Feeling tense or worried or critical? Then you are in a perfect mood to bid on eBay. Relaxed people were willing to bid higher prices than the non-relaxed.
NEW YORK – July 28, 2011 – A forthcoming paper in the American Marketing Association's Journal of Marketing Research by Professor Michel Tuan Pham, Kravis Professor of Business, Marketing, Columbia Business School; Iris W. Hung, Assistant Professor of Marketing, NUS Business School, National University of Singapore; and Gerald J. Gorn, Wang Seng Liang Professor of Business, Marketing Area Chair Professor at the School of Business, Faculty of Business and Economics, the University of Hong Kong, finds that states of relaxation consistently increase the monetary valuations of products, actually inflating these valuations by about 10 percent.
Relaxation methods used included music and video known to induce a state of greater relaxation. The result: A willingness to pay more for products than they are worth.
After being put in either of these two states, participants were asked to assess the monetary value of a variety products through various methods. In six studies involving more than 670 participants, relaxed individuals were consistently found to value the products more highly than their less relaxed counterparts. For example, in one simulated bidding study, relaxed participants bid about 11 percent higher for a digital camera than less-relaxed participants. Whereas the less-relaxed participants' bids were close to the product's estimated market price on online auction sites, relaxed participants' bids were about 15 percent higher than the estimated market price. The same effect was observed across a large variety of products in other studies.
We need to manage our own emotions in order to optimize our capacity to make decisions in our own interest. Meanwhile, in the opposing corner of the marketplace boxing match marketers are busy trying to achieve the opposite goal.
Less friction, less power, less fuel – plowshares coated with diamond-like carbon (DLC) slide through the soil like a hot knife through butter. As a result, the tractors pulling them need less power and fuel. In some tests the power required has been reduced by more than 30 percent.
Does this sound like a good development? Not so fast. If tilling becomes cheaper we'll get more tilling and therefore more soil run-off.
Even better: eliminate tilling altogether. Not only is energy saved but the vast bulk of soil run-off is halted. One purpose for tilling is to control weeds. But other methods to do that are available. Genetically modified crops that can survive weed killers do not need tilling. An article by Francis M. Epplin, Professor of Agricultural Economics at Oklahoma State University, highlights price changes and technological changes that have made no-till farming more cost competitive.
The second factor is a reduction in the price of glyphosate. Generic glyphosate became available in 2000 after the original patent expired. The price of glyphosate (four pounds of emulsifiable concentrate per gallon) has declined from a U.S. average of $45.50 per gallon in 1999 to less than $20 per gallon in 2007. This reduction in cost for controlling summer weeds in continuous monoculture no-till winter wheat is less than half of what it was in 1990 and substantially less when adjusted for price inflation. The development and adoption of glyphosate-resistant varieties of corn, soybeans, canola, and cotton has also advanced the adoption of no-till. The development and improvement of no-till grain drills and air seeders that increase the likelihood of good soil-to-seed contact in a variety of residue and soil conditions has also advanced the adoption of no-till. An additional factor is the price of diesel fuel increased from less than $1 per gallon in 2002 to more than $2 per gallon in 2006. This price change increases the relative cost of tillage, and tips the economic balance scales in favor of no-till.
Organic no-till with cover crops and other methods of weed control are in use as well.
One of the great hopes of agriculture is development of perennial grains which do not have to be planted each year. A National Geographic article on the potential for perennial grains describes the scale of the problem the world faces with soil erosion with plowed field farming.
No-till farming and other conservation practices have reduced the rate of soil loss in the U.S. by more than 40 percent since the 1980s, but it's still around 1.7 billion tons a year. Worldwide, one estimate put the rate of soil erosion from plowed fields at ten to a hundred times the rate of soil production. "Unless this disease is checked, the human race will wilt like any other crop," Jackson wrote 30 years ago. As growing populations force farmers in poor countries onto steeper, erodible slopes, the "disease" threatens to get worse.
So diamonds for lower energy till farming? Sounds like a good idea at first glance. But I think we need to move away from the plow rather than make it better.
This Slate piece brings up a morbid truth: Even the most long lived (female) humans reach the limits of their bodies to support further life at about 114 years. Male bodies, revved up by testosterone, hit the wall sooner.
Last month, a 114-year-old former schoolteacher from Georgia named Besse Cooper became the world's oldest living person. Her predecessor, Brazil's Maria Gomes Valentim, was 114 when she died. So was the oldest living person before her, and the one before her. In fact, eight of the last nine "world's oldest" titleholders were 114 when they achieved the distinction.
The unusual outliers reached 115.
Here's the morbid part: All but two were still 114 when they passed it on. Those two? They died at 115.
One woman reached 122. Not surprising. All the parts wear out. Then comes collapse.
Radical biogerontologist Aubrey de Grey thinks we will soon have the technology to lift that limit.
Dr De Grey said: 'I'd say we have a 50/50 chance of bringing ageing under what I'd call a decisive level of medical control within the next 25 years or so. 'And what I mean by decisive is the same sort of medical control that we have over most infectious diseases today.'
To extend the life of someone who is otherwise going to die at 70 or 75 is a lot easier than raising the limit on someone who is going to die at 115. Why? At age 70 probably only one or two components are failing. Your heart or lungs or liver gives out. A cancer spreads. If you can get a replacement organ or stem cells and gene therapy to repair an organ then that can be fixed. The ability to wipe out cancer cells will prevent cancer deaths. But at age 114 most parts are failing. The size of the intervention needed is orders of magnitude larger.
To go beyond 114 years we will need therapies stretching across decades and all the organs. We should not wait for organs to fail before replacing or repairing them because it will be too risky and too much of a strain on the body to let it get sick from organ failure before doing body upgrades. A still fairly healthy body is much better able to handle the stress of organ-replacement and organ-modification surgeries.
