Microfluidic chips are going to speed up the rate of biological experimentation by orders of magnitude. Here is another example of the power of microfluidics for studying biological systems.
CHAMPAIGN, Ill. — Researchers at the University of Illinois have developed a method for culturing mammalian neurons in chambers not much larger than the neurons themselves. The new approach extends the lifespan of the neurons at very low densities, an essential step toward developing a method for studying the growth and behavior of individual brain cells.
The technique is described this month in the journal of the Royal Society of Chemistry – Lab on a Chip.
“This finding will be very positively greeted by the neuroscience community,” said Martha Gillette, who is an author on the study and the head of the cell and developmental biology department at Illinois. “This is pushing the limits of what you can do with neurons in culture.”
The small scale allows much greater sensitivity of measurement.
First, the researchers scaled down the size of the fluid-filled chambers used to hold the cells. Chemistry graduate student Matthew Stewart made the small chambers out of a molded gel of polydimethylsiloxane (PDMS). The reduced chamber size also reduced – by several orders of magnitude – the amount of fluid around the cells, said Biotechnology Center director Jonathan Sweedler, an author on the study. This “miniaturization of experimental architectures” will make it easier to identify and measure the substances released by the cells, because these “releasates” are less dilute.
“If you bring the walls in and you make an environment that’s cell-sized, the channels now are such that you’re constraining the releasates to physiological concentrations, even at the level of a single cell,” Sweedler said.
The method used to create the microfluidic chambers
Second, the researchers increased the purity of the material used to form the chambers. Cell and developmental biology graduate student Larry Millet exposed the PDMS to a series of chemical baths to extract impurities that were killing the cells.
This technique allows measurement of cellular secretions.
Millet also developed a method for gradually perfusing the neurons with serum-free media, a technique that resupplies depleted nutrients and removes cellular waste products. The perfusion technique also allows the researchers to collect and analyze other cellular secretions – a key to identifying the biochemical contributions of individual cells.
This technique allows neurons to live longer in culture. Hence more experimental data can be collected and more kinds of processes studied.
This combination of techniques enabled the research team to grow postnatal primary hippocampal neurons from rats for up to 11 days at extremely low densities. Prior to this work, cultured neurons in closed-channel devices made of untreated, native PDMS remained viable for two days at best.
The development of microfluidic devices will bring changes in biotechnology as revolutionary as the changes which miniaturization have caused in the electronics industry. Microfluidics will enable massive parallelism and automation of experiments at very low cost.
Some people profess to be disgusted by the sight of old men seducing young fertile women. But some biologists and anthropologists at Stanford University and UC Santa Barbara argue that the success of old men managing to impregnant younger women drove human evolution to extend human life expectancy.
Evolutionary theory predicts that senescence, a decline in survival rates with age, is the consequence of stronger selection on alleles that affect fertility or mortality earlier rather than later in life. Hamilton quantified this argument by showing that a rare mutation reducing survival is opposed by a selective force that declines with age over reproductive life. He used a female-only demographic model, predicting that female menopause at age ca. 50 yrs should be followed by a sharp increase in mortality, a “wall of death.” Human lives obviously do not display such a wall. Explanations of the evolution of lifespan beyond the age of female menopause have proven difficult to describe as explicit genetic models. Here we argue that the inclusion of males and mating patterns extends Hamilton's theory and predicts the pattern of human senescence. We analyze a general two-sex model to show that selection favors survival for as long as men reproduce. Male fertility can only result from matings with fertile females, and we present a range of data showing that males much older than 50 yrs have substantial realized fertility through matings with younger females, a pattern that was likely typical among early humans. Thus old-age male fertility provides a selective force against autosomal deleterious mutations at ages far past female menopause with no sharp upper age limit, eliminating the wall of death. Our findings illustrate the evolutionary importance of males and mating preferences, and show that one-sex demographic models are insufficient to describe the forces that shape human senescence.
Read the full research paper (free access at Plos One) for all the details.
Older Canadian men need to try harder to apply selective pressures for longer life. The brutal Amazonian Yanomamo men show this can be done.
Male fertility is nonzero till ages 55 yrs in Canada and the !Kung, 65 yrs in the Ache, 70 yrs in the Yanomamo, 60 yrs in the Tsimane, and 75 yrs in the Gambia.
So, look, you have a life expectancy that extends into the 70s or 80s because old guys managed to knock up young hot babe women. Is this upsetting? Disgusting? Reality can sometimes be that way (to quote Jello Biafra of the Dead Kennedys).
Nowadays the best ways to extend life are to develop great stem cell therapies and gene therapies. We should pursue those therapies with all the determination and gusto that old men of yesteryear (and of today) spent trying to bed young fertile women.
Update: As regular readers know, I try to look for practical ways to apply lessons I learn from reading about scientific progress. This report is no exception. I now feel obliged to knock up a beautiful woman once I reach 65 years old. I'm going to do it because I support eugenics for a longer lived human species.
If you think you can trust your intuition you probably are making a mistake. Our intuitive judgments about food cause us to eat too much. We let our guards down in what we perceive as safer territory. People who eat at supposedly healthier restaurants consume more calories than those prudent people who wisely choose to eat at places with unhealthy food.
An important new study from the Journal of Consumer Research explains the “American obesity paradox”: the parallel rise in obesity rates and the popularity of healthier food. In a series of four studies, the researchers reveal that we over-generalize “healthy” claims. In fact, consumers chose beverages, side dishes, and desserts containing up to 131% more calories when the main dish was positioned as “healthy”.
“In our black and white view, most food is good or not good,” explain Pierre Chandon (INSEAD, France) and Brian Wansink (Cornell University). “When we see a fast-food restaurant like Subway advertising its low-calorie sandwiches, we think, ‘It’s OK: I can eat a sandwich there and then have a high-calorie dessert,’ when, in fact, some Subway sandwiches contain more calories than a Big Mac.”
In one study, Chandon and Wansink had consumers guess how many calories are in sandwiches from two restaurants. They estimated that sandwiches contain 35% fewer calories when they come from restaurants claiming to be healthy than when they are from restaurants not making this claim.
The result of this calorie underestimation: Consumers then chose beverages, side dishes, and desserts containing up to 131% more calories when the main course was positioned as “healthy” compared to when it was not—even though, in the study, the “healthy” main course already contained 50% more calories than the “unhealthy” one.
Do you need to lose weight? I'm sorry, you are going to have to shift your tastes toward thoroughly unhealthy restaurants so that you don't delude yourself about how many calories you are consuming. Eat unhealthy to be healthy.
A man of science might argue there must be a more rational option. The more rational option (know exactly how many calories are in what you are ordering) requires better information availability. Therein lies the problem. Marketers don't want to give you reasons to order fewer items on the menu. But if we had an automated way to know as we order how many calories we've racked up so far then we could pick and choose to lower calorie counts.
Calorie restriction extends life in most animals which have been studied well on calorie restricted diets. Calorie restriction is the only consistent way to extend life in lab animals that has been found to date. Some University of Florida scientists found that rats on low calorie diets might live longer because the calorie restriction causes cells to more rapidly chew up and recycle cellular components such as energy-producing mitochondria.
And a University of Florida study shows just how much the body benefits when it “goes green,” at least if you’re a rat: Cutting calories helps rodents live longer by boosting cells’ ability to recycle damaged parts so they can maintain efficient energy production.
“Caloric restriction is a way to extend life in animals. If you give them less food, the stress of this healthy habit actually makes them live longer,” said Christiaan Leeuwenburgh, Ph.D., chief of the division of biology of aging in UF’s Institute on Aging.
Understanding how the process works at the cellular level in rodents could help scientists develop drugs that mimic the process in humans, Leeuwenburgh added.
Some biogerontologists theorize that aging damaged mitochondria displace healthy mitochondria. Then those damaged mitochondria spew out free radicals that damage cells. These University of Florida researchers are speculating that if cells more aggressively chew up damaged mitochondria then those bad mitochondria won't take over and squeeze out healthier mitochondria.
Fortunately, younger cells are adept at reducing, recycling and rebuilding.
In this process, damaged mitochondria are quickly swallowed up and degraded. The broken down pieces are then recycled and used to build new mitochondria. However, older cells are less adept at this process, so damaged mitochondria tend to accumulate and contribute to aging.
Here is their core finding. Calorie restriction accelerated autophagy, the recycling of damaged cellular components.
UF scientists studied 22 young and old rats, comparing those allowed to eat freely with those fed a low-calorie, nutritious diet.
The stress of a low-calorie diet was enough to boost cellular cleaning in the hearts of older rats by 120 percent over levels seen in rats that were allowed to eat what they wanted. The diet had little or no effect on younger rats.
If drugs could be found that enhance autophagy (the chewing up of damaged cellular components) then those drugs might slow down the aging process by preventing bad damaged mitochondria from taking over cells and spewing free radicals into cells and into the environment around cells.
“Autophagy is a housekeeping mechanism that keeps cells free of damaged and thereby detrimental mitochondria and other toxic materials while recycling their building blocks — nutrients needed by the cell,” said Stephanie Wohlgemuth, Ph.D., a lecturer in UF’s department of aging and geriatrics and the study’s lead author. “So if that process is maintained with age – or even increased – that can only be beneficial.”
Gene therapy that could fix mitochondrial DNA might some day deliver an even bigger anti-aging benefit by fixing damaged mitochondria that spew free radicals.
Researchers have discovered that middle age spread seems to have an effect on waistlines but not weight as people get older.
Researchers, funded by the Medical Research Council, have found that people in early middle age seem to put on more weight more quickly than people slightly older. But the waistlines of the older group seem to grow more quickly.
The stage when the waistlines start expanding more rapidly is when the muscles wither.
One of the researchers Geoff Der, from the MRC’s Social and Public Health Sciences Unit in Glasgow explained:
“As people get older it seems that their bodies change… they lose muscle and get fatter – this explains why middle-age spread might not be reflected on the bathroom scales.”
He goes on: “This challenges the traditional method of measuring how fat a person is: the body mass index. The BMI is a good measure of lean body tissue, but an expanding waistline may be a more reliable measure of the amount of fatty tissue a person has gained. Although the people in the older middle age group in this study appeared to put on less weight than the younger people, their waist circumferences continued to grow over time. What appears to have been happening is that the increase in fat was being obscured by a loss of muscle mass.’’
So first you gain weight. Then your weight gain slows but some of your muscle mass gradually converts to fat. How disgusting. Really, we need rejuvenation therapies. Aging takes away your muscles and makes you fat. This is something we can do without. We should support bigger efforts to figure out how to avoid the decay of aging.
When you head into middle age the odds of keeping the weight off are definitely against you.
The researchers carried out a nine-year study of 1044 people aged either 39 or 59 in 1991. The height, waist circumference and weight of each participant was measured in 1991, 1995 and 2000, and used to measure changes in body mass index over time.
Only one in five (20%) of the people maintained a stable weight as the study progressed. Steady weight gain was measured in the younger group, more than 42% of study participants put on 10kg, 17% gained 5kg.
On average, both men and women in the younger group gained between 0.5kg and 1kg a year. This weight gain was fastest in their younger years. Those in the older age group gained least weight in the second half of the study, however, although their overall weight may not have changed their waist circumference did.
Aging is bad. The physical changes that come from the accumulation of damage to your body are a big and increasing negative. I'm talking downsides. I'm talking losses. Something to be avoided.
We need to seriously try to develop treatments that will reverse the aging process. The defeat of aging is an achievable goal and it is a goal that will be achieved in this century. But whether it comes soon enough for most of us depends on how hard we push to achieve it.
New noninvasive techniques to select embryos for in vitro fertilization (IVF) could boost pregnancy rates and lower the number of risky multiple births. Scientists are using proteomics and metabolomics to screen the liquid that embryos are grown in prior to implantation in order to search for telltale signs of a healthy--or unhealthy--embryo. Some screening tools could be commercially available within the next year.
At some point in the next 10 to 20 years we are going to turn a corner where the advantages of IVF for starting a pregnancy will outweigh the advantages of natural sexual intercourse as a way to start a pregnancy. Improved methods for screening lots of embryos for healthiness might prove sufficient to make that happen. Embryos selected with proteonomics and genetic testing for defects might result in lower defect rates than come from making babies the old fashioned way.
A number of groups are chasing the development of better methods to identify good embryos.
Scientists at Molecular Biometrics, a biotech startup in Chester, NJ, are taking a different approach. They use near-infrared spectroscopy to detect specific molecules involved in oxidative stress, which can be an indicator of health in some tissues. Rather than look at single markers, the researchers have developed a specialized algorithm that can detect differences in the molecular profiles of viable and nonviable embryos.
They are doing a clinical trial with 1,500 patients to look for patterns.
Even if refinements in embryo screening for defects does not by itself make IVF more compelling eventually more sophisticated genetic screening will provide so many advantages that IVF will definitely become the preferred method for starting pregnancies. Reaching that point will happen once we learn the effects of most genetic variations and genetic testing becomes cheap. Then starting a pregnancy via IVF will allow women to select between dozens of embryos to choose the embryo that has the combination of chromosomes most likely to provide desired traits.
Some countries will restrict the use of genetic testing of IVF embryos to only allow selection against genetic defects. Those countries will find their future generations falling behind in international economic competition as parents in less regulated countries choose genetic variations that boost the intelligence of their offspring. Genetic testing policy will therefore become industrial policy and national security policy.
Most parents will select for higher intelligence and physical attractiveness of their children (I'm expecting a lot more blond hair and blue eyed daughters). They will also seek to avoid genetic variations that increase the odds of diseases. But beyond that what other preferences will they exercise when choosing between embryos? How outgoing or shy? How empathetic? How analytical or artistic? How altruistic or selfish?
If robots or artificial intelligences on the web do not take over the world then IVF genetic screening choices made by prospective parents and governments will do more to determine the kind of world we live in in the future than any other area of human choice.
Angiogenesis inhibitors work against cancer by blocking the development of new blood vessels into tumors so that tumors can't grow. The hope with angiogenesis inhibitors is that they will have less side effects than conventional chemotherapy and radiation. Given that chemo and radiation cause severe side effects a treatment can be better and still have pretty substantial side effects. Angiogenesis inhibitors turn to out to be capable of causing lethal side effects.
Angiogenesis inhibitors, drugs that block a tumor's development of an independent blood supply, have been touted as effective cancer fighters that result in fewer side effects than traditional chemotherapy. However, a new study by researchers at UCLA's Jonsson Cancer Center has shown that one method of blocking blood-supply development could result in serious and potentially deadly side effects.
The UCLA researchers blocked angiogenesis factor VEGF in a type of cell in mice and found that the mice eventually suffered heart attacks as a result.
Several newly developed angiogenesis inhibitors work by blocking vascular endothelial growth factor (VEGF), an important signaling protein that spurs the growth of new blood vessels. Avastin, an angiogenesis inhibitor approved by the Food and Drug Administration for colon and lung cancers, inhibits angiogenesis by blocking VEGF signaling from outside the cell. UCLA researchers wanted to know what happened when VEGF signaling was blocked from within endothelial cells, a mechanism used by some small-molecule drugs currently being tested in late-phase clinical trials.
The result was unexpected and sobering. More than half of the mice in the study suffered heart attacks and fatal strokes, while those that remained alive developed serious systemic vascular illness, said Luisa Iruela-Arispe, a professor of molecular, cell and developmental biology and director of the Cancer Cell Biology program at UCLA's Jonsson Cancer Center.
The study appears Aug. 24 in the prestigious peer-reviewed journal Cell.
This result suggests humans might suffer more complications from the long term use of anti-angiogenesis compounds.
"This was an extremely surprising result," said Iruela-Arispe, past president of the North American Vascular Biology Organization and a national expert on angiogenesis. "I think this study is cause for some caution in the use of angiogenesis inhibitors in patients for very long periods of time and in particular for use of those inhibitors that block VEGF signaling from inside the cell."
Anti-angiogenesis compounds block the growth of cancers and therefore in many cases won't cure cancer. So people who take anti-angiogenesis compounds have to take them for many years. Hence long term side effects eventually become an issue. However, if you have an otherwise fatal cancer running a risk of blood clots or even a heart attack can be a price worth paying.
About 5 percent of patients taking Avastin develop blood clot-related side effects, Iruela-Arispe said. But because Avastin was approved only three years ago, it is unclear what side effects may occur when patients remain on the drug for many years, she said.
Anti-angiogenesis drugs side effects are acceptable only because those side effects are milder compared to even more undesirable alternatives such as dying sooner or experiencing even greater side effects from chemotherapy and still dying. We need anti-cancer treatments that are far milder while at the same time producing much higher cure rates.
