By doing counts of different types of blood cells a microfluidic device holds the potential to lower the cost of diagnosing some blood diseases.
Inexpensive, portable devices that can rapidly screen cells for leukemia or HIV may soon be possible thanks to a chip that can produce three-dimensional focusing of a stream of cells, according to researchers.
"HIV is diagnosed based on counting CD4 cells," said Tony Jun Huang, associate professor of engineering science and mechanics, Penn State. "Ninety percent of the diagnoses are done using flow cytometry."
Huang and his colleagues designed a mass-producible device that can focus particles or cells in a single stream and performs three different optical assessments for each cell. They believe the device represents a major step toward low-cost flow cytometry chips for clinical diagnosis in hospitals, clinics and in the field.
Microfluidic devices will cut the costs of most laboratory tests. They'll also accelerate the rate of advance of biological science and biotechnology. This bodes well for the development of rejuvenation therapies.
These researchers think they can eventually replace $100k machines with $1k machines.
"The full potential of flow cytometry as a clinical diagnostic tool has yet to be realized and is still in a process of continuous and rapid development," the team said in a recent issue of Biomicrofluidics. "Its current high cost, bulky size, mechanical complexity and need for highly trained personnel have limited the utility of this technique."
Flow cytometry typically looks at cells in three ways using optical sensors. Flow cytometers use a tightly focused laser light to illuminate focused cells and to produce three optical signals from each cell. These signals are fluorescence from antibodies bound to cells, which reveals the biochemical characteristics of cells; forward scattering, which provides the cell size and its refractive index; and side scattering, which provides cellular granularity. Processing these signals allows diagnosticians to identify individual cells in a mixed cell population, identify fluorescent markers and count cells and other analysis to diagnose and track the progression of HIV, cancer and other diseases.
"Current machines are very expensive costing $100,000," said Huang. "Using our innovations, we can develop a small one that could cost about $1,000."
We need huge reductions in medical testing costs so that medical testing can move into the home. You should be able to get tested daily in your bathroom with your test results uploaded to a diagnostic server. The diagnostic server should run a large set of expert systems for medical diagnosis and disease treatment recommendations.
This gene therapy only works on very young mice and more steps are needed to make it useful for reversing hearing loss in the aged.
Researchers at Emory University School of Medicine have shown that introducing a gene called Atoh1 into the cochleae of young mice can induce the formation of extra sensory hair cells.
I want this for a very important non-aged purpose: I want to turn up the volume on music much higher than I let myself listen to now. The ability to repair damage will enable us to get damaged in ways we (or at least the more prudent among us) avoid getting damaged today. We might even be able to identify genetic variants that make more robust hair cells. Then we could use gene therapy or cell therapy to grow cilia hair cells that can handle higher volume.
Their results show the potential of a gene therapy approach, but also demonstrate its current limitations. The extra hair cells produce electrical signals like normal hair cells and connect with neurons. However, after the mice are two weeks old, which is before puberty, inducing Atoh1 has little effect. This suggests that an analogous treatment in adult humans would also not be effective by itself.
Likely at some point in development changes happen to the genome (e.g. DNA methylation) that block gene activity so that Atoh1 can no longer initiate hearing hair cell growth. To grow replacement hearing hair will require turning on more genes than Atoh1 by itself can activate. Once scientists figure out how to turn on all the genes needed to grow replacement they'll still need techniques to safely deliver gene therapy. Or perhaps the repair will get done using cell therapy where cells are primed to do repair and then injected into the inner ear.
Human skin tissue, genetically reprogrammed into human-induced pluripotent stem cells (hiPSCs) , was able to inject the cells into rat hearts and get new heart tissue integrated to the rat hearts.
For the first time scientists have succeeded in taking skin cells from heart failure patients and reprogramming them to transform into healthy, new heart muscle cells that are capable of integrating with existing heart tissue.
The research, which is published online today (Wednesday) in the European Heart Journal , opens up the prospect of treating heart failure patients with their own, human-induced pluripotent stem cells (hiPSCs) to repair their damaged hearts. As the reprogrammed cells would be derived from the patients themselves, this could avoid the problem of the patients' immune systems rejecting the cells as "foreign". However, the researchers warn that there are a number of obstacles to overcome before it would be possible to use hiPSCs in humans in this way, and it could take at least five to ten years before clinical trials could start.
I think we need a legal environment that allows a more aggressive approach to human trials. For someone within 5 years of dying from heart failure the risks (notably cancer) of therapy using hiPSC should be weighed against otherwise inevitable death from heart failure.