Some Caltech researchers found that the dorsolateral prefrontal cortex (dlPFC) in the brain exerts self control to make people make healthier decisions and it is possible to make the dlPFC more active to improve your food choices.
When you decide what to eat, not only does your brain need to figure out how it feels about a food's taste versus its health benefits versus its size or even its packaging, but it needs to decide the importance of each of those attributes relative to the others. And it needs to do all of this more-or-less instantaneously.
Antonio Rangel, professor of economics and neuroscience at Caltech, has been studying this value-deriving and decision-making process for years now. Along with Todd Hare—a former postdoc at Caltech who is now an assistant professor of neuroeconomics at the University of Zurich in Switzerland—he published a paper in Science in 2009 describing differences in the brains of people who are better at exercising self-control than others. What they found was that while everyone uses the same area of the brain—the ventral medial prefrontal cortex, or vmPFC—to make value-laden decisions like what to munch on, there's a second brain area—the dorsolateral prefrontal cortex, or dlPFC—that seems to come to life when a person is using self-control during the decision-making process.
In other words, when the dlPFC is active, it allows the vmPFC to take into account health benefits as well as taste when it assigns a value to a particular food.
Imagine a gene therapy or cell therapy that long term boosts the level of dlPFC activity to basically change your preferences for food and likely for other things as well.
Before showing series of pictures of food to say yes or no to the researchers showed one of the messages "consider the healthiness," "consider the tastiness," or "make decisions naturally." The "consider the healthiness" image caused subjects to choose healthier foods and that image made their dorsolateral prefrontal cortex more active.
Things got interesting when the researchers looked at the other three categories, however. Among their findings:
- When thinking about healthiness, subjects were less likely to eat unhealthy foods, whether or not they deemed them to be tasty, and more likely to eat healthy-untasty foods.
- Being asked to think about healthiness led subjects to say "no" to foods more often than they did when asked to make decisions naturally.
- There were no real differences between the choices made during the "consider the tastiness" and "make decisions naturally" portions of the experiment.
When the researchers turned to the fMRI results, they found that the vmPFC was, as predicted, "more responsive to the healthiness of food in the presence of health cues," says Rangel. And, as they'd seen previously, the robustness of that response was due to the influence of the dlPFC—that bastion of self-control—which was much quieter when the study's subjects were thinking about taste or their own personal choice than when they were asked to throw healthiness into the equation.
How about "consider the healthiness" pasted in your refrigerator door? Where its really needed: on the entrance of fast food joints.
While the rabbits are still gloating about gene therapy to prevent clogged rabbit arteries the mice are are cheering development of the capability to grow replacement mouse teeth. Japanese researchers have successfully grown full teeth from stem cells in a mold and then transplanted the teeth into one month old mice. The teeth enabled the mice to chew and eat.
Here is the abstract from the Plos One research report. Note that you can read the full article for free.
Donor organ transplantation is currently an essential therapeutic approach to the replacement of a dysfunctional organ as a result of disease, injury or aging in vivo. Recent progress in the area of regenerative therapy has the potential to lead to bioengineered mature organ replacement in the future. In this proof of concept study, we here report a further development in this regard in which a bioengineered tooth unit comprising mature tooth, periodontal ligament and alveolar bone, was successfully transplanted into a properly-sized bony hole in the alveolar bone through bone integration by recipient bone remodeling in a murine transplantation model system. The bioengineered tooth unit restored enough the alveolar bone in a vertical direction into an extensive bone defect of murine lower jaw. Engrafted bioengineered tooth displayed physiological tooth functions such as mastication, periodontal ligament function for bone remodeling and responsiveness to noxious stimulations. This study thus represents a substantial advance and demonstrates the real potential for bioengineered mature organ replacement as a next generation regenerative therapy.
The significance here isn't just in the ability to grow teeth. The jaw responded to the teeth by growing supporting bone and nerves. The bone growth wasn't enough to restore full normal bone support. So there's still a need to develop methods to control bone growth. But the result suggests the potential to achieve full restoration of both bone and teeth after periodontal disease or trauma.
The era of regenerative medicine is drawing near.
Plastic feedstock made from sugar cane in Brazil might be competitive with oil-based plastic.
Making plastic from sugar can be just as cheap as making it from petroleum, says Dow Chemical. The company plans to build a plant in Brazil that it says will be the world's largest facility for making polymers from plants.
If transportation can be shifted to electric power and then biomass only gets used to make plastics can enough biomass starter material be grown for this purpose? Trying to move all transportation to biomass liquid fuels seems like a non-starter. Not enough tillable land to do that.
If electric vehicles are going to become cheaper that change hasn't started happening yet. Nissan raises the price on the EV Leaf in order to add features needed in colder states.
Nissan said the 2012 Leaf, which goes on sale in the fall, will cost at least $2,450 more than the 2011 model, but perform better in colder climates, with features like a battery warmer, heated seats and a heated steering wheel.
The new price, $36,050 will bring it closer to the new (and lower) $39,995 price for the Chevy Volt. That latter price cut was made possible by cutting out a nav system.
Maybe component costs for an EV are falling even as prices rise. Our ability to migrate away from oil depends heavily on a shift to electric power. Though fortunately we can get some pretty big improvements in fuel efficiency at price points below those for pure EVs. See more here. Caveat: We can't predict the costs of batteries, lighter materials, and other fuel savings technologies 10 or 15 years in advance. Commodity costs, energy costs, and innovations are all unknowns that far out.
