In 2011, more corn was used in ethanol production than for livestock feed for the first time ever. Ethanol accounted for 5.05 billion bushels which at 56 pounds per bushel (shelled) comes to 141.4 million tons. Worldwide corn production in 2011 was 867.5 million tons. That's over 16% of the global corn crop used for ethanol production.
The lack of human testing is a pretty big issue. I went to an early stages of drug discovery conference last year and remember one of the speakers referring to clinical trials as "the place where drug candidates go to die." However the articles linked to in TFA are very light on details so we don't really know what they have tested at all.
There are five different plasmodium species that can infect and cause disease in humans and we don't know which one(s) this group looked into. Probably P. malariae, and if effective on just one of the species it would still be wonderful news, but we don't know from TFA. The other problem is that the drug "killed resistant parasites instantly." What does that mean? Do they maintain drug resistant plasmodium strains in their lab and when you have them in some petri dish with tissue culture medium that you can instantly kill them by adding the compound? If that's all they've got then it's not nearly as impressive as the article lets on. Malarial pathogens spend a lot of time inside of cells, both inside of red blood cells and also inside of cells in the liver, hiding from the host immune system and any anti-malarial drugs. The life cycle inside the host is fairly complex with different malarial stages having different responses to any drug administered. This is why traditional malaria treatments are multiple doses over at least several days. The other problem is that the animal model for malaria disease isn't very good. Again, we don't know from the articles linked in TFA exactly what animal model they used, but it's probably a mouse model. In that case, it's already known to be easier to kill malarial infections in the model than in an actual infection in humans.
I share your wish that the research group has lots of luck in their upcoming clinical trials; it sounds like they've gone about as far as they can without testing on the actual disease in human patients. I'm just not optimistic as clinical trials are difficult to pass, a one pill cure just sounds too good to be true, and then your comments about the drug class itself.
Yes, there are a hundred coelacanth species, from dozens of genera, from a half dozen families, grouped into at least two suborders fitting into the order Coelacanthiformes. The taxonomic equivalent for dogs is the order Carnivora. Do you really wish to make a claim roughly equivalent to claiming that bears, badgers, and bobcats could all be due to variety existing in the same Carnivora genome? Keep in mind that Carnivora is only a little more than one-tenth the age of Coelacanthiformes, yet genetic basics like chromosome number can be wildly different. Just within family Ursidae the giant panda has 42 chromosomes, the spectacled bear 52, and the grizzly 74. From this comparison then it is a good bet that the coelacanth genomes of today are quite different from what existed 360 million years ago.
You're a bit muddled in your terms. Darwinian evolution is a collection of ideas which in Darwin's time didn't include mutation. He knew that species change over time, he knew that every group of organisms descended from a common ancestor, he knew that species multiplied by splitting into daughter species, he knew that speciation occurs through gradual processes rather than by saltation (sudden emergence of representatives of a new type), and he gave us one of the mechanisms of evolution: natural selection. Darwin didn't know the origin of new genetic information: mutation. In fact the merging of genetics and natural selection into the neo-Darwinian synthesis didn't happen until around 60 years after Darwin died. You're not getting genetic drift right either.
It is completely accurate to say that the only way species don't evolve is if they go extinct. At the most basic level evolution is simply the change in allele frequency in a population over time. Get a mutation, the allele frequency changes. Natural selection kills something off, ignoring clonal populations that's a change in allele frequency. Whether or not a change is necessary for survival is looking at it wrong. After all, other members of the species are getting along just fine without some specific mutation. A better way of looking at it is to ask if the mutation is compatible with survival. Does the mutation result in a nonviable organism? That's bad. Does it do nothing? Fine. Does it give you an advantage under some or all situations? That's good and as a result you might get more offspring and over time produce a large shift in allele frequency. These changes brought about by mutation and selection (and other evolutionary mechanisms) build up over time and new species inevitably result. There's nothing religious about it.
Of course biologists do: coelacanths (and insects, and everything else) are evolving. Over the 360 million years coelacanths have been around there have been countless new mutations and new environmental pressures that have shaped the coelacanths. We know of around a hundred coelacanth species that are grouped into not only multiple genera, but multiple families which we can identify from changes in skeletal structure and which we can use as index fossils. They hit upon a successful basic body form a long time ago but they've been evolving the whole time. The only way a species can't evolve is if it goes extinct.
Nice editing there. What Obama actually said was "...the next president, the next vice president of the United States of America, Joe Biden." Mediaite's clip from Fox News, of all places.
I've already got binoculars and a sheet of paper's pretty cheap. To me this looks like a good excuse to buy a welder's hood with #14 glass (as per the link in TFA). Once I've got the hood, that's an excuse to buy the torch...and presto! A new hobby is born!
OK, a welder's hood can be pricey. But you can buy the glass for less than $10.
Re:Check the party breakdowns ...
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House Passes CISPA
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· Score: 4, Informative
Damn it you made me laugh so hard I nearly pissed myself.