To cure cancer the key piece we need is much more selective ways to deliver treatments aimed precisely at cancer cells while leaving normal cells alone. That's the huge challenge that cancer researchers have been wrestling with for decades. Anti-angiogenesis drugs currently are delivered into the entire body. So they suffer from the same problem that chemotherapy suffers from: They affect too large a range of cells. A more selective way to deliver anti-angiogenesis compounds might involve attaching them to monoclonal antibodies that are targeted to cancer cells. That would get anti-angiogenesis compounds to concentrate near cancer cells. But the anti-angiogenesis compounds need to work their effects against blood vessel cells and blood vessel stem cells that are near cancer cells. A fancier monoclonal antibody mechanism of delivery might activate and release an anti-angiogenesis drug only once the monoclonal antibody attaches to a cancer cell.
The National Audobon Society of the United States says bird species are in decline.
Audubon's unprecedented analysis of forty years of citizen-science bird population data from our own Christmas Bird Count plus the Breeding Bird Survey reveals the alarming decline of many of our most common and beloved birds.
Since 1967 the average population of the common birds in steepest decline has fallen by 68 percent; some individual species nose-dived as much as 80 percent. All 20 birds on the national Common Birds in Decline list lost at least half their populations in just four decades.
The findings point to serious problems with both local habitats and national environmental trends. Only citizen action can make a difference for the birds and the state of our future.
What citizen action could work? I see a problem here which will prevent action on a scale needed to preserve large habitats: The human instinct to reproduce combined with our ability to generate more technology. We now out-compete a growing portion of all the species on the planet and our ability to harness a growing and very substantial portion of the world's land and biomass to our own purposes. If more environmentally minded people have fewer babies it won't matter because those with stronger genetic instincts to reproduce will make up a larger fraction of the next generation and fertility will eventually recover.
In his later years, my grandfather used to grumble that birds were becoming scarcer and scarcer. It was tempting to write off his gloom as the natural tendency of the elderly to romanticize the past, or maybe just an old man's deteriorating hearing and eyesight. But it was true that the whippoorwill that had kept me awake nights when I visited him as a boy had gone quiet, and the woods and fields of the Northeast felt emptier to me.
Earlier this summer, the National Audubon Society released a definitive study of population trends of North American birds, a monumental effort based on decades of Christmas bird counts and breeding bird surveys. The study confirms what my grandfather feared and what most of us now know. Birds that I used to see routinely growing up in New England – evening grosbeaks, eastern meadowlarks, northern bobwhites – are in free fall. The losses are mind-boggling. Since my grandfather introduced me to birds just half a lifetime ago, once-common species have declined by as much as 80 percent due to the usual suspects: habitat loss, pesticides, introduced species, and climate change. The songs of tens of millions of birds have been silenced. It feels as if the lights are dimming.
When some people read about cellulosic technology they think "environmentally friendly green energy". By contrast I think "yet another way to convert land from habitat for other species into biofactories to power cars and SUVs". The birdies are going bye bye because of human population expansion and economic growth. We need policies that decrease the human footprint. Or we have to accept the decline of most other species. My guess is we will continue to opt for the latter.
A plan to build 40 wind towers a few miles offshore of Long Island New York has been cancelled due to spiralling cost estimates.
According to LIPA, the study by Pace Global Energy Services, a consulting firm, found that the premium for wind-generated power from the Jones Beach project, over a 20-year period, would translate to about $2.50 per month to the typical residential consumer bill, or a total $66 million per year for all of LIPA. PACE arrived at the figure by comparing the cost of electricity produced in a combined-cycle natural gas power plant on Long Island, which is about $137 per megawatt hour, and a megawatt hour of power produced by the wind farm, which it said "could be $291."
Some locals opposed the project on esthetic grounds. But Long Island Power Authority Chairman Kevin Law says his decision was purely based on costs.
Costs for new electric generation plants of all types have been escalating sharply due to rising raw materials costs. Also, increased demand for wind power has been engineered by tax and regulatory changes and the resulting increase in demand has outstripped capacity of the wind tower makers to respond. Hence they've raised prices. Wind should become cheaper in a few years once makers have time to expand capacity.
Since nuclear, wind, and coal plants are all getting hit by higher costs due to higher steel prices I'd really like to know how long steel prices will remain high. Does anyone know how much the steel industry is increasing capacity and how soon we can expect to see a drop in steel prices?
I also wonder at the $137 per megawatt hour for the natural gas plant. That's a rather expensive 13.7 cents per kwh. What price of natural gas is that based on? What will happen to the price of natural gas once oil production peaks? My guess is the natural gas electric will end up costing more than they expect.
The original estimate for the windmills was about $200 million. The price increased to $356 million when FPL Energy of Florida won the bid for the project in 2003. Then last year, rising costs nearly doubled the estimate to $700 million.
Deep ocean offshore wind has been touted by some as a potential source of more reliable wind power. But even this Long Island project which was only a few miles offshore turned out to be too expensive. So I'm skeptical about the economic feasibility of deep offshore wind projects. Though ,aterials advances could some day make deep water wind towers more economically feasible.
Your genes seem like they are at war with each other. Very old ld people have genetic variations that protect them against other genetic variations they have.
August 24, 2007 – (BRONX, NY) – People who live to 100 or more are known to have just as many—and sometimes even more—harmful gene variants compared with younger people. Now, scientists at the Albert Einstein College of Medicine of Yeshiva University have discovered the secret behind this paradox: favorable “longevity” genes that protect very old people from the bad genes’ harmful effects. The novel method used by the researchers could lead to new drugs to protect against age-related diseases.
Next time someone marvels to you about the design of the human eye (which is really dumb if you look at the way nerves are routed to the light sensors called rods and cones) or other aspects of human anatomy keep in mind that you contain genetic variations that are bad for your health.
“We hypothesized that people living to 100 and beyond must be buffered by genes that interact with disease-causing genes to negate their effects,” says Dr. Aviv Bergman, a professor in the departments of pathology and neuroscience at Einstein and senior author of the study, which appears in the August 31 issue of PLoS Computational Biology.
A group of researchers are studying the genetics of some long-lived Ashkenazi Jews.
To test this hypothesis, Dr. Bergman and his colleagues examined individuals enrolled in Einstein’s Longevity Genes Project, initiated in 1998 to investigate longevity genes in a selected population: Ashkenazi (Eastern European) Jews. They are descended from a founder group of just 30,000 or so people. So they are relatively genetically homogenous, which simplifies the challenge of associating traits (in this case, age-related diseases and longevity) with the genes that determine them.
Participating in the study were 305 Ashkenazi Jews more than 95 years old and a control group of 408 unrelated Ashkenazi Jews. (Centenarians are so rare in human populations—only one in 10,000 people live to be 100—that “longevity” genes probably wouldn’t turn up in a typical control group. Longevity runs in families, so 430 children of centenarians were added to the control group to increase the number of favorable genes.)
The scale of their study was pretty limited. First, they only had 305 very old Ashkenazi Jews. Plus, they only looked at 66 genetic markers.
All participants were grouped into cohorts representing each decade of lifespan from the 50’s on up. Using DNA samples, the researchers determined the prevalence in each cohort of 66 genetic markers present in 36 genes associated with aging.
A far larger study with more centenarians and thousands of genetic markers tested would likely turn up many more genetic variations of interest. I repeat: We need a massive study of centenarian genetics that compares the entire genome of long lived and less long lived to find out which genetic variations boost life expectancy.
The researchers think they found a genetic variant of one gene, cholesteryl ester transfer protein (CETP), that protects against the genetic variant of another gene which codes for a lipoprotein, lipoprotein a (aka Lp(a)).
As expected, some disease-related gene variants were as prevalent or even more prevalent in the oldest cohorts of Ashkenazi Jews than in the younger ones. And as Dr. Bergman had predicted, genes associated with longevity also became more common in each succeeding cohort. “These results indicate that the frequency of deleterious genotypes may increase among people who live to extremely old ages because their protective genes allow these disease-related genes to accumulate,” says Dr. Bergman. The Einstein researchers were able to construct a network of gene interactions that contributes to the understanding of longevity. In particular, they found that the favorable variant of the gene CETP acts to buffer the harmful effects of the disease-causing gene Lp(a).
Elevated blood plasma Lp(a) is associated with increased risk of stroke and heart disease. That a CETP variant could reduce the risk posed by Lp(a) is not surprising. CETP variants appear to affect the size of LDL cholesterol particles and other research shows other influences that CETP has on apolipoprotein A1 concentrations.
We need much larger scale studies of centenarian gene expression and gene sequences to find genetic reasons why they live longer. We can use that knowledge to target genes for drug development. If genetic variations cause higher levels of expression of genes that turn out to allow us to live longer then we need to find out which genes those are and try to develop drugs that will turn up those genes. We also need drugs that will turn down the activity of genes that appear to accelerate aging.
The knowledge about which genes enable us to live longer only will allow us to slow the rate of aging. What we need even more are biotechnologies that let us reverse aging and rejuvenate the body. In particular, what I most want are stem cell therapies and tissue engineering technologies. Also, we need gene therapies and nanobots to use to repair the brain.
Melbourne, Australia; 20 August 2007: Australia's adult stem cell company, Mesoblast Limited (ASX:MSB;USOTC:MBLTY), today announced that preclinical trials of its patented adult stem cells had shown that the therapy significantly protected knee cartilage against damage in osteoarthritis.
Millions of people have osteoarthritis of the knee.
More than 10 million people in the US currently suffer from osteoarthritis of the knee, making it the most common joint disease. Osteoarthritis results in loss of cartilage which cannot repair itself after injury and for which there is no effective therapy. Current treatments attempt to alleviate painful symptoms but are unable to preserve the cartilage lining the joint. Moreover, many of the currently used pharmaceutical therapies are associated with severe side-effects and can even cause death. Joint replacement is often the only option for restoring function.
You may have knee osteoarthritis some day even if you don't now. Or you'll have it in your back or hands or shoulders or hips or some combination thereof. Your parts are wearing out. You need replacement parts.
People and dogs really suffer from decaying joints. We need stem cell therapies for joint rejuvenation and repair.
With the support of the Australian Government's Commercial Ready Grant award, Mesoblast's cartilage trials evaluated the effectiveness and safety of the company's allogeneic (donor unrelated) adult stem cells to treat osteoarthritis of the knee in 48 sheep arthritic joints. The results showed that joint cartilage in osteoarthritic knees of animals receiving Mesoblast's stem cells had significantly greater thickness, reduced breakdown, and greater biomechanical strength three months after injection into the knee than did control joints receiving injections of hyaluronic acid.
The trial's principal investigator, Professor Rick Read at the Murdoch University in Western Australia, said: "We are delighted with the significant cartilage protective effects of Mesoblast's allogeneic cells in our large animal model of knee osteoarthritis, without any adverse events of the cells at all".
We need this technology to work in humans. The benefits will be enormous. We need it faster.
An article by Chris Vernon at The Oil Drum notes we are close to the era of electric cars and that suggests to me we are close to the era of battery usage to store and provide home electricity.
These numbers are revolutionary. Even if your car has a small battery pack (plugin hybrid with 40 mile range) and you only drive it in town as an electric vehicle your battery is going to last 40x2300 miles (an amazing 86,000 miles on PHEV power alone) and the car will still go to 90% of the distance it could on a charge when new (36 miles instead of 40)! It seems the battery will outlast the life of the typical car on the road today. If your car is an electric car (with more batteries) and you can do 150 miles a charge it will be 90% as good-as-new after an astounding 345,000 miles! 2300 charges at one charge a day is also more than 6 years. The Phoenix SUT uses Altair Nano's battery and is expected to last 250,000 miles / 12+ years.
I see old PHEV car batteries eventually getting reallocated for use to store electricity for homes. Electricity collected when the wind blows or the sun shines will go into lithium ion car batteries that might have lost 30% or even 40% of their original charge capacity. But the remaining capacity will make a substantial difference to enable people to shift electric power from when it is cheap to generate to when they want to use it.
Suppose we see major volumes of pluggable hybrid electric vehicles onsale within 4 years. Seems plausible. GM is aiming for 2010 with their Volt car. Suppose it takes them till 2011. A Volt might go 20 years before its too old and its batteries at that point will still be in pretty good shape. If the Volt can go 40 miles on a charge and uses 250 watt-hours per mile (pretty close to what it will use) then the Volt might originally have 10 kwh of capacity. Well, even if it degrades 80% it will still have 8 kwh of capacity. For a house that uses 20 kwh per day the 8 kwh of storage capacity from old car lithium nanophosphate batteries would allow shifting of a substantial chunk of solar power from day time to night. Or it would allow shifting of nuclear electric power from night to day.
A big PHEV SUV will come with twice the battery capacity as a compact to drive the same difference. So the electric SUV might start with 20 kwh of battery capacity and end up with 16 kwh of capacity by the end of vehicle life. Such a battery could operate a house for a day after a power outage if the occupants became frugal with their electric usage. Throw in a second SUV and the house could go two days on the power of the old batteries.
But we don't need to wait for the cars to wear out to start using their batteries to save and use electric power. If you know you are staying home for a few days then why not plug the car into the house and use the car battery to let you grab electricity and store it in your car when it is cheap and use it from your car when the price of electricity goes up in late in the afternoon and early evening?
MIT researchers have developed a microfluidic chip that automates research on the worm Caenorhabditis elegans (C. elegans).
Genetic studies on whole animals can now be done dramatically faster using a new microchip developed by engineers at MIT.
The new "lab on a chip" can automatically treat, sort and image small animals like the 1-millimeter C. elegans worm, accelerating research and eliminating human error, said Mehmet Yanik, MIT assistant professor of electrical engineering and computer science.
The advance rate in biotechnology is going to accelerate because the technologies developed by the computer industry to work at increasingly smaller scales are getting reused to develop chips that can do biological research. The "lab on a chip" approach is going to allow an automation and acceleration of biological experiments that will speed up research by orders of magnitude.
Each worm can get routed through the chip and manipulated in different ways to do a very large variety of experiemnts in an automated fashion..
"Normally you would treat the animals with the chemicals, look at them under the microscope, one at a time, and then transfer them," Yanik said. "With this chip, we can completely automate that process."
The tiny worms are flowed inside the chip, immobilized by suction and imaged with a high resolution microscope. Once the phenotype is identified, the animals are routed to the appropriate section of the chip for further screening.
The worms can be treated with mutagen, RNAi or drugs before they enter the chip, or they can be treated directly on the chip, using a new, efficient delivery system that loads chemicals from the wells of a microplate into the chip.
"Our technique allows you to transfer the animals into the chip and treat each one with a different gene silencer or a different drug," Yanik said.
Chips can be mass produced at low cost. Chips that can manipulate whole worms can probably manipulate cells or small groups of cells. So this chip has application beyond C. elegans.
Really, I'm not joking. Max Krasnow and a team at Yale and UC Santa Barbara have found that women can navigate as well as men but their skills only show up when shopping.
The team asked the men and women to show the direction of a stall where they had bought a certain food, such as strawberries or tomatoes, using a compass.
A zero degree error meant the subjects were bang on target, while 90 degrees meant they were hopeless.“Men were making 33 degree pointing error, when women were around 25 degree, which is a 27 per cent improvement,” said Mr Krasnow.
Women also did better with a high-calorie food, such as a doughnut, compared with a stick of celery.
Women had much better accuracy for where to reach higher calorie foods as compared to vegetables and other lower calorie foods. Is it any wonder that we don't eat enough vegetables? Women have a hard time finding the produce section. Suddenly they find themselves in the pastry aisle.
Calorie malnutrition has been the biggest killer in human history. Women were the gatherers. They know how to get back to the places with the best food gathering potential. Whereas men had to know how to track prey over a larger range of areas.
How to make use of this knowledge? Depends on your motives. How about putting a women's clothing store next to Dunkin Donuts or International House of Pancakes?
So how to enhance the cognitive performance of both boys and girls? Put them in school together.
Vitamin D is the vitamin whose increased supplementation stands the best chances of reducing the incidence of major diseases. Here's more evidence for the cancer risk reduction achievable if only more people got enough daily vitamin D.
A new study looking at the relationship between vitamin D serum levels and the risk of colon and breast cancer across the globe has estimated the number of cases of cancer that could be prevented each year if vitamin D3 levels met the target proposed by researchers.
Cedric F. Garland, Dr.P.H., cancer prevention specialist at the Moores Cancer Center at the University of California, San Diego (UCSD) and colleagues estimate that 250,000 cases of colorectal cancer and 350,000 cases of breast cancer could be prevented worldwide by increasing intake of vitamin D3, particularly in countries north of the equator. Vitamin D3 is available through diet, supplements and exposure of the skin to sunlight.
