Yet another electric battery start-up touting a big advance in battery technology.
A start-up based in Menlo Park, CA, plans to sell a new type of anode for lithium-ion batteries that, the company says, will let electric vehicles travel farther and mobile devices last longer without a recharge. Amprius' lithium-ion anodes are made of silicon nanowires, which can store 10 times more charge than graphite, the material used for today's lithium-ion battery anodes. According to the company, electric vehicles that run 200 miles between charges could go 380 miles on its batteries, and laptops that have four hours of run time could last for seven hours between charges.
All of the start-up activity in battery technology makes me optimistic that we can shift away from liquid fuels for most ground transportation uses. But will the battery tech come soon enough for Peak Oil? The answer that question is still not clear.
Futuristic speculative questions sometimes become present day practical questions. Have you asked yourself what price you'd be willing to pay to get your genome fully sequenced?
Complete Genomics, a start-up based in Mountain View, CA, has again lowered the stick in the financial limbo dance of human genome sequencing, announcing in the journal Science that it has sequenced three human genomes for an average cost of $4,400. The most recently sequenced genome--which happens to be that of genomics pioneer George Church--cost just $1,500 in chemicals, the cheapest published yet.
This doesn't mean you can get your genome sequenced for $4400. They also had labor, equipment, and lab space costs as well as data post-processing costs. But the overall costs are still very low.
Their error rate exceeds that of previous efforts at complete genome sequencing.
In order to estimate their error rate, the researchers tested 291 random novel non-synonymous variants by targeted sequencing in sample NA07022. Based on the results, they calculated an error rate of about one in 100,000 bases, which the company claims "exceeds the accuracy rate achieved in other published complete genome sequences."
While the price keeps dropping the practical value of a person's genetic sequence is rising with more discoveries about what all the genetic differences mean. The rapid descent in genome sequencing costs has advanced so far that lower prices matter less than what you can do with the information. At this point the bigger improvements to the value equation for getting a full genome sequencing will come from scientific discoveries about what all the genetic variations mean.
The lower prices will lead to a flood of genetic data that will lead to discoveries about what the data means. In a few years knowing your full genetic sequence will become quite useful.
Recently Pauline C. Ng, Sarah S. Murray, Samuel Levy and J. Craig Venter sent genetic samples to genetic testing services Navigenics and 23andme and wrote a paper in nature comparing the results. The two companies were pretty accurate in their testing. But their interpretations of the results differed and were speculative. Click thru and read the details. We do not yet know enough about the real significance of the vast bulk of the genetic differences.
What is missing from climate models?
OAK RIDGE, Tenn., Oct. 9, 2009 -- For the first time, climate scientists from across the country have successfully incorporated the nitrogen cycle into global simulations for climate change, questioning previous assumptions regarding carbon feedback and potentially helping to refine model forecasts about global warming.
My own reaction: amazement. We are in the year 2009 and only now the nitrogen cycle gets added to climate models? What other important factors are not yet in climate models? Does anyone know? I'm looking for a knowledgeable reply, not a rant. What is the state of climate models? What are the prospects for more accurate models 5, 10, 20 years from now?
These scientists expect more rapid climate change as a result of adding the nitrogen cycle.
The results of the experiment at the Department of Energy's Oak Ridge National Laboratory and at the National Center for Atmospheric Research are published in the current issue of Biogeosciences. They illustrate the complexity of climate modeling by demonstrating how natural processes still have a strong effect on the carbon cycle and climate simulations. In this case, scientists found that the rate of climate change over the next century could be higher than previously anticipated when the requirement of plant nutrients are included in the climate model.
ORNL's Peter Thornton, lead author of the paper, describes the inclusion of these processes as a necessary step to improve the accuracy of climate change assessments.
You might think climate models can be really accurate even without the nitrogen cycle. But recall a recent post I did about biofuels boosting nitrous oxide emissions and thereby causing big warming effects. Where the nitrogen goes and in what form is very important for the climate.
MBL, WOODS HOLE, MA—A report examining the impact of a global biofuels program on greenhouse gas emissions during the 21st century has found that carbon loss stemming from the displacement of food crops and pastures for biofuels crops may be twice as much as the CO2 emissions from land dedicated to biofuels production. The study, led by Marine Biological Laboratory (MBL) senior scientist Jerry Melillo, also predicts that increased fertilizer use for biofuels production will cause nitrous oxide emissions (N2O) to become more important than carbon losses, in terms of warming potential, by the end of the century.
Fertilizer usage is going to rise anyway due to increasing human population and industrialization. So how much will nitrous oxide emissions increase in the 21st century? Also, how much will fertilizer run-off and phytoplankton blooms increase? Will the Antarctic continent become livable as a result? Always look on the bright side of life.
