In south Japan, Mie prefecture is rocking 7 million LED Christmas lights. Hence the awesome light tunnel above. "Illuminations" or Christmas light displays have been a big deal in Japan since the 1980s. But there's something a lot more contemplative about these lights compared to some of the spectacles
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Following tightly on rumors that it would release a stock tablet, LG has just announced the Google Play edition G Pad 8.3. The tablet looks nearly identical to the original version of the G Pad 8.3, but is of course running a stock version of Android 4.4 KitKat, as you would expect from a Google Play edition device.
The device is only available in black (rather than black and white), and packs the same 1.7GHz Snapdragon 600 processor, 2GB of RAM, 16GB of storage (expandable by MicroSD) and an 8.3-inch 1920 x 1200 IPS display.
The Google Play edition G Pad 8.3 is now available on the Play Store for $349.99, and at the moment shows 1-2 business day shipping. For the moment, Google and LG aren't releasing details on availability outside of the U.S.
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While everyone loves to beat up on Apple Maps - and not without justification - none of the existing maps apps are good enough yet. Whether it be data quality or user experience, they all still get it wrong too often to be acceptable, and that needs to change.
Apple, for all their data aggregation, cleansing, and sanitizing issues, gets a couple of things right. The interface, both pre- and post-iOS 7 is not only good looking but provides a a good amount of information about not only your next turn, but the turn after that. The voice directions also do a good job of keeping you informed over long stretches of road, and advising you to stay left or bear right so you're in the proper place for a turn sooner rather than too late. Unfortunately, while Apple Maps can often get you to the block you're going, it tends to break down when it comes to the exact place and entrance to it.
Google Maps nails the data, but almost to a fault. It's less human. It'll tell you you need to turn right without warning you to get right, or tell you to go left when there are three left options, and only get to the elaboration well after the proper one has past. (And lest you think their data is perfect, today they told me to pull a u-turn on a dead-end road when I was actually in the middle of a 4-lane highway. That only appeared after I passed the virtual dead end. On my way to Mountain View. Yeah.)
Nokia Here maps, TomTom, and everyone who licenses data from them all need to do a better job not only with that data but with presenting it in a more human way.
Well-verified, consistently presented location that doesn't just tell you where to turn and how to get some where, but makes sure you're in the right place to turn, and helps you get there.
Like far too many things, if I could somehow mash Apple and Google Maps back together, I'd get something approaching what I want - great data and great interface - but that's an option that no longer exists. For now it's a race to see who can become more like the other, better, faster.
Maps are hard, no doubt about it. But getting lost sucks. What's a reasonable level of accuracy? What's a reasonable level of experience? If you miss a turn, or get sent the wrong way, how often is too often?
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If you were bold enough to buy a Developer Edition HTC One or its unlocked sibling, today is your lucky day. HTC's US division has announced that it's rolling out an Android 4.4 KitKat upgrade to both One variants, weeks ahead of the expected update for carrier-locked models. Sense 5.5 should also be a part of the package. While the KitKat upgrade isn't reaching these units as quickly as it did for the Google Play Edition, it's safe to say that many One owners will have another reason to celebrate this Thanksgiving weekend.
It's Tuesday and time for the Engadget HD Podcast. We hope you'll join us live when the Engadget HD podcast starts recording at 9:30PM. Tonight we even more Xbox One and PS4 news, so if you want to catch up on the launch of the new consoles, this is the place. If you'll be joining us, take a peek at the topics after the break -- then do everything else you'll need to do in order to be ready to participate in the live chat.
Filed under: HD
Back in the day, the internet was hard. There weren't search engines or pretty HTML5 websites. There weren't address bars or social networks. You had to dial up other computers and make connections yourself. At least that's what they tell me.
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PUBLIC RELEASE DATE: 14-Nov-2013
ShareContact: Sarah McDonnell
s_mcd@mit.edu
617-253-8923
Massachusetts Institute of Technology
CAMBRIDGE, MA -- About half of all cancer patients have a mutation in a gene called p53, which allows tumors to survive and continue growing even after chemotherapy severely damages their DNA.
A new study from MIT biologists has found that tumor cells with mutated p53 can be made much more vulnerable to chemotherapy by blocking another gene called MK2. In a study of mice, tumors lacking both p53 and MK2 shrank dramatically when treated with the drug cisplatin, while tumors with functional MK2 kept growing after treatment.
The findings suggest that giving cancer patients a combination of a DNA-damaging drug and an MK2 inhibitor could be very effective, says Michael Yaffe, the David H. Koch Professor in Science and senior author of a paper describing the research in the Nov. 14 issue of the journal Cell Reports.
Several drugs that inhibit MK2 are now in clinical trials to treat inflammatory diseases such as arthritis and colitis, but the drugs have never been tested as possible cancer treatments.
"What our study really says is that these drugs could have an entirely new second life, in combination with chemotherapy," says Yaffe, who is a member of MIT's Koch Institute for Integrative Cancer Research. "We're very much hoping it will go into clinical trials" for cancer.
Sandra Morandell, a postdoc at the Koch Institute, is the paper's lead author.
To kill a tumor
P53 is a tumor-suppressor protein that controls cell division. Before cell division begins, p53 checks the cell's DNA and initiates repair, if necessary. If DNA damage is too extensive, p53 forces the cell to undergo programmed cell death, or apoptosis. Tumors that lack p53 can avoid this fate.
"Usually p53 is the main driver of cell death, and if cells lose this pathway they become very resistant to different treatments that cause cell death," Morandell says.
Several years ago, researchers in Yaffe's lab discovered that in cancer cells with mutated p53, the MK2 gene helps counteract the effects of chemotherapy. When cancer cells suffer DNA damage, MK2 puts the brakes on the cell division cycle, giving cells time to repair the damage before dividing.
"Our data suggested if you block the MK2 pathway, tumor cells wouldn't recognize that they had DNA damage and they would keep trying to divide despite having DNA damage, and they would end up committing suicide," Yaffe says.
In the new study, the researchers wanted to see if this would hold true in tumors in living animals, as well as cells grown in a lab dish. To do that, they used a strain of mice that are genetically programmed to develop non-small-cell lung tumors. The researchers further engineered the mice so they could reversibly turn the MK2 gene on or off, allowing them to study tumors with and without MK2 in the same animal.
This new approach allows them, for the first time, to compare different types of tumors in the same mice, where all genetic factors are identical except for MK2 expression.
Using these mice, the researchers found that before treatment, tumors lacking both MK2 and p53 grow faster than tumors that have MK2. This suggests that treating tumors with an MK2 inhibitor alone would actually do more harm than good, possibly increasing the tumor's growth rate by taking the brake off the cell cycle.
However, when these tumors are treated with cisplatin, the tumors lacking MK2 shrink dramatically, while those with MK2 continue growing.
'A nonobvious combination'
The potential combination of cisplatin and MK2 inhibitors is unlike other chemotherapy combinations that have been approved by the Food and Drug Administration, which consist of pairs of drugs that each show benefit on their own. "What we found is a combination that you would never have arrived at otherwise," Yaffe says. "It's a nonobvious combination."
While this study focused on non-small-cell lung tumors, the researchers have gotten similar results in cancer cells grown in the lab from bone, cervical, and ovarian tumors. They are now studying mouse models of colon and ovarian cancer.
###
The research was funded by the Austrian Science Fund, the National Institutes of Health, Janssen Pharmaceutical, the Koch Institute, MIT's Center for Environmental Health Sciences, the Volkswagenstiftung, the Deutsche Forschungsgemeinschaft, the German Ministry for Science and Technology, the Deutsche Jose Carreras Leukmie Stiftung, and the Anna Fuller Fund.
Written by Anne Trafton, MIT News Office
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| 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.
PUBLIC RELEASE DATE: 14-Nov-2013
ShareContact: Sarah McDonnell
s_mcd@mit.edu
617-253-8923
Massachusetts Institute of Technology
CAMBRIDGE, MA -- About half of all cancer patients have a mutation in a gene called p53, which allows tumors to survive and continue growing even after chemotherapy severely damages their DNA.
A new study from MIT biologists has found that tumor cells with mutated p53 can be made much more vulnerable to chemotherapy by blocking another gene called MK2. In a study of mice, tumors lacking both p53 and MK2 shrank dramatically when treated with the drug cisplatin, while tumors with functional MK2 kept growing after treatment.
The findings suggest that giving cancer patients a combination of a DNA-damaging drug and an MK2 inhibitor could be very effective, says Michael Yaffe, the David H. Koch Professor in Science and senior author of a paper describing the research in the Nov. 14 issue of the journal Cell Reports.
Several drugs that inhibit MK2 are now in clinical trials to treat inflammatory diseases such as arthritis and colitis, but the drugs have never been tested as possible cancer treatments.
"What our study really says is that these drugs could have an entirely new second life, in combination with chemotherapy," says Yaffe, who is a member of MIT's Koch Institute for Integrative Cancer Research. "We're very much hoping it will go into clinical trials" for cancer.
Sandra Morandell, a postdoc at the Koch Institute, is the paper's lead author.
To kill a tumor
P53 is a tumor-suppressor protein that controls cell division. Before cell division begins, p53 checks the cell's DNA and initiates repair, if necessary. If DNA damage is too extensive, p53 forces the cell to undergo programmed cell death, or apoptosis. Tumors that lack p53 can avoid this fate.
"Usually p53 is the main driver of cell death, and if cells lose this pathway they become very resistant to different treatments that cause cell death," Morandell says.
Several years ago, researchers in Yaffe's lab discovered that in cancer cells with mutated p53, the MK2 gene helps counteract the effects of chemotherapy. When cancer cells suffer DNA damage, MK2 puts the brakes on the cell division cycle, giving cells time to repair the damage before dividing.
"Our data suggested if you block the MK2 pathway, tumor cells wouldn't recognize that they had DNA damage and they would keep trying to divide despite having DNA damage, and they would end up committing suicide," Yaffe says.
In the new study, the researchers wanted to see if this would hold true in tumors in living animals, as well as cells grown in a lab dish. To do that, they used a strain of mice that are genetically programmed to develop non-small-cell lung tumors. The researchers further engineered the mice so they could reversibly turn the MK2 gene on or off, allowing them to study tumors with and without MK2 in the same animal.
This new approach allows them, for the first time, to compare different types of tumors in the same mice, where all genetic factors are identical except for MK2 expression.
Using these mice, the researchers found that before treatment, tumors lacking both MK2 and p53 grow faster than tumors that have MK2. This suggests that treating tumors with an MK2 inhibitor alone would actually do more harm than good, possibly increasing the tumor's growth rate by taking the brake off the cell cycle.
However, when these tumors are treated with cisplatin, the tumors lacking MK2 shrink dramatically, while those with MK2 continue growing.
'A nonobvious combination'
The potential combination of cisplatin and MK2 inhibitors is unlike other chemotherapy combinations that have been approved by the Food and Drug Administration, which consist of pairs of drugs that each show benefit on their own. "What we found is a combination that you would never have arrived at otherwise," Yaffe says. "It's a nonobvious combination."
While this study focused on non-small-cell lung tumors, the researchers have gotten similar results in cancer cells grown in the lab from bone, cervical, and ovarian tumors. They are now studying mouse models of colon and ovarian cancer.
###
The research was funded by the Austrian Science Fund, the National Institutes of Health, Janssen Pharmaceutical, the Koch Institute, MIT's Center for Environmental Health Sciences, the Volkswagenstiftung, the Deutsche Forschungsgemeinschaft, the German Ministry for Science and Technology, the Deutsche Jose Carreras Leukmie Stiftung, and the Anna Fuller Fund.
Written by Anne Trafton, MIT News Office
[
| 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.
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