Seriously though American universities are falling apart, salaries low, temporary and part-time positions (full time responsibilities for half pay! Yay!) are ever increasingly common, buildings in dire need of replacement, over $25 billion in deferred maintenance (ever have a ceiling cave in on you? I have. Not fun.), and university libraries everywhere have been slashing their journal subscriptions for years because they cost too much. Public funding of American universities has been slashed repeatedly over the last 30 years. A state university used to get 80% of its funds from the state. Now a state university usually gets around 20%, but some get single-digit support making them private schools in all but name. This is the cause of sky high tuition. Every time a state slashes university funding, tuition increases.
"That's the rub though- vaccines used to be for life threatening diseases like polio and smallpox but are now more and more prescribed for things that are merely a nuisance(chicken pox anyone?)."
Chicken pox vaccination is still worthwhile. From the link, before introduction of a vaccine chicken pox was annually responsible for 150 deaths, 11,000 hospitalizations, $330 million medical costs, and $1.5 billion in societal costs. Further the virus can later (even decades after initial infection) cause shingles, which typically involves a painful skin rash lasting several weeks but can also cause residual nerve pain lasting months or even years. Shingles is pretty common too, I found incidence rates of 2-3 per thousand per year, and you're at increased risk of developing shingles as you get older. Additionally you can have shingles more than once.
I have a hard time believing it's as good as your link says. Thinking about the funding opportunities I applied for in the last three years I'd say the funding success rate in my experience is much closer to 8% than 18%. I can think of two grants I wrote (one NIH, one USDA) where the success rate ended up less than 5%. If we went back to the 30% success rate of 2003 I'd be dancing buck-naked on top of the lab benches...so I guess there's an upside to the abysmal funding since nobody wants to see that.
Some of my work is referenced by wikipedia (just like a lot of other researchers) but it doesn't mean much of anything to me professionally. A wikipedia reference doesn't add on to the total number of citations a paper I wrote gets, only citations by other peer-reviewed papers does that. I doubt references on wikipedia gets me much in the way of other researchers' eyeballs on my papers either.
Maybe more in terms of TFA, I'm a biochemist and on the last paper I wrote I got the opposite pushback from the reviewers. They thought I had too many references for the length of the paper and asked me to try and cut it down if possible, but made no specific requests as to which references to remove or how many. So if I had more than one reference backing a statement I'd pick the more recent one, or use a review and add on "and references therein," pretty common stuff. I've never heard of a problem in my field of not getting past review due to not referencing prof smith or whoever. You might (rarely) get a reviewer's request for some statement to have a reference, but the reviewers don't care who you cite as long as it backs up the statement.
"The article explains NOTHING about how dangerous 2,3,4-T is, and simply replies upon "it's a part of Agent Orange" to assert the harmfulness of the chemical."
Well according to almighty wikipedia the oral LD50 of 2,4,5-T is 389 mg/kg in mice and 500 mg/kg in rats. That struck me as not being especially hideous, and on a whim I looked up the LD50 of aspirin: 250 mg/kg in mice and 200 mg/kg in rats. By this measure 2,4,5-T is less toxic than aspirin!. It's more complex than that however. It doesn't include low dose/persistent exposure effects of the compound and doesn't include degradation products or side products of synthesis, which could have different levels of toxicity. It's the synthesis byproducts that are a major issue with 2,4,5-T. As others have commented on, 2,3,7,8-Tetrachlorodibenzodioxin (TCDD) is a side product of synthesis, and according to wikipedia modern synthesis can knock its levels down to about 0.005 ppm (I've seen 0.1 ppm elsewhere in my quick search), but in earlier batches could be up to 60 ppm. The LD50 of TCDD is 1,000 times lower than 2,4,5-T; a few hundred micrograms ingested per kilogram of body weight was enough to kill rats (sorry about age of study). Nasty effects other than death naturally occur at lower amounts. Also keep in mind that we're just making rodents eat the stuff. I'm not a chemical engineer, but you do have to wonder what sort of waste products (TCDD included) were flushed out by that chemical plant and where it went, and how long TCDD and other nasties might persist in the environment. TCDD is unfortunately pretty resistant to biodegradation, one study in Italy I found gave a half-life in soil of 9.1 years. I've just spent a little bit of time working on insecticide development so these are some of the things I think about, although being a biochemist this is not a core area of expertise.
I can think of the SR-71, the A-12, YF-12 (although these three aircraft are related), and the XB-70 Valkyrie. If we include rocket powered aircraft that are launched from the air then there's the X-2, although the only one that made Mach 3 crashed shortly afterwards, and the X-15. Including the MiG-25 that's seven, but three are related, two can't really handle it, two are rocket-powered and require motherships, and four were experimental/prototypes. That leaves the SR-71 and its parent the A-12.
There might be a chance of 4,000 kph, but yeah 4,000 mph (6,437 kph) doesn't sound reasonable. 3,530 kph is the declassified SR-71 speed record but its true top speed remains classified.
Universities and other publicly-funded research institutions perform basic research for the most part. We study disease X, and find targets Y and Z that might be exploited for drug discovery by pharmaceutical companies. Starting about 10 years ago, a few of the largest universities started small high-throughput screening labs where university researchers could learn how to do some of the screening work done in the private sector. I've used one such facility at the University of Wisconsin. However the number of compounds available for screening is at least an order of magnitude smaller than what is available to pharmaceutical companies. More important than the number of compounds available for testing is the funds to do it. Pharma has it, academia doesn't.