“For the first time, we are saying that 600,000 cases of breast and colorectal cancer could be prevented each year worldwide, including nearly 150,000 in the United States alone,” said study co-author Garland. The paper, which looks at the dose-response relationship between vitamin D and cancer, will be published in the August edition of the journal Nutrition Reviews.
The study combined data from surveys of serum vitamin D levels during winter from 15 countries. It is the first such study to look at satellite measurements of sunshine and cloud cover in countries where actual blood serum levels of vitamin D3 had also been determined. The data were then applied to 177 countries to estimate the average serum level of a vitamin D metabolite of people living there.
The data revealed an inverse association of serum vitamin D with risk of colorectal and breast cancer. The protective effect began at levels ranging from 24 to 32 nanograms per milliliter of 25-hydroxyvitamin D concentration in the serum. The 25-hydroxyvitamin D level is the main indicator of vitamin D status. The late winter average 25-hydroxyvitamin D in the US is about 15-18 ng/ml. The researchers maintain that increasing vitamin D levels in populations, particularly those in northern climates, has the potential to both prevent and possibly serve as an adjunct to existing treatments for cancer.
The work builds on previous studies by Garland and colleagues (Journal of Steroid Biochemistry and Molecular, February 2007) which found that raising the serum 25(OH)D levels to 55 ng/mL was optimal for cancer prevention. This is the first study to recommend optimal vitamin D serum levels which, Garland said, are high enough to provide the needed benefit but which have been found by other scientists to be low enough to avoid health risks.
They recommend 2000 IU of vitamin D per day.
“This could be best achieved with a combination of diet, supplements and short intervals – 10 or 15 minutes a day – in the sun,” said Garland. It could be less for very fair-skinned individuals. He went on to say that “the appropriate dose of vitamin D in order to reach this level, could be very little in a lifeguard in Southern California… or quite a lot for someone in Northern Europe who tends to remain indoors most of the year.”
The serum level recommended by the study would correspond to intake of 2000 International Units per day of vitamin D3 for a meaningful reduction in colorectal cancer. The researchers recommend 2000 IU/day, plus, when weather allows, a few minutes in the sun with at least 40% of the skin exposed, for a meaningful reduction in breast cancer incidence, unless the individual has a history of skin cancer or a photosensitivity disease.
Unless you are taking supplements or spend a lot of time outdoors even in the winter you probably do not get enough vitamin D.
Life sometimes imitates cartoons and TV shows. Shades of the Bionic Woman and the Six Million Dollar Man:
Goldfarb decided on the miniaturized rocket propellant approach because batteries can't provide enough power to make strong prosthetic arms.
Combine a mechanical arm with a miniature rocket motor: The result is a prosthetic device that is the closest thing yet to a bionic arm.
A prototype of this radical design has been successfully developed and tested by a team of mechanical engineers at Vanderbilt University as part of a $30 million federal program to develop advanced prosthetic devices.
“Our design does not have superhuman strength or capability, but it is closer in terms of function and power to a human arm than any previous prosthetic device that is self-powered and weighs about the same as a natural arm,” says Michael Goldfarb, the professor of mechanical engineering who is leading the effort.
The prototype can lift (curl) about 20 to 25 pounds – three to four times more than current commercial arms – and can do so three to four times faster. “That means it has about 10 times as much power as other arms despite the fact that the design hasn’t been optimized yet for strength or power,” he says.
At a certain point, the weight of the batteries required to provide the energy to operate the arm for a reasonable period becomes a problem. It was the poor power-to-weight ratio of the batteries that drove Goldfarb to look for alternatives in 2000 while he was working on a previous exoskeleton project for DARPA. He decided to miniaturize the monopropellant rocket motor system that is used by the space shuttle for maneuvering in orbit. His adaptation impressed the Johns Hopkins researchers, so they offered him $2.7 million in research funding to apply this approach to the development of a prosthetic arm.
Goldfarb’s power source is about the size of a pencil and contains a special catalyst that causes hydrogen peroxide to burn. When hydrogen peroxide burns, it produces pure steam. The steam is used to open and close a series of valves. The valves are connected to the spring-loaded joints by belts made of a special monofilament used in appliance handles and aircraft parts. A small sealed canister of hydrogen peroxide that easily fits in the upper arm can provide enough energy to power the device for 18 hours of normal activity.
I'm expecting nanotubes designed to work more like muscles will eventually displace rockets and electric motors from arms. Though a rocket arm could some day support a rocket punch that would make a rocket-propelled fist and forearm pretty attractive to some.
Berkeley -- A compound found in broccoli and related vegetables may have more health-boosting tricks up its sleeves, according to a new study led by researchers at the University of California, Berkeley.
Veggie fans can already point to some cancer-fighting properties of 3,3'-diindolylmethane (DIM), a chemical produced from the compound indole-3-carbinol when Brassica vegetables such as broccoli, cabbage and kale are chewed and digested. Animal studies have shown that DIM can actually stop the growth of certain cancer cells.
This new study in mice, published online today (Monday, Aug. 20) in the Journal of Nutritional Biochemistry, shows that DIM may help boost the immune system as well.
"We provide clear evidence that DIM is effective in augmenting the immune response for the mice in the study, and we know that the immune system is important in defending the body against infections of many kinds and cancer," said Leonard Bjeldanes, UC Berkeley professor of toxicology and principal investigator of the study. "This finding bodes well for DIM as a protective agent against major human maladies."
Previous studies led by Bjeldanes and Gary Firestone, UC Berkeley professor of molecular and cell biology, have shown that DIM halts the division of breast cancer cells and inhibits testosterone, the male hormone needed for growth of prostate cancer cells.
In the new study, the researchers found increased blood levels of cytokines, proteins which help regulate the cells of the immune system, in mice that had been fed solutions containing doses of DIM at a concentration of 30 milligrams per kilogram. Specifically, DIM led to a jump in levels of four types of cytokines: interleukin 6, granulocyte colony-stimulating factor, interleukin 12 and interferon-gamma.
The scientists think the immune boosting effect of DIM might be one of the reasons why cruciferous vegetables seem to reduce the incidence of cancer.
"It is well-known that the immune system can seek out and destroy tumor cells, and even prevent tumor growth," said Xue. "An important type of T cell, called a T killer cell, can directly kill certain tumor cells, virally infected cells and sometimes parasites. This study provides strong evidence that could help explain how DIM blocks tumor growth in animals."
DIM was also able to induce higher levels of reactive oxygen species (ROS), substances which must be released by macrophages in order to kill some types of bacteria as well as tumor cells. The induction of ROS - three times that of a control culture - after DIM was added to the cell culture signaled the activation of macrophages, the researchers said.
"The effects of DIM were transient, with cytokine and lymphocyte levels going up and then down, which is what you'd expect with an immune response," said Bjeldanes. "Interestingly, to obtain the effects on the immune response, DIM must be given orally, not injected. It could be that the metabolism of the compound changes when it is injected instead of eaten."
I get a lot of people asking me what is the ideal diet. My answer: the kind of diet you probably don't like. That's the problem with the diet research. Mostly it turns up more reasons to eat huge amounts of vegetables. People don't want to hear that answer.
Here's yet another reason why people should stay home from work when they are sick. That wheezing and coughing guy over in the next cubicle might make you fat.
BOSTON, Aug. 20, 2007 — Scientists today reported new evidence that infection with a common virus may be a contributing factor to the obesity epidemic sweeping through the United States and other countries. In laboratory experiments they showed that infection with human adenovirus-36 (Ad-36), long recognized as a cause of respiratory and eye infections in humans, transforms adult stem cells obtained from fat tissue into fat cells. Stem cells not exposed to the virus, in contrast, were unchanged.
Vaccination against obesity. What a concept.
In addition, the study reported identification of a specific gene in the virus that appears to be involved in this obesity-promoting effect. The findings, which could lead to a vaccine or antiviral medication to help fight viral obesity in the future, were presented at the 234th national meeting of the American Chemical Society.
“We’re not saying that a virus is the only cause of obesity, but this study provides stronger evidence that some obesity cases may involve viral infections,” says study presenter Magdalena Pasarica, M.D., Ph.D., of the Pennington Biomedical Research Center, a campus of the Louisiana State University system.
Virus infection by itself is not sufficient to cause obesity.
“Not all infected people will develop obesity,” she notes. “We would ultimately like to identify the underlying factors that predispose some obese people to develop this virus and eventually find a way to treat it.”
Pasarica was part of the original research group which demonstrated that the Ad-36 virus was capable of causing animals infected with the virus to accumulate fat. Led by Nikhil Dhurandhar, Ph.D., now an associate professor at Pennington Biomedical Research Center, the group also conducted a noted epidemiologic study — the first to associate a virus with human obesity — showing 30 percent of obese people were infected with the Ad-36 virus in comparison to 11 percent of lean individuals. But evidence that the virus could actually cause fat levels to increase in human cells was lacking until now, Pasarica says.
This is more evidence for the argument of Paul Ewald and Greg Cochran that infections cause many more diseases than those historically thought to have infectious causes.
A study in the August 21st issue of Current Biology, a publication of Cell Press, reports some of the first conclusive evidence in support of the long-held notion that men and women differ when it comes to their favorite colors. Indeed, the researchers found that women really do prefer pink—or at least a redder shade of blue—than men do.
"Although we expected to find sex differences, we were surprised at how robust they were, given the simplicity of our test," said Anya Hurlbert of Newcastle University, UK. In the test, young adult men and women were asked to select, as rapidly as possible, their preferred color from each of a series of paired, colored rectangles.
Blue Man Group embody our basic human preference for blue.
The universal favorite color for all people appears to be blue, they found. "On top of that, females have a preference for the red end of the red-green axis, and this shifts their color preference slightly away from blue towards red, which tends to make pinks and lilacs the most preferred colors in comparison with others," she said.
So then when genetically engineered skin color becomes possible will anyone opt for blue skin or blue hair? Look at how popular blue eyes are.
Does it make more sense for women to die their hair blue to attract men and for men to go for a more reddish color to attract women? Or does the color preference not extend to preferences for mates? After all, blond hair is most desired in women. Yet blue eyes are too.
What I want to know: Does color preference vary at all according to sexual orientation? For example, do homosexual men lean more toward lilacs than hetero guys? Or do homosexual females lean more toward blue preference than hetero females? Also, does blood testosterone level influence color preference?
Overall, the differences between men and women were clear enough that the seasoned researchers can now usually predict the sex of a participant based on their favorite-color profile.
The color preference seems to track across at least 2 races.
To begin to address whether sex differences in color preference depend more on biology or culture, the researchers tested a small group of Chinese people amongst the other 171 British Caucasian study participants. The results among the Chinese were similar, Hurlbert said, strengthening the idea that the sex differences might be biological.
The question arises: Where does this color preference come from?
The explanation might go back to humans' hunter-gatherer days, when women—the primary gatherers--would have benefited from an ability to key in on ripe, red fruits.
"Evolution may have driven females to prefer reddish colors--reddish fruits, healthy, reddish faces," Hurlbert said. "Culture may exploit and compound this natural female preference."
Reddish faces as indicators of good nutrition and lots of red blood cells seems plausible. But reddish fruits? Seems like many more plant foods are green. Why would food gathering favor reddish foods? Are reddish plants more likely to be digestible for calories than, for example, green leaves?
Hurlbert suspects the preference for blue might be due to the desirability of blue skies for hunting or perhaps blue water for greater purity and safety. Can you think of another reason for the blue preference?
If rich people are so smart why do they sit in the front? Those first class seats in the front are relatively dangerous. To maximize your chance of survival sit it in the back.
The funny thing about all those expert opinions: They're not really based on hard data about actual airline accidents. A look at real-world crash stats, however, suggests that the farther back you sit, the better your odds of survival. Passengers near the tail of a plane are about 40 percent more likely to survive a crash than those in the first few rows up front.
That's the conclusion of an exclusive Popular Mechanics study that examined every commercial jet crash in the United States, since 1971, that had both fatalities and survivors. The raw data from these 20 accidents has been languishing for decades in National Transportation Safety Board files, waiting to be analyzed by anyone curious enough to look and willing to do the statistical drudgework.
Want to cut your transportation death rates much further? Don't travel. This applies to both short and long trips and it also saves time. Schedule trip activities to do them in batches so that you make few trips. Take jobs closer to home or move closer to your job. Telecommute. Use teleconferencing and email rather than road trips.
On the other hand, jet air travel is very safe as compared to car travel for equal distances. As Popular Mechanics points out, there's only been 1 fatal jet crash in the United States in the last 5 years. Car travel is most hazardous with over an order of magnitude more deaths per distance traveled than trains or planes. Curiously, trains and planes have almost the same rate of passenger deaths per distance traveled.
Car travel dangers are more controllable by individuals though. You can drive a safer car as measured by the US Insurance Institute for Highway Safety car ratings or the US government's car safety ratings. You can also avoid driving drunk or tired, avoid heavy traffic, don't speed, avoid driving in rain and snow, and use other safe driving techniques.
Another point about air travel: Take fewer hops and fly in jets. Take-offs and landings are where most accidents happen. The new Boeing Dreamliner jet that allows airlines to offer more direct flies that avoid hubs will reduce the number of times you have to take-off and land on a trip. Well, search on flights that take fewer hops.
The Popular Mechanics article above comes from a special issue on natural disaster survival. One complaint about their special issue: They emphasize after-disaster survival. For disasters that can happen to you at home the emphasis should be on locating and building a home in such a way that it can survive most disasters. No need to start camping if your roof doesn't fly off and your house doesn't flood or burn down. However, their articles have lots of useful tips.
COLUMBUS, Ohio – Understanding the molecular structures of compounds that give certain fruits and vegetables their rich colors may help researchers find even more powerful cancer fighters, a new study suggests.
Evidence from laboratory experiments on rats and on human colon cancer cells also suggests that anthocyanins, the compounds that give color to most red, purple and blue fruits and vegetables appreciably slow the growth of colon cancer cells.
The findings also bring scientists a step closer to figuring out what exactly gives fruits and vegetables their cancer-fighting properties.
“These foods contain many compounds, and we're just starting to figure out what they are and which ones provide the best health benefits,” said Monica Giusti, the lead author of the study and an assistant professor of food science at Ohio State University.
The plants vary both in the amount of anthocyanins they contain and in which particular anthocyanins they contain. The anthocyanins vary in their anti-cancer properties. Since they mostly do not get absorbed they seem like a fairly safe way to cut down on colon cancer risk.
If yellow corn is less potent than blue corn then do we need to get back to multi-colored corn?
The researchers determined the amount of extract needed from each plant to cut the growth of human colon cancer cells in half. Altering pigment structures slightly by adding an extra sugar or acid molecule changed the biological activity of these extracts.
The researchers added different extracts to flasks that contained colon cancer cells. They used an analytical technique called high-performance liquid chromatography – mass spectrometry in order to determine the exact chemical structure of each compound. They used biological tests to determine the number of cancer cells left after anthocyanin treatment.
The researchers found that the amount of anthocyanin extract needed to reduce cancer cell growth by 50 percent varied among the plants. Extract derived from purple corn was the most potent, in that it took the least amount of this extract (14 micrograms per milliliter of cell growth solution) to cut cell numbers in half. Chokeberry and bilberry extracts were nearly as potent as purple corn. Radish extract proved the least potent, as it took nine times as much (131 µg/ml) of this compound to cut cell growth by 50 percent.
“All fruits and vegetables that are rich in anthocyanins have compounds that can slow down the growth of colon cancer cells, whether in experiments in laboratory dishes or inside the body,” Giusti said.
In additional laboratory studies, she and her colleagues found that anthocyanin pigments from radish and black carrots slowed the growth of cancer cells anywhere from 50 to 80 percent. But pigments from purple corn and chokeberries not only completely stopped the growth of cancer cells, but also killed roughly 20 percent of the cancer cells while having little effect on healthy cells.
Note that they are not using whole corn or whole berries. So an ounce of blue corn won't necessarily have more potent anti-colon cancer activity than an ounce of radishes. We need to know what the concentration of the most active anthocyanin compounds are in each of these foods in order to say which will deliver the most benefit. Still, blue corn muffins or pancakes with berries for breakfast might reduce your odds of dying from colon cancer.
If you know someone recently diagnosed with colon cancer note that dietary changes can make a big difference on outcomes. Also see my post Western Diet Boosts Colon Cancer Recurrence.
In the long run genetic engineering of plants to boost their levels of the most potent anti-cancer anthocyanins seems like the ticket.
