Uber has been up against the ropes lately. For one, it's dealing with the fall out from an exec's suggestion it should be investigating critical journalists. Plus it's combating a report that claims a 'God Mode' allows its employees to track...
You can already check out Deezer Elite if you want high-quality streaming music, but it's only available on Sonos devices. That's not very useful when you're away from home, is it? Thankfully, Aspiro has stepped in to fill that void with a far more...
300 empty desks were placed in the street outside Los Angeles Unified School District headquarters earlier today as part of a protest demanding extra funding for disadvantaged youth. The 300 desks are meant to represent the approximate number of students who drop out of LAUSD every month. [Photo by Richard Vogel/AP]
The Lumia 820 just reached EOL at Delta. The airline's 20,000 flight attendants will be stepping up to the significantly larger Nokia Lumia 1520 "phablet" come this fall, matching the larger form factor that AA currently has in the sky. The 1520s...
Every day dozens and dozens of new and updated apps and games hit the iOS and Mac App Stores. It's impossible to keep up with them all, but it's not impossible to pick out the very best. Here they are! Today we have updates to a calendar app, a news reader, a text editor, and more.
If you try any of the apps or updates, let me know how they work for you. If you got any new or updated apps today that you loved, but don't see here, let us know about them!
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The Ultimate Fighter (TUF) 18 cast member Jessamyn Duke has kept a blog throughout the season. Duke's entry this week revealed something shocking about coach and UFC women's bantamweight champion Ronda Rousey.
Semi-finalists Anthony Gutierrez and David Grant never got to fight one another as scheduled on Wednesday's episode because Gutierrez did not make weight. After weighing in four pounds heavy the day before their scheduled fight, Gutierrez had another hour to make weight but chose not to try to do so.
As a result, he forfeited the fight and was kicked out of the TUF house. Rousey was the coach for both Gutierrez and Grant. The episode showed her talking with UFC president Dana White after Gutierrez was kicked out and telling the promoter that she herself was going to cut weight because she felt bad that she didn't guide Anthony through successfully.
The editing made it appear as if White talked her out of doing so. In an apparently entirely different part of the week, the episode showed Rousey beating opposing coach Miesha Tate in a wall-climbing challenge.
Jessamyn's blog entry this week reveals that Rousey did indeed go through with cutting weight to demonstrate to the fighters what is possible through strength of will, and she won the wall-climbing challenge while in the midst of that extreme weight cut.
[Rousey] jumped on the scale after Anthony missed weight and was 152 pounds. Without any sort of prep (diet, water loading, sodium loading/cutting, etc.) jumped in the sauna and was in there for FIVE hours before it was time to go to the coaches challenge. Yes, Ronda Rousey cut weight in the sauna for five hours, went to a rock climbing challenge, won, and then went BACK to the sauna that night and cut some more.
The next day when it was time for Jessica and Raquel to fight, she was at the gym before anyone else arrived and was back in the sauna cutting weight. When the rest of us arrived she was sitting at 136 pounds in the locker room. I watched her warm upRakoczy for her fight while on weight and then step on the scale in front of Dana and be 135 pounds. She did this to prove a point.
Wow.
Hopefully next week's episode will shine some light on that extraordinary occurrence as it is surely worth highlighting with actual air-time. Rousey is certainly a bundle of emotions and displayed that during this season of TUF but no one can say that the champion isn't willing to back up her words and outbursts.
Rousey defends her title December 28th against Tate. Chris Weidman also defends his middleweight strap against former champ Anderson Silva on the same card.
Follow Elias on Twitter @EliasCepeda
Source: http://sports.yahoo.com/blogs/mma-cagewriter/ronda-rousey-cut-17-pounds-one-day-prove-214523472--mma.html
Credit: Ireneusz Skorupa
Here's a hypothetical for you. Let's say you're a smart, plugged-in 20-something entrepreneur. You've come up with an idea for an app that proves insanely popular, though you have yet to figure out how to collect any money for it. This business is dependent entirely on the momentary whims of teenagers, many of whom may be breaking the law by using it.