A number of drugs can help lower dangerously high cholesterol, but as many as half a million people worldwide are resistant to existing therapies. Alnylam Pharmaceuticals, a leader in the development of therapies using RNA, aims to begin human tests of a treatment that could make a drastic dent in drug-resistant high cholesterol.
Another drug for lowering cholesterol is not so important in the long run. What is at stake: If an RNA drug can work then that opens the door to a huge number of highly effective drugs that can do things that conventional chemical compound drugs can never do. An RNA drug delivers more information and can alter the cell's execution of its own genetic programming in very precise ways. RNA drugs could lead to a huge surge in new therapies to instruct cells do cease harmful activities and instead do repair and clean-up.
A fluorescent dye injected into the skin will change its fluorescence based on concentrations of a target chemical in the blood (e.g. sodium or sugar) and then a smart phone add-on can read the dye to measure blood levels of a the chemical of interest.
Using a nanosensor "tattoo" and a modified iPhone, cyclists could closely monitor sodium levels to prevent dehydration, and anemic patients could track their blood oxygen levels.
Heather Clark, a professor in the Department of Pharmaceutical Sciences at Northeastern University, is leading a team working to make this possible. The team begins by injecting a solution containing carefully chosen nanoparticles into the skin.
You can imagine a series of small bars of dyes added to the skin to measure different chemicals. Reading it would be akin to doing bar code reading except each bar could indicate levels of a different blood chemical: sodium, potassium, glucose, etc.
This is part of a larger trend: direct consumer measurement of one's own body. Some of that measuring is going to be embedded in your environment. Imagine a toilet and sink that measure your excretions and logs them either to a home or cloud medical diagnostics server. Your bed stand will monitor your gases for signs of poor cardiovascular performance or sleep apnea. Will pillows monitor brain waves for sleep quality?
Rabbits the world over are celebrating the good news that a gene therapy for rabbits prevents clogging up of arteries. Rats and mice seethe in jealousy and resentment.
A one-dose method for delivering gene therapy into an arterial wall effectively protects the artery from developing atherosclerosis despite ongoing high blood cholesterol. The promising results, published July 19 in the journal Molecular Therapy, came from research in rabbits.
The gene therapy turns on a protein thought to be involved in delivering the benefits of high HDL blood cholesterol.
The deployed gene produces a protein that is likely responsible for the beneficial effects of high-density lipoprotein, or HDL, commonly known as good cholesterol.
This substance is apolipoprotein A-1, or apoA-1. It pumps out harmful cholesterol from the scavenger-type cells that ingest fats and congregate in early atherosclerotic lesions.
ApoA-1 appears to remove cholesterol from the lesions and is capable of transporting it to the liver, where it can be excreted from the body.
Why take daily drugs for decades when you can reprogram the body to do something better?
"Localized one-time gene therapy might someday be an alternative or an important adjunct to systemic drugs such as statins that patients take for decades," Dichek said. "In gene-therapy trials for other diseases, one-time treatments have shown efficacy for at least nine years and will likely continue to be effective indefinitely. Because atherosclerosis is a life-long threat, gene therapy that protects blood vessels for a lifetime makes a lot of sense."
What I'd like to see: a gene therapy that is tied to activator and deactivator drugs. If this gene therapy is done and lasts for decades you could find yourself with a serious problem if a dangerous side effect turned up 5 or 10 years later. Better to have some way to limit the duration of the therapy.
A pair of collections of cells known as the suprachiasmatic nucleus at the base of the brain in the hypothalamus regulate the body's circadian rhythm as the sun goes up and down. As we age those cells do a poorer job of putting out a wave signal that orchestrates the complex mechanisms that make us wake up and go to sleep.
A new study of the brain's master circadian clock — known as the suprachiasmatic nucleus, or SCN — reveals that a key pattern of rhythmic neural activity begins to decline by middle age. The study, whose senior author is UCLA Chancellor Gene Block, may have implications for the large number of older people who have difficulty sleeping and adjusting to time changes.
Can't sleep as well as you get older? A really small number of cells is at fault. Imagine how much better you'd sleep if several thousand cells could get rejuvenated or replaced.
Sleep quality declines as people age. This is yet another reminder: aging sucks. Really. Totally. There's no upside.
"Aging has a profound effect on circadian timing," said Block, a professor of psychiatry and biobehavioral sciences and of physiological science. "It is very clear that animals' circadian systems begin to deteriorate as they age, and humans have enormous problems with the quality of their sleep as they age, difficulty adjusting to time-zone changes and difficulty performing shift-work, as well as less alertness when awake. There is a real change in the sleep–wake cycle.
This result reminds me of the vicious cycles that drive much of aging. Deterioration of sleep quality reduces the repair that happens to the body as we sleep. This accelerates aging, including aging of components that regulate sleep.
With age the signal level from the SCN does not go down as far at night.
"In the middle-aged mice, they still have a circadian rhythm, but the amplitude is reduced," Block said. "During the nighttime, when electrical impulse activity levels are usually fairly low, the levels have increased. Thus, the difference between the highest levels of activity during the daytime and the lowest levels of activity during the nighttime is much smaller in the middle-aged mice."
We need a way to do periodic service on the SCN. Replace some worn out neurons and support cells perhaps. But that's going to be tricky to do in a highly targeted way. Another recent report shows that neural stem cells need a supporting cell type to enable them to replicate. Creating a local environment with the right supporting cells orchestrated to do the needed repair operations might turn out to be very difficult. Will it be enough to get the right cell type delivered to the right area? Or will 3-D scaffolding on a miniature scale be needed?
CHICAGO -- New research published online today in Circulation Research found that injections of adult patients' own CD34+ stem cells reduced reports of angina episodes and improved exercise tolerance time in patients with chronic, severe refractory angina (severe chest discomfort that did not respond to other therapeutic options).
