Vitamin K slowed the development of insulin resistance in elderly men in a study of 355 non-diabetic men and women ages 60 to 80 who completed a three-year clinical trial at the Jean Mayer Human Nutrition Research Center on Aging at Tufts University (USDA HNRCA).
“Men who received vitamin K supplementation had less progression in their insulin resistance by the end of the clinical trial,” said Sarah Booth, PhD, senior author and director of the Vitamin K Laboratory at the USDA HNRCA. “Conversely, we saw progression in insulin resistance in women who received vitamin K supplementation, and in the men or women who were not given vitamin K supplements.”
Among those given vitamin K, both men and women took daily multivitamins containing 500 micrograms of vitamin K, five times the Adequate Intake (AI) recommended by the Institute of Medicine’s Food and Nutrition Board, with instructions to maintain normal diets without any additional supplementation. They also received a calcium and vitamin D supplement. Men and women in the control group received no vitamin K supplementation but did receive the multivitamin and the calcium and vitamin D supplement. For the present study, insulin resistance was assessed by the homeostasis model (HOMA-IR). Additionally, participants’ blood glucose and blood insulin levels were measured following a minimum 10-hour fast. In addition to improved insulin resistance, the supplemented men had lower blood insulin levels compared to the unsupplemented men at the conclusion of the study.
Insulin resistance will accelerate your aging. Definitely worth avoiding.
The women might have needed a larger vitamin K dose to derive a benefit. Though cutting back on excess weight definitely would have helped.
Writing in the November issue of Diabetes Care, the authors speculate that weight might explain why only the vitamin K supplemented men improved their insulin resistance. “In our study, there was a higher prevalence of obese or overweight women in the vitamin K supplementation group compared to the male supplementation group,” Booth said. “Vitamin K is stored in fat tissue. If there is excess fat, vitamin K may not be readily available to cells that require it to process glucose.”
If you want to max out your dietary vitamin K then eat a cup a day of kale, collards, or spinach. Each will give you over 1000 mcg vitamin K or more than double the amount used in this study. See a longer list of good vitamin K food sources at that link.
Does your knee hurt? We need better methods for the repair of worn and aging body parts. With better ways to repair we could keep bodies running far beyond their original design life just like antique cars. The best knee cartilage repair surgery helps some but far from enough.
“A small hole is going turn into a big hole eventually, given enough time," says Riley Williams, M.D., orthopedic surgeon, Sports Medicine and Shoulder Service, Hospital for Special Surgery in New York, and director of the Institute for Cartilage Repair at HSS.
After an initial injury that has caused damage to a specific area of the cartilage, there are few options that can repair the damage which is likely to lead to severe osteoarthritis. The most popular current treatment for such lesions is called the microfracture procedure. In this surgery, a tiny 'pick' spikes holes into the base of the damaged cartilage area to promote bleeding. This allows the patient’s bone marrow cells to come to the surface of the damaged tissue. As a result, the cells then change into fibrocartilage cells and heal the defect.
While microfracture is minimally invasive and very quick, research has found that the defect may not always be fully repaired. The fibrocartilage does not hold up as well under everyday wear and tear as normal cartilage and has a much higher risk of breaking down again. As a result, surgeons in this area continue to pursue new methods of repairing cartilage injuries.
Some improvements in tissue engineering using a patient's own cells might produce a far more lasting layer of replacement cartilage.
A new multi-center clinical trial led by Dr. Williams at Hospital for Special Surgery uses a patient’s own cells to heal damaged cartilage, but in a much different way. First, a small piece of the patient’s healthy cartilage is taken and then the cells are grown in a laboratory. These cells are put into a piece of protein matrix, called NeoCart®, which has an internal structure shaped like a honeycomb. The cells use the NeoCart® as a scaffold and begin to grow over and around the structure. This creates a piece of new cartilage which is then, through a tiny incision, implanted into the patient’s joint over the damaged area, much like a living patch. The hope is that the new cartilage will repair the damage and integrate seamlessly with the surrounding cartilage.
Cell manipulation and tissue engineering technologies will produce much better results in the coming years. Some of the more mechanical parts of the body such as joints are lower lying fruit for repair and rejuvenation.
My biggest concern with the clinical trial above has to do with the age of the patients. Will the cells of older patients grow vigorously enough to create enough replacement cartilage? Will we need to wait for rejuvenating therapies for cells before an elderly patient's own cells can build replacement parts? The odds of success might be higher the younger you are.
A new national screening strategy in Denmark has halved the number of infants born with Down's syndrome and increased the number of infants diagnosed before birth by 30%, according to a study published on bmj.com today.
Many countries, including England, Australia and New Zealand, are trying to introduce national screening strategies for Down's syndrome, but are facing a variety of problems because of a lack of consensus about the screening policy and logistical challenges.
Owing to opposition to abortion by a substantial part of the American population do not expect to see such extensive systematic screening for Down's in the United States. This reduction in Down's births is coming as a result of abortions. Abortion opponents do not want women to know in advance they might be carrying a baby with a birth defect.
Since Denmark is a small country the number of Down's births is pretty small anyway. False positives and false negatives are both dropping.
They report that the number of infants born with Down's syndrome decreased from 55 per year during 2000, to 31 in 2005 and 32 in 2006. The total number of invasive tests fell sharply from 7524 in 2000 to 3510 in 2006.
The detection rate in the screened population was 86% in 2005 and 93% in 2006. With 3.9% (17) of women receiving a false positive result in 2005 and 3.3% (7) in 2006.
Down's will eventually become much rarer in the United States as a result of a much larger development. I predict a big shift toward in vitro fertilization (IVF) as we learn more about what all the genetic variations mean. Once genetic testing of embryos can provide enormous details about the future of potential offspring many prospective parents will opt to fertilize multiple eggs in vitro and then select the one that comes closest to matching their desires for offspring genetic inheritance.
Since the embryos will get screened for desired genes as a side effect major genetic problems will be avoided. The ability to select for smarter, better looking, more coordinated, stronger, more charming, and healthier children will lead to the widespread embrace of eugenics.
Breast cancer rates increased significantly in four Norwegian counties after women there began undergoing mammography every two years, according to a report in the November 24 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. Rates among regularly screened women remained higher than rates among women of the same age who were screened only once after six years, suggesting that some of the cancers detected by mammography may have spontaneously regressed had they not been discovered and treated.
The idea here is that if the women who were tested less often really had as much lasting breast cancer as that found in the more frequently tested group then the former group really should have had more breast cancer cases found when they were finally tested . But they did not show those "missing" breast cancer occurrences at the end of the trial.
Throughout Europe, the start of screening mammography programs has been associated with increased incidence of breast cancer, according to background information in the article. "If all of these newly detected cancers were destined to progress and become clinically evident as women age, a fall in incidence among older women should soon follow," the authors write. "The fact that this decrease is not evident raises the question: What is the natural history of these additional screen-detected cancers?"
Per-Henrik Zahl, M.D., Ph.D., of the Norwegian Institute of Public Health, Oslo, and colleagues examined breast cancer rates among 119,472 women age 50 to 64 who were all invited to participate in three rounds of screening mammograms between 1996 and 2001 as part of the Norwegian Breast Cancer Screening Program. They compared these to rates among a control group of 109,784 women age 50 to 64 in 1992, who would have been invited for screening if the program had existed at that time. Cancers were tracked for six years using a national registry, and at the end of that time all participants were invited to undergo a one-time screening to assess breast cancer prevalence.
As anticipated, breast cancer rates were higher among screened women than among the control group before the final prevalence screening. "Even after prevalence screening in controls, however, the cumulative incidence of invasive breast cancer remained 22 percent higher in the screened group," the authors write. Of every 100,000 screened women, 1,909 had breast cancer during the six-year period, compared with 1,564 of every 100,000 in the control group. Screened women were more likely to have breast cancer at every age.
An alternative explanation is that each test for breast cancer has false negatives and some of these women who are tested less often are having their breast cancer getting missed. Is that possible?
Suppose this finding holds up. It has some obvious implications. First off, some of the reported claimed progress in curing breast cancer might be a mirage. More frequent testing is turning up earlier stage breast cancer. Some of that earlier stage breast cancer might disappear naturally (perhaps via an immune response) if left alone. Treatment might even impair the immune system and leave it less able to defeat the breast cancer on its own.
This report suggests some women are going thru surgery, chemo, and radiation who would otherwise recover from breast cancer without ever knowing they even had it. Given the ravages of the treatments this is quite unfortunate. But perhaps scientists can discover characteristics of cancers or of patient immune systems that make regression more likely. Then those conditions could be induced in women with breast cancer in order to cause more regressions.
We can expect great advances in early detection. Microfluidic devices will test blood samples with great sensitivity and detect blood markers for cancer (and other diseases as well). The tests will become so sensitive that we are going to hit a problem: we have lots of very small cancers in our bodies (really) that are stuck at the stage of being unable to grow more blood vessels. These very small cancers are going to contribute to a sort of background noise of cancer signals. I expect as the blood assay tests become more sensitive to very low concentrations of cancer markers we will even find that as we age a gradual slow rise in cancer blood markers will be found.
On the bright side, the ability to detect very early stage cancer will lend itself to immune treatments against cancer. Caught early enough a cancer won't have as many mutations that protect it from an immune response. In particular, I'm hopeful that vaccines and monoclonal antibodies will be developed that will rid of cancers without our even having to know the exact location of each cancer. Perhaps as we age we will periodically go in for an anti-cancer immunotherapy that basically kills any early stage cancer cells that have grown up since a previous treatment.
The sirtuin genes activated by resveratrol seem to shift their behavior in stressed mouse cells in ways similar to how they behave in yeast. This provides an important clue about the causes of changes in gene regulation as we age. But is this an argument for taking resveratrol?
One function of the mouse version of Sir2, called SIRT1, is to regulate how genes are expressed in various tissues. Patterns of expression differ among organs--many genes that need to be active in the liver, for instance, must remain silent in the brain. By binding to regulatory regions alongside certain genes, SIRT1 helps dictate those patterns. Because SIRT1 has also been shown to participate in DNA repair, Sinclair and his colleagues wondered whether increasing DNA damage would compromise the protein's normal regulatory role, as is the case with Sir2 in yeast.
Sure enough, when the researchers treated mouse embryonic stem cells with DNA-damaging hydrogen peroxide, SIRT1 migrated away from regulatory regions of the genome and toward the many areas where DNA strands had broken. As a result, genes that were normally shut off suddenly became active. Gene expression patterns, once exquisitely fine-tuned, went haywire.
Lots of patterns of gene expression change as we age. Some of the genes that get turned on might be to try to do repair. Some are involved in inflammatory response. But the turning on of other genes might simply be mistakes that only cause harm.
"This is something that's eerily parallel to what we know in yeast," says Jan Vijg, chair of genetics at Albert Einstein College of Medicine, who was not involved in the study.
Okay, suppose the SirT1 moves to go deal with damaged DNA as we age. Suppose that leaves assorted genes no longer repressed. Then does the use of resveratrol redirect the genes back toward the genes it was originally bound to? If so, does that leave the damaged DNA unrepaired? Or does resveratrol make the SirT1 more active and therefore capable of handling more tasks at once? How can resveratrol allow SirT1 to perform both tasks at once? Anyone have an insight on this?
Connecting the dots, does the unrepression of lots of genes as SirT1 unbinds from them cause obesity?
Sirtris, a company Dr. Sinclair helped found, has developed a number of chemicals that mimic resveratrol and are potentially more suitable as drugs since they activate sirtuin at much lower doses than resveratrol. This month, one of these chemicals was reported in the journal Cell Metabolism to protect mice on fatty diets from getting obese and to enhance their endurance in treadmills, just as resveratrol does.
I am very tempted to start taking resveratrol. Haven't done it yet. I'm reluctant because I keep thinking there's no free lunch. If up-regulation of SirT1 activity will allow us to live longer why was this not selected for already? What is the cost of that higher SirT1 activity? There must be a cost or we'd already have mutations that make SirT1 more vigorous.
The researchers found in studies of mammalian stem cells that the protein SIRT1 controls the packaging of DNA into chromatin, thereby setting the youthful pattern of gene activity by keeping select genes switched off. In response to DNA damage, those SIRT1 proteins leave their posts to go off and assist in the necessary repairs. That change in SIRT1's job description leads to shifts in gene activity that parallel those seen in the aging mouse brain, they show. They suspect similar changes would also be found in other body tissues as well.
Again, do any readers follow the resveratrol research literature closely? What's the trade-off here when using resveratrol?
Resveratrol acts as a sirtuin activator. So does it make SirT1 do more things at once?
Resveratrol, a small molecule found in red wine, is reported to slow aging in simple eukaryotes and has been suggested as a potential calorie restriction mimetic. Resveratrol has also been reported to act as a sirtuin activator, and this property has been proposed to account for its anti-aging effects. We show here that resveratrol is a substrate-specific activator of yeast Sir2 and human SirT1.