The stem cells were derived from older patients with heart disease. This demonstrates a patient's own cells could be reprogrammed to restore damaged tissue.
Recent advances in stem cell biology and tissue engineering have enabled researchers to consider ways of restoring and repairing damaged heart muscle with new cells, but a major problem has been the lack of good sources of human heart muscle cells and the problem of rejection by the immune system. Recent studies have shown that it is possible to derive hiPSCs from young and healthy people and that these are capable of transforming into heart cells. However, it has not been shown that hiPSCs could be obtained from elderly and diseased patients. In addition, until now researchers have not been able to show that heart cells created from hiPSCs could integrate with existing heart tissue.
The danger is that the reprogrammed cells will become cancerous. But if you otherwise have but a few years left to live you should be allowed to throw the dice and try a stem cell therapy.
Ms Limor Zwi-Dantsis, who is a PhD student in the Sohnis Research Laboratory, Prof Gepstein and their colleagues took skin cells from two male heart failure patients (aged 51 and 61) and reprogrammed them by delivering three genes or "transcription factors" (Sox2, Klf4 and Oct4), followed by a small molecule called valproic acid, to the cell nucleus. Crucially, this reprogramming cocktail did not include a transcription factor called c-Myc, which has been used for creating stem cells but which is a known cancer-causing gene.
"One of the obstacles to using hiPSCs clinically in humans is the potential for the cells to develop out of control and become tumours," explained Prof Gepstein. "This potential risk may stem from several reasons, including the oncogenic factor c-Myc, and the random integration into the cell's DNA of the virus that is used to carry the transcription factors – a process known as insertional oncogenesis.
The researchers think we are still 5-10 years away from clinical trials of this approach. I think shows how the regulatory and legal environment causes an excessively conservative and slow approach to development of revolutionary therapies.
Energy analysts at Bernstein say the marginal cost of oil production, already $92 per barrel, is nearing $100 per barrel.
The marginal cost of the 50 largest oil and gas producers globally increased to US$92/bbl in 2011, an increase of 11% y-o-y and in-line with historical average CAGR growth. Assuming another double digit increase this year, marginal costs for the 50 largest oil and gas producers could reach close to US$100/bbl.
Their analysis does not include OPEC or former Soviet Union producers. But this does not matter. Since the former SU and OPEC aren't going to grow their production fast enough to meet rising world demand the marginal cost of the other producers will determine at what price rising demand and market price will meet.
This rapidly rising marginal cost of production is what Peak Oil looks like. Peak Oil is going to happen because marginal cost will go too high for the world economy to afford to pay what it takes to boost production. At that point oil production will start falling. I originally expected peak production to happen at a much higher price for oil. But the European debt crisis, the deceleration of Chinese economic growth, and the continued weak US economic recovery make me think peak global oil production will happen at a price not much higher than current oil prices.
The costs of tight shale oil is very high and high oil prices are needed to keep it flowing.
"The United States is producing an awful amount of oil from tight shale and tight sands reservoirs... If oil prices send a signal and drop below the $90-$80 level it is going to be uneconomic to drill those well. So drilling will stop immediately," said Michel Hulme, fund manager at Lombard Odier.
How high an oil price is needed to start world oil demand headed on a downward slope? Higher or lower than the current price range near $90-100?
Have modern sterile environments and antibiotics boosted the rate of cancer? Do we need to work ourselves into a fevered pitch once or twice a year?
There is an inverse relationship between febrile infection and the risk of malignancies. Interferon gamma (IFN-γ) plays an important role in fever induction and its expression increases with incubation at fever-range temperatures. Therefore, the genetic polymorphism of IFN-γ may modify the association of febrile infection with breast cancer risk.
Why? An immune system turned up to kill off invading bacteria might also react more vigorously to attack aberrant cells in your body that have mutated only part of the way toward becoming cancerous. Cells that have mutated all the way into becoming cancerous often have mutations that cause them to excrete substances that suppress the immune system. So vaccines against well developed cancers have fared poorly. But if the immune system could be stimulated into attacking pre-cancerous cells at much earlier stages then in some cases cancer could be prevented.
It might come down to genetic profiles. If you've got the right version of interferon gamma or other immune modulating molecules then a burning fever might keep the doctor away better than apples.
Chinese women who had at least 1 fever per year at a lower rate of breast cancer.