The phase II prospective, double-blind, randomized, controlled clinical trial was conducted at 26 centers in the United States, and is part of a long-term collaboration between researchers at Northwestern University Feinberg School of Medicine and Baxter International Inc. The objective of the trial was to determine whether delivery of autologous (meaning one's own) CD34+ stem cells directly into multiple targeted sites in the heart might reduce the frequency of angina episodes in patients suffering from chronic severe refractory angina, under the hypothesis that CD34+ stem cells may be involved in the creation of new blood vessels and increase tissue perfusion.
CD34+ cells are thought to be involved in capillary formation. Angina is caused by poor circulation of oxygen and nutrients to the heart.
By a few measures the treated groups did better.
At six months after treatment, patients in the low-dose treatment group reported significantly fewer episodes of angina than patients in the control group (6.8 vs. 10.9 episodes per week), and maintained lower episodes at one year after treatment (6.3 vs. 11 episodes per week). Additionally, the low-dose treatment group was able to exercise (on a treadmill) significantly longer at six months after treatment, as compared with those in the control group (139 seconds vs. 69 seconds, on average). Angina episodes and exercise tolerance rates were also improved in the high-dose treated group at six months and at one year post treatment compared to the control group.
Just growing up one's own stem cells outside of the body to be injected into disease sites can stimulate body repair. This seems like a rather blunt instrument approach even though it works. Treatments that involve creating local chemical signals to bring stem cells and other cells to a site to do repair will also some day accomplish the same outcome without the need for growing cells outside the body. But if stem cell therapies are easy to get going now then it makes sense to work on them first.
Want to get away from nuclear power and all that runs on nuclear power? Your only choice: move off planet. Half the heat energy from Earth's core comes from nuclear fission. Advocates of geothermal power are really advocates of nuclear fission power. By contrast, advocates of solar energy are really advocates of nuclear fusion power.
What spreads the sea floors and moves the continents? What melts iron in the outer core and enables the Earth's magnetic field? Heat. Geologists have used temperature measurements from more than 20,000 boreholes around the world to estimate that some 44 terawatts (44 trillion watts) of heat continually flow from Earth's interior into space. Where does it come from?
Radioactive decay of uranium, thorium, and potassium in Earth's crust and mantle is a principal source, and in 2005 scientists in the KamLAND collaboration, based in Japan, first showed that there was a way to measure the contribution directly. The trick was to catch what KamLAND dubbed geoneutrinos – more precisely, geo-antineutrinos – emitted when radioactive isotopes decay. (KamLAND stands for Kamioka Liquid-scintillator Antineutrino Detector.)
One thing that's at least 97-percent certain is that radioactive decay supplies only about half the Earth's heat. Other sources – primordial heat left over from the planet's formation, and possibly others as well – must account for the rest.
While the debate about the practicality of thorium nuclear energy still rages Earth is already getting as much energy from thorium as from uranium.
All models of the inner Earth depend on indirect evidence. Leading models of the kind known as bulk silicate Earth (BSE) assume that the mantle and crust contain only lithophiles ("rock-loving" elements) and the core contains only siderophiles (elements that "like to be with iron"). Thus all the heat from radioactive decay comes from the crust and mantle – about eight terawatts from uranium 238 (238U), another eight terawatts from thorium 232 (232Th), and four terawatts from potassium 40 (40K).
Suppose you want to get away from Earth's nuclear power. Where to go? Near as I can tell the the iron sulfur core of Mars has little or no nuclear fission going on. So Mars looks like a good zone for nuclear-free living. Though being so far from the Sun I'm wondering how life there can be made to work without fusion reactors. Does the Mars crust provide the materials needed to make massive solar panel installations and batteries?
Sam W. Lee and Anna Mandinova of Massachusetts General Hospital have accidentally discovered a compound that kills cancer cells by suppressing enzymes that detoxify free radicals.
A cancer cell may seem out of control, growing wildly and breaking all the rules of orderly cell life and death. But amid the seeming chaos there is a balance between a cancer cell's revved-up metabolism and skyrocketing levels of cellular stress. Just as a cancer cell depends on a hyperactive metabolism to fuel its rapid growth, it also depends on anti-oxidative enzymes to quench potentially toxic reactive oxygen species (ROS) generated by such high metabolic demand.
Scientists at the Broad Institute and Massachusetts General Hospital (MGH) have discovered a novel compound that blocks this response to oxidative stress selectively in cancer cells but spares normal cells, with an effectiveness that surpassed a chemotherapy drug currently used to treat breast cancer. Their findings, based on experiments in cell culture and in mice, appear online in Nature on July 13.
The plant-based compound piperlongumine (PL), derived from the fruit of a pepper plant found in southern India and southeast Asia, appears to kill cancer cells by jamming the machinery that dissipates high oxidative stress and the resulting ROS. Normal cells have low levels of ROS, in tune with their more modest metabolism, so they don't need high levels of the anti-oxidant enzymes that PL stymies once they pass a certain threshold.
Cancer cells generate a lot more toxic reactive oxygen species (ROS) because cancer cells grow at a fast rate. Cancer cells have faster rates of metabolism. So a drug that inhibits the cell's defenses against ROS will selectively cause much higher ROS concentration in cancer cells than in normal cells.
Since normal cells do not generate ROS in quantities that are immediately toxic the drug appears to be highly selective for cancer cells.
The scientists tested PL against cancer cells and normal cells engineered to develop cancer. In mice injected with human bladder, breast, lung, or melanoma cancer cells, PL inhibited tumor growth but showed no toxicity in normal mice. In a tougher test of mice that developed breast cancer spontaneously, PL blocked both tumor growth and metastasis. In contrast, the chemotherapy drug paclitaxel (Taxol) was less effective, even at high levels.
