From Simons Science News (find original story here).
In 1952, Alan Turing, a British mathematician best known for his work on code-breaking and artificial intelligence, was convicted of engaging in homosexual acts and sentenced to chemical castration. Amid that personal drama, he still found the time to publish a visionary paper on the mathematics of regularly repeating patterns in nature, which could be applied to the stripes on tigers and zebra fish, the spots on leopards and the spacing in rows of alligator teeth, to name a few.
Now, more than 60 years later, biologists are uncovering evidence of the patterning mechanisms that Turing proposed in his paper, prompting a resurgence of interest in them, with the potential to shed light on such developmental questions as how genes ultimately make a hand. ?That structure is there,? said Jeremy Green, a developmental biologist at King?s College London. ?We just need to put the chemistry onto the mathematics to get the biology.?
>> View the Tiger Stripes and Turing Patterns slide show
For the work that led to his 1952 paper, Turing wanted to understand the underlying mechanism that produces natural patterns. He proposed that patterns such as spots form as a result of the interactions between two chemicals that spread throughout a system much like gas atoms in a box do, with one crucial difference. Instead of diffusing evenly like a gas, the chemicals, which Turing called ?morphogens,? diffuse at different rates. One serves as an activator to express a unique characteristic, like a tiger?s stripe, and the other acts as an inhibitor, kicking in periodically to shut down the activator?s expression.
To explain Turing?s idea, James Murray, emeritus professor of mathematical biology at the University of Oxford and an applied mathematician at Princeton, imagined a field of dry grass dotted with grasshoppers. If the grass were set on fire at several random points and no moisture were present to inhibit the flames, Murray said, the fires would char the entire field. If this scenario played out like a Turing mechanism, however, the heat from the encroaching flames would cause some of the fleeing grasshoppers to sweat, dampening the grass around them and thereby creating periodic unburned spots in the otherwise burned field.
The notion was intriguing but speculative. Turing died two years after the publishing of his paper, which languished in relative obscurity for decades. ?He didn?t actually apply it to any real biological problem,? Murray said. ?It was mainly a boon for mathematicians looking for analytical problems.?
Although there was an explosion of theoretical work and computer modeling in the 1970s that successfully reproduced patterns like spots and stripes using Turing mechanisms, molecular biology was nowhere near the point where researchers could identify the specific molecules acting as activators and inhibitors.
The latest research suggests that Turing-type mechanisms may be responsible for the spacing between hair follicles in mice and feather buds on a bird?s skin, the ridges that form on a mouse?s palate and the digits on a mouse?s paw.
JUBA (Reuters) - More than 150 people have been killed in a battle between South Sudan's army and insurgents in the eastern Jonglei state, officials said on Thursday.
The African country's army earlier this month launched an offensive against rebels led by David Yau Yau in Jonglei where the government hopes to search for oil with the help of France's Total.
Since winning independence from Sudan in July 2011, South Sudan has been struggling to impose its authority across vast swathes of territory bristling with weapons after decades of civil war with Khartoum.
Yau Yau mounted a rebellion last year, with support from his Murle ethnic group, after losing local elections in 2010.
Army spokesman Philip Aguer told Reuters his forces had killed 143 fighters from Yau Yau's militia in a battle east of Pibor town on Tuesday. Twenty soldiers were killed and 70 people were wounded, he said.
Information Minister Barnaba Marial Benjamin said the army, or SPLA, had seized an air strip which had been used to drop ammunition and arms to Yau Yau's troops.
"The SPLA is moving in the area so as to put an end to the rebellion," he said.
South Sudan has accused arch rival Sudan of supporting Yau Yau and other rebel groups, a claim denied by Khartoum.
A shortwave radio station with links to the Yau Yau rebellion says the group is fighting the government in reaction to abuses committed during a state disarmament program in Jonglei.
Rights groups accuse South Sudan's army of human rights violations during a disarmament push aimed at ending a cycle of clashes between the Murle and Lou Nuer tribes.
Nearly 900 people died when about 7,000 armed youths of the Lou Nuer tribe attacked Murle villages in the Pibor area at the end of last year, according to the United Nations.