Increasing production of biofuels to combat climate change will release between two and nine times more carbon gases over the next 30 years than fossil fuels, according to the first comprehensive analysis of emissions from biofuels.
Does that sound counter-intuitive? Stop and think about where the land would come from to grow biomass crops: Places that are now forests. Those forest contain large quantities of carbon dioxide. The clearing of forests to turn them into biomass energy croplands releases so much CO2 that it takes several decades for the resulting reduction in fossil fuels use to cancel out the effects of CO2 release by destroyed forests.
What is more, environmentalists have expressed concerns that the growing political backing that biofuel is enjoying will mean forests will be chopped down to make room for biofuel crops such as maize and sugarcane. "When you do this, you immediately release between 100 and 200 tonnes of carbon [per hectare]," says Renton Righelato of the World Land Trust, UK, a conservation agency that seeks to preserve rainforests.
"Brazil, Paraguay, Indonesia among others have huge deforestation programmes to supply the world biofuel market", says the study's co-author Dominick Spracklen from Leeds University.
According to an article in the French monthly Le Monde Diplomatique, Brazil aims to supply 30% of the world's ethanol market by 2025. Last year it reclassified 200 million hectares as "degraded land" to release it for biofuel crop. Presently, it is growing crops such as sugar cane on land the size of Britain and the Benelux countries combined.
By 2025 the Brazilian government intends to expand that area fivefold to meet 10% of the world's petrol requirement. And last year it reclassified 200 million hectares as "degraded land" to release for crop cultivation.
I can see one way around this problem: Bury the biomass material in a sealed underground cavern. That way the CO2 from the destroyed forest won't make it into the atmosphere. Though that approach would still drastically shrink habitats available to all the species currently living in rain forests. Another alternative: Only grow biomass energy crops in areas which are currently barren with little plant life. Those areas tend to lack water. So how to irrigate? How about nuclear energy to drive massive desalination plants and to pump the water inland to deserts? Then deserts could bloom with plant life.
Destruction of rain forests to create land for biomass energy crops such as sugar cane ought to strike environmentalists as a bad idea before even considering effects on CO2 emissions. Yet so far the chorus against biomass energy is pretty quiet as compared to the chorus against CO2 emissions as a cause of climate change.
Near as I can tell the real oil reserves and natural gas reserves remaining are so low that world CO2 emissions are headed for a fall within a couple of decades. So the destruction of the rain forests to grow energy crops to displace fossil fuels isn't necessary in the first place. The fight against global warming is the wrong battle. Instead we should think a lot more on how to shift to wind, solar, and nuclear power as replacements for fossil fuels that aren't even going to exist to burn. The biggest challenge is how to make electric power more usable in transportation.
New research indicates that slowing tropical deforestation may play a much larger role in mitigating climate change than previously believed [1,2]. Carbon emissions from tropical deforestation are expected to increase atmospheric CO2 concentration by between 29 and 129 ppm within 100 years, much more than previously estimated . The parties to the United Nations Framework Convention on Climate Change are considering policy approaches and incentives for reducing emissions from deforestation (RED) in developing countries [4–6] that are timely, in light of these recent research findings. The leading proposals would enable trading of carbon saved by reducing tropical deforestation, just as carbon is currently traded from reducing industrial emissions. The state of these discussions suggests that a key group of countries are at risk of being omitted from a new framework—those with high forest cover and low rates of deforestation (HFLD).
Developing countries can be classified into four categories defined by two axes: remaining forest cover and deforestation rate (Figure 1). The HFLD countries in Quadrant IV harbor 18% of tropical forest carbon. Since current proposals would award carbon credits to countries based on their reductions of emissions from a recent historical reference rate , HFLD countries could be left with little potential for RED credits. Nor would they have the potential for reforestation credits under the Kyoto Protocol's Clean Development Mechanism that the countries in Quadrant II have. Without the opportunity to sell carbon credits, HFLD countries would be deprived of a major incentive to maintain low deforestation rates. Since drivers of deforestation are mobile, deforestation reduced elsewhere could shift to HFLD countries, constituting a significant setback to stabilizing global concentrations of greenhouse gases at the lowest possible levels.
The development of cellulosic technologies to generate ethanol from cellulose will also accelerate deforestation by increasing the demand for wood cellulose.
A typical solar cell generates only one electron per photon of incoming sunlight. Some exotic materials are thought to produce multiple electrons per photon, but for the first time, the same effect has been seen in silicon. Researchers at the National Renewable Energy Laboratory (NREL), in Golden, CO, showed that silicon nanocrystals can produce two or three electrons per photon of high-energy sunlight. The effect, they say, could lead to a new type of solar cell that is both cheap and more than twice as efficient as today's typical photovoltaics.
This approach might achieve 40% efficiency of conversion. That's more than double what you'll find on the market today. (someone correct me if they know about commercial photovoltaic cells above 20% conversion efficiency)
By generating multiple electrons from high-energy photons, solar cells made of silicon nanocrystals could theoretically convert more than 40 percent of the energy in light into electrical power, says Arthur Nozik, a senior research fellow at NREL.
These researchers think silicon nanocrystals will be cheaper to make than multijunction photovoltaics that have achieved even higher efficiency. Given the multitude of approaches for achieving higher efficiency and lower costs our chances of getting cheaper photovoltaics seem high.
Cheap solar will some day make noon time the cheapest time to buy electricity. But will stationary battery storage ever become cheap enough to allow solar to compete for baseload demand?
Update: Another report finds silicon nanoparticles improve solar cell efficiency.
CHAMPAIGN, Ill. — Placing a film of silicon nanoparticles onto a silicon solar cell can boost power, reduce heat and prolong the cell’s life, researchers now report.
“Integrating a high-quality film of silicon nanoparticles 1 nanometer in size directly onto silicon solar cells improves power performance by 60 percent in the ultraviolet range of the spectrum,” said Munir Nayfeh, a physicist at the University of Illinois and corresponding author of a paper accepted for publication in Applied Physics Letters.
A 10 percent improvement in the visible range of the spectrum can be achieved by using nanoparticles 2.85 nanometers in size, said Nayfeh, who also is a researcher at the university’s Beckman Institute.
In conventional solar cells, ultraviolet light is either filtered out or absorbed by the silicon and converted into potentially damaging heat, not electricity. In previous work, however, Nayfeh showed that ultraviolet light could efficiently couple to correctly sized nanoparticles and produce electricity. That work was reported in the August 2004 issue of the journal Photonics Technology Letters.
I hear the Beatles singing. "All the lonely people, where do they all come from? All the lonely people, where do they all belong?" University of Chicago psychologists Louise Hawkley and John Cacioppo find that lonely people find life more stressful.
However, when the psychologists looked at the lives of the middle-aged and old people in their study, they found that although the lonely ones reported the same number of stressful life events, they identified more sources of chronic stress and recalled more childhood adversity. Moreover, they differed in how they perceived their life experiences. Even when faced with similar challenges, the lonelier people appeared more helpless and threatened. And ironically, they were less apt to actively seek help when they are stressed out.
I also hear Mr. Mackey: "Stress is bad, mmmkay?" (not that he ever said that to my knowledge)
Loneliness cranks up a stressful flight-or-flight chemical state.
Hawkley and Cacioppo then took urine samples from both the lonely and the more contented volunteers, and found that the lonely ones had more of the hormone epinephrine flowing in their bodies. Epinephrine is one of the body’s “fight or flight” chemicals, and high levels indicate that lonely people go through life in a heightened state of arousal. As with blood pressure, this physiological toll likely becomes more apparent with aging. Since the body’s stress hormones are intricately involved in fighting inflammation and infection, it appears that loneliness contributes to the wear and tear of aging through this pathway as well.
Feeling lonely? That stress ages your body more rapidly.
Lonely people don't sleep as well.
There is more bad news. When we experience the depletion caused by stress, our bodies normally rely on restorative processes like sleep to shore us up. But when the researchers monitored the younger volunteers’ sleep, they found that the lonely nights were disturbed by many “micro awakenings.” That is, they appeared to sleep as much as the normal volunteers, but their sleep was of poorer quality. Not surprisingly, the lonelier people reported more daytime dysfunction. Since sleep tends to deteriorate with age anyway, the added hit from loneliness is probably compromising this natural restoration process even more.
You can read the original paper (paid access).
Seeking an end to your loneliness seems akin to seeking a medical treatment.
I also hear Roy Orbison singing "Only The Lonely".
There goes my baby, there goes my heart
They’re gone forever, so far apart
But only the lonely know wh-y-y I cry--only the lonely
Two recently discovered control networks that govern voluntary brain activity in adults start life as a single network in children, report neuroscientists at Washington University School of Medicine in St. Louis.
Researchers previously showed the networks supervise most goal-oriented brain activity, enlisting the specialized talents of multiple brain regions for goal-oriented tasks as diverse as reading a word, listening to music or searching for a star. They were surprised to find the two networks merged together in children.
Kids don't just know a lot less. They think differently. Okay, you already knew that. But it is still great when science confirms our observations about human nature. Also, this sort of research is a useful lesson for those who try to force kids to act like adults.
A new brain scanning method made this discovery possible.
Scientists used a new brain scanning technique called resting state functional connectivity MRI to identify the control networks. Instead of analyzing mental activity when a volunteer works on a cognitive task, the new technique scans their brains while they do nothing. The scans reveal changes in the levels of oxygen in blood flowing to different areas of the brain. Researchers interpret correlations in the rise and fall of blood oxygen to different brain areas during inactivity as a sign that those areas likely work together. In neuroscientist's terms, this means the regions have functional connectivity.
A team of researchers led by Petersen and M.D./Ph.D. student Nico Dosenbach analyzed scans of volunteers with an approach called graph theory. They represented various brain regions of interest as shapes, and when two regions met a threshold for functional connectivity, they drew a line between them. The two control networks were distinctly separate even when the connectivity threshold was set to a low level.
For the new study, scientists used the same techniques to analyze the brains of 210 children, adolescents and adults. They found the two control networks are merged in children but begin pulling apart in adolescents, establishing themselves as separate entities and becoming more complex.
Some people complain that adolescents are so weird. To those people I ask: How would you act if your brain was undergoing a major reorganization of how it controls itself?
The brain continues to change as we get older.
Fair notes that an interesting pattern emerged as scientists looked at their data from a big picture perspective.
"As we get older, connections that are getting weaker tend to be between brain regions located close to each other, while the connections that are getting stronger tend be those between regions that are far apart," he says.
I'm skeptical of claims that there's a single best standard for aesthetic issues. Given that humans differ so much in how their brains are wired up we should expect people to differ in their tastes in music, architecture, annoyance at noise, desire to drive fast, and in countless other ways. This isn't to argue that every state of mind is equally morally justifiable. Murderers aren't justified in murdering just because some might be wired up to strongly want to murder.
Brain research will eventually present challenges when some differences in values are found to derive from innate differences in brain architectures. Hard to argue that a disagreement is due to misunderstandings when the disagreement is the result of innate differences in how brains reason and form emotions.
Brain development research will probably change how we grant rights. Children have fewer rights (e.g. a very limited right to contract) in most societies. That's a recognition of the lower capacity of children to judge and to fulfill responsibilities. Well, once research can show that some fast developing 16 year olds have a greater capacity to evaluate and fulfill obligations in contracts than some 25 year olds why should all 25 year olds have more rights than all 16 year olds?
Instead of an all-or-little granting of rights might it make more sense to grant levels of rights and even categories of rights incrementally based on extent of cognitive capabilities? We lack the capability to measure small gradations in ability to respect rights or honor contracts. But that won't always be the case. I expect results of brain scans and other measurements of cognitive capability to some day get used by governments to determine when a person can get a driver's license, enlist in the military, or become an emancipated minor.
Natural selection can only select between mutations that occur naturally. The number of mutations that might occur naturally in humans is limited by the number of humans and by which mutations occur in each human. In theory if one could search through a much larger set of mutations one should be able to find genes which code for better enzymes and better versions of other components of our body. Some scientists have shown that they can generate and test a large number of potential enzymes to find new designs.
Living cells are not the only place where enzymes can help speed along chemical reactions. Industrial applications also employ enzymes to accelerate reactions of many kinds, from making antibiotics to removing grease from clothing. For the first time, scientists have created a completely new enzyme entirely in vitro, suggesting that industrial applications may one day no longer be limited to enzymes that can be derived from natural biological sources.
HHMI investigator Jack W. Szostak and Burckhard Seelig, a postdoctoral associate in his Massachusetts General Hospital and Harvard Medical School laboratory, show in a paper published in the August 16, 2007, issue of the journal Nature the steps they took to create the artificial enzyme, an RNA ligase that catalyzes a reaction joining two types of RNA chains.
This group at Harvard thinks they can develop better tools to select for enzymes that rise to a higher level of performance.
Szostak's approach relies instead on evolution. The technique enabled the researchers to generate a new RNA ligase without any pre-existing model of how it would work. According to Szostak, “There is no known biological enzyme that carries out this reaction.”
To create one, the researchers assembled a library of 4 trillion small protein molecules - each with slight variations on an initial protein sequence — then subjected those molecules to evolutionary selection in the laboratory. “Here,” Szostak says, “the hard work is in designing a good starting library, and an effective selection process. Since we do not impose a bias on how the enzyme does its job, whatever mechanism is easiest to evolve is what will emerge.”
The enzyme that emerged from the group's experiments is what Szostak characterizes as “small and not very stable, and not very active compared to most biological enzymes.” Nevertheless, Szostak's group is optimistic about their ability to select for versions of the enzyme that are more stable and more active.
Evolution by selection between whole organisms is too slow a way to turn up better designs. Computer simulations and automated lab equipment that generates more real life variations of proteins will some day allow us to search much more deeply through the space of all possible protein shapes to turn up much better genes. In order to give ourselves higher performing bodies we will some day replace some human genes with variants found in labs.
A Russian region best known as the birthplace of Vladimir Lenin has found a novel way to fight the nation's birthrate crisis: It has declared Sept. 12 the Day of Conception and for the third year running is giving couples time off from work to procreate.
The hope is for a brood of babies exactly nine months later on Russia's national day. Couples who ``give birth to a patriot'' during the June 12 festivities win money, cars, refrigerators and other prizes.
Ulyanovsk, a region on the Volga River about 550 miles east of Moscow, has held similar contests since 2005. Since then, the number of competitors, and the number of babies born to them, has been on the rise.
See the article for the full details on the promising results.
In his 7th state-of-the-nation address to the Russian Federal Assembly on May 10, 2006 President Vladimir Putin called Russia's declining birth rate the biggest problem facing Russia.
But the bulk of Putin's speech focused mainly on domestic issues. Chief among them was what Putin called "the main issue," to which he devoted one-fourth of his speech -- Russia's demographic crisis.
The Russian president decried the country's annual decline of nearly 700,000 people a year, and presented a detailed plan for improving child-care benefits in order to encourage women to have at least the two children needed to maintain a stable population.
"When planning to have a child, a woman is faced with the choice whether to have a child but lose her job, or not to have a child," Putin said. "This is a very difficult choice. The encouragement of childbirth should include a whole range of measures of administrative, financial, and social support for young families."
According to the most recent forecasts, Russia's population of 143 million people is expected to decrease by 22 percent between now and the year 2050. If the figures are borne out, Russia could lose up to 42 percent of its active working population.
The decline is being fueled primarily by two things: low birth rates, with Russian women increasingly choosing work over motherhood, and increased death rates among a rapidly aging population.
Some see the Russian state's pension system as removing an incentive to have kids who Russians used to have to depend on for retirement support.
The Russian president also rejected calls to abolish Russia's state pension fund and return to a more Soviet-style system, whereby the elderly would rely on their children, rather than the state, for essential support.
Modest proposal that would make a substantial difference: Make the state pension fund pay-outs bigger for people who have more kids. Make the act of procreation something that connects the tax revenues generated by offspring to how well off the parents will be. A number of variations on this are possible. For example, parents could get more government payments in their old age if their kids make more money and pay more in taxes.
The local leader, "Ataman" Viktor Vasilyevich, received me with open arms. He was dressed in traditional Cossack costume, which includes a full-length black coat, a sheepskin hat and a sword. He oozed authority, and it was immediately clear that he was held in deep respect by his family and the other villagers.
Cossack family life is a rigid, hierarchical system in which the eldest man's word is law. Unashamedly, the Ataman explained that Cossack families should be as large as possible. He introduced me to one of his own sons, already the father of seven children.
Will the Cossacks save Russia from demographic oblivion? I am reminded of Tolstoy's short story The Cossacks.
In what may be the first study to use brain imaging to look at the neural circuits involved in emotional control in patients with depression, researchers at the University of Wisconsin-Madison have found that brains of people with clinical depression react very differently than those of healthy people when trying to cope with negative situations.
