When T.J. Grant knocked out two-time title challenger Gray Maynard last May for his fifth straight win at lightweight – where he’s undefeated – the Canadian earned a shot at then-champion Benson Henderson. Unfortunately for him, Grant suffered a concussion in his training camp for Henderson and was forced to pull out.
Anthony Pettis would then step in for Grant and win the belt from Henderson this past August at UFC 164. Grant’s recovery from his concussion has been deliberate and justifiably long but he could at least conceivably comfort himself knowing that when he was ready, he’d get that coveted shot at the lightweight title he’d worked so hard for.
Turns out that Grant’s streak of bad luck is continuing. After Gilbert Melendez’s impressive win over Diego Sanchez this past weekend at UFC 166, promotion president Dana White said that “El Nino” very well could have bumped Grant back in the title contender’s line.
"T.J. Grant's in one of those unfortunate situations where he had the title shot and he had to pull out twice," White said, also calling Melendez’ win a “huge setback for T.J. Grant."
"He's in limbo. He might come back and have to fight another fight. We've got to keep this thing rolling."
Prior to beating Sanchez at UFC 166, Melendez lost a controversial decision to Henderson for the title in the former Strikeforce champ’s promotional debut. Melendez’s back to back impressive fights against Henderson and Sanchez, as well as a new champion in Pettis and Grant’s continuing recovery, may mean that Gilbert will get the first crack at the new champion in the near future.
What do you think? Is it fair for Grant to have to come back and fight someone else in order to get a title shot, and would you rather see Melendez fight Pettis first?
"Facebook users are reporting trouble logging in and posting updates Monday morning.
"Some users are seeing a 'temporary disruption of service' warning.
" 'Servers are down,' one user posted on Twitter.
" 'So, it's not just me,' posted another."
The site "Downrightnow" said, indeed (as of 10:40 a.m. ET) that Facebook was having some problems.
And here's an example of the sort of reaction trending on the rival Twitter under the hashtags #GetWellSoonFacebook and #RIPFacebook:
The Two-Way has reached out to Facebook for comment, but we haven't heard back yet.
Update At 11:50 a.m. ET. Facebook: 'Now Back To 100%'
"Earlier this morning, while performing some network maintenance, we experienced an issue that prevented some users from posting to Facebook for a brief period of time," a Facebook spokesman says in an email to NPR. "We resolved the issue quickly, and we are now back to 100%. We're sorry for any inconvenience we may have caused."
A spendy accessory aimed at corporate users on the go
Logitech is hoping to capitalize on the increasingly mobile workforce's needs for quality speakerphone audio with its latest Bluetooth speaker, the P710e. Built to be used with any phone or tablet over Bluetooth as well as your laptop over USB, the P710e brings enterprise-level speakerphone quality to any device that you connect it to.
On the mobile side, the P710e offers Bluetooth pairing over NFC, as well as a device dock in the top of the speaker for making video calls. When working wirelessly, Logitech is quoting 15 hours of battery life for the device, which should get you through even the longest conference calls with ease.
Logitech pegs the price of the P710e at a cool $169.99, but there isn't any easy way to buy one just yet — being that this is a enterprise-focused device we may be waiting a little while before anyone can buy them directly. This certainly isn't your average consumer-focused Bluetooth speaker.
Contact: Rachel Steinhardt rsteinhardt@licr.org 212-450-1582 Ludwig Institute for Cancer Research
A study of how cancer cells get energy and raw materials for growth from glucose opens doors to new therapies
October 21, 2013, New York, NY Ludwig researchers have elucidated a key mechanism by which cancer cells change how they metabolize glucose to generate the energy and raw materials required to sustain runaway growth.
Published online in Cell Metabolism, the Ludwig Cancer Research study also reveals how the aggressive brain cancer glioblastoma harnesses the mechanism to resist targeted therapies that should disrupt this capabilityknown as the Warburg effectand suggests how such resistance might be overcome. In detailing the molecular circuitry of the phenomenon, the researchers uncover several possible targets for new drugs that might disrupt cancer cell metabolism to destroy tumors.
"Cancer and other fast-growing cells extract energy from glucose using a process that ordinarily kicks in only when oxygen is in short supply," explains Ludwig scientist Paul Mischel, MD, who is based at the University of California, San Diego School of Medicine. "This allows them to thread the needle: they get the energy they need from glucose but also retain the carbon-based building blocks for molecules like lipids, proteins and DNA, which dividing cells need in large quantities."
