May 22, 2013 ? When turned on, the gene p53 turns off cancer. However, when existing drugs boost p53, only a few tumors die -- the rest resist the challenge. A study published in the journal Cell Reports shows how: tumors that live even in the face of p53 reactivation create more of the protein p21 than the protein PUMA; tumors that die have more PUMA than p21. And, for the first time, the current study shows a handful of genes that control this ratio.
"The gene p53 is one of the most commonly mutated cancer genes. Tumors turn it off and then they can avoid controls that should kill them. Fine: we have drugs that can reactivate p53. But the bad news is when we go into the clinic with these drugs, only maybe one in ten tumors actually dies. We wanted to know what genes fine-tune this p53 effectiveness," says Joaquin Espinosa, PhD, investigator at the University of Colorado Cancer Center, associate professor in the Department of Molecular, Cellular and Developmental Biology at CU Boulder, and the paper's senior author.
To answer that question, the group including first author Zdenek Andrisyk, PhD, postdoc in the Espinosa Lab, turned off every gene in the human genome in turn and asked if there were genes that, when deactivated, would tip the balance from p21 to PUMA, thus enhancing the likelihood of cell death.
"We found a couple dozen genes involved in this ratio -- genes that with p53 activated, lead to more p21 and better survival or more PUMA and more cell death," Espinosa says.
The hope is that in addition to drugs that reactivate the tumor-suppressor gene p53, patients could be given a second drug targeting genes that control this p21/PUMA ratio, thus making first drug more effective. Likewise, in cases in which toxicity in healthy tissue limits the use of p53 activating drugs, Espinosa's research could lead to new drugs that thumb the scale of the p21/PUMA ratio toward survival in these healthy tissues. Up or down: learning to adjust the ratio has immense promise.
The group's next step is likely repeating the genetic screen with additional tumor and healthy cell lines to discover which of their newly discovered candidate genes are common controllers of the p21/PUMA ratio across cancer types. And, interestingly, the same technique could be used to make many existing drugs more effective.
"With many of these molecularly targeted therapies, you want one effect but then you end up with many other possible effects," Espinosa says. (An example is the recently-reported side effect of low testosterone in male lung cancer patient taking the molecularly targeted drug crizotinib.) The genetic screening technique used in the Espinosa lab could help disentangle effect from side effect -- showing which secondary genes regulate the desired, tumor-killing response and which secondary genes lead to undesirable side-effects.
"Not only could this technique lead to drugs that decrease the side effects of targeted therapies, but if you're not limited by these side effects, you can simply give more drug, perhaps making existing drugs much more powerful," Espinosa says.
A study of an Allosaurus fossil found that the massive dinosaur dined more like a kestrel than a crocodile, tearing flesh from carcasses by pulling its head straight back.?
By Eoin O'Carroll,?Staff / May 22, 2013
At first glance, a nearly 30-foot long, 150-million-year-old dinosaur may not seem to have much in common with a modern-day bird of prey, but according to new research, the Allosaurus and the falcon at least had the same table manners.
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In a study published this week in the journal?Palaeontologia Electronica, Ohio University researchers used a CT scanner to create a digital image of an Allosaurus fragilis skull. After adding neck and jaw muscles, air sinuses, and a windpipe to the image, they then, using a physics simulator, modeled how the dinosaur would have moved its head.
They found that, unlike the Tyrannosaurus, which paleontologists say dismembered its victims by thrashing its head from side to side like a crocodile, the Allosaurus, which, like Tyrannosaurus walked on two legs and had stubby forelimbs, most likely dined by biting into its prey and then tearing the flesh retracting its head back and upward.
Their discovery hinged on a neck muscle that?was unusually positioned on the Allosaurus. On most predatory dinosaurs, such as the T. rex the longissimus capitis superficialis runs along the side of the neck, where it attaches to a bony protrusion at the base of the skull. But on the Allosaurus, the muscle is attached much lower on the skull.?
"This neck muscle acts like a rider pulling on the reins of a horse's bridle," said ?Ohio?University paleontologist Eric Snively, the study's lead author, in an Ohio University press release.?"If the muscle on one side contracts, it would turn the head in that direction, but if the muscles?on both sides pull, it pulls the head straight back."
Most Allosaurus specimens, including the one used in this study, have been unearthed in the western United States, in a fossil-rich region known as the Morrison Formation. During the late Jurassic period, about 150 million years ago, the Allosaurus sat at the top of the food chain. In 2005, paleontologists detailed?evidence?of combat between Allosaurus and Stegosaurus, suggesting that the armored quadroped was on the Allosaurus's menu.
The Tyrannosaurs lived much later, about 65 million years ago.
"Apparently one size doesn't fit all when it comes to dinosaur feeding styles," said Dr. Snively. "Many people think of Allosaurus as a smaller and earlier version of?T. rex, but our engineering analyses show that they were very different predators."
Both genuses are theropods, a group of two-legged dinosaurs that includes today's birds. In other words, the Allosaurus and the falcon have at least one more thing in common: they are both dinosaurs. ?
AMMAN (Reuters) - Western governments are ready to increase support to opponents of President Bashar al-Assad if he rejects a political solution to Syria's civil war, Secretary of State John Kerry said on Wednesday.
Kerry said recent military gains by Assad's forces were only temporary and that if he believed the counter-offensives against the rebels would be decisive, "then he is mis-calculating".
Kerry, speaking at a news conference in Amman before a meeting of the Friends of Syria group of nations, said several thousand fighters from the Lebanese group Hezbollah were taking part in the conflict with active Iranian support on the ground.
"Just last week, obviously, Hezbollah intervened very, very significantly. There are several thousands of Hezbollah militia forces on the ground in Syria who are contributing to this violence and we condemn that."
He said U.S. President Barack Obama had made clear he did not intend to despatch U.S. forces to Syria but that Washington would discuss continued and growing support to help rebel fighters if Assad was unwilling to negotiate a political solution to the two-year-old crisis.
Wednesday's meeting in Amman, which gathers ministers from 11 Western and Middle Eastern countries who have led international opposition to Assad, aimed to promote efforts to end the bloodshed in Syria, he added.