Why is H1N1 influenza vaccine coming out so slowly in the United States? Dr. Scott Gottlieb, a former FDA deputy commissioner, says a few policy decisions slow the production of vaccine.
Why do adjuvants matter? An adjuvanted H1N1 vaccine being used in Europe contains 3.75 micrograms of vaccine stock. The same vaccine in the U.S., without the adjuvant, requires 15 micrograms of vaccine for equal potency. If we used adjuvants, we could have had four times the number of shots with the same raw material.
Our regulators are more risk-averse. If a much more lethal pandemic flu strain popped up would the regulators continue to be so conservative?
We need to move beyond the use of chicken eggs to produce virus proteins for vaccine. The much more rapid and scalable approach using mammalian cells is already in use in Europe, not so in the US. Again, regulatory conservatism makes a difference.
The third policy decision was to stick for too long with a proven, but slow process for making flu shots that uses chicken eggs to grow the raw vaccine material. Shots can be made much faster using mammalian cells to grow vaccine, and this process is already being used in Europe. The cell-based vaccines are unlikely to be approved in the U.S. Our precaution when it comes to vaccines means we don't easily embrace novel technologies, even if the Europeans would part with some of their limited supply.
Luckily H1N1 isn't lethal to all that many people. Tens of thousands might die. But a repeat of 1918 levels of lethality would require a far far less conservative approach to vaccine approvals. Would the US government make the needed changes in regulatory policy when tens of millions of lives are at stake?
Forget global free trade when lives are at stake. Where the vaccine manufacturing plants are located also matters.
In 2004, only two companies were licensed to sell flu vaccine in the United States; now there are five, but only one, Sanofi-Pasteur, has a domestic plant. The others — GlaxoSmithKline, Novartis, CSL Ltd. and Medimmune — use plants in England, Germany and Australia.
The drawback of relying on foreign plants was made clear recently when the Australian government pressured CSL to keep its vaccine at home instead of fulfilling its contract for 36 million doses of swine flu vaccine for the United States.
H1N1 vaccine production is late.
Frieden said the CDC had a cumulative 26.6 million doses of vaccine available -- far short of the 40 to 80 million that had been forecast for the end of October.
My advice: take vitamin D and clean your hands more often.
Yet another claimant to the future best battery throne.
A spinoff from Arizona State University says it can develop a metal-air battery that dramatically outperforms the best lithium-ion batteries on the market, and now it has the funding it needs to prove it.
The amount of battery innovation seems to have really picked up in recent years. Clamor for better batteries for cell phones and laptop computers provides big demand today. At the same time, a big push by car companies to develop more hybrids and pluggable hybrids provides assurances that a far larger source of demand is building. Government policy provides incentives for the latter as well as money for research. Hence lots of start-ups.
An order of magnitude higher energy density? That'd be a game changer if it can work well in real world use.
The U.S. Department of Energy last week awarded a $5.13-million research grant to Scottsdale, AZ-based Fluidic Energy toward development of a metal-air battery that relies on ionic liquids, instead of an aqueous solution, as its electrolyte.
The company aims to build a Metal-Air Ionic Liquid battery that has up to 11 times the energy density of the top lithium-ion technologies for less than one-third the cost.
With great batteries the looming threat of Peak Oil becomes a lot less menacing. 95% of all transportation energy comes in the form of liquid fossil fuels and transportation is the sector most vulnerable to declining oil production. Electric power for cars and trucks would let keep flowing the goods and people even as less oil flows.
Update: Here's an ultracapacitor start-up.
An MIT spinoff just getting off the ground received a huge helping hand from the U.S. Department of Energy on Monday. FastCAP Systems, of Cambridge, MA, received a two-and-a-half-year, $5.35 million grant in the first round of funding ever issued by the new Advanced Research Projects Agency-Energy (ARPA-E). The company aims to commercialize a nanotube-enhanced ultracapacitor, an energy storage device that could greatly reduce the cost of hybrid and electric vehicles and of fast-responding grid-scale energy storage, making it easier to integrate renewable energy sources such as solar and wind-based power.
Capacitors can deliver current faster than batteries and stand between the batteries and the engine and regenerative braking system.
A judge's decision to reduce a killer's sentence because he has genetic mutations linked to violence raises a thorny question – can your genes ever absolve you of responsibility for a particular act?
Regards the idea of genes absolving someone of responsibility: If they do then I think the genes reduce a person's rights at the same time. If a person has genes that compel him to violate the rights of others then that person lacks attributes needed to make that person into a full rights-possessing being.
