Superstar musician and accused drug hander-outer CeeLo Green went to court today and assured the world he is NOT GUILTY of charges stemming from an evening in 2012 that may or may not have involved sex and ecstasy.
The Voice judge — who we told you will not lose his chair — submitted his plea in court today and denied giving a woman ecstasy at an El Lay restaurant last year before having sex with her.
Prosecutors reportedly flirted with the idea of filing sexual assault charges against the Forget You singer, but earlier today decided they didn't have enough evidence.
CeeLo's bail was set at $30K. He is due back in court on November 20th.
Audio for this story from Morning Edition will be available at approximately 9:00 a.m. ET.
At the White House on Monday, President Obama acknowledged widespread problems with his health care law's website while still defending the Affordable Care Act. NPR White House Correspondent Scott Horsley talks with Steve Inskeep about the president's remarks.
NPR's business news starts with an acknowledgement of trouble by President Obama.
(SOUNDBITE OF MUSIC)
INSKEEP: OK, the president is speaking right now to reporters and others in the White House Rose Garden. Our White House correspondent Scott Horsley has been listening in. He's in our studios. Hi, Scott.
SCOTT HORSLEY, BYLINE: Good to be with you, Steve.
INSKEEP: OK, the president's talking about Obamacare. What's he saying?
HORSLEY: Well, this is really the first big acknowledgement by the president that the problems with the website, healthcare.gov, that people are using to access the new insurance marketplaces are more than the glitches. He'd said all along there would be glitches. It's now become clear that the problems are more deep-seeded than that.
The president said there's no sugar coating that, and that he's as frustrated as anybody else. He also said the government is working to fix those problems. They're bringing in some top IT talent from the private sector to help out. He also says some of those private sector folks anticipated this kind of problem with a big undertaking like this.
INSKEEP: They might have anticipated it but they weren't ready for it...
(LAUGHTER)
INSKEEP: ..but it's going to be a problem here, isn't it, to get it fixed on the fly?
HORSLEY: Absolutely. You're trying to fix the airplane while flying the airplane, as the saying goes. But the president also stressed that what he calls the underlying product, the insurance that's available through these marketplaces is still good, even if it's tough to get access to it. And he stressed that the Affordable Care Act is more than just this website and that there are ways for people to access that insurance offline, either by the telephone or in person.
INSKEEP: OK, Scott, thanks very much.
HORSLEY: My pleasure.
INSKEEP: We'll be hearing more about this. NPR's Scott Horsley.
NPR transcripts are created on a rush deadline by a contractor for NPR, and accuracy and availability may vary. This text may not be in its final form and may be updated or revised in the future. Please be aware that the authoritative record of NPR's programming is the audio.
No evidence to support stem cell therapy for pediatric optic nerve hypoplasia
PUBLIC RELEASE DATE:
22-Oct-2013
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Contact: Eileen Leahy e.leahy@elsevier.com 732-238-3628 Elsevier Health Sciences
US experts report on their independent study of Chinese stem cell treatment protocol in the journal of AAPOS
San Francisco, CA, October 22, 2013 A study performed at Children's Hospital Los Angeles found no evidence that stem cell therapy improves vision for children with optic nerve hypoplasia (ONH). Their results are reported in the Journal of the American Association for Pediatric Ophthalmology and Strabismus (AAPOS).
ONH, an underdevelopment of optic nerves that occurs during fetal development, may appear either as an isolated abnormality or as part of a group of disorders characterized by brain anomalies, developmental delay, and endocrine abnormalities. ONH is a leading cause of blindness in children in North America and Europe and is the only cause of childhood blindness that shows increasing prevalence. No treatments have been shown to improve vision in these children.
With no viable treatment options available to improve vision, ophthalmologists are becoming aware that families with children affected by ONH are travelling to China seeking stem cell therapy, despite lack of approval in the United States and Europe or evidence from controlled trials. The American Association for Pediatric Ophthalmology and Strabismus has also expressed its concern about these procedures. In response to this situation, pediatric neuro-ophthalmologist Mark Borchert, MD, Director of both the Eye Birth Defects and Eye Technology Institutes in The Vision Center at Children's Hospital Los Angeles, realized that a controlled trial of sufficient size was needed to evaluate whether stem cell therapy is effective at improving optic nerve function in children with ONH. He agreed to conduct an independent study when asked by Beike Biotech, a company based in Shenzhen, China, that offers treatment for ONH using donor umbilical cord stem cells injected into the cerebral spinal fluid.