Even in the rare cases where the universities do come up with something that shows efficacy, that doesn't necessarily make it a good compound. How well does it inhibit? How easy is it to make? How stable is it? How soluble is it? What else does the compound inhibit? Does it show undesirable side effects? How easy is it to formulate? Modification of lead compounds is pretty much the middle third of drug discovery, and can take three years or more. Some universities have medicinal chemists, but at least in my experience they do not have time, interest (running their own labs they've naturally got their own projects and interests), personnel, or funds to take a compound discovered at a different lab and work it over for a few years. Even if they did, no university has the funds to get a compound through clinical trials.
Biotech and pharmaceuticals companies fund all the phase I, II, and III clinical trials. The amount of time and money spent on compound modification by biotech and pharma dwarfs the universities, to put it mildly. The same is true for the time and money spent on screening chemical libraries and preclinical trials. Biotech and pharma also have involvement in the very earliest stage of target identification and verification. Universities are important in the drug discovery process. They provide some of the targets, do the vast majority of the basic research needed before you can even tease out a target, and provide all of the early (BS/MS/PhD) and most of the middle (postdoctoral) training of the personnel that biotech and pharma need. But for the majority of drug or drug candidate the bulk of the time and money spent is from biotech and pharmaceuticals companies, not the universities.
"Anything that is trivial to reverse engineer and steal in such a manner probably didn't require that much R&D and isn't worth a patent, certainly for the length of time current patents grant a monopoly."
Once a new drug is on the market its exact formulation is known, so reverse engineering is a trivial matter. However the required R&D for a new drug is typically around 10 years and $1 billion.
There is no maximum age, although hires and employees can get weeded out by the "must lift 40 lbs box" or "stand for long periods of time" requirements that pop up routinely even for office work. You've probably heard jokes about geriatric Walmart greeters, but many Americans work well into their 60's and beyond. The earliest you're eligible for Social Security is 62 with reduced benefits, or 65-67 with full benefits (the eligibility depends on birth date, born after 1960 and you must be 67). Since Social Security doesn't pay that much many Americans work longer, or work longer because retirement is unappealing. My uncle didn't retire from trucking until his early 70's despite having to unload the semi himself, and that's after doing that job for 40 years and having a bad back, bad shoulder, and a hip replacement. My mom (68) and an aunt (70) are still office workers. Farmers also tend to hang on, in the USA 40% of them are age 55+ and every farmer out there knows some crazy old bastard still at it deep into their 80's.
More on topic, for scientists and retirement there's a big difference between those who work in academia and those who work in private enterprise. For the latter, unless you've moved up very high in the corporate ladder you're going to retire in your 60's, assuming you haven't gotten canned and replaced with a younger, cheaper scientist. For academic scientists there's tenured professors and then there's everybody else. Postdocs either find an industry job, quit science, or move up to an academic staff science job (tenure track jobs account for much less than 1%). Academic staff scientists either transition to industry, quit science, or are forced into retirement when their professor boss retires/can't get grants. Tenured professors rarely retire. Eventually they get demoted to Professor Emeritus, typically with restrictions on their ability to recruit grad students. There will be pressure on them to downsize their lab from the university and their department, but some can continue for many years winning grants and employing postdocs, techs, staff scientists, and undergrads. Eventually their lab will shrink in numbers and they may be reduced to a tiny space nobody else wants, or just an office. I know several professors who worked/are working into their 80's with reduced lab personnel and/or space, and have heard of a few who went into their 90's. Ernst Mayr never retired, instead going out feet first at 100.
There used to be the Office of Technology Assessment, a highly respected (so much so that it has been imitated by other governments) body whose function was to advise Congress on science and technology matters. Newt Gingrich lead the Republicans in killing it off as a part of their Contract with America back in 1995. The OTA would have denied Congress the cover of ignorance when it came time to vote on this SOPA monstrosity.
"They were simply the fastest cells that were among those that were raced; many cells from various species of protists, not to mention sperm cells are capable of faster speeds than that."
The first thing that came to me was Listeria. These bacteria are intracellular pathogens, using the host cell's cytoskeleton (actin filaments) to shoot around the interior of the cell (and eventually punch through the cell wall IIRC) at 0.12-1.46 microns/sec, faster than the cells tested.
This is outside of my area of expertise, but I would think the risk to be somewhere between very low and nonexistent. Definition of species can be squishy, and ability to interbreed with members of different species in the same genus is known in mosquitoes. For example Aedes aegypti has been known to produce offspring when it mates with Aedes mascarensis, at least under laboratory conditions, but a large portion of the offspring have developmental abnormalities. So if you have these two species overlapping when this GM Ae. aegypti is released you might see some small knockdown of the Ae. mascarensis population size. Keep introducing the GM Ae. aegypti long enough and you amplify an already strong evolutionary pressure on Ae. mascarensis females to avoid mating with Ae. aegypti males. Similarly the effect of the GM Ae. aegypti on mosquito species belonging to different genera would be greatly reduced or nil; I'm not aware of any mosquitoes mating outside their genus. Again, outside my area of expertise: I'm a protein biochemist who just happens to work in a mosquito lab.