(Reporting by Arshad Mohammed; Editing by Angus MacSwan)
Japan finance minister reluctant to cut corporate tax
Jiji Press -- May 21
Japanese Finance Minister Taro Aso expressed his reluctance Tuesday to meet the business community's request for a cut in corporate taxes. "Tax cut demands by companies that do not currently pay taxes are little convincing," Aso said at a press conference after the day's cabinet meeting.
About 1.86 million of all 2.57 million companies in Japan in fiscal 2011 were in the red and thus exempted from corporate tax payments, according to the Finance Ministry.
20 May 2013Last updated at 19:08 ETBy Helen BriggsBBC News
A vaccine to protect sheep and cattle from a virus spread by midges has been approved by government vets.
The virus, which emerged in the Netherlands and Germany in 2011, can lead to sheep and cattle having stillborn or deformed offspring.
The disease has spread to every county in England and Wales, and was recently reported in Scotland.
Schmallenberg virus (SBV) causes fever, diarrhoea and loss of milk production in adult cattle.
The first SBV vaccine, developed by the animal health company Merck MSD, is expected to be available to UK farmers in the summer.
Continue reading the main story
?Start Quote
It is welcome news for British farmers to have the choice to vaccinate their animals. ?
End QuoteAlick Simmons Deputy chief veterinary officer, Defra
The vaccine is of most use before sheep and cattle become pregnant, as exposure to the virus during pregnancy can cause birth defects in the unborn animal.
Alick Simmons, deputy chief veterinary officer at the Department for Environment, Food and Rural Affairs (Defra) said in a statement:
"It is welcome news for British farmers to have the choice to vaccinate their animals.
"The vaccine will give extra assurance against this disease on top of the natural immunity we expect sheep and cattle to develop after initial exposure."
Continue reading the main story
Schmallenberg virus
Discovered in the German town of Schmallenberg in November 2011
Spread rapidly to many European countries, including the Netherlands, Belgium, France and the UK
Thought to be spread by infected midges
SBV causes relatively mild illness in adult cattle and sheep, but where infection takes place during the early stages of pregnancy it can result in congenital disorders of lambs and calves, and stillbirths
One of a class of emerging viruses spread by insects (arboviruses)
The European Centre for Disease Prevention and Control suggests that there is a low likelihood of any risk to public health
NFU livestock board chairman and sheep farmer, Charles Sercombe, lost 40% of his early lambing flock to the virus.
He said the vaccine would give added reassurance to farmers who were concerned about losing lambs to the disease.
"Everybody in farming who wants to use it will welcome it as soon as possible," he told BBC News.
"Some flocks need it in the next few weeks to fit in with their breeding programmes."
Reports from farmers suggest that at least 1,700 farms throughout the UK have now tested positive for the SBV virus.
UK farmers will be the first in the EU with access to the vaccine, according to Defra.
Phil Stocker, chief executive of the National Sheep Association, said farmers should speak to their vet about the timing of vaccination.
"The decision about whether to vaccinate or not will be down to each individual farmer, their business model, infection history, lambing pattern and location," he said.
Brad Pitt looks amazing, but he can't always see so well. In the new issue of Esquire, the actor cops to an unusual problem: he has "face blindness," or prosopagnosia, meaning he doesn't recognize faces that he's seen before. If you're guessing this creates problems in schmooze-happy Hollywood, then you're correct.
Memphis Grizzlies' Mike Conley (11) and Zach Randolph react to a call during the second half of Game 1 of the Western Conference final NBA basketball playoff series against the San Antonio Spurs, Sunday, May 19, 2013, in San Antonio. San Antonio won 105-83. (AP Photo/Darren Abate)
Memphis Grizzlies' Mike Conley (11) and Zach Randolph react to a call during the second half of Game 1 of the Western Conference final NBA basketball playoff series against the San Antonio Spurs, Sunday, May 19, 2013, in San Antonio. San Antonio won 105-83. (AP Photo/Darren Abate)
San Antonio Spurs' Tim Duncan, left, drives around Memphis Grizzlies' Marc Gasol, of Spain, during the second half of Game 1 of the Western Conference final NBA basketball playoff series Sunday, May 19, 2013, in San Antonio. (AP Photo/Darren Abate)
San Antonio Spurs' Kawhi Leonard, right, fights for a loose ball with Memphis Grizzlies' Quincy Pondexter (20), Tony Wroten, left, and Tony Allen during the second half of Game 1 of the Western Conference final NBA basketball playoff series Sunday, May 19, 2013, in San Antonio. San Antonio won 105-83. (AP Photo/Darren Abate)
San Antonio Spurs' Manu Ginobili, left, of Argentina, defends against Memphis Grizzlies' Tony Allen during the second half of Game 1 of the Western Conference final NBA basketball playoff series on Sunday, May 19, 2013, in San Antonio. San Antonio won 105-83. (AP Photo/Darren Abate)
Memphis Grizzlies' Tony Allen scores during the second half of Game 1 of the Western Conference final NBA basketball playoff series against the San Antonio Spurs Sunday, May 19, 2013, in San Antonio. San Antonio won 105-83. (AP Photo/Darren Abate)
SAN ANTONIO (AP) ? Mike Conley wouldn't let Zach Randolph take the blame for the Memphis Grizzlies' blowout loss in Game 1 of the Western Conference finals.
No one on either team expects him to play so poorly the rest of the series.
Tony Parker had 20 points and nine assists, Kawhi Leonard scored 18 points and the Spurs neutralized Randolph in beating the Grizzlies 105-83 on Sunday. Randolph had just two points ? less than in any game this season, regular season or playoffs ? after playing brilliantly to lead Memphis past defending West champion Oklahoma City in the last round.
"It's not just him. It is all of us," Conley said. "He was telling us that he is going to do better, but we all have to do better defensively. Offensively, we have to move the ball and get guys open."
The NBA's stingiest defense wasn't up to its usual standards, allowing the Spurs to hit 53 percent of their shots and a franchise postseason-record 14 3-pointers.
San Antonio raced out to a 17-point lead in the first quarter, then came up with a response when Memphis rallied to get within six in the second half. Both teams pulled their starters with over 5 minutes left and the Spurs leading by 21.