I'd like to prevent or reverse gene regulation changes associated with aging. But can this be done with a net benefit using a single chemical compound? I'm skeptical but open to evidence.
Update: Giving extra copies of SirT1 to mice which get lymphoma causes them to live longer. But would an extra copy of the SirT1 gene cause standard lab mice to live longer? Would it cause humans to live longer?
The researchers also discovered that lab mice with an excess of SIRT1 showed fewer unwanted changes in gene expression and improved ability to repair DNA. Perhaps this is a way to slow down the aging process; by developing a drug that stimulates SIRT1, said the researchers. There is already evidence that the red wine ingredient resveratrol works via SIRT1, as do several other targeted drugs that are in various stages of development. Following a calorie restricted diet is also thought to slow aging and improve health via SIRT1.
They showed this by using mice genetically altered to model lymphoma. They gave them extra copies of SIRT1, or fed them the SIRT1 activator resveratrol, and found this extended their lifespan by between 24 and 46 per cent.
If youthful patterns of gene expression could be restored would that cause us to live longer? Or are some of the age-related changes in gene expression necessary for adjustment to accumulated damage?
What's not yet clear is how much youthful patterns of gene expression matter. Scientists not involved in the study pointed out that even if that particular aspect of aging is reversible, it is not clear that keeping gene expression young is the key to staying young.
"The paper says you might be able to maintain or go back to a younger gene expression profile, but does that mean you will be younger? You may have passed through that gate already, and you can't go back," said Dr. Stephen Helfand, a professor in the department of molecular biology, cell biology and biochemistry at Brown University.
I am especially interested in sirtuin enhancement drugs for the brain since the brain is going to be the hardest organ to rejuvenate.
Obesity gradually numbs the taste sensation of rats to sweet foods and drives them to consume larger and ever-sweeter meals, according to neuroscientists. Findings from the Penn State study could uncover a critical link between taste and body weight, and reveal how flab hooks the brain on sugary food.
"When you have a reduced sensitivity to palatable foods, you tend to consume it in higher amounts," said Andras Hajnal, associate professor of neural and behavioral sciences at Penn State College of Medicine. "It is a vicious circle."
Previous studies have suggested that obese persons are less sensitive to sweet taste and crave sweet foods more than lean people. However, little is known about the specific differences between obese and lean individuals in their sense of taste and the pleasure they derive from sweet foods.
Hajnal and his Penn State colleague Peter Kovacs, a post-doctoral fellow, investigated these differences by studying the taste responses of two strains -- OLETF and LETO rats.
Compared to the lean and healthy LETO rats, the taste responses in OLETF rats mirror those in obese humans. These rats have normal body weight at first, but they tend to chronically overeat due to a missing satiety signal, become obese and develop diabetes. The obese rats also show an increased preference for sweet foods and also are willing to work harder to obtain sweet solutions as a reward for their learning.
Obese rats react less to weaker concentrations of sucrose sugar but more to stronger concentrations - as compared to non-obese rats.
The researchers implanted electrodes in the rodents' brains to record the firing of nerve cells when the rats' tongues were exposed to various tastes -- salt, citric acid, plain water and six different concentrations of sucrose.
Hajnal and Kovacs specifically looked at differences in processing taste in the pontine parabrachial nucleus (PBN), a part of the brain that uses nerve cells to relay information from the surface of the tongue to the brain.
"We found that compared to the LETO rats, the OLETF rats had about 50 percent fewer neurons firing when their tongues were exposed to sucrose, suggesting that obese rats are overall less sensitive to sucrose," explained Hajnal, whose findings appeared in a recent issue of the Journal of Neurophysiology. The response to salt was the same for both strains.
However, when the obese rats were fed a stronger concentration of sucrose, their nerve cells fired more vigorously than in the lean rats. In other words, obese rats have a weaker response to weak concentrations and a stronger response to strong concentrations.
This probably at least partially explains human obesity. If one could increase the neural response to less sugary foods while dampening the neural response to stronger sugar concentrations one could make it much easier for people to eat less food.
Currently, solar cells are difficult to handle, expensive to purchase and complicated to install. The hope is that consumers will one day be able to buy solar cells from their local hardware store and simply hang them like posters on a wall.
A new study by researchers at the UCLA Henry Samueli School of Engineering and Applied Science has shown that the dream is one step closer to reality. Reporting in the Nov. 26 edition of the Journal of the American Chemical Society, Yang Yang, a professor of materials science and engineering, and colleagues describe the design and synthesis of a new polymer, or plastic, for use in solar cells that has significantly greater sunlight absorption and conversion capabilities than previous polymers.
The research team found that substituting a silicon atom for carbon atom in the backbone of the polymer markedly improved the material's photovoltaic properties.
Yang's lab has reached 5.6% efficiency. Yang thinks 10% efficiency is achievable with plastic photovoltaics.
The new polymer created by Yang's team reached 5.1 percent efficiency in the published study but has in a few months improved to 5.6 percent in the lab. Yang and his team have proven that the photovoltaic material they use on their solar cells is one of the most efficient based on a single-layer, low-band-gap polymer.
While the efficiency is low the use of plastics can deliver a couple of benefits. First off, low cost is a possibility. Second, the light weight and flexibility creates the possibility of installation in locations which could not support heavier weight photovoltaics. For example, long lightweight PV sheets could be hung on the sides of buildings.
The biggest potential downside of a plastic is degradation in response to prolonged light exposure. The product would need to be extremely cheap to make frequent replacement economical.
In the Baycrest study, 12 younger adults (average age 26) and 12 older adults (average age 70) took part in a face recognition task that involved having their brains scanned with fMRI while they were shown pictures of faces and later again when trying to recall whether they'd seen each face before. Researchers found that when younger and older adults had difficulty encoding a new memory (certain face), this was marked by decreased activity in brain regions important for encoding, such as the hippocampus. The researchers weren't surprised by this based on an abundance of scientific evidence indicating the importance of hippocampus for making memories.
But the older brains showed additional increased activation in certain regions during memory encoding failure that was not found in younger brains!
"The older brains showed increased activation in certain regions that normally should be quieter or tuned down," said Dale Stevens, who led the study as a psychology graduate at Baycrest's Rotman Research Institute, with senior scientists Drs. Cheryl Grady and Lynn Hasher, both of whom are distinguished researchers in aging, memory, attention and distraction.
"The auditory cortex and prefrontal cortex, which are associated with external environmental monitoring, were idling too high. The older brains were processing too much irrelevant information from their external environment – basically the scanner noise," said Dr. Stevens, who is now a post-doctoral fellow in the Department of Psychology and Cognitive Neuroscience at Harvard University. The younger brains did not show this abnormal high idling during their failed memory encoding.
The practical take-home lesson here: As you get older cut back on environmental distractions when you need to concentrate.
Another take-home lesson for employers: Cubicles are especially productivity draining for older employees. The noise and distractions of unwalled workplaces exact a greater cost in lost productivity as your employees age. Put up some sound-deadening walls and increase profits.
The better solution we need: brain rejuvenation therapies. We need remyelination to restore the neuron insulation which deteriorates with age.
University of Chicago scientists have documented that the ocean is growing more acidic faster than previously thought. In addition, they have found that the increasing acidity correlates with increasing levels of atmospheric carbon dioxide, according to a paper published online by the Proceedings of the National Academy of Sciences on Nov. 24.
"Of the variables the study examined that are linked to changes in ocean acidity, only atmospheric carbon dioxide exhibited a corresponding steady change," said J. Timothy Wootton, the lead author of the study and Professor of Ecology and Evolution at the University of Chicago.
These scientists collected the most detailed dataset of ocean pH.
The increasingly acidic water harms certain sea animals and could reduce the ocean's ability to absorb carbon dioxide, the authors said. Scientists have long predicted that higher levels of atmospheric carbon dioxide would make the ocean more acidic. Nevertheless, empirical evidence of growing acidity has been limited.
The new study is based on 24,519 measurements of ocean pH spanning eight years, which represents the first detailed dataset on variations of coastal pH at a temperate latitude—where the world's most productive fisheries live.
"The acidity increased more than 10 times faster than had been predicted by climate change models and other studies," Wootton said. "This increase will have a severe impact on marine food webs and suggests that ocean acidification may be a more urgent issue than previously thought, at least in some areas of the ocean."
The temperature rise due to CO2 build-up seems avoidable with fairly cheap climate engineering. But I do not see how we can prevent the oceans from becoming too acidic as atmospheric CO2 increases. The ocean acidity problem seems to me the most compelling argument for cutting CO2 emissions from fossil fuels burning.
Within 50 to 100 years, there could be severe consequences for marine calcifying organisms, which build their external skeletal material out of calcium carbonate, the basic building block of limestone. Most threatened are cold-water calcifying organisms, including sea urchins, cold-water corals, coralline algae, and plankton known as pteropods—winged snails that swim through surface waters. These organisms provide essential food and habitat to others, so their demise could affect entire ocean ecosystems.
The loss of shelled creatures at the lower end of the food chain could have disastrous consequences for larger marine animals. North pacific salmon, mackerel, herring, cod and baleen whales all feed on pteropods or sea butterflies, one of the species under imminent threat.
CAMBRIDGE, Mass. — New ways of squeezing out greater efficiency from solar photovoltaic cells are emerging from computer simulations and lab tests conducted by a team of physicists and engineers at MIT.
Using computer modeling and a variety of advanced chip-manufacturing techniques, they have applied an antireflection coating to the front, and a novel combination of multi-layered reflective coatings and a tightly spaced array of lines — called a diffraction grating — to the backs of ultrathin silicon films to boost the cells' output by as much as 50 percent.
The carefully designed layers deposited on the back of the cell cause the light to bounce around longer inside the thin silicon layer, giving it time to deposit its energy and produce an electric current. Without these coatings, light would just be reflected back out into the surrounding air, said Peter Bermel, a postdoctoral researcher in MIT's physics department who has been working on the project.
But what was the absolute efficiency of conversion? Is the 50% an increase over ultrathin silicon film PV efficiency and not over conventional thicker silicon PV?
The thinnest of this design cuts the cost of expensive silicon crystal.
And the potential for savings is great, because the high-quality silicon crystal substrates used in conventional solar cells represent about half the cost, and the thin films in this version use only about 1 percent as much silicon, Bermel said.
This project, along with other research work going on now in solar cells, has the potential to get costs down "so that it becomes competitive with grid electricity," Bermel said. While no single project is likely to achieve that goal, he said, this work is "the kind of science that needs to be explored in order to achieve that."
I am increasingly optimistic that the cost of PV is going to plummet. Now if only technological advances for lightweight batteries suitable for cars could cause similar cost reductions for electric cars we'd gain a major piece of the puzzle needed for migration away from fossil fuels.
Children of people who live to 100 suffer less from heart disease, stroke, and diabetes. So choose your parents wisely.
Boston, Mass. – November 20, 2008 - A recent study appearing in the November issue of Journal of American Geriatrics Society revealed that centenarian offspring (children of parents who lived to be at least 97 years old) retain important cardiovascular advantages from their parents compared to a similarly-aged cohort. The study is the first to assess the health of centenarian offspring over time and could be important for future research, as the subjects may be used as a model of healthy aging.
The findings show that centenarian offspring have a 78 percent lower risk for heart attacks, 83 percent lower likelihood of stroke and an 86 percent lower risk of developing diabetes mellitus.
Additionally, the study found that centenarian offspring who were followed in the study were 81 percent less likely to die than the reference group of similarly-aged patients during the follow-up period. The survival rate is evidence that longevity runs in families, and the results reinforce the notion that there may be physiological and genetic reasons that longevity runs in families.
The identification of genes that influence longevity will lead to drugs that alter genetic regulation in order to produce the same life-extending effects as the right genetic variations provide. Life extending drugs made to act like resveratrol will probably hit the market ahead of drugs made to mimic life-extending genes. I expect drugs that slow aging to have a fairly short-lived run before stem cell therapies and gene therapies eclipse such drugs by repairing and reversing the aging process.
The first aging decelerator drug is already on the horizon. It will get approved for diabetes but many will ask their doctor for it to slow down aging.
Harvard gerontologist David Sinclair, who co-founded Sirtris Pharmaceuticals and first showed resveratrol's effect on mice, says the drug will be inexpensive. Since the company is testing its own formulation as a diabetes drug, it will need to be priced at just a few dollars per dose, competitive with other diabetes treatments. People who use it off-label for other diseases would pay the same price.
I'm tempted to start taking resveratrol now. Anyone want to comment on their experiences using it?
Measuring proteins in the blood can help doctors determine patients' cancer risk and monitor the health of the elderly and people with chronic diseases. But current methods for testing these proteins are too expensive and require too much blood to be performed regularly. A microfluidic chip in clinical trials does on a single chip in 10 minutes what normally takes multiple technicians hours to do--and with just a single drop of blood. Researchers hope to make bedside diagnostics based on blood proteins a reality by bringing down the cost of such tests by at least an order of magnitude.
