Thirteen years ago, on an idyllic summer?s afternoon, I stood by the side of a road in the cheesemaking region of Cantal and watched Lance Armstrong speed by, tucked into the peloton, on his way to his first victory in the Tour de France.
It was 1999. A year earlier the Tour had been in tatters, devastated by a doping scandal that had seen police and judges raiding riders? hotel rooms in the middle of the night, seizing drugs. Armstrong?s successful arrival on the scene after overcoming cancer ?is symbolic of the way the Tour de France is emerging from its own battle against disappearance,? said the tour director at the time.
His victory would be ?highly symbolic of the combat he fought against death, and that we are fighting against doping,? promised Jean-Marie Leblanc.
[Think you know Europe? Take our geography quiz.]
It turns out that Mr. Armstrong beat the Tour de France organizers just as he had beaten death. Today the International Cycling Union (UCI), accepting evidence gathered by the US Anti-Doping Agency that Armstrong was a serial drug-taker, stripped the US ?champion? of all his titles.
Even back in 1999, people suspected something was wrong. ?Armstrong is very strong, too strong, incredibly strong,? commented one French TV journalist the evening that the US rider won a punishing stage in the Alps.
But that could be dismissed as sour grapes, as an American charged into a sport long dominated by the French and swept all before him, ?winning? a record seven Tours.
And we all wanted to believe in Armstrong, from the UCI ? for whom he was a magnificent money-spinning mascot for his sport ? down to the lowliest spectator standing by the side of the road who admired his comeback courage.
Well, not all of us. My (French) wife never believed Armstrong was clean. She never believed that any of the top riders were clean. In argument after argument over the years I called her cynical, pointing out that my hero had never failed a drug test. Now I know that she was just clear-eyed.
Everybody who followed Lance during his ?glory days? will have his or her own way of feeling disappointed now that the truth, it seems, is out. (Armstrong has not acknowledged any guilt but says he will not challenge the USADA report.)
For me, the news has tainted some of my happiest memories of reporting in France. I used to love covering the Tour, driving halfway up an Alp one July afternoon, parking my car near a steep hairpin bend, picnicking sociably with whomever I found parked next to me (and there were always crowds of families waiting for the Tour to come by), sleeping in the car, and then the next day enjoying the hoopla of the publicity caravan before the riders themselves came by, just an arm?s length away, thighs straining, sweat pouring from their chins, teeth gritted.
It was an annual treat for me, the most fun I have ever had at work. And watching these men at the outer edges of endurance even inspired me to take up cycling myself: I had a go at one of the Tour?s mountain stages in 2005 and I spend my weekends now cycling up and down mountains. (You can imagine what my wife thinks about that?.)
Lance Armstrong, whose feats excited a lot of interest in American newspaper readers, was my passport to this kind of fun, and now that we know he was cheating, it feels almost as though I was piggyback cheating by having that fun.
Even at the time though, I realize, I could not entirely ignore my wife?s doubts. That evening in July 1999, as I dictated my article over the phone to my editor, I ended it with something the spokesman for Credit Lyonnais bank, the Tour?s leading sponsor, had told me.
?We cannot be certain that a scandal won?t drop on our heads,? he said. ?I have just one hope: that the rumors about Lance Armstrong are not true.?
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If you?re trying to generate ideas for article writing, it can be easy to think that this all has to be done by sitting and researching online. Although the internet is an enormous and wonderful resource for finding out information and stimulating new ideas, if you?re creating content on a regular basis it can also be useful to step away from your computer and in the course of your day take note of things around you that can stimulate ideas. Try and be flexible and allow your mind just to have fun and finding ideas for article writing will come from the most surprising places.
Other peoples conversations
I?m sure you?re thinking that you don?t make a habit of listening to other people?s conversations, but often it?s very difficult not to. People talking on their phones, in the street, on public transport. People holding conversations in doctor?s waiting rooms, dentists, hospital waiting rooms, hairdressers, in cafes and bars. You don?t need to listen to hear whole conversations, even small snippets can generate ideas. What are their fears, their worries, the problems they have and need solving?
Shop window displays
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Flyers and posters
Sometimes it seems you can?t walk down a street without someone trying to press a flyer in your hand. As tempting as it may be to just put it in the nearest bin, take a quick look. Similarly instead of just walking on past advertising hoardings, see if there?s anything that stimulates your interest.
Public announcements
Yes even public announcements in train, bus, or coach stations or ones inside shops can be interesting. Quite often one hears poor examples of communication skills, customer service, time management, organisational skills or even funny announcements that can spark ideas and help you find ideas for article writing.
Hustle and bustle of life
Just in the course of a normal day you will be interacting with lots of different people. Some of these interactions whether they be positive or negative can be used to generate further ideas. Sometimes it may be conversations, it may be the manner of someone, it may be the way their dressed, it may be something that they?re doing. And of course ? although I?ve said about the hustle and bustle of life they are just as many times to gain ideas at quieter times such as a walk in the country, a jog along the beach...