Depressed people and normal people were monitored for how their brains responded to negative pictures when they were told to try to imagine positive outcomes.
Participants were asked to consciously work to decrease their emotional responses to some of the negative images, using techniques such as envisioning a more positive outcome than the one implied or by imagining the situation was acted out rather than real.
"We ask them to reframe the content of what they're seeing," rather than divert their attention or distract themselves with unrelated thoughts, Johnstone says. "We hope to engage cognitive areas in re-interpreting the emotional content of a stimulus — to either increase or decrease its impact."
In both healthy and depressed individuals, they found that such efforts increased brain activity in prefrontal cortical areas known to help regulate the emotional centers of the brain, as they expected.
The big difference was seen in the reactions of the emotional centers themselves, including a small almond-shaped structure called the amygdala located deep in the brain.
In nondepressed individuals, high levels of regulatory activity correlated with low activity in the emotional response centers - in effect, the healthy subjects' efforts successfully quelled their emotional responses. In depressed patients, however, high levels of activity in the amygdala and other emotional centers persisted despite intense activity in the regulatory regions.
This finding suggests that healthy people are able to effectively regulate their negative emotions through conscious effort, but that the necessary neural circuits are dysfunctional in many patients with depression, the researchers say.
Attempts by depressed people to suppress their negative responses actually backfire. They think even more negative thoughts.
The difference becomes even more pronounced the harder the patients try.
"Those [healthy] individuals putting more cognitive effort into it are getting a bigger payoff in terms of decreasing activation in these emotional centers," Johnstone explains. "In the depressed individuals, you find the exact opposite relationship - it seems the more effort they put in, the more activation there is in the amygdala."
Depressed people should avoid negative images and negative information. Maybe depressed people shouldn't watch the news. I also wonder whether distraction could work as a strategy against depression. Thinking about something negative? Watch a comedy movie or TV show. Or play a game that is very engrossing. Just leave no room for the negative thoughts.
What the depressed people of the world need: A happy news channel. All happy, all the time. But that might not work. The depressed might resent happy news.
“I met a girl who sang the blues, And I asked her for some happy news; But she just smiled and turned away”.
Patients treated for colon cancer who had a diet high in meat, refined grains, fat and desserts had an increased risk of cancer recurrence and death compared with patients who had a diet high in fruits and vegetables, poultry and fish, according to a study in the August 15 issue of JAMA.
But most people really like meat, refined grains, fat, and desserts. What good is this research result when it tells people to ignore their cravings?
Previous research has indicated that diet and other lifestyle factors have a significant influence on the risk of developing colon cancer. However, few studies have assessed the influence of diet on colon cancer recurrence and survival, according to background information in the article.
Jeffrey A. Meyerhardt, M.D., M.P.H., of the Dana-Farber Cancer Institute, Boston, and colleagues examined the influence of two distinct dietary patterns on cancer recurrence and survival in a group of 1,009 stage III colon cancer patients (cancer present in the colon and lymph nodes) enrolled in a clinical trial of postoperative chemotherapy in addition to other treatment. Patients reported dietary intake using a food frequency questionnaire during and six months after supplemental chemotherapy. Two major dietary patterns were identified, prudent and Western. The prudent pattern was characterized by high intakes of fruits and vegetables, poultry, and fish; the Western pattern was characterized by high intakes of meat, fat, refined grains, and dessert.
Patients were followed up for cancer recurrence or death. During a median (midpoint) follow-up of 5.3 years, 324 patients had cancer recurrence, 223 patients died with cancer recurrence, and 28 died without documented cancer recurrence.
Recurrence rates are way higher if you eat a bad Western diet.
The researchers found that a higher intake of a Western dietary pattern after cancer diagnosis was associated with a significant increase in the risk of cancer recurrence or death. Compared with patients in the lowest Western dietary pattern quintile (bottom 20 percent), those in the highest quintile (top 20 percent) experienced a 3.3 times higher risk for cancer recurrence or death. Patients in the highest quintile of Western dietary pattern were 2.9 times more likely to have cancer recur than those in the lowest quintile. Similarly, a significantly higher overall risk of death with increasing Western dietary pattern was observed. In contrast, the prudent dietary pattern was not significantly associated with cancer recurrence or death.
A “prudent” pattern characterized by high intakes of fruits and vegetables, poultry, and fish, and a “Western” pattern characterized by high amounts of red and processed meats, sweets and desserts, French fries, and refined grains. Participants didn’t fall neatly into one category or the other, but were scored in each by how closely they matched the Western and prudent models.
The survival benefit for those whose diets least resembled the Western pattern held true even after researchers controlled for factors such as gender, age, body mass, degree of cancer spread to lymph nodes, and physical activity level. Investigators do not know why such a diet is associated with a poorer outcome, but speculate that it may be related to increased insulin levels and insulin-like growth factors. Insulin and related growth factors have been linked to the formation and growth of some types of tumors.
Eat a lower glycemic index diet. Or watch metastatic colon cancer lodge in your bones and cause excruciating pain until you die an emaciated shadow of your former self. Hey, I'm not going to sugar coat the news for you. Doing that would boost your insulin level. I'm trying to write a low insulin blog here.
Fruits and veggies do not lower the rate of recurrence of all types of cancers though. Fruits and veggies failed to lower breast cancer recurrence in a recent study (more here and here).
Antioxidant vitamins C, E, and beta carotene failed to cut risk of heart attacks in women. (but remember that you probably need more vitamin D)
Vitamins C and E and beta carotene, either individually or in combination, do not appear to reduce the risk of cardiovascular events or death among women at high risk for heart disease, according to a report in the August 13/27 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
The search for why vegetables and fruits improve your health isn't finding that antioxidant vitamins are the cause.
Oxidative damage—harm to cells caused by exposure to oxygen—may contribute to the development of cardiovascular disease, according to background information in the article. In addition, compounds known as free radicals may damage artery linings, encourage blood clots and alter the function of blood vessels. “Antioxidants scavenge free radicals and limit the damage they can cause,” the authors write. “Diets high in fruit and vegetable intake, and thus rich in such antioxidants, have been associated with reduced rates of coronary heart disease and stroke. Vitamins C and E and beta carotene are potential mediators of the apparent protective effect of a plant-based diet on cardiovascular disease.”
Nancy R. Cook, Sc.D., of Brigham & Women’s Hospital and Harvard Medical School, Boston, and colleagues tested the effects of these compounds in the Women’s Antioxidant Cardiovascular Study, which followed 8,171 women 40 years or older (average age 60.6) beginning in 1995 to 1996. The women, who either had a history of cardiovascular disease or three or more risk factors, were randomly assigned to take 500 milligrams of ascorbic acid (vitamin C) or placebo every day; 600 international units of vitamin E or placebo every other day; and 50 milligrams of beta carotene or placebo every other day. Participants were followed up for the occurrence of heart events (including stroke, heart attack and bypass surgery) or death through 2005.
Vitamin C and E in combination might cut risk of stroke.
During the average study period of 9.4 years, 1,450 women had one or more cardiovascular events, including 274 heart attacks, 298 strokes, 889 coronary revascularization procedures (bypass surgery or angioplasty) and 395 cardiovascular deaths (out of a total 995 deaths). “There was no overall effect of ascorbic acid, vitamin E or beta carotene on the primary combined end point or on the individual secondary outcomes of myocardial infarction, stroke, coronary revascularization or cardiovascular disease death,” the authors write. “There were no significant interactions between agents for the primary end point, but those randomized to both active ascorbic acid and vitamin E experienced fewer strokes.”
While scientists try to figure out what exactly in fruits and vegetables extend the lives of many people your best bet is to eat more fruits and vegetables. Vegetables are boring. But vegetables are good for you. They are probably good for you for the same reason they are boring: They have low glycemic index and so do not taste as sweet as other higher glycemic index foods. Also, their fibers have tastes that aren't as appealing as starchy grains. If you want to live longer then find ways to make vegetables more palatable.
If you can't find it in you to eat lots of vegetables (and few people can) then you should find the time to promote accelerated research into the development of therapies that reverse the damage caused by eating lots of meat and grains. Donate to research. Ask your government to fund more research into stem cells and gene therapy. Invest in biotech start-ups.
12 people in the whole world are known to lack the appetite regulation hormone leptin. 2 leptin deficient teens were found to rate even broccoli as very tasty.
Without leptin, the two teens wanted to eat non-stop. The boy weighed 103 kilograms by age 14 and the girl weighed 128 kilograms at 19 years old. As part of the study, the researchers asked them to rate how much they liked various foods, ranging from chocolate cake to broccoli, and discovered that they rated bland foods unusually highly.
These teens had unusual activation patterns in an area of the brain called the nucleus accumbens. Leptin therapy caused their appetites to become more normal. They also lost their appetite for broccoli.
Farooqi then began treating the two leptin-deficient teens with the hormone and tested their brain response to various foods one week later. After receiving leptin therapy, the nucleus accumbens of the subjects only became activated by foods when they had not eaten for several hours.
If you can't keep your weight down then blame it on your genes.
Studies suggest that genetics accounts for 40 to 70 percent of adult body weight, but researchers don't know all the culprits. Four years ago, Farooqi's group discovered that a separate mutation in the gene for melanocortin-4 receptor shows up in 1 percent of obese people and 5 to 6 percent of severely obese children.
Offspring genetic engineering will eventually make obesity very rare. Even before then better appetite control drugs will greatly reduce problems with excess weight. This study suggests that a leptin mimic drug might reduce appetite and make weight control much easier.
The rabbit-proof fence — or bunny fence — in Western Australia was completed in 1907 and stretches about 2,000 miles. It acts as a boundary separating native vegetation from farmland. Within the fence area, scientists have observed a strange phenomenon: above the native vegetation, the sky is rich in rain-producing clouds. But the sky on the farmland side is clear.
Within the last few decades, about 32 million acres of native vegetation have been converted to croplands west of the bunny fence. On the agricultural side of the fence, rainfall has been reduced by 20 percent since the 1970s.
The article lists a few hypotheses for why this has happened. But the real interesting thing about this is what it portends for the future. As population growth and rising affluence increase the demand for food more land will get worked by farmers. Will this cause droughts? Will increased farming of land reduce rain enough to cause a reduction in total production in areas which become the most heavily farmed?
The human footprint on the Earth grows larger every year. Think about it.
The key to the whole process is Wnt, a protein traditionally thought to help promote maintenance and proliferation of stem cells in many tissues. But in this instance, Wnt appears to block proper communication.
"That was a total surprise," said Thomas Rando, MD, PhD, associate professor of neurology and neurological sciences. "We had no idea that the Wnt signaling pathway would have a negative effect on stem cell function." Rando, who also does research and clinical work at the Veterans Affairs Palo Alto Health Care System, is senior author of the research that will be published in the Aug. 10 issue of Science.
Rando previously discovered (and the link below is to a previous post I did on that report) that old stem cells will act younger if exposed to younger blood. That's very troubling news for efforts to develop rejuvenating cell therapies. If the whole body is full of chemical signals that suppress growth then just replacing older stem cells with younger stem cells won't yield as much increase in healing and repair as our aging bodies need.
It was while the researchers were testing the opposite situation - how the repair capabilities of young muscle stem cells were affected by being placed in an aged environment - that the Wnt pathway came to light. The work was done with live mice whose circulatory systems were joined, and in lab dishes with young cells immersed in serum from old blood.
As expected, the young muscle stem cells were influenced negatively by the aged environment, repairing damaged muscle tissue just as slowly and poorly as old stem cells in the same surroundings. This confirmed their earlier research showing that the ability of muscle stem cells to regenerate tissue depends on the age of the cells' environment (including the age of the blood supplying the tissue), not the age of the stem cell.
The stem cells exposed to too much Wnt failed to produce needed replacement muscle cells. Worse yet, the muscle stem cells formed scar tissue instead.
Rando also found that the misdirected stem cells - the ones that failed to generate new muscle cells in the old environment - were instead differentiating into scar-tissue-producing cells called fibroblasts. The stem cells weren't just failing to respond to the garbled instructions, they were actually giving rise to daughter cells that turned into the wrong thing. The consequence of muscle stem cells producing fewer muscle cells (myoblasts) and more fibroblasts is that the healing muscle had more scar tissue, also known as fibrosis.
"That says something about how cells decide who they're going to be. Even if they start off knowing they're supposed to be a muscle cell, they can change," said Rando. "If you're exposed to the wrong environment, it will change your fate."
Rando said the type of fibrosis that occurs in the aging muscle tissue is the same type seen in muscular dystrophy. He is already exploring how inhibiting Wnt signaling might help provide therapy for that disease.
So as you age your muscles accumulate scar tissue. We need ways to get rid of that scar tissue and replace it with youthful muscle cells produced from youthful and properly instructed stem cells.
Another research group has just discovered that Wnt is able to suppress mouse stem cell activity because as mice age their bodies make less of another protein called klotho. Well, klotho restrains Wnt and the absence of klotho causes Wnt to suppress stem cell division.
Wnt has also popped up unexpectedly in work by researchers at the National Institutes of Health, published in the same issue of Science, who were studying the effects of a deficiency of a hormone called klotho. Klotho deficiency causes a syndrome that resembles extremely rapid aging in mice, which end up dying very young compared with normal mice. In seeking to understand why that happens, the NIH researchers discovered that klotho inhibits Wnt activity. The hypothesis is that klotho production declines with age, and thus its effectiveness against Wnt decreases, allowing Wnt activity to pick up and disrupt the normal signaling to the stem cells in a variety of tissues studied.
You might think hey, why not deliver klotho hormone replacement therapy to slow or reverse cellular aging? Good question. Let me put the question another way: Why does klotho production decline with age? Is it just due to accumulation of damage to klotho-making machinery? My guess: the decline of klotho happens in order to reduce the risk of cancer. As cells age they accumulate mutations that could become cancerous. By slowing cell division by reducing klotho the body reduces healing but on average that reduction in healing becomes a net benefit due to avoided cancer.
Here is the abstract of that NIH study that Rando mentioned. Klotho suppresses Wnt whereas continuous exposure to Wnt causes cells to go into a senescent (old, much lower level of function) state.
The contribution of stem and progenitor cell dysfunction and depletion in normal aging remains incompletely understood. We explored this concept in the Klotho mouse model of accelerated aging. Analysis of various tissues and organs from young Klotho mice revealed a decrease in stem cell number and an increase in progenitor cell senescence. Because klotho is a secreted protein, we postulated that klotho might interact with other soluble mediators of stem cells. We found that klotho bound to various Wnt family members. In a cell culture model, the Wnt-klotho interaction resulted in the suppression of Wnt biological activity. Tissues and organs from klotho-deficient animals showed evidence of increased Wnt signaling, and ectopic expression of klotho antagonized the activity of endogenous and exogenous Wnt. Both in vitro and in vivo, continuous Wnt exposure triggered accelerated cellular senescence. Thus, klotho appears to be a secreted Wnt antagonist and Wnt proteins have an unexpected role in mammalian aging.
We need to know whether other genes signal klotho's gene to stop expressing itself. We also need to know what upstream event starts the sequence of gene activations and deactivations that lead to too little klotho.
Wnt is an obvious candidate for drug development. A drug that binds to Wnt and blocks its action will probably have the effect of making your stem cells divide more vigorously and to form more types of needed cells. Though such a drug probably would increase your risk of cancer. For someone who is suffering from, say, life threatening cardiovascular disease the trade-off from drug use of getting more repair cell activity with more cancer risk would probably be worth it.
We need much more progress toward the goal of understanding how stem cells interact with aging bodies. In spite of all the news above about Wnt and klotho it seems likely that replacing aged stem cells with more youthful stem cells will yield many therapeutic benefits. The aged stem cells are at greater risk of becoming cancerous. Their replacement by stem cells that have far fewer accumulated genetic defects will reduce the risk of cancer from stem cells as well as provide stem cells that can divide more times. Older stem cells have shortened telomeres that become obstacles in the way of stem cell division.
If we could only find ways to keep stem cells active as the years go by we would develop degenerative diseases of old age much less frequently.
Over at The Oil Drum Professor Cutler Cleveland has an essay "Energy Transitions Past and Future that is well worth the time to read. One of the points he makes is about biomass energy and the amount of land needed for biomass to displace oil:
The low energy and power density of most renewable alternatives collides with a second global environmental imperative: human use of the Earth's plant life for food, fiber, wood and fuelwood. Satellite measurements have been used to calculate the annual net primary production (NPP)—the net amount of solar energy converted to plant organic matter through photosynthesis—on land, and then combined with models to estimate the annual percentage of NPP humans consume (Figure 12). Humans in sparsely populated areas, like the Amazon, consume a very small percentage of locally generated NPP. Large urban areas consume 300 times more than the local area produced. North Americans use almost 24 percent of the region's NPP. On a global scale, humans annually require 20 percent of global NPP.
