Mozilla's Gary Kovacs has been harping on this idea of connecting the next billion or so people to the internet all week -- it's one of the driving philosophies behind Firefox OS. Nokia is looking to bring down the cost of entry to the mobile web with the 105 and 301. Then there are operations like Qtel and Bharti Airtel, that provide cellular service across the developing world and in emerging markets. These companies are all looking to put the democratizing power of the web in the pockets of people across the globe, and they're all here at Mobile World Congress 2013 to discuss just how they plan to do that and why it's so important. To find out what these CEOs, including Stephen Elop, Dr. Nasser Marafih (Qtel) and Sunil Mittal (Bharti Airtel) have to say, check back in at the time below.
Feb. 25, 2013 ? Even dying stars could host planets with life -- and if such life exists, we might be able to detect it within the next decade. This encouraging result comes from a new theoretical study of Earth-like planets orbiting white dwarf stars. Researchers found that we could detect oxygen in the atmosphere of a white dwarf's planet much more easily than for an Earth-like planet orbiting a Sun-like star.
"In the quest for extraterrestrial biological signatures, the first stars we study should be white dwarfs," said Avi Loeb, theorist at the Harvard-Smithsonian Center for Astrophysics (CfA) and director of the Institute for Theory and Computation.
When a star like the Sun dies, it puffs off its outer layers, leaving behind a hot core called a white dwarf. A typical white dwarf is about the size of Earth. It slowly cools and fades over time, but it can retain heat long enough to warm a nearby world for billions of years.
Since a white dwarf is much smaller and fainter than the Sun, a planet would have to be much closer in to be habitable with liquid water on its surface. A habitable planet would circle the white dwarf once every 10 hours at a distance of about a million miles.
Before a star becomes a white dwarf it swells into a red giant, engulfing and destroying any nearby planets. Therefore, a planet would have to arrive in the habitable zone after the star evolved into a white dwarf. A planet could form from leftover dust and gas (making it a second-generation world), or migrate inward from a larger distance.
If planets exist in the habitable zones of white dwarfs, we would need to find them before we could study them. The abundance of heavy elements on the surface of white dwarfs suggests that a significant fraction of them have rocky planets. Loeb and his colleague Dan Maoz (Tel Aviv University) estimate that a survey of the 500 closest white dwarfs could spot one or more habitable Earths.
The best method for finding such planets is a transit search -- looking for a star that dims as an orbiting planet crosses in front of it. Since a white dwarf is about the same size as Earth, an Earth-sized planet would block a large fraction of its light and create an obvious signal.
More importantly, we can only study the atmospheres of transiting planets. When the white dwarf's light shines through the ring of air that surrounds the planet's silhouetted disk, the atmosphere absorbs some starlight. This leaves chemical fingerprints showing whether that air contains water vapor, or even signatures of life, such as oxygen.
Astronomers are particularly interested in finding oxygen because the oxygen in Earth's atmosphere is continuously replenished, through photosynthesis, by plant life. Were all life to cease on Earth, our atmosphere would quickly become devoid of oxygen, which would dissolve in the oceans and oxidize the surface. Thus, the presence of large quantities of oxygen in the atmosphere of a distant planet would signal the likely presence of life there.
NASA's James Webb Space Telescope (JWST), scheduled for launch by the end of this decade, promises to sniff out the gases of these alien worlds. Loeb and Maoz created a synthetic spectrum, replicating what JWST would see if it examined a habitable planet orbiting a white dwarf. They found that both oxygen and water vapor would be detectable with only a few hours of total observation time.
"JWST offers the best hope of finding an inhabited planet in the near future," said Maoz.
Recent research by CfA astronomers Courtney Dressing and David Charbonneau showed that the closest habitable planet is likely to orbit a red dwarf star (a cool, low-mass star undergoing nuclear fusion). Since a red dwarf, although smaller and fainter than the Sun, is much larger and brighter than a white dwarf, its glare would overwhelm the faint signal from an orbiting planet's atmosphere. JWST would have to observe hundreds of hours of transits to have any hope of analyzing the atmosphere's composition.
