Powertrains: 4 AC electric motors, 740 hp, 738 lb-ft; 60-kwh lithium-ion battery pack; direct drive, AWD
EPA Fuel Economy (city/hwy): N/A
What's New: On the outside it looks like almost exactly like a gas-powered SLS AMG, but underneath lies a completely different powertrain that is hand-assembled at the AMG headquarters in Affalterbach, Germany. There are four electric motors, one for each wheel, making a total of 740 hp. In between, along the center of the car where the engine, propshaft, and transmission used to be, is the 60-kilowatt-hour battery pack encased in a thick carbon-fiber shell. To fit the front axles and motors, AMG reengineered the front suspension, going from the double-wishbone setup in the gas-powered version to a multilink with racing-style pushrod dampers.
At a glance the interior of the SLS AMG Electric Drive reveals no major differences, though the dashboard is slightly reconfigured to show the total energy usage or regen. The steering-wheel paddle shifters, which still have Up and Down stampings, are repurposed?in the electric version, they toggle the regenerative braking between four levels, displayed in the row of lights in the instrument cluster that used to show engine RPM.
In Europe, with the appropriate high-voltage charger, the SLS AMG Electric Drive can charge in as little as 3 hours. Using the onboard charger takes quite a bit longer: 20 hours. On the European combined test, which is more conservative than U.S. tests, the range is 155 miles.
Tech Tidbit: The Electric Drive features AMG Torque Dynamics, which allows the power to be adjusted individually for each motor depending on what the car is supposed to do. In a turn, for instance, the outside motors will drive the car while the inside motors will drag with a regenerative force, helping to turn the car. It's similar to the torque-vectoring system used on some AWD cars, except with faster responses and control at all four corners instead of just two.
Driving Character: The SLS AMG Electric Drive proves that an EV can be just as exciting as a gas-powered supercar. We can't decide what's more mind-blowing about this car: the way it changes character between driving modes or just how easy and fun it can be.
As with other AMG cars, a rotary lets you choose between C, S, and S+. In C, or Controlled Efficiency mode, the SLS feels reserved and corners with a bit of understeer. Punch it up to Sport Plus and the car feels completely different, with instantaneous reactions to steering inputs and a cornering attitude that borders on oversteer. With 740 hp on tap and 738 lb-ft of instantaneous torque available, we thought the Electric Drive would do two things: shred the tires and scare us straight to a Nissan Leaf. But in reality, the SLS is smooth, and the torque-vectoring system makes the car so responsive that the gas-powered SLS AMG seems piggish.
Favorite Detail: Neither the bright yellow nor the ultrashiny blue hues that adorned the cars on hand for our test session at Paul Ricard Circuit in southern France are actually paint?they're wraps. We're not concerned with how they come to look that way?we just love that a nearly silent car comes with the loudest color scheme in the world.
Driver's Grievance: Sure, we accept that this is a special car, but the 155-mile range illustrates that electric cars still have serious limitations, even ones that cost megabucks.
Bottom Line: With a 0-to-100-kilometers-per-hour (0-to-62-mph) time of 3.9 seconds and a top speed of 155 mph, the SLS Electric Drive is a stunning piece of engineering. Sadly, it's for sale only in Europe, and the price (more than double that of a gas-powered SLS) guarantees that this will be a rare car. Plus, it makes even less practical sense than its conventional counterpart.
Yet, that's a considerable part of the charm. Mercedes-Benz didn't need to build an electric supercar. The SLS Electric Drive is the best kind of automaker bravado, the kind that shows what can be done at the limits of technology, where reason and rationality are of little importance.
Study pinpoints, prevents stress-induced drug relapse in ratsPublic release date: 6-Mar-2013 [ | E-mail | Share ]
Contact: David Orenstein david_orenstein@brown.edu 401-863-1862 Brown University
PROVIDENCE, R.I. [Brown University] All too often, stress turns addiction recovery into relapse, but years of basic brain research have provided scientists with insight that might allow them develop a medicine to help. A new study in the journal Neuron pinpoints the neural basis for stress-related relapse in rat models to an unprecedented degree. The advance could accelerate progress toward a medicine that prevents stress from undermining addiction recovery.
In the paper published March 6, researchers at Brown University and the University of Pennsylvania demonstrated specific steps in the sequence of neural events underlying stress-related drug relapse and showed that they take place within a brain region called the ventral tegmental area (VTA), which helps reinforce behaviors related to fulfilling basic needs. They also showed that a closely related neural process believed to be crucial to stress-related relapse may not be involved after all.
