Oh stop. The captain is a big party schmoozer and paper pusher. They don't do all of those silly things on a non military vessel.
Create a problem? Some largish persons will escort you to a nice little jail cell. There you will sit until the company lawyers figure out what to do with you.
I might invite you to look at a brochure on any Cruise Line in the world. They've solved all of these little problems and more. And some of them make money doing so.
This is basically a cross between a cruise line trip and a short jail sentence.
Oh, it's a big enough ship to have basic medical facilities and a doctor that mostly sort of speaks English (whether or not they speak whatever language you happen to speak is another question).
At the moment, there are probably 100,000 people on this planet 'suffering' under similar situations in cruise ships everywhere. People do occasionally die on cruise ships when they would have survived if they were in a bigger city, but it's an edge case.
China has enough land, just needs more technology to increase yields. They will continue to import food, they don't need to "own Dakota". That is just weird right wing talk. Besides if you want good farming land with plenty of water i don't think Dakota is high on your target list. Grow a lot of rice there?
Won't really help in the long run - you are just changing one scarce resource (rice) for a couple of others (water, petrochemicals). It's still a resource problem.
Of note in the Nature article is that none of the breathless claims in the PR bit are even alluded to. The abstract (which is typically available):
Protein synthesis involves the translation of ribonucleic acid information into proteins, the building blocks of life. The initial step of protein synthesis is the binding of the eukaryotic translation initiation factor 4E (eIF4E) to the 7-methylguanosine (m7-GpppG) 5cap of messenger RNAs1, 2. Low oxygen tension (hypoxia) represses cap-mediated translation by sequestering eIF4E through mammalian target of rapamycin (mTOR)-dependent mechanisms3, 4, 5, 6. Although the internal ribosome entry site is an alternative translation initiation mechanism, this pathway alone cannot account for the translational capacity of hypoxic cells7, 8. This raises a fundamental question in biology as to how proteins are synthesized in periods of oxygen scarcity and eIF4E inhibition9. Here we describe an oxygen-regulated translation initiation complex that mediates selective cap-dependent protein synthesis. We show that hypoxia stimulates the formation of a complex that includes the oxygen-regulated hypoxia-inducible factor 2 (HIF-2), the RNA-binding protein RBM4 and the cap-binding eIF4E2, an eIF4E homologue. Photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP)10 analysis identified an RNA hypoxia response element (rHRE) that recruits this complex to a wide array of mRNAs, including that encoding the epidermal growth factor receptor. Once assembled at the rHRE, the HIF-2–RBM4–eIF4E2 complex captures the 5cap and targets mRNAs to polysomes for active translation, thereby evading hypoxia-induced repression of protein synthesis. These findings demonstrate that cells have evolved a program by which oxygen tension switches the basic translation initiation machinery.
Is certainly consistent with your thoughts on apoptosis but there is scant discussion in TFA.
Interestingly the Nature article doesn't make mention of this mechanism in cancer cells other than to show it exists in a particular brain cancer clone. As the saying goes, 'extraordinary claims require extraordinary data' - at this point we're at the mercy of the idiot PR summary and a single statement from one of the researchers.
The idea that you could wipe out cancer cells selectively (if this pathway is indeed common to malignant cells AND not required by normal cells) is nice but lets hold our breath, shall we.
I've lost count on how many times cancer has been cured according to various and sundry press releases. Of interest perhaps, is that there isn't an editorial note on the paper. Nature tends to do this for papers that they perceive to have a major result. The editorial typically gives some background and insight to the paper to allow people who aren't in the field to understand it's significance.
Most people wouldn't know a desktop manager if it came up and bit them in the ass. They would not have any idea that they could be more or less productive. It's not on their radar..
Anybody who thinks China isn't 'the enemy' is smoking something good (come on, share it, dude). The next set of wars will be resource wars (just like the last ones). Likely by proxy and likely 'low intensity' but they will be wars nonetheless. The chance of the US and China going full out turn-the-the-guy-into-molten-glass is pretty low (but non zero).
There will be too much competition for oil (and possibly water) in the next 50 years. We're not doing anything to mitigate growth - our economy requires growth to survive - and so does China's.
That said, the idea that we need half billion dollar UAV bombers to pound somebody's jungle into a parking lot seems a tad over the top. TFA was really just an exercise in Pentagon babble, full of sound and fury, signifying nothing....
True to a point. EU law isn't binding on an American company operating in the US, but the various appellate courts often cite foreign courts for reasoning. There are good reasons for laws to consistent between sovereign nations. Doesn't always happen that way, but you can be certain that the US Supreme Court (which will likely hear the case no matter who wins this round) will review the EU decision.
tl;dr Maybe yes, maybe no. Likely there is something Prion like in Alzheimer's dementia. Cause or effect is uncertain. More research needed. Stay tuned.
More caveats (come on Slashdot, allow unicode and editing ferchristsakes) - I just quickly scanned the article. It's not my field. Any mouse neurodevelopmental geneticists in the audience?