Some guy comes up to you driving a Brink's truck filled with greenbacks. He offers you $3 billion on the spot, in cash, for your company.
[ Also on InfoWorld: 10 signs the dot-com tech bubble is back. | For a humorous take on the tech industry's shenanigans, subscribe to Robert X. Cringely's Notes from the Underground newsletter and follow Cringely on Twitter. | Check out InfoWorld TechBrief, your source for quick, smart views on the news you'll be talking about -- subscribe today. ]
Do you:
A) Look behind him for the guys in the white coats with the nets
B) Take the money, buy your own island, and stock it with supermodels
C) See if Google will make you a better offer
D) Say, "Meh, I think I'll pass"
If you're 23-year-old Evan Spiegel, co-founder of Snapchat -- or you're out of your flippin' mind -- you choose options C and/or D. Why? That is the $3 billion question, or possibly the $4 billion one, if the rumors about Google's counteroffer are to be believed.
Sexts and the single URL
Snapchat is based on a very simple premise: You can take any kind of naughty photo you want, send it to any other Snapchat user, and have the thing go poof within 10 seconds. No harm, no foul, and no incriminating evidence are left behind.
Nearly one out of every 10 U.S. cellphone users has installed Snapchat, according to the latest Pew Research Center survey, 95 percent of them under the age of 29. It's a concept so appealing to a certain demographic that an alleged 350 million Snapchats are sent each day. That's a lot of self-destructing selfies.
The problem? A large percentage of those narcissistic shutterbugs are under the age of 18 -- which makes Snapchat a big, fat target for law enforcement agencies trying to combat kiddie porn. The service has already published a guide telling police what they need to do to get their hands on Snapchat user data. Last month, Snapchat admitted it has passed on "about a dozen" photos to the feds. That "about a dozen" number is likely to zoom upward very soon, I suspect.
Also, that bit about Snapchats quickly disappearing? Not so much. The service recently unveiled Stories, a feature that makes Snapchat sessions available for up to 24 hours. Even the quickly disappearing kind can be captured by someone with fast enough fingers, as evidenced by any Google search for nude Snapchat pix. (Or so I've heard.)
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PUBLIC RELEASE DATE: 8-Nov-2013
ShareContact: David Orenstein
[email protected]
401-863-1862
Brown University
PROVIDENCE, R.I. [Brown University] The story of why we are all so different goes well beyond the endless mixing and matching of DNA through breeding. A new study in the journal Nature Communications, for instance, reports a new molecular mechanism of individual variation found in fruit flies that uses components operating in a wide variety of species, including humans.
The new mechanism is based in a surprising genetic oddity. Nearly all genomes those of humans, fruit flies, and even corn and rice are constantly grappling with parasitic snippets of genetic material called "transposons." These snippets copy themselves, move around, and embed themselves within DNA. If left unchecked, transposons can alter how genetic instructions are carried out in the body,usually for the worse, sometimes for the better. But genomes don't leave transposons unchecked. They "look" for tell-tale double-stranded RNA associated with the transposons, chop the strands up and use the pieces to "silence" the invaders.
In the new paper, scientists show that an enzyme called ADAR, which edits RNA in humans, flies, and many other creatures, edits double-stranded RNAs. This loosens the system that keeps "Hoppel" transposons silenced in fruit flies. When transposons are silenced, it's done by keeping them locked tight around tiny balls of material called chromatin.
Since the amount of ADAR varies from one individual to the next, the amount of jailbreaking from those chromatin prison varies too, and that should lead to altered gene expression. After showing that an abundance of ADAR reduces silencing of a common transposon in the flies and that a lack of ADAR meant widespread silencing the researchers measured two consequences of different levels of ADAR activity: a 20-percent difference in life span and difference in eye color (red rather than white).
The study was focused on fruit flies, ADAR, and the double-stranded RNA of the Hoppel transposon, but the ability of RNA editors to loosen the silencing of at least some transposons may be a source of individual variation in humans and other species too, said Brown University biologist Robert Reenan, senior author of the new study published online. Editing of double-stranded RNA or a lack of editing has already been linked to diseases in people, including amyloid lateral sclerosis and, specifically in the case of ADAR, Aicardi-Goutires syndrome.