In my view human rights do not come about as a result of our having spirits or souls. We do not have rights because we all just up and decided we had rights either. A rights-based system requires that the rights-possessing conscious intelligent beings have the capacity to act as moral agents. Someone who is compelled to murder or steal lacks attributes needed in a rights-possessing being. The ability to reason is not by itself sufficient to make a being have the attributes needed to possess rights.
Cutting the sentence of a genetically driven killer by a year is nuts. If someone really can't prevent themselves from carrying out murder then that person needs to be permanently removed from civilized society.
In 2007, Abdelmalek Bayout admitted to stabbing and killing a man and received a sentenced of 9 years and 2 months. Last week, Nature reported that Pier Valerio Reinotti, an appeal court judge in Trieste, Italy, cut Bayout's sentence by a year after finding out he has gene variants linked to aggression. Leaving aside the question of whether this link is well enough understood to justify Reinotti's decision, should genes ever be considered a legitimate defence?
If a lion or tiger kills a human we do not consider it a murderer because we do not view lions and tigers and bears (oh my) as moral agents. I expect genetic research and neuroscience to continue to produce results that leave less room for free will as the agent for decision-making in humans. To the extent that compulsions and drives pull people toward engaging in behaviors those people become less rights-deserving.
Will cutting your cholesterol lower your cancer risk?
PHILADELPHIA – A pair of studies in Cancer Epidemiology, Biomarkers & Prevention, lay to rest the decades-long concern that lower total cholesterol may lead to cancer, and in fact lower cholesterol may reduce the risk of high-grade prostate cancer.
Demetrius Albanes, M.D., a senior investigator at the National Cancer Institute, said early studies suggested that low cholesterol could increase the risk of certain types of cancer.
"Our study affirms that lower total cholesterol may be caused by undiagnosed cancer. In terms of public health message, we found that higher levels of 'good cholesterol' (HDL) seem to be protective for all cancers, which is in line with recommendations for cardiovascular health," said Albanes.
Lowering cholesterol cuts cancer risk 15% overall.
In Platz's study, cholesterol levels had no significant effect on the entire spectrum of prostate cancer incidence, only those that were high-grade, she says.
Platz cautions that, while the group took into account factors that could bias the results, such as smoking history, weight, family history of prostate cancer, and dietary cholesterol, other things could have affected their results. One example is whether men in the study were taking cholesterol-lowering drugs at the time of the blood collections, a data point the researchers expect to analyze soon.
Results of the current study are expected to be published online Nov. 3 in the journal Cancer Epidemiology, Biomarkers & Prevention. Also in the journal is an accompanying paper from the National Cancer Institute showing that lower cholesterol in men conferred a 15 percent decrease in overall cancer cases.
If you want to lower your cholesterol go paleo and make like an ape man.
Could the conventional mainstream wisdom about diet (more carbo, less fat) be, like, totally wrong? Researchers at the Sahlgrenska Academy in Sweden find that children who drink full-fat milk have lower body mass index.
Eight-year-old children who drink full-fat milk every day have a lower BMI than those who seldom drink milk. This is not the case for children who often drink medium-fat or low-fat milk. This is one conclusion of a thesis presented at the Sahlgrenska Academy.
The study showed that children who drink full-fat milk every day weigh on average just over 4 kg less.
"This is an interesting observation, but we don't know why it is so. It may be the case that children who drink full-fat milk tend also to eat other things that affect their weight. Another possible explanation is that children who do not drink full-fat milk drink more soft drinks instead", says dietician Susanne Eriksson, author of the thesis.
Better deep fat than the high fructose corn syrup found in soda.
The scientists also discovered a difference between overweight children who drink full-fat milk every day and those who do not. Children who often drink milk with a fat content of 3% are less overweight. The thesis shows also that the children eat more saturated fat than recommended, but those children who have a high intake of fat have a lower BMI than the children with a lower intake of fat.
For some children there is no deep fat. The children of Woody Allen's futuristic Sleeper knew (or will know) better.
The team, led by Assistant Clinical Professor of Public Health at Warwick Medical School Dr Oscar Franco, has discovered that simultaneously having obesity, high blood pressure and high blood sugar are the most dangerous combination of health factors when developing metabolic syndrome.
How dangerous are these factors? Way more.
In his study, published in the American Heart Association journal Circulation, Dr Franco has identified the most dangerous combination of these conditions to be central obesity, high blood pressure and high blood sugar. People who have all three of these conditions are twice as likely to have a heart attack and three times more likely to die earlier than the general population.
His team looked at 3,078 people to track the prevalence and progress of Metabolic Syndrome as part of the Framingham Offspring Study.
What to do about it? Exercise and a better diet of course.