"This compound is selectively reducing the enzyme activity involved in oxidative stress balance in cancer cells, so the ROS level can go up above the threshold for cell death," said Lee, a Broad associate member and associate director of CBRC at MGH. "We hope we can use this compound as a starting point for the development of a drug so patients can benefit."
It'll probably be years before this drug (or drugs like it) get tried in humans in clinical trials. But since this compound is found in pepper plants it might be possible to get the compound outside of medical channels of distribution. If I had fatal cancer I would try to get some of it to try.blockquote>
Maybe we are in a "supersymmetric multiverse with vanishing cosmological constant" where the multiverse is the same as quantum mechanics idea of the universe being a range of probabilities.
Today, Leonard Susskind at Stanford University in Palo Alto and Raphael Bousso at the University of California, Berkeley, put forward the idea that the multiverse and the many worlds interpretation of quantum mechanics are formally equivalent.
But there is a caveat. The equivalence only holds if both quantum mechanics and the multiverse take special forms.
Could this theory be true? I have no idea. Neither do these guys at Berkeley and Stanford. But that isn't the point, is it? The point is that a multiverse would be really fun (though risky) if you could imagine to cruise around between universes.
One of my favorite fantasies: traveling between parallel universes in the multiverse. Imagine worlds that were causally identical to current Earth until 500 or 1000 or 2000 years ago. How might they differ starting with the smallest quantum fluctuation? Go back further. Imagine an Earth that split off from our Earth some millions of years ago that does not have humans on it. Would it be in an ice age now due to lower atmospheric CO2? The real estate would be very cheap.
If one could find worlds more technologically advanced one could use that tech (e.g. robots, AI, nanotech factories, rejuvenation tech using microfluidic devices) to an unpopulated world and create a luxurious community in a clean environment with no terrorism or pollution or resource depletion. On the other hand, if multiverse travel is possible how soon till multiverse invasions by hostile species?
Travel between stars looks so hard that theories about the multiverse become much more appealing. If we can' travel around at warp speed then we need a way to slide between universes.
Christopher Mims says The Internet Is Filling Up with Dead People and There's Nothing We Can Do About It. Why this is coming up: One's GMail email history gets used by Google+ (which I had to join just to be a chic early adopter) to recommend putting into social circles. So suddenly a piece of software is recommending adding dead people and old lovers to circles.
Naturally this sent my mind on a tangent: When will algorithms for processing the text history of social media discussion forums become powerful enough to basically fake being you? Imagine years of your postings on Facebook or Google+ (G+) processed by some fancy algorithms that use all that material to try to act like a Turing machine and fool others into thinking they are really interacting with you.
I can see how to sort of wade into this in a way that is pretty cool. Suppose you write something on your G+ stream and friends comment. You could click some button to ask for assistance in writing a response. The server software could suggest jokes or bring up points you've previously made and it could even suggest recent news articles that have points you could use.
Take this even further and before you even write in your stream (or blog as the case might be) the tool could suggest topics to comment about. In a way this is what Google News is already doing when it suggests news items that match with your previous clicking history. But combine your posting history with your clicking history and it should be possible to suggest more appropriate articles to read and points to make to your social circles about them.
So the development of the Turing Machine could come gradually. At some point you could die (or just go on a sailing trip off the web) and the Turing Machine would carry on generating content like you were still there. So the internet would really fill up with content generated by dead people - or at least simulations of dead people.
Kyle Munkittrick argues we need cognitive enhancement to deal with existential threats.
The reason I use Ender’s Game as an example is that we human beings face a lot of existential threats. We have our current challenges such as climate change, over-population, the looming health care crisis, and the ever present threat of global nuclear war (forgot about that one for a while there, didn’t ya?); not to mention the improbable but possible future-threats of asteroid impact, AI uprising, or alien invasion. Having more rather than less great minds to work together to solve these problems could be the difference between human survival and extinction.
But, as it stands, the number of geniuses among humanity is a result of genetic statistical probability. Even in Ender’s Game, the generals fear that if Ender is hurt or killed there will be no one to replace him, dooming humanity. That’s where human cognitive enhancement comes in. Be it by genetic engineering, cognition-enhancing drugs, cybernetic-augmentation or some combination of the three, we will have the ability within this century to make most, if not all people, more intelligent. The emergent benefits for humanity that would result of an intelligence boom of this scale could be immense.
This brings up a question I've wondered about: Can genetic engineering to enhance IQ make us smart enough to avoid getting wiped out by artificial intelligences? If genetic engineering can do that (big if) will the genetic engineering come soon enough? Can we create and mature enough human geniuses to build anti-AI defenses (or controls inside of A.I.s) before A.I.s emerge that look at us as little dummies to be snuffed out?
The BGI-Shenzhen project to try to identify IQ genes is practical to try due to an acceleration in the rate of decline in DNA sequencing costs. The sudden acceleration in decline of DNA sequencing costs that started in October 2007 might give us the edge we need to find ways to make geniuses who can defeat killer A.I.s. It depends on how soon A.I. emerges. When will that happen? I'm thinking genetic engineering of offspring starts in about 20 years or less. But even after the first genetically engineered genius baby is born that baby is many years away from becoming a matrix warrior.
We face other existential threats as well. Asteroids, massive volcanic eruptions, and other natural threats come to mind. Geniuses are a big help against natural threats. But the creation of huge numbers of geniuses will enable many more technological threats too such as mass killer pathogens and even A.I. So will a hundred million 160+ IQ geniuses help or hurt assure our survival? Even if they are genetically engineered to feel strong empathy for humans at least geniuses will want to protect us from A.I. So once A.I.s exist more geniuses seem like an asset overall. But will they accidentally create dangerous A.I.s that will be all that more effective because of the geniuses who did the design work that will make A.I.s possible?