Summary
When you?re out and about on an everyday basis you will come across many things which can help you in finding and generating ideas for article writing. The connections may not seem obvious, but be flexible. Oh and I never said earlier, but always have a way of jotting down any idea that comes into your head. There?s nothing worse than having a great idea and then not being able to remember it later.
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Salk scientists pinpoint key player in Parkinson's disease neuron lossPublic release date: 19-Oct-2012 [ | E-mail | Share ]
Contact: Andy Hoang ahoang@salk.edu 619-861-5811 Salk Institute
Stem cell study may help to unravel how a genetic mutation leads to Parkinson's symptoms
LA JOLLA, CA---- By reprogramming skin cells from Parkinson's disease patients with a known genetic mutation, researchers at the Salk Institute for Biological Studies have identified damage to neural stem cells as a powerful player in the disease. The findings, reported online October 17th in Nature, may lead to new ways to diagnose and treat the disease.
The scientists found that a common mutation to a gene that produce the enzyme LRRK2, which is responsible for both familial and sporadic cases of Parkinson's disease, deforms the membrane surrounding the nucleus of a neural stem cell. Damaging the nuclear architecture leads to destruction of these powerful cells, as well as their decreased ability to spawn functional neurons, such as the ones that respond to dopamine.
The researchers checked their laboratory findings with brain samples from Parkinson's disease patients and found the same nuclear envelope impairment.
"This discovery helps explain how Parkinson's disease, which has been traditionally associated with loss of neurons that produce dopamine and subsequent motor impairment, could lead to locomotor dysfunction and other common non-motor manifestations, such as depression and anxiety," says Juan Carlos Izpisua Belmonte, a professor in Salk's Gene Expression Laboratory, who led the research team. "Similarly, current clinical trials explore the possibility of neural stem cell transplantation to compensate for dopamine deficits. Our work provides the platform for similar trials by using patient-specific corrected cells. It identifies degeneration of the nucleus as a previously unknown player in Parkinson's."
Although the researchers say that they don't yet know whether these nuclear aberrations cause Parkinson's disease or are a consequence of it, they say the discovery could offer clues about potential new therapeutic approaches.
For example, they were able to use targeted gene-editing technologies to correct the mutation in patient's nuclear stem cells. This genetic correction repaired the disorganization of the nuclear envelope, and improved overall survival and functioning of the neural stem cells.
They were also able to chemically inhibit damage to the nucleus, producing the same results seen with genetic correction. "This opens the door for drug treatment of Parkinson's disease patients who have this genetic mutation," says Belmonte.
The new finding may also help clinicians better diagnose this form of Parkinson's disease, he adds. "Due to the striking appearance in patient samples, nuclear deformation parameters could add to the pool of diagnostic features for Parkinson's disease," he says.
The research team, which included scientists from China, Spain, and the University of California, San Diego, and Scripps Research Institute, made their discoveries using human induced pluripotent stem cells (iPSCs). These cells are similar to natural stem cells, such as embryonic stem cells, except that they are derived from adult cells. While generation of these cells has raised expectations within the biomedical community due to their transplant potential----the idea that they could morph into tissue that needs to be replaced----they also provide exceptional research opportunities, says Belmonte.
"We can model disease using these cells in ways that are not possible using traditional research methods, such as established cell lines, primary cultures and animal models," he says.
In this study, the researchers used skin fibroblast cells taken from Parkinson's disease patients who have the LRRK2 mutation, and they reprogrammed them to iPSC stem cells and developed them into neural stem cells.
Then, by using an approach to model what happens when these neural stem cells aged, they found that older Parkinson disease neural stem cells increasingly displayed deformed nuclear envelopes and nuclear architecture. "This means that, over time, the LRRK2 mutation affects the nucleus of neural stem cells, hampering both their survival and their ability to produce neurons," Belmonte says.
"It is the first time to our knowledge that human neural stem cells have been shown to be affected during Parkinson's pathology due to aberrant LRRK2," he says. "Before development of these reprogramming technologies, studies on human neural stem cells were elusive because they needed to be isolated directly from the brain."
Belmonte speculates that the dysfunctional neural stem cell pools that result from the LRRK2 mutation might contribute to other health issues associated with this form of Parkinson's disease, such as depression, anxiety and the inability to detect smells.
Finally, the study shows that these reprogramming technologies are very useful for modeling disease as well as dysfunction caused by aging, Belmonte says.
###
Other researchers on the study were: Guang-Hui Liu, Jing Qu, Keiichiro Suzuki, Emmanuel Nivet, Mo Li, Nuria Montserrat, Fei Yi. Xiuling Xu, Sergio Ruiz, Weiqi Zhang, Bing Ren, Ulrich Wagner, Audrey Kim, Ying Li, April Goebl, Jessica Kim, Rupa Devi Soligalla, Ilir Dubova, James Thompson, John Yates III, Concepcion Rodriguez Esteban, and Ignacio Sancho-Martinez.
The research was supported by Glenn Foundation for Medical Research, G. Harold and Leila Y. Mathers Charitable Foundation, Sanofi, The California Institute of Regenerative Medicine, Ellison Medical Foundation and Leona M. and Harry B. Helmsley Charitable Trust, MINECO and Fundacion Cellex.
