwide have made the show their own with brilliant results. Now Les Misérables has, to my surprise, taken over the mantle of the world’s longest-running musical from another of my productions, Cats. As well as celebrating this milestone in London, we simultaneously opened a new production on Broadway.

A bolt out of the blue came when Susan Boyle sang “I Dreamed a Dream” on television’s Britain’s Got Talent. Almost overnight it became the world’s most popular song with now over 200 million YouTube hits and counting! The connection of this song with extraordinary worldwide exposure means that LesMisérables is a hit all over again. Cosette never fails to surprise us.

To mark its quarter-century at the end of 2010 I presented a special 25th anniversary production of Les Misérables in a new staging by Laurence Connor and James Powell. Victor Hugo’s extraordinary and revolutionary paintings, previously little known, proved a wonderful inspiration to designers Matt Kinley and Paule Constable and exciting new orchestrations and sound design brought Hugo’s story to even more colourful life. This production has been wonderfully received and is following in the footsteps of the original and opening up all over the world. The Queen’s Theatre is now the only place that audiences can see the brilliant original production. The 25th anniversary UK tour was an amazing sell-out success around the country with audiences and critics alike. It came full circle and finished with three weeks at the Barbican Theatre where the show had first opened 25 years before.

WORLDWIDE SUCCESS

The culmination of 2010’s celebration was the staging of two spectacular Les Misérables concerts at The O2, in front of over 30,000 devoted fans. An international cast of stars, including Alfie Boe, Norm Lewis, Lea Salonga, Jenny Galloway, Matt Lucas, Nick Jonas, Katie Hall, Ramin Karimloo and Samantha Barks, together with performers from London’s Queen’s and the tour, and many of the show’s original cast, came together to mark this momentous occasion on 3 October. I would like to thank them and my tirelessly inventive production team for making sure that every performance of Les Misérables is, as described in The Times, “still like going to a First Night”.

Les Misérables is proving more successful than ever with the original London production holding record-breaking advance box office figures. The 25th Anniversary staging of the show with its new design, direction and orchestrations is also breaking box office records wherever it plays. It has already opened in the USA and Spain and is planned to open in South Africa, Canada, Japan, Korea, South America and Australia. So successful has the new sound design and orchestration been that I decided to install it at the Queen’s so the original production could also enjoy the tremendous benefit of the revitalised musical score. The DVD of the marvellous 25th Anniversary Concert at The O2 continues to be a bestseller and at long last a film version of the show, produced by myself and Working Title for Universal, is underway, under the helm of director Tom Hooper.

There is no doubt that Les Misérables will be storming the barricades for many years to come. I know that when I go “beyond the barricade”, the part I played in bringing Les Misérables to life as a musical will remain one of my proudest achievements.

http://www.youtube.com/watch?v=ePaZ-tK07v4

Lance Armstrong's confession by Andrea Carmona

Posted by: Andrea Carmona

http://www.guardian.co.uk/commentisfree/2013/jan/20/observer-editorial-lance-armstrong-confession-flawed

Lance Armstrong's confession was too little and far too late

The cyclist's appearance on Oprah still leaves many questions unanswered

 

Sunday 20 January 2013

 

What was the old, cancer-surviving, rival-bashing Lance Armstrong like? He was, he revealed to Oprah Winfrey last week, "a guy who expected to get whatever he wanted and control every outcome". But here was the problem: that old Lance Armstrong bore more than a passing resemblance to the new, flawed, semi-contrite one. By choosing the medium of the TV confessional, Armstrong believed he could manipulate the discussion once again. His failure to recognise quite how deep a hole he's in is hubris on an epic scale.
It is hard to think of anyone in public life who has lied as Armstrong has. Everything about his cycling career has been built on a persistently restated deception: I did not take performance-enhancing drugs. He became a really world-class liar and there is evidence that even now he is finding the habit a hard one to give up. His claim that he never doped after 2005 is strongly contested by the United States Anti-Doping Agency. There are numerous other unanswered questions from the Oprah interview that need to be addressed now by legal and anti-doping authorities.
Armstrong was right on one point: he may have been a kingpin, but he is only one guy. It's worth remembering just how ingrained drug use is in professional cycling. In the very first races, in the late 19th century, riders took morphine, cocaine, even bull's blood and the crushed testicles of wild animals. There has never been an era that has not been tainted by doping.
All of which should give us hope – and caution – for the future of the sport. Armstrong hogged the headlines last week, but on Thursday there was a cheerier announcement when the routes for three British stages of the 2014 Tour de France were revealed. Millions of Britons will turn out to watch. Will they be able to believe what they are watching? A full, explicit confession from Armstrong is essential for everyone to move on. Cycling may be the boom sport of the new century, but the people who love it don't have infinite patience.

Here you have the confession on tv:

http://www.nytimes.com/video/playlist/front-business-media/1194811622251/index.html#100000002008911