"ADAR in humans functions the same way it does in flies, and double-stranded RNAs are made in humans the same way," said Reenan, professor of biology in the Department of Molecular Biology, Cell Biology and Biochemistry. "They are all generic, off the shelf staples of the biological toolkit. This is not anything that is particular to flies."
Picking the double strand
Many of Reenan's studies focus on ADAR's editing activity in the development of the nervous system, but this investigation began years ago when lead author and then graduate student Yiannis Savva happened to overexpress ADAR in fruit fly salivary gland cells. He found some bound in an unexpected place: one specific site on chromosome four.
Reenan recalled: "I told him that's either an artifact or it will be the centerpiece of your thesis."
Various tests revealed that the chromosome four site was a home for several Hoppel transposons making a double-stranded RNA.
Savva and Reenan were curious about what business ADAR had with the transposon. A series of experiments in ensuing years did just that. They relocated the transposons to places where they weren't and found that ADAR followed. They deleted the double-stranded RNA from chromosome four and found that ADAR was no longer there. They identified specific editing sites and signs of editing on the double stranded RNA.
Savva and his collaborators then measured silencing of tranposons with varying levels of ADAR and found that the more ADAR there was, the less silencing there was.
Then, working with Stephen Helfand, an expert on the biology of aging, they noticed that a reduction of editing increases life span.
"As a loss of silencing has been associated with aging in Drosophila and other organisms, we performed lifespan analyses on [low-ADAR] adults and wild-type controls and found a ~20-percent increase in the median life span of [low-ADAR] males and females," the authors wrote in Nature Communications.
Look in their eyes
Later they looked at eye color, using natural (wild-type) flies and those where ADAR activity was either artificially hamstrung or excessively active. The natural flies have eyes that run a full continuum from red to white with various "variegating" blends in between that reflect the silencing state of their eye color gene. In the excessively ADAR-active flies there was little silencing and eyes turned out red much more often than normal. In the ADAR-hamstrug flies, virtually all of the eyes were white (reflecting a lot of silencing of the red color gene).
Ultimately, Savva said, ADAR appears to be allowing transposons like Hoppel to exercise their capacity to regulate gene expression, even though they are really just uninvited guests in the genome.
"What ADAR does is fine tune this regulatory network," Savva said. "In cells where you have ADAR, the network is activated. In cells where you don't it's silenced. It provides dynamicity."
In other words, some of the differences among us may be apparent in the eyes of flies.
###
In addition to Savva, Reenan, and Helfand, authors on the paper are James Jepson, Yoah-Jen Chang, Rachel Whitaker, Brian Jones, Nian Jiang, and Guyu Du of Brown; Georges St. Laurent of Brown and the St. Laurent Institute; and Michael Tackett and Phillipp Kapranov of the St. Laurent Institute.
The National Institute on Aging (grants: AG16667, AG24353, AG25277) and the Ellison Medial Foundation funded the research.
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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.
PUBLIC RELEASE DATE: 8-Nov-2013
ShareContact: David Orenstein
[email protected]
401-863-1862
Brown University
PROVIDENCE, R.I. [Brown University] The story of why we are all so different goes well beyond the endless mixing and matching of DNA through breeding. A new study in the journal Nature Communications, for instance, reports a new molecular mechanism of individual variation found in fruit flies that uses components operating in a wide variety of species, including humans.
The new mechanism is based in a surprising genetic oddity. Nearly all genomes those of humans, fruit flies, and even corn and rice are constantly grappling with parasitic snippets of genetic material called "transposons." These snippets copy themselves, move around, and embed themselves within DNA. If left unchecked, transposons can alter how genetic instructions are carried out in the body,usually for the worse, sometimes for the better. But genomes don't leave transposons unchecked. They "look" for tell-tale double-stranded RNA associated with the transposons, chop the strands up and use the pieces to "silence" the invaders.