Intensive lifestyle changes aimed at modest weight loss reduced the rate of developing type 2 diabetes by 34 percent over 10 years in people at high risk for the disease.
My own advice: eat lots and lots of vegetables, drug no sweet drinks, and avoid food that has high fructose corn syrup or sugar in it. Start reading labels.
I suspect the benefit of frequent interaction with health-care professionals mainly came in the form of repetitive encouragement to lose weight and eat better and less food.
The DPP results showed that intensive lifestyle changes, including exercise, reducing calories and fat intake and frequent interaction with health-care professionals, reduced the development of type 2 diabetes by 58 percent after three years. Those assigned to two daily doses of metformin but no lifestyle changes reduced the development of the disease by 31 percent over the same period.
Of course you could just take the drug. It'll only deliver about half the benefit but with much less effort.
Decreased physical activity may have little to do with the recent spike in obesity rates among U.S. adolescents, according to researchers at the Johns Hopkins Bloomberg School of Public Health. Prompted by growing concern that the increase was due to decreased physical activity associated with increased TV viewing time and other sedentary behaviors, researchers examined the patterns and time trends in physical activity and sedentary behaviors among U.S. adolescents based on nationally representative data collected since 1991. The review found signs indicating that the physical activity among adolescents increased while TV viewing decreased in recent years. The results are featured in the October 30 online issue of Obesity Reviews.
"Although only one third of U.S. adolescents met the recommended levels of physical activity, there is no clear evidence they had become less active over the past decade while the prevalence of obesity continued to rise," said Youfa Wang, MD, PhD, MS, senior author of the study and an associate professor with the Bloomberg School's Center for Human Nutrition and the Department of International Health. "During the recent decade, U.S. adolescents had greater access to TV, but significantly fewer of them watched TV for three or more hours per day. In addition, daily physical education attendance rates improved along with the use of physical education class in engaging in physical activity. However, there are considerable differences in the patterns by age, sex and ethnicity."
If less exercise isn't the cause of the obesity epidemic then what is? Some people say it is cheaper food. I'm skeptical. Lots of middle class kids had all the food they could eat in the 1960s. Refrigerators were full. Why did the obesity epidemic come later?
A study in Vancouver BC finds that very few people live in ideal neighborhoods that feature both high walkability and clean air.
A new study compares neighborhoods' walkability (degree of ease for walking) with local levels of air pollution and finds that some neighborhoods might be good for walking, but have poor air quality. Researchers involved in the study include University of Minnesota faculty member Julian Marshall and University of British Columbia faculty Michael Brauer and Lawrence Frank.
I find these results to be important reminders on the value of electric vehicles. Cities and suburbs would both become better for our health if more vehicles were battery powered.
If we had finer granularity maps of pollution I bet it would change housing prices. Just what is the health cost of living 50 yards, 100 yards, or 200 yards from a busy freeway? Also, just driving to work during the busy part of the day is bad because you are right in the lanes breathing soot.
The research team found that, on average, neighborhoods downtown are more walkable and have high levels of some pollutants, while suburban locations are less walkable and have high levels of different pollutants. Neighborhoods that fare well for pollution and walkability tend to be a few miles away from the downtown area. These "win-win" urban residential neighborhoods--which avoid the downtown and the suburban air pollution plus exhibit good walkability--are rare, containing only about two percent of the population studied. Census data indicate that these neighborhoods are relatively high-income, suggesting that they are desirable places to live. Neighborhoods that fare poorly for both pollution and walkability tend to be in the suburbs and are generally middle-income.
I just hate it when an old smelly diesel truck drives by when I'm out for a walk. I see them coming and alter my path to reduce the fume exposure. Sometimes I suck in a big breath just before they pass so I can get upwind of the exhaust before I breathe again.
"The finding that nitric oxide concentrations are highest downtown, while ozone concentrations are highest in the suburbs, is not surprising," said Marshall. "Motor vehicle exhaust is most concentrated downtown, leading to the high nitric oxide concentrations downtown. In contrast, ozone takes time to form. Air masses have moved away from downtown--often, to suburban areas--by the time ozone concentrations reach their highest levels. Thus, reductions in vehicle emissions can benefit people who live near high-traffic areas and also people living in less dense areas."
I think more people who live in polluted areas ought to get HEPA filters. Also, again, this report is an argument for electric cars and trucks.
Fat around your internal organs is thought to be a much bigger risk factor for heart disease than fat near the surface of the skin. Well, if you go on a diet, exercise, get your weight down, and then eventually go off the diet continued exercise will prevent the resulting weight gain from happening where the risk factor is greatest.