"It's as good as we could ever expect," said Spurs cornerstone Tim Duncan, who didn't need a big game with so many outside shots falling. "We shot the ball incredibly well from the 3. Tony controlled the game all around: scoring, passing the ball, on defense.
"We know they're going to play better. They're going to change some things. We know we're not going to shoot the ball as well as we did. We have to be prepared for that. For tonight, right now, that's as well as it could have gone."
Game 2 is Tuesday night in San Antonio.
The Grizzlies will surely be trying to tinker and get back to the formula that got them to the conference finals for the first time: a combination of a suffocating defense and Randolph rumbling for points and rebounds inside.
He had a playoff-best 28 points and 14 rebounds in his last game, when Memphis eliminated the Thunder in Game 5 on Wednesday night.
"Obviously, he's their best scorer. He's a beast inside," Parker said. "We know he's not going to play like that every game. It's just sometimes it happens."
Randolph, who missed his first seven shots before a tip-in for his only bucket, said he told his teammates he has "to do better for them."
"A lot of my shots were just off," he said. "I didn't get the good looks I wanted to."
The Grizzlies started to rally as soon as Randolph came out of the game for the first time in the second half.
Quincy Pondexter made a baseline cut for a layup off Darrell Arthur's pass, then hit back-to-back 3-pointers during a 10-0 burst. Jerryd Bayless' two-handed, fast-break dunk off a steal got the Grizzlies within 62-56 with 3:43 left in the third quarter.
The comeback was short-lived.
Bayless missed a 3-pointer on the next trip, and Manu Ginobili was able to make one at the opposite end to spark an 11-1 response that restored the Spurs' lead to 16 by end of the quarter. Leonard hit a pair of 3-pointers and Gary Neal had one as San Antonio kept pouring it on in the fourth.
The four regular-season meetings were all won by the team with more points in the paint, but perimeter shooting proved to be a bigger factor in the playoff opener. Memphis, which was second in the NBA by holding opponents to 33.8 shooting on 3-pointers, let San Antonio make 13 of its first 24 from behind the arc and finish 14 of 29.
Danny Green connected three times and scored 16, and Matt Bonner hit four of his five attempts for 12 points.
"It was just one of those nights. Pretty much, everyone was shooting well," Bonner said. "We won't expect that to continue every game."
Pondexter led Memphis with 17 points, Marc Gasol scored 15 and Conley had 14 points and eight assists. The Grizzlies hadn't allowed 14 3-pointers in a game all season.
"We were just so hyper, just running all over the place on defense," coach Lionel Hollins said. "We'd have four guys in the paint and nobody would be out on the perimeter guarding anybody. And that's not how we play defense."
The Spurs asserted themselves early, scoring on their first seven possessions and also getting a couple head-to-head defensive stops from their veterans while claiming a quick 23-8 lead. Parker swiped the ball from Conley on Memphis' second possession, running out for a layup, and Hollins burned a timeout in the first 2 minutes.
Tim Duncan snuffed out the ensuing play by blocking Randolph's shot, and the Spurs' strong start continued. Bonner hit back-to-back 3-pointers for a 17-point edge late in the first quarter, and San Antonio pushed out to a 43-23 advantage following consecutive baskets by Parker with 6:06 left before halftime.
It was the largest first-half deficit for the Grizzlies during the playoffs.
Memphis has lost its opener in each round in this year's playoffs, recovering from an 0-2 hole in the first round against the Los Angeles Clippers and an 0-1 deficit against Oklahoma City in the West semifinals.
Two years ago in the first round, Memphis won Game 1 in San Antonio and went on to knock the top-seeded Spurs out of the playoffs. San Antonio had a 2-0 lead on Oklahoma city in last year's West finals before losing four in a row.
"I can promise you this: Nobody's happy in our locker room, because we were up 2-0 (in the West finals) last year and we lost," Parker said. "It's just one game. It means nothing. We still have a long way to go."
NOTES: Memphis' only previous deficit larger than 20 this postseason came in the first-round opener against the Los Angeles Clippers. L.A. didn't lead by 20 until the final minute of a 112-91 victory. ... Tracy McGrady got a standing ovation when he checked in with the Spurs up by 20 midway through the fourth quarter. ... The Spurs had 13 3-pointers in Game 1 of their second-round series against the Clippers in last year's playoffs.
United launched their new?Small Business Network, where small businesses can earn bonus United miles when shopping at the program?s network partners.? Small business members can now earn award miles for day-to-day?spending, like paying utilities, buying office supplies or for shipping packages etc.
This program is separate from United?s PerksPlus business frequent flyer program, and is intended for small business owners or those who work in small businesses. However to join it?s a pretty informal process since they do not ask for a tax ID number, so anyone can join this as long as you consider yourself a sole?proprietor. Right now they have a special offer where once you join the network and make a purchase that earns 100 miles with a partner,?you?ll earn 1,000 bonus United miles.
United Small Business Network
To take advantage of this offer, you must first enroll in the MileagePlus Small Business Network and then complete qualifying earning activity for 100 miles or more with Small Business Network partners. This offer runs now through August 17, 2013. Some of the partners that you can earn miles at include Staples, The UPS store, Dell, Avis and Vistaprint to name a few.
Earning rates vary and can be anything from 1-6 miles per $1 spent, to 75 per car rental with Avis to individual bonuses worth well over 1,000 miles.
Earn bonus United miles through their Small Business Network.
Terms and Conditions: This account will be separate from personal MileagePlus member accounts *Enrollment bonus terms and conditions
To qualify for 1,000 mile bonus, prior to 11:59PM CENTRAL on August 17, 2013, a business must:
Enroll in MileagePlus Small Business Network
Complete qualifying earning activity for 100 miles or more with Small Business Network partners
Member must be a business that is duly organized and validly existing in the United States under the laws of the jurisdiction of its organization
Offer?subject to terms & conditions?of the MileagePlus Small Business Network
Bonus offer available one time per member account
Earning points in connection with United PerksPlus will not count as qualified earning activity toward earning the enrollment bonus.