In the new paper, scientists show that an enzyme called ADAR, which edits RNA in humans, flies, and many other creatures, edits double-stranded RNAs. This loosens the system that keeps "Hoppel" transposons silenced in fruit flies. When transposons are silenced, it's done by keeping them locked tight around tiny balls of material called chromatin.
Since the amount of ADAR varies from one individual to the next, the amount of jailbreaking from those chromatin prison varies too, and that should lead to altered gene expression. After showing that an abundance of ADAR reduces silencing of a common transposon in the flies and that a lack of ADAR meant widespread silencing the researchers measured two consequences of different levels of ADAR activity: a 20-percent difference in life span and difference in eye color (red rather than white).
The study was focused on fruit flies, ADAR, and the double-stranded RNA of the Hoppel transposon, but the ability of RNA editors to loosen the silencing of at least some transposons may be a source of individual variation in humans and other species too, said Brown University biologist Robert Reenan, senior author of the new study published online. Editing of double-stranded RNA or a lack of editing has already been linked to diseases in people, including amyloid lateral sclerosis and, specifically in the case of ADAR, Aicardi-Goutires syndrome.
"ADAR in humans functions the same way it does in flies, and double-stranded RNAs are made in humans the same way," said Reenan, professor of biology in the Department of Molecular Biology, Cell Biology and Biochemistry. "They are all generic, off the shelf staples of the biological toolkit. This is not anything that is particular to flies."
Picking the double strand
Many of Reenan's studies focus on ADAR's editing activity in the development of the nervous system, but this investigation began years ago when lead author and then graduate student Yiannis Savva happened to overexpress ADAR in fruit fly salivary gland cells. He found some bound in an unexpected place: one specific site on chromosome four.
Reenan recalled: "I told him that's either an artifact or it will be the centerpiece of your thesis."
Various tests revealed that the chromosome four site was a home for several Hoppel transposons making a double-stranded RNA.
Savva and Reenan were curious about what business ADAR had with the transposon. A series of experiments in ensuing years did just that. They relocated the transposons to places where they weren't and found that ADAR followed. They deleted the double-stranded RNA from chromosome four and found that ADAR was no longer there. They identified specific editing sites and signs of editing on the double stranded RNA.
Savva and his collaborators then measured silencing of tranposons with varying levels of ADAR and found that the more ADAR there was, the less silencing there was.
Then, working with Stephen Helfand, an expert on the biology of aging, they noticed that a reduction of editing increases life span.
"As a loss of silencing has been associated with aging in Drosophila and other organisms, we performed lifespan analyses on [low-ADAR] adults and wild-type controls and found a ~20-percent increase in the median life span of [low-ADAR] males and females," the authors wrote in Nature Communications.
Look in their eyes
Later they looked at eye color, using natural (wild-type) flies and those where ADAR activity was either artificially hamstrung or excessively active. The natural flies have eyes that run a full continuum from red to white with various "variegating" blends in between that reflect the silencing state of their eye color gene. In the excessively ADAR-active flies there was little silencing and eyes turned out red much more often than normal. In the ADAR-hamstrug flies, virtually all of the eyes were white (reflecting a lot of silencing of the red color gene).
Ultimately, Savva said, ADAR appears to be allowing transposons like Hoppel to exercise their capacity to regulate gene expression, even though they are really just uninvited guests in the genome.
"What ADAR does is fine tune this regulatory network," Savva said. "In cells where you have ADAR, the network is activated. In cells where you don't it's silenced. It provides dynamicity."
In other words, some of the differences among us may be apparent in the eyes of flies.
###
In addition to Savva, Reenan, and Helfand, authors on the paper are James Jepson, Yoah-Jen Chang, Rachel Whitaker, Brian Jones, Nian Jiang, and Guyu Du of Brown; Georges St. Laurent of Brown and the St. Laurent Institute; and Michael Tackett and Phillipp Kapranov of the St. Laurent Institute.
The National Institute on Aging (grants: AG16667, AG24353, AG25277) and the Ellison Medial Foundation funded the research.
[
| 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.