Male mosquitoes feed on nectar from flowers, in the lab we feed them sugar water. Female mosquitoes on the other hand require a blood meal for the proper development of their eggs. Mosquitoes live in the water as free swimming larvae, which will develop into similarly free-swimming pupae. When development is complete, the pupae floats to the water surface and the adult mosquito emerges. The adult mosquito stands on the water surface while its new exoskeleton and wings dry and harden. The adult mosquito can't swim, and while it can walk on water it only does so when emerging from the pupae and for some species when depositing eggs. It minimizes water walking in both cases and flies away as soon as possible. That's what makes this so cool. The female, and only the female mosquito, is stuck on the water unable to fly and practically motionless. It's a free lunch to any mosquito-eating predator around. The males on the other hand are free to escape and then free to mate and pass that gene on to their offspring--again fatal to their daughters, and no harm to their sons, who repeat the cycle.
"My question isn't so much "what could possibly go wrong", but rather "What right gives you to make such a decision for the whole world to live by".
The best source that I can find is Scientific American, and from what I've been reading over the last couple hours I wouldn't be surprised to see a book written on this project. It's got everything: oooh scary genetically engineered mosquitoes! Exotic and tropical locations! International intrigue in law, politics, academia! Skulduggery, intellectual theft, backstabbing! And possibly world-changing success in eradicating dengue!
The quick summary is that there are multiple parties involved: the Genetic Strategies for Control of Dengue Virus Transmission, an international and public-private organization that is behind the GM mosquitoes. Key members are Prof. Anthony James at UC-Irvine, and Dr. Luke Alphey at Oxitec, a UK-based biotech company. While sterile insect technique has been used in the past to eradicate one species of screwworm in the US, that same technique did not work on mosquitoes. James' group identified a gene specific to the female of the mosquito species that if targeted via genetic engineering could have a sterile insect effect analogous to the screwworms. Actual engineering of the mosquito was contracted out to Oxitec, who according to SciAm were the ones responsible for the release of the GM mosquitoes on Grand Cayman island without the knowledge of other members of the dengue control group. Prof. James apparently didn't know until Dr. Alphey publicly disclosed it 14 months after the fact. Where the regulations come in is complex. As a US-based academic researcher Prof. James is subject to ethical and biosafety guidelines of his department, UC-Irvine, the state of California, and the Federal government, plus that of the agencies that granted the funds for his research and the government of whatever country he is conducting research in. UK-based Oxitec has to play by the rules of the UK at least for work done in the UK, but the initial release of the mosquitoes was in the Caymans. Environmental regulations regarding GM mosquitoes didn't exist there according to one source I read, according to another they were brand new and it was implied that Oxitec had some involvement in their crafting. The other researchers are pissed, and Oxitec's actions threaten the extremely careful, conservative, and highly regulated GMO work that has been done in the US and other parts of the world.
"Folks, the mosquito could get extinct in a few years. Scary indeed."
Well, A mosquito species could be come extinct. According to TFA, Aedes aegypti to be exact. This particular mosquito can carry several major human pathogens including dengue hemorrhagic fever, yellow fever, and chickungunya, which are all viral diseases. Ae. aegypti originated in Africa but is now found throughout tropical and subtropical regions including the USA, where it used to be in only Florida and the southeast but has since spread north to New York and Illinois. Especially alarming is the fact that there have been outbreaks of dengue recently (in 2010 at least) in Florida.
Eradication of Ae. aegypti might not necessarily be that big of a deal environmentally. While mosquitoes are an important part of the diet of many predators, there are over 40 genera comprising thousands of species of mosquitoes. Any reasonably sized chunk of land probably has more than one species of mosquito, for example here in Wisconsin we have not less than 58 species. Even tiny Rhode Island is home to at least 46 mosquito species!
Just adding on to what PCM2 wrote, the banana variety you're thinking of was the Gros Michel, a triploid hybrid banana. There was no genetic engineering, the variety existed over a hundred years ago. It used to be the main variety of banana eaten, being sweeter and better tasting than the Cavendish, currently the most common banana. In all those old cartoons of people slipping and falling due to a banana peel, it wasn't much of an exaggeration since the peel of the Gros Michel is much slippier than the Cavendish. The Gros Michel was highly susceptible to Panama disease, a highly virulent fungal infection, and today the Gros Michel is practically extinct. A problem with bananas is that they are propagated asexually. A banana plant will last for about 25 years, but it will send out lateral roots (rhizomes) that will develop into a clone of the parent plant. There is no genetic diversity so if a fungus can parasitize and kill one plant it'll take the entire crop, which was what happened to the Gros Michel. However the Cavendish cultivar is also a clone, and is susceptible to new strains of the fungus that caused Panama disease. It's probably just a manner of time before the Cavendish goes the way of the dodo...er...Gros Michel.
There are limitations to what you can do with plants through selective breeding, particularly for crop species which have extremely low genetic diversity, which leads us to genetic engineering. Corn is the most common GMO, but rice and cotton are definitely on the upswing. As for bananas there are field trials in the USA, Australia, Israel, and Uganda for plants with engineered resistance to viral and fungal diseases, including Panama disease. Research on nutritional enhancement of bananas, resistance to bacterial disease, and nematode pests is ongoing.
Slashdot Mirror
"Let's face it, even the scientists don't know what quantum spin is all about."
MRI scans couldn't exist without a thorough understanding of what quantum spin states are. Ditto for NMR spectroscopy.