Miles accrued, awards, and benefits issued are subject to change and are subject to the rules of the United MileagePlus program. Please allow 6-8 weeks after completed qualifying activity for bonus miles to post to your account. United may change the MileagePlus program including, but not limited to, rules, regulations, travel awards and special offers or terminate the MileagePlus program at any time and without notice. Bonus award miles, award miles and any other miles earned through non-flight activity do not count or qualify for Premier? status unless expressly stated otherwise. United and its subsidiaries, affiliates and agents are not responsible for any products and services of other participating companies and partners. Taxes and fees related to award travel are the responsibility of the member. The accumulation of mileage or Premier status or any other status does not entitle members to any vested rights with respect to the program. United and MileagePlus are registered service marks. For complete details about the MileagePlus program, go to www.united.com.
Though this might not be your primary means of earning United miles, business frequent flyer programs can still be a good way to rack up a lot of miles on small business purchases and to take advantage of category spending bonuses as well as double dipping on your purchases and travel.
Disclaimer: This content is not provided or commissioned by the credit card issuer. Opinions expressed here are author.s alone, not those of the credit card issuer, and have not been reviewed, approved or otherwise endorsed by the credit card issuer. This site may be compensated through the credit card issuer Affiliate Program.
The planets beyond Mars exhibit the highest winds speeds of any other planets in the solar system. It's a puzzle, because less energy from the sun is available there to drive higher winds.?
By Pete Spotts,?Staff writer / May 17, 2013
This image of Neptune was taken during the August 16-17, 1989, period as Voyager 2 photographed the planet almost continuously, but had no way to measure the winds or how deep they reach into the atmosphere. Now, scientists have turned to subtle changes in the planet's gravity for clues.
NASA/AP
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Astronomers have long marveled that the fastest wind speeds in the solar system have been clocked on the planets farthest from the sun.
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Now, they may be a step closer to figuring out the energy source that drives these mighty winds.
In a new study, a team of scientists from Israel and the US finds that on Uranus and Neptune the winds appear to be confined to the top 680 miles of the atmosphere ? and may actually involve a thinner layer than that.
The results not only reveal new information about Uranus and Neptune, the researchers say. They also provide insights into the mechanisms driving the atmospheres of planets orbiting other stars, says William Hubbard, a researcher at the University of Arizona's Lunar and Planetary Laboratory and a member of the team reporting the results in Thursday's issue of the journal Nature.
Up to now, researchers have posited two possible sources: processes confined to the top layer of the atmosphere or heat welling up from deep in the planets' interiors. Both planets emit more heat than they receive from the sun, with Neptune radiating twice as much. And while 680 miles of atmosphere seems towering by Earthly standards, it's only skin deep for Uranus and Neptune.
The winds in the planets' wide equatorial jet streams rip along at speeds of up to 450 miles an hour on Uranus and as high as 1,300 miles an hour on more-distant Neptune. Still, the flows "seem to be rather shallow, so the amount of energy that has to be supplied to keep them going is much less than might have been thought," Dr. Hubbard says.
The planets beyond Mars exhibit the highest winds speeds of any other planets in the solar system. Yet from Jupiter on out, wind speeds increase with distance, even though less energy is available from the sun to drive atmospheric circulation at each orbit along the way.
The reasons for this trend "are not well understood, actually," says Adam Showman, also with the Lunar and Planetary Laboratory and a member of the study's team. But the prime suspect is atmospheric drag, or rather, the lack of it.
The outer planets' atmospheres behave more like liquids deep in their interiors, so there is virtually no surface roughness to act as a drag on winds, as there is on Earth. And as the distance between a planet and the sun increases, there is less solar energy to impart turbulence to the atmosphere, which also acts as a drag.
We?re for sale too-BUT we are in a rural part of Central Oregon, so it takes a while for anything to sell here-we are 45 minutes from Bend, Or which is great-all the shopping and restaurants and etc you could want; snow bunnies will love the skiing and snowboarding on Mt Bachelor; our town is about 6000 people-so you know your neighbors, etc.
We are ready to go For Sale By Owner on June 1st and our price will go to 145,000. Our house is also the home that was built for the first mayor of Madras, OR in 1948
By Rehanna Ramsay ?Remove the stigma and discrimination often attached to those who are visually impaired and more so differently abled, see our potential, give us a chance, and help us to make our mark in society? This is Anthony Robinson?s message to the public as Guyana shares another observance of Blind Awareness Month. At just 22 years old, Robinson is completely blind but says he ?is prepared for any challenge that life tosses his way.? Robinson is currently a student of Guyana?s Society for the Blind?s Caribbean Secondary Examination Council?s, (CSEC) class. He explains that ?it is people?s lack of confidence and support that assists in further crippling persons with disabilities.? Robinson views the development of disabled persons, as playing a pivotal role in
Anthony Robinson at his work desk
shaping the country?s future. ?Disabled people are just like everybody else. It is just that their lives have been altered in one way or another. This doesn?t mean that you have the right to write them off or exclude them from civilisation.? Characterized by drive and ambition, Robinson oozes confidence. He reminisced that the most difficult part of his life was accepting that he would never be able to see again. Robinson was not born blind. ?I was preparing to sit the common entrance exam to go into Secondary School when I did the surgery; I became completely blind afterwards. At first I had difficulty accepting it but my family and friends, at that time, gave me support and showed me that it?s not the end of the world. They encouraged me not to give up. ?Although being blind hindered me for a while, I decided to fight, to face the world again.?? The surgical intervention he underwent was to remove cataract. Robinson, who hails from Plaisance, would then attend the St Roses institute for the blind and study Braille for three years.? There, he met students like himself, who further fostered his desire to develop. Robinson recalled that those years were somewhat challenging since his mother was a single parent raising eight children on her own. None-the- less he persevered. ?I looked at this as an opportunity to nurture my independence I learnt to do everything on my own.? The unit later transferred Robinson to the Guyana Society for the Blind, where he is under the mentorship of Ganesh Singh, a visually impaired tutor. At present, Robinson is being taught courses in Human and Social Biology, Office Administration, Social Studies, English Language, and Principles of Business while computer training is a bonus feature of the course. These courses are preparing him for the upcoming CSEC exams. These lessons are made possible through the use of JAWS, a software technology designed to teach the blind. Curious about how a blind person can write any exam, Robinson told me that in such instances, the student can request a writer or type the answers using the same software technology. Upon successfully completing the CSEC exams, Robinson plans to enter the world of work. His desire is to become a teacher but not just any teacher. He says, ?I want to be able to impart to people with disabilities like me the same knowledge that I was given.? Once again, the young man who loves dogs, noted that he plans to lead a normal life and future despite his lack of sight. ?I want to teach and have my own property and family like everyone else. I cook, I cut up meat and vegetables, I do my laundry, I wash the dishes, I clean the house and everything on my own. If my family and those around didn?t believe in me I would never have been able to do these simple things? Robinson?s desire is to change people?s attitude towards the blind and differently abled.