Information on potential breast cancer risk factors, history of fever during the last 10 years, and blood specimens were collected from 839 incident breast cancer cases and 863 age-matched controls between October 2008 and June 2010 in Guangzhou, China. IFN-γ (rs2069705) was genotyped using a matrix-assisted laser desorption/ionization time-of-flight mass spectrometry platform. Odds ratios (OR) and 95% confidence intervals (CIs) were calculated using multivariate logistic regression. We found that women who had experienced ≥1 fever per year had a decreased risk of breast cancer [ORs and 95% CI: 0.77 (0.61–0.99)] compared to those with less than one fever a year.
The effect of the fever appears to be dependent on which genetic variant of interferon gamma the women carried. Interferons play roles in immune regulation. So this comparison of interferon gamma variants was not randomly chosen.
This association only occurred in women with CT/TT genotypes [0.54 (0.37–0.77)] but not in those with the CC genotype [1.09 (0.77–1.55)]. The association of IFN-γ rs2069705 with the risk of breast cancer was not significant among all participants, while the CT/TT genotypes were significantly related to an elevated risk of breast cancer [1.32 (1.03–1.70)] among the women with <1 fever per year and to a reduced risk of breast cancer [0.63 (0.40–0.99)] among women with ≥1 fever per year compared to the CC genotype. A marked interaction between fever frequencies and the IFN-γ genotypes was observed (P for multiplicative and additive interactions were 0.005 and 0.058, respectively).
The idea that lower infectious disease incidence is associated with higher rates of cancer is not new.
Since the 19th century, it has been repeatedly observed that spontaneous cancer regressions were coincided with acute infections and the cancer patients had a remarkable disease-free history before the onset of cancer –. In the 20th century, an inverse association between infectious diseases, particularly febrile ones, and cancer risk has also been consistently found for malignant melanoma and glioma using modern epidemiological methods , , –.
With the widespread introduction of antibiotics and antipyretics since the beginning of the last century, however, the critical role played by fever has often been overlooked, resulting in considerable changes to the clinical course and magnitude of the immune response that develops following acute infections , . These changes may be part of the reasons for the substantial increase in the age-adjusted incidences or mortalities of malignant diseases during the early part of the last century in western countries  and in the late of the last century in China . It has been observed that every 2% reduction in infectious disease mortality was followed by a 2% increase in cancer mortality over a 10-year interval from 1895 to 1963 in Italy .
It would be handy to have a way to periodically turn up the knob on one's immune system to get it to kill pre-cancerous cells. Genetic engineering might eventually help once we figure out what causes some people to have extremely powerful anti-cancer immune systems. See my previous post. Rare People Have Extreme Anti-Cancer Immune Cells.
An Australian study published in the New England Journal of Medicine finds Assisted Reproduction Technologies (ART) substantially increase birth defect risks.
"The unadjusted risk of any birth defect in pregnancies involving assisted conception was 8.3% (513 defects), compared with 5.8% for pregnancies not involving assisted conception (17,546 defects)," Associate Professor Davies says.
"The risk of birth defects for IVF was 7.2% (165 birth defects); and the rate for ICSI was higher at 9.9% (139 defects).
"A history of infertility, either with or without assisted conception, was also significantly associated with birth defects. While factors associated with the causes of infertility explained the excess risk associated with IVF, the increased risk for a number of other treatments could not readily be explained by patient factors. ICSI, for instance, had a 57% increase in the odds of major defect, although the absolute size of the risk remained relatively small," he says.
Of course the researchers tried to adjust for other causes of defects. For example, older women have greater risks of birth defects even without using ART. But note that since we do not all age at the same rate the women who need ART in order to conceive probably have effectively older reproductive tracts than other women at the same age who are still fertile.
But use of cryopreservation is associated with a reduction in risk of birth defects.
Associate Professor Davies says cryopreservation (freezing) of embryos was associated with a substantially reduced risk of birth defects, particularly for ICSI. "This may be due to developmentally compromised embryos failing to survive the freeze/thaw process," he says.
That's encouraging because it suggests better technologies for embryo selection could lower the rate of birth defects.
A drug that stimulates ovulation raises birth defect risks.
Also of concern was the tripling of risk in women using clomiphene citrate to stimulate ovulation outside of a closely supervised clinical setting.
I expect ART will eventually advance to the point where it will enable lower rates of birth defects than occur naturally. This will happen a few ways:
Note that even for younger women smarter embryo selection will some day make the use of assisted reproduction technologies preferable to the natural way to start pregnancies. ART will lower birth defect rates while also providing the ability to select for embryos that have desired combinations of genetic traits from the two (or more) genetic parents.