Until recently, relatively little was known about the biochemical circuits that induce this vital metabolic shift in cancer cells. Earlier this year, however, Mischel and his colleagues published a study describing how an aberrant growth signal found in many glioblastomas is channeled to induce the Warburg effect. That signaling cascade, which involves the key proteins PI3 kinase (PI3K), Akt and mTORC1, culminates in the activation of a transcription factora controller of gene expressionnamed c-Myc. "In many cancer cells," says Mischel, "c-Myc seems to be a lever that links growth signaling pathways with the machinery that controls the uptake and use of nutrients."
In the current study, Mischel, who did the research in collaboration with Ludwig researchers Kenta Masui, MD, PhD and Web Cavenee, PhD, both also at UC San Diego, identifies a second interacting biochemical cascade that is independent of the PI3K-Akt-mTORC1 signal and uses distinct biochemical circuits and an unusual mechanism to turn on c-Myc. This pathway, Mischel and his colleagues report, depends on signals from a protein complex named mTORC2. The researchers show that when mTORC2 is switched on, it silences two other transcription factors, FoxO1 and FoxO3, which would otherwise suppress the activation of c-Myc in the nucleus of the cell. Further, they learned that the silencing of the FoxOs occurs through a chemical modificationknown as acetylationa process that has not been well understood.
The study has significant implications for cancer therapy. "Many drugs have recently been devised to block PI3K-Akt-mTORC1 signaling," explains Mischel. "What we show is that when you use those drugs, you will probably drive the acetylation of the FoxOs through mTORC2, and inadvertently fuel the Warburg effect. In other words, this new pathway is likely to be responsible for resistance to those drugs. Our data suggest that to disrupt the Warburg effect and kill cancer cells, you have to develop therapies that target both signaling pathways. That's the main clinical ramification of this finding."
Mischel and his colleagues find that glioblastomas that rely predominantly on the mTORC2-mediated pathway tend to have the worse prognosis. Further, their studies suggest that lung cancer cells, too, use this pathway to induce the Warburg effect.
"Increasingly," says Mischel, "we're using glioblastoma as a system to understand a variety of other cancers and, in fact, this finding has broader relevance because the signaling pathways identified here are conserved across cancer types." Different cancers, he explains, are fueled by different types of mutations to growth factor receptors, but the signals these mutated receptors transmit tend to converge on a subset of signaling proteins.
"Our identification of the key moleculesand novel signaling mechanismsinvolved in this pathway, has opened up a landscape rich in possible targets for novel cancer drugs," says Mischel. His laboratory, he says, is now working with other Ludwig researchers to identify small drug-like molecules that might disrupt key steps of the mTORC2-mediated pathway.
###
About Ludwig Cancer Research
Ludwig Cancer Research is an international collaborative network of acclaimed scientists with a 40-year legacy of pioneering cancer discoveries. Ludwig combines basic research with the ability to translate its discoveries and conduct clinical trials to accelerate the development of new cancer diagnostics and therapies. Since 1971, Ludwig has invested more than $1.6 billion in life-changing cancer research through the not-for-profit Ludwig Institute for Cancer Research and the six U.S.-based Ludwig Centers. http://www.ludwigcancerresearch.org
Paul Mischel is a member of the Ludwig Institute for Cancer Research and is based at the University of California, San Diego. Lead author Kenta Masui is a post-doctoral fellow in the Mischel lab. Web Cavenee is the director of Ludwig San Diego.
For further information please contact Rachel Steinhardt, rsteinhardt@licr.org or +1-212-450-1582.
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Targeting cancer's sweet tooth
PUBLIC RELEASE DATE:
21-Oct-2013
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Contact: Rachel Steinhardt rsteinhardt@licr.org 212-450-1582 Ludwig Institute for Cancer Research
A study of how cancer cells get energy and raw materials for growth from glucose opens doors to new therapies
October 21, 2013, New York, NY Ludwig researchers have elucidated a key mechanism by which cancer cells change how they metabolize glucose to generate the energy and raw materials required to sustain runaway growth.
Published online in Cell Metabolism, the Ludwig Cancer Research study also reveals how the aggressive brain cancer glioblastoma harnesses the mechanism to resist targeted therapies that should disrupt this capabilityknown as the Warburg effectand suggests how such resistance might be overcome. In detailing the molecular circuitry of the phenomenon, the researchers uncover several possible targets for new drugs that might disrupt cancer cell metabolism to destroy tumors.