While you are hanging out on the Internet (in your underwear, maybe?) on a Saturday, kids that are smarter than either of us are out there getting ready to change the world. 18-year-old Eesha Khare (left), for instance, not only invented a supercapacitor that could someday be a phone battery that charges in just a couple of seconds; she also won $50,000 for it.
Khare is one of the three big winners from the Intel International Science and Engineering Fair. She and 17-year-old Henry Lin (right)?who created a model that simulates thousands of galaxies?picked up Intel Foundation Young Scientist Awards. Meanwhile, 19-year-old Ionut Budisteanu won the Gordon E. Moore Award and $75,000 for his AI model that could lead to a cheaper self-driving car. Khare's invention is the one with some really immediate potential though, and quick-charging phones is something we all want.
So far, the supercapcitor has only been tested to light up a LED, but it was able to do that wonderfully and the prototypes new format holds potential to be scaled. It's also flexible and tiny, and should be able to handle 10,000 recharge cycles, more than normal batteries by a factor of 10.
It's a great step in the right direction, especially since we all know that battery life is the most important feature a phone can have. But like all supercapcitor tech, it's not exactly close to commercial development yet. But hey, if an (admittedly super smart) 18-year-old can get this stuff figured out, multi-national corporations with an even bigger cash profit incentive on the table should be able to as well, right? Hurry up already. I'll take either solution so long as one comes soon. [Intel via NBC News]
A derailed Metro-North rail car is hoisted back on to the tracks in Bridgeport. Conn. on Sunday, May 19, 2013. Crews will spend days rebuilding 2,000 feet of track, overhead wires and signals following the collision between two trains Friday evening that injured 72 people, Metro-North President Howard Permut said Sunday. (AP Photo/The Connecticut Post,Brian A. Pounds ) MANDATORY CREDIT
A derailed Metro-North rail car is hoisted back on to the tracks in Bridgeport. Conn. on Sunday, May 19, 2013. Crews will spend days rebuilding 2,000 feet of track, overhead wires and signals following the collision between two trains Friday evening that injured 72 people, Metro-North President Howard Permut said Sunday. (AP Photo/The Connecticut Post,Brian A. Pounds ) MANDATORY CREDIT
Metro-North employees work at the site of Friday's train derailment in Bridgeport. Conn. on Sunday, May 19, 2013. Crews will spend days rebuilding 2,000 feet of track, overhead wires and signals following the collision between two trains Friday evening that injured 72 people, Metro-North President Howard Permut said Sunday. (AP Photo/The Connecticut Post,Brian A. Pounds ) MANDATORY CREDIT
Map locates Bridgeport, Conn
BRIDGEPORT, Conn. (AP) ? Tens of thousands of commuters are bracing for a difficult trip around southwest Connecticut and to New York City beginning Monday as workers repair the Metro-North commuter rail line crippled by a derailment and crash.
Crews will spend days rebuilding 2,000 feet of track, overhead wires and signals following the collision between two trains Friday evening that injured 72 people, Metro-North President Howard Permut said Sunday. Nine remained hospitalized.
"This amounts to the wholesale reconstruction of a two-track electrified railroad," he said.
Several days of around-the-clock work will be required, including inspections and testing of the newly rebuilt system, Permut said. The damaged rail cars were removed from the tracks on Sunday, the first step toward making the repairs.
Service disruptions on the New Haven line between South Norwalk and New Haven are expected to continue "well into the coming week," Permut said.
Each day, approximately 30,000 Metro-North customers use the stations where service has been shut down, according to the Metropolitan Transportation Authority, which operates Metro-North.
Amtrak service between New York and New Haven also was suspended, and there was no estimate on service restoration. Limited service was available between New Haven and Boston.
Jim Cameron, chairman of the Connecticut Rail Commuter Council, said he's asked officials in numerous towns to suspend parking rules to accommodate what could be tens of thousands of motorists driving to unaffected train stations. Twelve stations are affected by the shutdown.
Starting with the Monday morning rush-hour, a shuttle train will operate about every 20 minutes between New Haven and Bridgeport and two shuttle buses will run between Bridgeport and Stamford stations, state transportation officials said.
For morning and evening peak commutes, limited train service will operate between Grand Central Terminal and Westport.
State officials say travel times will be significantly longer than normal and trains will be crowded. Commuters are advised to use the Harlem line in New York.
Cameron said he doubts many commuters will use three modes of transportation to get to work: driving their cars to catch a bus to get to a train station for the final leg.
Commuters will more likely rely on their cars, leading to massive traffic problems on highways that are already clogged on normal days, Cameron said. He suggested that local and regional officials post highway signs directing motorists to available parking so motorists "don't get off the highway and drive in circles looking for where to dump their cars."
About 700 people were on board the trains Friday evening when one heading east from New York City's Grand Central Terminal to New Haven derailed just outside Bridgeport. It was hit by a train heading west from New Haven.
Dan Solomon, a trauma surgeon who lives in Westport and was headed to work at Yale-New Haven Hospital in New Haven, was on the train that derailed. He said he treated several injured passengers, including a woman with severely broken ankles.
He said he was in a front car that was not as badly affected as cars in the rear of the train.
"I hardly lost my iced tea," Solomon said in an interview.
He said walls were torn off both trains and he quickly checked injured passengers to separate the most badly injured from others.
"When the EMS arrived, I was covered in everyone's blood," he said.
Investigators are looking at a broken section of rail to see if it is connected to the derailment and collision.
NTSB investigators arrived Saturday and are expected to be on site for seven to 10 days. They will look at the brakes and performance of the trains, the condition of the tracks, crew performance and train signal information, among other things.