"Although the closest habitable planet might orbit a red dwarf star, the closest one we can easily prove to be life-bearing might orbit a white dwarf," said Loeb.
Their paper has been accepted for publication in the Monthly Notices of the Royal Astronomical Society.
Headquartered in Cambridge, Mass., the Harvard-Smithsonian Center for Astrophysics (CfA) is a joint collaboration between the Smithsonian Astrophysical Observatory and the Harvard College Observatory. CfA scientists, organized into six research divisions, study the origin, evolution and ultimate fate of the universe.
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The above story is reprinted from materials provided by Harvard-Smithsonian Center for Astrophysics.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Abraham Loeb, Dan Maoz. Detecting bio-markers in habitable-zone earths transiting white dwarfs. Arxiv, 2013 [link]
Note: If no author is given, the source is cited instead.
Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
Brooklyn: Drunk Driver Who Killed Moshe Berkowitz Z?L Gets Convicted
(Monday, February 25th, 2013)
Kings County District Attorney Charles J. Hynes today announced the conviction of Anel Kolenovic, 25, on charges of Manslaughter in the Second Degree, Operating a Motor Vehicle While Impaired, and Assault in the Second Degree. He was charged with killing the driver of a car he struck while speeding down Ocean Avenue drunk in November 2010. He faces a maximum of five to 15 years in prison when he is sentenced on March 18 before Brooklyn Supreme Court Justice John Ingram.
On November 29, 2010, Kolenovic was speeding down Ocean Avenue and ran a red light at Avenue N, in Midwood, where he hit Moshe Berkowitz?s car, killing Berkowitz. Two passengers in Kolenovic?s car were injured. Kolenovic was intoxicated at the time of the incident.
The case was prosecuted by Gayle Dampf, Chief of the Vehicular Crimes Bureau and Assistant District Attorney Seth Zuckerman from the Trial Bureau Orange Zone.
(YWN Desk ? NYC)
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The U.S. Supreme Court today essentially put the government's expanded terror surveillance program beyond legal challenge, tossing out a lawsuit filed by a group of lawyers, journalists, and civil rights groups who claimed they were improperly swept up in the law's reach.
By a 5-4 ruling, the court said the challengers couldn't show that they were actually harmed by the government's foreign terrorist surveillance program, set up during the George W. Bush administration to allow the monitoring of suspected terrorists overseas. Congress eventually approved the program, with some changes.
The issue in this case was what happens when targets of the program talk by phone or e-mail with people in the United States. The challengers claimed that because their jobs required them to talk with people overseas likely to be targeted by the program, they've had to change how they operate ? traveling overseas to meet with potential clients and sources instead of talking to them by phone.
In other words, while the challengers said they couldn't prove their conversations were intercepted, because the expanded terror surveillance program is classified, it was so likely that they had the legal standing to sue.
Not so, said the five-member majority, in an opinion written by Justice Samuel Alito. Their theory, he said, "is too speculative." And even though the challengers say they've had to take expensive measures to avoid the surveillance they fear is taking place, they "cannot manufacture standing by choosing to make expenditures based on hypothetical future harm."
Writing for the dissenters, Justice Stephen Breyer said the harm the challengers claim "is as likely to take place as are most future events that commonsense inference and ordinary knowledge of human nature tell us will happen."
Contact: Rachel Steinhardt rsteinhardt@licr.org 212-450-1582 Ludwig Institute for Cancer Research
February 26, 2013, New York, N.Y. and San Diego, Calif. Glioblastoma, the most common and lethal form of brain tumor in adults, is challenging to treat because the tumors rapidly become resistant to therapy. As cancer researchers are learning more about the causes of tumor cell growth and drug resistance, they are discovering molecular pathways that might lead to new targeted therapies to potentially treat this deadly cancer.