To put it another way: The existence of more geniuses accelerate the development of A.I. On the other hand, once A.I. exists we are better off with more geniuses to manage A.I.s. Yet more geniuses means more innovation to make A.I.s more intellectually capable. I'm not clear on how this will balance out in terms of risks.
Even if more human geniuses get produced by genetic engineering before artificial intelligence is realized does AI doom us anyhow because geniuses will underestimate the threat? This becomes a plausible idea if even geniuses suffer from the Dunning-Kruger Effect. The Dunning-Kruger Effect? Yes, the Dunning-Kruger Effect. It could doom us to being wiped out by hostile A.I.'s.
As you can read at that link, Cornell professor of social psychology David Dunning and his then grad student Justin Kruger did some cool experiments showing that incompetent people are not competent enough in self evaluation to know they are incompetent. People don't know their limits. People assume they can model what's important about their place in the world and make decisions wisely.
What I want to know about the Dunning-Kruger Effect: At higher levels of human intelligence does the mind do a much better job of understanding its own limitations? Will geniuses develop deep enough understandings of limits of their software development skills that they won't overestimate their ability to control artificial intelligences? Or will their excessive regard for their own abilities doom us as they try to make systems too complex for them to understand and control?
Some U Penn researchers injected RNA from heart cells into astrocytes and fibroblasts and in each case the cells converted into the cell type that the RNA came from.
PHILADELPHIA - For the past decade, researchers have tried to reprogram the identity of all kinds of cell types. Heart cells are one of the most sought-after cells in regenerative medicine because researchers anticipate that they may help to repair injured hearts by replacing lost tissue. Now, researchers at the Perelman School of Medicine at the University of Pennsylvania are the first to demonstrate the direct conversion of a non-heart cell type into a heart cell by RNA transfer. Working on the idea that the signature of a cell is defined by molecules called messenger RNAs (mRNAs), which contain the chemical blueprint for how to make a protein, the investigators changed two different cell types, an astrocyte (a star-shaped brain cell) and a fibroblast (a skin cell), into a heart cell, using mRNAs.
James Eberwine, PhD, the Elmer Holmes Bobst Professor of Pharmacology, Tae Kyung Kim, PhD, post-doctoral fellow, and colleagues report their findings online this week in the Proceedings of the National Academy of Sciences. This approach offers the possibility for cell-based therapy for cardiovascular diseases.
Note that the starting cell types were not stem cells. Neither adult or embryonic stem cells were needed as a starting point. This opens up a much longer list of sources of cells to make cell therapies. Continued refinements of techniques to convert cells into other cell types will lead to cell therapies for a great many diseases. Got a bad joint or muscle? Cell therapies are the ticket.
This opens up the possibility of converting just about any cell type to any other cell type.
"What's new about this approach for heart-cell generation is that we directly converted one cell type to another using RNA, without an intermediate step," explains Eberwine. The scientists put an excess of heart cell mRNAs into either astrocytes or fibroblasts using lipid-mediated transfection, and the host cell does the rest. These RNA populations (through translation or by modulation of the expression of other RNAs) direct DNA in the host nucleus to change the cell's RNA populations to that of the destination cell type (heart cell, or tCardiomyocyte), which in turn changes the phenotype of the host cell into the destination cell.
I see potential downsides: If the RNA is from the same person who needs, say, a heart cell therapy it is possible that an undesirable expression pattern of RNA in that person's diseased heart could be replicated in the converted cells. So can one use RNA from a different person's cells to cause the conversion?
Transcriptome Induced Phenotype Remodeling, or TIPeR:
The method the group used, called Transcriptome Induced Phenotype Remodeling, or TIPeR, is distinct from the induced pluripotent stem cell (iPS) approach used by many labs in that host cells do not have to be dedifferentiated to a pluripotent state and then redifferentiated with growth factors to the destination cell type. TIPeR is more similar to prior nuclear transfer work in which the nucleus of one cell is transferred into another cell where upon the transferred nucleus then directs the cell to change its phenotype based upon the RNAs that are made. The tCardiomyocyte work follows directly from earlier work from the Eberwine lab, where neurons were converted into tAstrocytes using the TIPeR process.
There are still more hurdles to making a useful cell therapy. How thorough and complete is the change in cell type? Is there a need to carefully select starting cells to screen out mutations? Does old age of the starter cells make the new cells less able to replicate and function in a heart or other organ?
My guess is that the need to screen the starter cells to identify cells that are not aged is going to be a key problem to solve to make the most effective therapies for older people.
John M. Logsdon, a member of the 2003 Columbia Accident Investigation Board, ays it is doubtful that the US Space Shuttle was worth the money spent on it.
But were these considerable benefits worth the $209.1 billion (in 2010 dollars) that the program cost? I doubt it. The shuttle was much more expensive than anyone anticipated at its inception. Then-NASA administrator James Fletcher told Congress in 1972 that the shuttle would cost $5.15 billion to develop and could be operated at a cost of $10.5 million per flight. NASA only slightly overran development costs, which is normal for a challenging technological effort, but the cost of operating the shuttle turned out to be at least 20 times higher than was projected at the program's start.
The Shuttle came nowhere close to the cheap space bus image used to promote its construction.
The Columbia Accident Investigation Board (CAIB) found that the technical goals of the Shuttle made it riskier to operate than a design with more limited objectives.