(Reporting by Andrew Green in Juba; Writing by Ulf Laessing in Cairo; Editing by Michael Roddy)
The best way to deal with smog is to make less of it, but it's too late to just do that. And when it comes to cleaning up your already polluted air, mesh structures like this one in Mexico City are a stylish way to filter a whole city's worth of air. More »
Some people will tell you that pain is the basis of spiritual growth. Sorrow, regret and eventually letting go are life lessons we all go through at some point.
But not all of us experience those painfully emotional moments in association with our wisdom teeth. And even fewer have had to deal with the moment being captured on video and posted to the delight of countless strangers.
But that?s exactly what Kansas teen Abbie Kritz is going through, after her boyfriend posted a video of Kritz lamenting the loss of her wisdom teeth while under the influence of pain medication.
"I did it against my own will, I would have kept you," Kritz says earnestly to the removed wisdom teeth, which she is holding inside a plastic jar while being driven home by her mother.
"I loved you from the first moment on."
Her boyfriend and mom can be heard laughing in disbelief as Kritz continues the soliloquy to her lost choppers.
"They were just trying to help me chew and I didn't accept them," she explains." I could have accepted them."
Eventually, Kritz came to terms with the situation. Or, put another way, the dentist?s drugs wore off. And for her part, Kritz appears to be taking in all the attention with a toothy smile.
?Oh my goodness it was awful,? she wrote on her Twitter account. ?I just remember wanting to stop crying the whole time but I couldn't!?
Still, there?s no word on whether Kritz stands by her previous offer of putting the wisdom teeth back in place.
"They just wanted to be a part of my body and I said 'No, get out,'" she said tearfully in the video after making it back home. "I didn't meant it. You can come back if you want."
Then again, Kritz might be onto something, not just previously on something. While many people eventually have their wisdom teeth removed, there is growing opposition to having them removed without a clinical reason to do so.
We saw the teasers yesterday, and today Gameloft has announced that Iron Man 3 is coming to Android. It's set to launch on April 25, and it looks like a new breed of endless runner.
Before you complain about yet another endless running game, be sure to check the trailer above. Flying above city streets, firing a lazer at obstacles and enemies is a far cry from Temple Run. This looks like a ton of fun, and even if you're not a fan of Iron Man, who doesn't love to blow the bad guys out of the sky?
No news on what this one's going to cost, all Gameloft is telling us is the date and where to see the trailer. When it comes, we'll have a good look at it.
Contact: marla Paul marla-paul@northwestern.edu 312-503-8928 Northwestern University
Viral protein hijacks cellular machinery and grabs the wheel
(Chicago) Northwestern Medicine scientists have identified a component of the herpesvirus that "hijacks" machinery inside human cells, allowing the virus to rapidly and successfully invade the nervous system upon initial exposure.
Led by Gregory Smith, associate professor in immunology and microbiology at Northwestern University Feinberg School of Medicine, researchers found that viral protein 1-2, or VP1/2, allows the herpesvirus to interact with cellular motors, known as dynein. Once the protein has overtaken this motor, the virus can speed along intercellular highways, or microtubules, to move unobstructed from the tips of nerves in skin to the nuclei of neurons within the nervous system.
This is the first time researchers have shown a viral protein directly engaging and subverting the cellular motor; most other viruses passively hitch a ride into the nervous system.
"This protein not only grabs the wheel, it steps on the gas," says Smith. "Overtaking the cellular motor to invade the nervous system is a complicated accomplishment that most viruses are incapable of achieving. Yet the herpesvirus uses one protein, no others required, to transport its genetic information over long distances without stopping."
Herpesvirus is widespread in humans and affects more than 90 percent of adults in the United States. It is associated with several types of recurring diseases, including cold sores, genital herpes, chicken pox, and shingles. The virus can live dormant in humans for a lifetime, and most infected people do not know they are disease carriers. The virus can occasionally turn deadly, resulting in encephalitis in some.
Until now, scientists knew that herpesviruses travel quickly to reach neurons located deep inside the body, but the mechanism by which they advance remained a mystery.
Smith's team conducted a variety of experiments with VP1/2 to demonstrate its important role in transporting the virus, including artificial activation and genetic mutation of the protein. The team studied the herpesvirus in animals, and also in human and animal cells in culture under high-resolution microscopy. In one experiment, scientists mutated the virus with a slower form of the protein dyed red, and raced it against a healthy virus dyed green. They observed that the healthy virus outran the mutated version down nerves to the neuron body to insert DNA and establish infection.