The diagnostic chip is being developed by Caltech chemistry professor James Heath and by Leroy Hood, the president and founder of the Institute for Systems Biology, in Seattle. Heath and Hood have founded a company called Integrated Diagnostics to commercialize the blood chip.
Microfluidic chips will eventually show up at home and people will test themselves using a home lab kit at very low cost. A laptop or smart phone will display the test results. The number of diseases these chips can detect will grow enormously and the chips will allow diagnosis at much earlier stages of disease development. This will of course help cure cancer before it metastasizes. But it will also enable much earlier and successful intervention in many other disease processes.
Home testing will lead to computer expert systems for home diagnosis. The data will be at home. Why not upload the daily test results to a web site that monitors for trends and detects bad test results? This will tend to decrease the role of doctors as diagnosticians and leave them more in the role of treatment deliverers. Though eventually automated systems for preparation of stem cell and gene therapies will cut back the need for doctors to deliver treatments.
Rejuvenation therapies and therapies that boost the immune system will cut the incidence of disease. In the long run doctors will spend almost all their time delivering rejuvenation therapies, enhancement therapies (including for appearances, athletics, and even cognitive function), and emergency treatments for accidents and assaults.
The chip offers a significant improvement over the cost and speed of standard laboratory tests to analyze proteins in the blood. In traditional tests, one or more vials of blood are removed from a patient's arm and taken to a laboratory, where the blood is centrifuged to separate whole blood cells from the plasma. The plasma is then assayed for specific proteins. "The process is labor intensive, and even if the person doing the testing hurries, the tests will still take a few hours to complete," says Heath. A kit to test for a single diagnostic protein costs about $50.
"We wanted to dramatically lower the cost of such measurements, by orders of magnitude," he says. "We measure many proteins for the cost of one. Furthermore, if you reduce the time it takes for the test, the test is cheaper, since time is money. With our barcode chip, we can go from pinprick to results in less than 10 minutes."
A single chip can simultaneously test the blood from eight patients, and each test measures many proteins at once. The researchers reported on devices that could measure a dozen proteins from a fingerprick of blood, and their current assays are designed for significantly more proteins. "We are aiming to measure 100 proteins per fingerprick within a year or so. It's a pretty enabling technology," Heath says.
Microfluidic chip power will continue to increase rapidly. More tests will be done in a doctor's office while you wait. Further out more tests will be done routinely at home at much more frequent intervals. Costs will plummet by orders of magnitude and the tests will become far more sensitive.
Good news for future human settlement of Mars: a supply of water for Mars colonists will not be a problem.
AUSTIN, Texas—Vast Martian glaciers of water ice under protective blankets of rocky debris persist today at much lower latitudes than any ice previously identified on Mars, says new research using ground-penetrating radar on NASA's Mars Reconnaissance Orbiter.
Because water is one of the primary requirements for life as we know it, finding large new reservoirs of frozen water on Mars is an encouraging sign for scientists searching for life beyond Earth.
The concealed glaciers extend for tens of miles from edges of mountains or cliffs and are up to one-half mile thick. A layer of rocky debris covering the ice may have preserved the glaciers as remnants from an ice sheet covering middle latitudes during a past ice age.
"Altogether, these glaciers almost certainly represent the largest reservoir of water ice on Mars that's not in the polar caps. Just one of the features we examined is three times larger than the city of Los Angeles, and up to one-half-mile thick, and there are many more," said John W. Holt of The University of Texas at Austin's Jackson School of Geosciences, lead author of a report on the radar observations in the Nov. 21 issue of the journal Science.
"In addition to their scientific value, they could be a source of water to support future exploration of Mars," said Holt.
So would it be better to melt all that ice? Some of the water would evaporate into the atmosphere providing Mars with a higher atmospheric pressure. But it is not clear to me that would help. The amount of radiation reaching the surface would probably still be so high that underground colonies would continue to make the most sense. If the water is kept frozen then colonies could be located around glaciers and only melt as much water as needed.
To make Mars a full outside-living planet where can the oxygen come from? The outer planets seem to have little oxygen. Can anyone point to abundant sources of oxygen in this solar system outside of the Earth? The Mars glaciers are mostly oxygen since water is made from 2 hydrogens and an oxygen. But I doubt enough oxygen is in that water to support a high atmospheric pressure.
Neptune's moon Triton seems like the best place to go (leaving aside energy costs and time) to get oxygen and nitrogen for a Mars atmosphere. We could remove Triton's surface and transport it to Mars for the nitrogen and oxygen.
As with Pluto, 55% of Triton's surface is covered with frozen nitrogen, with water ice comprising 15–35% and dry ice (frozen carbon dioxide) forming the remaining 10–20%.
But does anyone know how much mass of nitrogen and oxygen are on Triton as compared to how much would be needed to give Mars an atmospheric pressure similar to that of Earth?
Or does anyone have a good source for how else enough oxygen and nitrogen could be found to make the Mars atmosphere capable of supporting humans outside?
Update: James Bowery points me to a problematic report on why Mars lost its atmosphere in the first place. David Brain of UC Berkeley says irregular magnetic fields on Mars cause pieces of the Martian atmosphere to pinch off and get blown away by the solar wind.
Brain was scrolling through archival data from Global Surveyor's particles and fields sensors. "We have measurements from 25,000 orbits," he says. During one of those orbits, MGS passed through the top of a magnetic umbrella. Brain noticed that the umbrella's magnetic field had linked up with the magnetic field in the solar wind. Physicists call this "magnetic reconnection." What happened next is not 100% certain, but Global Surveyor's readings are consistent with the following scenario: "The joined fields wrapped themselves around a packet of gas at the top of the Martian atmosphere, forming a magnetic capsule a thousand kilometers wide with ionized air trapped inside," says Brain. "Solar wind pressure caused the capsule to 'pinch off' and it blew away, taking its cargo of air with it." Brain has since found a dozen more examples. The magnetic capsules or "plasmoids" tend to blow over the south pole of Mars, mainly because most of the umbrellas are located in Mars' southern hemisphere.
So how can we create a strong consistent magnetic field on Mars capable of retaining an atmosphere for a long time? Bring iron in from elsewhere in the solar system? If so, where?
WASHINGTON, D.C. - The cancer preventive properties of broccoli and other cruciferous vegetables appear to work specifically in smokers, according to data presented at the American Association for Cancer Research's Seventh Annual International Conference on Frontiers in Cancer Prevention Research.
Cruciferous vegetables have been shown to be protective in numerous studies, but this is the first comprehensive study that showed a protective benefit in smokers, specifically in former smokers, according to lead author Li Tang, Ph.D., a post-doctoral fellow at Roswell Park Cancer Institute.
If you can't stop smoking at least eat lots of cabbage and broccoli.
Among smokers, the protective effect of cruciferous vegetable intake ranged from a 20 percent reduction in risk to a 55 percent reduction in risk depending on the type of vegetable consumed and the duration and intensity of smoking.
For example, among current smokers, only the consumption of raw cruciferous vegetables was associated with risk reduction of lung cancer. No significant results were found for consumption of vegetables in general and fruits.
Eating vegetables is one of the few things you can do that will slow the aging process and make you feel better. If you do not like vegetables wolf them down quickly at the beginning of a meal just to get them out of the way.
Boys with Attention Deficit Hyperactivity Disorder (ADHD) have brain shapes that differ from those kids who aren't hyperactive.
November 17, 2008 (Baltimore, MD)—A study published today in the online advance edition of The American Journal of Psychiatry for the first time reveals shape differences in the brains of children with ADHD, which could help pinpoint the specific neural circuits involved in the disorder. Researchers from the Kennedy Krieger Institute in Baltimore, Md. and the Johns Hopkins Center for Imaging Science used a new analysis tool, large deformation diffeomorphic mapping (LDDMM), which allowed them to examine the precise shape of the basal ganglia. The study found boys with ADHD had significant shape differences and decreases in overall volume of the basal ganglia compared to their typically developing peers. Girls with ADHD did not have volume or shape differences, suggesting sex strongly influences the disorder's expression.
Once again another discovery is made possible by a new measurement technique. The ability to more accurately scan and measure brain volumes allows scientists to discern differences in brain shapes that are correlated with behavioral differences.
Previous studies examining the basal ganglia in children with ADHD were limited to volume analysis and had conflicting results, with some reporting a smaller volume and some reporting no difference in volume. LDDMM provides detailed analysis of the shape of specific brain regions, allowing for precise examination of brain structures well beyond what has been examined in previous MRI studies of ADHD. In this study, LDDMM was used to map the brains of typically developing children in order to generate a basal ganglia template. This is the first reported template of the basal ganglia. After creating LDDMM mappings of the basal ganglia of each child with ADHD, statistical analysis was conducted to compare them to the template.
In this study, the initial volume analysis revealed boys with ADHD had significantly smaller basal ganglia volumes compared with typically-developing boys. Moving beyond the standard volume analysis, the LDDMM revealed shape abnormalities in several regions of the basal ganglia. Comparison of the standard volume and LDDMM analysis of girls with ADHD and their typically developing peers failed to reveal any significant volume or shape differences.
The multiple shape differences found in boys with ADHD suggests that the disorder may not be associated with abnormalities in one specific neural circuit. Rather, it appears the disorder involves abnormalities in parallel circuits, including circuits important for the control of complex behavior and more basic motor responses, such as hitting the brake pedal when a traffic light turns yellow. Findings revealing abnormalities in circuits important for basic motor response control may be crucial to understanding why children with ADHD have difficulty suppressing impulsive actions.
If this finding holds up it suggests that permanent reduction in ADHD behavior might require large scale changes in brain shape.
Scientists at Penn State are leaders of a team that is the first to report the genome-wide sequence of an extinct animal, according to Webb Miller, professor of biology and of computer science and engineering and one of the project's two leaders. The scientists sequenced the genome of the woolly mammoth, an extinct species of elephant that was adapted to living in the cold environment of the northern hemisphere. They sequenced four billion DNA bases using next-generation DNA-sequencing instruments and a novel approach that reads ancient DNA highly efficiently.
"Previous studies on extinct organisms have generated only small amounts of data," said Stephan C. Schuster, Penn State professor of biochemistry and molecular biology and the project's other leader. "Our dataset is 100 times more extensive than any other published dataset for an extinct species, demonstrating that ancient DNA studies can be brought up to the same level as modern genome projects."
The researchers suspect that the full woolly-mammoth genome is over four-billion DNA bases, which they believe is the size of the modern-day African elephant's genome. Although their dataset consists of more than four-billion DNA bases, only 3.3 billion of them -- a little over the size of the human genome -- currently can be assigned to the mammoth genome. Some of the remaining DNA bases may belong to the mammoth, but others could belong to other organisms, like bacteria and fungi, from the surrounding environment that had contaminated the sample. The team used a draft version of the African elephant's genome, which currently is being generated by scientists at the Broad Institute of MIT and Harvard, to distinguish those sequences that truly belong to the mammoth from possible contaminants.
Of course you know where this leads: Recreation of living breathing woolly mammoths wandering around the cooler parts of United States and Canada.
What I'd most like to see in terms of species recovery: recreation of Neanderthals from sequenced Neanderthal genome samples.
Update: Nicholas Wade of the New York Times reports that scientists are already considering ways to bring back the woolly mammoth.
Scientists are talking for the first time about the old idea of resurrecting extinct species as if this staple of science fiction is a realistic possibility, saying that a living mammoth could perhaps be regenerated for as little as $10 million.
The same technology could be applied to any other extinct species from which one can obtain hair, horn, hooves, fur or feathers, and which went extinct within the last 60,000 years, the effective age limit for DNA.
How? Take all the genetic differences between elephants and woolly mammoth and start doing genetic engineering to elephant embryos to introduce woolly mammoth genetic segments. Maybe a few generations of elephant-woolly mammoth hybrids would be required to do the complete transformation. This is doable for an affordable price of about $12 million. Lots of millionaires and billionaires could afford to do this. Even if that is a lowball cost estimate of course the price will fall. 20 years from now this sort of genetic engineering will be incredibly cheap.
The coming of incredibly cheap genetic engineering will usher in an era of genetically engineered pets. Want a super smart dog that is incredibly loyal, obedient, beautiful, and very long lived? This will become affordable first for very wealthy people and then later for the middle class.
High magnesium intake has been associated with low risk of colorectal cancer. Americans have similar average magnesium intake as East Asian populations. If that were all that were involved, observers might expect both groups to have similar risk for colorectal cancer.
However, the United States has seen a much higher colorectal cancer incidence rate than East Asian populations. Furthermore, when East Asians immigrated to the United States, their incidence rates for colorectal cancer increased. This led researchers at Vanderbilt University to suspect there was something else at work.
Calcium supplementation has been shown to inhibit colorectal carcinogenesis although high calcium may simultaneously be preventing the body from absorbing magnesium. United States patients have a higher calcium intake and higher colorectal cancer incidence. "If calcium levels were involved alone, you'd expect the opposite direction. There may be something about these two factors combined – the ratio of one to the other – that might be at play", said Qi Dai, M.D., Ph.D., assistant professor of medicine at Vanderbilt University.