Human appropriation of NPP, apart from leaving less for other species to use, alters the composition of the atmosphere, levels of biodiversity, energy flows within food webs, and the provision of important ecosystem services. There is strong evidence from the Millennium Ecosystem Assessment and other research that our use of NPP has seriously compromised many of the planet's basic ecosystem services. Replacing energy-dense liquid fuels from crude oil with less energy dense biomass fuels will require 1,000- to 10,000-fold increase in land area relative to the existing energy infrastructure, and thus place additional significant pressure on the planet's life support systems.
Note that the current human use of global NPP is only going to go up as populations expand and more affluent populations use more land for plant crops, livestock, and also for biomass energy and wood for structures.
The already extensive harnessing of biomass to produce useful products for humans strikes me as a strong argument against biomass energy. The only compelling argument for biomass is the ability to produce liquid fuels from biomass suitable for use in vehicles. But we can develop ways to use more electricity in transportation including better batteries and methods to make synthetic liquid fuels.
Imagine you have a fatal disease (for a few of you the imagining is unfortunately not necessary). You are going to check out of the Life Hotel. You are either going to cease to exist or move on to some sort of afterlife. Imagine that before you die every day you continue to live you will become weaker, more incapacitated, lose control of more bodily functions, and experience increasing pain. Imagine that, like most people, you'd rather not die of that fatal disease. But no approved drug or other treatment can save your life or even extend it very much. Faced with a painful downhill slide to death would you want to try experimental therapies? Count me in the "Yes! Hell Yes!" column on that one.
In the United States the Food & Drug Administration does not want you to try unapproved drugs outside of clinical trials. Effectively, for most people that means you won't be able to try unapproved drugs at all. At best you'll be able to use just one unapproved drug. A federal court ruled 15 months ago that, contra the FDA, American citizens have a fundamental right to try drugs when they are going to die. But a (dare I say stupid and imperious? yes, I do) D.C. Circuit Court of Appeals have decided you do not have the right to try to save your life in ways not approved by the FDA. (commentary here by Roger Pilon of the libertarian Cato Institute)
The wheels of justice turn slowly, especially for the dying. On Tuesday the D.C. Circuit, sitting en banc, reversed a 15-month-old decision by a panel of the court that had recognized a constitutional right of terminally ill patients to access potentially life-saving drugs not yet finally approved by the Food and Drug Administration. Given the poor quality of Tuesday's opinion in Abigail Alliance for Better Access to Developmental Drugs v. Eschenbach — "startling," said the dissent — one wonders why it took so long. The opinion's one virtue is that it brings out clearly how far modern "constitutional law" has strayed from the Constitution, a document written to protect liberty, not federal regulatory schemes.
Represented by the Washington Legal Foundation, Abigail Alliance is named for Abigail Burroughs, a 21-year-old college student who died of cancer in 2001. Their argument could not be more simple or straightforward, nor could Tuesday's dissent, written by Judge Judith Rogers and joined by Chief Judge Douglas Ginsburg, the majority in the earlier opinion. Citing the Fifth Amendment's right to life, the Ninth Amendment's assurance to the Constitution's ratifiers that the rights retained by the people far exceed those named in the document, and the Supreme Court's "fundamental rights" jurisprudence, Judge Rogers argued that the right to life, the right to self-preservation, and the right against interference with those rights — which the FDA is guilty of — are of one piece. They are deeply rooted in common law and the nation's history and traditions, implicit in the concept of ordered liberty, and thus "fundamental."
Indeed, it is startling, she noted, that the rights "to marry, to fornicate, to have children, to control the education and upbringing of children, to perform varied sexual acts in private, and to control one's own body have all been deemed fundamental, but the right to try to save one's life is left out in the cold despite its textual anchor in the right to life." Because the rights at issue here are "fundamental," she concluded, the court must apply, in judicial parlance, "strict scrutiny." The burden is on the FDA to show why its interference is justified — to show that its regulatory interests are compelling and its means narrowly tailored to serve those interests.
Here's what I want to know: Who do the FDA and these judges think they are protecting and from what exactly? Think of the downsides to using experimental treatments. You might spend more money on treatments and leave your heirs with less money. You might die sooner. But earlier death not always a bad thing if your cancer has spread to your bones and just getting touched causes excruciating pain. You might suffer pain from the way the experimental treatments are administered. But you've decided to accept that pain or else you wouldn't get the treatments.
The upsides to allowing people to try experimental drugs are considerable. First off, how about the value of letting each individual make personal decisions about what they can control over their ultimate fate? Even if you are going to die might you die with more peace of mind if you die knowing that you tried everything possible and died fighting the good fight?
At The Huffington Post Adam Freedman thinks the DC Circuit misrepresented the nature of the right that is at stake.
The first panel of the DC Circuit found that the FDA's actions (in denying drugs to terminally-ill patients) interfered with the "right to life," which implicitly includes the right to preserve one's life through medication. Stated this way, the right is "fundamental" because it is - as constitutional jurisprudence requires - "deeply rooted in the nation's history and traditions." So in the first Abigail decision, the DC Circuit held that the FDA could not justify its meddling with this fundamental right.
But in the second Abigail holding, the DC Circuit described the contested right differently: "the right to access experimental and unproven drugs in an attempt to save one's life." Stated in these terms, the right hardly seems fundamental - indeed, the court's words conjure up the image of some deluded sicko grasping for the nearest bottle of snake oil. So much for respect for the terminally ill.
Sounds like the court is saying that the odds that experimental drugs will help are so low that attempts to save one's life with experimental drugs don't have to be counted as exercises of one's right to life.
Yaron Brook of the Ayn Rand Institute says patients aren't just guinea pigs for clinical trials.
Some claim that allowing individuals to take unapproved drugs will make effective clinical testing impossible, since, as they say, no rational person would willingly submit to the double-blind, randomized tests that are currently used in clinical trials required by the FDA. In such tests, some of the participants are unknowingly given a placebo, which, it's said, no one would chance if he could ensure that he received the drug by paying for it. But, contrary to those who make this argument, individuals are not lab rats who may be blackmailed by the government into becoming test subjects. It is chilling that defenders of the FDA's current trial system are, in effect, advocating as an incentive to take part in such trials: 'join or die.'
Yes, those placebo recipients are basically human sacrifices for future patients who get the same diseases.
I see utilitarian arguments for the right to try experimental treatments. First off, if developers of new drugs can start selling them at earlier stages they can get revenue sooner to develop more drugs and to do so faster. We will get effective treatments sooner if the terminally ill can try new and unproven drugs. Also, for each new drug since more patients will take it sooner we'll find out if it works sooner and if it doesn't we can abandon it and move on to other drugs sooner.
Despite the popular notion that antioxidants, such as vitamins C and E, offer health-promoting benefits by protecting against damaging free radicals, a new study in the August 10 issue of the journal Cell reveals that, in fact, balance is the key. The researchers show in mice that an overload of natural antioxidants can actually lead the heart to failure.
There is plenty of evidence about the damaging effects of oxidative stress, but “there is another side to the coin,” said Ivor Benjamin of the University of Utah, Salt Lake City. “There has been so much emphasis on free radicals to the exclusion of the potential consequences of reductants. Our study provides the first bona fide example of the role that reductive stress can play in disease.”
Reductants, sometimes referred to as antioxidants, are elements or compounds that easily give up an electron to become “oxidized,” while oxidizing agents readily accept electrons. In the body, such oxidation-reduction (redox) reactions are integral to the release and storage of energy. Many cellular pathways are also sensitive to the prevailing redox condition.
In a nutshell: A human mutation that causes muscle damage was added to mice. The scientists discovered that in mice this mutation causes an excess amount of glutathione in reduced form. They think that reductive stress (the opposite of oxidative stress) causes the protein clumping and muscle damage which accompany this mutation.
In the current study, the researchers examined mice carrying a human mutation earlier linked to so-called protein aggregation skeletal myopathies and cardiomyopathies, in which weakening skeletal and heart muscle contain clumps of proteins. Although the genetic basis for the disease had been linked to mutations in one of two genes, the mechanism responsible remained mysterious.
The researchers now show that mice with one of the mutant genes, áB-crystallin, specifically in the heart develop the same symptoms seen in human patients, including heart enlargement, progressive heart failure, and an early death. They further show that the animals’ hearts are under reductive stress.
The find initially took Benjamin by surprise, he said. They had conducted a test traditionally used to measure the level of oxidative stress in the animals, expecting they might see higher than normal levels. Instead, they found the mice had “markedly reduced” oxidative stress levels due to an abundance of a natural antioxidant known as glutathione.
The mutant mouse hearts exhibited a heightened stress response, including higher activity of heat shock proteins that have been documented in human heart failure, Benjamin explained. Such stress responses yield reactive oxygen species, triggering antioxidative pathways to kick in. In the diseased animals, however, that pathway—in which oxidized glutathione is recycled to its reduced, antioxidant form—soon got out of hand, producing excess levels of the reduced glutathione and a condition of reductive stress.
Too much of a good thing becomes a bad thing.
Less of an enzyme involved in generation of reductive compounds allowed the mice to avoid heart disease.
Moreover, they showed that the offspring of the heart-diseased animals and mice with lower levels of one of the antioxidant enzymes, glucose-6-phosphate dehydrogenase (G6PD), were relieved of their symptoms.
G6PD appears to help restore glutathione back to its reduced state. So a reduction in G6PD likely shifts glutathione back toward its reduced form. Cutting back G6PD lowered the amount of reduced glutathione in cells and doing that avoided heart disease.
Biogerontologist Aubrey de Grey has long argued that antioxidant vitamins would provide little life extension benefit. Why? Because antioxidant compounds are easy for cells to synthesize and if more of the antioxidant (aka reductant) compounds provided a net benefit then very likely selective pressures would have caused us to make more of these antioxidants.
There's no easy magic bullet to slow down the rate of aging. We need treatments that will repair the damage caused by aging. Those rejuvenating repair treatments will come in the form of cell therapies, gene therapies, and replacement organs.
Telomeres, pronounced TEE-low-meres, are DNA caps. They protect genes at the tips of chromosomes — all 23 pairs that reside in the nucleus of each of our trillions of cells. They are kind of like the tips that keep your shoelaces from unraveling.
A handful of studies indicate that telomeres are shorter in the immune cells of older people in comparison with the young. Now, a research team led by UCSF’s Wen-Chi Hsueh, MPH, PhD, suggests that telomere length might be associated with life span itself. Hsueh and colleagues published their very preliminary findings in the July 17 issue of the Proceedings of the National Academy of Sciences (PNAS).
The PNAS study co-authors believe they are the first to report an association between telomere length and life span. But the finding needs to be confirmed, Hsueh says, as more data on life span become available. Only 35 study participants have died so far.
Telomeres are caps on the ends of chromosomes. Current thinking is that every time a cell divides its telomere caps get shorter. Once the telomeres get short enough cells have a hard time dividing and perhaps become senescent. The telomere cap length shortening might be a mechanism for reducing the incidence of cancer. So if we could find a way to lengthen telomere caps of cells in our bodies any resulting rejuvenation might come at the expense of greater incidence of cancers. So you die from your cells not dividing enough or you die from your cells dividing too much.
At least in this Old Order Amish population the telomere lengths in fathers appear to correlate with the telomere lengths in their offspring.
The researchers discovered that average telomere length in fathers — but not mothers — was related to telomere length in children. Moreover, the researchers found an association between daughters’ telomere length and how long their fathers lived. This suggests that life span and telomere length may share some genetic determinants.
“It’s very rare to observe such a paternal inheritance phenomenon for complex traits, so I was very surprised,” Hsueh says.
The likely explanation is a biological phenomenon known as imprinting, Hsueh says. In imprinting, the activity of certain genes depends on whether they were passed down through one’s mother or one’s father. The maternal gene copies are not active. The exact mechanism by which imprinting might affect the inheritance of telomere length remains mysterious, Hsueh says.
I'm even more interested in the "Why?" than the "How?" about this effect. What advantage is there (if any) to having the father's telomere lengths exert a stronger influence on offspring than the mother's telomere lengths? Does some adaptive advantage come from this? Or is it a side effect of something else that was selected for?
The study was done on Old Order Amish in Pennsylvania because they are genetically fairly homogeneous and live very similar lifestyles to each other.
The Amish fit the bill. They have a small number of ancestors — about 200 Amish families came to the United States from Europe about 14 generations ago, during the early to mid-1700s. Now, there are about 30,000 Old Order Amish living in Lancaster County. They do not marry outsiders. As a result, they have little variability in their genes — a small gene pool. That reduces the complexity of finding genetic variants that may be associated with particular traits or diseases within the population.
There also is little variation in lifestyle and environment to complicate the study of genetic influences on aging, Hsueh notes. Amish women do not smoke or drink, and those behaviors also are very rare among Amish men. The Amish eat together in large groups and have similar schedules.
Highly homogeneous populations are very handy for teasing out various potential causes of differences in development and diseases.
Even though telomere lengthening would probably increase risk of cancer that will not always be the case. Picture, say, 10 or 20 years from now. Suppose an effective and controllable technique for telomere lengthening is found (probably a gene therapy that includes telomerase genes). How can telomere lengthening get used to increase life expectancy without increased death from cancer?
First off, we might have 100% effective cures for cancer 20 years from now. Certainly we will sooner or later. Whenever we develop the ability to cure cancer we'll be able to make use of many treatments that have the side effect of increasing cancer risk.
Second, we will gain the ability to selectively apply telomere lengthening only to cells which have no mutations that increase risk of cancer. Hiow? Take a bunch stem cells out of a body. Put each individually in a small tube with nutrients. Send in gene therapy to fix each cell's telomeres. Let each cell divide. Take just one cell out of each tube. Test for DNA mutations that increase cancer risk. Go back to the small tubes that contain cells which have no detectable cancer risk and let them replicate in much larger numbers. Then reinject those stem cells back into the body.
Third, repair the genes that have accumulated mutations that contribute to cancer. The third approach is similar to the second approach except more extensive gene therapy will get placed into each cell in order to repair the genes that have dangerous mutations. Basically, repair all the mutations that could contribute to cancer. Then telomere lengthening could be done safely without boosting cancer risk.
We need greater efforts to start testing out stem cell rejuvenation therapies such as telomere lengthening. This work could get done in rats, mice, and other non-human species and would provide useful indications on what kinds of stem cell rejuvenation therapies will work best.
If we could find a way to rejuvenate stem cells without boosting cancer risk then we could probably prevent and even reverse many degenerative old age diseases. See, for example, my previous post Bone Marrow Stem Cell Aging Key In Atherosclerosis.
Also see my previous posts "Telomere Length Indicates Mortality Risk" and "Chronic Stress Accelerates Aging As Measured By Telomere Length" and New Telomere Lengthening Technique Developed and Telomeres Wear Down Quicker In Men Than Women and Aged Blood Stem Cells Indicator For Cardiovascular Disease Risk.
Two researchers working at the Department of Mechanical Engineering at Iowa State University set out to compare the capital and operating costs of generating fuel from starch and cellulose-containing materials.
They showed that the capital costs for 150 million gallon gasoline equivalent capacity range from around $111 million for a conventional grain ethanol plant to $854 million for an advanced (Fischer Tropsch) plant. The difference in the final cost of the fuel, however, was less severe, being $1.74 for grain ethanol when corn costs $3.00 per bushel and $1.80 for cellulosic biofuel when biomass costs $50 per ton.
The authors compared biochemical and thermochemical approaches to biofuels. They showed that both have much higher capital costs than conventional grain ethanol plants, but that neither had a significant cost advantage over the other.
The assumption of $3 for a bushel of corn seems low given that a bushel of corn for December 2007 delivery is above $3.50 at the time of this writing. However, $50 as the price of a ton of biomass material seems realistic:
Biomass Program analysts estimate that 512 million dry tons of biomass equivalent to 8.09 quads of primary energy could initially be available at less than $50/dry ton delivered (Walsh et al. 2000, 2003, Ugarte et al. 2003). Of this, 36.8 million dry tons (0.63 Quads) of urban wood wastes were available in 1999. In the wood, paper, and forestry industrial sectors, they estimate that 90.5 million dry tons (1.5 Quads) of primary mill residues were available in 1999 and 45 million dry tons (0.76 Quads) of forest residues were available at a delivered price of less than $50/dry ton. An estimated 150.7 million dry tons (2.3 Quads) of agricultural residues (corn stover and wheat straw) would be available annually. A joint U.S. Department of Agriculture and Department of Energy evaluation of the potential to produce biomass energy crops (Ugarte et al. 2003) estimated 188 million dry tons (2.9 Quads) of biomass could be available annually at delivered prices of less than $50/dry ton by the year 2008. A county-level database of potential energy crop resources is available at Oak Ridge National Laboratory and a county-level database of multiple resources will be available soon. State-level information can also be obtained at the EERE website.