"Remarkably, this viral protein can be artificially activated, and in these conditions it zips around within cells in the absence of any virus. It is striking to watch," Smith says.
He says that understanding how the viruses move within people, especially from the skin to the nervous system, can help better prevent the virus from spreading.
Additionally, Smith says, "By learning how the virus infects our nervous system, we can mimic this process to treat unrelated neurologic diseases. Even now, laboratories are working on how to use herpesviruses to deliver genes into the nervous system and kill cancer cells."
Smith's team will next work to better understand how the protein functions. He notes that many researchers use viruses to learn how neurons are connected to the brain.
"Some of our mutants will advance brain mapping studies by resolving these connections more clearly than was previously possible," he says.
###
This work was funded by grants R01 AI056346, R01 EY017809, T32AI07476 from the National Institute of Allergy and Infectious Diseases of the National Institutes of Health.
It was published in the journal Cell Host & Microbe and is available online at http://www.sciencedirect.com/science/article/pii/S1931312813000401.
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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.
Contact: marla Paul marla-paul@northwestern.edu 312-503-8928 Northwestern University
Viral protein hijacks cellular machinery and grabs the wheel
(Chicago) Northwestern Medicine scientists have identified a component of the herpesvirus that "hijacks" machinery inside human cells, allowing the virus to rapidly and successfully invade the nervous system upon initial exposure.
Led by Gregory Smith, associate professor in immunology and microbiology at Northwestern University Feinberg School of Medicine, researchers found that viral protein 1-2, or VP1/2, allows the herpesvirus to interact with cellular motors, known as dynein. Once the protein has overtaken this motor, the virus can speed along intercellular highways, or microtubules, to move unobstructed from the tips of nerves in skin to the nuclei of neurons within the nervous system.
This is the first time researchers have shown a viral protein directly engaging and subverting the cellular motor; most other viruses passively hitch a ride into the nervous system.
"This protein not only grabs the wheel, it steps on the gas," says Smith. "Overtaking the cellular motor to invade the nervous system is a complicated accomplishment that most viruses are incapable of achieving. Yet the herpesvirus uses one protein, no others required, to transport its genetic information over long distances without stopping."
Herpesvirus is widespread in humans and affects more than 90 percent of adults in the United States. It is associated with several types of recurring diseases, including cold sores, genital herpes, chicken pox, and shingles. The virus can live dormant in humans for a lifetime, and most infected people do not know they are disease carriers. The virus can occasionally turn deadly, resulting in encephalitis in some.
Until now, scientists knew that herpesviruses travel quickly to reach neurons located deep inside the body, but the mechanism by which they advance remained a mystery.
Smith's team conducted a variety of experiments with VP1/2 to demonstrate its important role in transporting the virus, including artificial activation and genetic mutation of the protein. The team studied the herpesvirus in animals, and also in human and animal cells in culture under high-resolution microscopy. In one experiment, scientists mutated the virus with a slower form of the protein dyed red, and raced it against a healthy virus dyed green. They observed that the healthy virus outran the mutated version down nerves to the neuron body to insert DNA and establish infection.
"Remarkably, this viral protein can be artificially activated, and in these conditions it zips around within cells in the absence of any virus. It is striking to watch," Smith says.
He says that understanding how the viruses move within people, especially from the skin to the nervous system, can help better prevent the virus from spreading.
Additionally, Smith says, "By learning how the virus infects our nervous system, we can mimic this process to treat unrelated neurologic diseases. Even now, laboratories are working on how to use herpesviruses to deliver genes into the nervous system and kill cancer cells."
Smith's team will next work to better understand how the protein functions. He notes that many researchers use viruses to learn how neurons are connected to the brain.
"Some of our mutants will advance brain mapping studies by resolving these connections more clearly than was previously possible," he says.
###
This work was funded by grants R01 AI056346, R01 EY017809, T32AI07476 from the National Institute of Allergy and Infectious Diseases of the National Institutes of Health.
It was published in the journal Cell Host & Microbe and is available online at http://www.sciencedirect.com/science/article/pii/S1931312813000401.
[ | E-mail | Share ]
?
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: 27-Mar-2013
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