Any word, as yet, on what eventually happens to the cells thus saved from early death?
Hard to say. It's a complicated, limited, experimental model using a fairly aggressive prion (infection to death in 12 weeks) so ringing this out to the slower neurodegenerative diseases in humans is a bit of stretch and likely limited by a number of caveats. They did find a 'window' of ability to rescue the cells - after around 9 weeks the rescue didn't work. But it did increase 'survival' in the mice so it's possible that it would have a clinically useful improvement in other similar diseases (assuming lots of things).
Remember, Prion disease in humans tends to be a very slow process. Timing could well be reflected in different mechanisms. Or not. This is really just an opening wedge rather than a robust look into the process.
Well yes, the switch isn't there just to make zombies (although it does suggest a mechanism). But identifying the switch at a molecular and / or genetic level allows one to start playing with it and work out the feedback mechanisms, etc. It's really unlikely that someone is going to find a drug that magically stops Alzheimer's or Prion disease simply by studying this one switch.
But I, for one, welcome our new hyper-intelligent, prion resistant, immortal rodentia overlords.
Legitimate question: 65 million years ago, were trees/plants as efficient at converting carbon dioxide to Oxygen? I assume trees have evolved since then to become better at what they do.
Once you had 'trees' you have modern photosynthesis. There might have been some qualitative differences with more surface area, etc, but the higher temps and just plain more organic matter would have likely trumped any later 'efficiencies'. Basically, once photosynthesis jumped out of the cyanobacteria (about 3+ billion years ago), the molecular mechanism has been highly conserved.
Fun office game for the younger crowd: Let the old geezers think you can't find the source of the sound. Let them have their little fun now at the end of their lives, this is pretty much the high point for them.
You're really gonna be hurting when I clobber you with my shuffleboard cue.
er, 'software engineers', sorry.
The oceans are full of cruise liners which seem to cope with these issues perfectly adequately not to mention oil platforms.
But this will be different. It will be a boat full of programmers.
Oh stop. The captain is a big party schmoozer and paper pusher. They don't do all of those silly things on a non military vessel.
Create a problem? Some largish persons will escort you to a nice little jail cell. There you will sit until the company lawyers figure out what to do with you.
Of course, then you're really in trouble.
I might invite you to look at a brochure on any Cruise Line in the world. They've solved all of these little problems and more. And some of them make money doing so.
This is basically a cross between a cruise line trip and a short jail sentence.
You get to decide which parts fit which theme.
Oh, it's a big enough ship to have basic medical facilities and a doctor that mostly sort of speaks English (whether or not they speak whatever language you happen to speak is another question).
At the moment, there are probably 100,000 people on this planet 'suffering' under similar situations in cruise ships everywhere. People do occasionally die on cruise ships when they would have survived if they were in a bigger city, but it's an edge case.
Malcolm Reynolds was a top dog?
In that thing he was flying around in? The one with recycled junkyard control boxes?
You're just looking at the women and projecting.
China has enough land, just needs more technology to increase yields. They will continue to import food, they don't need to "own Dakota". That is just weird right wing talk. Besides if you want good farming land with plenty of water i don't think Dakota is high on your target list. Grow a lot of rice there?
Won't really help in the long run - you are just changing one scarce resource (rice) for a couple of others (water, petrochemicals). It's still a resource problem.
Of note in the Nature article is that none of the breathless claims in the PR bit are even alluded to. The abstract (which is typically available):
Protein synthesis involves the translation of ribonucleic acid information into proteins, the building blocks of life. The initial step of protein synthesis is the binding of the eukaryotic translation initiation factor 4E (eIF4E) to the 7-methylguanosine (m7-GpppG) 5cap of messenger RNAs1, 2. Low oxygen tension (hypoxia) represses cap-mediated translation by sequestering eIF4E through mammalian target of rapamycin (mTOR)-dependent mechanisms3, 4, 5, 6. Although the internal ribosome entry site is an alternative translation initiation mechanism, this pathway alone cannot account for the translational capacity of hypoxic cells7, 8. This raises a fundamental question in biology as to how proteins are synthesized in periods of oxygen scarcity and eIF4E inhibition9. Here we describe an oxygen-regulated translation initiation complex that mediates selective cap-dependent protein synthesis. We show that hypoxia stimulates the formation of a complex that includes the oxygen-regulated hypoxia-inducible factor 2 (HIF-2), the RNA-binding protein RBM4 and the cap-binding eIF4E2, an eIF4E homologue. Photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP)10 analysis identified an RNA hypoxia response element (rHRE) that recruits this complex to a wide array of mRNAs, including that encoding the epidermal growth factor receptor. Once assembled at the rHRE, the HIF-2–RBM4–eIF4E2 complex captures the 5cap and targets mRNAs to polysomes for active translation, thereby evading hypoxia-induced repression of protein synthesis. These findings demonstrate that cells have evolved a program by which oxygen tension switches the basic translation initiation machinery.