Scientists at the Ludwig Institute for Cancer Research in San Diego worked collaboratively across the laboratories of Drs. Paul Mischel, Web Cavenee and Frank Furnari to investigate one such molecular pathway called the mammalian target of rapamycin or mTOR. This signaling pathway is hyperactivated in close to 90 percent of glioblastomas and plays a critical role in regulating tumor growth and survival. Therapies that inhibit mTOR signaling are under investigation as drug development targets, but results to date have been disappointing: mTOR inhibitors halt the growth but fail to kill the tumor cells.
A study published this week in the Proceedings of the National Academy of Sciences uncovers an unexpected but important molecular mechanism of mTOR inhibitor resistance and identifies a novel drug combination that reverses this resistance.
The story begins with a closer look at a gene-encoded protein called promyleocytic leukemia gene or PML. The study investigators explored the role of PML in causing resistance to mTOR inhibitor treatment. They found that when glioblastoma patients are treated with drugs that target the mTOR pathway, the levels of PML rise dramatically. Further, they showed that PML upregulation made the tumor cells resistant to mTOR inhibitors, and that if they suppressed the ability of the tumor cells to upregulate the PML protein, the tumor cells died in response to the mTOR inhibitor therapy.
"When we looked at cells in in vivo models and patients treated in the clinic, it became clear that the glioblastoma cells massively regulated PML enabling them to escape the effects of mTOR inhibitor therapy," reported senior author Paul Mischel, MD, Ludwig Institute member based at the University of California at San Diego.
"Our team hypothesized that if we could use a pharmacological approach to get rid of PML and combine it with an mTOR inhibitor, it could change the response from halting growth to cell death. The question was how?" added Mischel.
Previous research had shown that the use of low-dose arsenic could cause degradation of the PML protein in patients with leukemia. The team hypothesized that if arsenic could degrade PML, it may reverse resistance to mTOR inhibitors. The combination of mTOR and low-dose arsenic in mice indeed showed a synergistic effect, with massive tumor cell death along with very significant shrinkage of the tumor in mice with no ill side effects.
"Current therapy upregulates PML, turning off the mTOR signaling pathway. The tumor cells hide, waiting for the target signal to return," said Mischel. "When low-dose arsenic is added, not only does it stop the cell from returning, it shuts down the escape route killing the tumor cell."
These results present the first clinical evidence that mTOR inhibition promotes PML upregulation in mice and patients, and that it mediates drug resistance. The clinical relevance was confirmed when researchers looked at before- and after-treatment tissue samples from patients treated with mTOR inhibitors, confirming that PML goes up significantly in post treatment of mTOR inhibitors.
"These data suggest a new approach for potential treatment of glioblastoma," said
Mischel. "We are moving forward to test that possibility in people."
Post-doctoral students Akio Iwanami and Beatrice Gini from the Mischel lab as well as Ciro Zanca from the Furnari/Cavenee lab, also contributed significantly to this paper.
###
This work was supported by the Japan Society for the Promotion of Science, the Uehara Memorial Foundation, three NIH grants: NS73831, CA 119347 and P01-CA95616, the Ziering Family Foundation in Memory of Sigi Ziering and the Ben and Catherine Ivy Foundation.
About The Ludwig Institute for Cancer Research
The Ludwig Institute for Cancer Research is an international non-profit organization committed to improving the understanding and control of cancer through integrated laboratory and clinical discovery. Leveraging its worldwide network of investigators and the ability to sponsor and conduct its own clinical trials, Ludwig is actively engaged in translating its discoveries into applications for patient benefit. Since its establishment in 1971, the Ludwig Institute has expended more than $1.5 billion on cancer research.
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.
Contact: Rachel Steinhardt rsteinhardt@licr.org 212-450-1582 Ludwig Institute for Cancer Research
February 26, 2013, New York, N.Y. and San Diego, Calif. Glioblastoma, the most common and lethal form of brain tumor in adults, is challenging to treat because the tumors rapidly become resistant to therapy. As cancer researchers are learning more about the causes of tumor cell growth and drug resistance, they are discovering molecular pathways that might lead to new targeted therapies to potentially treat this deadly cancer.