The MTA operates the Metro-North Railroad, the second-largest commuter railroad in the nation. The Metro-North main lines ? the Hudson, Harlem, and New Haven ? run northward from New York City's Grand Central Terminal into suburban New York and Connecticut.
The last significant train collision involving Metro-North occurred in 1988 when a train engineer was killed in Mount Vernon, N.Y., when one train empty of passengers rear-ended another, railroad officials said.
FILE ? In this March 4, 2013 file photo President Barack Obama talks to media at the start of a cabinet meeting at the White House in Washington. With Obama, from left are Health and Human Services Secretary Kathleen Sebelius, Obama, Defense Secretary Chuck Hagel, and Transportation Secretary Ray LaHood. Saturday, May 18, 2013, Obama took Sebelius and LaHood to Andrews Air Force Base for round of golf, in the rain. LaHood is running the Transportation Department until the Senate confirms Obama's choice of Charlotte, N.C., Mayor Anthony Foxx as successor. (AP Photo/Pablo Martinez Monsivais, File)
FILE ? In this March 4, 2013 file photo President Barack Obama talks to media at the start of a cabinet meeting at the White House in Washington. With Obama, from left are Health and Human Services Secretary Kathleen Sebelius, Obama, Defense Secretary Chuck Hagel, and Transportation Secretary Ray LaHood. Saturday, May 18, 2013, Obama took Sebelius and LaHood to Andrews Air Force Base for round of golf, in the rain. LaHood is running the Transportation Department until the Senate confirms Obama's choice of Charlotte, N.C., Mayor Anthony Foxx as successor. (AP Photo/Pablo Martinez Monsivais, File)
WASHINGTON (AP) ? President Barack Obama has taken two Cabinet secretaries out for a round of golf ? in the rain.
The White House said Health and Human Services Secretary Kathleen Sebelius (seh-BEEL'-yuhs) and outgoing Transportation Secretary Ray LaHood joined the president Saturday at Andrews Air Force Base. LaHood is running the Transportation Department until the Senate confirms Obama's choice of Charlotte, N.C., Mayor Anthony Foxx as successor.
Reporters saw Sebelius climb into the president's SUV before the motorcade left the White House. She's overseeing the president's health care law.
Before he got into the vehicle, Obama looked up at the grey sky with an outstretched hand. A steady rain was falling by the time he arrived about a half hour later.
White House assistant chef Sam Kass completes the foursome.
Study identifies new approach to improving treatment for MS and other conditionsPublic release date: 17-May-2013 [ | E-mail | Share ]
Contact: Charles Casey charles.casey@ucdmc.ucdavis.edu 916-734-9048 University of California - Davis Health System
(SACRAMENTO, Calif.) Working with lab mice models of multiple sclerosis (MS), UC Davis scientists have detected a novel molecular target for the design of drugs that could be safer and more effective than current FDA-approved medications against MS.
The findings of the research study, published online today in the journal EMBO Molecular Medicine could have therapeutic applications for MS as well as cerebral palsy and leukodystrophies, all disorders associated with loss of white matter, which is the brain tissue that carries information between nerve cells in the brain and the spinal cord.
The target, a protein referred to as mitochondrial translocator protein (TSPO), had been previously identified but not linked to MS, an autoimmune disease that strips the protective fatty coating off nerve fibers of the brain and spinal cord. The mitrochronical TSPO is located on the outer surface of mitochondria, cellular structures that supply energy to the cells. Damage to the fatty coating, or myelin, slows the transmission of the nerve signals that enable body movement as well as sensory and cognitive functioning.
The scientists identified mitochondrial TSPO as a potential therapeutic target when mice that had symptoms of MS improved after being treated with the anti-anxiety drug etifoxine, which interacts with mitochondrial TSPO. When etifoxine, a drug clinically available in Europe, was administered to the MS mice before they had clinical signs of disease, the severity of the disease was reduced when compared to the untreated lab animals. When treated at the peak of disease severity, the animals' MS symptoms improved.
"Etifoxine has a novel protective effect against the loss of the sheath that insulates the nerve fibers that transmit the signals from brain cells," said Wenbin Deng, principal investigator of the study and associate professor of biochemistry and molecular medicine at UC Davis.
"Our discovery of etifoxine's effects on an MS animal model suggests that mitochondrial TSPO represents a potential therapeutic target for MS drug development," said Deng.
"Drugs designed to more precisely bind to mitochondrial TSPO may help repair the myelin sheath of MS patients and thereby even help restore the transmission of signals in the central nervous system that enable normal motor, sensory and cognitive functions," he said.
Deng added that better treatments for MS and other demyelinating diseases are needed, especially since current FDA-approved therapies do not repair the damage of immune attacks on the myelin sheath.
The UC Davis research team hopes to further investigate the therapeutic applications of mitochondrial TSPO in drug development for MS and other autoimmune diseases. To identify more efficacious and safer drug candidates, they plan to pursue research grants that will enable them to test a variety of pharmacological compounds that bind to mitochondrial TSPO and other molecular targets in experimental models of MS and other myelin diseases.
The journal paper is entitled, "A TSPO ligand is protective in a mouse model of multiple sclerosis."
###
In addition to Wenbin Deng, co-authors of the paper are Daniel J. Daugherty, Vimal Selvaraj, Olga V. Chechneva, Xiao-Bo Liu and David E. Pleasure.
The study was in part supported by grants from the National Institutes of Health, National Multiple Sclerosis Society, Feldstein Medical Foundation and Shriners Hospitals for Children. NIH grant numbers R01 NS059043 and R01 ES015988.
UC Davis Health System is improving lives and transforming health care by providing excellent patient care, conducting groundbreaking research, fostering innovative, interprofessional education, and creating dynamic, productive partnerships with the community. The academic health system includes one of the country's best medical schools, a 619-bed acute-care teaching hospital, a 1000-member physician's practice group and the new Betty Irene Moore School of Nursing. It is home to a National Cancer Institute-designated comprehensive cancer center, an international neurodevelopmental institute, a stem cell institute and a comprehensive children's hospital. Other nationally prominent centers focus on advancing telemedicine, improving vascular care, eliminating health disparities and translating research findings into new treatments for patients. Together, they make UC Davis a hub of innovation that is transforming health for all. For more information, visit http://healthsystem.ucdavis.edu.