Beike Biotech agreed to identify 10 children with bilateral ONH (ages 7-17 years) who had volunteered to travel to China for stem cell therapy and who agreed to participate in the study; Children's Hospital was to find case matched controls from their clinic. However, only two case-controlled pairs were evaluated because Beike Biotech was only able to recruit two patients. Treatments consisted of six infusions over a 16-day period of umbilical cord-derived mesenchymal stem cells and daily infusions of growth factors. Visual acuity, optic nerve size, and sensitivity to light were to be evaluated one month before stem cell therapy and three and nine months after treatment.
No therapeutic effect was found in the two case-control pairs that were enrolled. "The results of this study show that children greater than 7 years of age with ONH may have spontaneous improvement in vision from one examination to the next. This improvement occurs equally in children regardless of whether or not they received treatment. Other aspects of the eye examination included pupil responses to light and optic nerve size; these did not change following treatment. The results of this research do not support the use of stem cells in the treatment of ONH at this time," says lead author Cassandra Fink, MPH, program administrator at The Vision Center, Children's Hospital Los Angeles.
Confounding the trial was that subjects received additional alternative therapies (acupuncture, functional electrical stimulation, and exercise) while receiving stem cell treatments, which was contrary to the trial protocol. The investigators could not determine the effect of these additional therapies.
"This study underscores the importance of scientifically testing these procedures to validate them and also to ensure their safety. Parents of afflicted children should be aware that the science behind the use of stem cell technology is unclear. This study takes a step toward testing this technology and finds no beneficial effect," says William V. Good, MD, Senior Associate Editor, Journal of AAPOS and Clinical Professor of Ophthalmology and Senior Scientist at the Smith-Kettlewell Eye Research Institute.
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No evidence to support stem cell therapy for pediatric optic nerve hypoplasia
PUBLIC RELEASE DATE:
22-Oct-2013
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Contact: Eileen Leahy e.leahy@elsevier.com 732-238-3628 Elsevier Health Sciences
US experts report on their independent study of Chinese stem cell treatment protocol in the journal of AAPOS
San Francisco, CA, October 22, 2013 A study performed at Children's Hospital Los Angeles found no evidence that stem cell therapy improves vision for children with optic nerve hypoplasia (ONH). Their results are reported in the Journal of the American Association for Pediatric Ophthalmology and Strabismus (AAPOS).
ONH, an underdevelopment of optic nerves that occurs during fetal development, may appear either as an isolated abnormality or as part of a group of disorders characterized by brain anomalies, developmental delay, and endocrine abnormalities. ONH is a leading cause of blindness in children in North America and Europe and is the only cause of childhood blindness that shows increasing prevalence. No treatments have been shown to improve vision in these children.
With no viable treatment options available to improve vision, ophthalmologists are becoming aware that families with children affected by ONH are travelling to China seeking stem cell therapy, despite lack of approval in the United States and Europe or evidence from controlled trials. The American Association for Pediatric Ophthalmology and Strabismus has also expressed its concern about these procedures. In response to this situation, pediatric neuro-ophthalmologist Mark Borchert, MD, Director of both the Eye Birth Defects and Eye Technology Institutes in The Vision Center at Children's Hospital Los Angeles, realized that a controlled trial of sufficient size was needed to evaluate whether stem cell therapy is effective at improving optic nerve function in children with ONH. He agreed to conduct an independent study when asked by Beike Biotech, a company based in Shenzhen, China, that offers treatment for ONH using donor umbilical cord stem cells injected into the cerebral spinal fluid.
Beike Biotech agreed to identify 10 children with bilateral ONH (ages 7-17 years) who had volunteered to travel to China for stem cell therapy and who agreed to participate in the study; Children's Hospital was to find case matched controls from their clinic. However, only two case-controlled pairs were evaluated because Beike Biotech was only able to recruit two patients. Treatments consisted of six infusions over a 16-day period of umbilical cord-derived mesenchymal stem cells and daily infusions of growth factors. Visual acuity, optic nerve size, and sensitivity to light were to be evaluated one month before stem cell therapy and three and nine months after treatment.
No therapeutic effect was found in the two case-control pairs that were enrolled. "The results of this study show that children greater than 7 years of age with ONH may have spontaneous improvement in vision from one examination to the next. This improvement occurs equally in children regardless of whether or not they received treatment. Other aspects of the eye examination included pupil responses to light and optic nerve size; these did not change following treatment. The results of this research do not support the use of stem cells in the treatment of ONH at this time," says lead author Cassandra Fink, MPH, program administrator at The Vision Center, Children's Hospital Los Angeles.
Confounding the trial was that subjects received additional alternative therapies (acupuncture, functional electrical stimulation, and exercise) while receiving stem cell treatments, which was contrary to the trial protocol. The investigators could not determine the effect of these additional therapies.