BIRMINGHAM, Ala. - A study conducted by exercise physiologists in the University of Alabama at Birmingham (UAB) Department of Human Studies finds that as little as 80 minutes a week of aerobic or resistance training helps not only to prevent weight gain, but also to inhibit a regain of harmful visceral fat one year after weight loss.
The study was published online Oct. 8 and will appear in a future print edition of the journal Obesity.
Unlike subcutaneous fat that lies just under the skin and is noticeable, visceral fat lies in the abdominal cavity under the abdominal muscle. Visceral fat is more dangerous than subcutaneous fat because it often surrounds vital organs. The more visceral fat one has, the greater is the chance of developing Type 2 diabetes and heart disease.
80 minutes per week of either aerobic or resistance training prevents any fat weight gain around the internal organs. This is good news.
"What we found was that those who continued exercising, despite modest weight regains, regained zero percent visceral fat a year after they lost the weight," Hunter said. "But those who stopped exercising, and those who weren't put on any exercise regimen at all, averaged about a 33 percent increase in visceral fat.
It takes at least an hour a day of exercise to prevent weight gain. But 80 minutes per week to prevent the harmful form of weight gain is only 19% of the hour per day amount. So this is a lot easier.
You've heard that we shouldn't judge people by their appearances and that appearances are only skin deep. Well no. People can predict the aggressiveness of other people after viewing their facial pictures for less than a second.
Angry words and gestures are not the only way to get a sense of how temperamental a person is. According to new findings in Psychological Science, a journal of the Association for Psychological Science, a quick glance at someone's facial structure may be enough for us to predict their tendency towards aggression.
Facial width-to-height ratio (WHR) is determined by measuring the distance between the right and left cheeks and the distance from the upper lip to the mid-brow. During childhood, boys and girls have similar facial structures, but during puberty, males develop a greater WHR than females. Previous research has suggested that males with a larger WHR act more aggressively than those with a smaller WHR. For example, studies have shown that hockey players with greater WHR earn more penalty minutes per game than players with lower WHR.
Psychologists Justin M. Carré, Cheryl M. McCormick, and Catherine J. Mondloch of Brock University conducted an experiment to see if it is possible to predict another person's propensity for aggressive behavior simply by looking at their photograph. Volunteers viewed photographs of faces of men for whom aggressive behavior was previously assessed in the lab. The volunteers rated how aggressive they thought each person was on a scale of one to seven after viewing each face for either 2000 milliseconds or 39 milliseconds.
We have the innate ability to read faces and know things about a person's personality.
The photographs were very revealing: Volunteers' estimates of aggression correlated highly with the actual aggressive behavior of the faces viewed, even if they saw the picture for only 39 milliseconds. Even more interestingly, the volunteers' estimates were also highly correlated with WHR of the faces—the greater the WHR, the higher the aggressive rating, suggesting that we may use this aspect of facial structure to judge potential aggression in others. These findings indicate that subtle differences in face shape may affect personality judgments, which may, in turn, guide how we respond to certain individuals.
Some day these results will lead to an important offspring genetic engineering question: Genetically engineer your kid to look more aggressive than he is in order to intimidate would-be challengers? Or genetically engineer him (or her) to look meek while being ready, willing, and able to aggressively pursue goals?
You don't want to engineer your kid to be physically aggressive but weak or poorly coordinated. Though it'll probably be possible to genetically engineer more for an aggressiveness useful for success in business and less for aggressiveness that leads to time in prison for assault and murder.
Update: Most personality traits are readable from facial expressions. We really are open books.
AUSTIN, Texas—First impressions do matter when it comes to communicating personality through appearance, according to new research by psychologists Laura Naumann of Sonoma State University and Sam Gosling of The University of Texas at Austin.
Despite the crucial role of physical appearance in creating first impressions, until now little research has examined the accuracy of personality impressions based on appearance alone. These findings will be published in the December 2009 issue of Personality and Social Psychology Bulletin, co-written with Simine Vazire (Washington University in St. Louis) and Peter J. Rentfrow (University of Cambridge).
"In an age dominated by social media where personal photographs are ubiquitous, it becomes important to understand the ways personality is communicated via our appearance," says Naumann. "The appearance one portrays in his or her photographs has important implications for their professional and social life."
In the study, observers viewed full-body photographs of 123 people they had never met before. The targets were viewed either in a controlled pose with a neutral facial expression or in a naturally expressed pose. The accuracy of the judgments was gauged by comparing them to the aggregate of self-ratings and that of three informants who knew the targets well, a criterion now widely regarded as the gold standard in personality research.