About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world's preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer's, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.
Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Salk scientists pinpoint key player in Parkinson's disease neuron lossPublic release date: 19-Oct-2012 [ | E-mail | Share ]
Contact: Andy Hoang ahoang@salk.edu 619-861-5811 Salk Institute
Stem cell study may help to unravel how a genetic mutation leads to Parkinson's symptoms
LA JOLLA, CA---- By reprogramming skin cells from Parkinson's disease patients with a known genetic mutation, researchers at the Salk Institute for Biological Studies have identified damage to neural stem cells as a powerful player in the disease. The findings, reported online October 17th in Nature, may lead to new ways to diagnose and treat the disease.
The scientists found that a common mutation to a gene that produce the enzyme LRRK2, which is responsible for both familial and sporadic cases of Parkinson's disease, deforms the membrane surrounding the nucleus of a neural stem cell. Damaging the nuclear architecture leads to destruction of these powerful cells, as well as their decreased ability to spawn functional neurons, such as the ones that respond to dopamine.
The researchers checked their laboratory findings with brain samples from Parkinson's disease patients and found the same nuclear envelope impairment.
"This discovery helps explain how Parkinson's disease, which has been traditionally associated with loss of neurons that produce dopamine and subsequent motor impairment, could lead to locomotor dysfunction and other common non-motor manifestations, such as depression and anxiety," says Juan Carlos Izpisua Belmonte, a professor in Salk's Gene Expression Laboratory, who led the research team. "Similarly, current clinical trials explore the possibility of neural stem cell transplantation to compensate for dopamine deficits. Our work provides the platform for similar trials by using patient-specific corrected cells. It identifies degeneration of the nucleus as a previously unknown player in Parkinson's."
Although the researchers say that they don't yet know whether these nuclear aberrations cause Parkinson's disease or are a consequence of it, they say the discovery could offer clues about potential new therapeutic approaches.
For example, they were able to use targeted gene-editing technologies to correct the mutation in patient's nuclear stem cells. This genetic correction repaired the disorganization of the nuclear envelope, and improved overall survival and functioning of the neural stem cells.
They were also able to chemically inhibit damage to the nucleus, producing the same results seen with genetic correction. "This opens the door for drug treatment of Parkinson's disease patients who have this genetic mutation," says Belmonte.
The new finding may also help clinicians better diagnose this form of Parkinson's disease, he adds. "Due to the striking appearance in patient samples, nuclear deformation parameters could add to the pool of diagnostic features for Parkinson's disease," he says.
The research team, which included scientists from China, Spain, and the University of California, San Diego, and Scripps Research Institute, made their discoveries using human induced pluripotent stem cells (iPSCs). These cells are similar to natural stem cells, such as embryonic stem cells, except that they are derived from adult cells. While generation of these cells has raised expectations within the biomedical community due to their transplant potential----the idea that they could morph into tissue that needs to be replaced----they also provide exceptional research opportunities, says Belmonte.
"We can model disease using these cells in ways that are not possible using traditional research methods, such as established cell lines, primary cultures and animal models," he says.
In this study, the researchers used skin fibroblast cells taken from Parkinson's disease patients who have the LRRK2 mutation, and they reprogrammed them to iPSC stem cells and developed them into neural stem cells.
Then, by using an approach to model what happens when these neural stem cells aged, they found that older Parkinson disease neural stem cells increasingly displayed deformed nuclear envelopes and nuclear architecture. "This means that, over time, the LRRK2 mutation affects the nucleus of neural stem cells, hampering both their survival and their ability to produce neurons," Belmonte says.
"It is the first time to our knowledge that human neural stem cells have been shown to be affected during Parkinson's pathology due to aberrant LRRK2," he says. "Before development of these reprogramming technologies, studies on human neural stem cells were elusive because they needed to be isolated directly from the brain."
Belmonte speculates that the dysfunctional neural stem cell pools that result from the LRRK2 mutation might contribute to other health issues associated with this form of Parkinson's disease, such as depression, anxiety and the inability to detect smells.
Finally, the study shows that these reprogramming technologies are very useful for modeling disease as well as dysfunction caused by aging, Belmonte says.
###
Other researchers on the study were: Guang-Hui Liu, Jing Qu, Keiichiro Suzuki, Emmanuel Nivet, Mo Li, Nuria Montserrat, Fei Yi. Xiuling Xu, Sergio Ruiz, Weiqi Zhang, Bing Ren, Ulrich Wagner, Audrey Kim, Ying Li, April Goebl, Jessica Kim, Rupa Devi Soligalla, Ilir Dubova, James Thompson, John Yates III, Concepcion Rodriguez Esteban, and Ignacio Sancho-Martinez.
The research was supported by Glenn Foundation for Medical Research, G. Harold and Leila Y. Mathers Charitable Foundation, Sanofi, The California Institute of Regenerative Medicine, Ellison Medical Foundation and Leona M. and Harry B. Helmsley Charitable Trust, MINECO and Fundacion Cellex.
About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world's preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer's, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.
Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
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Public release date: 19-Oct-2012
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