Once cellulosic technologies mature to the point that costs drop then the demand for biomass ethanol will rise. What I wonder: Will this increase or decrease the demand for land to make ethanol? On the one hand ethanol yield per acre will rise. On the other hand, lower prices will cause demand for ethanol to displace more gasoline. That might boost the demand for ethanol so much that land usage for biomass ethanol will rise. The ability to use more types of land to grow various biomass ethanol feedstock plants could allow biomass ethanol agriculture to grow far beyond the lands currently used to grow corn.
I do not want to see more habitats shifted into biomass energy production. I'd rather we develop better battery technologies so we can switch from gasoline to electric power rather than to ethanol.
Toyota Motor Corp., which used the green image of its gasoline-electric Toyota Prius to propel a U.S. sales surge, has decided to delay by one to two years the launches of new high-mileage hybrids with lithium-ion battery technology because of potential safety problems. The slowdown could offer General Motors Corp. and other rivals a chance to narrow the gap in the race to define future clean-vehicle technology.
Until recently, Toyota was preparing to roll out a dozen new and redesigned hybrids using new lithium-ion battery technology in the U.S. between 2008 and 2010. Its hybrids now use nickel-metal-hydride batteries. But safety concerns with the lithium-ion technology have forced Toyota to back away from that timetable, people familiar with the company's strategy say.
Toyota is also slipping plans for hybrids for other models including the Tundra and Sequoia.
Officially, the car was not postponed because Toyota had never published an introduction date, but such a decision would have major implications: reverting to nickel-metal hydride batteries in today's Prius means finding room for a larger and heavier power pack. A Toyota spokesman, John Hanson, said that while the company saw "huge potential" in lithium-ion batteries, it wanted to assure future Prius buyers the same levels of affordability and reliability they experience in today's models.
Speaking in February, Toyota chief Katsuaki Watanabe told BusinessWeek that the next-generation Prius, expected in late 2008 or early 2009, would use li-ions (see BusinessWeek.com, 3/5/07, "Toyota's Bid for a Better Battery"). But in recent months, Toyota appears to be having difficulties meeting that timeline.
General Motors Corp. (GM) said Thursday it has an agreement with battery developer A123 Systems to create a battery cell for the auto maker's planned Chevrolet Volt electric car, a move that could help the auto maker win a global hybrid-electric vehicle race that currently is dominated by Toyota Motor Corp. (TM).
During a speech here, GM Vice Chairman Bob Lutz said A123 will be a key supplier for GM's E-Flex system, which essentially is the propulsion designed to power the Volt and other electric cars the auto maker hopes to make. E-Flex uses an electric motor to drive a vehicle, backed up by a more traditional engine for when battery power is not adequate.
Bob Lutz says the A123 Systems battery design avoids the thermal issues that cause some lithium ion batteries to catch fire. If A123 Systems can pull this off - and at an affordable price - then pluggable hybrids will take off in a big way. GM would score big time.
We need some big steps forward in battery technology so that electric power can replace gasoline and diesel fuel for most transportation needs. With great batteries the peak in world oil production will be easy to handle. Without great batteries our post-peak living standards will take much bigger hits as oil production declines.
DURHAM, N.C. – Scientists examining the relationship between the intensity and length of a workout and the duration of its benefits have made a surprising discovery: More isn't necessarily better, and none may be worse than we ever imagined.
"On the surface, it seems to make sense that the harder we exercise, the better off we'll be, and by some measures that's true," says lead author Cris Slentz, Ph.D, an exercise physiologist at Duke University Medical Center. "But our studies show that a modest amount of moderately intense exercise is the best way to significantly lower the level of a key blood marker linked to higher risk of heart disease and diabetes. More intense exercise doesn't seem to do that."
What may be even more remarkable, he says, is that some of the benefits derived from a modest exercise regimen appear to last much longer than those gained from a more rigorous program.
Triglyceride lowering benefits of exercise were longer lasting for those who only exercised moderately.
The researchers found that for the most part, no amount of exercise significantly changed LDL levels. HDL levels, however, tended to improve with the length and intensity of the workout, and that the benefit was sustained over time.
But perhaps the most interesting finding was that a modest, low-intensity workout – walking just 30 minutes per day, for example, dramatically lowered triglyceride levels. Triglycerides are the particles that carry fat around in the body, and they're also a good indicator of insulin resistance, a marker for diabetes. Lowering triglyceride levels lowers risk of heart disease and diabetes.
"A proper exercise program appears to be able to lower a person's insulin resistance in just a matter of days," says Kraus. "We were also amazed to see that the lower triglyceride levels stayed low even two weeks after the workouts ended." Longer, more intense workouts didn't have nearly the same impact, they say.
An organization called Partnership for Prevention claims 5 preventive measures could save over 100,000 lives per year
I'm skeptical of the wisdom behind the first claim about aspirin use. The evidence on aspirin use for low risk patients is ambiguous. Though prolonged aspirin use might lower the risk of cancer. Also, I'm surprised to see the claim about flu vaccines. Influenza vaccination might not reduce mortality in the elderly. (more here) Though if everyone got vaccinated then the elderly would face less risk of getting exposed to an infected person. The best vaccination strategy depends on the transmissibility of each strain.
Screening for cancer is probably a net benefit. Cancers caught and removed sooner are cancers less likely to have metastatized before removal. So their cancer recommendations (at least for colonoscopy) are probably at least approximately correct. What would really benefit us: implantable cancer detector devices. Detect cancer every day with embedded sensors that could use radio waves to report to an external computer whether a cancer has been detected.
For your heart my advice is to improve your diet and get more exercise. Exercise and better diet are more assured methods of reducing heart disease risk. Eat like an ape man.
Harvard labor economics prof George Borjas points to a National Public Radio story on the trend toward larger families among the most affluent:
The newest status symbol for the nation's most affluent families is fast becoming a big brood of kids.
Historically, the country-club set has had the smallest number of kids. But in the past 10 years, the number of high-end earners who are having three or more kids has shot up nearly 30 percent.
Some say the trend is driven by a generation of over-achieving career women who have quit work and transferred all of their competitive energy to baby making.
They call it "competitive birthing."
Gotta keep up with the Joneses, especially when you and the Joneses are investment bankers. But if you want to compete Jim Bob and Michelle Duggar of Arkansas have set the bar for competitive birthing very high.
I don't know if the rise in the number of children among more affluent families is due to "competitive birthing" or not. But the data, and many anecdotal observations, clearly suggest that there's something going on.
It is not unusual, for instance, to find families in the Boston suburbs where the mother has an advanced academic degree, obviously can earn a high wage in the labor market, but has instead decided to be a stay-at-home mom for a brood of 3 or 4 children. I would not classify these families as part of the "country-club set." These families are often making a substantial financial sacrifice.
I keep saying that natural selection will turn around the decline in fertility rates in Western nations. The people having babies are more likely to carry genes that make them want to have babies. So those genes are getting selected for. But selective pressures aren't the only force at work that can drive up fertility in some segments of populations. The desire to own and experience and consume in large amounts will drive some around to the thought "But we haven't had the experience of raising children and controlling and shaping them. We've got to have kids if we are going to have it all." Also, children (especially if driven to expensive private schools in a new Range Rover) are a way to signal one's ability to engage in conspicuous consumption. Children confer status. The desire for higher status is an innate drive of humans.
Once we develop the ability to turn back the biological aging clock and make ourselves young again will the desire for children interact with the huge reduction in deaths from aging to cause a massive population explosion? I think so.
The idea that biomass energy can become a substantial source of new energy production is based on the assumption that plenty of land is available to shift into agricultural uses. Well, land prices seem like a good test of this idea. If the United States had a large amount of surplus land suitable for expansion of corn ethanol or soy biodiesel production then the prices of farm land wouldn't be going up so much.
In central Illinois, prime farmland is selling for about $5,000 an acre on average, up from just over $3,000 an acre five years ago, a study showed. In Nebraska, meanwhile, land values rose 17 percent in the first quarter of this year over the same time last year, the swiftest such gain in more than a quarter century, said Jason R. Henderson, an economist at the Federal Reserve Bank in Kansas City.
A federal-government analysis of farm real estate values released Friday showed record average-per-acre values across the country. The analysis said property prices averaged $2,160 an acre at the start of 2007, up 14 percent from a year earlier.
We aren't getting much useful energy out of biomass energy and the cost of farm lands is already going up a lot. That suggests we don't have enough farm lands to really scale up biomass energy production - at least not with corn ethanol. Now, maybe other types of land which can't grow corn could get used for biomass energy production using other types of plants. For example, cellulosic technologies applied to miscanthus or switchgrass plants might so expand the range of usable lands and yield per acre enough to make contribution from biomass energy substantial. Of course, if that comes to pass then less land will be available for wild plants and animals.
DURHAM, N.C. -- Researchers have shown for the first time that putting two specific types of neural cells directly into an aging brain can kick-start creation of brain cells linked to learning and memory.
In older people and people with Alzheimer's disease "neural stem cells are sitting there but not dividing, so they are not making new neurons," said Ashok K. Shetty, Ph.D., professor of neurosurgery at Duke and medical research scientist at the Durham Veterans Affairs (VA) Medical Center. "We hope that by making more neurons, we can improve learning and memory" in compromised patients.
Shetty and colleagues have shown that implanting specific brain cell precursors into the hippocampus region of aging rats increases neurogenesis, a first step in working toward therapies for humans. The results of their work appear in the August issue of the journal Stem Cells.
Two types of cells were harvested from the spinal cords of rats and then grafted into the aging rat hippocampus. After three weeks researchers saw an increase in neurogenesis in the rats that received the cell implants compared to rats that did not receive any treatment and rats that received implantation surgery but not receive stem cells. This is the first evidence that introduction of these two kinds of neural stem cells stimulate neurogenesis in the hippocampus.
The hippocampus has been linked to not just memory formation and storage in the brain, but also depression and neurodegenerative diseases such as Alzheimer's.
"Any strategies for improving neurogenesis in aging animals may be helpful to humans," said Shetty. The research was supported by the National Institutes of Health (NIH) National Institute on Aging as well as the National Institute of Neurological Disorders and Stroke and the Department of Veterans Affairs.
The researchers believe that the precursor cells secreted nerve growth factors that stimulated the inactive stem cells of the aging hippocampus to start dividing again. They also did a study that injected nerve growth factors directly to see if they would stimulate neurogenesis. Publication of study results is expected by the end of the year.
We need biotechnology that can take our cells, repair them, and then turn them into various types of stem cells. Once we can produce an assortment of types of youthful stem cells then we'll be able to start slowing and reversing the aging process. How soon will this happen? I do not know. But it would happen sooner if we tried harder to make it happen.
DALLAS — Aug. 6, 2007 — The longstanding idea that the entire human face ages uniformly is in need of a facelift, say researchers at UT Southwestern Medical Center who have found that multiple, distinct compartments of fat in the face age at different rates.
The findings, published in a recent issue of Plastic and Reconstructive Surgery, challenge previously held theories regarding aging and may offer new ways to help turn back the clock, UT Southwestern plastic surgeons say.
“For hundreds of years, everyone has believed that the fat on the face is one confluent mass, which eventually gets weighed down by gravity, creating sagging skin,” said Dr. Joel Pessa, assistant professor of plastic surgery and the study’s lead author. “In our studies, however, we were surprised to find that this is not the case; the face is made up of individual fat compartments that gain and lose fat at different times and different rates as we age.”
We lose the smooth continuous appearance of our faces as the compartments shift, shrink, and grow in size.
The study involved injecting different types of dye into facial cavities of 30 cadavers. Despite at least 24 hours of settling time, the dye, rather than permeating the entire face, stayed in separate areas — showing that individual facial compartments have boundaries between them that act like fences. These fences, which seem to be composed of fibrous tissue, allow the face to maintain its blood supply should it become injured.
Dr. Pessa said the face resembles a three-dimensional puzzle, with fat divided into distinct units around the forehead, eyes, cheeks and mouth. Facial aging is, in part, characterized by how these separate compartments change as we grow older.
A youthful face is characterized by a smooth transition between these compartments. As people age, contour changes occur between these regions due to volume losses and gains as well as repositioning of the compartments. Eventually, this can result in sagging or hollowed skin and wrinkles.
We need youthful fat cells to put into the facial cavities that hold our aging facial fat tissue. Plastic surgeons of the future are going to become stem cell therapists who deliver rejuvenated stem cells into many parts of the body. We need a more rapid rate of advance in stem cell research so that we get these youthful stem cells sooner.
A recurring FuturePundit theme: The toughest part of the body to rejuvenate is going to be the brain. Therefore anything that slows brain aging is especially valuable for those who want to survive until the reversal of aging becomes possible. With that thought in mind: Looks like a cup of coffee might slow your brain aging.
ST. PAUL, MN- Caffeine may help older women protect their thinking skills, according to a study published in the August 7, 2007, issue of Neurology®, the medical journal of the American Academy of Neurology.
The study found that women age 65 and older who drank more than three cups of coffee (or the equivalent in tea) per day had less decline over time on tests of memory than women who drank one cup or less of coffee or tea per day. The results held up even after researchers adjusted for other factors that could affect memory abilities, such as age, education, disability, depression, high blood pressure, medications, cardiovascular disease, and other chronic illnesses.
“Caffeine is a psychostimulant which appears to reduce cognitive decline in women,” said study author Karen Ritchie, PhD, of INSERM, the French National Institute for Health and Medical Research, in Montpellier, France. “While we have some ideas as to how this works biologically, we need to have a better understanding of how caffeine affects the brain before we can start promoting caffeine intake as a way to reduce cognitive decline. But the results are interesting – caffeine use is already widespread and it has fewer side effects than other treatments for cognitive decline, and it requires a relatively small amount for a beneficial effect.”
The study involved 7,000 people whose cognitive abilities and caffeine consumption were evaluated over four years. Compared to women who drank one cup or less of coffee per day, those who drank over three cups were less likely to show as much decline in memory. Moreover, the benefits increased with age – coffee drinkers being 30 percent less likely to have memory decline at age 65 and rising to 70 percent less likely over age 80.
Now, do I have to take up coffee drinking or watch my mental lights go out? I'd really like to know whether the caffeine or some other compound in the coffee delivers the protective benefit.
There are other ways to get the caffeine of course. For example, 3.5 ounces of dark chocolate has as much caffeine as 8 ounces of instant coffee. Yet another reason to eat chocolate. Black tea contains more than twice as much caffeine as green tea.
Currently a diagnosis of pancreatic cancer is almost always a death sentence. Pancreatic cancer causes little or no symptoms until it has spread and mutated so much that it can't be stopped. If we could only diagnose this cancer much sooner the potential exists to go remove it in a small area and get a cure in most cases. Well, some scientists and technologists at Northwestern University have discovered that a biopsy of the duodenum (the top part of the small intestine which the stomach empties into) can provide a method to do very early diagnosis for pancreatic cancer.
EVANSTON, Ill. --- Optical technology developed by a Northwestern University biomedical engineer shown to be effective in the early detection of colon cancer now appears promising for detecting pancreatic cancer, the fourth most common cause of cancer deaths in the United States.
Known as a silent killer, with no method of early detection, pancreatic cancer spreads rapidly and seldom is detected in its early stages. The new technique could lead to the first screening method for pancreatic cancer in asymptomatic patients, said Vadim Backman, developer of the technology and professor of biomedical engineering at Northwestern’s Robert R. McCormick School of Engineering and Applied Science.
Backman and Yang Liu, a former graduate student of Backman’s, teamed up with physicians at Evanston Northwestern Healthcare (ENH) to test the technique in a pilot study of 51 patients. The researchers found they could detect both early- and advanced-stage pancreatic cancer without touching or imaging the pancreas.
The extraordinarily sensitive technique, which is minimally invasive and takes advantage of certain light-scattering effects, can detect abnormal changes in cells lining the duodenum even though the cells appear normal when examined with a conventional microscope. The results, which will be published in the Aug. 1 issue of the journal Clinical Cancer Research, show that the changes accurately predict the presence of cancer.
So they developed a better way to examine cells to identify abnormal cells. Then they used that better technology to examine duodenal cells because it is easier to reach the duodenum to get the cell sample than it is to reach the pancreas. Luckily, the duodenum shows abnormal cells when the pancreas (which connects to the duodenum) has early stage cancer cells. All very good.
What I want to know: How did they reach the duodenum? Can this be done by snaking a tube through the mouth and down through the stomach?
In the study, biopsies of normal-looking tissue were taken from the duodenum near the opening of the pancreatic duct for analysis. For each sample, light is shined on the tissue. The light scatters and some of it bounces back to sensors in the fiber-optic probe. A computer analyzes the pattern of light scattering, looking for the “fingerprint” of carcinogenesis in the nanoarchitecture of the cells.
The researchers found the technique identified with 100 percent accuracy each person who had a resectable cancerous tumor in the pancreas. (Resectable means the tumor can be removed surgically, which in this study is defined as stage 1 or 2 tumors.) Some people were identified who did not have a tumor; it is uncertain whether this is a false finding or if it means those people could be at risk for developing pancreatic cancer and need to be watched closely.
This pair of optical tests also produced excellent results in detecting colon cancer.
The method combines two complementary technologies developed by Backman and colleagues in his lab: four-dimensional elastic light-scattering fingerprinting (4D-ELF) and low-coherence enhanced backscattering spectroscopy (LEBS). The researchers found that the two combined work better than one alone in pancreatic cancer screening.
The success of the pancreatic cancer screening study follows on the heels of extremely positive results in studies using the two optical technologies for the early detection of colon cancer.
What I want to know: How often would we need to get tested for pancreatic and colon cancer to assure that new cancers would always get caught at early enough stages to be curable? How fast does a pancreatic cancer pass through its first stage into later stages? My guess is that the answer varies considerably from case to case.
What we really need are cancer tests for the entire body that can work pretty close to continuously. Imagine an injection of a cancer detection nanobot that would produce a visible symptom (how about blue and green spots on your hand or face?) when it found a cancer. Then a blood sample could isolate some nanobots and an instrument could download the collected information from the nanobots.
We face another problem with highly sensitive techniques for early cancer detection: We have lots of very small cancers in tiny nodes that are stuck at very small sizes because they have not mutated to generate new blood vessels (ie they do not secrete angiogenesis compounds). The most sensitive methods imaginable for detecting cancers would detect too many. The vast majority of detected abnormal cells would not constitute a threat - at least not for many years. Attempts to find and remove all these very small cancers would involve surgery on many organs and the little cancer nodes might be hard for surgeons to find. So we need cancer finding technology that can discriminate between high and low risk cancers.
WESTCHESTER, Ill. -- People who work rotating shifts have significantly lower levels of serotonin, a hormone and neurotransmitter in the central nervous system believed to play an important role in the regulation of sleep, according to a study published in the August 1st issue of the journal SLEEP.
Heard of anti-depressant drugs like Prozac, Celexa, Lexapro, Zoloft, or Paxil? They are all selective serotonin reuptake inhibitors (SSRIs). They work by preventing neurons from pulling serotonin back onto the internal side of neural cell membranes. That leaves more serotonin to bind to receptors which boosts certain types of neural signalling which somehow lifts people out of depression. But if you do something that lowers the amount of serotonin available (and working the night shift does this) then you are going to be more prone to depression.
Night shift workers are probably not asking for enough additional compensation to make it worth the effect on their bodies.
The study, authored by Carlos J. Pirola, PhD, of the Universidad de Buenos Aires, Argentina, focused on 683 men of self-reported European ancestry, in which 437 day workers were compared with 246 rotating shift workers. Day and night work periods started at 6 a.m. and 6 p.m. respectively. None of the subjects interchanged their job schedule.
The results showed that serotonin content differed greatly between day workers and rotating shift workers, with levels of serotonin significantly higher in day workers.
“These findings may be important not only to understand the mechanisms related to the circadian rhythm desynchronization imposed by the rotating shift work regime, but also to target truly effective therapeutic strategies that may ameliorate the associated comorbidities and behavioral problems in rotating shift workers,” said Pirola.
In addition to sleep problems, low levels of serotonin are also associated with other conditions such as anger, depression and anxiety.
What would be interesting follow-up experiments: Can high intensity lights, melatonin, or some other treatment or style of living allow people to work late shifts without lowered serotonin? Also, is some fraction of the populace able to do late shift work without getting lowered levels of serotonin?
Brian Wang of the Advanced Nano blog has figures that answer a question that comes up here on occasion: How big a strain on productive capacity would a massive nuclear power plant construction program impose? Not much.
Building 1,000 one gigawatt nuclear plants per year would use less than 10% of the worlds annual concrete and steel. Modern nuclear reactors need less than 40 metric tons of steel and 190 cubic meters of concrete per megawatt of average capacity. 1,000 one gigawatt nuclear plants per year would need 40 million metric tons of steel and 190 million cubic meters of concrete. World supplies in 2006 are 1.24-billion tons of steel per year & 2.283 billion tons of coal per year.
So what do these raw materials cost? A short ton (2000 lb) of steel costs about $600. (and the metric ton used above equals 2,204.6 pounds)
Spot prices for cold-rolled steel in June averaged $602.24 a short ton, down from $672.95 a year earlier, according to Dow Jones Indexes.
Then (2204.6/2000)*602.24 equals $663.85 per metric ton of steel. Then times 40 metric tons per megawatt of capacity we get to $26554 worth of steel per megawatt of nuclear electric power plant capacity. So then the steel cost for a 1 gigawatt nuclear power plant is only 1000 times that amount or about $26 to $27 million at current steel prices. That's not much for a plant that costs perhaps nearly $2 billion to build. However, note that steel comes in many forms and the steel used in some parts of nuclear power plants is more expensive. A table of highway construction materials costs shows that structural steel can cost as much as double the cost of reinforcing steel. I'm not sure how expensive the most expensive types of nuclear reactor steel get. So my rough steel cost calculation has a large margin of error.
I couldn't come up with good data on concrete costs. Does concrete or steel cost more for nuclear power plant construction?
I am suspicious of the cost numbers I came up with above because they do not fit with the news stories about the rising costs of coal and nuclear power plant construction. A recent New York Times story by Matthew Wald drives home the effects that rising raw materials costs are having on power plant construction:
NEW YORK: When General Electric called in reporters for a briefing on its new nuclear partnership with Hitachi, it said that atomic power plants could be built faster than before, operated reliably and had a vanishingly small chance of an accident.
But what will they cost? After some hemming and hawing, company executives Monday gave figures by the standard industry metric, dollars per kilowatt of capacity, but in a huge range: $2,000 to $3,000.
"There's massive inflation in copper and nickel and stainless steel and concrete," said John Krenecki, president and chief executive of GE Energy. The uncertainty is not just in nuclear plants, he said. Coal plant prices are similarly unstable.
At $3000 per kilowatt that is $3 billion for a 1 Gigawatt nuclear power plant. Seems expensive. Is it? Does anyone know how to get from that to pennies per kilowatt-hour (kwh)? The answer depends on operating costs, fuel costs, interest rate for the capital, and still other factors. A kilowatt of capacity translates into 1 kwh every hour, right? So then 24 kwh per day times 365 days a year or 8760 kwh. But then assume operation of the plant 90% of the time and it goes down to 7884 kwh per year. If that sells for, say, 5 cents per kwh at wholesale (how close is that to actual in various parts of the US) then $3000 of investment generates about $400 in revenue per year. At about 13% of the $3000 that sounds like it more than covers the cost of capital. Is my method of calculation roughly correct?
If my calculation approach above is close to correct then nuclear power at $2000 per kilowatt capacity looks pretty competitive. A $2000 investment generates $400 in revenue at 5 cents per kwh.
Some argue against nuclear power by claiming that nuclear power plant construction requires large amounts of energy usage. But compared to what? How about wind? Brian also quotes Per Peterson of the UC Berkeley Dept. of Nuclear Engineering on the steel and concrete needs per megawatt for wind.
Modern wind energy systems, with good wind conditions, take 460 metric tons of steel and 870 cubic meters of concrete per megawatt.
Does wind power really require 11.5 times as much steel as nuclear power per megawatt? Does wind power really require 4.5 times as much concrete per megawatt? Wind is making strides in terms of size of blades and materials in blades. Do these numbers really represent the state of play right now? Given wind's rapid rate of growth I'm having a hard time believing it takes so much steel and concrete (i.e. so much money) to build.
If anyone has high quality original sources on materials needs per megawatt capacity for various electrical power sources please post in the comments.
I am also looking for authoritative sources on Energy Return On Energy Invested (EROEI) for nuclear and wind. I've come across claims that nuclear power plants pay back their energy invested within the first 6 months of operation.
I also want to know how much steel and concrete costs can fall as a result of expansion of production facilities. Can nickel's price come down as a result of expanded mining operations? Can copper's price come down or is the world running out of copper? How much of the current high costs of new power generation capacity are long term and how much due to a transitory period where many sources of demand are peaking?
One might argue that China's rapid rate of growth has temporarily caused demand to exceed supply. But isn't China going to continue to expand rapidly? If so, can the mining and raw materials processing industries (e.g. steel, cement) start growing at rates that will prevent Chinese demand from holding prices high for an extended period of time?
Those of you moved by my story Heroic Wolves Save Glorious Aspens From Evil Elks about how the carnivores are the good guys will no doubt be delighted to learn that carnivore birds protect trees from evil vegetarian insects.
Chickadees, nuthatches and warblers foraging their way through forests have been shown to spur the growth of pine trees in the West by as much as one-third, according to a new University of Colorado at Boulder study.
The study showed birds removed various species of beetles, caterpillars, ants and aphids from tree branches, increasing the vigor of the trees, said study author Kailen Mooney. Mooney, who conducted the study as part of his doctoral research in CU-Boulder's ecology and evolutionary biology department, said it is the first study to demonstrate that birds can affect the growth of conifers.
"In a nutshell, the study shows that the presence of these birds in pine forests increased the growth of the trees by helping to rid them of damaging insects," said Mooney. "From the standpoint of the trees, it appears that the old adage, 'the enemy of my enemy is my friend,' holds true."
A paper on the subject by Mooney was published in the August issue of Ecology, a monthly science journal. Mooney, who received his doctorate from CU-Boulder in 2004, will become a biology department faculty member at the University of California, Irvine, in fall 2007.
In the study, Mooney used mesh netting to exclude birds from ponderosa pine limbs in the U.S. Forest Service-managed Manitou Springs Experimental Forest northwest of Colorado Springs for three years. The results showed that branches on 42 trees rigged to exclude birds had 18 percent less foliage and 34 percent less wood growth by the end of the study.Mooney collected about 150,000 insect specimens from the mountain study area, identifying more than 300 separate spider and insect species collectively known as arthropods. The trees used in the study were set up to exclude birds, ants, or both, since ants also can have significant impacts on other arthropods, he said.
Carnivorous birds and wolves toil to protect forests from their natural enemies. What great animals. Cheer them on as they kill, kill, kill!
WASHINGTON, July 30 — A one-sentence provision buried in the Senate’s recently passed energy bill, inserted without debate at the urging of the nuclear power industry, could make builders of new nuclear plants eligible for tens of billions of dollars in government loan guarantees.
As regular readers know, I'm a supporter of nuclear power and see it as a desirable replacement for dwindling fossil fuels supplies. But I'm skeptical of an argument that every nuclear power plant that gets built should receive federal loan guarantees. What's the justification for this?.
All those plans for new nuclear power plant construction? Well, now we find out that the nuclear power industry says it won't build them without loan guarantees.
Power companies have tentative plans to put the 28 new reactors at 19 sites around the country. Industry executives insist that banks and Wall Street will not provide the money needed to build new reactors unless the loans are guaranteed in their entirety by the federal government.
Um, are they serious or bluffing? Surely, capitalists want to reduce risks and increase returns on investment. Loan guarantees will lower the cost of capital and therefore increase profits. But is the nuclear power industry saying that the cost of capital for nuclear plants is so high that without lowered interest rates that new nuclear power plants can't be profitable?
I am skeptical of the claimed need for loan guarantees. The cost of fossil fuel competitors is going to keep going up. North American natural gas production is headed for a downhill slope. World coal and oil supplies are looking pretty limited. (and Saudi Arabia's Ghawar oil field looks like it has peaked) Well, nuclear's long term competitors end up being wind and solar. Unless wind and solar can out-compete nuclear why won't new nuclear power plants turn a profit even if operators borrow money at market rates?
Update: To clarify: I happen to think it is a good idea for a subsidy for the next few reactors that get built to test out the licensing process and to come up with a few reactor designs. All the utilities otherwise sit around waiting for other utilities to go first. The Nuclear Regulatory Commission doesn't know what it is going to decide during a review of any of the new designs. So the industry can get stuck with regulatory uncertainty.
Also, this loan program is supposed to apply to all energy sources that will not generate carbon dioxide from fossil fuels. There's an argument to be made for pushing along all the non-fossil fuels energy sources. Currently the dumbest and most damaging non-fossil fuel source - biomass corn ethanol - gets huge subsidies and gets used instead of far smarter choices. We need to level the playing field. I'd rather level it by ending all subsidies for corn ethanol. But the grain farmer lobby and numerous Congressional whores make that impossible.
Writing in the Journal of the National Cancer Institute, researchers from Canada and the US report that an increased intake of cruciferous vegetables was associated with a 40 per cent reduction in prostate cancer risk, with broccoli and cauliflower singled out as offering most protection.
Men who reported eating cauliflower more than once per week were 52 percent less likely to be diagnosed with aggressive prostate cancer than men who reported eating cauliflower less than once a month.
Men who reported eating broccoli more than once per week were 45 percent less likely to be diagnosed with aggressive prostate cancer than men who reported eating broccoli less than once a month.
Eat more cabbage, cauliflower, kale, collars, rutabaga, kohlrabi, Brussel sprouts, and other members of the Brassicaceae (aka Cruciferae) family of veggies.
Rutgers researchers have found that the curry spice turmeric holds real potential for the treatment and prevention of prostate cancer, particularly when combined with certain vegetables.
The scientists tested turmeric, also known as curcumin, along with phenethyl isothiocyanate (PEITC), a naturally occurring substance particularly abundant in a group of vegetables that includes watercress, cabbage, winter cress, broccoli, Brussels sprouts, kale, cauliflower, kohlrabi and turnips. "The bottom line is that PEITC and curcumin, alone or in combination, demonstrate significant cancer-preventive qualities in laboratory mice, and the combination of PEITC and curcumin could be effective in treating established prostate cancers," said Ah-Ng Tony Kong, a professor of pharmaceutics at Rutgers, The State University of New Jersey.
A variation in a gene called GRIK4 appears to make people with depression more likely to respond to the medication citalopram (Celexa) than are people without the variation, a study by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, has found. The increased likelihood was small, but when people had both this variation and one in a different gene shown to have a similarly small effect in an earlier study, they were 23 percent more likely to respond to citalopram than were people with neither variation.
The finding addresses a key issue in mental health research: the differences in people’s responses to antidepressant medications, thought to be based partly on differences in their genes. Some patients respond to the first antidepressant they attempt, but many don’t. Each medication takes weeks to exert its full effects, and patients’ depression may worsen while they search for a medication that helps. Genetic studies, such as the one described here, may lead to a better understanding of which treatments are likely to work for each patient.
The ability to avoid the use of drugs that will fail will reduce time until effective treatments are used and therefore, reduce suffering, speed recovery, and reduce costs.
Genetic variations for serotonin and glutamate neuotransmitter receptors influenced how well people responded to citalopram.
In the newest study, researchers examined the genetic material of more of the patients who had participated in STAR*D, for a total of 1,816 samples, and repeated the comparison of DNA from citalopram responders and nonresponders. They discovered that people with the variation in the GRIK4 gene had a higher likelihood of response, and again found that the variation in the HTR2A gene also made people more likely to respond. The results were reproduced, strengthening their validity.
The protein produced by HTR2A acts as a receptor on brain cells for the chemical messenger serotonin, one of several neurotransmitters that enable the cells to communicate with each other. The discovery that a variation in a serotonin-related gene could affect response to citalopram was not entirely surprising, since the serotonin system is known to be involved in depression. Citalopram targets this system.
But GRIK4 makes a protein that acts as a receptor in a different neurotransmitter system, the glutamate system. Recent studies suggest that the glutamate system also is involved in depression, an assertion supported by the new finding.
Genetic testing for drug selection will also help to avoid drugs that will cause patients side effects. For each drug genetic profiles will be found that put one at much higher risk of adverse reactions,. Everyone will have a complete genetic profile that will help guide drug selection for most effect results with least risk of side effects.