[ | E-mail | Share ]
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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.
Study identifies new approach to improving treatment for MS and other conditionsPublic release date: 17-May-2013 [ | E-mail | Share ]
Contact: Charles Casey charles.casey@ucdmc.ucdavis.edu 916-734-9048 University of California - Davis Health System
(SACRAMENTO, Calif.) Working with lab mice models of multiple sclerosis (MS), UC Davis scientists have detected a novel molecular target for the design of drugs that could be safer and more effective than current FDA-approved medications against MS.
The findings of the research study, published online today in the journal EMBO Molecular Medicine could have therapeutic applications for MS as well as cerebral palsy and leukodystrophies, all disorders associated with loss of white matter, which is the brain tissue that carries information between nerve cells in the brain and the spinal cord.
The target, a protein referred to as mitochondrial translocator protein (TSPO), had been previously identified but not linked to MS, an autoimmune disease that strips the protective fatty coating off nerve fibers of the brain and spinal cord. The mitrochronical TSPO is located on the outer surface of mitochondria, cellular structures that supply energy to the cells. Damage to the fatty coating, or myelin, slows the transmission of the nerve signals that enable body movement as well as sensory and cognitive functioning.
The scientists identified mitochondrial TSPO as a potential therapeutic target when mice that had symptoms of MS improved after being treated with the anti-anxiety drug etifoxine, which interacts with mitochondrial TSPO. When etifoxine, a drug clinically available in Europe, was administered to the MS mice before they had clinical signs of disease, the severity of the disease was reduced when compared to the untreated lab animals. When treated at the peak of disease severity, the animals' MS symptoms improved.
"Etifoxine has a novel protective effect against the loss of the sheath that insulates the nerve fibers that transmit the signals from brain cells," said Wenbin Deng, principal investigator of the study and associate professor of biochemistry and molecular medicine at UC Davis.
"Our discovery of etifoxine's effects on an MS animal model suggests that mitochondrial TSPO represents a potential therapeutic target for MS drug development," said Deng.
"Drugs designed to more precisely bind to mitochondrial TSPO may help repair the myelin sheath of MS patients and thereby even help restore the transmission of signals in the central nervous system that enable normal motor, sensory and cognitive functions," he said.
Deng added that better treatments for MS and other demyelinating diseases are needed, especially since current FDA-approved therapies do not repair the damage of immune attacks on the myelin sheath.
The UC Davis research team hopes to further investigate the therapeutic applications of mitochondrial TSPO in drug development for MS and other autoimmune diseases. To identify more efficacious and safer drug candidates, they plan to pursue research grants that will enable them to test a variety of pharmacological compounds that bind to mitochondrial TSPO and other molecular targets in experimental models of MS and other myelin diseases.
The journal paper is entitled, "A TSPO ligand is protective in a mouse model of multiple sclerosis."
###
In addition to Wenbin Deng, co-authors of the paper are Daniel J. Daugherty, Vimal Selvaraj, Olga V. Chechneva, Xiao-Bo Liu and David E. Pleasure.
The study was in part supported by grants from the National Institutes of Health, National Multiple Sclerosis Society, Feldstein Medical Foundation and Shriners Hospitals for Children. NIH grant numbers R01 NS059043 and R01 ES015988.
UC Davis Health System is improving lives and transforming health care by providing excellent patient care, conducting groundbreaking research, fostering innovative, interprofessional education, and creating dynamic, productive partnerships with the community. The academic health system includes one of the country's best medical schools, a 619-bed acute-care teaching hospital, a 1000-member physician's practice group and the new Betty Irene Moore School of Nursing. It is home to a National Cancer Institute-designated comprehensive cancer center, an international neurodevelopmental institute, a stem cell institute and a comprehensive children's hospital. Other nationally prominent centers focus on advancing telemedicine, improving vascular care, eliminating health disparities and translating research findings into new treatments for patients. Together, they make UC Davis a hub of innovation that is transforming health for all. For more information, visit http://healthsystem.ucdavis.edu.
[ | 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.
725.35 meters. A whoppumental 2,379.75 feet. That's how big the new super-sized Enterprise is. Here you can see it compared against the Galactica, the good old Enterprise, the Blockade Runner, and the ISS.
When JJ Abrams said that he wanted to put some Star Wars into Star Trek, apparently it also applied to the scale of spaceships. And while the new Enterprise doesn't even reach half of the 1,600 meters?that's a mile long?of an Imperial Star Destroyer, it's still amazingly big compared to the 288 meters of the old Enterprise. Maybe now you would be able to take down an Star Destroyer with a couple of these.
How much would it cost to build this thing today? This much.
Soccer fans in America often have a chip on their shoulder about football.? And for good reason.? Football is the dominant sport in the country, soccer isn?t.
Then again, soccer is boring.? Football isn?t.
It creates potential friction where an NFL team also owns a professional soccer team.? In New England, the Krafts are getting the brunt of some of that friction via fans of the soccer team the Krafts own.
Julian Cardillo of the Boston Globe (via SportsBusiness Daily) writes that ?[i]t appears to many that the Revolution are the Kraft family?s second priority, rather than an equal investment, to the New England Patriots.?
If it appears that way, that appearance would be accurate.? The Patriots have become one of the elite franchises in the NFL, the premier professional sports league in the United States.? The Revolution are an also-ran, at best, in a league that is an also-ran, at best.
Revolution Brian Bilello seems to think that the griping comes from soccer?s anti-football bias.
?I think both the Kraft family and the Hunt family, because they have NFL sides as well, I think there?s a weird perception,? Bilello told Cardillo.? ?Both families have been involved with the sport since the very beginning.? The fact that they?re involved in the NFL, that hurts them.?
Still, a Sports Illustrated poll of anonymous players pegged the Krafts as the worst owners in the MLS, and players like Thierry Henry and David Beckham have balked at playing on the FieldTurf at Gillette Stadium.
?There?s a lot of great things about having the Krafts as owners,? Bilello said.? ?They?ve supported this league.? They do things behind the scenes not just for the Revolution, but for the sport of soccer in this country.?