Genes play a greater role in forming character traits - such as self-control, decision making or sociability - than was previously thought, new research suggests.
A study of more than 800 sets of twins found that genetics were more influential in shaping key traits than a person's home environment and surroundings.
Psychologists at the University of Edinburgh who carried out the study, say that genetically influenced characteristics could well be the key to how successful a person is in life.
The study of twins in the US – most aged 50 and over– used a series of questions to test how they perceived themselves and others. Questions included "Are you influenced by people with strong opinions?" and "Are you disappointed about your achievements in life?"
The results were then measured according to the Ryff Psychological Well-Being Scale which assesses and standardises these characteristics.
By tracking their answers, the research team found that identical twins - whose DNA is exactly the same - were twice as likely to share traits compared with non-identical twins.
My recurring thought in genetic control of personality: Once it becomes possible for prospective parents to choose brain gene variations for their offspring what sorts of minds will they choose to make? The answer to that question will some day start to determine the future of the human race. My guess is that offspring genetic engineering will become very popular within 20 years at most.
Finally genetic testing costs have fallen far enough to chase after the genetic variants that influence cognitive traits. What makes this chase hard: each genetic variant that influences cognitive traits has only a very small effect. Our brain-altering genetic variants are large in number and each has only small impact.
ITHACA, N.Y. – Genetic factors explain some of the variation in a wide range of people's political attitudes and economic decisions – such as preferences toward environmental policy and financial risk taking – but most associations with specific genetic variants are likely to be very small, according to a new study led by Cornell University economics professor Daniel Benjamin.
The research team arrived at the conclusion after studying a sample of about 3,000 subjects with comprehensive genetic data and information on economic and political preferences. The researchers report their findings in "The Genetic Architecture of Economic and Political Preferences," published by the Proceedings of the National Academy of Sciences Online Early Edition, May 7, 2012.
The study showed that unrelated people who happen to be more similar genetically also have more similar attitudes and preferences. This finding suggests that genetic data - taken as a whole – could eventually be moderately predictive of economic and political preferences. The study also found evidence that the effects of individual genetic variants are tiny, and these variants are scattered across the genome. Given what is currently known, the molecular genetic data has essentially no predictive power for the 10 traits studied, which included preferences toward environmental policy, foreign affairs, financial risk and economic fairness.
This conclusion is at odds with dozens of previous papers that have reported large genetic associations with such traits, but the present study included ten times more participants than the previous studies.
"An implication of our findings is that most published associations with political and economic outcomes are probably false positives. These studies are implicitly based on the incorrect assumption that there are common genetic variants with large effects," said Benjamin. "If you want to find genetic variants that account for some of the differences between people in their economic and political behavior, you need samples an order of magnitude larger than those presently used," he added.
I'm looking forward to the day when I can identify thru genetic testing all the people who are lucky enough to share with me the cognitive traits that enable us to share the same profound understanding of why everyone is wrong when they disagree with us.
Attention, college students cramming between midterms and finals: Binging on soda and sweets for as little as six weeks may make you stupid.
A new UCLA rat study is the first to show how a diet steadily high in fructose slows the brain, hampering memory and learning — and how omega-3 fatty acids can counteract the disruption. The peer-reviewed Journal of Physiology publishes the findings in its May 15 edition.
"Our findings illustrate that what you eat affects how you think," said Fernando Gomez-Pinilla, a professor of neurosurgery at the David Geffen School of Medicine at UCLA and a professor of integrative biology and physiology in the UCLA College of Letters and Science. "Eating a high-fructose diet over the long term alters your brain's ability to learn and remember information. But adding omega-3 fatty acids to your meals can help minimize the damage."
While earlier research has revealed how fructose harms the body through its role in diabetes, obesity and fatty liver, this study is the first to uncover how the sweetener influences the brain.
High-fructose corn syrup makes rats dumber.
The UCLA team zeroed in on high-fructose corn syrup, an inexpensive liquid six times sweeter than cane sugar, that is commonly added to processed foods, including soft drinks, condiments, applesauce and baby food. The average American consumes more than 40 pounds of high-fructose corn syrup per year, according to the U.S. Department of Agriculture.
"We're not talking about naturally occurring fructose in fruits, which also contain important antioxidants," explained Gomez-Pinilla, who is also a member of UCLA's Brain Research Institute and Brain Injury Research Center. "We're concerned about high-fructose corn syrup that is added to manufactured food products as a sweetener and preservative."
I eat a lot of berries,cherries, and dark grapes. They've got lots of antioxidants along with the fructose.