"Cancer and other fast-growing cells extract energy from glucose using a process that ordinarily kicks in only when oxygen is in short supply," explains Ludwig scientist Paul Mischel, MD, who is based at the University of California, San Diego School of Medicine. "This allows them to thread the needle: they get the energy they need from glucose but also retain the carbon-based building blocks for molecules like lipids, proteins and DNA, which dividing cells need in large quantities."
Until recently, relatively little was known about the biochemical circuits that induce this vital metabolic shift in cancer cells. Earlier this year, however, Mischel and his colleagues published a study describing how an aberrant growth signal found in many glioblastomas is channeled to induce the Warburg effect. That signaling cascade, which involves the key proteins PI3 kinase (PI3K), Akt and mTORC1, culminates in the activation of a transcription factora controller of gene expressionnamed c-Myc. "In many cancer cells," says Mischel, "c-Myc seems to be a lever that links growth signaling pathways with the machinery that controls the uptake and use of nutrients."
In the current study, Mischel, who did the research in collaboration with Ludwig researchers Kenta Masui, MD, PhD and Web Cavenee, PhD, both also at UC San Diego, identifies a second interacting biochemical cascade that is independent of the PI3K-Akt-mTORC1 signal and uses distinct biochemical circuits and an unusual mechanism to turn on c-Myc. This pathway, Mischel and his colleagues report, depends on signals from a protein complex named mTORC2. The researchers show that when mTORC2 is switched on, it silences two other transcription factors, FoxO1 and FoxO3, which would otherwise suppress the activation of c-Myc in the nucleus of the cell. Further, they learned that the silencing of the FoxOs occurs through a chemical modificationknown as acetylationa process that has not been well understood.
The study has significant implications for cancer therapy. "Many drugs have recently been devised to block PI3K-Akt-mTORC1 signaling," explains Mischel. "What we show is that when you use those drugs, you will probably drive the acetylation of the FoxOs through mTORC2, and inadvertently fuel the Warburg effect. In other words, this new pathway is likely to be responsible for resistance to those drugs. Our data suggest that to disrupt the Warburg effect and kill cancer cells, you have to develop therapies that target both signaling pathways. That's the main clinical ramification of this finding."
Mischel and his colleagues find that glioblastomas that rely predominantly on the mTORC2-mediated pathway tend to have the worse prognosis. Further, their studies suggest that lung cancer cells, too, use this pathway to induce the Warburg effect.
"Increasingly," says Mischel, "we're using glioblastoma as a system to understand a variety of other cancers and, in fact, this finding has broader relevance because the signaling pathways identified here are conserved across cancer types." Different cancers, he explains, are fueled by different types of mutations to growth factor receptors, but the signals these mutated receptors transmit tend to converge on a subset of signaling proteins.
"Our identification of the key moleculesand novel signaling mechanismsinvolved in this pathway, has opened up a landscape rich in possible targets for novel cancer drugs," says Mischel. His laboratory, he says, is now working with other Ludwig researchers to identify small drug-like molecules that might disrupt key steps of the mTORC2-mediated pathway.
###
About Ludwig Cancer Research
Ludwig Cancer Research is an international collaborative network of acclaimed scientists with a 40-year legacy of pioneering cancer discoveries. Ludwig combines basic research with the ability to translate its discoveries and conduct clinical trials to accelerate the development of new cancer diagnostics and therapies. Since 1971, Ludwig has invested more than $1.6 billion in life-changing cancer research through the not-for-profit Ludwig Institute for Cancer Research and the six U.S.-based Ludwig Centers. http://www.ludwigcancerresearch.org
Paul Mischel is a member of the Ludwig Institute for Cancer Research and is based at the University of California, San Diego. Lead author Kenta Masui is a post-doctoral fellow in the Mischel lab. Web Cavenee is the director of Ludwig San Diego.
For further information please contact Rachel Steinhardt, rsteinhardt@licr.org or +1-212-450-1582.
[
| 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.
In case you missed it, late Friday afternoon Microsoft pulled the Windows RT 8.1 update. Enough customers complained about BSODs and completely bricked machines -- including, notably, Microsoft Surface RT machines -- after applying the RT-to-RT 8.1 upgrade, that the update was yanked entirely.
There's also been a steady stream of complaints about the Win8-to-Win8.1 update, including an inability to connect with Remote Access Website connections. Here's an overview of what we know so far has happened, and how you may be able to recover.
Microsoft released the Windows 8.1 upgrade early in the morning (U.S. time) on Oct. 17. For consumers and others who don't have Volume License agreements with Microsoft, the update was directly accessible through the Microsoft Store. Volume Licensees had access through the VLSC. And, of course, MSDN and TechNet members have had access to the Windows 8.1 Enterprise (but not the Windows RT 8.1) bits for a month.