Dai and colleagues examined this hypothesis in a large clinical trial and found indeed that supplementation of calcium only reduced the risk of adenoma recurrence if the ratio of calcium to magnesium was low and remained low during treatment. "The risk of colorectal cancer adenoma recurrence was reduced by 32 percent among those with baseline calcium to magnesium ratio below the median in comparison to no reduction for those above the median," said Qi.
Parenthetically, magnesium is one of the few supplements I take and I never take calcium without magnesium. The magnesium delivers other benefits including lowered risk of the metabolic syndrome and type 2 diabetes.
Men with facial scars are more attractive to women seeking short-term relationships, scientists at the University of Liverpool have found.
It was previously assumed that in Western cultures scarring was an unattractive facial feature and in non-Western cultures they were perceived as a sign of maturity and strength. Scientists at Liverpool and Stirling University, however, have found that Western women find scarring on men attractive and may associate it with health and bravery.
What I wonder: Do the scars really increase attraction? Or are more masculine men more likely to get into fights and other dangerous behavior and have facial scars as result?
Researchers investigated how scarring might impact on mate choice for men and women seeking both long-term and short-term relationships. They found that women preferred men with facial scars for short-term relationships and equally preferred scarred and un-scarred faces for long-term relationships. Men, however, regarded women with and without facial scars as equally attractive for both types of relationship.
Dr Rob Burriss, from the University's School of Biological Sciences, explains: "Male and female participants were shown images of faces that displayed scarring from injury or illness, and were asked to rate how attractive they found the person for long-term and short-term relationships.
"Women may have rated scarring as an attractive quality for short-term relationships because they found it be a symbol of masculinity, a feature that is linked to high testosterone levels and an indicator of good genetic qualities that can be passed on to offspring. Men without scars, however, could be seen as more caring and therefore more suitable for long-term relationships.
What I'd like to know: Do more feminine or more masculine women have a greater attraction to men who have facial scars? I'm expecting the most feminine women to feel the most attraction to scarred men.
Roissy's Love In The Time Of Game has me thinking Darwinian thoughts about the attraction between the sexes. Were scarred men in the past seen as proven fighters? How was this female pattern of attraction selected for?
Muscle exercise might be good for your brain. Exercise boosts brain stem cell generation in both middle-aged and young mice.
BETHESDA, Md. (Nov. 18, 2008) − A new study confirms that exercise can reverse the age-related decline in the production of neural stem cells in the hippocampus of the mouse brain, and suggests that this happens because exercise restores a brain chemical which promotes the production and maturation of new stem cells.
The researchers trained young (3 months), adult (7 months), early middle-aged (9 months), middle-aged (13 months) and old (24 months) mice to run a treadmill for up to one hour a day.
The study tracked neurogenesis, age, exercise, serum corticosterone levels and brain-derived neurotrophic factor (BDNF) and its receptor TrkB levels in the hippocampus. The researchers focused on middle age as a critical stage for the decline of neurogenesis in the mice.
As expected, the study found that neurogenesis drops off sharply in middle-aged mice. For example, the number of neural progenitor and mitotic (dividing) cells in the hippocampus of middle-aged mice was only 5% of that observed in the young mice.
The researchers also found that exercise significantly slows down the loss of new nerve cells in the middle-aged mice. They found that production of neural stem cells improved by approximately 200% compared to the middle-aged mice that did not exercise. In addition, the survival of new nerve cells increased by 170% and growth by 190% compared to the sedentary middle-aged mice. Exercise also significantly enhanced stem cell production and maturation in the young mice. In fact, exercise produced a stronger effect in younger mice compared to the older mice.
What I wonder: once we can replace aged neural stem cells with younger stem cells will we hit a problem with excessive crowding of neurons and other brain cells as the reproduction of neural stem cells uses up all available space?
Some people experience slower brain aging. Are you one of the lucky ones?
Now they have a preliminary answer. Scientists examined the brains of five deceased people considered super aged because of their high performance on memory tests when they were more than 80 years old and compared them to the brains of elderly, non-demented individuals. Researchers found the super aged brains had many fewer fiber-like tangles than the brains of those who had aged normally. The tangles consist of a protein called tau that accumulates inside brain cells and is thought to eventually kill the cells. Tangles are found in moderate numbers in the brains of elderly and increase substantially in the brains of Alzheimer's disease patients.
These results suggest that treatments for Alzheimer's disease that aim to prevent tangle formation will provide benefit to all people as their brains age. That's good news. A lot of effort is going into Alzheimer's treatment and the treatment development efforts aimed at tangles strike me as having a good chance of succeeding.
"This new finding in super aged brains is very exciting," said Changiz Geula, principal investigator of the study and a research professor of neurology at the Cognitive Neurology and Alzheimer's Disease Center at Northwestern's Feinberg School. "It was always assumed that the accumulation of these tangles is a progressive phenomenon through the aging process. But we are seeing that some individuals are immune to tangle formation and that the presence of these tangles seems to influence cognitive performance." Individuals who have few tangles perform at superior levels, while those who have more tangles appear to be normal for their age, Geula noted.
This begs the question: why are some people immune to tangle formation? Do they have immune systems that attack the tangles? Or do they have some genetic variant that lowers oxidative stress in the brain?
Geula will present his findings Sunday, November 16, at the Society for Neuroscience annual meeting in Washington, D.C.
The number of plaques in the brains of the super aged was similar to that in the brains of the normally aging group. The plaque is an aggregation of protein called amyloid that becomes deposited outside the brain cell and disrupts communication between neurons. Like tangles, plaques also are found in modest numbers in the brains of aged individuals and show a dramatic increase in number in Alzheimer's disease.
Geula said the lower number of tangles in the super aged appears to be the critical difference in maintaining memory skills.
Some of the super aged in the study performed memory tasks at the level of people who were about 50 years old. For example, after being told a story, they were able to remember it immediately after and still accurately recall its details 30 minutes later. They also remembered a list of 15 words and recalled these words equally well when tested after 30 minutes.
Stopping brain aging at age 50 wouldn't be ideal. But I'd take it as a good starter. Prevention of tangles won't stop all brain aging though. For example, demyelination (loss of insulation on neurons) would still proceed. We probably need some sort of cell therapy to reverse that process.
An interesting article in MIT's Technology Review reports on a generator for wind turbines that can harvest electric power over a wider range of wind speeds.
ExRo Technologies, a startup based in Vancouver, BC, has developed a new kind of generator that's well suited to harvesting energy from wind. It could lower the cost of wind turbines while increasing their power output by 50 percent.
The new generator runs efficiently over a wider range of conditions than conventional generators do. When the shaft running through an ordinary generator is turning at the optimal rate, more than 90 percent of its energy can be converted into electricity. But if it speeds up or slows down, the generator's efficiency drops dramatically.
If the cost delta for this generator design is small enough then the 50% boost in electric power could greatly improve the economics of wind electric power. The generator works by switching in more magnetic coils as turbine speed increases.
ExRo's new design replaces a mechanical transmission with what amounts to an electronic one. That increases the range of wind speeds at which it can operate efficiently and makes it more responsive to sudden gusts and lulls.
Rather than layering individual legacy machines one on top of the next, the VIEG uses a series of coils, configured in "balanced stages".The magnetic balancing allows the use of permanent magnets, yet still reduces cogging torque to a bare minimum, which allows the VIEG to operate at extremely low wind speeds (near zero).As available energy increases, the VIEG matches generator resistance to source energy by electronically adding generator stages. Conversely, the VIEG is able to drop stages as available energy (wind speed) drops, cycling up and down without hesitation and without mechanical friction.The need for a gearbox is eliminated, and a single VIEG generator scales up and down with available energy in a way that would take almost 70 individual generators to match.
My guess is that wipespread deployment of this generator would also reduce the problem of wind intermittency since wind power wouldn't drop off suddenly below a threshold. The power supplied would decay more slowly. This would tend to make load balancing easier I would think. Anyone know if this intuition is correct?
Andrew Revkin of the New York Times reports on a new paper that argues from a climate model that the Earth's climate will shift toward a colder world.
A new analysis of the dramatic cycles of ice ages and warm intervals over the past million years, published in Nature, concludes that the climatic swings are the gyrations of a system poised to settle into a quasi-permanent colder state — with expanded ice sheets at both poles.In essence, says one of the two authors, Thomas J. Crowley of the University of Edinburgh, the ice age cycles over the past million years are a super-slow-motion variant of the dramatic jostlings recorded by a seismograph in an earthquake before the ground settles into a new quiet state. He and William T. Hyde of the University of Toronto used climate models and other techniques to assess the chances that the world is witnessing the final stages of a 50-million-year transition from a planet with a persistent warm climate and scant polar ice to one with greatly expanded ice sheets at both poles.
This isn't expected to happen in the next 100 years. At this point the result probably doesn't have any policy implications. But for those of us who live long enough to receive rejuvenation therapies if the robots or nanobots do not wipe us out at some point we'll need to argue about whether to engineer the climate to prevent another ice age.
Revkin posted a series of responses to this paper. Here's part of a response from NASA climate scientist James Hansen arguing that humans could easily prevent a deeper freezing by producing chloro flouro carbons. I agree. But CFCs are a bad choice due to their effects on the ozone hole.
Another ice age cannot occur unless humans go extinct. It would take only one CFC factory to avert any natural cooling tendency. Our problem is the opposite: we cannot seem to find a way to keep our GHG forcing at a level that assures a climate resembling that of the past 10,000 years.
Introduction of greenhouse gases isn't the only way to prevent a new ice age. We also could make all our buildings black on the outside and our roads too. That'd make the planet absorb more light.
This model does not prove the future. Carl Wunsch of MIT complains this model isn't science because the model is too simple and unproven.
Surely this isn’t science in any conventional sense. Taking a toy model and using it to make a “prediction” about something nearly a million years in the future, is a form of science fiction—maybe interesting in the same way a novel is, but it isn’t science. The prediction itself is untestable—except a million years from now, and the model “tests” that quoted are carefully chosen to be those things that the model has been tuned to get “right,” with no mention of the huge number of things it gets wrong. How many times do “if”, and “may” get used in the paper?
While this is simpler than the average climate model all climate models are simple (at least compared to the system they attempt to model) and unproven. A planetary scientist of my acquaintance tells me that all climate models have large errors in them and aren't really science because they can't predict. But they are the best available and we need to make decisions based on incomplete understanding.
Update: Lest anyone miss the point: The reason this model has no present day policy implications is that the time line for this projected cooling is not in this century. Whereas models that project global warming due to carbon dioxide emissions do project warming in this century. I do not know whether the latter models are correct. I'm told they have large sources of error in them. But they might be correct. We deal with large uncertainties with regard climate. We need to make decisions based on incomplete and partially erroneous information.
Once we have rejuvenation therapies some of us might some day need to consider policy changes in response to some future more refined model that will project cooling changes at some point some of us might just live to see.
In vitro maturation (IVM) is a variation on conventional in vitro fertilization (IVF) where no hormones are administered to a woman to mature eggs before removal. IVM has yielded lower success rates as compared to IVF. But advances in IVM technique have raised IVM success rates for assisted reproduction.
A form of IVF that does not require women to take powerful drugs has a success rate similar to conventional IVF, according to data from the only UK fertility clinic licensed to carry out the treatment.
The team at the Oxford Fertility Unit followed 40 women who received the treatment known as in vitro maturation – including those who had the first babies born in Britain using the technique in October last year. Nine of the women became pregnant – a pregnancy rate of 33% in under 35s.
IVF hormone treatment can cause pain, sickness, and an acute deadly complication. Plus, it might raise risks of other problems with ovaries later on. Plus, it costs more. In the future these differences will matter to to many more women than just those who have problems starting pregnancy. More powerful genetic testing techniques will make the use of assisted reproduction more popular as prospective parents try to select which genes to pass along to their offspring.
Among women under 35 - all of whom had an ovary condition that affects fertility - 48% became pregnant with IVM using their own fresh eggs and the percentage achieving a clinical pregnancy, where the baby's heart beat is detected, was 33%. This compares with a UK national average of 31% for those in the same age group having conventional IVF.
As well as being more successful, the new technique is also cheaper than the standard IVF as it largely avoids the need for drugs, which cost around £1,500 per cycle.
Historically success rates of IVM have been lower than standard IVF, at 25 per cent compared to around 36 per cent on average.
IVM avoids the risk of ovarian hyperstimulation syndrome where in some cases cysts form on the ovaries, fluid accumulates in the abdominal cavity and lungs, and function of kidneys and other organs can be compromised. IVM will probably replace IVF for the masses when many millions of women embrace genetic selection for offspring.
Also see my previous posts Lower Fertility Drug Doses Just As Effective For IVF and In Vitro Maturation Advantages Over IVF As Pregnancy Starter.
The only known genetic risk factor for Alzheimer's disease slows down the brain's ability to export a toxic protein known as amyloid-beta that is central to the damage the disease causes, scientists have found.