Even when viewing the targets in the controlled pose, the observers could accurately judge some major personality traits, including extraversion and self-esteem. But most traits were hard to detect under these conditions. When observers saw naturally expressive behavior (such as a smiling expression or energetic stance), their judgments were accurate for nine of the 10 personality traits. The 10 traits were extraversion, agreeableness, conscientiousness, emotional stability, openness, likability, self-esteem, loneliness, religiosity and political orientation.
Does the personality shape the face? Or do genetic factors shape them both?
The brain downshifts to simpler ways of processing information when lacking sleep.
Westchester, Ill. —A study in the Nov.1 issue of the journal Sleep shows that sleep deprivation causes some people to shift from a more automatic, implicit process of information categorization (information-integration) to a more controlled, explicit process (rule-based). This use of rule-based strategies in a task in which information-integration strategies are optimal can lead to potentially devastating errors when quick and accurate categorization is fundamental to survival.
The experimental subjects were West Point cadets. So they were at similar ages, pretty healthy, and smarter than the average population. The decay here is an average. I would be curious to know what the outliers looked like. Likely a subset suffered more severe cognitive decay when sleep-deprived.
Results show that sleep deprivation led to an overall performance deficit on an information-integration category learning task that was held over the course of two days. Performance improved in the control group by 4.3 percent from the end of day one to the beginning of day two (accuracy increased from 74 percent to 78.3 percent); performance in the sleep-deprived group declined by 2.4 percent (accuracy decreased from 73.1 percent to 70.7 percent) from the end of day one to the beginning of day two.
According to co-principal investigators W. Todd Maddox, PhD, professor of psychology, and David M. Schnyer, PhD, associate professor of psychology at the Institute for Neuroscience at the University of Texas in Austin, fast and accurate categorization is critical in situations that could become a matter of life or death. However, categorization may become compromised in people who often experience sleep deprivation in fast-paced, high pressure roles such as doctors, firefighters, soldiers and even parents. Many tasks performed on a daily basis require information-integration processing rather than rule-based categorization. Examples include driving, making a medical diagnosis and performing air-traffic control.
It would be useful to know for each person how rapidly their brain function deteriorates with lack of sleep. Even more useful: an easily administered sleep impairment test that would let one know whether one is currently sleep impaired and if so by how much. Think of it as akin to an alcohol breath test to determine whether you are safe to drive. Some who is both sleep impaired and alcohol impaired especially ought not drive.
Here's the part I find especially interesting: Not all of the sleep-deprived subjects shifted to rules-based strategies for processing information. Would a more severe degree of sleep deprivation eventually cause everyone to shift to less effective approaches for cognitive processing?
Maddox and Schnyer were surprised to find that the source of the information-integration deficit was a subgroup of sleep-deprived individuals who shifted from information-integration strategies when rested to rule-based strategies when sleep deprived. Sleep-deprived participants who used information-integration strategies in both sessions showed no drop in performance in the second session, mirroring the behavior of control participants.
A brain scan that measures white matter distribution might provide predictive results over how each person's brain will respond to sleep deprivation.
The study cites previous research suggesting that differences in cortical white matter predict cognitive vulnerability to the effects of sleep deprivation.
What I want: a watch that would let me know with a sliding bar or color coding just how sleep-deprived I am at the moment. While I'm wishing: the watch also ought to tell me about nutrient deficiencies detected by nanosensors embedded in my body. When will we get such a capability? 2020? 2025?
30% of the American public carry a gene that probably makes them more dangerous on the road. Hey, these people ought to move to cities and take mass transit.
Bad drivers may in part have their genes to blame, suggests a new study by UC Irvine neuroscientists.
People with a particular gene variant performed more than 20 percent worse on a driving test than people without it - and a follow-up test a few days later yielded similar results. About 30 percent of Americans have the variant.
"These people make more errors from the get-go, and they forget more of what they learned after time away," said Dr. Steven Cramer, neurology associate professor and senior author of the study published recently in the journal Cerebral Cortex.
We are not all as well adapted genetically to industrialized civilization. This one gene, brain-derived neurotrophic factor (BDNF), is just one of many genes where we differ from each other in our ability to handle the many products and environmental niches we've created with industrialization. Some people can't handle beer or cocaine or addictive drugs. Some other people can't handle the sleep deprivation made easier by Thomas Edison's invention of the light bulb. Still others can't handle easy access to online gambling or online porn.
Not enough BDNF means your brain functions less well behind the wheel.
This gene variant limits the availability of a protein called brain-derived neurotrophic factor during activity. BDNF keeps memory strong by supporting communication among brain cells and keeping them functioning optimally. When a person is engaged in a particular task, BDNF is secreted in the brain area connected with that activity to help the body respond.
I wonder whether 29 people can provide enough data points to demonstrate an effect. But if the effect is strong maybe it can.