Gomez-Pinilla and study co-author Rahul Agrawal, a UCLA visiting postdoctoral fellow from India, studied two groups of rats that each consumed a fructose solution as drinking water for six weeks. The second group also received omega-3 fatty acids in the form of flaxseed oil and docosahexaenoic acid (DHA), which protects against damage to the synapses — the chemical connections between brain cells that enable memory and learning.
"DHA is essential for synaptic function — brain cells' ability to transmit signals to one another," Gomez-Pinilla said. "This is the mechanism that makes learning and memory possible. Our bodies can't produce enough DHA, so it must be supplemented through our diet."
One gram of DHA per day.
Still planning to throw caution to the wind and indulge in a hot-fudge sundae? Then also eat foods rich in omega-3 fatty acids, like salmon, walnuts and flaxseeds, or take a daily DHA capsule. Gomez-Pinilla recommends one gram of DHA per day.
This is a useful reminder to get on daily DHA.
The progressive disappearance of seed-dispersing animals like elephants and rhinoceroses puts the structural integrity and biodiversity of the tropical forest of South-East Asia at risk. With the help of Spanish researchers, an international team of experts has confirmed that not even herbivores like tapirs can replace them.
"Megaherbivores act as the 'gardeners' of humid tropical forests: They are vital to forest regeneration and maintain its structure and biodiversity", as was explained to SINC by Ahimsa Campos-Arceiz, the lead author of the study that was published in the 'Biotropica' journal and researcher at the School of Geography of the University of Nottingham in Malaysia.
In these forests in East Asia, the large diversity of plant species means that there is not enough space for all the trees to germinate and grow. As well as the scarce light, seed dispersion is made more complicated by the lack of wind due to the trees that are up to 90 metres high. Plant life is then limited to seeds dispersed by those animals that eat pulp. They either scatter seeds by dropping their food, regurgitating it or by defecating later on.
The Asian elephant (Elephas maximus) occupies just 5% of its historical range and its range will likely continue to shrink as more forests get cut down.
With the input of hundreds of experts worldwide, the primate review provides scientific data to show the severe threats facing animals that share virtually all DNA with humans. In both Vietnam and Cambodia, approximately 90 percent of primate species are considered at risk of extinction. Populations of gibbons, leaf monkeys, langurs and other species have dwindled due to rampant habitat loss exacerbated by hunting for food and to supply the wildlife trade in traditional Chinese medicine and pets.
A team of researchers from Singapore, Australia, Switzerland, the UK and the USA has carried out a comprehensive assessment to estimate the impact of disturbance and land conversion on biodiversity in tropical forests. In a recent study published in Nature, they found that primary forests – those least disturbed old-growth forests – sustain the highest levels of biodiversity and are vital to many tropical species.
As the human population grows toward 9 billion people and Asia continues to industrialize habitat loss is going to drive many more species to extinction.
Born between 1945 and 1965? The CDC says you should get tested for a virus that might be destroying your liver.
Anyone born from 1945 to 1965 should get a one-time blood test to see if they have the liver-destroying virus, the Centers for Disease Control and Prevention said in draft recommendations issued Friday.
If one is going to take the time to go visit a doctor what other tests or perhaps vaccinations should one get done? With my car I like to build up a list and get several things done at once. So what about one's body? Should we get revaccinated for stuff we were last vaccinated for as kids? Or any other diseases worth getting tested for?
Longer telomere caps on chromosomes enable cells to divide more times, replace lost cells, and do repairs. Lengthening the caps on telomeres increases life expectancy in mice.
A number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals' genes permanently from the embryonic stage – an approach impracticable in humans. Researchers at the Spanish National Cancer Research Centre (CNIO), led by its director María Blasco, have proved that mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal's genes. And they have done so using gene therapy, a strategy never before employed to combat ageing. The therapy has been found to be safe and effective in mice.
The results are published today in the journal EMBO Molecular Medicine. The CNIO team, in collaboration with Eduard Ayuso and Fátima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Autònoma de Barcelona (UAB), treated adult (one-year-old) and aged (two-year-old) mice, with the gene therapy delivering a "rejuvenating" effect in both cases, according to the authors.
Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals' health, delaying the onset of age-related diseases – like osteoporosis and insulin resistance – and achieving improved readings on ageing indicators like neuromuscular coordination.
This is an interesting result for a number of reasons. First off, why don't mice just have longer telomeres at the start? If the increased life expectancy has no cost in fitness why aren't mouse telomeres longer already?