In 2011, more corn was used in ethanol production than for livestock feed for the first time ever. Ethanol accounted for 5.05 billion bushels which at 56 pounds per bushel (shelled) comes to 141.4 million tons. Worldwide corn production in 2011 was 867.5 million tons. That's over 16% of the global corn crop used for ethanol production.
The lack of human testing is a pretty big issue. I went to an early stages of drug discovery conference last year and remember one of the speakers referring to clinical trials as "the place where drug candidates go to die." However the articles linked to in TFA are very light on details so we don't really know what they have tested at all.
There are five different plasmodium species that can infect and cause disease in humans and we don't know which one(s) this group looked into. Probably P. malariae, and if effective on just one of the species it would still be wonderful news, but we don't know from TFA. The other problem is that the drug "killed resistant parasites instantly." What does that mean? Do they maintain drug resistant plasmodium strains in their lab and when you have them in some petri dish with tissue culture medium that you can instantly kill them by adding the compound? If that's all they've got then it's not nearly as impressive as the article lets on. Malarial pathogens spend a lot of time inside of cells, both inside of red blood cells and also inside of cells in the liver, hiding from the host immune system and any anti-malarial drugs. The life cycle inside the host is fairly complex with different malarial stages having different responses to any drug administered. This is why traditional malaria treatments are multiple doses over at least several days. The other problem is that the animal model for malaria disease isn't very good. Again, we don't know from the articles linked in TFA exactly what animal model they used, but it's probably a mouse model. In that case, it's already known to be easier to kill malarial infections in the model than in an actual infection in humans.
I share your wish that the research group has lots of luck in their upcoming clinical trials; it sounds like they've gone about as far as they can without testing on the actual disease in human patients. I'm just not optimistic as clinical trials are difficult to pass, a one pill cure just sounds too good to be true, and then your comments about the drug class itself.
Yes, there are a hundred coelacanth species, from dozens of genera, from a half dozen families, grouped into at least two suborders fitting into the order Coelacanthiformes. The taxonomic equivalent for dogs is the order Carnivora. Do you really wish to make a claim roughly equivalent to claiming that bears, badgers, and bobcats could all be due to variety existing in the same Carnivora genome? Keep in mind that Carnivora is only a little more than one-tenth the age of Coelacanthiformes, yet genetic basics like chromosome number can be wildly different. Just within family Ursidae the giant panda has 42 chromosomes, the spectacled bear 52, and the grizzly 74. From this comparison then it is a good bet that the coelacanth genomes of today are quite different from what existed 360 million years ago.
You're a bit muddled in your terms. Darwinian evolution is a collection of ideas which in Darwin's time didn't include mutation. He knew that species change over time, he knew that every group of organisms descended from a common ancestor, he knew that species multiplied by splitting into daughter species, he knew that speciation occurs through gradual processes rather than by saltation (sudden emergence of representatives of a new type), and he gave us one of the mechanisms of evolution: natural selection. Darwin didn't know the origin of new genetic information: mutation. In fact the merging of genetics and natural selection into the neo-Darwinian synthesis didn't happen until around 60 years after Darwin died. You're not getting genetic drift right either.
It is completely accurate to say that the only way species don't evolve is if they go extinct. At the most basic level evolution is simply the change in allele frequency in a population over time. Get a mutation, the allele frequency changes. Natural selection kills something off, ignoring clonal populations that's a change in allele frequency. Whether or not a change is necessary for survival is looking at it wrong. After all, other members of the species are getting along just fine without some specific mutation. A better way of looking at it is to ask if the mutation is compatible with survival. Does the mutation result in a nonviable organism? That's bad. Does it do nothing? Fine. Does it give you an advantage under some or all situations? That's good and as a result you might get more offspring and over time produce a large shift in allele frequency. These changes brought about by mutation and selection (and other evolutionary mechanisms) build up over time and new species inevitably result. There's nothing religious about it.
Of course biologists do: coelacanths (and insects, and everything else) are evolving. Over the 360 million years coelacanths have been around there have been countless new mutations and new environmental pressures that have shaped the coelacanths. We know of around a hundred coelacanth species that are grouped into not only multiple genera, but multiple families which we can identify from changes in skeletal structure and which we can use as index fossils. They hit upon a successful basic body form a long time ago but they've been evolving the whole time. The only way a species can't evolve is if it goes extinct.
Nice editing there. What Obama actually said was "...the next president, the next vice president of the United States of America, Joe Biden." Mediaite's clip from Fox News, of all places.
I've already got binoculars and a sheet of paper's pretty cheap. To me this looks like a good excuse to buy a welder's hood with #14 glass (as per the link in TFA). Once I've got the hood, that's an excuse to buy the torch...and presto! A new hobby is born!
OK, a welder's hood can be pricey. But you can buy the glass for less than $10.
Obama has issued a veto threat.
"...the universities have the money..."
Damn it you made me laugh so hard I nearly pissed myself.