Windows RT customers (those with retail copies of Windows RT, not volume licensees) encountered unresolved Blue Screen 0xc000000d errors with notification that "Your PC needs to be repaired / The Boot Configuration Data file is missing some required information / File: \BCD". On Oct. 19 -- two days after the update was released -- Microsoft MVP Wesley_P posted on the Answers Forum: "Why isn't the Windows RT 8.1 upgrade available in the Microsoft store?"
Apparently it took Microsoft about 48 hours to pull the upgrade. In a post without a time stamp, on a rather obscure site , Microsoft issued this advisory:
Microsoft is investigating a situation affecting a limited number of users updating their Windows RT devices to Windows RT 8.1. As a result, we have temporarily removed the Windows RT 8.1 update from the Windows Store. We are working to resolve the situation as quickly as possible and apologize for any inconvenience. We will provide updates as they become available.
I have seen no further comment from Microsoft, no acknowledgment or description of the problem, and certainly no fix.
Ozzie Scott Williams, on his technical blog kickthatcomputer ("Annoying stuff I figured out / I really hate computers"), has come up with an ingenious workaround. Big problem: the method requires a USB recovery drive for your Windows RT computer, and few people have one sitting around.
However, following the steps he outlines, if you trust him (disclaimer: I don't know Williams), you can create a Windows RT recovery USB drive. Using the recovery USB drive, there's a way to bring up an old-fashioned command prompt, and type in a one-line command to rebuild the trashed BCD. Once the BCD is fixed, apparently Windows RT 8.1 will boot.
Score one for the DOS command line. Hard to believe it would bring a borked Surface RT back to life.
The other major, solvable Windows 8.1 bug I've seen makes it impossible to connect Internet Explorer to a Remote Web Access website running on a Small Business Server 2011 server. Poster Yves describes it on the TechNet forum:
We still haven't heard anything official about Google's next Nexus phone, but tonight some people are already seeing the Nexus 5 as an option in the Play Store. Just among our editors, some see the outgoing Nexus 4 while others get the result shown after the break, with a 16GB (from the link in the ...
China's media watchdog has cut back the number of foreign TV formats allowed to be broadcast in the country, with satellite broadcasters restricted to airing one per year beginning in 2014. The new guideline is part of a campaign aimed at "building morality" and boosting educational programming.
The rules are bad news for Hollywood and overseas TV companies seeking a foothold in China. They step up a raft of regulations introduced in February, which capped the broadcast of foreign television series to 50 episodes, and will result in fewer foreign series being aired in China.
This is expected to result in more TV viewers abandoning the traditional TV format and watching on other platforms, such as computers, tablets and mobile devices.
Chinese audiences have warmly embraced overseas formats like "China’s Got Talent" and "The Voice," but now the State Administration of Radio, Film and Television says satellite broadcasters will be allowed to buy only one format per year.
The Chinese government regularly bemoans what it sees as the rising level of vulgarity in domestic TV programming, while trying to keep overseas shows to a minimum.
Overseas formats cannot be aired during prime time from 7:30 p.m. to 10:00 p.m. within the year they are imported. And only one domestic musical talent show will be approved every three months by the administration to be aired during prime time.
The new order is aimed at pushing domestically-produced and "morality-building programs," the People's Daily reported. The vacated slots will have to be filled with news, education programs and service shows, according to the state directive.
The government watchdog has ordered broadcasters to air at least 30 minutes of domestically made documentaries between 6 a.m. to 1 a.m., and 30 minutes of children’s programs or cartoons between 8 a.m. and 9:30 p.m. every day.
"It is really a headache on how we can make up for the seven and a half hours of time. Many TV stations are used to airing TV dramas, shows and films," one TV station staffer told China's Southern Metropolis Daily.
The People's Daily quoted Liu Yuan, deputy director of the chief editing office with Jiangsu Satellite TV, as admitting that the new regulations would make it tougher for them, while Wu Chaoyang, publicity director of Shanghai’s Dragon TV, told the newspaper the television station has always tried to localize overseas programs and already has four and a half hours of news programs daily.
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We still haven't heard anything official about Google's next Nexus phone, but tonight some people are already seeing the Nexus 5 as an option in the Play Store. Just among our editors, some see the outgoing Nexus 4 while others get the result shown after the break, with a 16GB (from the link in the ...
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