Second, I am surprised that the longer telomeres didn't enable more cancer growth and therefore cause shorter life expectancy. Telomere shortening every time a cell divides acts like a counter on the max number of times a cell can divide. This functions as a defense against cancer. Some cancers mutate their way past this defense (e.g. by turning on telomerase to make telomeres longer). But presumably others get stopped by cells with telomeres too short to allow further cell division.
The researchers address the cancer issue in a way that suggests to me this would not work for humans.
In 2007, Blasco's group proved that it was feasible to prolong the lives of transgenic mice, whose genome had been permanently altered at the embryonic stage, by causing their cells to express telomerase and, also, extra copies of cancer-resistant genes. These animals live 40% longer than is normal and do not develop cancer.
The mice subjected to the gene therapy now under test are likewise free of cancer. Researchers believe this is because the therapy begins when the animals are adult so do not have time to accumulate sufficient number of aberrant divisions for tumours to appear.
Mice do not live that long to begin with. Humans at middle age given telomerase gene therapy would have decades in which to accumulate aberrant cells that can turn cancerous. So
Third, on the bright side the gene therapy was able to reach a large enough fraction of the cells in the bodies of mice to make a big difference. Very good news because we have need for lots of types of gene therapy to do rejuvenation of our bodies. I wonder what fraction of all the cells in the mice got the gene therapy.
As for the implications for humans: Keep in mind that we already live many times longer than mice. We've got an assortment of optimizations for longer life that might reduce the value of longer telomeres and our cancer risk from longer telomeres might be greater than for mice.
But even if telomere lengthening would boost our all cause mortality today that does not mean this must always be so. Once cancer becomes easily curable the risks from longer telomeres will go way down and we'll left with just the benefits. So gene therapy for telomere lengthening will likely become a useful technique for life extension in about 10 to 20 years.
We will gain another and safer way to get the benefits of longer telomeres: Cell therapy. Separate out cells. Then test different cell lines for mutations. Then extend the telomeres of the safest cells. Then grow up those cells in large numbers and inject those cells back into the body.
A report from the International Monetary Fund predicts a doubling in oil prices.
The International Monetary Fund (IMF) has been warned by its internal research team that there could be a permanent doubling of oil prices in the coming decade with profound implications for global trade.
"This is uncharted territory for the world economy, which has never experienced such prices for more than a few months," the report warns.
Here is the IMF report: The Future of Oil: Geology v Technology Its writers are very up on the debate happening between economists and geologists over future oil production potential. They are familiar with the work of UCSD energy economist James Hamilton, Robert Hirsch's Dept of Energy report on Peak Oil, and geologists who have put forth models predicting future oil production including M. King Hubbert, Colin Campbell, and Ken Deffeyes.
Hamilton (2009), on the other hand, ﬁnds that temporary disruptions in physical oil supply have already had a major role in explaining historical dynamics of oil price movements. And furthermore, he argues that stagnating world oil production, meaning a very persistent reduction in oil supply growth, may have been one of the reasons for the run-up in oil prices in 2007-08. The main reasons why oil supply shocks aﬀect output according to Hamilton is their disruptive eﬀect on key industries such as automotive manufacturing, and their eﬀect on consumers’ disposable incomes. In other words, the main eﬀect is on aggregate demand. As for aggregate supply eﬀects, his view is that there may be short-run impacts due to very low short-run elasticities of substitution between oil and other factors of production. But he assumes that such elasticities get larger over longer horizons, as agents ﬁnd possibilities to substitute away from oil. This is because high prices start to stimulate technological change that can both increase the recovery of oil, and the availability of substitutes for oil. Therefore, even though Hamilton is closest among mainstream economists to seeing real problems emanating from the physical, geological availability of oil, he nevertheless subscribes to the economic or technological view whereby prices must eventually have a decisive impact on production levels.
The IMF authors point out that both the optimists (those expecting continued production increases) and pessimists (those expecting a decline off a production peak) have been wrong. But Ken Deffeyes's 2005 oil production peak prediction is not as wrong as it looks at first glance. When reading and listening to talk about oil production be very aware of difference between oil production (where we get black liquid out of the ground) and all liquids production. Usually when a story in the press refers to oil production they are really reporting on all liquids production. The quite small growth in liquids production since 2005 has come in the form of non-conventionals such as natural gas-to-liquid, corn ethanol, and tar sands oil. These non-conventionals have lower Energy Return On Energy Invested (EROEI) and they can not scale. Also, the maintenance of conventional oil production has come from a large scale up in drilling activity. The oil industry is exploiting smaller fields, smaller left-overs of big old fields. and deep sea fields. These trends are really end games.