Seriously though American universities are falling apart, salaries low, temporary and part-time positions (full time responsibilities for half pay! Yay!) are ever increasingly common, buildings in dire need of replacement, over $25 billion in deferred maintenance (ever have a ceiling cave in on you? I have. Not fun.), and university libraries everywhere have been slashing their journal subscriptions for years because they cost too much. Public funding of American universities has been slashed repeatedly over the last 30 years. A state university used to get 80% of its funds from the state. Now a state university usually gets around 20%, but some get single-digit support making them private schools in all but name. This is the cause of sky high tuition. Every time a state slashes university funding, tuition increases.
"That's the rub though- vaccines used to be for life threatening diseases like polio and smallpox but are now more and more prescribed for things that are merely a nuisance(chicken pox anyone?)."
Chicken pox vaccination is still worthwhile. From the link, before introduction of a vaccine chicken pox was annually responsible for 150 deaths, 11,000 hospitalizations, $330 million medical costs, and $1.5 billion in societal costs. Further the virus can later (even decades after initial infection) cause shingles, which typically involves a painful skin rash lasting several weeks but can also cause residual nerve pain lasting months or even years. Shingles is pretty common too, I found incidence rates of 2-3 per thousand per year, and you're at increased risk of developing shingles as you get older. Additionally you can have shingles more than once.
I have a hard time believing it's as good as your link says. Thinking about the funding opportunities I applied for in the last three years I'd say the funding success rate in my experience is much closer to 8% than 18%. I can think of two grants I wrote (one NIH, one USDA) where the success rate ended up less than 5%. If we went back to the 30% success rate of 2003 I'd be dancing buck-naked on top of the lab benches...so I guess there's an upside to the abysmal funding since nobody wants to see that.
Some of my work is referenced by wikipedia (just like a lot of other researchers) but it doesn't mean much of anything to me professionally. A wikipedia reference doesn't add on to the total number of citations a paper I wrote gets, only citations by other peer-reviewed papers does that. I doubt references on wikipedia gets me much in the way of other researchers' eyeballs on my papers either.
Maybe more in terms of TFA, I'm a biochemist and on the last paper I wrote I got the opposite pushback from the reviewers. They thought I had too many references for the length of the paper and asked me to try and cut it down if possible, but made no specific requests as to which references to remove or how many. So if I had more than one reference backing a statement I'd pick the more recent one, or use a review and add on "and references therein," pretty common stuff. I've never heard of a problem in my field of not getting past review due to not referencing prof smith or whoever. You might (rarely) get a reviewer's request for some statement to have a reference, but the reviewers don't care who you cite as long as it backs up the statement.
"The article explains NOTHING about how dangerous 2,3,4-T is, and simply replies upon "it's a part of Agent Orange" to assert the harmfulness of the chemical."
Well according to almighty wikipedia the oral LD50 of 2,4,5-T is 389 mg/kg in mice and 500 mg/kg in rats. That struck me as not being especially hideous, and on a whim I looked up the LD50 of aspirin: 250 mg/kg in mice and 200 mg/kg in rats. By this measure 2,4,5-T is less toxic than aspirin!. It's more complex than that however. It doesn't include low dose/persistent exposure effects of the compound and doesn't include degradation products or side products of synthesis, which could have different levels of toxicity. It's the synthesis byproducts that are a major issue with 2,4,5-T. As others have commented on, 2,3,7,8-Tetrachlorodibenzodioxin (TCDD) is a side product of synthesis, and according to wikipedia modern synthesis can knock its levels down to about 0.005 ppm (I've seen 0.1 ppm elsewhere in my quick search), but in earlier batches could be up to 60 ppm. The LD50 of TCDD is 1,000 times lower than 2,4,5-T; a few hundred micrograms ingested per kilogram of body weight was enough to kill rats (sorry about age of study). Nasty effects other than death naturally occur at lower amounts. Also keep in mind that we're just making rodents eat the stuff. I'm not a chemical engineer, but you do have to wonder what sort of waste products (TCDD included) were flushed out by that chemical plant and where it went, and how long TCDD and other nasties might persist in the environment. TCDD is unfortunately pretty resistant to biodegradation, one study in Italy I found gave a half-life in soil of 9.1 years. I've just spent a little bit of time working on insecticide development so these are some of the things I think about, although being a biochemist this is not a core area of expertise.
I can think of the SR-71, the A-12, YF-12 (although these three aircraft are related), and the XB-70 Valkyrie. If we include rocket powered aircraft that are launched from the air then there's the X-2, although the only one that made Mach 3 crashed shortly afterwards, and the X-15. Including the MiG-25 that's seven, but three are related, two can't really handle it, two are rocket-powered and require motherships, and four were experimental/prototypes. That leaves the SR-71 and its parent the A-12.
There might be a chance of 4,000 kph, but yeah 4,000 mph (6,437 kph) doesn't sound reasonable. 3,530 kph is the declassified SR-71 speed record but its true top speed remains classified.
Universities and other publicly-funded research institutions perform basic research for the most part. We study disease X, and find targets Y and Z that might be exploited for drug discovery by pharmaceutical companies. Starting about 10 years ago, a few of the largest universities started small high-throughput screening labs where university researchers could learn how to do some of the screening work done in the private sector. I've used one such facility at the University of Wisconsin. However the number of compounds available for screening is at least an order of magnitude smaller than what is available to pharmaceutical companies. More important than the number of compounds available for testing is the funds to do it. Pharma has it, academia doesn't.
