From Maine to Florida, from Virginia to Missouri, as much as half the United States confronts the possibility that harshly cold weather will lead to restrictions of natural-gas supplies. In some places - areas heavily dependent on natural gas to produce electricity - the prospect of "rolling blackouts," or controlled power outages, is much higher than in previous winters.
Any natural-gas cutoffs would primarily affect electric-power plants and factories fueled by gas, not homes, and be most likely in the Northeast.
If cold deepens for prolonged periods, the likelihood of interrupted natural-gas supplies rises to 30 percent in the Northeast and to 10 percent as far south as Florida and as far west as Missouri, according to a recent report by the Interstate Natural Gas Association of America (INGAA), a trade association representing gas pipeline companies. In a "worst-case" scenario, chances of interrupted gas rise to 40 percent for the Northeast and 25 percent across the eastern seaboard.
Nuclear power anyone?
New England is more dependent on natural gas.
Overall, 23 percent of America's electricity-generating capacity is fueled by natural gas. In New England, however, fully 40 percent of electricity is drawn from natural-gas-fired power plants, up from just 17 percent in 1999.
Rolling blackouts would probably lessen opposition to liquified natural gas terminals for off-loading LNG ships. The United States has much higher natural gas prices than most of the world because US production is declining and we do not have enough LNG terminals.
The main energy choices for the future are coal and nuclear. Opposition to nuclear amounts to support for coal. In Britain the debate is now on for whether to re-open long closed coal mines. Many of Britain's nuclear power plants will close by the 2020s. Wind power can't make up for those losses combined with increased demand from economic growth. Hence Tony Blair keeps bringing up nuclear power in speeches. In the last month natural gas prices in Britain have more than quintupled.
On the face of it, this winter's rocketing gas prices look a simple problem with simple causes. A drop in North Sea gas production combined with cold temperatures has led to prices soaring since the start of the month, from about 30p a therm (a unit of energy) to a peak of just over 160p.
Britain's political debate on energy seems to be advancing faster than America's at the moment. They know they face a huge problem between aging nuclear plants, declining North Sea production, rising imports costs, political instability in the Middle East, and worries about greenhouse gas emissions. Check out this opinion piece for nuclear power by Henry Porter in the UK's Observer. That's a publication on the left side of the political spectrum over there.
I only wish a huge research push by government was part of their debate.
A University of Minnesota study indicates that the nicotine vaccine NicVax, which is now being tested in humans, appears safe, well-tolerated, and a potentially effective method for helping smokers kick the habit.
Dorothy Hatsukami, Ph.D., director of the University of Minnesota Cancer Center's Transdisciplinary Tobacco Use Research Center (TTURC), is the lead author on this study. The 38-week study included 68 active smokers who were randomly assigned to receive one of three different doses of the vaccine or a placebo. The findings are published in the current issue of the journal Clinical Pharmacology and Therapeutics.
"The vaccine works by producing antibodies that specifically bind to nicotine and thereby prevent much of the nicotine from entering the brain," Hatsukami said. "This process potentially reduces the pleasurable effects from smoking and reduces the addiction to nicotine."
The vaccine may become a new option for helping the approximately 45 million people in the United States who smoke. In 2004, the rate for smoking in Minnesota was about the same as the national average of 20.9 percent.
"More research needs to be done, but at this point, our results show the vaccine is safe and well-tolerated," Hatsukami said. "We found the vaccine has few side effects on the central nervous system because the antibody itself is targeted specifically for nicotine and does not alter any functions of the brain."
Additionally, she says that while this study was not designed to test the treatment effect, 38 percent of the participants in the high-dose vaccine group quit smoking for at least 30 days.
"This result was an impressive and completely unexpected finding because the study was not focused on helping smokers quit smoking," she noted. "In fact, to participate in the study, smokers had to attest that they did not have a planned quit date for the next six months."
This is really an ideal addiction treatment because it can just as easily prevent addiction as cure it. However, some drugs might not make good immune system targets. In that case what we need are nanobots that are smart enough to recognize and destroy specific drug targets. Nanobots are a more distant prospect than vaccines though. Another possibility would be to develop gene therapies for the liver that would up a liver's ability to break down a drug compound. Make the drug have a very short half-life in the body. Though people could still get high by use of nasal delivery or other delivery mechanisms that take the drugs to the brain without passing through the liver first.
We also need gene and/or cell therapies that will reverse the effects of addictive drugs on the brain. Also, since some people are genetically more prone to addiction we need gene therapies that will modify the brain to make it less prone to addiction.
Social and economic circumstances do not explain why twins have significantly lower IQ in childhood than single-born children, according to a study in this week's BMJ.