Scientists at the Ludwig Institute for Cancer Research in San Diego worked collaboratively across the laboratories of Drs. Paul Mischel, Web Cavenee and Frank Furnari to investigate one such molecular pathway called the mammalian target of rapamycin or mTOR. This signaling pathway is hyperactivated in close to 90 percent of glioblastomas and plays a critical role in regulating tumor growth and survival. Therapies that inhibit mTOR signaling are under investigation as drug development targets, but results to date have been disappointing: mTOR inhibitors halt the growth but fail to kill the tumor cells.
A study published this week in the Proceedings of the National Academy of Sciences uncovers an unexpected but important molecular mechanism of mTOR inhibitor resistance and identifies a novel drug combination that reverses this resistance.
The story begins with a closer look at a gene-encoded protein called promyleocytic leukemia gene or PML. The study investigators explored the role of PML in causing resistance to mTOR inhibitor treatment. They found that when glioblastoma patients are treated with drugs that target the mTOR pathway, the levels of PML rise dramatically. Further, they showed that PML upregulation made the tumor cells resistant to mTOR inhibitors, and that if they suppressed the ability of the tumor cells to upregulate the PML protein, the tumor cells died in response to the mTOR inhibitor therapy.
"When we looked at cells in in vivo models and patients treated in the clinic, it became clear that the glioblastoma cells massively regulated PML enabling them to escape the effects of mTOR inhibitor therapy," reported senior author Paul Mischel, MD, Ludwig Institute member based at the University of California at San Diego.
"Our team hypothesized that if we could use a pharmacological approach to get rid of PML and combine it with an mTOR inhibitor, it could change the response from halting growth to cell death. The question was how?" added Mischel.
Previous research had shown that the use of low-dose arsenic could cause degradation of the PML protein in patients with leukemia. The team hypothesized that if arsenic could degrade PML, it may reverse resistance to mTOR inhibitors. The combination of mTOR and low-dose arsenic in mice indeed showed a synergistic effect, with massive tumor cell death along with very significant shrinkage of the tumor in mice with no ill side effects.
"Current therapy upregulates PML, turning off the mTOR signaling pathway. The tumor cells hide, waiting for the target signal to return," said Mischel. "When low-dose arsenic is added, not only does it stop the cell from returning, it shuts down the escape route killing the tumor cell."
These results present the first clinical evidence that mTOR inhibition promotes PML upregulation in mice and patients, and that it mediates drug resistance. The clinical relevance was confirmed when researchers looked at before- and after-treatment tissue samples from patients treated with mTOR inhibitors, confirming that PML goes up significantly in post treatment of mTOR inhibitors.
"These data suggest a new approach for potential treatment of glioblastoma," said
Mischel. "We are moving forward to test that possibility in people."
Post-doctoral students Akio Iwanami and Beatrice Gini from the Mischel lab as well as Ciro Zanca from the Furnari/Cavenee lab, also contributed significantly to this paper.
###
This work was supported by the Japan Society for the Promotion of Science, the Uehara Memorial Foundation, three NIH grants: NS73831, CA 119347 and P01-CA95616, the Ziering Family Foundation in Memory of Sigi Ziering and the Ben and Catherine Ivy Foundation.
About The Ludwig Institute for Cancer Research
The Ludwig Institute for Cancer Research is an international non-profit organization committed to improving the understanding and control of cancer through integrated laboratory and clinical discovery. Leveraging its worldwide network of investigators and the ability to sponsor and conduct its own clinical trials, Ludwig is actively engaged in translating its discoveries into applications for patient benefit. Since its establishment in 1971, the Ludwig Institute has expended more than $1.5 billion on cancer research.
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.
Kings County District Attorney Charles J. Hynes today announced the conviction of Anel Kolenovic, 25, on charges of Manslaughter in the Second Degree, Operating a Motor Vehicle While Impaired, and Assault in the Second Degree. He was charged with killing the driver of a car he struck while speeding down Ocean Avenue drunk in November 2010. He faces a maximum of five to 15 years in prison when he is sentenced on March 18 before Brooklyn Supreme Court Justice John Ingram.
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Public release date: 26-Feb-2013
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