The driving test was taken by 29 people - 22 without the gene variant and seven with it. They were asked to drive 15 laps on a simulator that required them to learn the nuances of a track programmed to have difficult curves and turns. Researchers recorded how well they stayed on the course over time. Four days later, the test was repeated.
Results showed that people with the variant did worse on both tests than the other participants, and they remembered less the second time. "Behavior derives from dozens and dozens of neurophysiologic events, so it's somewhat surprising this exercise bore fruit," Cramer said.
In the future will some people look at their brain gene test results and decide to live next to a subway stop?
Update: If this discovery holds up under further investigation it will be unusual. In the search for genes that influence cognitive ability the researchers are finding that it is hard to find the genetic variants which contribute to differences. They know the variants are there from twins studies and other studies on populations. The thinking now is that bulk of the variants which influence cognitive ability each have only a small influence. So much larger populations are needed to find them.
Researcher Robert Plomin comments that so far the genetic differences influencing IQ appear to each contribute very little to the total differences.
Failing to find genes for intelligence has, in itself, been very instructive for Plomin. Twin studies continue to persuade him that the genes exist. “There is ultimately DNA variation responsible for it,” he says. But each of the variations detected so far only makes a tiny contribution to differences in intelligence. “I think nobody thought that the biggest effects would account for less than 1 percent,” Plomin points out.
That means that there must be hundreds--perhaps thousands--of genes that together produce the full range of gene-based variation in intelligence.
Check out this brief essay by Plomin about IQ and genes in Technology Review.
You can cut your risk of death from swine flu H1N1 with cholesterol-lowering statin drugs.
Overall, 2.1 percent of patients taking statins died, compared to 3.2 percent of patients not taking statins. That means patients taking statins were just under 50 percent less likely to die.
But how quickly do the statins exercise protective effects? Few people will start taking statins before they get the flu in order to cut an already pretty low risk of dying from H1N1.
Update: Someone points out that the real reduction in the risk of dying is 35%. But the 50% figure would be (almost) correct if one used the lower rate as the reference point. The people not taking statins are 47.6% more likely to die.
Another commenter recommends vitamin D. Vitamin D does reduce respiratory infections in children and other lines of evidence point toward an anti-influenza effect from vitamin D. Knowing all this I decided some weeks ago to become more consistent about taking 2000 IU of vitamin D daily.
Recently a commenter asserted (with no evidence - correction: some evidence but not quantitative) that wind power has big reliability problems due to blades and the mechanical assemblies suffering high failure rates. No quantitative data was provided. This got me wondering if there is any publically available data on mean time between failures for assorted wind farms. Anyone know of such sources? Or are the operating companies tight-lipped about their problems? An article in Technology Review about the development of continuously variable transmissions for wind turbines mentions a number of hours that wind turbines are expected to operate: 80,000 hours.
The question is whether the CVT is tough enough. Viryd parent company Fallbrook Technologies has already commercialized its technology as a smooth-shifting alternative to gears and derailleurs in high-end bicycles and is working on larger vehicle applications. Wind power, however, is a particularly demanding application, according to Jason Cotrell, a senior engineer at the Department of Energy's National Wind Technology Center in Golden, CO. "Wind turbines are subject to very high torque for 80,000 hours of operation, so it's a very challenging environment," Cotrell says. "CVTs tend to be complex, and we haven't yet verified that they're suitably robust."
Well, there are 8760 hours per year. A wind farm that operated every hour of the year would run up 80,000 hours in about 9 years and 2 months. But if a wind farm only spins, say, 30 percent of the time then 80,000 hours of operation would occur over a period of 30 years.
I would be very surprised if a wind turbine's transmission could run for 80,000 hours without service. The spinning, vibration, temperature variations, humidity, and other stresses must take their toll. So do wind turbine transmissions last 80,000 hours before total replacement? How much maintenance gets done before total replacement? Do the transmissions or blades tend to fail first? Anyone know?
While I'm asking: What's more expensive, the blades, the transmission, or the generator?
Beware a diet high in fructose.
A diet high in fructose increases the risk of developing high blood pressure (hypertension), according to a paper being presented at the American Society of Nephrology’s 42nd Annual Meeting and Scientific Exposition in San Diego, California. The findings suggest that cutting back on processed foods and beverages that contain high fructose corn syrup (HFCS) may help prevent hypertension.
Over the last 200 years, the rate of fructose intake has directly paralleled the increasing rate of obesity, which has increased sharply in the last 20 years since the introduction of HFCS. Today, Americans consume 30% more fructose than 20 years ago and up to four times more than 100 years ago, when obesity rates were less than 5%. While this increase mirrors the dramatic rise in the prevalence of hypertension, studies have been inconsistent in linking excess fructose in the diet to hypertension.