What we need: technological advances that will let us substitute away from oil. If we are lucky the current oil production plateau will continue long enough for substitutes to mature. We especially need much lower cost battery technologies to enable our migration away from liquid hydrocarbons for most transportation needs.
The computer power doublings in successive generations of computer chips will come to a halt some time in the 2020s.
High Performance Computing expert Thomas Sterling would like you to know that a computing goal you've never heard of will probably never be reached. The reason you should care is that it means the end of Moore's Law, which says that roughly every 18 months the amount of computing you get for a buck doubles.
The problem: devices can't shrink down below the size of individual atoms. Can quantum computing or some other method allow the doublings to keep going on? If not, the end of the doublings will slow economic growth. Though the biotech revolution will likely have the opposite effect. What's the economic value of a rejuvenated body? I hope I live long enough to find out.
Physicist Michio Kaku foresees the end of the age of silicon.
"In about ten years or so, we will see the collapse of Moore’s Law. In fact, already, already we see a slowing down of Moore’s Law," says world-renowned physicist, Michio Kaku. "Computer power simply cannot maintain its rapid exponential rise using standard silicon technology."
Kaku thinks protein computers or quantum computers might let us go further with more computing power.
Back in 2007 Gordon Moore predicted about 15 years left to run for computer power doublings, at least by shrinking of silicon devices.
Back in 1959 physicist Richard Feynman gave a talk entitled There's Plenty of Room at the Bottom where he outlined the potential of technologies at very small scale. Well, there's still plenty of room for innovation with very small devices, but a lot less than there used to be.
STANFORD, Calif. — The cells that slough off from a cancerous tumor into the bloodstream are a genetically diverse bunch, Stanford University School of Medicine researchers have found. Some have genes turned on that give them the potential to lodge themselves in new places, helping a cancer spread between organs. Others have completely different patterns of gene expression and might be more benign, or less likely to survive in a new tissue. Some cells may even express genes that could predict their response to a specific therapy. Even within one patient, the tumor cells that make it into circulating blood vary drastically.
The finding underscores how multiple types of treatment may be required to cure what appears outwardly as a single type of cancer, the researchers say. And it hints that the current cell-line models of human cancers, which showed patterns that differed from the tumor cells shed from human patients, need to be improved upon.
The new study, which will be published online May 7 in PLoS ONE, is the first to look at so-called circulating tumor cells one by one, rather than taking the average of many of the cells. And it's the first to show the extent of the genetic differences between such cells.
I do not find this at all surprising. A tumor has large numbers cells undergoing rapid division and more mutations happen in each cell division. Many of those cancer cells are sick and dying, making room for cells with mutations that provide advantages for spreading. Natural selection operates very strongly for cancer cells which secrete more angiogenesis factors to promote blood vessel growth needed for tumor growth, which secrete factors that dampen immune response against them, and which have greater ability to move around in the blood stream and land in other parts of the body and divide. So a tumor becomes genetically very diverse.
What's more interesting: the tools used to do the study. Those tools will some day help to identify all the important genetic subpopulations of cancer cells in each cancer patient.
First the researchers used a technology they developed to separate the literally 1-in-a-million circulating tumor cells (CTCs) from normal blood cells.
To make their latest discovery, Jeffrey, along with an interdisciplinary team of engineers, quantitative biologists, genome scientists and clinicians, relied on a technology they developed in 2008. Called the MagSweeper, it's a device that lets them isolate live CTCs with very high purity from patient blood samples, based on the presence of a particular protein — EpCAM — that's on the surface of cancer cells but not healthy blood cells.
Then they used microfluidic chips to look at each individual cancer cells.
So once Jeffrey and her collaborators isolated CTCs using the MagSweeper, they turned to a different kind of technology: real-time PCR microfluidic chips, invented by a Stanford collaborator, Stephen Quake, PhD, professor of bioengineering. They purified genetic material from each CTC and used the high-throughput technology to measure the levels of all 95 genes at once. The results on the cell-line-derived cells were a success; the genes in the CTCs reflected the known properties of the mouse cell-line models. So the team moved on to testing the 95 genes in CTCs from 50 human breast cancer patients — 30 with cancer that had spread to other organs, 20 with only primary breast tumors.
To defeat cancer we need cheap and highly powerful microfluidic devices to identify every trick each cancer is using to survive and spread. While in this study only at most 5 individual CTCs were analyzed in the future costs will drop. Cheaper microfluidic devices will enable analysis of many more CTCs per patient yielding more detailed analyses.