Researchers studied 9,832 single-born children and 236 twins born in Aberdeen, Scotland between 1950 and 1956, using a previous child development survey as a base. They also gathered further information on mother's age at delivery, birth weight, at what stage of the child's gestation they were born, their father's occupational social class, and information on other siblings.
They found that at age seven, the average IQ score for twins was 5.3 points lower than that for single-born children of the same family, and 6.0 points lower at age nine.
The study also showed that taking into account factors such as the child's sex, mother's age, and number of older siblings made little difference to the IQ gap.
Despite advances in recent years in obstetric practice and neonatal care, the authors argue that the likely explanation is because some twins have a shorter length of time in the womb than other children and are prone to impaired fetal growth.
I've been expecting this finding for years. It makes perfect sense. Mom can't feed two fetuses as well as she can feed one. I wonder if diet and perhaps exercise could at least partially compensate for this effect.
I also wonder if the use of drugs to prolong pregnancy could raise average IQ. If pregnancies could be stretched out a few extra weeks would the resulting babies grow up to be smarter? Anything that could raise average IQ a few points would do more to boost economic growth and lower social pathologies than increased educational spending or the other typical liberal or free market libertarian nostrums.
Another point: IVF therapies ought to be aimed to reduce the odds of multiple fetus pregnancies. Each baby is going to pay a steep cognitive cost from not being the sole pregnancy.
Canadian scientists have developed some clever molecular trickery that is helping to reduce the drug cravings of addicted rats. One of the problems in addiction is that neurons in some parts of the brain lose glutamate receptors from the cell surface, and those receptors are important for communication between neurons. The researchers have sidestepped this problem by crafting a peptide that mimics a portion of the tail of the glutamate receptor and, once inside a neuron, serves as a decoy to prevent the loss of glutamate receptors.
Yu Tian Wang, an HHMI international research scholar, and colleagues at the University of British Columbia in Vancouver report their findings in the November 25, 2005, issue of the journal Science.
In addicted rats, cell-to-cell communication is compromised as a result of certain long-term changes at the level of individual neurons. Their research has produced a targeted drug that tricks brain cells into preventing those changes. "We think this is a good candidate for a drug against addiction that has very few side effects," said Wang, a neuroscientist . Although the initial studies are promising, Wang cautioned that the drug is in the early stages of development and is years away from testing in humans.
One obvious problem with this approach is that peptides are hard to deliver. Diabetics have to take insulin shots because the insulin peptide would get digested and broken up if taken orally. So a peptide treatment would probably have to be taken by syringe. Still, diabetics manage to do this and some addicts have plenty of experience with syringes.
Another potential problem is that the peptide might interfere with normal learning or other normal on-going neuronal processes. But such an interference might be worth it given the damage that amphetamine use causes to people's brains and their lives and the lives of other people around them.
The biggest question I see here is whether the peptide will work on existing addicts. Most people aren't going to go to the doctor and say "Hey, I'm about to spend several months abusing amphetamine. Could you prescribe me that peptide drug that'll prevent addiction from developing?". I suspect the peptide will do less to reverse addiction than it will to prevent it. However, the press release isn't clear enough on the protocol used to tell if that is the case.
The peptide has a piece that looks like the glutamate receptor and so competes with the glutamate receptor for getting pulled into the cell.
Wang's team developed a peptide that serves as a decoy to prevent the cell from pulling glutamate receptors in from their surfaces.
The researchers began by building a peptide – a long molecule made from a string of amino acids – with a structure similar to the tail of the glutamate receptor that is anchored inside the cell. In addiction, cellular machinery tugs on this tail, pulling the entire receptor into the cell. Without its business end sticking out into the synapse, or space between neurons, the receptor no longer works.
Wang's peptide tricks the cellular machinery into tugging on it instead of the receptor's tail. "Once it gets inside the neuron, the peptide competes with the receptor for binding to the machinery," Wang explained. With the cellular machinery otherwise occupied, the glutamate receptors stay on the cell surface, where they continue to receive signals.
The peptide prevented sensitization of the rats to amphetamine and therefore probably would block the development of cravings.
After confirming these results in cell cultures, Wang and colleagues tested the peptide in rats that had been given amphetamine once every other day for 20 days. During this period, the animals displayed stereotypical behavior such as repeated sniffing, licking, and grooming, indicating a craving for the drug. Such behavior parallels the compulsive thought patterns that people addicted to drugs experience, said Anthony Phillips, Wang's colleague at the University of British Columbia and a co-author of the article.
After keeping the rats drug-free for 21 days, the researchers gave the animals a small amount of drug again. The rats immediately displayed intense stereotypical behavior – a sign of behavioral sensitization. The behavior meant that the glutamate receptors in the animals' neurons were rapidly internalized, said Wang. "It's the trigger that leads to sustained motivation to seek a drug."