Even in the rare cases where the universities do come up with something that shows efficacy, that doesn't necessarily make it a good compound. How well does it inhibit? How easy is it to make? How stable is it? How soluble is it? What else does the compound inhibit? Does it show undesirable side effects? How easy is it to formulate? Modification of lead compounds is pretty much the middle third of drug discovery, and can take three years or more. Some universities have medicinal chemists, but at least in my experience they do not have time, interest (running their own labs they've naturally got their own projects and interests), personnel, or funds to take a compound discovered at a different lab and work it over for a few years. Even if they did, no university has the funds to get a compound through clinical trials.
Biotech and pharmaceuticals companies fund all the phase I, II, and III clinical trials. The amount of time and money spent on compound modification by biotech and pharma dwarfs the universities, to put it mildly. The same is true for the time and money spent on screening chemical libraries and preclinical trials. Biotech and pharma also have involvement in the very earliest stage of target identification and verification. Universities are important in the drug discovery process. They provide some of the targets, do the vast majority of the basic research needed before you can even tease out a target, and provide all of the early (BS/MS/PhD) and most of the middle (postdoctoral) training of the personnel that biotech and pharma need. But for the majority of drug or drug candidate the bulk of the time and money spent is from biotech and pharmaceuticals companies, not the universities.
"Anything that is trivial to reverse engineer and steal in such a manner probably didn't require that much R&D and isn't worth a patent, certainly for the length of time current patents grant a monopoly."
Once a new drug is on the market its exact formulation is known, so reverse engineering is a trivial matter. However the required R&D for a new drug is typically around 10 years and $1 billion.
There is no maximum age, although hires and employees can get weeded out by the "must lift 40 lbs box" or "stand for long periods of time" requirements that pop up routinely even for office work. You've probably heard jokes about geriatric Walmart greeters, but many Americans work well into their 60's and beyond. The earliest you're eligible for Social Security is 62 with reduced benefits, or 65-67 with full benefits (the eligibility depends on birth date, born after 1960 and you must be 67). Since Social Security doesn't pay that much many Americans work longer, or work longer because retirement is unappealing. My uncle didn't retire from trucking until his early 70's despite having to unload the semi himself, and that's after doing that job for 40 years and having a bad back, bad shoulder, and a hip replacement. My mom (68) and an aunt (70) are still office workers. Farmers also tend to hang on, in the USA 40% of them are age 55+ and every farmer out there knows some crazy old bastard still at it deep into their 80's.
More on topic, for scientists and retirement there's a big difference between those who work in academia and those who work in private enterprise. For the latter, unless you've moved up very high in the corporate ladder you're going to retire in your 60's, assuming you haven't gotten canned and replaced with a younger, cheaper scientist. For academic scientists there's tenured professors and then there's everybody else. Postdocs either find an industry job, quit science, or move up to an academic staff science job (tenure track jobs account for much less than 1%). Academic staff scientists either transition to industry, quit science, or are forced into retirement when their professor boss retires/can't get grants. Tenured professors rarely retire. Eventually they get demoted to Professor Emeritus, typically with restrictions on their ability to recruit grad students. There will be pressure on them to downsize their lab from the university and their department, but some can continue for many years winning grants and employing postdocs, techs, staff scientists, and undergrads. Eventually their lab will shrink in numbers and they may be reduced to a tiny space nobody else wants, or just an office. I know several professors who worked/are working into their 80's with reduced lab personnel and/or space, and have heard of a few who went into their 90's. Ernst Mayr never retired, instead going out feet first at 100.
There used to be the Office of Technology Assessment, a highly respected (so much so that it has been imitated by other governments) body whose function was to advise Congress on science and technology matters. Newt Gingrich lead the Republicans in killing it off as a part of their Contract with America back in 1995. The OTA would have denied Congress the cover of ignorance when it came time to vote on this SOPA monstrosity.
"I'm sure someone will figure out a way to reflect (mirror?) back to the source."
I guess this means mirrored sunglasses are going to make a comeback. Or did they already? I don't pay attention to fashion.
"They were simply the fastest cells that were among those that were raced; many cells from various species of protists, not to mention sperm cells are capable of faster speeds than that."
The first thing that came to me was Listeria. These bacteria are intracellular pathogens, using the host cell's cytoskeleton (actin filaments) to shoot around the interior of the cell (and eventually punch through the cell wall IIRC) at 0.12-1.46 microns/sec, faster than the cells tested.
This is outside of my area of expertise, but I would think the risk to be somewhere between very low and nonexistent. Definition of species can be squishy, and ability to interbreed with members of different species in the same genus is known in mosquitoes. For example Aedes aegypti has been known to produce offspring when it mates with Aedes mascarensis, at least under laboratory conditions, but a large portion of the offspring have developmental abnormalities. So if you have these two species overlapping when this GM Ae. aegypti is released you might see some small knockdown of the Ae. mascarensis population size. Keep introducing the GM Ae. aegypti long enough and you amplify an already strong evolutionary pressure on Ae. mascarensis females to avoid mating with Ae. aegypti males. Similarly the effect of the GM Ae. aegypti on mosquito species belonging to different genera would be greatly reduced or nil; I'm not aware of any mosquitoes mating outside their genus. Again, outside my area of expertise: I'm a protein biochemist who just happens to work in a mosquito lab.