The research, published Nov. 13 by the Journal of Clinical Investigation, provides new clues into the workings of a protein known as apolipoprotein E4, or ApoE4. People who carry two copies of the gene have roughly eight to 10 times the risk of getting Alzheimer's disease than people who do not.
The new results mark a step toward resolving a longstanding question that scientists have had about exactly how ApoE4 increases a person's risk for the disease. The findings point to differences in the way that amyloid-beta is removed from the brain depending on which ApoE protein is involved.
Scientists found that when ApoE4 is present, the brain is less efficient at ridding itself of the toxic material, because a molecule that is much slower at removing the substance becomes much more involved.
Biogerontologist Aubrey de Grey argues that one of the major causes of cellular aging is the accumulation of toxic junk inside of aging cells. The body lacks enzymes to break down some kinds of intracellular junk. Therefore Aubrey argues for development of therapies to transplant into aging human cells the genes for enzymes that break down intracellular junk in other species. This report that Alzheimer's risk is boosted by a gene involved in intracellular trash removal underscores the importance of intracellular trash accumulation in brain aging. If we could remove more of the trash that accumulates in cells as we age then we wouldn't age as rapidly.
Why do people who eat a lot of meat and milk products get cancer more often? A glycan (a type of polysaccharide) molecule present in red meat and milk products might elicit an immune response that stimulates tumor growth.
Researchers at the University of California, San Diego School of Medicine, led by Ajit Varki, M.D., have shown a new mechanism for how human consumption of red meat and milk products could contribute to the increased risk of cancerous tumors. Their findings, which suggest that inflammation resulting from a molecule introduced through consumption of these foods could promote tumor growth, are published online this week in advance of print publication in the Proceedings of the National Academy of Sciences (PNAS).
Varki, UC San Diego School of Medicine distinguished professor of medicine and cellular and molecular medicine, and co-director of the UCSD Glycobiology Research and Training Center, and colleagues studied a non-human cellular molecule called N-glycolylneuraminic acid (Neu5Gc). Neu5Gc is a type of glycan, or sugar molecule, that humans don't naturally produce, but that can be incorporated into human tissues as a result of eating red meat. The body then develops anti-Neu5Gc antibodies – an immune response that could potentially lead to chronic inflammation, as first suggested in a 2003 PNAS paper by Varki.
In mice the combination of the Neu5Gc glycan and immune antibodies against Neu5Gc caused tumors to grow quicker. Drugs that reduce inflammation might cut cancer risk by suppressing an immune response to Neu5Gc.
Using specially bred mouse models that lacked the Neu5Gc molecule – mimicking humans before the molecule is absorbed into the body through ingesting red meat – the researchers induced tumors containing Neu5Gc, and then administered anti-Neu5Gc antibodies to half of the mice. In mice that were given antibodies inflammation was induced, and the tumors grew faster. In the control mice that were not treated with antibodies, the tumors were less aggressive
Others have previously shown that humans who take non-steroidal anti-inflammatory drugs (commonly known as NSAIDs) have a reduced risk of cancer. Therefore, the mice with cancerous tumors facilitated by anti-Neu5Gc antibodies were treated with an NSAID. In these animals, the anti-inflammatory treatment blocked the effect of the Neu5Gc antibodies and the tumors were reduced in size.
"Taken together, our data indicate that chronic inflammation results from interaction of Neu5Gc accumulated in our bodies from eating red meat with the antibodies that circulate as an immune response to this non-human molecule – and this may contribute to cancer risk," said Varki.
This result is important because it suggests you probably can't neutralize all the cancer risk associated with greater meat and milk consumption. As long as you are eating sources of Neu5Gc you are boosting your risk of cancer.
Though not all studies find a strong link between cancer and red meat consumption. Another recent study found that the risk small intestine cancer seemed to be boosted by saturated fat consumption and not by red meat. Of course a lot of red meat is high in saturated fat. This result holds out the hope that lean red meat might not boost your cancer risk.
Cross and other researchers from the National Cancer Institute used food frequency questionnaires to track food intake in a half million men and women enrolled in the NIH -AARP Diet and Health study over an eight-year period. Through state cancer registries and national death indexes researchers noted the development of 60 adenocarcinomas and 80 carcinoid tumors of the small intestine.
While findings showed no clear connection between red and processed meat and these tumors, they suggested a noticeably elevated risk for carcinoid tumors in the small intestine in association with saturated fat intake.
If you eat more fruits and vegetables they will displace less healthy foods from your diet. Add omega 3 fatty acids since they probably counteract the harmful effects of too much omega 6 fats from red meat and dairy.
A 38-year-old woman from London has given birth to the world’s first baby conceived after a full ovary transplant.
The patient, who received an ovary donated by her identical twin sister, had a healthy daughter weighing 7lb 15oz today, delivered by Caesarean section.
The birth is the ninth reported worldwide after ovarian tissue was transplanted from one sister to another, but the first in which an entire ovary was used.
The woman who received the ovary went into menopause at age 15 for some reason. The ovary transplant is amazing. But also note the age of the woman. That the donor ovary could produce viable eggs really goes against the odds.
Dr. Sherman Silber, who carried out the ovary transplant at the Infertility Center in St. Louis Missouri, argues that young women should consider getting one of their ovaries removed and frozen for replacement when they get older.
I see no reason why this technique to prolong reproductive life should not be routine for all women who want it. The cancer patients who we have frozen ovaries for say they feel really lucky they had cancer, which is an odd thing to say. But they say 'I'm getting older and am not in a relationship and all my friends are worried about their biological clock. But I'm not worried because I've got a young ovary frozen'.
They wouldn't have done this if they were not confronted by the immediate situation of losing their fertility because of their cancer treatment but then they think about it a couple of years later and they are glad they did it because of the simple biological clock reasons.
Dr. Silber says this will extend the fertile period and also delay the symptoms of menopause.
What comes next? Once it becomes possible to grow ovaries from stem cells the logical next step will be for a woman to get some adult cells removed from her, genetically manipulated to become stem cells, and then further genetically manipulated with assorted improvements. Then the stem cells will get grown up into ovaries and implanted into her so she can have better babies than she'd have with her unenhanced genetic endowment.
NEW ORLEANS, La., Nov. 11, 2008 – The neck arteries of obese children and teens look more like those of 45-year-olds, according to research presented at the American Heart Association’s Scientific Sessions 2008.
“There’s a saying that ‘you’re as old as your arteries,’ meaning that the state of your arteries is more important than your actual age in the evolution of heart disease and stroke,” said Geetha Raghuveer, M.D., M.P.H., associate professor of pediatrics at the University of Missouri Kansas City School of Medicine and cardiologist at Children’s Mercy Hospital. “We found that the state of the arteries in these children is more typical of a 45-year-old than of someone their own age.”
Researchers used ultrasound to measure the thickness of the inner walls of the neck (carotid) arteries that supply blood to the brain. Increasing carotid artery intima-media thickness (CIMT) indicates the fatty buildup of plaque within arteries feeding the heart muscle and the brain, which can lead to heart attack or stroke.
We are not designed for the environment we have created for ourselves. Some of our responses to that environment are maladaptive. Historically calorie malnutrition was the biggest killer of our ancestors. So we have genes that make us like food, especially fatty sweet food. As a result some kids have vascular systems that are undergoing accelerated aging.
The children’s “vascular age” — the age at which the level of thickening would be normal for their gender and race — was about 30 years older than their actual age, Raghuveer said.
A high fat diet for pregnant rats predisposes the rat offspring for obesity. If this same phenomenon is at work in humans then childhood obesity will probably get worse and cause more adult obesity in a vicious cycle.
A study in rats shows that exposure to a high-fat diet during pregnancy produces permanent changes in the offspring's brain that lead to overeating and obesity early in life, according to new research by Rockefeller University scientists. This surprising finding, reported in the Nov. 12 issue of the Journal of Neuroscience, provides a key step toward understanding mechanisms of fetal programming involving the production of new brain cells that may help explain the increased prevalence of childhood obesity during the last 30 years.
"We've shown that short-term exposure to a high-fat diet in utero produces permanent neurons in the fetal brain that later increase the appetite for fat," says senior author Sarah F. Leibowitz, who directs the Laboratory of Behavioral Neurobiology at Rockefeller. "This work provides the first evidence for a fetal program that links high levels of fats circulating in the mother's blood during pregnancy to the overeating and increased weight gain of offspring after weaning."
We need the ability to control human appetite and to activate cells to burn off excess calories.
PITTSBURGH, Nov. 6 – A new study suggests that genetic factors influence size variations in a certain region of the brain, which could in turn be partly responsible for increased susceptibility to alcohol dependence.
It appears that the size of the right orbitofrontal cortex (OFC), an area of the brain that is involved in regulating emotional processing and impulsive behavior, is smaller in teenagers and young adults who have several relatives that are alcohol dependent, according to a study led by Dr. Shirley Hill, Ph.D., professor of psychiatry, University of Pittsburgh School of Medicine.
In the research, which was published this week in the early online version of Biological Psychiatry, Dr. Hill and her team imaged the brains of 107 teens and young adults using magnetic resonance imaging. They also examined variation in certain genes of the participants and administered a well-validated questionnaire to measure the youngsters' tendency to be impulsive.
The participants included 63 individuals who were selected for the study because they had multiple alcohol-dependent family members, suggesting a genetic predisposition, and 44 who had no close relatives dependent on drugs or alcohol. Those with several alcohol-dependent relatives were more likely to have reduced volume of the OFC.
When the investigators looked at two genes, 5-HTT and BDNF, they found certain variants that led to a reduction in white matter volume in the OFC, and that in turn was associated with greater impulsivity.
The 5-HTT is a transporter gene for the neurotransmitter serotonin. The gene has been linked to depression, hyperactivity, and disruptive behavior in boys. Low levels of BDNF, or Brain-derived neurotrophic factor, have been linked to assorted problematic cognitive phenomena as well. So a role for these genes in influencing the degree of impulsivity is plausible.
If you pride yourself in your self-control don't feel too smug about the wisdom of your free will in choosing to be so controlled. You probably just have a large right orbitofrontal cortex due to getting genes that code for a large right OFC.
The kinase enzyme cdk5 controls how well new neurons connect to other neurons. Neural stem cells developed for brain cell therapies will need very precise adjustments so that they go and connect only where they ought to.
In a paper published in the Nov. 11 issue of PLoS Biology, the team, led by Fred H. Gage, Ph.D., professor in the Laboratory of Genetics, discovered that a protein called cdk5 is necessary for both correct elaboration of highly branched and complex antennae, known as dendrites, which are extended by neurons, and the proper migration of cells bearing those antennae.
Previously described functions of cdk5 are manifold, among them neuronal migration and dendritic pathfinding of neurons born during embryonic development. "The surprising element was that the dendrites of newborn granule cells in the adult hippocampus lacking cdk5 stretched in the wrong direction and actually formed synapses with the wrong cells," explains Gage. Synapses are the specialized contact points where dendrites receive input from the long processes, or axons, of neighboring neurons.
These findings offer extremely valuable, although unanticipated, input for investigators whose goal is to develop transplantation strategies to treat brain injuries or neurodegeneration.
Replacement neurons which are not correctly programmed to migrate and connect at the right places will likely mess up cognitive processes. Stem cell therapies for the brain will not be easy to develop.
"Our data shows that cells that fail to find their 'right spot' might actually become integrated into the brain and possibly interfere with normal information processing," says the study's lead author Sebastian Jessberger, M.D., a former postdoc in the Gage lab and now an assistant professor at the Swiss Federal Institute of Technology in Zurich, Switzerland.
Gage agrees that this is a possibility, noting that therapeutic targeting of new tissue—which would presumably be derived from stem cells—to the brain or spinal cord may demand extreme accuracy. "Our findings reflect the need for therapeutic approaches that will assure that cells used in regenerative medicine are strategically placed so that they will make appropriate rather than promiscuous connections."
Whatever the precise mechanism, the discovery of cdk5's role in guiding new neurons to their proper place improves the understanding of neurogenesis in the adult hippocampus, a process that is believed to be aberrant in cognitive aging, Alzheimer disease, and some forms of epilepsy and depression. In addition, it may suggest ways to improve prospects for neural transplantation for neurodegenerative diseases such as Parkinson disease. The clinical benefits of experimental transplants have been inconsistent and largely disappointing to date, with most transplanted neurons unable to integrate into existing brain circuits. A better understanding of what neurons need to find their way and fit into their new surroundings may increase the chances of success for this treatment.
The brain is going to be the toughest organ in the body to rejuvenate. It is extremely complex and large. It requires repair and not replacement. For many organs the growth of new young replacement organs will serve as very effective ways to upgrade and reverse the effects of accumulated damage from aging. But for the brain we need to develop therapies that fix cells and replace individual cells. That's much harder. This latest research sheds light on the signaling systems which biomedical scientists and engineers will need to manipulate in order to deliver rejuvenating cell therapies to the brain.