In contrast, addicted animals who received an intravenous injection of the artificial peptide displayed no sensitized behavior. "The effect was immediate and very noticeable," said Wang.
An ideal anti-addiction drug would allow someone in the early stages of addiction to pull out when they realize they've become hooked. But if such a drug existed how many early stage addicts could be convinced to use it before they racked up a lot of brain damage?
Countries whose leaders like to pose as environmentalist Miss Goodie Two Shoes forgot that moral posturing eventually fails if countries fail to honor their treaty commitments.
Canada is among those countries most likely to run into difficulty implementing its commitments, as in 2003 the country had increased its emissions by 24.2 pct from the base 1990 level, far from its 2012 target of a 6 pct reduction.
Japan, meanwhile, recorded a 12.8 pct increase over the 13 years to 2003 and is headed for an increase of 12 pct by 2010 instead of the intended 6 pct reduction.
And although the 15-member European Union, which ratified the treaty en bloc in 1997, achieved a reduction of 1.4 pct in emissions from 1990 to 2003 -- it is still a long way from the 8 pct target in 2012 -- most of the 15 countries have seen emissions increasing.
Read the full article for more details about the more egregious treaty violators. Spain's emissions have risen 41.7% since 1990. I'm guessing Spain has seen some very hefty increases in per capita income due to economic liberalization post-Franco. But that's just the problem: Economic growth makes more more able to afford energy consumption. As long as increased energy demand is satisfied by fossil fuels carbon dioxide emissions will rise with expanding economies.
Last year nearly half of all CO2 emissions increases came from China. Attempts to deal with CO2 emissions with a regulatory approach are hopelessly naive. Every country is going to point away toward other countries and suggest others should sacrifice.
Instead of a regulatory approach what we need is a massive effort at energy research and development across a wide range of energy technologies. The recently deceased Nobelist Richard Smalley proposed that the United States spend $10 billion per year on energy research and development with nuclear, solar photovoltaics, and an assortment of other approaches all as elements of the big drive to develop new energy technologies.
I think Smalley's approach makes far more sense than moralizing and signing of treaties. But too many groups are intent upon fighting yesterday's battles over who to blame or who to make suffer or which energy technology to stop. Why advocate useful measures when you can spend the same amount of time demonizing SUVs, Hummers, George W. Bush or oil companies? Why take the rise in atmospheric CO2 seriously when you can point at environmentalists as a bunch of crack-pots? Political activists enjoy partisan mudslinging ("mostly say 'hoo-ray for our side'") a lot more than they do solving problems. So the more reasonable approach which could produce cheaper and cleaner energy technologies remains the road not taken. How long is this state of affairs going to last? Isn't it getting old? Why not solve the problem?
Two new studies of gases trapped in Antarctic ice cores have extended the record of Earth’s past climate almost 50 percent further, adding another 210,000 years of definitive data about the makeup of the Earth’s atmosphere and providing more evidence of current atmospheric change.
The research is being published in the journal Science by participants in the European Project for Ice Coring in Antarctica. It’s "an amazing accomplishment we would not have thought possible" as recently as 10 years ago, said Ed Brook, a professor of geosciences at Oregon State University, who analyzed the studies in the same issue of this professional journal.
"Not long ago we thought that previous ice studies which go back about 500,000 years might be the best we could obtain," said Brook, who is also the co-chair of the International Partnerships in Ice Coring Sciences, a group that’s helping to plan future ice core research efforts around the world.
650,000 years is a long time to have such a history of the Earth's' atmosphere's constituents. But the scientists now think they can go back further than 1 million years.
"Now we have a glimpse into the past of up to 650,000 years, and we believe it may be possible to go as much as one million years or more," Brook said. "This will give us a fuller picture of Earth’s past climates, the way they changed and fluctuated, and the forces that caused the changes. We’ll be studying this new data for years."
As the data become more solid about the atmospheric conditions of the past, it’s becoming increasingly clear that the current conditions of the past 200 years are a distinct anomaly, Brook said."The levels of primary greenhouse gases such as methane, carbon dioxide and nitrous oxide are up dramatically since the Industrial Revolution, at a speed and magnitude that the Earth has not seen in hundreds of thousands of years," Brook said. "There is now no question this is due to human influence."
Humans have created atmospheric conditions unlike any seen in the last 650,000 years. That ought to give anyone pause. We should be concerned about what this portends for the future. It could be good. Or it could be bad. It will certainly be different. Shouldn't we at least be trying a lot harder to develop energy technologies that do not use fossil fuels?
Last night I was watching an excellent History Channel TV show about climate changes on the Earth from the early Middle Ages to today. The warming period that preceded the 14th century cooling was an amazing period. Food production surged. Fish populations surged near Europe. Grapes for wine were grown in Britain 300 miles north of where grapes are grown in France today. Europe's population surged by 50%. Swamps dried out and this led to a big decrease in malaria. Climate change is not necessarily automatically bad in its effects.