Is certainly consistent with your thoughts on apoptosis but there is scant discussion in TFA.
Interestingly the Nature article doesn't make mention of this mechanism in cancer cells other than to show it exists in a particular brain cancer clone. As the saying goes, 'extraordinary claims require extraordinary data' - at this point we're at the mercy of the idiot PR summary and a single statement from one of the researchers.
The idea that you could wipe out cancer cells selectively (if this pathway is indeed common to malignant cells AND not required by normal cells) is nice but lets hold our breath, shall we.
I've lost count on how many times cancer has been cured according to various and sundry press releases. Of interest perhaps, is that there isn't an editorial note on the paper. Nature tends to do this for papers that they perceive to have a major result. The editorial typically gives some background and insight to the paper to allow people who aren't in the field to understand it's significance.
Most people wouldn't know a desktop manager if it came up and bit them in the ass. They would not have any idea that they could be more or less productive. It's not on their radar..
Anybody who thinks China isn't 'the enemy' is smoking something good (come on, share it, dude). The next set of wars will be resource wars (just like the last ones). Likely by proxy and likely 'low intensity' but they will be wars nonetheless. The chance of the US and China going full out turn-the-the-guy-into-molten-glass is pretty low (but non zero).
There will be too much competition for oil (and possibly water) in the next 50 years. We're not doing anything to mitigate growth - our economy requires growth to survive - and so does China's.
That said, the idea that we need half billion dollar UAV bombers to pound somebody's jungle into a parking lot seems a tad over the top. TFA was really just an exercise in Pentagon babble, full of sound and fury, signifying nothing....
True to a point. EU law isn't binding on an American company operating in the US, but the various appellate courts often cite foreign courts for reasoning. There are good reasons for laws to consistent between sovereign nations. Doesn't always happen that way, but you can be certain that the US Supreme Court (which will likely hear the case no matter who wins this round) will review the EU decision.
Well no wonder they blow out - you're running them at twice the rated voltage!
Step away from the computer for a while. Remember your blood pressure!
Just channel Dr. Bob, DC for a bit - you'll feel better in a jiffy.
So, in other words, he would be destitute.
Cat got your tongue?
YOU aren't Boeing / Lockheed / Northrup-Grumman , et. al.
THEY need lots of money for this sort of thing. Government regulations, security, terrorism and all that.
YOU shut the fuck up. THEY will protect America!
It's complicated
tl;dr Maybe yes, maybe no. Likely there is something Prion like in Alzheimer's dementia. Cause or effect is uncertain. More research needed. Stay tuned.
More caveats (come on Slashdot, allow unicode and editing ferchristsakes) - I just quickly scanned the article. It's not my field. Any mouse neurodevelopmental geneticists in the audience?
Any word, as yet, on what eventually happens to the cells thus saved from early death?
Hard to say. It's a complicated, limited, experimental model using a fairly aggressive prion (infection to death in 12 weeks) so ringing this out to the slower neurodegenerative diseases in humans is a bit of stretch and likely limited by a number of caveats. They did find a 'window' of ability to rescue the cells - after around 9 weeks the rescue didn't work. But it did increase 'survival' in the mice so it's possible that it would have a clinically useful improvement in other similar diseases (assuming lots of things).
Remember, Prion disease in humans tends to be a very slow process. Timing could well be reflected in different mechanisms. Or not. This is really just an opening wedge rather than a robust look into the process.
Well yes, the switch isn't there just to make zombies (although it does suggest a mechanism). But identifying the switch at a molecular and / or genetic level allows one to start playing with it and work out the feedback mechanisms, etc. It's really unlikely that someone is going to find a drug that magically stops Alzheimer's or Prion disease simply by studying this one switch.
But I, for one, welcome our new hyper-intelligent, prion resistant, immortal rodentia overlords.
The problem of dinosaurs causing climate change has been around for 150 million years and we haven't fixed it yet?
Maybe somebody already did. Think about this:
TIme travel is invented.
First thing they do is send back a thermite grenade.
Poof, the entire atmosphere blows up. No more big dinos.
Problem solved until the Industrial Revolution. Now, you have to worry about:
Somebody set us up the bomb?
Legitimate question: 65 million years ago, were trees/plants as efficient at converting carbon dioxide to Oxygen? I assume trees have evolved since then to become better at what they do.
Once you had 'trees' you have modern photosynthesis. There might have been some qualitative differences with more surface area, etc, but the higher temps and just plain more organic matter would have likely trumped any later 'efficiencies'. Basically, once photosynthesis jumped out of the cyanobacteria (about 3+ billion years ago), the molecular mechanism has been highly conserved.
Are you sure? Most politicians seem to be talking out their ass all of the time.
Fun office game for the younger crowd: Let the old geezers think you can't find the source of the sound. Let them have their little fun now at the end of their lives, this is pretty much the high point for them.
You're really gonna be hurting when I clobber you with my shuffleboard cue.