It is the Board's view that, in retrospect, the increased complexity of a Shuttle designed to be all things to all people created inherently greater risks than if more realistic technical goals had been set at the start. Designing a reusable spacecraft that is also cost-effective is a daunting engineering challenge; doing so on a tightly constrained budget is even more difficult. Nevertheless, the remarkable system we have today is a reflection of the tremendous engineering expertise and dedication of the workforce that designed and built the Space Shuttle within the constraints it was given.
In the end, the greatest compromise NASA made was not so much with any particular element of the technical design, but rather with the premise of the vehicle itself. NASA promised it could develop a Shuttle that would be launched almost on demand and would fly many missions each year. Throughout the history of the program, a gap has persisted between the rhetoric NASA has used to market the Space Shuttle and operational reality, leading to an enduring image of the Shuttle as capable of safely and routinely carrying out missions with little risk.
General rocket failure rates are so high that manned flight needs capsules or small spacecraft for humans that can survive failure of rockets.
But with the end of the Shuttle program we lose some capabilities. James Oberg points to a half dozen capabilities unique to the shuttle.
Robert K. Kaufmann of Boston University and a few other researchers have proposed a theory to explain why global warming basically stopped for about 10 years: sulfur aerosols emissions from China's big surge in coal burning (doubling from 2003 to 2007!) have canceled out most of the warming effects of higher carbon dioxide. Accidental large-scale climate engineering. What a fascinating experiment. Massive sulfur never would have been politically approved as an intentional intervention for cooling.
Given the widely noted increase in the warming effects of rising greenhouse gas concentrations, it has been unclear why global surface temperatures did not rise between 1998 and 2008. We find that this hiatus in warming coincides with a period of little increase in the sum of anthropogenic and natural forcings. Declining solar insolation as part of a normal eleven-year cycle, and a cyclical change from an El Nino to a La Nina dominate our measure of anthropogenic effects because rapid growth in short-lived sulfur emissions partially offsets rising greenhouse gas concentrations.
CO2's half-life in the atmosphere is decades (centuries?) longer than sulfur's. So these effects of sulfur are short-lived. Worse, attempts to reduce sulfur emissions to cut ground-level pollution can cause a rapid decrease in sulfur aerosol cooling effects.
This idea is at least plausible because sulfur aerosols have a cooling effect. In fact, Nobel Prize winning chemist Paul Crutzen has proposed injecting sulfur into the atmosphere to cool the planet. By using airplanes to inject sulfur aerosols at high altitudes the half-life of sulfur in the atmosphere can be boosted to a year and a half.
There are downsides to this approach to climate engineering. For example, by making more light diffuse sulfur will reduce the output of concentrating solar power by as much as a fifth. But it beats melting all the ice in Greenland.
I realize many are skeptics about the role of CO2 in warming the planet. But if sulfur's role as a cooler is real then China's big burst in dirty coal burning has to have prevented a warmer planet.
WHAT: A trio of large-scale genome-wide association studies, or GWAS, have identified more than 15 gene variants responsible for the diversity of white blood cell counts among whites, African-Americans, and Japanese. Supported in part by the National Institutes of Health, each study examined the genomes of tens of thousands of people. Combined, the studies offer the first comprehensive analysis into why some people, and some populations, have more or fewer white blood cells than others.
All three articles will be published online June 30 in PLoS Genetics.
White blood cells are part of the immune system, which fights infections and diseases. Measuring white blood cell levels is a common diagnostic test that can reveal underlying infections, cancers, or immune system disorders. Some scientific studies have also linked higher levels of white blood cells to increased risk of disease, including heart disease.
Different genetic variants influence immune function in different ways. One of the benefits of studying genetic variants is that it leads to the identification of which genes play a role in which metabolic subsystems and organs.
Some of the identified gene variants were responsible for altering total numbers of white blood cells, while other variants affected only one specific cell subtype, such as neutrophils, basophils, eosinophils, lymphocytes, and monocytes.
The findings could lead to important clinical advances. For example, these gene variants could be tested to pinpoint disease risks earlier in life. In addition, understanding the genetic basis behind altered white blood cell counts might also lead to gene therapies, such as boosting white blood cells in immune compromised people or reducing them in leukemia patients.
What is so important about genetic variants that influence immune function? Researchers at Wake Forest U found that mice differ greatly in how well their immune systems attack cancer cells and so do humans. So one reason to care about immune system genetic variants is that some variants could probably substantially reduce our risk of cancer if we could get our immune systems upgraded with some gene therapy.We need immune system upgrades anyway just to reverse the effects of immune system aging. That immune system aging doesn't just put us at greater risk of death from infection. As the immune system ages it becomes less able to kill cancer cells. It probably also becomes less able to remove intercellular debris. So immune system rejuvenation would cut our death risk from multiple causes.
You can read the 3 papers on genetic variants in immune systems: Multiple Loci Are Associated with White Blood Cell Phenotypes, Genome-Wide Association Study of White Blood Cell Count in 16,388 African Americans: the Continental Origins and Genetic Epidemiology Network (COGENT), and Identification of Nine Novel Loci Associated with White Blood Cell Subtypes in a Japanese Population.
BOSTON (July 1) -- Eating a diet high in vitamin D, as well as the nutrients betaine and methionine, might help reduce the risk of macular degeneration, according to new research conducted by Tufts Medical Center scientists. Their study of identical twins from the US World War II Twin Registry also found that the more a person smoked, the higher their risk of developing macular degeneration. The study, "Smoking, Dietary Betaine, Methionine, and Vitamin D in Monozygotic Twins with Discordant Macular Degeneration: Epigenetic Implications” published in the journal Ophthalmology on July 1, is the first to look at identical twin pairs in which one twin had early age-related macular degeneration (AMD), and the other had late stage AMD.
Eat your spinach with fish or poultry.