"This study underscores the importance of scientifically testing these procedures to validate them and also to ensure their safety. Parents of afflicted children should be aware that the science behind the use of stem cell technology is unclear. This study takes a step toward testing this technology and finds no beneficial effect," says William V. Good, MD, Senior Associate Editor, Journal of AAPOS and Clinical Professor of Ophthalmology and Senior Scientist at the Smith-Kettlewell Eye Research Institute.
###
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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.
It's 2013, the era of the cloud. But for whatever reason — it really doesn't matter why — BlackBerry's still stuck in a one-device frame of mind.
We live in a world of multiple screens. Some of us use more than one phone. More likely, however, is the combination of using a phone and a tablet. Being able to access your data anywhere is the crux of everything Google — and therefore Android — does. Apple's stumbled with iCloud, but damned if it's not trying. And for all its faults in the past, even Microsoft had this one figured out long ago with its "Three screens and the cloud" strategy.
And then there's BlackBerry. BBM — BlackBerry Messenger — is finally available for iOS and Android. Sort of. You can download the app, then get on a waiting list, as BlackBerry's ramping things up slowly. But know this: You can only use one BBM ID on one device at a time. One ID, one phone. Or one tablet.
And not at all (yet — it's coming) on a desktop or laptop computer.
Anyhoo. This isn't a surprise to anyone who's used BBM before. (Or the popular WhatsApp, for that matter.) But for those of us used to accessing our conversations on any connected device, it's a bit of a shock.
St. Louis Rams' Sam Bradford (8) is helped into the locker room after being injured in the second half of an NFL football game against the Carolina Panthers in Charlotte, N.C., Sunday, Oct. 20, 2013. (AP Photo/Chuck Burton)
St. Louis Rams' Sam Bradford (8) is helped into the locker room after being injured in the second half of an NFL football game against the Carolina Panthers in Charlotte, N.C., Sunday, Oct. 20, 2013. (AP Photo/Chuck Burton)
St. Louis Rams' Sam Bradford (8) is pushed out of bounds by Carolina Panthers' Mike Mitchell (21) in the second half of an NFL football game in Charlotte, N.C., Sunday, Oct. 20, 2013. Bradford was injured on the play. (AP Photo/Mike McCarn)
ST. LOUIS (AP) — Sam Bradford is done for the season, and the burden for the St. Louis Rams has just become a whole lot bigger.
The quarterback will have will have season-ending surgery for a torn ligament in his left knee, a major blow to a team seeking its first winning record in a decade. He was hurt in the fourth quarter of Sunday's 30-15 loss at Carolina that dropped the Rams to 3-4.
"Even if Sam wasn't hurt, we'd still have some heavy lifting to do," center Scott Wells said after the game. "But this adds extra to it."
The extent of the injury was revealed on an MRI exam late Sunday after the return flight, and the team announced the results Monday. Coach Jeff Fisher was to provide details at an afternoon news conference.
Bradford tore his anterior cruciate ligament when he landed on his knee after being shoved out of bounds by safety Mike Mitchell. Fisher said after the game that Bradford was in "significant pain" on the sideline. Teammates feared the worst once they saw him carted off the field and on crutches in the locker room.
Kellen Clemens filled in for Bradford and is the only other quarterback on the roster, with the team a week away from a Monday night home game against the Seahawks. Austin Davis, released late in training camp, is perhaps the leading potential backup.
Bradford has 14 touchdown passes and just four interceptions this season. Still, he has his detractors, critics who insist he has not measured up to the billing of a No. 1 overall pick.
But now in his fourth season out of Oklahoma, Bradford has been nudging his way up the ladder, surely among the top half of the league's best quarterbacks. He's been taking charge and minimizing mistakes — exactly what the youngest team in the NFL needed.
Bradford threw for 255 yards and a score Sunday, with one interception and two sacks. He has thrown a touchdown pass in 11 consecutive games. St. Louis had won its previous two games, with Bradford throwing three TD passes in each.
Bradford is no stranger to injuries. He missed six games with a high left ankle sprain in 2011. He had season-ending shoulder surgery in 2009 when he was at Oklahoma.
Clemens made three starts in 2011 but hadn't played this year until replacing Bradford against Carolina. He has made 12 career starts, seven of them with the New York Jets in 2007.
"It's never easy when you see a teammate go down," he said after the game. "When you see a person that you spend as much time with as I do with Sam and genuinely care about as a person. ... I have great respect for what he does on the field, but just as genuine concern for him as a person."
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.
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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.
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