Next we need microfluidic devices that can construct agents (e.g. gene therapies, antibodies, specialized immune cells) that will target each of the cancer subpopulations.
Even better: Imagine early stage cancer detection by periodic blood tests fed into very microfluidic devices installed in a fully automated home medical test lab. Earlier stage discovery brings the advantage that the cancer hasn't yet mutated adaptations for metastasis.
Beware the demon car exhaust. Long range commuters probably face a similar risk.
BOSTON – Living close to a major highway poses a significant risk to heart attack survivors, reinforcing the need to isolate housing developments from heavy traffic areas, a Beth Israel Deaconess Medical Center study concludes.
Writing in the May 7 edition of Circulation, researchers found heart attack survivors living less than 100 meters or 328 feet from a roadway have a 27 percent higher risk of over within 10 years than survivors living at least 1,000 meters away. That risk recedes to 13 percent for those living between 200 and 1,000-meter or 656 to 3,277-feet from the roadway.
"Living close to a highway is associated with adverse cardiovascular outcomes in those with underlying cardiac disease," says Murray Mittleman, MD, DrPH, a physician in the CardioVascular Institute at Beth Israel Deaconess Medical Center, an Associate Professor of Medicine at Harvard Medical School and director of BIDMC's cardiovascular epidemiological research program. "Besides air pollution, exposure to noise could be a possible mechanism underlying this association."
I have a HEPA air filter unit running as I type this. I wonder how much it reduces health risk from living near a moderately busy nearby roadway.
Also see a previous post on why green acres is the place to be.
Dopamine is a neurotransmitter and genetic variants for it influence behavior in a number of ways. If you are a slacker you probably have a lot of dopamine activity in your insula. If you are motivated and work really hard you probably have a lot activity in your striatum and ventromedial prefrontal cortex. Blame your dopamine if you can't make yourself work hard enough.
Whether someone is a "go-getter" or a "slacker" may depend on individual differences in the brain chemical dopamine, according to new research in the May 2 issue of The Journal of Neuroscience. The findings suggest that dopamine affects cost-benefit analyses.
The study found that people who chose to put in more effort — even in the face of long odds — showed greater dopamine response in the striatum and ventromedial prefrontal cortex, areas of the brain important in reward and motivation. In contrast, those who were least likely to expend effort showed increased dopamine response in the insula, a brain region involved in perception, social behavior, and self-awareness.
Researchers led by Michael Treadway, a graduate student working with David Zald, PhD, at Vanderbilt University, asked participants to rapidly press a button in order to earn varying amounts of money. Participants got to decide how hard they were willing to work depending on the odds of a payout and the amount of money they could win. Some accepted harder challenges for more money even against long odds, whereas less motivated subjects would forgo an attempt if it cost them too much effort.
My guess is there's genetic differences play a large role in differences in brain dopamine activity. Once it becomes possible to choose offspring genetic variants will people opt make babies who will be more motivated than their parents? My guess is yes, genetically engineered future generations of humans will be more motivated by design.
Brain PET scans were used to determine individual responsiveness to dopamine.
In a separate session, the participants underwent a type of brain imaging called positron emission tomography (PET) that measured dopamine system activity in different parts of the brain. The researchers then examined whether there was a relationship between each individual's dopamine responsiveness and their scores on the motivational test described earlier.
Imagine a country where employers are allowed to require a PET scan as a condition of employment. If PET scan costs were cheap enough some employers would use them.
“The point of view we have is that we are all going to be paying more for energy worldwide.”
With oil producing countries consuming more oil domestically and developing Asian countries such as China and India importing more oil the West has less available net exports of oil to buy, as Jeffrey Brown points out.
Mulally says batteries for electric vehicles (EV) still are very expensive.
“Right now a battery costs $15,000 for a 100-mile range,” Mulally says. “Now, as energy goes up, you can start to make a case for the economics of all-electric. But the most important thing is finding a way to manufacture electric batteries in a cost-efficient way.”
A few years back we had debates in the comments about how far and how fast electric battery prices would fall. I was on the pessimistic side on those debates. $15k for enough battery capacity to provide 100 mile EV range in 2012 seems like confirmation of the more pessimistic view.
Hybrids still seem like the way to go even up around $7 and $8 per gallon gasoline. A huge reduction in battery costs would change that calculation. But when will enough batteries for 100 mile range hit a more reasonable $5000?