A new study in the November issue of the journal Appetite finds that obese women display significantly weaker impulse control than normal-weight women, but between obese and normal-weight men, the impulsivity levels are nearly the same. The study was conducted by researchers in the University of Alabama at Birmingham (UAB) Department of Psychology.
UAB researchers conducted the study to see how obese and normal-weight men and women differed in their decision-making skills, specifically in delay discounting, the measure of how much an individual is driven by immediate gratification versus the willingness to wait for delayed but greater rewards.
In the study of 95 men and women, UAB researchers gave the participants the choice of receiving varying hypothetical amounts of money immediately or fixed hypothetical amounts of money to be received after delays of two weeks, one month, six months or one, three, five or 10 years. The hypothetical rewards ranged from $1,000 to $50,000.
The researchers found that obese women discounted the value of future rewards at a rate three-to-four times greater than that of normal-weight women, suggesting greater impulsivity. Obese men, however, and the male and female control subjects all showed similar levels of delay discounting. The results were the same even when the researchers controlled for differences in IQ and income, both of which have been found to be related to measures of impulsivity.
First off, what's the evolutionary explanation for this result? Are the women more obese because they were selected for to be more obese in order to avoid starvation? Or is the obesity a modern side effect of selection for impulsivity which provided a reproductive fitness advantage some other way?
Also, why the difference between men and women? Also, if impulsivity doesn't contribute to male obesity then what other factor does? In the United States the prevalence of obesity is higher among females than among males. But the difference isn't large.
Among men, the prevalence of obesity increased significantly between 1999-2000 (27.5%) and 2003-2004 (31.1%). Among women, no significant increase in obesity was observed between 1999-2000 (33.4%) and 2003-2004 (33.2%). The prevalence of extreme obesity (body mass index > or =40) in 2003-2004 was 2.8% in men and 6.9% in women.
For people with normal cholesterol but high scores in a test for the inflammation marker high-sensitivity C-reactive protein (hs-CRP) the statin drug rosuvastatin (Crestor) very substantially cuts cardiovascular disease risks and mortality risks. So getting an hs-CRP test is a good idea.
Montreal, November 9th 2008 - A team of international researchers – including scientists from the McGill University Health Centre (MUHC) and McGill University – have discovered that having high levels of particular protein puts patients at increased risk of developing cardiovascular disease. The results of the study were so conclusive that the clinical trial had to be stopped before its scheduled completion date.
Researchers associated with the international JUPITER Project have demonstrated that high levels of high-sensitivity C-reactive protein (hs-CRP) leads to increased risk of cardiovascular disease. This risk decreases by up to 44% if the patients are treated with statin medications.
Dr. Jacques Genest, of the Research Institute of the MUHC and McGill's Faculty of Medicine led the Canadian component of the JUPITER clinical study, which was initiated by Dr. Paul Ridker of the Harvard University Faculty of Medicine.
"The risk of cardiovascular disease due to increased hs-CRP levels has been greatly underestimated until now," according to Dr Genest. "Our results show that this is an extremely important indicator that doctors will have to consider in the future."
"We hope that this study will prompt a review of current clinical practices, especially in terms of screening and prevention in adults," he added. "However, we still need to do more research to establish specific standards."
A 21% decrease in mortality in just a couple of years treatment is impressive.
The JUPITER study included 17,802 patients from 27 different countries. All had normal levels of cholesterol (LDL-c) and high levels of hs-CRP, and according to current standards, were not considered "at risk" for cardiovascular events, and were therefore not receiving any treatment. During the study, participants received a daily dose of the statin drug rosuvastin, and its consequences were striking: a 44% decrease in the risk of cardiovascular disease and a 21% decrease in mortality.
"These results definitely surpassed our predictions," said Dr. Genest. "We had to stop the study before its scheduled completion, as the benefit of the treatment for the selected patients was so great that we needed to present our findings to the medical community as soon as possible."
Since statins have a cholesterol-lowering effect, they are currently used to prevent cardiovascular disease in patients who are at-risk due to high LDL-c levels. But cardiovascular disease is also caused by vascular inflammation, which is marked by levels of hs-CRP. This study shows that statins indeed act on both cholesterol and inflammation, an effect that has long been suspected but not proven.
The researchers planned to follow the subjects for five years, but an independent panel monitoring the study stopped the trial in March after an average follow-up of less than two years, concluding that the benefit was so striking that it would be unethical to continue withholding the real drug from those taking the placebo. But no details were released at the time.
But these results do not prove all cause mortality will be lowered if statins are taken for decades by those with high hs-CRP. Still, these results are very suggestive.
Dr. Ridker said an analysis by study statistician Robert Glynn of Brigham estimated that applying the Jupiter findings to medical practice for six million Americans for five years would prevent 250,000 major cardiovascular events. The study suggests 25 patients would need to be treated for five years to prevent one major event, a number Dr. Ridker says appears at least as cost effective as strategies screening for high LDL.
Reports of serious adverse events were evenly divided -- 1,352 on the drug and 1,377 on placebo -- as were reports of muscle weakness -- 1,421 on the drug and 1,375 on placebo. Muscle side effects cause some patients to go off statins. There were 270 cases of diabetes among Crestor patients, compared with 216 on placebo.
The higher rate of diabetes among statin users is troubling. Muscle problems and memory problems also show up as side effects. Statins are not risk free. My hope is that cheap widespread genetic testing will eventually allow much more precise targeting of statin use. Those with high genetic risks of side effects will be able to steer clear of statins while those at great risk can know to take the drugs.
Some of you might have read that C-Reactive Protein (CRP) isn't looking as useful for identifying those at risk for heart disease as originally thought. However, this latest study use a more telling CRP test called the highly sensitive C-reactive protein (hs-CRP) assay. This hs-CRP assay sounds like it really picks up on risks that cholesterol tests miss.
C-reactive protein (CRP) is one of the acute phase proteins that increase during systemic inflammation. It’s been suggested that testing CRP levels in the blood may be an additional way to assess cardiovascular disease risk. A more sensitive CRP test, called a highly sensitive C-reactive protein (hs-CRP) assay, is available to determine heart disease risk.
What I'd like to know: What diet and lifestyle factors will lower hs-CRP? My guess is all the usual suspects: vegetables, fruits, fish, exercise. Anybody up for some googling (or maybe Pub Med searching) on this question?
Update: Writing in a New England Journal of Medicine editorial Mark A. Hlatky, M.D. observes that long term safety is unproven.
On the other side of the balance, of concern are the significantly higher glycated hemoglobin levels and incidence of diabetes in the rosuvastatin group in JUPITER (3.0%, vs. 2.4% in the placebo group; P=0.01). There are also no data on the long-term safety of lowering LDL cholesterol to the level of 55 mg per deciliter (1.4 mmol per liter), as was attained with rosuvastatin in JUPITER, which is lower than in previously reported trials. Long-term safety is clearly important in considering committing low-risk subjects without clinical disease to 20 years or more of drug treatment. Finally, the cost of rosuvastatin (roughly $3.45 per day) is much higher than that of generic statins.
Update: Stephen Colbert weighs in on the Jupiter Crestor trial:
Well worth a watch.
Two advances in pre-implantation testing of in vitro fertilization (IVF) embryos offer advantages for higher pregnancy rates and more desired genetic features in offspring. First off, at least for some categories of women having reproductive problems a new embryo screening technique called comparative genomic hybridization (CGH) can double the rate of successful pregnancies when using IVF.
The new approach improves on this by testing IVF embryos when they reach the blastocyst stage of 100 to 150 cells. This allows extra cells to be removed for genetic analysis, giving increased accuracy.
It also employs a more advanced profiling system called comparative genomic hybridisation, which can screen all 23 pairs of chromosomes, against only ten with existing techniques.
The technique involves letting the embryos divide more times before cells are extracted for testing. Unlike in previous techniques all 23 chromosomes are tested for aneuploidy (where the wrong number of chromosomes is present rather than a pair of each chromosome type).
In the new approach the test is conducted on blastocysts, embryos grown for five days until they have 100 to 150 cells. These are larger and stronger, allowing cells to be removed more safely
So more cells are removed later and then fancier tests are done on them.
Oxford Fertility Unit has applied for a licence that would allow them to carry out sophisticated screening of embryos to look for defects which reduce the chances of them leading to a successful pregnancy.
Current techniques mean that only half of the embryo's DNA can be checked for problems before being implanted in the womb.
A new method, which is being used in America, can check 23 pairs of chromosomes, meaning many more defects can be found and those embryos discarded so only the perfect ones – with the best chance of creating a baby – are then implanted in the womb.
Analysing the embryos using the latest technique meant that all 23 had at least one normal blastocyst for transfer. A total of 50 embryos were transferred in 23 cycles.
Of the women, 21 fell pregnant (91%) and 20 (87%) had a clinical pregnancy (where a foetal heartbeat is confirmed by ultrasound).
Experts predict the live birth rate will be 78%. This compares with an anticipated 60% for the same patients without embryo screening.
Research team members Dr Mandy Katz-Jaffe at the Colorado Centre for Reproductive Medicine and Dr Dagan Wells of Oxford both think this testing technique works much better.
"The pregnancy rates we've got so far are absolutely phenomenal," said Dr Dagan Wells at Oxford University and Reprogenetics UK, who led the study. "We're ready to begin a trial in the UK, and we have a couple of licence applications in to the Human Fertilisation and Embryology Authority to start offering CGH to patients." The HFEA is the UK's regulator of fertility clinics.
Another advance in embryo genetic testing will have greater impact in the long run: Karyomapping allows checking of all known genetic conditions.
“What we’re basically doing is mapping family trees, so you can work out which parts of your chromosomes came from which grandparents,” Professor Handyside said. “This turns out to provide a truly universal method for PGD – that’s why we’re excited about it.
“At the moment, there are preimplantation tests for only a small fraction of the 15,000 genetic conditions that are known. This test is capable of detecting any of them. There is no need to find the mutation that is affecting a family, and work up a test. You do the analysis, and just read off the results.”
As the technique maps all the embryo’s chromosomes, it can check any gene, allowing several to be screened at once. It could also be used retrospectively, once an embryo has become a child, to provide wider information about its genetic inheritance.
With declining costs for genetic testing just about any genetic variation that has functional significance will be testable before embryos are implanted. Combine that testing ability with understandings of what more genetic variations mean and very suddenly we are going to reach a stage where embryo selection offers huge advantages to anyone who wants to make their offspring smarter, better looking, healthier, or possessing of any other most desired genetic features of each parent.
Once we know the meaning of enough different genetic variants the use of natural sexual relations to start pregnancies will pass out of favor for large segments of many populations. In nations where governments allow people to select embryos for reasons other than disease avoidance (and I expect the US to fall into this category) the advantages for couples who want smarter kids, kids with desired personality characteristics, kids with better looks, and other qualities will be so incredibly compelling that IVF with genetic testing will become very common very quickly. I expect it to take off first with the most educated and most affluent and ambitious.
By the year 2020 I predict at least 10% of all pregnancies in the United States will involve IVF and embryo genetic testing. Governments that restrict this testing are setting up their populations to fall behind in intelligence and other measures.
Swiss and Chinese researchers lifted the conversion efficiency of a bendable and thin type of solar cell.
Researchers in China and Switzerland are reporting the highest efficiency ever for a promising new genre of solar cells, which many scientists think offer the best hope for making the sun a mainstay source of energy in the future. The photovoltaic cells, called dye-sensitized solar cells or Grätzel cells, could expand the use of solar energy for homes, businesses, and other practical applications, the scientists say. Their study is scheduled for the November 13 issue of ACS’ The Journal of Physical Chemistry C, a weekly publication.
The research, conducted by Peng Wang and colleagues — who include Michael Grätzel, inventor of the first dye-sensitized solar cell — involves photovoltaic cells composed of titanium dioxide and powerful light-harvesting dyes. Grätzel cells are less expensive than standard silicon-based solar cells and can be made into flexible sheets or coatings. Although promising, Grätzel cells until now have had serious drawbacks. They have not been efficient enough at converting light into electricity. And their performance dropped after relatively short exposures to sunlight.
In the new study, researchers describe lab tests of solar cells made with a new type of ruthenium-based dye that helps boost the light-harvesting ability. The new cells showed efficiencies as high as 10 percent, a record for this type of solar cell. The new cells also showed greater stability at high temperatures than previous formulas, retaining more than 90 percent of their initial output after 1,000 hours in full sunlight.
These cells offer two potential advantages: First off, they should be lower cost due to expected ease in manufacturing. Second, both their flexibility and their light weight will allow installation in places which otherwise would not support the presence of solar cells. For example, cars could have them on their roofs without a big weight penalty. Also, side walls and other vertical surfaces could be covered with lightweight solar cells whereas much heavier weight silicon photovoltaics would weigh too much for easy installation. Skyscrapers might some day get covered with Grätzel solar cell sheeting.
While they achieved 10% efficiency they only achieved 9.1% efficiency using materials that can be incorporated into a plastic.