None of that matters to the average soccer fan, who can?t understand why Americans haven?t embraced the sport the way the rest of the world has.
Meanwhile, we can?t understand why the rest of the world hasn?t embraced football the way Americans have.
A fundamental property of the rarest element on Earth, astatine, has been discovered for the first time, scientists say.
Astatine occurs naturally; however, scientists estimate much less than an ounce in total exists worldwide. For a long time, the characteristics of this elusive element were a mystery, but physicists at the CERN physics laboratory in Switzerland have now measured its ionization potential ? the amount of energy needed to remove one electron from an atom of astatine, turning it into an ion or a charged particle.
The measurement fills in a missing piece of the periodic table of elements, because astatine was the last naturally occurring element for which this property was unknown. Astatine, which has 85 protons and 85 electrons per atom, is radioactive, and half of its most stable version decays in just 8.1 hours, a time called half-life. In 1953, Isaac Asimov estimated the worldwide total of astatine in nature was 0.002 ounces (0.07 grams). [Graphic: Nature's Tiniest Particles Explained]
To measure astatine's ionization potential, physicists at CERN's ISOLDE (Isotope Separator On Line-Detector) Radioactive Ion Beam facility created artificial isotopes of astatine (atoms with different numbers of neutrons than those occurring in nature) by shooting beams of energetic protons at a target of uranium (which has 92 protons and electrons). The collisions created a shower of new particles, some of which were astatine.
The physicists then shined laser beams of varying wavelengths at the atoms to ionize them. By isolating the astatine ions, and checking which wavelength of laser had created them, the researchers determined astatine's ionization potential to be 9.31751 electronvolts (the ionization potential of hydrogen, for example, is 13.6 electronvolts).
The value will serve as a benchmark for studying exotic superheavy elements, which don't occur naturally, but can be created at specialized labs. For example, researchers want to compare the properties of astatine with those of the newly discovered element 117, first created at Russia's Joint Institute for Nuclear Research (JINR) in 2010. This element, the second-heaviest ever created, is a homologue of astatine, meaning that it sits right below astatine on the periodic table and likely shares similar properties.
"In-source laser spectroscopy today is a most sensitive method to study atomic properties of exotic short-lived isotopes," Valentin Fedosseev, team leader of ISOLDE's resonance ionization laser ion source, said in a statement. "It is well-suited to explore the spectra of artificially produced elements, like the superheavy ones. The success in this study of astatine has added confidence for similar projects started recently at GANIL, France, and at JINR, Russia." (GANIL stands for Grand Acc?l?rateur National d'Ions Lourds, or the Large Heavy Ion National Accelerator.)
The new discovery could also help scientists develop medical applications for artificial astatine, which might be useful in radiotherapy treatments for cancer called alpha therapy.
"None of the many short-lived isotopes used in medicine exist in nature; they have to be artificially produced by nuclear reactions," said Bruce Marsh, a resonance ionization laser ion source team member. "The possible medical isotopes of astatine are not so different in this respect. What is different about astatine is that its scarcity in nature makes it difficult to study by experiment, which is why this measurement of one of the fundamental properties is a significant achievement."
Follow Clara Moskowitz on Twitter?and Google+. Follow us?@livescience,?Facebook?&?Google+. Original article on?LiveScience.com.
Copyright 2013 LiveScience, a TechMediaNetwork company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
May 15, 2013 ? Melbourne scientists have made the surprise discovery that malaria parasites can 'talk' to each other -- a social behaviour to ensure the parasite's survival and improve its chances of being transmitted to other humans.
The finding could provide a niche for developing antimalarial drugs and vaccines that prevent or treat the disease by cutting these communication networks.
Professor Alan Cowman, Dr Neta Regev-Rudzki, Dr Danny Wilson and colleagues from the Walter and Eliza Hall Institute's Infection and Immunity division, in collaboration with Professor Andrew Hill from the University of Melbourne's Bio21 Institute and Department of Biochemistry and Molecular Biology showed that malaria parasites are able to send out messages to communicate with other malaria parasites in the body. The study was published today in the journal Cell.
Professor Cowman said the researchers were shocked to discover that malaria parasites work in unison to enhance 'activation' into sexually mature forms that can be picked up by mosquitoes, which are the carriers of this deadly disease.
"When Neta showed me the data, I was absolutely amazed, I couldn't believe it," Professor Cowman said. "We repeated the experiments many times in many different ways before I really started to believe that these parasites were signalling to each other and communicating. But we came to appreciate why the malaria parasite really needs this mechanism -- it needs to know how many other parasites are in the human to sense when is the right time to activate into sexual forms that give it the best chance of being transmitted back to the mosquito."
Malaria kills about 700,000 people a year, mostly children aged under five and pregnant women. Every year, hundreds of millions of people are infected with the malaria parasite, Plasmodium, which is transmitted through mosquito bites. It is estimated that half the world's population is at risk of contracting malaria, with the disease being concentrated in tropical and subtropical regions including many of Australia's near neighbours.
Dr Regev-Rudzki said the malaria parasites inside red blood cells communicate by sending packages of DNA to each other during the blood stage of infection. "We showed that the parasites inside infected red blood cells can send little packets of information from one parasite to another, particularly in response to stress," she said.
The communication network is a social behaviour that has evolved to signal when the parasites should complete their lifecycle and be transmitted back to a mosquito, Dr Regev-Rudzki said. "Once they receive this information, they change their fate -- the signals tell the parasites to become sexual forms, which are the forms of the malaria parasite that can live and replicate in the mosquito, ensuring the parasites survives and is transmitted to another human."
Professor Cowman said he hopes to see the discovery pave the way to new antimalarial drugs or vaccines for preventing malaria. "This discovery has fundamentally changed our view of the malaria parasite and is a big step in understanding how the malaria parasite survives and is transmitted," he said. "The next step is to identify the molecules involved in this signalling process, and ways that we could block these communication networks to block the transmission of malaria from the human to the mosquito. That would be the ultimate goal."
This project was supported by the National Health and Medical Research Council of Australia, Howard Hughes Medical Institute and the Victorian Government.
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Public release date: 17-May-2013
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