Moreover, this new understanding allowed the researchers to prevent relapse to drug seeking in the animal model. When they treated rats that had recovered from cocaine addiction with a chemical that blocks the "kappa opioid receptors" that stress activates in the VTA, the rats did not relapse to cocaine use under stress. Untreated rats who had also recovered from addiction did relapse after the same stress.
The chemical that helped the rats, "nor-BNI," may be one that would someday be tried in humans, said study senior author Julie Kauer, professor of biology in Brown's Department of Molecular Pharmacology, Physiology, and Biotechnology. By deepening scientists' understanding of the stress-related relapse mechanism, she and her co-authors hope to identify multiple possible targets for eventual patient treatments.
"If we understand how kappa opioid receptor antagonists are interfering with the reinstatement of drug seeking we can target that process," said Kauer, who is affiliated with the Brown Institute for Brain Science. "We're at the point of coming to understand the processes and possible therapeutic targets. Remarkably, this has worked."
The neural crux of relapse
Exactly how stress acts in the brain to trigger relapse is a complicated sequence that is still not fully understood, but the new study focuses on and elucidates three key players at the crux of the phenomenon in the VTA: GABA-releasing neurons, dopamine-releasing neurons, and the kappa opioid receptors that affect their connections.
Fulfilling natural needs such as hunger or thirst results in a rewarding release of dopamine from the VTA's dopamine neurons, Kauer said. Unfortunately, so does using drugs of abuse.
In normal brain function, GABA applies the brakes on the rewarding dopamine release, slowing it back to a normal level. It achieves this by forging and then strengthening the connections, called synapses, with the dopamine neuron. The strengthening process is called long-term potentiation (LTP).
In the first of their experiments, the team at Brown, including lead author Nicholas Graziane, showed that stress interrupts the LTP process, hindering GABA's ability to slam the brakes on dopamine release.
Previous research implicated kappa opioid receptors as one of many neural entities that could have a role in stress-related relapse. Kauer, Graziane, and co-author Abigail Polter investigated that directly by blocking the receptors in some rats with a treatment of nor-BNI in the VTA and leaving others untreated. Then they subjected the rats to a standardized five-minute stress exercise. After 24 hours they looked at the cells in the VTA and found that LTP was hindered in the untreated rats but still present and underway in the rats whose receptors had been blocked with nor-BNI.
With the role of stress and the receptors in the GABA-dopamine dynamic both confirmed and then mitigated, the question remained: Could this knowledge be used to prevent relapse?
To answer that, Penn co-authors Lisa Briand and Christopher Pierce performed the experiment demonstrating that nor-BNI delivered directly to the VTA prevented stressed rats from relapsing to cocaine seeking, while untreated rats subjected to the same stress did relapse.
"Our results indicate that the kappa receptors within the VTA critically control stress-induced drug seeking in animals," the authors wrote in Neuron.
Along the way, the team also discovered evidence that another stress-affected synapse in the VTA one that excites dopamine release rather than inhibits it does not play a role in the stress-related relapse as many researchers have thought. The nor-BNI treatment that prevented stress-related relapse, for example, did not affect those synapses.
Kauer emphasized that her lab's findings of therapeutic potential are the product of more than a decade of essential basic research on the importance of how changes in synapses relate to behaviors including addiction.
"If we can figure out how not only stress, but the whole system works, then we'll potentially have a way to tune it down in a person who needs that," she said.
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The National Institutes of Health supported the research with several grants: DA011289, MH019118, AA007459, DA026660, DA15214, and DA18678.
[ | 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.
Study pinpoints, prevents stress-induced drug relapse in ratsPublic release date: 6-Mar-2013 [ | E-mail | Share ]
Contact: David Orenstein david_orenstein@brown.edu 401-863-1862 Brown University
PROVIDENCE, R.I. [Brown University] All too often, stress turns addiction recovery into relapse, but years of basic brain research have provided scientists with insight that might allow them develop a medicine to help. A new study in the journal Neuron pinpoints the neural basis for stress-related relapse in rat models to an unprecedented degree. The advance could accelerate progress toward a medicine that prevents stress from undermining addiction recovery.
In the paper published March 6, researchers at Brown University and the University of Pennsylvania demonstrated specific steps in the sequence of neural events underlying stress-related drug relapse and showed that they take place within a brain region called the ventral tegmental area (VTA), which helps reinforce behaviors related to fulfilling basic needs. They also showed that a closely related neural process believed to be crucial to stress-related relapse may not be involved after all.