Fructose is starting to look like a more plausible villain than fat. Perhaps Diane Keaton in Sleeper was right to praise "Deep fat".
Diana Jalal, MD (University of Colorado Denver Health Sciences Center), and her colleagues studied the issue in a large representative population of US adults. They examined 4,528 adults 18 years of age or older with no prior history of hypertension. Fructose intake was calculated based on a dietary questionnaire, and foods such as fruit juices, soft drinks, bakery products, and candy were included. Dr. Jalal’s team found that people who ate or drank more than 74 grams per day of fructose (2.5 sugary soft drinks per day) increased their risk of developing hypertension. Specifically, a diet of more than 74 grams per day of fructose led to a 28%, 36%, and 87% higher risk for blood pressure levels of 135/85, 140/90, and 160/100 mmHg, respectively. (A normal blood pressure reading is below 120/80 mmHg.)
I've gradually become more concerned about fructose. Robert H. Lustig, MD, a UCSF Professor of Pediatrics in the Division of Endocrinology, takes a look at the harms that come from excessive fructose consumption. Note that he says we are eating an order of magnitude more fructose than our ancestors did historically.
Is high fructose consumption from high fructose corn syrup and sucrose sugar responsible for the obesity epidemic? He says our ancestors got about 15 grams per day. Well, a medium sized apple has about 10 grams. So 2 apples will give you more fructose than most of our ancestors consumed. Our bodies are probably not well adapted to handle 150 grams of fructose per day.
Anyone know of a good detailed list of fructose levels in various foods? I've only found short lists of fructose levels in foods.
Might a widely available cholesterol-lowering drug slow or stop the progression of Parkinson's?
(CHICAGO) –Simvastatin, a commonly used, cholesterol-lowering drug, may prevent Parkinson's disease from progressing further. Neurological researchers at Rush University Medical Center conducted a study examining the use of the FDA-approved medication in mice with Parkinson's disease and found that the drug successfully reverses the biochemical, cellular and anatomical changes caused by the disease.
If this happens in humans surely some doctors would have noticed by now? Since Simvastatin is sold by Merck as Zocor and since at least some older patients with Parkinson's also have high cholesterol I wonder how difficult it would be to measure Parkinson's progression in patients already taking Zocor. Ditto for the other statin drugs such as lovastatin (Mevacor), rosuvastatin (Crestor), atorvastatin (Lipitor), and other statins.
"Statins are one of the most widely used cholesterol-lowering drugs throughout the world," said study author Kalipada Pahan, PhD, professor of neurological sciences at Rush University Medical Center. "This may be a safer approach to halt the disease progression in Parkinson's patients."
Pahan and colleagues from Rush, along with researchers at the University of Nebraska Medical Center in Omaha published these findings in the October 28 issue of the Journal of Neurosciences.
The authors have shown that the activity of one protein called p21Ras is increased very early in the midbrain of mice with Parkinson's pathology. Simvastatin enters into the brain and blocks the activity of the p21Ras protein and other associated toxic molecules, and goes on to protect the neurons, normalize neurotransmitter levels, and improves the motor functions in the mice with Parkinson's.
25 million people world-wide use statins including 13 million in the United States (yes, the US uses more statins than the rest of the world combined). So if statins are providing a benefit against Parkinson's does this show up in Parkinson's incidence data?
I would be reluctant to take statins just to cut my risk of Parkinson's. Though for someone with a lot of genetic risk factors for Parkinson's running the other risks from statin side effects (e.g. a skeletal myopathy that damages muscles) might be worth it. My guess is that as genetic risk factors for statin side effects become known it should be possible to accurately predict your individual costs and benefits from statin usage.
Update: In the comments Dave Gore points to a 2007 study that found the protective effect is specific to simvastatin. Thanks Dave.
The researchers examined data from the Decision Support System database of the United States Veterans Affairs Medical System, a database of medical centers throughout the United States which contains diagnostic, pharmaceutical and demographic information on approximately 4.5 millions people.
Using three different models for analysis, the researchers examined the effects of three different statins (atorvastatin, lovastatin and simvastatin) and found that simvastatin showed a strong reduction in the incidence of Alzheimer’s disease in each of the models. The data also showed the same statin was associated with a reduced incidence of Parkinson’s disease.
The researchers speculate that the selective benefit observed with simvastatin might be due to the combination of high potency and the ability to enter the brain.
“The strength of reduction of incidence of dementia with simvastatin is striking,” said lead author Benjamin Wolozin, MD, PhD, a professor of pharmacology at BUSM.
Sounds promising. A good genetic test that would predict side effects might allow many people to take simvastatin for protection.