Similarly, Dr. Seddon’s research team also found that higher intakes of betaine and methionine were linked to a slower progression of the disease. These nutrients have also been linked to epigenetic mechanisms, which is a change in DNA, not attributable to a change in the actual DNA sequence. Betaine is found in fish, grains and spinach, while methionine is found in poultry, fish and dairy foods.
Light Emitting Diodes (LEDs) are expected by some observers to become so cheap, efficient, and long-lasting that they will displace fluorescent light bulbs. Francis Rubinstein, a scientist in the Lawrence Berkeley National Laboratory's Environmental Energy Technologies Division, says the imminent death of fluorescent lighting at the hands of LEDs has been exaggerated.
"The common view," says Francis Rubinstein, a scientist and energy-efficient lighting expert at Lawrence Berkeley National Laboratory's Environmental Energy Technologies Division, "is that LED lighting is replacing fluorescent lighting with the same inevitability that mammals replaced dinosaurs as the dominant large life forms on Earth."
But wait, says Rubinstein, who has been delivering a talk to lighting industry audiences titled "Why Fluorescent Lighting Isn't Dead." He believes that modern fluorescent lighting will continue to dominate the general lighting market and that solid-state LED lighting will coexist in the marketplace with fluorescent lighting for some time to come. Rubinstein sees a near-term future in which LED and fluorescent lighting coexist in hybrid systems that will be more adaptable to the lighting needs of a wide variety of residential, commercial, and industrial building types and space configurations.
Established technologies often last way longer than expected. Look at the 4 stroke internal combustion engine (ICE). The Wankel rotary failed to displace it. Hydrogen fuel cells are still a long way off. Previous attempts to commercialize electric vehicles have failed. This time around high oil prices and advances in battery tech suggest better prospects for EV. But while projections for electric vehicle sales in 2020 vary over a wide range none of the estimates I've found have EVs replacing the ICE from the top spot by 2020. It is hard to unseat the incumbent because incumbent technologies generate huge cash flows that help fund refinements and improvements to the incumbent's design and manufacture.
In the comments of Green Tech Media's coverage of this report you can read a few people who work in the lighting industry explaining obstacles to more widespread uptake of LEDs. Cost is not the only concern. Color quality, existing fixtures designed for fluorescents, and continued improvements in fluorescent technologies all slow down the adoption of LEDs.
Is the universe just a big computer simulation running in another universe? Suppose it is. Then I've got some questions:
Imagine the purpose of the sim is entertainment or decision-making. Either way, it could be that out-of-universe sentient beings actually enter this universe and interact with some of its intelligent entities. Interact with simulated people for fun. Or interact in order to try out different experiments of political development. In the latter case I would expect more rerunning of the same sim backed up to restart at the same point but with some alteration of what some people say or do.
So what's your (simulated) gut feeling? Are you in a sim? If so, what's it for?
Update: Some commenters wonder why simulate a whole universe unless you want to simulate intelligence? Maybe the outer universe is many orders of magnitude larger in numbers of stars and planets and they want to see what a less crowded universe would be like.
Here's an even better idea: Suppose the real outer universe has massive planets all in close proximity. Suppose they have quintillions of people who are all very similar in this highly interconnected universe. So there's no diversity of intelligent life forms. So they decided to create a universe sim where the stars are so far apart that each intelligent life form evolves separately and is different in many ways. This provides the homogeneous simulator people experience of greater differences than they can see in their own universe.
Update II: Maybe we all suffer from the Dunning-Kruger Effect and can't grasp the extent of our mental deficiencies that render us unable to grasp the motives of the sim writers. There could be motives beyond our ability to suspect or conceive.
A couple of UCSD Scripps Institute grad students find nearly a tenth of the fish in the North Pacific Subtropical Gyre have plastic in their stomachs.
Two graduate students with the Scripps Environmental Accumulation of Plastic Expedition, or SEAPLEX, found evidence of plastic waste in more than nine percent of the stomachs of fish collected during their voyage to the North Pacific Subtropical Gyre. Based on their evidence, authors Peter Davison and Rebecca Asch estimate that fish in the intermediate ocean depths of the North Pacific ingest plastic at a rate of roughly 12,000- to 24,000 tons per year.
On the bright side, Peak Oil is going to make plastic more expensive and therefore less used. Otherwise I hold out little hope for a big reduction in the amount of plastic finding its way into rivers and the ocean. Asian industrialization is boosting demand for plastic in a region where the most populated countries haven't achieved living standards high enough to spawn big environmental movements.
You can see my previous post on the plastic build-up in the Gyre. Also, the Wikipedia Great Pacific Garbage Patch page is pretty good on the topic. Lots of detail and diagrams.
A couple of physicists at Imperial College London think it is possible to create event cloaks to hide events.
In this month's special issue of Physics World, which examines the science and applications of invisibility, Martin McCall and Paul Kinsler of Imperial College London describe a new type of invisibility cloak that does not just hide objects – but events.
Using the ultimate bank heist as an example, McCall and Kinsler explain how a thief could, in principle, use an "event cloak" to steal money from a safe, without even the CCTV surveillance cameras being aware.
So what event do you most want to hide? Got something you want to do or something you want someone else to do that requires invisibility?
An event cloak could emulate a Star Trek transporter. But it still wouldn't let you beam down from an orbiting space station.
If a high-performance, macroscopic-size, fully functional space–time cloak could be developed, one potential "party trick" could be a Star Trek-type transporter, in which a person could appear to instantly relocate from one point to another.
Although no-one has yet tried to build a space–time cloak in the lab, McCall and Kinsler argue that "there is no obvious reason why such a cloak could not be achieved quite soon, perhaps even within a few years".
What I'd do with an event cloak: