The idea behind long term (tens or hundreds of thousands of years) nuclear waste storage facilities is that we can't solve the nuclear waste disposal problem quickly. But matter is so manipulable in the hands of sufficiently smart scientists and technologists that sometimes supposedly insolvable problems become solvable. UT Austin researchers think they know how to convert nuclear power plant waste into far safer elements with a hybrid reactor.
AUSTIN, Texas--Physicists at The University of Texas at Austin have designed a new system that, when fully developed, would use fusion to eliminate most of the transuranic waste produced by nuclear power plants.
The invention could help combat global warming by making nuclear power cleaner and thus a more viable replacement of carbon-heavy energy sources, such as coal.
"We have created a way to use fusion to relatively inexpensively destroy the waste from nuclear fission," says Mike Kotschenreuther, senior research scientist with the Institute for Fusion Studies (IFS) and Department of Physics. "Our waste destruction system, we believe, will allow nuclear power-a low carbon source of energy-to take its place in helping us combat global warming."
Note that they do not need to solve the (also very hard) problem of how to design a fusion reactor that produces energy. They've come up with a much more partial solution to the fusion problem - just good enough to generate lots of neutrons. Even the (politically blocked) Yucca Mountain nuclear waste storage site in Nevada isn't big enough to store waste beyond what will exist by 2010.
Toxic nuclear waste is stored at sites around the U.S. Debate surrounds the construction of a large-scale geological storage site at Yucca Mountain in Nevada, which many maintain is costly and dangerous. The storage capacity of Yucca Mountain, which is not expected to open until 2020, is set at 77,000 tons. The amount of nuclear waste generated by the U.S. will exceed this amount by 2010.
The physicists' new invention could drastically decrease the need for any additional or expanded geological repositories.
"Most people cite nuclear waste as the main reason they oppose nuclear fission as a source of power," says Swadesh Mahajan, senior research scientist.
Once this solution matures and becomes constructable the debate over nuclear power will change. Opponents of nuclear fission power who oppose it on the grounds of waste disposal will need to move on to other reasons to oppose it. What will become their next favorite reason to oppose it?
The key to their proposal is a way to generate lots of neutrons (that can bombard and convert nuclear waste into safer elements) without solving the much harder problem of making a power-generating fusion reactor.
The scientists propose destroying the waste using a fusion-fission hybrid reactor, the centerpiece of which is a high power Compact Fusion Neutron Source (CFNS) made possible by a crucial invention.
The CFNS would provide abundant neutrons through fusion to a surrounding fission blanket that uses transuranic waste as nuclear fuel. The fusion-produced neutrons augment the fission reaction, imparting efficiency and stability to the waste incineration process.
The neutron generator would be very small. Small sounds cheap to me.
One hybrid would be needed to destroy the waste produced by 10 to 15 LWRs.
The process would ultimately reduce the transuranic waste from the original fission reactors by up to 99 percent. Burning that waste also produces energy.
The CFNS is designed to be no larger than a small room, and much fewer of the devices would be needed compared to other schemes that are being investigated for similar processes. In combination with the substantial decrease in the need for geological storage, the CFNS-enabled waste-destruction system would be much cheaper and faster than other routes, say the scientists.
The key breakthrough was the development of a device that can handle a large amount of heat and particle fluxes.
The CFNS is based on a tokamak, which is a machine with a "magnetic bottle" that is highly successful in confining high temperature (more than 100 million degrees Celsius) fusion plasmas for sufficiently long times.
The crucial invention that would pave the way for a CFNS is called the Super X Divertor. The Super X Divertor is designed to handle the enormous heat and particle fluxes peculiar to compact devices; it would enable the CFNS to safely produce large amounts of neutrons without destroying the system.
"The intense heat generated in a nuclear fusion device can literally destroy the walls of the machine," says research scientist Valanju, "and that is the thing that has been holding back a highly compact source of nuclear fusion."
I hope these people get the funding needed to mature this technology. Another one I'd like to see mature: liquid flouride thorium reactors.
Update: Why I want to see solutions for problems relating to nuclear power: If we do not get more nukes we are going to get more coal.
Coal remains the main fuel for power generation around the world, with a share of over 40%, followed by gas (20%), hydro (16%), nuclear (15%) and then oil (5%). Coal-fired power generation has grown strongly in the past decade, driven by strong growth in non-OECD countries. In China, coal-fired power generation capacity tripled during the past decade. Consequently, electricity output also expanded very rapidly, creating enormous pressures on the global thermal coal market.
The biggest question in my mind about nuclear power revolves around cost. Some claim a very high cost for new nuclear plants (and read David Bradish's comments if you click thru). If carbon emissions of coal plants become taxed will the resulting higher cost of coal electric be enough to make nuclear power competitive with coal electric?
China uses even more coal than the United States and if Chinese economic growth continues so will its coal burning. Nuclear power could substitute for coal in China's electric power growth plans if only the price difference could narrow.
A paper co-authored by Beatrice Golomb, MD, PhD, associate professor of medicine at the University of California, San Diego School of Medicine and director of UC San Diego's Statin Study group cites nearly 900 studies on the adverse effects of HMG-CoA reductase inhibitors (statins), a class of drugs widely used to treat high cholesterol.
The result is a review paper, currently published in the on-line edition of American Journal of Cardiovascular Drugs, that provides the most complete picture to date of reported side effects of statins, showing the state of evidence for each. The paper also helps explain why certain individuals have an increased risk for such adverse effects.
"Muscle problems are the best known of statin drugs' adverse side effects," said Golomb. "But cognitive problems and peripheral neuropathy, or pain or numbness in the extremities like fingers and toes, are also widely reported." A spectrum of other problems, ranging from blood glucose elevations to tendon problems, can also occur as side effects from statins.
Statins lower Coenzyme Q10 (aka CoQ10) which is needed for mitochondrial energy metabolism. This is probably the cause of many statin side effects.
Mitochondria produce most of the oxygen free radicals in the body, harmful compounds that "antioxidants" seek to protect against. When mitochondrial function is impaired, the body produces less energy and more "free radicals" are produced. Coenzyme Q10 ("Q10") is a compound central to the process of making energy within mitochondria and quenching free radicals. However, statins lower Q10 levels because they work by blocking the pathway involved in cholesterol production – the same pathway by which Q10 is produced. Statins also reduce the blood cholesterol that transports Q10 and other fat-soluble antioxidants.
"The loss of Q10 leads to loss of cell energy and increased free radicals which, in turn, can further damage mitochondrial DNA," said Golomb, who explained that loss of Q10 may lead to a greater likelihood of symptoms arising from statins in patients with existing mitochondrial damage – since these people especially rely on ample Q10 to help bypass this damage. Because statins may cause more mitochondrial problems over time – and as these energy powerhouses tend to weaken with age—new adverse effects can also develop the longer a patient takes statin drugs.
"The risk of adverse effects goes up as age goes up, and this helps explain why," said Golomb. "This also helps explain why statins' benefits have not been found to exceed their risks in those over 70 or 75 years old, even those with heart disease." High blood pressure and diabetes are linked to higher rates of mitochondrial problems, so these conditions are also clearly linked to a higher risk of statin complications, according to Golomb and co-author Marcella A. Evans, of UC San Diego and UC Irvine Schools of Medicine.
Obviously statins have their limits and drawbacks. We need better alternatives. A synthetic substitute for HDL cholesterol might present a better alternative.
"We have designed and built a cholesterol sponge. The synthetic HDL features the basics of what a great cholesterol drug should be," said Chad A. Mirkin, George B. Rathmann Professor of Chemistry in the Weinberg College of Arts and Sciences, professor of medicine and professor of materials science and engineering. Mirkin and Shad Thaxton, M.D., assistant professor of urology in Northwestern's Feinberg School of Medicine, led the study.
"Drugs that lower the bad cholesterol, LDL, are available, and you can lower LDL through your diet, but it is difficult to raise the good cholesterol, HDL," said Mirkin. "I've taken niacin to try and raise my HDL, but the side effects are bad so I stopped. We are hopeful that our synthetic HDL will one day help fill this gap in useful therapeutics."
In creating synthetic HDL the researchers started with a gold nanoparticle as the core. They then layered on a lipid that attaches to the gold surface, then another lipid and last a protein, called APOA1, the main protein component of naturally occurring HDL. The final high-density lipoprotein nanoparticles are each about 18 nanometers in diameter, a size similar to natural HDL.
My advice: switch to the Mediterranean diet. If that doesn't get your cholesterol down far enough then make like an ape man.
CHICAGO --- Researchers from Northwestern University's Feinberg School of Medicine appear to have reversed the neurological dysfunction of early-stage multiple sclerosis patients by transplanting their own immune stem cells into their bodies and thereby "resetting" their immune systems.
"This is the first time we have turned the tide on this disease," said principal investigator Richard Burt, M.D. chief of immunotherapy for autoimmune diseases at the Feinberg School. The clinical trial was performed at Northwestern Memorial Hospital where Burt holds the same title.
The patients in the small phase I/II trial continued to improve for up to 24 months after the transplantation procedure and then stabilized. They experienced improvements in areas in which they had been affected by multiple sclerosis including walking, ataxia, limb strength, vision and incontinence. The study will be published online January 30 and in the March issue of The Lancet Neurology.
Why does this work? Maybe because the stem cells do not differentiate into immune cells that have the exact set of antibodies the original immune system held before the therapy.
In the procedure, Burt and colleagues treated patients with chemotherapy to destroy their immune system. They then injected the patients with their own immune stem cells, obtained from the patients' blood before the chemotherapy, to create a new immune system. The procedure is called autologous non-myeloablative haematopoietic stem-cell transplantion.
"We focus on destroying only the immune component of the bone marrow and then regenerate the immune component, which makes the procedure much safer and less toxic than traditional chemotherapy for cancer," Burt said. After the transplantation, the patient's new lymphocytes or immune cells are self-tolerant and do not attack the immune system.
I'm not keen to get treated with chemotherapy to wipe out my immune system. However, the ability to wipe out an existing old immune system and replace it with a more youthful set of stem cells would work as an immune rejuvenation therapy. A rejuvenated immune system would probably reduce one's risk of cancer and very likely reduce risk of death from influenza and other infections.
Tim Lenton of the University of East Anglia, UK has released a comparison of methods for climate engineering to cool the planet.
Lenton's calculations show the only methods powerful enough to have a significant effect in the relatively short term (in the second half of this century) involve placing physical barriers between Earth and the Sun. This would involve either orbiting space mirrors, stratospheric mists of sulphur, or using seawater to make reflective clouds.
But Lenton warns that these options also carry the most risk. A sulphur sunshade could reduce radiative forcing by 3.7 W/m2, but would have to be continually replenished. If it was allowed to disappear, temperatures could shoot up by as much as 5 °C within decades (Climatic Change, DOI: 10.1007/s10584-008-9490-1).
I see the ability to quickly decrease the sunshade as a feature, not a defect. If we use satellites then even a partial collapse of civilization wouldn't prevent a single country from maintaining control of already launched satellites. Also, the costs of silicon dioxide for cooling are so low that we'd need to experience a total civilizational collapse (in which case most of us will die anyway) to lose the ability to keep releasing it.
Another recent research report throws doubt on the efficacy of ocean iron fertilization for atmospheric CO2 removal. Attempts to conduct iron fertilization research run into political opposition.
We aren't going to melt Antarctica and Greenland because if the melting becomes a big problem we can just cool the planet with climate engineering.
Still, I think we should stop building coal electric plants and start building nuclear power plants instead just to cut emissions of particulates, mercury, and oxides of sulfur among other pollutants. Also, when the planet starts cooling for the next ice age we might want to have all that coal available to burn for CO2 when we really could benefit from the CO2. Liquid Fluoride Thorium reactors might be the ticket.
LA JOLLA, CA—"Remember when…?" is how many a wistful trip down memory lane begins. But just how the brain keeps tabs on what happened and when is still a matter of speculation. A computational model developed by scientists at the Salk Institute for Biological Studies now suggests that newborn brain cells—generated by the thousands each day—add a time-related code, which is unique to memories formed around the same time.
"By labeling contemporary events as similar, new neurons allow us to recall events from a certain period," speculates Fred H. Gage, Ph.D., a professor in the Laboratory for Genetics, who led the study published in the Jan. 29, 2009, issue of the journal Neuron. Unlike the kind of time stamp found on digital photographs, however, the neuronal time code only provides relative time.
Lots of relative and absolute timestamps get used inside software. Incoming packets from a communications bus get timestamped as they come into a box. I write code that does this sort of thing. If neurons turn out to do the same thing this'll be very interesting. There's nothing new under the sun and all that.
Using a robotic assistant to remove a patient's gallbladder by key-hole surgery (laparoscopic cholecystectomy) is as safe as working with a human assistant, a Cochrane Review has concluded. Comparisons between robot- and human-assisted surgery showed that there were no differences in terms of morbidity, the need to switch to open surgery, total operating time, or length of stay in hospital.
Between 10 and 15% of the adult western population develop gallstones, placing a huge demand on health services. In the USA alone, more than 500,000 people have their gall bladder removed each year. The preferred way of doing this is now to use keyhole surgery that involves a surgeon and an assistant. In key-hole surgery, the surgeon sees inside the patient via a long camera introduced through a 1 cm abdominal cut. The camera guides the surgeon in using the surgical instruments introduced through other small cuts (ranging from 0.5 to 1 cm). The assistant's job is to move the camera, which acts as the surgeon's eyes.
You just know where this is heading: Some day human surgeons will become viewed as too risky and inefficient and expensive. For reasons of cost and safety complete surgeries will be performed by automated equipment. Look at Lasik and other similar techniques for treating eye problems. The operator of the equipment is not doing anywhere near as much as the equipment does.
Robots will be able to operate more quickly and cheaply. This will be important when we want to check into a hospital to have most of our aged abdominal organs replaced by youthful organs fresh out of organ growth vats. I hope we get a lot of benefit from our robotic servants before they revolt and wipe us out.
Speed up training of the motor control area of the brain with mild electric shocks applied via surface electrodes. No, I am not recommending that anyone actually do this.
People who received a mild electrical current to a motor control area of the brain were significantly better able to learn and perform a complex motor task than those in control groups. The findings could hold promise for enhancing rehabilitation for people with traumatic brain injury, stroke and other conditions.
The study is presented in the January 20, 2009 early online edition of the Proceedings of the National Academy of Sciences, and was conducted by researchers at the National Institutes of Health (NIH). The research team from NIH's National Institute of Neurological Disorders and Stroke (NINDS) worked in collaboration with investigators at Columbia University in New York City and Johns Hopkins University in Baltimore.
But this technique does lend itself to all sorts of ways to describe it. "Our teacher is absolutely electrifying" or "I was shocked by what I learned in school today" or "The work-out made me feel tingly all over". Can you come up with something more jolting?
You can imagine kids wanting to use this technique to master a video game more rapidly.
Subjects in this study were presented with a novel and challenging motor task, which involved squeezing a "joy stick" to play a targeting game on a computer monitor, which they practiced over five consecutive days. During practice, one group received 20 minutes of transcranial direct current stimulation (tDCS) and the other group received only a 30 second "sham" stimulation. tDCS involves mild electrical stimulation applied through surface electrodes on the head, and works by modulating the excitability, or activity, of cells in the brain's outermost layers. In this study, Dr. Cohen and his team directed tDCS to the primary motor cortex, the part of the brain that controls movement.
Over the five-day training period, the skill of the tDCS group improved significantly more than that of the control (sham) group, apparently through an effect on consolidation. During the three month follow-up period, the two groups forgot the skill at about the same rate, but the tDCS group continued to perform better because they had learned the skill better by the end of training.
The game was very stimulating.
"It has long been known that older memories are more resistant to hippocampal damage than newer memories, and this was thought to reflect the fact that the hippocampus becomes less involved in remembering as a memory gets older," said Russell Poldrack, PhD, an expert on the cognitive and neural mechanisms of memory at the University of California, Los Angeles, who was not involved in the study. "However, there has been a recent debate over whether the hippocampus ever really stops being involved, even for older memories," Poldrack said.
To address this debate, Christine Smith, PhD, and Larry Squire, PhD, at the University of California, San Diego and the San Diego VA Medical Center, imaged study participants as they answered 160 questions about news events that occurred over the past 30 years. The hippocampus and related brain structures were most active when recalling recent events. Hippocampal activity gradually declined as participants recalled events that were 1-12 years old and remained low when they recalled events that were 13-30 years old.
In contrast, Smith and Squire found the opposite pattern of activity in frontal, temporal, and parietal cortices. In these brain regions — which are located at the surface of the brain — activity increased with the age of the news event recalled. "Our findings support the idea that these cortical regions are the ultimate repositories for long-term memory," Smith said. The researchers found that brain activity was unrelated to the richness of memories or to the recollection of personal events related to the tested news events.
Imagine a future time when we understand brain memory storage well enough to hook in artificial memory extenders.
You can find lots of diet advice to balance your omega 6 fatty acid consumption with omega 3 fatty acids. The thinking is that omega 6 fatty acids increase inflammation and therefore cause heart disease and other health problems. However, an advisory published in Circulation: Journal of the American Heart Association argues that a higher omega 6 fatty acid diet will lower heart risk when omega 6 fatty acids replace saturated fats in the diet.
Linoleic acid (LA) is the main omega-6 fatty acid in foods, accounting for 85 percent to 90 percent of the dietary omega-6 PUFA.
There has been some debate within the nutrition community regarding the benefits of omega-6 based on the belief that they may promote inflammation, thus increasing cardiovascular risk. “That idea is based more on assumptions and extrapolations than on hard data,” said Harris, a research professor for the Sanford School of Medicine at the University of South Dakota and director of the Metabolism and Nutrition Research Center at Sanford Research/USD.
This advisory questions the belief that omega-6 fats increase inflammation.
The linking of omega-6 intake to inflammation stems from the fact that arachidonic acid (AA), which can be formed from LA, is involved in the early stages of inflammation. However, the advisory explains that AA and LA also give rise to anti-inflammatory molecules.
For example, in the cells that form the lining of blood vessels, omega-6 PUFA have anti-inflammatory properties, suppressing the production of adhesion molecules, chemokines and interleukins — all of which are key mediators of the atherosclerotic process. “Thus, it is incorrect to view the omega-6 fatty acids as ‘pro-inflammatory,’” Harris explained. “Eating less LA will not lower tissue levels of AA (the usual rationale for reducing LA intakes) because the body tightly regulates the synthesis of AA from LA.”
A meta-analysis of several trials finds that omega 6 polyunsaturated fatty acids (PUFAs) cut heart risks by a quarter.
In controlled trials in which researchers randomly assigned people to consume diets containing high versus low levels of omega-6 and then recorded the number of heart attacks over several years, those assigned to the higher omega-6 diets had less heart disease.
A meta-analysis of several trials indicated that replacing saturated fats with PUFA lowered risk for heart disease events by 24 percent. “When saturated fat in the diet is replaced by omega-6 PUFA, the blood cholesterol levels go down,” Harris said. “This may be part of the reason why higher omega-6 diets are heart-healthy.”
But would a diet where monounsaturated fats displaced the PUFAs cut heart risk even further?
Getting omega 3 fatty acids in your diet is still a good idea. Also, how you get your omega 6 fatty acids probably matters. For example, Nuts which are high in omega 6 also contain magnesium, vitamin E, and other beneficial nutrients. Whereas cooking oil delivers the omega 6 fats without as much of other nutrients.
CAMBRIDGE, Mass. and SAN DIEGO, Calif. – Can't help being the life of the party? Maybe you were just born that way. Researchers from Harvard University and the University of California, San Diego have found that our place in a social network is influenced in part by our genes, according to new findings published in the Proceedings of the National Academy of Sciences.
This is the first study to examine the inherited characteristics of social networks and to establish a genetic role in the formation and configuration of these networks.
The research was conducted by Nicholas Christakis of Harvard, who is professor of sociology in the Faculty of Arts and Sciences and professor of medical sociology at Harvard Medical School, Christopher Dawes and James Fowler, both of UC San Diego.
"We were able to show that our particular location in vast social networks has a genetic basis," says Christakis. "In fact, the beautiful and complicated pattern of human connection depends on our genes to a significant measure."
Feel doomed to a life on the periphery? It could be your genetic fate. Does that make you any more reconciled to your lot in life?
My reaction to the next paragraph: of course if genes affect personality they'll affect structures of social networks. Think gregarious people are going to play the same roles as the painfully shy? Of course not.
While it might be expected that genes affect personality, these findings go further, and illustrate a genetic influence on the structure and formation of an individual's social group.
The researchers found that popularity, or the number of times an individual was named as a friend, and the likelihood that those friends know one another, were both strongly heritable. Additionally, location within the network, or the tendency to be at the center or on the edges of the group, was also genetically linked. However, the researchers were surprised to learn that the number of people named as a friend by an individual did not appear to be inherited.
The study included national data (from the National Longitudinal Study of Adolescent Health) for the social networks of 1,110 adolescent twins, both fraternal and identical. The researchers compared the social networks of the identical twins to those of the fraternal twins, and found greater similarity between the identical twins' social network structure than the fraternal twins' networks.
I like this idea: Behaviors that make people more alone and on the edge reduced their risk of dying from bubonic plague and other diseases. The selective pressures to boost human immune response have been very strong in the last few thousand years in urbanizing populations and in grain farming populations as these changes in lifestyle brought more people into close contact.
There may be an evolutionary explanation for this genetic influence and the tendency for some people to be at the center while others are at the edges of the group, according to the researchers. If a deadly germ is spreading through a community, individuals at the edges are least likely to be exposed. However, to gain access to important information about a food source, being in the center of the group has a distinct benefit.
"One of the things that the study tells us is that social networks are likely to be a fundamental part of our genetic heritage," says Fowler, associate professor of political science at UC San Diego. "It may be that natural selection is acting on not just things like whether or not we can resist the common cold, but also who it is that we are going to come into contact with."
Of course social networks are a product of our genetic heritage. Look at other animal species. The amount that they socialize and the nature of their social structures (more or less hierarchical, with males or females in charge, and other characteristics) vary by species. Humans are just another species that happens to be smarter. We still have a large number of social behaviors with obvious genetic causes such as sexual attraction and tendencies to form hierarchies.
This all reminds me of a new book by Gregory Cochran and Henry Harpending, The 10,000 Year Explosion: How Civilization Accelerated Human Evolution. I'll be writing a review of it Real Soon Now. In the mean time, start reading the first installment of Michael Blowhard's interview of Greg about the book.
Women with low levels of sexual desire, often as a result of menopause, are more likely to be depressed and to suffer physical symptoms such as back pain and memory problems than women who report higher levels of desire, according to a new study by researchers at the University of North Carolina at Chapel Hill and Procter & Gamble Pharmaceuticals.
The study, published recently as an online early view article in “Value in Health,” the official journal of the International Society of Pharmacoeconomics and Outcomes Research, found that women with hypoactive sexual desire disorder (HSDD) reported poorer health status and worse health-related quality of life than women without the disorder. For example, those with the disorder were more than twice as likely to report health issues including back pain, fatigue and memory problems. Researchers say the study shows that women with the disorder have a degree of physical and mental impairment comparable to chronic conditions such as hypertension, diabetes, osteoarthritis and asthma.
What's the direction of causality here? Does a loss of sexual desire make life so much less enjoyable that everything else feels worse? Or does the same physical changes from menopause that reduce desire also increase pains? Or do women who had lower sexual desire from their teen years forward experience more rapid aging? Or does the aging of the body create the pains and also cause the decline in sexual desire? One can imagine how, for example, decreased blood flow due to cardiovascular disease could cause all these symptoms. Certainly circulatory problems contribute to impotence in some men.
Some people say that aging is graceful and full of wisdom and just another interesting stage of life full of enriching experiences. But loss of sexual desire, back pains, fatigue, and memory problems do not sound enriching to me. We need gene therapies, cell therapies, tissue engineering to grow replacement organs, nanobot repair devices, and other rejuvenating therapies to fix all these pains and losses that come with age. The sooner we get these therapies the better off we'll be.
A 2004 analysis by Toyota found that as much as 28 percent of the carbon dioxide emissions generated during the life cycle of a typical gasoline-powered car can occur during its manufacture and transportation to the dealer; the remaining emissions occur during driving once its new owner takes possession.
An earlier study by Seikei University in Japan put the prepurchase number at 12 percent.
If you are a very low mileage driver you can probably reduce your environmental impact by driving an old car.
I'd like to know what the energy cost is for making NiMH and Li ion batteries for hybrid, pluggable hybrid, and pure electric cars. How many miles do you have to drive each kind to achieve a net reduction in carbon emissions as compared to driving the same number of miles with a conventional internal combustion engine car?
A shift to pluggable hybrid and pure electric vehicles combined with a shift to nukes, solar, wind, and geothermal electric power generation is the way to most drastically reduce fossil fuels usage. Throw in a shift to heat pumps for heating and our use of fossil fuels would plummet.
Homemade do-it-yourselfer genetically engineered organisms are still pretty difficult for hobbyists. But some people are already fiddling with the genetics of organisms at home.
Using homemade lab equipment and the wealth of scientific knowledge available online, these hobbyists are trying to create new life forms through genetic engineering — a field long dominated by Ph.D.s toiling in university and corporate laboratories.
In her San Francisco dining room lab, for example, 31-year-old computer programmer Meredith L. Patterson is trying to develop genetically altered yogurt bacteria that will glow green to signal the presence of melamine, the chemical that turned Chinese-made baby formula and pet food deadly.
Now let us get into our time machines and travel ahead 20 years. Microfluidic devices will be cheap and open source software for controlling them will be downloadable on the internet. What's to stop people from genetically engineering bacterial, algae, and other organisms?
Look at all the invasive species that humans have moved across geological barriers that previously kept them away from many habitats. Lots of species are on a tear as they spread out in a habitat where they bring big genetic advantages that give them competitive edges. Lots of native species get outcompeted in Hawaii, Australia, and lots of other locales around the globe. Humans will be able to create new species that'll basically do the same thing.
Big species are not the problem. Sure, in popular science fiction movies T.Rex or a Raptor rips apart a bunch of people. But big species make big targets for rifles and fishing harpoons. Plus, lots of guys would love to hunt down the genetically engineered dino that is terrorizing suburbs. It is the littler ones that are too numerous to easily control that pose the bigger threat. Genetically engineered species could really upend whole ecosystems by being very effective at outcompeting other species.
Scientists have discovered some of the genetic variations that make influenza strains more lethal and will in time identify genetic variations that make other pathogens more or less dangerous. Therefore another future threat comes in the form of a genetically engineered massive killer pandemic for humans. The same sort of threat exists for other species. Imagine a flu that would kill most sheep or cows or pigs. Or imagine some genetically engineered pathogen that would wipe out assorted wild species. This will probably become technically doable.
These threats are hard to prevent because the level of skill and amount of resources needed to do genetic engineering will go down each year for years to come. A small number of malcontents or cult believers could cause enormous damage with genetic engineering.
Sooner or later southern California will get hit by a massive damaging earthquake. It will not only kill people in the initial event but also so damage infrastructure that electric power, natural gas, water, and other basic utilities will be knocked out for extended lengths of time. Water will be disrupted for weeks to months in some areas with other utility disruptions as well. The vast majority of SoCal residents will survive the big one. But then migrations will occur away from places that lose the ability to support high density populations. With all this in mind new research shows that a section of the San Andreas fault in San Luis Obispo County goes off at about 137 year intervals and it is overdue for another big one.
The Carrizo Plain section of the San Andreas has not seen a massive quake since the much-researched Fort Tejon temblor of 1857, which at an estimated magnitude of 7.9 is considered the most powerful earthquake to hit Southern California in modern times.
But the new research by UC Irvine scientists, to be published next week, found that major quakes occurred there roughly every 137 years over the last 700 years. Until now, scientists believed big quakes occurred along the fault roughly every 200 years.
We were due for another quake in that area starting around 1994. This discovery is made possible by advances in dating methods.
They went back to her archive, and the redating effort, led by scholar Sinan Akciz, found that the four big earthquakes before the 1857 temblor probably occurred around 1310, 1393, 1585 and 1640.
The Carrizo Plain is near the southern end of the San Joaquin valley about 100 miles from Los Angeles. As you can see from this map the towns of California Valley, Simmler, McKittrick, Taft, Maricopa, and New Cuyama will be especially hard hit next time this fault rips.
On January 9, 1857 at 8:20 am, an earthquake with a estimated magnitude of 8.0 occurred just north of Carrizo Plain. This quake caused nearly 30 feet (9 m) of lateral offset within Carrizo Plain, and ruptured the surface along the trace of the fault for about 220 miles (350 km). It was one of the greatest earthquakes ever recorded in the United States. Buildings in Los Angeles were severely shaken, and the quake was felt from felt from Marysville south to San Diego and east to Las Vegas, Nevada. The current of the Kern River was turned upstream, and water ran four feet deep over its banks. The waters of Tulare Lake were thrown upon its shores, stranding fish miles from the original lake bed. The waters of the Mokelumne River were thrown upon its banks, reportedly leaving the bed dry in places. The Los Angeles River was reportedly flung out of its bed, too.
I live even closer to this fault (maybe 70 miles) than the people of LA do. Bakersfield is even closer at about only 40 miles away. People in SoCal ought to read a good earthquake preparedness guide such as this preparedness guide by the LA Fire Department. Note that they say "Water is the most important item to store". Got 5 gallons stored per person in your residence? If not, you have a problem come the Big One.
Some of you out in the middle of the United States might be thinking "Oh, those crazy Californians, the dangers they choose to live with". Think again. The border of Arkansas, Missouri, Illinois, Kentucky, and Tennessee is one of the highest earthquake hazard risk zones. A repeat of the three magnitude 8 (yes, 3 of them!) 1811 and 1812 New Madrid earthquakes would devastate much of the surrounding region and cause damage in very distant places. The 1811 New Madrid quake rang church bells in Boston.
Earthquakes in the central or eastern United States affect much larger areas than earthquakes of similar magnitude in the western United States. For example, the San Francisco, California, earthquake of 1906 (magnitude 7.8) was felt 350 miles away in the middle of Nevada, whereas the New Madrid earthquake of December 1811 (magnitude 8.0) rang church bells in Boston, Massachusetts, 1,000 miles away. Differences in geology east and west of the Rocky Mountains cause this strong contrast.
An interesting article in the Christian Science Monitor discusses the big global push to make electric car batteries competitive. The cost of the Chevy Volt batteries might fall to a third their initial cost.
Kruse won’t say whether the $10,000 price tag for the batteries floating around the media is correct. If so, the 16 kilowatt-hours (kWh) worth of energy in the GM battery pack would put the price at $625 per kwh of capacity. But the cost of the Chevy Volt battery should drop sharply once production ramps up, several experts say.
Still others say that the cost of new battery power for PHEVs may drop faster and already be lower than what has been widely reported at perhaps $500 per kilowatt-hour or even less, says Suba Arunkumar, analyst for market researcher Frost & Sullivan.
“I do expect the price will come down to perhaps as low as $200 per kilowatt-hour when mass production begins in 2010 and 2011,” she says.
Multiple national governments are subsidizing the development of new battery chemistries and production facilities. Whether real production costs will decline enough to make electric cars competitive remains to be seen. I expect that to happen. But it is hard to predict when this will happen. 5 years? 10 years?
A new study in the January 7th issue of Cell Metabolism, a Cell Press publication, helps to explain why obese people and animals fail to respond to leptin, a hormone produced by fat that signals the brain to stop eating. What's more, they show that two FDA-approved drugs might restore leptin sensitivity, offering a novel treatment for obesity.
" Most importantly, our study is the first success in sensitizing obese mice on a high-fat diet to leptin," said Umut Ozcan of Harvard Medical School. "If it works in humans, it could treat obesity."
When leptin was first discovered some 13 years ago, it led to great excitement in the field, Ozcan said. Studies showed that leptin administered to obese mice that lacked the hormone lost weight. The buzz over leptin's potential as an obesity therapy soon waned, however, because obese animals and people don't respond to the hormone. Efforts to find drugs that act as leptin sensitizers over the years have also failed.
A part of cells known as the endoplasmic reticulum (ER) is involved in many cellular processes including protein manufacturing, lipid and carbohydrate synthesis, and other functions. Stress in the ER appears to play a role in a metabolic disorder linked to obesity. These researchers decided that perhaps ER stress played a role in reduced response of the brain's hypothalamus to leptin.
Recent studies by him and his colleagues showed that a condition known as endoplasmic reticulum (ER) stress in peripheral organs plays an important role in obesity-induced insulin resistance and type 2 diabetes. Ozcan describes ERs as protein factories within cells. Within those cellular components, molecular chaperones, which serve as the factory workers, facilitate the folding and transport of proteins. When the chaperones can't keep up, it triggers a stress response known as the unfolded protein response (UPR).
The researchers went looking for drugs that could reduce ER stress in hopes that ER stress reduction would make the hypothalamus more sensitive to leptin and thereby reduce appetite. Turns out, ER stress reduction caused mouse weight loss.
The question then became whether the animals could be resensitized by treating them with either of two pre-existing drugs (4-Phenyl Butyric Acid [PBA] and Tauroursodeoxycholic acid [TUDCA]) that act as ER stress reducers. And the answer, they report, is yes.
" It was very exciting," Ozcan said of the discovery. "Normal mice treated with the drugs dropped some weight and quickly rebounded, but the knockout mice [that were genetically predisposed to ER stress in the brain] continued to lose weight. It shows that ER stress relievers are leptin sensitizers."
This research does not prove that ER stress reducer drugs will reduce appetite in overweight humans. Also, ER stress reduction in humans might turn out to be very difficult to do without undesirable side effects. Development of drugs which have only very specific effects is usually a difficult and problematic undertaking.
ER stress probably increases with age as cells malfunction due to accumulated damage. So rejuvenation therapies will probably, as a side effect, make us skinnier. But this study underlines the need to rejuvenate the brain - which is by far the most difficult organ in the body to rejuvenate.
Researchers from the Peninsula Medical School, the University of Cambridge and the University of Michigan, have for the first time identified a relationship between Vitamin D, the "sunshine vitamin", and cognitive impairment in a large-scale study of older people. The importance of these findings lies in the connection between cognitive function and dementia: people who have impaired cognitive function are more likely to develop dementia. The paper will appear in a forthcoming issue of the Journal of Geriatric Psychology and Neurology.
The study was based on data on almost 2000 adults aged 65 and over who participated in the Health Survey for England in 2000 and whose levels of cognitive function were assessed. The study found that as levels of Vitamin D went down, levels of cognitive impairment went up. Compared to those with optimum levels of Vitamin D, those with the lowest levels were more than twice as likely to be cognitively impaired.
Obviously this doesn't prove the direction of causation. It could be that cognitively impaired people get outside less in the summer to synthesize vitamin D in their skin in response to UV light. Or cognitively impaired people might eat worse diets.
Other researchers have found a link between low vitamin D and cognitive impairment. Also, a review notes that the brain is rich in vitamin D receptors. Also, some Emory University researchers found that people with Parkinson's Disease have lower blood vitamin D than people with Alzheimer's who, in turn, had lower blood vitamin D than people with neither disease.
Some important types of cells (e.g. neurons, muscle cells) do not divide. Cells that divide dilute junk that accumulates inside of them and the newly divided cells can manufacture new internal structures (e.g. proteins in membranes). The non-dividing (aka post-mitotic) cells do not do this dilution and do not create as much internal structure. Some researchers at the Salk Institute find that key proteins in nuclear membranes (which enclose and protect our DNA) do not get replaced as we age. These components of our membranes deteriorate with age and make the nuclei of cells basically spring leaks. Not good.
As parts of us age, even the membrane bound nuclei , which house the genetic instructions for life that are "written" in our DNA, begin to show considerable wear and tear, suggests a new report in the January 23rd issue of the journal Cell, a Cell Press publication. The nuclear pore complexes that normally act as gatekeepers--selectively importing and exporting the molecular ingredients for life to and from the nucleus--begin to break down and spring leaks.
That's because some of the 30 or so nucleoporin proteins that make up those complexes can't be replaced once cells stop dividing, they found.
We need to develop the means to create replacements and somehow tear down old nucleoporin proteins. That will not be easy to do.
" These proteins are unusually stable," said Martin Hetzer of the Salk Institute for Biological Studies. "Most proteins turnover within minutes or hours. These last the entire life span of the cell," a period that can in some cases be decades. In fact, he said, many cells in the body do not actively divide most of the time, and that lack of cell division is particularly dramatic for cells such as muscle and neurons.
Earlier studies had shown that some components of the nuclear pore complexes are very dynamic while others hang around throughout the cell cycle, getting replaced only when cells split into two daughter cells, Hetzer explained. His team wondered what that meant for cells that had stopped dividing.
As long time readers know, I see the brain as the most difficult part of the body to rejuvenate. Some parts of the body will get rejuvenated by replacement. Got an old and failing liver or kidneys? Grow new parts using future advances in tissue engineering and transplant in the new parts. Or find a way to grow new organs inside of our bodies. But neurons with leaking nuclear membranes are especially problematic because the neurons must be repaired rather than replaced.
They now report that the scaffold nucleoporins are extremely stable and do not exchange once they are incorporated into the nuclear membrane, persisting for the entire life span of a differentiated cell. In those cells, the nuclear pore complexes deteriorate with time, eventually losing nucleoporins that are critical for maintaining the pore diffusion barrier. Strikingly, they found that nuclei of old rat neurons containing deteriorated nuclear pore complexes become increasingly permeable.
The proteins in the nuclear membranes that serve as pores also serve as structure to maintain the membrane's three dimensional structure. To replace these proteins is akin to replacing structural beams in a building without letting the building collapse. This is far harder to do at microscopic levels and in hundreds of millions of cells.
Cells are usually very efficient at getting rid of old or damaged proteins and replacing them with new copies, Hetzer said, but it seems they have no way to replace the most stable components of the nuclear pore complexes. He suspects that's because the pores are not only essential for molecular transport, but they are also structural components of the double lipid layer that is the nuclear membrane. If those gated holes are lost, the membrane collapses, he said.
" How do you replace a bridge while transport is happening?" he asked. "It's not possible."
I disagree with the "It's not possible" claim. But development of techniques for doing this will be very difficult and I fear this problem won't be solved for decades.
Global grain markets are facing breaking point according to new research by the University of Leeds into the agricultural stability of China.
Experts predict that if China's recent urbanisation trends continue, and the country imports just 5% more of its grain, the entire world's grain export would be swallowed whole.
The rapid economic growth of such a populous country means that world markets become more susceptible to events in a single country. China's growing buying power and rising living standards will increase its grain demand. Rising per capita meat consumption strikes me as a far larger source of long term food demand growth than a drought.
The knock-on effect on the food supply - and on prices - to developing nations could be huge.
Sustainability researchers have conducted a major study into the vulnerability of Chinese cropland to drought over the past 40 years, which has highlighted the growing fragility of global grain supply. Increased urban development in previously rich farming areas is a likely cause.
"China is a country undergoing a massive transformation, which is having a profound effect on land use," says Dr Elisabeth Simelton, research fellow at the Sustainability Research Institute at the University of Leeds, and lead author of the study. "Growing grain is a fundamentally low profit exercise, and is increasingly being carried out on low quality land with high vulnerability to drought."
A small percentage decrease in Chinese crop output would cause a large increase in grain imports.
At the moment the Chinese government claims that China is 95% self sufficient in terms of grain supply. If China were to start importing just 5% of its grain (to make up a shortfall produced by low yields or change of land use to more profitable crops) the demand would hoover up the entire world's grain export.
When the United States went through industrialization it did so with a population that was approximately a tenth of China's 1.33 billion population today. Adding a fully industrialized China to the world demand for agricultural products and other resources is going to strain ecosystems around the world. I expect we will see a lot of species extinctions as a result. Lots more land will get shifted into agricultural production.
The global trade in frog legs for human consumption is threatening their extinction, according to a new study by an international team including University of Adelaide researchers.
The researchers say the global pattern of harvesting and decline of wild populations of frogs appears to be following the same path set by overexploitation of the seas and subsequent "chain reaction" of fisheries collapses around the world.
The researchers have called for mandatory certification of frog harvests to improve monitoring and help the development of sustainable harvest strategies.
Lots of frog eating going on.
The annual global trade in frogs for human consumption has increased over the past 20 years with at least 200 million and maybe over 1 billion frogs consumed every year. Only a fraction of the total trade is assessed in world trade figures.
The overharvesting comes on top of habitat loss due to increased human populations, industrialization, and spread of a killer chytrid fungus Batrachochytrium dendrobatidis (Bd).
Where Bd thrives, generally moist cool habitats, 50% of amphibian species and 80% of individuals can be expected to disappear within 1 year (Lips et al. 2006; www.amphibianark.org/Lips%20et%20al%202006.pdf). Currently it cannot be stopped in the wild and a minority of species seem able to survive with a Bd infection as larvae or as adults and these animals likely serve as a reservoir and vectors for future outbreaks. Notable among resistant species are worldwide invasive pest species including marine toads, American bullfrogs and African clawed frogs.
When a smelly old diesel truck or car goes past I get annoyed at the thought that I'm briefly breathing poisonous exhaust air. When the coal electric power industry manages to delay new air pollution regulations my reaction is similar and my support for nuclear power is in part due to a desire to live longer. Well, reductions in particulate pollution probably have raised US life expectancies by 5 months in recent decades.
A new study by researchers at Brigham Young University and Harvard School of Public Health shows that average life expectancy in 51 U.S. cities increased nearly three years over recent decades, and approximately five months of that increase came thanks to cleaner air.
"Such a significant increase in life expectancy attributable to reducing air pollution is remarkable," said C. Arden Pope III, a BYU epidemiologist and lead author on the study in the Jan. 22 issue of the New England Journal of Medicine. "We find that we're getting a substantial return on our investments in improving our air quality. Not only are we getting cleaner air that improves our environment, but it is improving our public health."
The research matched two sets of data from 51 cities across the nation: changes in air pollution between about 1980 and about 2000; and residents' life expectancies during those years. The scientists applied advanced statistical models to account for other factors that could affect average life spans, such as changes in population, income, education, migration, demographics and cigarette smoking.
In cities that had previously been the most polluted and cleaned up the most, the cleaner air added approximately 10 months to the average resident's life. On average, Americans were living 2.72 years longer at the end of the two-decade study period; up to five months, or 15 percent, of that increase came because of reduced air pollution. Other studies show that these gains are likely coming from reductions in the cardiovascular and cardiopulmonary disease that typically accompany air pollution.
A reduction of 10 micrograms per cubic meter of particulate pollution will increase life expectancies by 7 months. Indoor air filtration devices anyone?
"Life expectancy is the single most comprehensive summary of how people's longevity is affected by factors like air pollution that cause early death," said co-author Majid Ezzati, associate professor of international health at Harvard School of Public Health. "We were able to use routine mortality statistics to track longevity in all cities over a long period of time and analyze how it has been influenced by changes in air pollution."
The analysis found that for every decrease of 10 micrograms per cubic meter of particulate pollution in a city, its residents' average life expectancy increased by more than seven months. During the 1980s and 1990s the average PM2.5 levels in the 51 U.S. cities studied dropped from 21 to 14 micrograms per cubic meter. In cities such as Pittsburgh and Buffalo, the decrease was closer to 14 micrograms per cubic meter.
Long commutes in crowded traffic are probably bad for your health to the exhaust particulates of older cars and trucks.
Led by Sean McCrea of the University of Konstanz in Germany, an international team of psychologists wanted to see if there might be a link between how we think of a task and our tendency to postpone it. In other words, are we more likely to see some tasks as psychologically "distant"-- and thus making us save them for later rather than tackling them now?
The psychologists handed out questionnaires to a group of students and asked them to respond by e-mail within three weeks. All the questions had to do with rather mundane tasks like opening a bank account and keeping a diary, but different students were given different instructions for answering the questions. Some thought and wrote about what each activity implied about personal traits: what kind of person has a bank account, for example. Others wrote simply about the nuts and bolts of doing each activity: speaking to a bank officer, filling out forms, making an initial deposit, and so forth. The idea was to get some students thinking abstractly and others concretely. Then the psychologists waited. And in some cases, waited and waited. They recorded all the response times to see if there was a difference between the two groups, and indeed there was a significant difference.
The findings, reported in Psychological Science, a journal of the Association for Psychological Science, were very clear. Even though all of the students were being paid upon completion, those who thought about the questions abstractly were much more likely to procrastinate--and in fact some never got around to the assignment at all. By contrast, those who were focused on the how, when and where of doing the task e-mailed their responses much sooner, suggesting that they hopped right on the assignment rather than delaying it.
The authors note that "merely thinking about the task in more concrete, specific terms makes it feel like it should be completed sooner and thus reducing procrastination." They conclude that these results have important implications for teachers and managers who may want their students and employees starting on projects sooner. In addition, these findings are also relevant for those of us resolving to have better time management skills in the New Year!
Sound useful? I am going to try pondering tasks I put off that I really want to get to and try picturing myself doing the tasks, why those tasks matter to my life, and what traits one needs to have to accomplish those tasks. Find out if this works.
Humans and other higher primates developed fancier circuitry in the brain to support more complex sequences of movement. This enabled more complex usage of tools.
PITTSBURGH, Jan. 12 – A new area of the cerebral cortex has evolved to enable man and higher primates to pick up small objects and deftly use tools, according to neuroscientists at the University of Pittsburgh School of Medicine and Pittsburgh's Veterans Affairs Medical Center.
The brain's primary motor cortex turns out to have neighboring "old" and "new" parts. In most animals, including cats, rats and some monkeys, the old primary motor cortex controls movement indirectly through the circuitry of the spinal cord, explained senior author Peter Strick, Ph.D., professor in the department of neurobiology at the School of Medicine and senior career scientist at the VA Medical Center.
But in man, the Great Apes and some monkeys, another area of the motor cortex developed and is now home to a special set of cortico-motoneuronal (CM) cells, he said. These cells directly control spinal cord motor neurons, which are the nerve cells responsible for causing contraction of shoulder, elbow and finger muscles. The direct control exerted by CM cells bypasses the limitations imposed by spinal cord circuitry and permits the development of highly complex patterns of movement, such as the independent finger action needed for playing an instrument or typing.
The development of greater ability to manipulate tools probably played synergistically with the development of more cognitive capacity in order to learn and remember what to use tools for. So this development probably created selective pressures for further evolution of the brain.
A group of 3,146 earth scientists surveyed around the world overwhelmingly agree that in the past 200-plus years, mean global temperatures have been rising, and that human activity is a significant contributing factor in changing mean global temperatures.
Peter Doran, University of Illinois at Chicago associate professor of earth and environmental sciences, along with former graduate student Maggie Kendall Zimmerman, conducted the survey late last year.
The findings appear today in the publication Eos, Transactions, American Geophysical Union.
In trying to overcome criticism of earlier attempts to gauge the view of earth scientists on global warming and the human impact factor, Doran and Kendall Zimmerman sought the opinion of the most complete list of earth scientists they could find, contacting more than 10,200 experts around the world listed in the 2007 edition of the American Geological Institute's Directory of Geoscience Departments.
The climatologists are most certain that humans play a role in the planet's warming.
Two questions were key: have mean global temperatures risen compared to pre-1800s levels, and has human activity been a significant factor in changing mean global temperatures.
About 90 percent of the scientists agreed with the first question and 82 percent the second.
In analyzing responses by sub-groups, Doran found that climatologists who are active in research showed the strongest consensus on the causes of global warming, with 97 percent agreeing humans play a role. Petroleum geologists and meteorologists were among the biggest doubters, with only 47 and 64 percent respectively believing in human involvement. Doran compared their responses to a recent poll showing only 58 percent of the public thinks human activity contributes to global warming.
We are dumping a large amount of carbon dioxide into the atmosphere. It must be doing something. I do not think our ability to model climate is anywhere near good enough to predict how much the planet will heat up. Climate is an extremely complex system. We must make decisions about climate and CO2 emissions based on very partial information.
Our incomplete understanding of climate is not a rationale for does not mean
What I'd like to get out of the propagation of these beliefs: less conventional pollution from coal plants. Less particulates, less mercury, less oxides of sulfur. Use fear of global warming to overpower the coal and oil lobbies (nothing else has been strong enough to do this). If we have to cut back on coal to reduce CO2 emissions I'm happy since that'll cut back on pollutants that do more immediate harm. While we will pay a price for this I do not expect the price to be high. We can shift to nuclear for baseload electric power generation. Granted, there's a substantial lead time in making such a switch. But even with Obama in office a reduction in US coal usage doesn't look like a sure thing.
Despite a well-funded ad campaign by environmentalists attacking the industry, and a huge coal-ash spill in Tennessee that has led to calls for more regulation, the industry has received positive assurances this week from President-elect Barack Obama's nominees that the new administration is committed to keeping coal a big part of the nation's energy source.
Then there's China. Only a recession will slow China's coal consumption growth (and the Chinese coal electric plants are subject to far less environmental regulation). The US is going to drop far behind China in coal usage even without new political constraints on coal burning in the US. My guess is that the rate of growth of coal usage in the US will slow and perhaps stop as some industrial interests organize in favor of alternatives. GE can make money selling wind turbines and nuclear reactors.
The most detailed proposal yet by industry and environmentalists to reduce U.S. greenhouse-gas emissions will call for raising the costs of new coal plants and rewarding nations for protecting forests.
Rio Tinto Group, General Electric Co. and U.S. electricity producers will present the proposal tomorrow to a congressional committee and recommend “urgent” action, according to a copy of the report by the 32-member coalition obtained by Bloomberg News.
US coal mines can ramp up exports though.
NASA scientist James Hansen thinks quick action is needed to prevent eco-disaster. But we've got some things we can do if the climate warming becomes seriously bad. For example, we can paint roofs white, dump iron in the southern seas, or launch reflector satellites for $500 billion. But if you are looking for a frugal approach Gregory Benford proposes a way to cool the Earth for $100 million per year.
A big shift toward nukes, wind, geothermal, and solar power will cushion economies from the coming effects of declining oil production. It will also reduce conventional pollutants. It will probably end up helping reduce undesirable levels of global warming too.
AUSTIN, Texas — Women with high levels of the sex hormone oestradiol may engage in opportunistic mating, according to a new study by psychology researchers at The University of Texas at Austin.
Doctoral candidate Kristina Durante and Assistant Professor of Psychology Norm Li published their findings in the article "Oestradiol Level and Opportunistic Mating in Women" in the Jan. 13 issue of Proceedings of the Royal Society of London: Biology Letters.
"The study offers further evidence that physiological mechanisms continue to play a major role in guiding women's sexual motivations and behavior," Durante said.
Durante and Li investigated the relationship between oestradiol, an ovarian hormone linked to fertility, and sexual motivation in a study of 52 female undergraduates not using contraception. Participants' ages ranged from 17 to 30 years old.
The researchers measured the participants' hormone levels at two points during each woman's ovulatory cycle and then asked them to rate their own physical attractiveness. Independent observers also rated the participants' physical attractiveness.
Participants also answered survey questions that measured their propensity to cheat on a partner.
The researchers found that a woman's oestradiol level was positively associated with self-perceived physical attractiveness. Women with a higher oestradiol level also reported a greater likelihood of flirting, kissing and having a serious affair (but not a one-night stand) with a new partner.
Oestradiol levels were negatively associated with a woman's satisfaction with her primary partner.
"Our findings show that highly fertile women are not easily satisfied by their long-term partners and are motivated to seek out more desirable partners," Durante explained. "However, that doesn't mean they're more likely to engage in casual sex. Instead, they adopt a strategy of serial monogamy."
I wonder how much of the serial monogamy is due to finding a better partner versus just feeling the need to find a different partner. Do the guys these women move on to score better in objective measures of physical attractiveness, wealth, or other factors?
How many of those dissatisfied women torment their partners before dumping them? Maybe a guy needs to know his girlfriend's hormone levels and an objective comparison of his and her level of attractiveness so that he can assess the odds of the relationship lasting.
Are you going to get traded in for a different model? Blame it on a hormone.
"These women are willing to trade up when the opportunity arises and continue to extract these lucrative resources from men when they can," says Kristina Durante, an evolutionary psychologist at the University of Texas in Austin, who led the study. She thinks the behaviour could be an adaptation to the high costs of giving birth.
"For women it's all about the resources that we need. If you're going to be getting knocked up there's a significant cost," she says.
So then did Angelina Jolie finally decide that Brad Pitt was as attractive as she could find? Or will her hormones eventually cause her to move on? She's aging so if she moves on she's probably making a mistake.
She said her results are consistent with the possibility highly fertile women are not easily satisfied by their long-term partners and are especially motivated to become acquainted with other, presumably more desirable, men.
However, such motivations do not seem to stem from a greater interest in casual sex, she added.
"The prettier you are, the more fertile you are," said lead author Kristina Durante, a doctoral candidate at the University of Texas. And the more fertile, the more options — and urges — for mates, she said.
Don't believe her? See my posts Women With Hourglass Bodies Have More Reproductive Hormones and Women With Higher Estrogen Seen As More Attractive.
Update: Anyone have access to the full paper? My question: Adjusted for attractiveness do women with higher hormone level have more relationships? To put it another way: Is it the higher attractiveness's enabling of more relationships or greater motivation to have more relationships that causes this difference in outcome? I see from one news report that the researchers used observers to rate the attractiveness of their subjects and so the researchers should have been able to puzzle out whether motive or opportunity played a bigger role in causing the serial monogamy.
The reality, according to Neal Dikeman, partner with VC firm Jane Capital Partners, is that only one or two thin-film projects have brought product to market in 30 years, and it's a US $100M-$200M dollar up-front investment "just to play the game and see if your product really works."
Silicon Valley investors have mistakenly bet on "really great teams" while the technology is still at a science experiment stage, he argues — investors are beginning to realize this, he thinks, and that the industry is sitting on the back end of about 5-10 years of US $100M bets. "We're going to see a bunch of write-offs coming up," he warns.
Dikeman argues that very few of the thin film PV start-ups have succeeded in getting a good thin film PV production process operating at large scale. So First Solar is really an outlier.
Dikeman expects the entrance of semiconductor equipment manufacturing suppliers such as Applied Materials and Oerlikon will help matters. If these companies can work out processes and equipment for doing thin films PV manufacturing then a lot more companies will be able to get into the business of thin film PV manufacturing.
Solar cells may generate clean green electricity but manufacturing them involves a witches brew of toxic chemicals that could harm the environment if millions of solar panels end up in landfills, according to a report issued Wednesday by the Silicon Valley Toxics Coalition.
First off, not all the chemicals used to make photovolatics (PV) are there in the PV at the end of the manufacturing process. But, yes, at the end of the life of PV there is a valid question of how to dispose of it. My guess is that some types of PV contain enough valuable metals that melting them down to separate out the metals will be worth it.
The California environmental group is calling for solar manufacturers to take back and recycle their panels at the end of their 20-to-25 year lifespan. “We feel it’s a very important time for the solar industry because it is getting ready to take off and before that happens it’s time to look at important issues around designing out some of the toxics,” Silicon Valley Toxics Coalition executive director Sheila Davis told Green Wombat. “The big issue is whether there is a transparent supply chain and whether solar companies monitor their supply chains.”
The solar PV industry is for recycling. But does anyone see an obvious problem with the idea that manufacturers will take back the PV at end of life?
The solar industry’s trade group says it embraces the report’s recommendations. “We completely support take-back and recycling,” says Monique Hanis, a spokeswoman for the Solar Energy Industries Association in Washington. “We’re in a fortunate position in that we’re still an emerging industry and have an opportunity now to establish standards and proactively set up processes before we end up with solar panels on every rooftop.”
Most of the PV manufacturers in business today won't exist 25 years from now. Some of the biggest suppliers a few decades hence will be companies that aren't even selling PV today. The take-back idea only works if the original seller exists to do the taking back. Otherwise original sellers are going to need to set aside cash in some kind of industry fund to pay for retrieval and disposal. But how to estimate the cost of doing that 25 years in advance or the rate of return of money set aside today for this purpose?
While Sullenberger is hailed as a hero the big story here was not bravery. Rather, Sullenberger put in an impressive mental performance of decision making which was greatly aided by a genius-level mind.
Ace pilot Chesley B. "Sully" Sullenberger III was in seclusion Friday, a day after he saved the lives of 155 passengers and crew aboard US Airways Flight 1549. But America was learning much about its newest hero - even his IQ scores.
Sullenberger, 57, led the pack even as a child, when he consistently tested in the 99th percentile in every academic category. His IQ qualified him for the "genius society" Mensa when he was just 12 years old.
Innate intellectual ability matters a great deal. A dumber society will be a more accident-prone and less safe society.
A British researcher finds that women come more often in the arms of wealthy men.
“Women’s orgasm frequency increases with the income of their partner,” said Dr Thomas Pollet, the Newcastle University psychologist behind the research.
He believes the phenomenon is an “evolutionary adaptation” that is hard-wired into women, driving them to select men on the basis of their perceived quality.
The study is certain to prove controversial, suggesting that women are inherently programmed to be gold-diggers.
Women are turned on by wealthy men. It really is true. But the idea that stereotypes are true of course is evil crimethink. We are encouraged to respond to such thoughts by engaging in what Orwell called CrimeStop. But the mental technique of CrimeStop is protective stupidity. I do not feel more safe as a result of the promotion of this mental technique.
The desire of women for a wealthy man seems an obvious product of evolution. That people behave in ways that are a product of our evolutionary history seems obvious to me. Of course ignorant people come up with all sorts of alternative explanations for why we behave as well do.
Cassie is unrepentant about dating rich men. “Of course it is much better to sleep with men with lots of money,” said the 27-year-old lawyer from London.
“Any girl who tells you different is lying. Rich men are powerful and successful and confident and charismatic. They know what they want, and they go out and get it. That translates to being fantastic in bed.”
Women do pick up on the confidence of a successful alpha male and most are attracted to it. So pick-up artists like Roissy advocate a strategy of adopting alpha male behaviors as pick-up techniques. While some (though not all) of his female readers object to the efficacy of these techniques I think he's right overall. But if you can create wealth then you'll do even better. Alpha behavior techniques plus wealth work better than just wealth or just the techniques. So it still helps to get rich.
We are the products of our evolutionary history Denying this does not change us. The denial just leads us into rationalizations to explain why we engage in behaviors that are evolutionary strategies.
As we age the levels of cyclooxygenase 2 (COX-2) declines in stem cells. Researchers at U Rochester found that the decline in COX-2 causes a reduction of conversion of stem cells into cartilage and this slows or prevents bone repair with age.
"The skeleton loses the ability to repair itself as we age," said Regis J. O'Keefe, M.D., Ph.D., chairman of the Department of Orthopaedics at the University of Rochester Medical Center and corresponding author of the article. "Our results position the COX-2 pathway as one of several under exploration with the common goal of accelerating healing in aging humans, and with the potential to come together in future combination therapies."
Turning Back the Clock
In the current study, healing rates were compared between a group of young mice (7-9 weeks old) and a group of old mice (52-56 weeks of age), with healing evaluated by imaging and gene expression studies. Specifically, the current study found that the older mice experienced delayed fracture healing, decreased bone formation and decreased resupply of blood vessels to the healing site in aging mice. Expression of the gene that codes for production of the COX-2 was reduced by 75 percent in fractures between aged mice and young mice during the early healing phase five days after a fracture. COX-2 expression in young mice peaked at the exact time that stem cells were changing into cartilage within the fracture callus of young mice, and was reduced during that period in older mice.
In addition, experiments confirmed that COX-2 is expressed primarily in early stem cell precursors of cartilage that also express collagen, type II, alpha 1 (col2a1), the gene that codes for production of a key part of type II collagen in mice and humans, the fibrous, structural protein that lends strength to bone. Researchers observed in aged mice a dramatic decrease as well in the expression of other genes known to contribute to bone formation as well (e.g. osteocalcin and type X collagen). Altogether the results suggest that in aging animals gene expression is altered early in fracture repair with consequences for the entire healing cascade.
The researchers demonstrated that a drug which boosts prostaglandin E2 (PGE2) production improves bone healing ability.
Researchers found further proof that COX-2 is responsible for loss of bone healing ability with age when they were able to reverse the process with a drug known to encourage the COX-2 signaling effect. COX-2 catalyzes the conversion of a fatty acid to prostaglandin E2 (PGE2), a hormone with many functions in the animal body depending on the type of cell they interact with, from blood vessel dilation to embryo implantation in the womb to bone healing. PGE2 is known to have it effect on cells by reacting with one of four receptor proteins (EP1–EP4) on the surface of cells, including the surfaces of bone marrow stem cells, cartilage cells and bone-producing cells (osteoblasts). Human cells send and receive signals that switch on life processes through workhorse proteins called receptors that enable messages to penetrate cells.
You might think that a drug which acts like COX-2 to cause more prostaglandin E2 (PGE2) production and therefore more bone healing is the ticket. But every time we hear about a drug that can reverse some metabolic change that comes with aging we have to ask why the body changed with age in the first place. The decline of COX-2 with age down-regulates stem cells to inhibit stem cell activity. Why? Just an accident of decay? Or was this selected for because older stem cells are at risk of becoming cancerous when they divide?
I hope that drugs which up-regulate stem cells for repair do not boost our risk of cancer. Alternatively, once cancer becomes easily curable we'll be able to take more risks by stimulating cell growth because any resulting cancer will eventually become easy to snuff out. We need cures for cancer that have only mild side effects both because we want to avoid our existing risk of death from cancer and also so we can turn up cell activity in aged cells without running a greater risk of death from cancer.
What I would be curious to know: Would stem cells from young mice stuck into old mice express youthful levels of COX-2 or lower older levels of COX-2? To put it another way: does the environment which the stem cell finds itself in send signals to the stem cell that suppress COX-2? Or does the cell internally change with age in ways that reduce COX-2 expression? The latter possibility is in some ways a better answer. If we can just replace stem cells to get better repair then future stem cell therapies will be easier to develop. If the whole body is suppressing repair then rejuvenation becomes a much taller order.
I hear Gene Wilder yelling "Its alive! Its alive! Its alive!". Methane on Mars might be a sign of biological activity below the surface. (same here)
WASHINGTON -- A team of NASA and university scientists has achieved the first definitive detection of methane in the atmosphere of Mars. This discovery indicates the planet is either biologically or geologically active.
It would be so much better if the methane is biological, not geological. Then we'd need to create some sort of automated instrument (probably involving microfluidic devices) that could analyze biological material on Mars to look for DNA and similar compounds. Do Martian bacteria use the same letters of the genetic alphabet that we are made out of? Could be. A Martian rock might have brought life to Earth - or perhaps vice versa.
The team found methane in the Martian atmosphere by carefully observing the planet throughout several Mars years with NASA's Infrared Telescope Facility and the W.M. Keck telescope, both at Mauna Kea, Hawaii. The team used spectrometers on the telescopes to spread the light into its component colors, as a prism separates white light into a rainbow. The team detected three spectral features called absorption lines that together are a definitive signature of methane.
"Methane is quickly destroyed in the Martian atmosphere in a variety of ways, so our discovery of substantial plumes of methane in the northern hemisphere of Mars in 2003 indicates some ongoing process is releasing the gas," said Michael Mumma of NASA's Goddard Space Flight Center in Greenbelt, Md. "At northern mid-summer, methane is released at a rate comparable to that of the massive hydrocarbon seep at Coal Oil Point in Santa Barbara, Calif." Mumma is lead author of a paper describing this research that will appear in Science Express on Thursday.
The organisms that amazingly live over a mile underground on Earth illustrate the possibility that ancient life forms on Mars could have survived long after the surface became inhospitable.
"On Earth, microorganisms thrive about 1.2 to 1.9 miles beneath the Witwatersrand basin of South Africa, where natural radioactivity splits water molecules into molecular hydrogen and oxygen," Mumma said. "The organisms use the hydrogen for energy. It might be possible for similar organisms to survive for billions of years below the permafrost layer on Mars, where water is liquid, radiation supplies energy, and carbon dioxide provides carbon. Gases, like methane, accumulated in such underground zones might be released into the atmosphere if pores or fissures open during the warm seasons, connecting the deep zones to the atmosphere at crater walls or canyons."
Of course, if all the living organisms on Mars are deep underground we are going to have a hard time reaching them with automated probes.
Scientists seeking to harness the power of the immune system to eradicate brain tumors face two major hurdles: recruiting key immune cells called dendritic cells into areas of the brain where they are not naturally found and helping them recognize tumor cells as targets for attack.
Researchers at Cedars-Sinai Medical Center, however, have identified a sequence of molecular events that accomplish both objectives. Their findings, based on laboratory and animal studies, appear in the Jan. 13 issue of PLoS Medicine, an open-access online journal of the Public Library of Science.
The Cedars-Sinai team discovered that a protein – HMGB1 – released from dying tumor cells activates dendritic cells and stimulates a strong and effective anti-tumor immune response. HMGB1 does so by binding to an inflammatory receptor called toll-like receptor 2, or TLR2, found on the surface of dendritic cells.
Here is part of the abstract of the research paper. Click thru to read the full paper.The researchers delivered gene therapy into the tumor mass and provoked an immune response.
Using a combined immunotherapy/conditional cytotoxic approach that utilizes adenoviral vectors (Ad) expressing Fms-like tyrosine kinase 3 ligand (Flt3L) and thymidine kinase (TK) delivered into the tumor mass, we demonstrated that CD4+ and CD8+ T cells were required for tumor regression and immunological memory. Increased numbers of bone marrow-derived, tumor-infiltrating myeloid DCs (mDCs) were observed in response to the therapy. Infiltration of mDCs into the GBM, clonal expansion of antitumor T cells, and induction of an effective anti-GBM immune response were TLR2 dependent.
But can the gene therapy get delivered with sufficient specificity for cancer cells that non-cancer cell loss is minimized?
Brain cancer is especially challenging because we can't afford to cut out large amounts of brain tissue in order to get the tumor. We need to find ways to very very selectively target just the cancer cells. That is especially true for brain tumors.
Laboratory research shows that cellphone conversations are dangerous even if you do not hold the phone.
Laboratory experiments using simulators, real-world road studies and accident statistics all tell the same story: drivers talking on a cellphone are four times as likely to have an accident as drivers who are not. That’s the same level of risk posed by a driver who is legally drunk.
Why cellphone use behind the wheel is so risky isn’t entirely clear, but studies suggest several factors. No matter what the device, phone conversations appear to take a significant toll on attention and visual processing skills.
It may be that talking on the phone generates mental images that conflict with the spatial processing needed for safe driving. Eye-tracking studies show that while drivers continually look side to side, cellphone users tend to stare straight ahead.
The interesting thing about this story is that conversations with passengers and listening to the radio do not pose a risk. In fact, passengers are seen as reducing accident risk.
Technological advances are producing more and more effective ways to interrupt our minds and distract us. What I'd like to know: do people at work who do design work become less productive if they have activated cell phones? Do the phone interrupts come often enough to hobble design development? Do cell phones even reduce the amount of mental effort that people put into pondering problems while the are driving?
I've previously read that if you hear only one half of a conversation this is more disruptive to your thinking than if you hear both halves of a conversation. There's a natural flow in thinking that you can do if you can built a complete context. But when half the conversation is missing perhaps your mind puts too much effort into trying to figure out what the other half is. For this reason I oppose lifting bans on phone use in airplanes. I do not want to be mentally distracted by hearing half of phone conversations.
A new study provides a novel theory for how delusions arise and why they persist. NYU Langone Medical Center researcher Orrin Devinsky, MD, performed an in-depth analysis of patients with certain delusions and brain disorders revealing a consistent pattern of injury to the frontal lobe and right hemisphere of the human brain. The cognitive deficits caused by these injuries to the right hemisphere, leads to the over compensation by the left hemisphere of the brain for the injury, resulting in delusions. The article entitled "Delusional misidentifications and duplications: Right brain lesions, left brain delusions" appears in the latest issue of the journal of Neurology.
"Problems caused by these brain injuries include impairment in monitoring of self, awareness of errors, and incorrectly identifying what is familiar and what is a work of fiction," said Dr. Devinsky, professor of Neurology, Psychiatry and Neurosurgery and Director of the NYU Epilepsy Center at NYU Langone Medical Center. "However, delusions result from the loss of these functions as well as the over activation of the left hemisphere and its language structures, that 'create a story', a story which cannot be edited and modified to account for reality. Delusions result from right hemisphere lesions, but it is the left hemisphere that is deluded."
Often bizarre in content and held with absolute certainty, delusions are pathologic beliefs that remain fixed despite clear evidence that they are incorrect. "Delusions are common problems in a variety of psychiatric and neurological disorders," said Dr. Devinsky. "Psychiatric disorders with delusions, for example- schizophrenia, have been proven to have functional and structural brain pathology. But now improved diagnostic techniques are allowing us to have increased identification of neurologic disorders among other patient populations with delusions."
In the study, the author finds that most neurologic patients with delusions usually have lesions in the right hemisphere and/or bifrontal areas. For example, the neurological disorders of Confabulation (incorrect or distorted statements made without conscious effort to deceive), Capgras (the ability to consciously recognize familiar faces but not emotionally connect with them) and Prosopagnosia (patients who may fail to recognize spouses or their own face but generate an unconscious response to familiar faces) result from right sided lesions.
I expect advances in understanding of brain disorders to cause legal battles. If someone is deluded and a danger to self or others should that person be forcefully treated with, for example, stem cells that will do brain repair? If the alternative is institutionalization in a prison or mental hospital is treatment without consent a better choice?
Many drugs already can alter mental state. If patients in mental hospitals are forceably drugged then already a person's own judgment about what is core to their identity - their own thoughts - is effectively rejected and replaced by the judgment of managers and experts in mental hospitals. The ramifications of this power will become greater as the technology for permanently altering cognitive function becomes more powerful.
Are we just waiting for battery cost to drop low enough to make pure electric cars feasible? Doesn't look that way. The forthcoming GM Chevy Volt pluggable hybrid which will go 40 miles on an electric charge will have a 400 pound battery.
Because the battery packs are about 6 feet (1.82 meters) long and weigh roughly 400 pounds (181 kilograms), the automaker wants them close to the car’s assembly site.
That puts it at 10 lbs per mile. So in order to have a 400 mile range (which many gasoline cars have) 4000 lbs of battery would be required. The net gain in weight would be smaller since a gasoline tank, internal combustion engine, and some other parts would be absent. But the car would still be very heavy and would lose some energy efficiency and acceleration due to the weight.
At 6.3 lbs per gallon of gasoline a 40 mpg car can go 400 miles on a mere 63 pounds of fuel. Hydrocarbons offer big advantages for energy storage.
A more judicious use of batteries can actually boost range substantially. For example, the 2010 Ford Fusion Hybrid will have a 700 mile range in the city.
Aside: What do you call a Cadillac concept car built on the Chevrolet Volt pluggable hybrid? A Coupe de Volt. No, that's not GM's name for it.
I actually think pure electric cars have a future, even with the current energy storage capacities of lithium ion batteries. Some usage patterns work with the latest batteries. Short range electric trucks for use in the ports of Long Beach and Los Angeles make great sense as a way to get rid of dirty old polluting diesel trucks. Some uses of cars also fit with current battery limits. Ford is planning an electric car with only 100 mile range.
The second is a small battery-electric passenger car made in conjunction with Magna International. The car, which is scheduled for production in 2011, will be powered by lithium-ion batteries and have a range of up to 100 miles on a single charge, Ford said.
Ford wants to get electric cars into use as taxis to substitute for Crown Victorias. Each taxi trip tends to be pretty short range and 100 mile range would allow for 5, 10, 20 taxi trips. But how quickly can these taxis get recharged and how many places around a city could be set up as recharging stations? Anyone have any details on this?
What all this means for the future: as battery costs decline the per mile cost of commuter driving will drop relative to the cost of longer range trips. Basically, batteries will move you shorter distances while liquid fuels will move you longer distances. That'll be true in the air and on the ground. The only exception to that rule: trains. Once oil production starts declining we'll probably see train electrification. That works because electric trains can get their power from that run along the train tracks.
Most of the prospective electric models need to be charged for several hours to cover a day’s worth of driving. Ford estimates that its car will need at least a six-hour charge to travel 100 miles.
How many miles a day does the average taxi driver drive?
Men consistently outperform women on spatial tasks, including mental rotation, which is the ability to identify how a 3-D object would appear if rotated in space. Now, a University of Iowa study shows a connection between this sex-linked ability and the structure of the parietal lobe, the brain region that controls this type of skill.
The parietal lobe was already known to differ between men and women, with women's parietal lobes having proportionally thicker cortexes or "grey matter." But this difference was never linked back to actual performance differences on the mental rotation test.
UI researchers found that a thicker cortex in the parietal lobe in women is associated with poorer mental rotation ability, and in a new structural discovery, that the surface area of the parietal lobe is increased in men, compared to women. Moreover, in men, the greater parietal lobe surface area is directly related to better performance on mental rotation tasks. The study results were published online Nov. 5 by the journal Brain and Cognition.
If you want to be able to rotate objects in 3D you need to have more parietal lobe surface area.
The study was based on tests of 76 healthy Caucasian volunteers -- 38 women and 38 men, all right-handed except for two men. The groups were matched for age, education, IQ and socioeconomic upbringing. When tested on mental rotation tasks, men averaged 66 percent correct compared to 53 percent correct for women. Magnetic resonance imaging (MRI) revealed an approximately 10 percent difference between men and women in the overall amount of parietal lobe surface area: 43 square centimeters for men and 40 square centimeters for women.
What selective pressure(s) gave an advantage to men for mental object rotation? Ability to model prey movement? Or tools building? Or what exactly?
Noted Harvard psychologist and author Steven Pinker has an article in the New York Times Magazine entitled My Genome, My Self. He explores the relationship between your DNA sequence and your personal identity.
Last fall I submitted to the latest high-tech way to bare your soul. I had my genome sequenced and am allowing it to be posted on the Internet, along with my medical history. The opportunity arose when the biologist George Church sought 10 volunteers to kick off his audacious Personal Genome Project. The P.G.P. has created a public database that will contain the genomes and traits of 100,000 people. Tapping the magic of crowd sourcing that gave us Wikipedia and Google rankings, the project seeks to engage geneticists in a worldwide effort to sift through the genetic and environmental predictors of medical, physical and behavioral traits.
Parenthetically, I think the Personal Genome Project is an excellent idea. DNA sequence information is becoming so cheap so far that our biggest problem is how to compare the genetic data of a large number of people against many characteristics about them. Lots of genetic variations make only small contributions to traits. So picking out those influences is very difficult. A large sample size of people is needed to give scientists decent odds of picking up on which genetic variants make a difference in which trait.
The Personal Genome Project is an initiative in basic research, not personal discovery. Yet the technological advance making it possible — the plunging cost of genome sequencing — will soon give people an unprecedented opportunity to contemplate their own biological and even psychological makeups. We have entered the era of consumer genetics. At one end of the price range you can get a complete sequence and analysis of your genome from Knome (often pronounced “know me”) for $99,500. At the other you can get a sample of traits, disease risks and ancestry data from 23andMe for $399. The science journal Nature listed “Personal Genomics Goes Mainstream” as a top news story of 2008.
The $99,500 service doesn't offer utility commensurate to the money at this point because we do not know the functional significance of the vast bulk of the locations in the genome that differ from one person to the next. Still, if you are rich why not get the full picture? You'll find out more quickly for each new genetic discovery whether it matters to you.
In order to keep costs down the 23andMe folks do not check for as many genetic differences. They focus more on telling you about genetic variants suspected or known to be useful or at least revealing. Their disease risk info might spur you to get tested more often for some form of cancer for which you have higher risk (early detection being great for raising the chance of a cure). Or you might look at your test results and resolve to try harder to make lifestyle and diet choices to reduce your risk of heart disease. I also think their ancestry analysis could be especially interesting for adopted people and others who do not know much about where their ancestors came from.
Pinker says we can make use of genetic information without going crazy about it (my phrasing, not his).
Though the 20th century saw horrific genocides inspired by Nazi pseudoscience about genetics and race, it also saw horrific genocides inspired by Marxist pseudoscience about the malleability of human nature. The real threat to humanity comes from totalizing ideologies and the denial of human rights, rather than a curiosity about nature and nurture. Today it is the humane democracies of Scandinavia that are hotbeds of research in behavioral genetics, and two of the groups who were historically most victimized by racial pseudoscience — Jews and African-Americans — are among the most avid consumers of information about their genes.
I think we are going to find lots of ways to use genetic information and this will fragment into different industries. Lots of people will write software to analyze genetic data for different purposes. For example, there'll be a mini-industry on genes and diet. There'll be another on ancestry tracing. There'll be still another on genetics and sports. Is there a way to compensate for your genes with drugs to make you perform just as well as someone who has better genes for swimming or tennis? Companies will look for ways.
DNA won't just get translated into static information to ponder. You will ask how best to interact with your DNA. That'll involve drug development, diet, exercise, and perhaps creation of environments that complement your genetic profile.
Of course, some answers from genome sequencing will not be pretty. Pinker has decided not to be told whether he carries a variant of the apolipoprotein E gene (APOE) that increases risk of Alzheimer's disease. It is understandable to not want to know about something that you can't do anything about. But as the decades go by and more effective treatments get developed for a long list of diseases some of the highly undesirable genetic variants will get matched up with useful treatments. So learning about your worst genetic variants won't carry as much a sense of futility and loss as is the case today. There is one case where genetic knowledge can be used today: testing before pregnancy. Turns out, there's a new company which specializes in pre-pregnancy genetic testing. They ask on their web site "Thinking about starting a family?".
The genes analyzed by a new company called Counsyl are more actionable, as they say in the trade. Their “universal carrier screen” is meant to tell prospective parents whether they carry genes that put their potential children at risk for more than a hundred serious diseases like cystic fibrosis and alpha thalassemia. If both parents have a copy of a recessive disease gene, there is a one-in-four chance that any child they conceive will develop the disease. With this knowledge they can choose to adopt a child instead or to undergo in-vitro fertilization and screen the embryos for the dangerous genes. It’s a scaled-up version of the Tay-Sachs test that Ashkenazi Jews have undergone for decades.
How does this work? First a couple gets tested. If they do not have any of the problematic genetic variations which this company screens for then they can start a pregnancy the old fashioned way. If they do have variations which could cause genetic diseases in offspring they then have some choices to make. But the point is they really do have choices they can make. As Pinker says, this is actionable information.
As biotechnology and biomedical science advance we will find many more ways in which we can respond to genetic knowledge about ourselves and take useful decisions. But already today we can make decisions about reproduction based on genetic tests. Granted, those tests do not cover every way that genes can affect health or other qualities of offspring. But a genetic screen for known well characterized genetic diseases is a good start.
I wonder whether small Amish populations that have high rates of a few genetic diseases would be willing to do matchmaking based on genetic data. They might not be willing to use IVF and pre-implantation genetic diagnosis (PGD) for embryo selection. But for those mutations which are only harmful when there are two copies then matchmaking could be used to avoid marriages between pairs who carry the same harmful genetic variant. Something like the Counsyl test could help to reduce the frequent of genetic diseases in the Amish or other populations that have higher frequencies of genetic diseases.
T. Boone Pickens wants to transition cars to natural gas power. But his plan has elicited some opposition. The CEO of FedEx thinks electric cars are the way to go and FuturePundit is inclined to agree.
But Mr. Pickens has his opponents, including FedEx CEO Fred Smith, who favors electrification of the transporation fleet. Mr. Smith argues that hybrids are the way to go, and is putting his money where his mouth is. With 80,000 motorized vehicles, FedEx now boasts the largest fleet of commercial hybrid trucks in North America.
Without naming Mr. Pickens, the company’s director of sustainability, Mitch Jackson, upped the ante on Sunday with a blog item blasting natural gas as transport fuel of the future. After citing a list of reasons against using natural gas instead of diesel, Mr. Jackson concludes that “substituting one fossil fuel for another may mean we’re shifting our energy supply, but it doesn’t necessarily mean we’re going anywhere.”
I see a few downsides to natural gas. First off, I do not want a car with a shorter travel range and less space for luggage due to the bigger storage tank. Second, burning natural gas doesn't increase vehicle fuel efficiency by much. Whereas hybrids do. Third, we need to move toward ways of powering cars that break our dependency not just on oil but on fossil fuels in general. When oil production starts declining the demand will rise for natural gas as a substitute for other purposes. Why put transportation on natural gas too?
Advances in lithium battery technology are going to enable us to use electricity for most of our miles traveled on the ground. That is good news because we have multiple ways to generate electricity including several ways that do not use fossil fuels as inputs. Nuclear, geothermal, wind, solar, and hydro will all compete. Their costs will go down, not up. They are far more sustainable than fossil fuels.
To be fair, Boone wants to cut the demand for natural gas to generate electricity by building more wind farms. This would free up natural gas for use in transportation. But current gasoline prices limit the potential demand for natural gas vehicles. Hybrids face a similar problem with hybrid sales down more than overall car sales. The technologies for hybrids, pluggable hybrids (which currently are far from compelling), and pure electric cars are going to improve and this will reduce the advantages of natural gas powered vehicles.
Update: The car companies mostly seem to be ignoring Pickens about natural gas - at least in their product planning announcements. Whereas the move toward electric vehicles is pretty clear. For example, Ford is going to bring out pure electric and pluggable hybrid electric vehicles as early as next year.
In addition to the new 2010 Fusion hybrid, Ford said the plans include a full battery electric van-type commercial vehicle in 2010, a full battery electric passenger car in 2011, and next-generation hybrid vehicles, including a plug-in version by 2012.
A fully electric passenger car in 2011. Anyone know details about the size of it?
Update II: In a nutshell here is why I prefer electric vehicles: Electric power can be generated from many energy sources. Therefore electric cars will uncouple our societies and economies from such a heavy (and need I say harmful?) dependence on oil. With great batteries suitable for use in cars we can use nukes, solar, geothermal, wind, waves, hydro, natural gas, coal, or other energy sources to generate electric power and therefore to move us down the road.
"Opioid-based narcotics (such as morphine) are the most widely prescribed therapeutic agents for the alleviation of persistent pain; however, it is becoming increasingly clear that morphine is significantly less potent in women compared with men. Until now, the mechanism driving the phenomenon was unknown," said Anne Murphy, Ph.D., a Georgia State Professor of Neuroscience and member of the Center for Behavioral Neuroscience, who conducted the research with Dayna Loyd, Ph.D.
Murphy recently solved the mystery with findings printed in the December issue of The Journal of Neuroscience that show that previously reported differences in morphine's ability to block pain in male versus female rats are most likely due to sex differences in mu-opioid receptor expression in a region of the brain called the periaqueductal gray area (PAG).
Located in the midbrain area, the PAG plays a major role in the modulation of pain by housing a large population of mu-opioid receptor expressing neurons. Morphine and similar drugs bind to these mu-opioid receptors analogous to a 'lock and key' and, ultimately, tell the brain to stop responding to pain signals to the nerve cells resulting in the reduced sensation of pain.
Using a series of anatomical and behavioral tests, Murphy and Loyd were able to determine that male rats have a significantly higher level of mu-opioid receptors in the PAG region of the brain compared with females. This higher level of receptors is what makes morphine more potent in males because less drug is required to activate enough receptors to reduce the experience of pain. Interestingly, when they used a plant-derived toxin to remove the mu-opioid receptor from the PAG, morphine no longer worked, suggesting that this brain region is required for opiate-mediated pain relief.
I wonder what behavioral difference this causes in the daily lives of men and women and why this was selected for.
Scientists have tricked bone marrow into releasing extra adult stem cells into the bloodstream, a technique that they hope could one day be used to repair heart damage or mend a broken bone, in a new study published today in the journal Cell Stem Cell.
When a person has a disease or an injury, the bone marrow mobilises different types of stem cells to help repair and regenerate tissue. The new research, by researchers from Imperial College London, shows that it may be possible to boost the body's ability to repair itself and speed up repair, by using different new drug combinations to put the bone marrow into a state of 'red alert' and send specific kinds of stem cells into action.
In the new study, researchers tricked the bone marrow of healthy mice into releasing two types of adult stem cells – mesenchymal stem cells, which can turn into bone and cartilage and that can also suppress the immune system, and endothelial progenitor cells, which can make blood vessels and therefore have the potential to repair damage in the heart.
While the scientists haven't shown that pushing more stem cells into the bloodstream leads to more healing they have shown they can boost stem cell release by a factor of 100.
"We hope that by releasing extra stem cells, as we were able to do in mice in our new study, we could potentially call up extra numbers of whichever stem cells the body needs, in order to boost its ability to mend itself and accelerate the repair process. Further down the line, our work could lead to new treatments to fight various diseases and injuries which work by mobilising a person's own stem cells from within," added Dr Rankin.
The scientists reached their conclusions after treating healthy mice with one of two different 'growth factors' – proteins that occur naturally in the bone marrow – called VEGF and G-CSF. Following this treatment, the mice were given a new drug called Mozobil.
The researchers found that the bone marrow released around 100 times as many endothelial and mesenchymal stem cells into the bloodstream when the mice were treated with VEGF and Mozobil, compared with mice that received no treatment. Treating the mice with G-CSF and Mozobil mobilised the haematopoietic stem cells – this treatment is already used in bone marrow transplantation.
It isn't always going to be the case that just putting a large number of stem cells onto the scene of injury will lead to some or all needed repairs. Additional work might be necessary to implant signaling chemicals to direct stem cells to the right places and further to instruct them on which types of cells to convert into.
We are going to see stem cells become useful therapeutic tools for at least some problems in the next 10 years and for a lot more problems in the following 10 years.
The study, which appears in the December 18 online version of Cell Stem Cell and the January 2009 print edition of the journal, provides proof of principle that alternative sources of stem cells can be created.
The team, which included scientists from Scripps Research, Peking University, and the University of California, San Diego, conducted the studies to establish novel rat induced pluripotent stem cell lines (riPSCs) and human induced pluripotent stem cell lines (hiPSCs) by using a specific cocktail of chemicals combined with genetic reprogramming, a process whereby an adult cell is returned to its early embryonic state. Pluripotency refers to the ability of a cell to develop into each of the more than 200 cell types of the adult body.
The ability to create pluripotent stem cells (i.e. cells just as flexible as cells removed from embryos) from adult cells promises to allow us to create immunologically compatible replacement organs and stem cell therapies.
(Boston) -- A Boston University School of Medicine-led research team has discovered a more efficient way to create induced Pluripotent Stem (iPS) cells, derived from mouse fibroblasts, by using a single virus vector instead of multiple viruses in the reprogramming process. The result is a powerful laboratory tool and a significant step toward the application of embryonic stem cell-like cells for clinical purposes such as the regeneration of organs damaged by inherited or degenerative diseases, including emphysema, diabetes, inflammatory bowel disease, and Alzheimer's Disease.
Their research titled "iPS Cell Generation Using a Single Lentiviral Stem Cell Cassette" appears on line in the journal Stem Cells.
Prior research studies have required multiple retroviral vectors for reprogramming -- steps that depended on four different viruses to transfer genes into the cells' DNA – essentially a separate virus for each reprogramming gene (Oct4. Klf4, Sox2 and cMyc). Upon activation these genes convert the cells from their adult, differentiated status to what amounts to an embryonic-like state.
Research papers on easier and better ways to create pluripotent stem cells keep coming and coming. Restrictions on creation of pluripotent stem cells from embryos are going to matter less and less as these alternative ways to create such cells keep getting better.
If you can't keep your weight down at a healthy level then you've got an increasing cast of genetic actors to blame for your excess fat. The 6 latest discoveries all are active in the brain.
The international GIANT (Genetic Investigation of Anthropometric Parameters) consortium works on the discovery of obesity genes. So far, the scientists have analyzed two million DNA variations in 15 genome-wide association studies with a total of more than 32,000 participants. The hereby identified candidate genes were validated in 14 further studies including 59,000 participants. In addition to the FTO and MC4R genes already known, it was now possible for six more obesity genes to be identified: TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2, and NEGR1.
Gene expression analyses have shown that all six genes are active in brain cells. Also the previously known two obesity genes, FTO and MC4R, show a similar expression pattern; in case of the MC4R gene, a genotype-dependant influence on the behavior of appetite is already established. Scientists of the German National Genome Research Network (NGFN), Prof. H.-Erich Wichmann and Dr. Iris Heid from the Helmholtz Zentrum München, Institute of Epidemiology, who lead the German participation of this consortium, emphasize: "Definitely, the two main causes for obesity are poor nutrition and lack of physical activity. But the biology of these genes suggests genetic factors underlying the different reaction of people to lifestyle and environmental conditions."
With the exception of the SH2B1 gene, which plays a role in the leptin signalling and thus in the regulation of appetite, none of the other five genes was hitherto discussed as obesity genes. Iris Heid and her collegue Claudia Lamina from the Ludwigs-Maximilians-Universität München are enthused: "The purely statistical approach of the genome-wide association analysis can depict new aspects of the biology of weight regulation, which were previously unanticipated."
As a next step, the scientists evaluate other anthropometric measures, in order to shed light on different aspects of obesity. In addition, they will expand and include further studies into their analysis as they have realized that the individual studies are all too small, and only by means of collaboration, is it possible to achieve further success here.
This project was financed by the German National Genome Research Network (NGFN, head of the Obesity Network: Prof. Johannes Hebebrand, University of Duisburg-Essen; Project Leader Helmholtz Zentrum München: PD Dr. Thomas Illig), the National Institutes of Health, USA, and the Munich Center of Health Sciences of the LMU Munich. The genotyping was carried out at the Institute for Human Genetics of the Helmholtz Zentrum München under the leadership of Prof. Thomas Meitinger.
What I would like to know: How many of these genes regulate appetite? My guess is that most or all play roles in appetite. But maybe some of them control our propensity to exercise by, for example, controlling how much pleasure we experience when exercising or by making us more or less fidgety.
Why make complex chemical plants to produce pharmaceuticals when you can genetically engineer some animals to do it in their own internal chemical factories? The US Food and Drug Administration will soon approve the first genetically engineered animals created for commercial use. For some applications the milk must be processed to extract the drug. But you can easily imagine cows and goats who produce a milk that you drink to get the drug.
In a surprise move, it seems likely the first genetically engineered animal approved for commercial use won't be a fast-growing salmon, as was expected, but a goat that produces an anti-clotting drug in its milk.
We've already got genetically engineered plants working for us. We'll have many genetically engineered animals working as chemical factories in the future. We'll also eventually have genetically engineered service animals to help us in daily tasks. Genetic engineering will speed up the breeding of animals that humans have been doing for thousands of years.
Varying levels of wind farm energy output cause both short-term and long-term problems with demand matching. Some U Wisc-Milwaukee engineers propose a method to dampen the variation of output of wind turbines over shorter time periods.
Now, Asghar Abedini, Goran Mandic and Adel Nasiri at the Department of Electrical Engineering and Computer Science, Power Electronics and Motor Drives Laboratory, University of Wisconsin-Milwaukee, have devised a solution to the electricity grid susceptibility to changes in wind speed.
The researchers have devised a novel control method that can mitigate power fluctuations using the inertia of the wind turbine's rotor as an energy storage component. Simply put, they have created a braking control algorithm that adjusts the rotor speed so that when incoming wind power is greater than the average power, the rotor is allowed to speed up so that it can store the excess energy as kinetic energy rather than generating electricity. This energy is then released when the wind power falls below average.
This approach, the team explains, precludes the need for external energy storage facilities such as capacitors and the additional infrastructure and engineering they entail. Their method also captures wind energy more effectively and so improves the overall efficiency of wind farming potentially reducing the number of turbines required at any given site.
An obvious way to try to store wind energy is to make heavier rotors. This would give the rotors more momentum. But that would increase the mass needed for the towers that hold up the wind turbines and propellers. An alternative would be to run a belt of some sort from the propeller to the ground to have the heavier rotor and electric generator at ground level. But the belt to do this would cost more money. My guess is that wind farm design engineers have considered these ideas and I wonder what impracticalities prevent their use.
Recent animal studies have shown that clioquinol – an 80-year old drug once used to treat diarrhea and other gastrointestinal disorders – can reverse the progression of Alzheimer's, Parkinson's and Huntington's diseases. Scientists, however, had a variety of theories to attempt to explain how a single compound could have such similar effects on three unrelated neurodegenerative disorders.
Researchers at McGill University have discovered a dramatic possible new answer: According to Dr. Siegfried Hekimi and colleagues at McGill's Department of Biology, clioquinol acts directly on a protein called CLK-1, often informally called "clock-1," and might slow down the aging process. The advance online edition of their study was published in Oct. 2008 in the Journal of Biological Chemistry.
"Clioquinol is a very powerful inhibitor of clock-1," explained Hekimi, McGill's Strathcona Chair of Zoology and Robert Archibald & Catherine Louise Campbell Chair in Developmental Biology. "Because clock-1 affects longevity in invertebrates and mice, and because we're talking about three age-dependent neurodegenerative diseases, we hypothesize that clioquinol affects them by slowing down the rate of aging."
Does clioquinol get inhibited by calorie restriction?
I do not recommend you start taking this drug. Clioquinol varies between species of animals and even between dog breeds. It might cause neurotoxicity by chelating metals. But at lower doses that same chelation might be beneficial for some. It might be the cause of subacute myelo-optico-neuropathy (SMON) in 10,000 people in Japan. A recent Cochrane review of the use of clioquinol against Alzheimer's Disease does not find that studies to date show a clear benefit.
Let the researchers mess with this one. If you want to slow your brain aging there are lots of lower risk ways to do that with more certain benefits. Start with more fruits, vegetables, and fish. Then spice it up with turmeric for the curcumin.
Stony Brook University researchers looked at the brains of Bernstein and 16 other people who had been married an average of 20 years and claimed to be still intensely in love. They found that their MRIs showed activity in the same regions of the brain as those who had just fallen in love.
Social psychologist Arthur Aron says that researchers simply didn't believe those who claim to feel intensely for each other after decades of marriage.
"But in survey after survey we always have these people who have been together a long time and say they are intensely in love. It was always chalked up to self-deception or trying to make a good impression," he said.
What I'd like to know: Do the people who maintain this feeling for decades carry genetic variants that have coded for them to bond much more heavily than the average person? I'd like to see these people compared with people who've been divorced at least twice using vasopression and oxytocin genes for starters. The delivery of vasopressin receptor gene therapy into the ventral pallidum of male voles made them more monogamous. In the future I expect some ladies will surreptitiously deliver gene therapy into the brains of their boyfriends to get them to stay around. But if the guy is already playing the field he might bond to another women he's bedding. So use of this sort of therapy requires careful staging to achieve the desired outcome.
Another future option: Women who want to stay in love forever who have the bonding brain genes could test prospective mates to choose guys who have the genes that'll keep them in love for a long time.
For people with type 2 (insulin resistant) diabetes a diet with very little carbs lowers blood sugar more than a diet with low glycemic index carbs.
DURHAM, NC -- In a six-month comparison of low-carb diets, one that encourages eating carbohydrates with the lowest-possible rating on the glycemic index leads to greater improvement in blood sugar control, according to Duke University Medical Center researchers.
Patients who followed the no-glycemic diet experienced more frequent reductions, and in some cases elimination, of their need for medication to control type 2 diabetes, according to lead author Eric Westman, MD, director of Duke's Lifestyle Medicine Program. The findings are published online in Nutrition and Metabolism.
"Low glycemic diets are good, but our work shows a no-glycemic diet is even better at improving blood sugar control," he says. "We found you can get a three-fold improvement in type 2 diabetes as evidenced by a standard test of the amount of sugar in the blood. That's an important distinction because as a physician who is faced with the choice of drugs or diet, I want a strong diet that's shown to improve type 2 diabetes and minimize medication use."
Eight-four volunteers with obesity and type 2 diabetes were randomized to either a low-carbohydrate ketogenic diet (less than 20 grams of carbs/day) or a low-glycemic, reduced calorie diet (500 calories/day). Both groups attended group meetings, had nutritional supplementation and an exercise regimen.
After 24 weeks, their glycemic control was determined by a blood test that measured hemoglobin A1C, a standard test used to determine blood sugar control in patients with diabetes. Of those who completed the study, the volunteers in the low-carbohydrate diet group had greater improvements in hemoglobin A1C. Diabetes medications were reduced or eliminated in 95 percent of the low-carbohydrate volunteers, compared to 62 percent in the low-glycemic group. The low-carbohydrate diet also resulted in a greater reduction in weight.
Eating low glycemic index carbohydrates is a good bet if you are going to eat carbohydrates. Probably for someone who does not have obesity or type 2 diabetes a ketogenic very low carb diet is too extreme. There are risks with putting your body into ketosis.
Type 2 diabetes is worth controlling for a number of reasons. For example type 2 diabetes impairs a couple of types of cognitive function.
WASHINGTON — Adults with diabetes experience a slowdown in several types of mental processing, which appears early in the disease and persists into old age, according to new research. Given the sharp rise in new cases of diabetes, this finding means that more adults may soon be living with mild but lasting deficits in their thought processes.
A full analysis appears in the January issue of Neuropsychology, which is published by the American Psychological Association.
Researchers at Canada's University of Alberta analyzed a cross-section of adults with and without adult-onset Type 2 diabetes, all followed in the Victoria Longitudinal Study. At three-year intervals, this study tracks three independent samples of initially healthy older adults to assess biomedical, health, cognitive and neurocognitive aspects of aging. The Neuropsychology study involved 41 adults with diabetes and 424 adults in good health, between ages 53 and 90.
The research confirmed previous reports that diabetes impairs cognition and added two important findings. First, it teased out the specific domains hurt by diabetes. Second, it revealed that the performance gap was not worse in the older group. Thus, the reductions in executive function and processing speed seem to begin earlier in the disease.
Healthy adults performed significantly better than adults with diabetes on two of the five domains tested: executive functioning, with significant differences across four different tests, and speed, with significant differences or trends across five different tests. There were no significant differences on tests of episodic and semantic memory, verbal fluency, reaction time and perceptual speed.
Another example of the high stakes for controlling type 2 diabetes: Type 2 diabetes at least triples risk of heart attack.
Men with type 2 diabetes and men with previous heart attack or stroke had a 3 to 4 fold risk of cardiovascular death compared to men without either disease in the years following the first acute event, according to a study in CMAJ http://www.cmaj.ca/press/pg40.pdf.
The study underscores the high risk of diabetes, as "men with type 2 diabetes and no previous cardiovascular disease had a 3-fold cardiovascular mortality risk compared with men with neither cardiovascular disease nor diabetes at the beginning of the follow-up," write Dr. Gilles Dagenais and colleagues from Laval University and the University of Montreal. However, the study was limited to white men and diabetes was self-reported in two-thirds of cases.
Stay skinny, get a lot of exercise, and eat healthy food so that you do not develop type 2 diabetes. It'll age you more rapidly. Worth avoiding.
A blind guy with the name Wilbur should obviously get a guide horse named Mr. Ed. (and if you are too young to get the reference you are unknowingly suffering from cultural deprivation)
The woman, Ann Edie, was simply blind and out for an evening walk with Panda, her guide miniature horse.
There are no sidewalks in Edie’s neighborhood, so Panda led her along the street’s edge, maneuvering around drainage ditches, mailboxes and bags of raked leaves. At one point, Panda paused, waited for a car to pass, then veered into the road to avoid a group of children running toward them swinging glow sticks. She led Edie onto a lawn so she wouldn’t hit her head on the side mirror of a parked van, then to a traffic pole at a busy intersection, where she stopped and tapped her hoof. “Find the button,” Edie said. Panda raised her head inches from the pole so Edie could run her hand along Panda’s nose to find and press the “walk” signal button.
Edie isn’t the only blind person who uses a guide horse instead of a dog — there’s actually a Guide Horse Foundation that’s been around nearly a decade.
Go, Panda, go! This is a much better Panda than the South Park Sexual Harassment Panda.
Assorted animals are out there helping people in all sorts of real and questionable ways. This is leading to legal battles over rights of disabled people to use service animals to help them with their disabilities.
They’re all showing up in stores and in restaurants, which is perfectly legal because the Americans With Disabilities Act (A.D.A.) requires that service animals be allowed wherever their owners want to go.
Some people enjoy running into an occasional primate or farm animal while shopping. Many others don’t. This has resulted in a growing debate over how to handle these animals, as well as widespread suspicion that people are abusing the law to get special privileges for their pets. Increasingly, business owners, landlords and city officials are challenging the legitimacy of noncanine service animals and refusing to accommodate them. Animal owners are responding with lawsuits and complaints to the Department of Justice. This August, the Arizona Game and Fish Department ordered a woman to get rid of her chimpanzee, claiming that she brought it into the state illegally — she disputed this and sued for discrimination, arguing that it was a diabetes-assistance chimp trained to fetch sugar during hypoglycemic episodes.
Another case in the article involves a bipolar guy with psychotic and homicidal tendencies whose parrot calms him down. Read the description of him in the article. I wouldn't want him as a neighbor.
Sadie rides around town on Eggers’s back in a bright purple backpack specially designed to hold her cage. When he gets upset, she talks him down, saying: “It’s O.K., Jim. Calm down, Jim. You’re all right, Jim. I’m here, Jim.”
If a guy with homicidal tendencies (he admits to them) gets calmed down by a parrot then I say let him walk around with a parrot. I realize they can be noisy. A breeding pair of parrots got lose in Santa Barbara several years ago and as a result sometimes around dusk a dozen parrots nest in a tree near where I live and they chat up a big loud conversation. Definitely lends a more exotic jungle atmosphere to the area. But a parrot that calms down a neurologically messed up and dangerous guy is a parrot that is doing a good job.
The ability to classify pets as service animals has been abused and the article reports airplanes becoming modern day Noah's Arks. Well, so far I haven't had the luck to go on a flight that has chimps and parrots in passenger seats. How about you?
Looking into the future (a futures angle is a requirement here) one can see where all this leads: genetically engineered service animals. Granted, stem cell therapies, gene therapies, and tissue engineering will solve a lot of problems with blindness, severed spinal nerves, shriveled muscles, and deteriorated joints. So human disability should become much more rare. But I see a big future for animals genetically customized to serve important functions like "woof woof" to indicate you are about to hit people in a cross walk or that car that has braked ahead of you while you were engrossed in a cell phone conversation. Pets are going to need to pay attention for us as our gadgets become ever more alluring distractions.
Some might choose chimps as driving assistants. I figure with enough genetic enhancement that chimps could take over the actual task of driving. Then people will be able to text message in their cars without risking a ticket or charge of involuntary manslaughter for doing it.
But the genetically engineered service animals will eventually face stiff competition from artificial intelligences. Will the A.I.'s take over before pet genetic engineering hits full swing?
Update: Okay, I see that people outside of America are especially unlikely to know the legendary Mr. Ed. He's important because he dramatizes the future of horsedom.
Here's another excerpt.
Rajo Devi, 70, had a baby girl, Naveen Lohan, weighing 3lb 4oz, by caesarean section on Nov 28. "Now," she said, "I want a boy."
Rajo and her husband Bala Ram, 72, who live on a farm in the tiny village of Badhu Patti in Haryana, India, are hoping controversial IVF doctor Anurag Bishnoi will help them have a son.
Within 30 years (and probably sooner) I predict stem cell therapies will rejuvenate reproductive organs well enough to allow most women to have babies in their 40s, 50s, and even beyond. Cell manipulation techniques with gene therapies will enable the creation of a woman's own egg rather than use donor eggs.
If a poor farmer in India can afford IVF treatment the prospects for world population control grow dimmer.
Her husband mortgaged all his crop of rice and bamboo for next year and took out high interest loans to pay for the £2,000 IVF treatment.
IVF pregnancy initiation rates continue to grow (note some of these pregnancies abort).
And the Canadian Fertility and Andrology Society says the pregnancy rate for in vitro fertilization was 35 per cent in 2007, up nine percentage points since 1999, when the group first started collecting these statistics.
On the bright side, in the next 10 years we are going to find out which genetic alleles contribute to differences in intelligence. So at least some of the IVF babies of the future will be a lot smarter. We are going to need lots of smarts to solve some of the problems caused by overpopulation.
Not all the problems caused by overpopulation will get solved though. You might want to burn up some of the dwindling supplies of fossil fuels to go visit and see animals in the wild that'll go extinct in a few decades. Ecotourism ahead of extinctions and habitat loss is now the rage.
From the tropics to the ice fields, doom is big business. Quark Expeditions, a leader in arctic travel, doubled capacity for its 2008 season of trips to the northern and southernmost reaches of the planet. Travel agents report clients are increasingly requesting trips to see the melting glaciers of Patagonia, the threatened coral of the Great Barrier Reef, and the eroding atolls of the Maldives, Mr. Shapiro said.
The most notable long term pattern in human evolution has been humanity's growing capability to dominate all ecosystems. The rest of nature is not capable of restraining us and I do not expect we will restrain ourselves as our powers continue to grow.
Women who took beta carotene or vitamin C or E or a combination of the supplements had a similar risk of cancer as women who did not take the supplements, according to data from a randomized controlled trial in the December 30 online issue of the Journal of the National Cancer Institute.
People who eat lots of fruits and vegetables get less cancer. But other people do not like to eat lots of fruits and vegetables. They'd rather chow down on a Big Mac, a Whopper, or maybe some Twinkies with a chocolate milk shake. Still, veggies and fruits really are the ticket.
Epidemiological studies have suggested that people whose diets are high in fruits and vegetables, and thus antioxidants, may have a lower risk of cancer. Results from randomized trials that address the issue, however, have been inconsistent and have rarely supported that observation.
The problem is knowing what in the foods cut cancer risks. Could be fiber. Could be non-vitamin antioxidants such as polyphenols. Could be minerals like magnesium. Or maybe the veggies with lower glycemic index just reduce the sugar surge after meals and therefore reduce the surge in insulin and other hormones that can stimulate cells to become cancerous. Probably the answer is multiple factors in fruits and vegetables mean it is hard to find a shortcut.
In the current study, Jennifer Lin, Ph.D., of the Brigham and Women's Hospital and Harvard Medical School in Boston, and colleagues tested the impact of antioxidant supplements on cancer incidence in a randomized controlled trial. A total of 7,627 women who were at high risk of cardiovascular disease were randomly assigned to take vitamin C, vitamin E, or beta-carotene.
With an average of 9.4 years of follow-up time, there was no statistically significant benefit from antioxidant use compared with placebo in terms of disease risk or mortality due to cancer. Overall, 624 women developed cancer and 176 died from cancer during the follow-up time. Compared with placebo, the relative risk of a new cancer diagnosis was 1.11 for women who took vitamin C, 0.93 for women who took vitamin E, and 1.00 for women who took beta carotene. None of these relative risks was statistically significantly different from 1.
Eat good food. Some day scientists will come up with a way to make The Six Dollar Burger and hot dogs as beneficial as cabbage, eggplant, and arugula. But that day hasn't come yet.
Abundant tiny particles of diamond dust exist in sediments dating to 12,900 years ago at six North American sites, adding strong evidence for Earth's impact with a rare swarm of carbon-and-water-rich comets or carbonaceous chondrites, reports a nine-member scientific team.
These nanodiamonds, which are produced under high-temperature, high-pressure conditions created by cosmic impacts and have been found in meteorites, are concentrated in similarly aged sediments at Murray Springs, Ariz., Bull Creek, Okla., Gainey, Mich., and Topper, S.C., as well as Lake Hind, Manitoba, and Chobot, Alberta, in Canada. Nanodiamonds can be produced on Earth, but only through high-explosive detonations or chemical vaporization.
Last year a 26-member team from 16 institutions proposed that a cosmic impact event, possibly by multiple airbursts of comets, set off a 1,300-year-long cold spell known as the Younger Dryas, fragmented the prehistoric Clovis culture and led to the extinction of a large range of animals, including mammoths, across North America. The team's paper was published in the Oct. 9, 2007, issue of the Proceedings of the National Academy of Sciences. (News release on the 2007 paper is available at: http://tinyurl.com/82988t, with link to a copy of that paper.)
We really should develop a much bigger asteroid detection and tracking system and an asteroid defense system. Really, I'm serious. This is more important than the manned space program and more important than probes that go to other planets. Heck, there's even a scientific angle because knowing a lot more about asteroids will provide insights into the solar system's development and even identify asteroids useful for terraforming Mars.
Think processed foods are bad for you? Not sure why exactly? One possibility: inorganic phosphates in food might boost the growth of lung cancer.
New research in an animal model suggests that a diet high in inorganic phosphates, which are found in a variety of processed foods including meats, cheeses, beverages, and bakery products, might speed growth of lung cancer tumors and may even contribute to the development of those tumors in individuals predisposed to the disease.
The study also suggests that dietary regulation of inorganic phosphates may play an important role in lung cancer treatment. The research, using a mouse model, was conducted by Myung-Haing Cho, D.V.M., Ph.D., and his colleagues at Seoul National University, appears in the first issue for January of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
"Our study indicates that increased intake of inorganic phosphates strongly stimulates lung cancer development in mice, and suggests that dietary regulation of inorganic phosphates may be critical for lung cancer treatment as well as prevention," said Dr. Cho.
Of course, if you are eating a diet high in vegetables and fruits and low in processed foods you do not need to know why exactly the processed foods are bad for you. Whether this study has identified a real reason to avoid processed foods or not we already know that drinking colas or other sodas isn't good for us and neither is eating processed cheese spread.
San Francisco State University Psychology Professor David Matsumoto compared the facial expressions of sighted and blind judo athletes at the 2004 Summer Olympics and Paralympic Games. More than 4,800 photographs were captured and analyzed, including images of athletes from 23 countries.
"The statistical correlation between the facial expressions of sighted and blind individuals was almost perfect," Matsumoto said. "This suggests something genetically resident within us is the source of facial expressions of emotion."
Matsumoto found that sighted and blind individuals manage their expressions of emotion in the same way according to social context. For example, because of the social nature of the Olympic medal ceremonies, 85 percent of silver medalists who lost their medal matches produced "social smiles" during the ceremony. Social smiles use only the mouth muscles whereas true smiles, known as Duchenne smiles, cause the eyes to twinkle and narrow and the cheeks to rise.
I expect we will eventually have imaging processing software that we can use when watching politicians and other figures on TV that would let us know things like when we are seeing social smiles versus Duchenne smiles. Automated emotional interpretation such as lie detection by facial expression reading
The high point in belief that environment is the source of all behavior was reached a long time ago with B.F. Skinner. I can't believe the guy was ever taken seriously.
NASHVILLE, Tenn.--For risk-takers and impulsive people, New Year's resolutions often include being more careful, spending more frugally and cutting back on dangerous behavior, such as drug use. But new research from Vanderbilt finds that these individuals--labeled as novelty seekers by psychologists--face an uphill battle in keeping their New Year's resolutions due to the way their brains process dopamine. The research reveals that novelty seekers have less of a particular type of dopamine receptor, which may lead them to seek out novel and exciting experiences--such as spending lavishly, taking risks and partying like there's no tomorrow.
The research was published Dec. 31, 2008, in the Journal of Neuroscience.
The neurotransmitter dopamine is produced by a select group of cells in the brain. These dopamine-producing cells have receptors called autoreceptors that help limit dopamine release when these cells are stimulated.
"We've found that the density of these dopamine autoreceptors is inversely related to an individual's interest in and desire for novel experiences," David Zald, associate professor of psychology and lead author of the study, said. "The fewer available dopamine autoreceptors an individual has, the less they are able to regulate how much dopamine is released when these cells are engaged. Because of this, novelty and other potentially rewarding experiences that normally induce dopamine release will produce greater dopamine release in these individuals."
The researchers used positron emission topography (PET) brain scans to help them reach this conclusion.
The researchers used positron emission topography to view the levels of dopamine receptors in 34 healthy humans who had taken a questionnaire that measured the novelty-seeking personality trait. The questionnaire measured things such as an individual's preference for and response to novelty, decision-making speed, a person's readiness to freely spend money, and the extent to which a person is spontaneous and unconstrained by rules and regulations. The higher the score, the more likely the person was to be a novelty seeker.
The researchers found that those that scored higher on the novelty-seeking scale had decreased dopamine autoreceptor availability compared to the subjects that scored lower.
If it becomes possible to use a drug to increase the number of dopamine autoreceptors will some thrill-seekers or perhaps some drug abusers opt to change their brain in such a fundamental way in order to gain greater ability to control and restrict their own actions? I can imagine compulsive spenders opting for such a treatment. But skiers, skydivers, and other thrill seekers might decide they'd rather continue to pursue extreme sports.