The new dye absorbs light far better than the conventional dye. Because the dye absorbs light so well, it's possible to cut the thickness of the active material in the solar cell in half, which makes it easier for electrons to escape the solar cell and reach an external circuit. That, in turn, increases efficiency, in this case to 9.1 percent.
The researchers also paired the new dye with a nonvolatile solvent-based electrolyte. It's not quite as stable as an ionic liquid, and it can't be used with plastic. But it allowed slightly higher efficiencies--up to 10 percent.
With advances happening that cut costs for such a large variety of solar photovoltaic materials I am optimistic about the future of solar energy. PV electric power will come down in cost so far that it will compete with grid power during the day first in high sunlight areas such as the US southwest and gradually in lower and lower light areas. This will slow and eventually stop and reverse the growth of coal burning for electric power. It will also cut natural gas consumption and save it for more valuable space heating and fertilizer production.
Our biggest future energy problem continues to be for transportation. While the world recession has cut oil demand and oil prices the eventual resumption of economic growth will push oil prices back up again and the peak in world oil production is not many years away. I'm still not clear on whether advances in battery technology will happen soon enough to make the transition away from liquid fuels.
Duke Energy Carolinas has raised the expected construction costs of its proposed Lee Nuclear Station to $11 billion, excluding financing costs. That’s roughly twice the company’s original estimates.
Based on the financing costs for Duke’s new coal-powered unit at Cliffside Steam Station, financing expenses would increase the nuclear plant’s price to more than $14 billion.
The utility had originally estimated costs at $4 billion to $6 billion to build the two 1,117-megawatt reactors planned for the plant near Gaffney, S.C.
That works out to about $6.3 billion per gigawatt. Anyone have a good idea on how that translates into pennies per kilowatt hour sold on the wholesale market?
The price of nuclear power plant construction might be in decline since steel prices have declined greatly since the July 2008 commodity price peak.
In China, the world's largest steel producer, prices of benchmark hot-rolled coil dropped to a one-year low of $595 a tonne, down 1 percent on the week and 42 percent from a record high of $1,030 hit in July, data from Metal Bulletin shows.
But nuclear power plant planning and construction takes so long that steel prices could be much higher by the time construction starts on Duke's plants. Nuclear power plant construction costs are therefore hard to forecast.
Okay puppets, who among you are sadists? Some people are wired up with a puppeteer in their brains that makes them enjoy seeing pain in others. Sadists are wired up to be sadists.
Unusually aggressive youth may actually enjoy inflicting pain on others, research using brain scans at the University of Chicago shows.
Scans of the aggressive youth's brains showed that an area that is associated with rewards was highlighted when the youth watched a video clip of someone inflicting pain on another person. Youth without the unusually aggressive behavior did not have that response, the study showed.
"This is the first time that fMRI scans have been used to study situations that could otherwise provoke empathy," said Jean Decety, Professor in Psychology and Psychiatry at the University of Chicago. "This work will help us better understand ways to work with juveniles inclined to aggression and violence."
Some kids are just bad to the bone. Once it becomes possible to precisely identify such kids I expect some private schools to reject them as applicants. Though in some jurisdictions governments will try to prevent the screening out of bullies.
The youth were tested with fMRI while looking at video clips in which people endured pain accidentally, such as when a heavy bowl was dropped on their hands, and intentionally, such as when a person stepped on another's foot.
"The aggressive youth activated the neural circuits underpinning pain processing to the same extent, and in some cases, even more so than the control participants without conduct disorder," Decety said.
"Aggressive adolescents showed a specific and very strong activation of the amygdala and ventral striatum (an area that responds to feeling rewarded) when watching pain inflicted on others, which suggested that they enjoyed watching pain," he said.
Unlike the control group, the youth with conduct disorder did not activate the area of the brain involved in self-regulation (the medial prefrontal cortex and the temporoparietal junction).
I bet people who have committed murder are more likely to show this brain activation pattern than law-abiding people. So them could brain implants be devised that will block these feelings of pleasure from pain?
That’s because parts of your brain are actually asleep, according to a new theoretical paper by sleep scientists at Washington State University.
Contrary to conventional wisdom, the researchers say, there’s no control center in your brain that dictates when it’s time for you to drift off to dreamland. Instead, sleep creeps up on you as independent groups of brain cells become fatigued and switch into a sleep state even while you are still (mostly) awake. Eventually, a threshold number of groups switch and you doze off.
So when you are fighting sleep you are really just keeping only part of your brain awake. Parts of your mind have already gone missing. You find yourself working more or less effectively without those parts? (maybe some hyperactive people work more effectively sleep-deprived? I'm just asking.)
This isn't a proven theory. But it makes a lot of sense.
Lead author James Krueger said the view of sleep as an “emergent property” explains familiar experiences that the top-down model doesn’t, such as sleepwalking, in which a person is able to navigate around objects while being unconscious, and sleep inertia, the sluggishness we feel upon waking up in the morning.
“If you explain it in terms of bits and pieces of the brain, instead of a top-down phenomenon, all of a sudden you can make sense of these things,” said Krueger. “The old paradigm doesn’t even address these things.”
Krueger teamed with fellow neurobiologists David Rector, Hans Van Dongen, Gregory Belenky, Jaak Panksepp and electrical engineer Sandip Roy on the work. Their paper, “Sleep as a fundamental property of neuronal assemblies,” will appear in the December issue of Nature Reviews/Neuroscience. It is available online at http://www.nature.com/nrn/journal/vaop/ncurrent/pdf/nrn2521.html.
If sleep were being directed by a control center, the whole brain would respond at the same time, said Krueger. Instead, it behaves like a self-directing orchestra in which most sections are more-or-less in sync, but a few race ahead or lag behind at any given time.
Click thru and read some of the evidence for why they think their theory makes sense. Interesting stuff.
A year ago James Thomson's lab at U Wisc Madison used the genes OCT4, SOX2, NANOG, and LIN28 to turn adult cells into pluripotent stem cells. It was an experiment that the scientists could have done years sooner if they'd only thought the problem could be that easy. Since then other researchers have found safer ways to do the cell conversion. Here's yet another paper showing a way to convert adult fibroblast cells into pluripiotent stem cells by substituting small molecules for those of the genes used by Thomson's lab.
In the study, the scientists screened known drugs and identified small molecules that could replace conventional reprogramming genes, which can have dangerous side effects. This new process offers a new way to generate stem cells from fibroblasts, a general cell type that is abundant and easily accessible from various tissues, including skin.
The study was published in the November 6, 2008 edition (Volume 3, Issue 5) of the journal Cell Stem Cell.
"Our study shows for the first time that somatic or general cell types can be reprogrammed with only two genes and small molecules, and that these small molecules can replace one of the two most essential reprogramming genes," said Sheng Ding, a Scripps Research scientist and Associate Professor in the Department of Chemistry, who led the study with colleagues from Scripps Research and the Max Planck Institute for Molecular Biomedicine in Germany. "In this case, we replaced the Sox2 gene, which had previously always been regarded as absolutely essential for the reprogramming process."
A reduction in the number of genes used probably decreases the risk that the converted cells will go cancerous.
For the first time, the new study showed that BIX, an inhibitor of enzymes involved in regulating gene expression, enables fibroblast cell reprogramming in the absence of Sox2 gene overexpression. However, by itself, BIX's reprogramming efficiency is relatively low.
"As a result, we performed a second screen to find a compound that would synergize with BIX to further increase the reprogramming efficiency of general cells" Ding said. "Besides providing an improvement in reprogramming, we believed that these newly identified molecules might lead to discovery of different reprogramming mechanisms."
The second screen identified BayK, a calcium channel agonist, which was selected because it had no observable reprogramming activity on general cells in the absence of BIX. In addition, BayK was not known to affect the cell directly at the epigenetic level—changes in gene expression without any DNA or DNA-associated packaging protein modification—but rather at the cell signal transduction level.
The scientists found that when transduced general cells were treated with both BIX and BayK, a significant increase in the number of pluripotent cells resulted compared to transduced general cells treated with BIX alone.
Expect more research papers that reduce the risk and difficulty of converting adult cells to pluripotent stem cells. Your own cells will become convertible into cells usable in therapies.
Boston, MA—Silencing natural growth inhibitors may make it possible to regenerate nerves damaged by brain or spinal cord injury, finds a study from Children's Hospital Boston. In a mouse study published in the November 7 issue of Science, researchers temporarily silenced genes that prevent mature neurons from regenerating, and caused them to recover and re-grow vigorously after damage.
Because injured neurons cannot regenerate, there is currently no treatment for spinal cord or brain injury, says Zhigang He, PhD, Associate Professor of Neurology at Children's and senior author on the paper. Previous studies that looked at removing inhibitory molecules from the neurons' environment, including some from He's own lab, have found only modest effects on nerve recovery. But now He's team, in collaboration with Mustafa Sahin, MD, PhD, Assistant Professor of Neurology at Children's, demonstrates that re-growth is primarily regulated from within the cells themselves.
"We knew that on completion of development, cells stop growing due to genetic mechanisms that prevent overgrowth," explains He. "We thought that this kind of mechanism might also prevent regeneration after injury."
Keep in mind that aging basically amounts to a slow accumulation of injury. The ability to make cells grow is also essential to the development of rejuvenation therapies. Brain rejuvenation is the hardest challenge for aging reversal therapies. So the development of techniques for turning on neuron growth has special importance.
By blocking inhibiting genes that suppress the mTOR pathway the scienists were able to boost brain repair in injured mice.
The key pathway for controlling cell growth in neurons, known as the mTOR pathway, is active in cells during development, but is substantially down-regulated once neurons have matured. Moreover, upon injury, this pathway is almost completely silenced, presumably for the cell to conserve energy to survive. He and colleagues reasoned that preventing this down-regulation might allow regeneration to occur.
He and his team used genetic techniques to delete two key inhibitory regulators of the mTOR pathway, known as PTEN and TSC1, in the brain cells of mice. After two weeks, the mice were subjected to mechanical damage of the optic nerve. Two weeks post-injury, up to 50 percent of injured neurons in the mice with gene deletions of PTEN or TSC1 survived, compared to about 20 percent of those without the deletions. And of the surviving mutant mice, up to 10 percent showed significant re-growth of axons, the fiber-like projections of neurons that transmit signals, over long distances. This re-growth increased over time.
Tired of waiting for solar photovoltaics costs to finally drop? Looks like the wait is almost up. Average Selling Prices (ASPs) of solar photovoltaic modules are expected to decline 20% in 2009 and 25% in 2010.
After subsidies, Plan B for module makers is to sell products at a discount to keep inventory moving. It helps that manufacturing costs continue to decline about 10% each year, thanks to design improvements and benefits of scale. But it seems a little coincidental that most solar companies happened to predict the ASP for their products will decline at the exact same rate.
Analysts from Deutsche Bank (nyse: DB - news - people ), UBS (nyse: UBS - news - people ), Hapoalim Securities and Goldman Sachs all reached a different consensus, namely that ASPs will need to decline closer to 20% in 2009 to absorb excess inventory, and as much as 25% the following year.
Commerzbank said the impact of tougher financing conditions would affect returns seven times more than would module prices. It puts next year's financing needs for global photovoltaic projects at 33 billion euros, of which 20 billion would need debt financing.
But all indications pointed to a near halt in debt financing for large-scale solar power parks outside Germany, Commerzbank added, which would last until at least the second quarter of 2009.
The credit crunch will also cause delays and cancellations of new solar photovoltaic manufacturing plants. That will tend to boost prices by reducing future supply.
First Solar and some of the PV manufacturers are claiming costs much lower than current prices. As production capacity expands the prices should drop down closer to manufacturing costs.
CHENGDU, Nov. 5 (Xinhua) -- China may raise its total installed nuclear power generating capacity to 70 million kilowatts by 2020,75 percent higher than government target set in 2006, says a senior energy official.
China's projected future carbon dioxide emissions are causing concern in the Chinese government. If China opted for a big nuclear build that would slow the rate of growth of Chinese CO2 emissions.
A potential longevity-enhancing drug has passed its final animal testing challenge, pushing closer to reality the dream of all-purpose drugs against diseases of aging.
Mice given the new drug, called SRT1720, gorged on high-fat food for four months without gaining weight or developing diabetes, and ran twice as far on a treadmill as their control-group counterparts. Similar drugs are expected to follow down the pipeline.
SRT1720 targets the gene SIRT1 also targeted by resveratrol while being far more potent.
The drug's side effects aren't yet apparent, but resveratrol has proven safe in animals and — anecdotally, at least — in humans. Since SRT1720 works at doses 1000 times lower than resveratrol, said Lambert, it should prove even safer if effective.
The synthetic drug, called SRT1720, shifted the animals' metabolism into a mode normally seen only when they are calorie-deprived, reported Johan Auwerx, M.D., of the Ecole Polytechnique Federale de Lausanne, and colleagues.
The agent directly activates the so-called SIRT1 pathway, which is believed to account for at least some of the beneficial effects of resveratrol, the health-giving component of red wine.
