Researchers have found that chunks of dry ice, jetting around on cushions of gas, may be responsible for mysterious channels on the Martian surface
By Christopher Crockett
Linear gullies on Mars Gullies like these appear on pole-facing slopes at mid-latitudes on Mars. Are chunks of dry ice carving them?Image: NASA/JPL-Caltech/Univ. of Arizona
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Some things are uniquely Martian. And dry ice hovercraft may be one of them.
For 10 years, scientists have been trying to understand what causes ?linear gullies? on Mars?long, thin canals carved into sandy slopes and crater walls. Flowing water doesn?t quite work as an explanation. Water should carry rocks and dirt downstream, dumping it in a fan-shaped apron at the bottom. But these gullies don?t have debris deposits. They abruptly stop.
New gullies appear?and old ones grow?every spring as the winter ice thaws. And some researchers noticed that the sinuous, leveed ditches looked like trails carved by blocks sliding down the hills. That led astronomers to consider an intriguing possibility for the gullies? origin: chunks of dry ice?frozen carbon dioxide?plowing through the sand while riding cushions of gas. But the idea had never been tested.
Researchers at NASA?s Jet Propulsion Laboratory (JPL) spent a couple of days in Coral Pink Sand Dunes State Park in Utah to see if ice, on its own, could carve out a furrow on the shallow slopes. Water ice?the same stuff you put in your lemonade?didn?t do much. Mostly, it just melted. The dry ice, however, came alive. ?The dry ice behaved dramatically different,? says JPL systems engineer Serina Diniega, lead author on a paper in Icarus. ?The water ice blocks didn?t move at all, but the dry ice just took off!? After a small nudge, the dry ice glided down the dune, blowing away sand as it did. When the block stopped, the sand beneath it writhed as jets of carbon dioxide escaped from under the ice. ?We were surprised,? she adds.
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Dry ice doesn?t melt; that?s what makes it ?dry.? Instead, it changes from a solid to a gas via sublimation. And that?s the secret ingredient. The gas collects in a very thin, flat bubble under the block. Like a hovercraft, the gas cushion makes the ice highly mobile. Something similar happens when you flick water onto a hot pan: the bubbles dance around on miniature cushions of steam.
Frozen CO2 is prevalent on Mars. During the Martian winter the polar caps grow as carbon dioxide condenses out of the atmosphere. Ice sheets form a couple of meters thick. In the spring the ice breaks up. Blocks jutting out from overhangs and crater lips, weakened by warming temperatures, can break off and land on the shallow slopes below. The fall serves the same purpose as the nudge from the researchers?it gets the blocks going. From here, sublimation takes over and the ice rides its way to the bottom of the hill, carving out a groove as it goes.
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Hawke and Delpy remain as charming as ever, and their combined goofiness is more endearing than annoying.
Love is messy here, life cannot be controlled, satisfaction is far from guaranteed. Romance is rocky at best. But romance still is.
Though "Before Midnight" is often uncomfortable to watch, it's never less than mesmerizing - and ultimately, a joy to walk with this prickly but fascinating couple again.
"Before Midnight" is heartbreaking, but not because of Jesse and Celine. It's the filmmakers' passions that seem to have cooled.
Before Midnight is fascinating to watch, and so long as Celine and Jesse are communicating, there's still hope.
How (Jesse and Celine) try to rekindle that flame is what drives Midnight, a film that feels so authentic it's like overhearing a conversation you're not sure you should be hearing.
Hawke and Delpy, who are both credited on the script too, have never found co-stars to bounce off more nimbly or bring out richer nuances in their acting.
The performances and dialogue are wonderfully naturalistic; a reminder that the best special effects are often the cheapest.
Before Midnight is about the nature of long-term relationships, and the way love deepens and grows but also finds itself subject to the complications of maturity. Smart, insightful, and poignant.
For those who witnessed Jesse and Celine's tentative getting together as inter railing students almost twenty years ago, it's reassuring to see them still in love.
Brilliantly directed, superbly written and impeccably acted, this is a thoroughly enjoyable, thought-provoking and emotionally engaging drama that perfectly complements the previous two films.
It remains as engaging, illuminating, honest and funny as its predecessor; here's hoping we revisit Jesse and C?line in another decade or so.
Nine-year gaps between films would sink a studio franchise, but the unforgiving impact of time and the slipperiness of its mysterious mental record, memory, are the very subjects of 'Before Midnight.'
Contains more shrewd and candid insights than many Hollywood midlife crisis dramas.
A couple persistently digging at each other might have been insufferable to watch except that Hawke and Delpy manage to be goofy, funny, witty and charming, even while they're fighting.
A bit tarter than its predecessors, but not skimping on their woozy, chatty charm, this perfectly played, gently incisive film is a welcome new chapter in one of cinema's most beguiling ongoing romances.
Director Richard Linklater's life-affirming Before trilogy is the Lord of the Rings of the art-house experience, the Toy Story of the American indie movement.
Whatever wins Best Picture for 2013 ... long after that film's glory fades, actors, writers, cinephiles, and lovers will still lavish Before Midnight with praise.
It's a brutal parade of heartbreak and mind-rake that leaves you curled up and wound up in a ball, covering your eyes but peeking through parted fingers.
"Before Midnight" presents a paradox: It's the best entry in director Richard Linklater's romantic trilogy, but it's also the first in the series that doesn't leave me dying to know what happens next.
Awesome, authentic examination of a constantly evolving romantic relationship, it's a definite 'must see' for adult audiences.
Before Midnight is a beautiful reminder that a movie with nothing more than two people talking can have just as many explosions and fireworks as any high-tech summer blockbuster.
Before Midnight understands that when love falters it isn't with a bang but a long protracted sigh. It's a perceptive and humbling view of romance that debunks all notions of fairy tale endings.
...We are not likely to get a more thoughtful or thought-provoking film than Before Midnight.
"Before Midnight" puts us in the same position with Jesse and Celine that they are in with each other. The romantic idealism has evaporated, and now we see them for who they are - real, deeply flawed, sometimes selfish people. Can we still love them?
I got my iPhone 4s a few days ago and whenever I listen to music it plays normally but whenever I get a text it doesent play the default ringtone for the text. So whenever I text somebody I have to check every second to make sure they texted me back because I won?t know when they do. Same thing with when someone calls me. And no, the mute button isn?t on. It isn?t orange. Someone please explain how to fix? TY
An article in 'Cell' reveals a new resistance mechanism to chemotherapy in breast and ovarian cancerPublic release date: 18-Jun-2013 [ | E-mail | Share ]
Contact: Press Office comunicacion@cnio.es Centro Nacional de Investigaciones Oncologicas (CNIO)
CNIO researchers take part in an international project that describes the molecular bases of resistance to a new chemotherapeutic agent in familial breast and ovarian cancers
It is estimated that between 5% and 10% of breast and ovarian cancers are familial in origin, which is to say that these tumours are attributable to inherited mutations from the parents in genes such as BRCA1 or BRCA2. In patients with these mutations, PARP inhibitors, which are currently in clinical trials, have shown encouraging results that make them a new option for personalised cancer treatment, an alternative to standard chemotherapy. Nevertheless, the latest studies indicate that a fraction of these patients generate resistance to the drug and, therefore, stop responding to the new treatment.
The team led by Spanish National Cancer Research Centre researcher scar Fernndez-Capetillo, head of the Genomic Instability Group, together with researchers from the National Cancer Institute in the US, have participated in a study that describes the causes that explain why tumours with BRCA1 and BRCA2 mutations stop responding to PARP inhibitor drugs.
"PARP inhibitors are only toxic in tumours that have an impaired DNA repair mechanism, such as those that contain BRCA1/2 mutations" says Mara Nieto-Soler, a researcher from Fernndez-Capetillo's team.
According to the researchers, the problem arises when these tumours, in addition to having BRCA1 and/or BRCA2 mutations, also contain secondary mutations in other proteins such as 53BP1 or PTIP, whose function is to restrain DNA repair. In these cases, the mutations mutually compensate for each other, the tumour cells recover the ability to repair their DNA and the drug stops working.
Fernndez-Capetillo says: "This is one of the first studies to demonstrate that secondary mutations can make tumours resistant when faced with specific treatments like, in this case, PARP inhibitors".
NEW DIAGNOSTIC TESTS WITH SECONDARY MUTATIONS
When the researchers compared different treatments, they observed that for those tumours with BRCA1 and/or BRCA2 mutations that also presented mutations in 53BP1 or PTIP, standard treatment with cisplatin was more efficient than personalised therapy.
"These data indicate that only patients containing mutations in BRCA1 and/or BRCA2, but not in the secondary genes we have described, would be candidates for an effective personalised therapy with PARP inhibitors", explains Fernndez-Capetillo, concluding that: "Our results suggest that 53BP1 and PTIP genes would need to be evaluated in patients with familial breast and ovarian cancer when deficiencies in the BRCA genes were present before deciding on their treatment".
In this context, researchers intend to warn healthcare providers in personalised medicine that the challenge, in addition to the search for markers of drug sensitivity for new pharmacological compounds, also encompasses the search for secondary resistance markers. The aim would be to bring about significant improvements in treatment outcomes.
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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.
An article in 'Cell' reveals a new resistance mechanism to chemotherapy in breast and ovarian cancerPublic release date: 18-Jun-2013 [ | E-mail | Share ]
Contact: Press Office comunicacion@cnio.es Centro Nacional de Investigaciones Oncologicas (CNIO)
CNIO researchers take part in an international project that describes the molecular bases of resistance to a new chemotherapeutic agent in familial breast and ovarian cancers
It is estimated that between 5% and 10% of breast and ovarian cancers are familial in origin, which is to say that these tumours are attributable to inherited mutations from the parents in genes such as BRCA1 or BRCA2. In patients with these mutations, PARP inhibitors, which are currently in clinical trials, have shown encouraging results that make them a new option for personalised cancer treatment, an alternative to standard chemotherapy. Nevertheless, the latest studies indicate that a fraction of these patients generate resistance to the drug and, therefore, stop responding to the new treatment.
The team led by Spanish National Cancer Research Centre researcher scar Fernndez-Capetillo, head of the Genomic Instability Group, together with researchers from the National Cancer Institute in the US, have participated in a study that describes the causes that explain why tumours with BRCA1 and BRCA2 mutations stop responding to PARP inhibitor drugs.
"PARP inhibitors are only toxic in tumours that have an impaired DNA repair mechanism, such as those that contain BRCA1/2 mutations" says Mara Nieto-Soler, a researcher from Fernndez-Capetillo's team.
According to the researchers, the problem arises when these tumours, in addition to having BRCA1 and/or BRCA2 mutations, also contain secondary mutations in other proteins such as 53BP1 or PTIP, whose function is to restrain DNA repair. In these cases, the mutations mutually compensate for each other, the tumour cells recover the ability to repair their DNA and the drug stops working.
Fernndez-Capetillo says: "This is one of the first studies to demonstrate that secondary mutations can make tumours resistant when faced with specific treatments like, in this case, PARP inhibitors".
NEW DIAGNOSTIC TESTS WITH SECONDARY MUTATIONS
When the researchers compared different treatments, they observed that for those tumours with BRCA1 and/or BRCA2 mutations that also presented mutations in 53BP1 or PTIP, standard treatment with cisplatin was more efficient than personalised therapy.
"These data indicate that only patients containing mutations in BRCA1 and/or BRCA2, but not in the secondary genes we have described, would be candidates for an effective personalised therapy with PARP inhibitors", explains Fernndez-Capetillo, concluding that: "Our results suggest that 53BP1 and PTIP genes would need to be evaluated in patients with familial breast and ovarian cancer when deficiencies in the BRCA genes were present before deciding on their treatment".
In this context, researchers intend to warn healthcare providers in personalised medicine that the challenge, in addition to the search for markers of drug sensitivity for new pharmacological compounds, also encompasses the search for secondary resistance markers. The aim would be to bring about significant improvements in treatment outcomes.
###
[ | 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.
There's a reason that many eyes were on Plaza Towers Elementary as Moore, Oklahoma began to assess the damage from a deadly, devastating tornado that blasted through the town Monday evening?and killed at least 51 people: the school was leveled, with dozens of children still inside. And so far, some of the most emotionally charged news has emerged from the story unfolding there.?