Male mosquitoes feed on nectar from flowers, in the lab we feed them sugar water. Female mosquitoes on the other hand require a blood meal for the proper development of their eggs. Mosquitoes live in the water as free swimming larvae, which will develop into similarly free-swimming pupae. When development is complete, the pupae floats to the water surface and the adult mosquito emerges. The adult mosquito stands on the water surface while its new exoskeleton and wings dry and harden. The adult mosquito can't swim, and while it can walk on water it only does so when emerging from the pupae and for some species when depositing eggs. It minimizes water walking in both cases and flies away as soon as possible. That's what makes this so cool. The female, and only the female mosquito, is stuck on the water unable to fly and practically motionless. It's a free lunch to any mosquito-eating predator around. The males on the other hand are free to escape and then free to mate and pass that gene on to their offspring--again fatal to their daughters, and no harm to their sons, who repeat the cycle.
"My question isn't so much "what could possibly go wrong", but rather "What right gives you to make such a decision for the whole world to live by".
The best source that I can find is Scientific American, and from what I've been reading over the last couple hours I wouldn't be surprised to see a book written on this project. It's got everything: oooh scary genetically engineered mosquitoes! Exotic and tropical locations! International intrigue in law, politics, academia! Skulduggery, intellectual theft, backstabbing! And possibly world-changing success in eradicating dengue!
The quick summary is that there are multiple parties involved: the Genetic Strategies for Control of Dengue Virus Transmission, an international and public-private organization that is behind the GM mosquitoes. Key members are Prof. Anthony James at UC-Irvine, and Dr. Luke Alphey at Oxitec, a UK-based biotech company. While sterile insect technique has been used in the past to eradicate one species of screwworm in the US, that same technique did not work on mosquitoes. James' group identified a gene specific to the female of the mosquito species that if targeted via genetic engineering could have a sterile insect effect analogous to the screwworms. Actual engineering of the mosquito was contracted out to Oxitec, who according to SciAm were the ones responsible for the release of the GM mosquitoes on Grand Cayman island without the knowledge of other members of the dengue control group. Prof. James apparently didn't know until Dr. Alphey publicly disclosed it 14 months after the fact. Where the regulations come in is complex. As a US-based academic researcher Prof. James is subject to ethical and biosafety guidelines of his department, UC-Irvine, the state of California, and the Federal government, plus that of the agencies that granted the funds for his research and the government of whatever country he is conducting research in. UK-based Oxitec has to play by the rules of the UK at least for work done in the UK, but the initial release of the mosquitoes was in the Caymans. Environmental regulations regarding GM mosquitoes didn't exist there according to one source I read, according to another they were brand new and it was implied that Oxitec had some involvement in their crafting. The other researchers are pissed, and Oxitec's actions threaten the extremely careful, conservative, and highly regulated GMO work that has been done in the US and other parts of the world.
"Folks, the mosquito could get extinct in a few years. Scary indeed."
Well, A mosquito species could be come extinct. According to TFA, Aedes aegypti to be exact. This particular mosquito can carry several major human pathogens including dengue hemorrhagic fever, yellow fever, and chickungunya, which are all viral diseases. Ae. aegypti originated in Africa but is now found throughout tropical and subtropical regions including the USA, where it used to be in only Florida and the southeast but has since spread north to New York and Illinois. Especially alarming is the fact that there have been outbreaks of dengue recently (in 2010 at least) in Florida.
Eradication of Ae. aegypti might not necessarily be that big of a deal environmentally. While mosquitoes are an important part of the diet of many predators, there are over 40 genera comprising thousands of species of mosquitoes. Any reasonably sized chunk of land probably has more than one species of mosquito, for example here in Wisconsin we have not less than 58 species. Even tiny Rhode Island is home to at least 46 mosquito species!
Just adding on to what PCM2 wrote, the banana variety you're thinking of was the Gros Michel, a triploid hybrid banana. There was no genetic engineering, the variety existed over a hundred years ago. It used to be the main variety of banana eaten, being sweeter and better tasting than the Cavendish, currently the most common banana. In all those old cartoons of people slipping and falling due to a banana peel, it wasn't much of an exaggeration since the peel of the Gros Michel is much slippier than the Cavendish. The Gros Michel was highly susceptible to Panama disease, a highly virulent fungal infection, and today the Gros Michel is practically extinct. A problem with bananas is that they are propagated asexually. A banana plant will last for about 25 years, but it will send out lateral roots (rhizomes) that will develop into a clone of the parent plant. There is no genetic diversity so if a fungus can parasitize and kill one plant it'll take the entire crop, which was what happened to the Gros Michel. However the Cavendish cultivar is also a clone, and is susceptible to new strains of the fungus that caused Panama disease. It's probably just a manner of time before the Cavendish goes the way of the dodo...er...Gros Michel.
There are limitations to what you can do with plants through selective breeding, particularly for crop species which have extremely low genetic diversity, which leads us to genetic engineering. Corn is the most common GMO, but rice and cotton are definitely on the upswing. As for bananas there are field trials in the USA, Australia, Israel, and Uganda for plants with engineered resistance to viral and fungal diseases, including Panama disease. Research on nutritional enhancement of bananas, resistance to bacterial disease, and nematode pests is ongoing.