It would be hard to get a drug such as this approved to slow general aging. But fortunately the benefits against weight gain and insulin resistance mean the drug has very specific clinical benefits that make approval for disease treatment easier.
The drug called SRT1720, which acts through the protein SIRT1, enhances running endurance in exercised mice and protects the animals against weight gain and insulin resistance even when they eat a high-fat diet, the researchers report. The drug works by shifting the metabolism to a fat-burning mode that normally takes over only when energy levels are low.
The findings bolster the notion that SIRT1 may be a useful target in the fight again metabolic disorders, including obesity and type 2 diabetes. It also helps lay to rest a long-standing controversy in the scientific world over the metabolic benefits of the red wine ingredient known as resveratrol. Resveratrol also acts on SIRT1, but its influence on other metabolic actors had left room to question exactly how it works.
Once one of these SIRT1 activators get approved expect to see many people asking for a prescription even if they do not have one of the diseases it treats.
Resveratrol is available now. Whether SRT1720 or another drug which mimics resveratrol will it make it to market remains to be seen. If you want to buy something that might deliver this sort of benefit now resveratrol is the only game in town.
An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.
“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”
Nicotinamide even boosted cognitive abilities in normal mice. Hmmm...
The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.
Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.
Nicotinamide is pretty low toxicity. So it is worth consideration for Alzheimer's sufferers.
If you've put off scheduling a Mars trip due to the threat from solar particle events and other sources of radiation a portable magnetosphere might some day make a trip to Mars much safer.
The solar energetic particles, although just part of the 'cosmic rays' spectrum, are of greatest concern because they are the most likely to cause deadly radiation damage to the astronauts.
Large numbers of these energetic particles occur intermittently as "storms" with little warning and are already known to pose the greatest threat to man. Nature helps protect the Earth by having a giant "magnetic bubble" around the planet called the magnetosphere.
....Researchers at the Science and Technology Facilities Council's Rutherford Appleton Laboratory, the Universities of York, Strathclyde and IST Lisbon, have undertaken experiments, using know-how from 50 years of research into nuclear fusion, to show that it is possible for astronauts to shield their spacecrafts with a portable magnetosphere - scattering the highly charged, ionised particles of the solar wind and flares away from their space craft.
Computer simulations done by a team in Lisbon with scientists at Rutherford Appleton last year showed that theoretically a very much smaller "magnetic bubble" of only several hundred meters across would be enough to protect a spacecraft.
Now this has been confirmed in the laboratory in the UK using apparatus originally built to work on fusion. By recreating in miniature a tiny piece of the Solar Wind, scientists working in the laboratory were able to confirm that a small "hole" in the Solar Wind is all that would be needed to keep the astronauts safe on their journey to our nearest neighbours.
Dr. Ruth Bamford, one of the lead researchers at the Rutherford Appleton Laboratory, said, "These initial experiments have shown promise and that it may be possible to shield astronauts from deadly space weather".
Energetic protons are mainly produced during solar particle events, sporadic showers that usually coincide with maximum sunspot activity. More dangerous is galactic cosmic radiation (GCR), atomic nuclei produced during supernova explosions that travel at almost the speed of light. GCR arrives from all directions, and induces cancer as it hurtles through the body. On Earth, the planet's magnetic field and atmosphere combine to deter and block these particles. But shielding a spacecraft requires mass, and the mass of shielding that can practically be launched on a spaceship will only reduce GCR by 20% to 30%, says Frank Cucinotta, of NASA's Space Radiation Health Project at the Johnson Space Center.
We need better robot tech in order to colonize Mars. The robots could go first and do lots of work to create living quarters and enclosed farms before humans arrived. We also need better photovoltaics or workable fusion reactors for energy. Plus, we need lots of genetic engineering to create organisms to provide a variety of products for colonists. Most of this tech will get developed for other reasons. So colonization of Mars will become much easier with time.
Researchers at Rensselaer Polytechnic Institute have discovered and demonstrated a new method for overcoming two major hurdles facing solar energy. By developing a new antireflective coating that boosts the amount of sunlight captured by solar panels and allows those panels to absorb the entire solar spectrum from nearly any angle, the research team has moved academia and industry closer to realizing high-efficiency, cost-effective solar power.
“To get maximum efficiency when converting solar power into electricity, you want a solar panel that can absorb nearly every single photon of light, regardless of the sun’s position in the sky,” said Shawn-Yu Lin, professor of physics at Rensselaer and a member of the university’s Future Chips Constellation, who led the research project. “Our new antireflective coating makes this possible.”
Note that these numbers do not indicate the percentage of the light that gets converted into electricity. But solar cells that absorb more photons will probably increase their electric power output roughly proportionate to the amount of additional light absorbed. I say roughly because the light that would otherwise get reflected away might be at frequencies that do not convert well to electrons.
An untreated silicon solar cell only absorbs 67.4 percent of sunlight shone upon it — meaning that nearly one-third of that sunlight is reflected away and thus unharvestable. From an economic and efficiency perspective, this unharvested light is wasted potential and a major barrier hampering the proliferation and widespread adoption of solar power. After a silicon surface was treated with Lin’s new nanoengineered reflective coating, however, the material absorbed 96.21 percent of sunlight shone upon it — meaning that only 3.79 percent of the sunlight was reflected and unharvested. This huge gain in absorption was consistent across the entire spectrum of sunlight, from UV to visible light and infrared, and moves solar power a significant step forward toward economic viability.
Increased absorption combined with solar concentrators could greatly reduce the amount of PV material needed per amount of electricity produced. This will work in favor of more expensive high conversion efficiency PV materials. So the cheaper thin film PV will effectively face more competition from the more expensive and more efficient silicon-based PV.
Puppets, your environment yanks your chain down in winter if you have a mutation in your eye pigment that lets light intensity play puppeteer with your emotions. A mutation of a photopigment of the eye might contribute to the development of the form of depression called seasonal affective disorder (SAD).
A new study indicates that SAD may be linked to a genetic mutation in the eye that makes a SAD patient less sensitive to light.
"These individuals may require brighter light levels to maintain normal functioning during the winter months," said Ignacio Provencio, a University of Virginia biology professor who studies the genetics of the body's biological clock, or circadian rhythms.
Provencio and his colleagues have discovered that melanopsin, a photopigment gene in the eye, may play a role in causing SAD in people with a recently discovered mutation.
"We believe that the mutation could contribute to increasing the amount of light needed for normal functioning during winter for people with SAD," Provencio said. "Lack of adequate light may be a trigger for SAD, but not the only explanation for the disorder."
This mutation might not by itself cause winter depression. But it seems to boost the chances of SAD.
The study was conducted with several other institutions, including the National Institute of Mental Health. It involved 220 participants, 130 of whom had been diagnosed with SAD and 90 participants with no history of mental illness.
Using a genetics test, the study authors found that seven of the 220 participants carried two copies of the mutation that may be a factor in causing SAD, and, strikingly, all seven belonged to the SAD group.
"While a person diagnosed with SAD does not necessarily carry the melanopsin mutation, what we found strongly indicates that people who carry the mutation could very well be diagnosed with SAD," Provencio said. "We think that if an individual has two copies of this gene, he or she has a reasonable chance of having the disorder."
The researchers found that a person with two copies of the gene is five times more likely to have symptoms of SAD than a person without the mutation.
These results only strengthen the argument for using a bright light box to treat SAD. Do you get depressed in winter? Think about getting a light box to wake up to in the morning.
The amount of blood flowing in two areas of the brain differs in people who feel musculoskeletal pain characteristic of fibromyalgia. So even though the sufferers of this disorder feel pain in their muscles and bones the actual pain might be originating in the brain.
Reston, Va.—Using single photon emission computed tomography (SPECT), researchers in France were able to detect functional abnormalities in certain regions in the brains of patients diagnosed with fibromyalgia, reinforcing the idea that symptoms of the disorder are related to a dysfunction in those parts of the brain where pain is processed.
"Fibromyalgia is frequently considered an 'invisible syndrome' since musculoskeletal imaging is negative," said Eric Guedj, M.D., and lead author of the study. "Past imaging studies of patients with the syndrome, however, have shown above-normal cerebral blood flow (brain perfusion) in some areas of the brain and below-normal in other areas. After performing whole-brain scans on the participants, we used a statistical analysis to study the relationship between functional activity in even the smallest area of the brain and various parameters related to pain, disability and anxiety/depression."
In the study, which was reported in the November issue of The Journal of Nuclear Medicine, 20 women diagnosed with fibromyalgia and 10 healthy women as a control group responded to questionnaires to determine levels of pain, disability, anxiety and depression. SPECT was then performed, and positive and negative correlations were determined.
The researchers confirmed that patients with the syndrome exhibited brain perfusion abnormalities in comparison to the healthy subjects. Further, these abnormalities were found to be directly correlated with the severity of the disease. An increase in perfusion (hyperperfusion) was found in that region of the brain known to discriminate pain intensity, and a decrease (hypoperfusion) was found within those areas thought to be involved in emotional responses to pain.
In the past, some researchers have thought that the pain reported by fibromyalgia patients was the result of depression rather than symptoms of a disorder. "Interestingly, we found that these functional abnormalities were independent of anxiety and depression status," Guedj said.
According to Guedj, disability is frequently used in controlled clinical trials to evaluate response to treatment. Because molecular imaging techniques such as SPECT can help predict a patient's response to a specific treatment and evaluate brain-processing recovery during follow-up, it could prove useful when integrated into future pharmacological controlled trials.
"Fibromyalgia may be related to a global dysfunction of cerebral pain-processing," Guedj added. "This study demonstrates that these patients exhibit modifications of brain perfusion not found in healthy subjects and reinforces the idea that fibromyalgia is a 'real disease/disorder.'"
I wonder whether niacin flushing or drugs that dilate capillaries might lessen the symptoms of fibromyalgia. Does the hyperperfusion cause pain just as much as the hypoperfusion? Or is the altered blood flow a result of the same underlying cause of the pain?
By 2020, China's burning of fossil fuels could annually emit carbon dioxide equal in mass to 2.5 billion metric tonnes of pure carbon and up to 2.9 billion tonnes, depending on varying scenarios for development and technology, the new report states. By 2030, those annual emissions may reach 3.1 billion tonnes a year and up to 4.0 billion tonnes.
That compares with global carbon emissions of about 8.5 billion tonnes in 2007.
...The U.S. Oak Ridge National Laboratory estimated that the United States emitted about 1.6 billion tonnes of carbon in 2007, compared to China's 1.8 billion tonnes.
I expect Peak Oil will cut into the rate of growth of Chinese CO2 emissions. But most Chinese emissions come from burning coal, not from oil. In fact, the International Atomic Energy Agency estimates that as of 2003 77.1% of China's CO2 emissions came from coal. Almost 9% of China's CO2 emissions come from cement. That puts coal and cement together at 86% of Chinese carbon emissions meaning that little of current emissions comes from oil. But how much of this projected surge in Chinese CO2 emissions is projected to come from oil? If most of it is from oil then I do not expect most of the CO2 emissions surge to happen. World oil production will be way down by 2030.
On the bright side, declining costs of solar photovoltaics and wind farms should cut into the demand for coal to generate electricity. But our problem is that coal power plants last a long time and so solar's price has to fall lower than the fuel cost of a coal plant to shut down existing coal electric plants.
"The problem is that power plants, once built, are meant to last for 40 to 75 years," Carson said. "Our forecast incorporates the fact that much of China is now stuck with power plants that are dirty and inefficient."
If it turns out that increased CO2 concentrations cause a large warming effect then we will likely need to do climate engineering. Though maybe technological advances will make photovoltaics very cheap by the 2020s. Or maybe China's dwindling coal reserves might put a limit on their rate of coal consumption.
Quebec City, October 28, 2008—A team of Université Laval researchers has shown that the main neurological markers for Alzheimer's disease are exacerbated in the brains of mice fed a diet rich in animal fat and poor in omega-3s. Details of the study—which suggests that diets typical of most industrialized countries promote the development of Alzheimer's—are outlined in the latest online edition of Neurobiology of Aging.
To demonstrate this, the team led by Frédéric Calon used a type of transgenic mice that produce two proteins found in the brains of Alzheimer patients—tau proteins, which prevent proper neuron functioning, and amyloid-beta, associated with the formation of senile plaques within the brains of afflicted patients.
The researchers fed transgenic and regular mice different diets for nine months, after which they compared the effects on the animals' brains.
The mice whose diet was poor in omega-3s and rich in fat (60% of consumed calories) showed amyloid-beta and tau protein concentrations respectively 8.7 and 1.5 times higher than the control group mice, whose food contained 7 times less fat. The high-fat diet also reduced drebrin protein levels in the brain, another characteristic of Alzheimer's disease.
I'd like to see this study repeated with other types of fats. Exactly which types of fats are okay? Monunsaturates and polyunsaturates of all types? Also, do all types of saturated fats boost tau and amyloid-beta proteins?