Moreover, this new understanding allowed the researchers to prevent relapse to drug seeking in the animal model. When they treated rats that had recovered from cocaine addiction with a chemical that blocks the "kappa opioid receptors" that stress activates in the VTA, the rats did not relapse to cocaine use under stress. Untreated rats who had also recovered from addiction did relapse after the same stress.
The chemical that helped the rats, "nor-BNI," may be one that would someday be tried in humans, said study senior author Julie Kauer, professor of biology in Brown's Department of Molecular Pharmacology, Physiology, and Biotechnology. By deepening scientists' understanding of the stress-related relapse mechanism, she and her co-authors hope to identify multiple possible targets for eventual patient treatments.
"If we understand how kappa opioid receptor antagonists are interfering with the reinstatement of drug seeking we can target that process," said Kauer, who is affiliated with the Brown Institute for Brain Science. "We're at the point of coming to understand the processes and possible therapeutic targets. Remarkably, this has worked."
The neural crux of relapse
Exactly how stress acts in the brain to trigger relapse is a complicated sequence that is still not fully understood, but the new study focuses on and elucidates three key players at the crux of the phenomenon in the VTA: GABA-releasing neurons, dopamine-releasing neurons, and the kappa opioid receptors that affect their connections.
Fulfilling natural needs such as hunger or thirst results in a rewarding release of dopamine from the VTA's dopamine neurons, Kauer said. Unfortunately, so does using drugs of abuse.
In normal brain function, GABA applies the brakes on the rewarding dopamine release, slowing it back to a normal level. It achieves this by forging and then strengthening the connections, called synapses, with the dopamine neuron. The strengthening process is called long-term potentiation (LTP).
In the first of their experiments, the team at Brown, including lead author Nicholas Graziane, showed that stress interrupts the LTP process, hindering GABA's ability to slam the brakes on dopamine release.
Previous research implicated kappa opioid receptors as one of many neural entities that could have a role in stress-related relapse. Kauer, Graziane, and co-author Abigail Polter investigated that directly by blocking the receptors in some rats with a treatment of nor-BNI in the VTA and leaving others untreated. Then they subjected the rats to a standardized five-minute stress exercise. After 24 hours they looked at the cells in the VTA and found that LTP was hindered in the untreated rats but still present and underway in the rats whose receptors had been blocked with nor-BNI.
With the role of stress and the receptors in the GABA-dopamine dynamic both confirmed and then mitigated, the question remained: Could this knowledge be used to prevent relapse?
To answer that, Penn co-authors Lisa Briand and Christopher Pierce performed the experiment demonstrating that nor-BNI delivered directly to the VTA prevented stressed rats from relapsing to cocaine seeking, while untreated rats subjected to the same stress did relapse.
"Our results indicate that the kappa receptors within the VTA critically control stress-induced drug seeking in animals," the authors wrote in Neuron.
Along the way, the team also discovered evidence that another stress-affected synapse in the VTA one that excites dopamine release rather than inhibits it does not play a role in the stress-related relapse as many researchers have thought. The nor-BNI treatment that prevented stress-related relapse, for example, did not affect those synapses.
Kauer emphasized that her lab's findings of therapeutic potential are the product of more than a decade of essential basic research on the importance of how changes in synapses relate to behaviors including addiction.
"If we can figure out how not only stress, but the whole system works, then we'll potentially have a way to tune it down in a person who needs that," she said.
###
The National Institutes of Health supported the research with several grants: DA011289, MH019118, AA007459, DA026660, DA15214, and DA18678.
[ | 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.
James Mangold has frequently stated that The Wolverine will be influenced by more than just the X-Men comics, and has taken to his Twitter feed to make his point in picture form.
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The director tweeted a series of images from ten films that have influenced him while making The Wolverine, and very interesting reading they make too.
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You can see all 10 below, and for a bit of amusement, you can see how many you recognise. They?re not labelled you see? there?s at least ten minutes of fun right there!
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Take a look at the images below??
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For those of you wondering, those images are from?
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1) Chungking Express
2) The Outlaw Josey Wales
3) The Samurai Trilogy
4) Floating Weeds
5) Black Narcissus
6) Happy Together
7) 13 Assassins
8) The French Connection
9) Chinatown
10) Shane
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Co-starring Hugh Jackman, Will Yun Lee and Rila Fukushima, The Wolverine will open in the UK on 26 July 2013.?
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Public release date: 6-Mar-2013
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