However, that warming might have triggered a flow of melting glacial water into the North Atlantic that then caused the Atlantic Conveyor to stop bringing warm water up from the south and that might have triggered the cooling that started in the 14 century (said cooling had the River Thames freezing solid every winter in England). But then again, that cooling might have been caused by volcanic eruptions, lower solar output, and other natural phenomena. The take-home lesson I got from the show was that if you have had fairly stable climate for a few centuries then best you start expecting a big shift. The climate is just not stable for many centuries running.
EPICA is the European Project for Ice Coring in Antarctica. The new ice core, initially described in 2004, is from a site in East Antarctica known as EPICA Dome C. This work represents a long-term European research collaboration and appears in two studies and an accompanying “Perspective” article in the 25 November 2005 issue of the journal Science, published by AAAS the nonprofit science society.
One study chronicles the stable relationship between climate and the carbon cycle during the Pleistocene (390,000 to 650,000 years before the present). The second one documents atmospheric methane and nitrous oxide levels over the same period.
The analysis highlights the fact that today’s rising atmospheric carbon dioxide concentration, at 380 parts per million by volume, is already 27 percent higher than its highest recorded level during the last 650,000 years, said Science author Thomas Stocker of the Physics Institute of the University of Bern, in Bern, Switzerland, who serves as the corresponding author for both papers.
I do not favor immediate regulations on CO2 emissions that would put a big damper on global economic growth. However, the continued rise in CO2 emissions really ought to be reason for serious concern by all prudent and rational people. We do not know what this rise in CO2, methane, and other greenhouse gassess is going to do to the global climate system. We really ought to make a very large push to develop technologies that would allow us to generate large amounts of cheap energy from non-fossil fuels energy sources.
The human-caused changes in the atmosphere have been made in a short period of time as compared to the length of most natural climate cycles.
“We have added another piece of information showing that the timescales on which humans have changed the composition of the atmosphere are extremely short compared to the natural time cycles of the climate system,” Stocker explained.
Though the recorded record made by humans does contain incidents of large climate changes that came on within the space of a single year. So the climate does sometimes shift very rapidly.
A half million years ago the interglacials were warmer and longer lasting.
The new work confirms the stable relationship between Antarctic climate and the greenhouse gasses carbon dioxide and methane during the last four glacial cycles. The new ice core analysis also extends this relationship back another two glacial cycles, to a time when the warm “interglacial” periods were milder and longer than more recent warm periods, according to the European researchers.
The fact that carbon dioxide and methane levels were lower during the relatively mild warm periods of the two additional cycles, compared to the warmer warm periods of the last 400,000 years, is especially interesting for the study of climate sensitivity, which is a measure of how the climate system reacts when atmospheric carbon dioxide concentrations double, explained Science author Dominique Raynaud from LGGE in Grenoble, France.
The new atmospheric and climate records from the EPICA Dome C ice core also indicate that the response of the natural carbon cycle to climate warming remains the same over time – in terms of the mechanism involved and the degree to which greenhouse gasses further amplify climate change, explained Science author Jean Jouzel from LSCE and Institut Pierre Simon Laplace in France.
Recent interglacial warming periods have been only 10,000 or so years long. Worryingly, we are already 10,000 years into the current interglacial. Anyone feel a chill coming on?
The new ice core analysis provides insights on our present interglacial warm period through a glimpse into Antarctic climate and greenhouse gas concentrations during the most recent warm period that is relatively similar to our current warm period. Known as Marine Isotope Stage 11 or MIS 11, this analog warm period occurred between 420,000 and 400,000 years and is not completely covered by the Vostok record.
The similarities between our current warm period and MIS 11 are primarily due to a similar configuration of the orbits of the Earth around the Sun: the relative positions of the Earth and Sun are thought to be the key driver of ice age cycles.
On an optimistic note, the MIS 11 warming period which was during a period with a similar orientation between the Earth and Sun wasted at least 20,000 years and so maybe we don't face an massive cooling any time soon.
“MIS 11 shows us that the climate system can indeed reside in a warm period for 20,000 or 30,000 years, something that we can’t say based on the last three warm phases which are no longer than about 10,000 years each,” said Stocker.
We are currently about 10,000 years into our current warm period.
The new papers also document MIS 13 and 15 -- two warm periods more distant than MIS 11 that may have been about as long. The idea that MIS 13 and 15 were long warm periods contrasts the argument scientists have made in the past suggesting that our current warm period is exceptionally long.
Sooner or later natural processes will kick the Earth's climate into a state greatly changed from what it is today. When that happens do you favor or oppose measures to engage in massive scale climate engineering to dampen the extent of the changes either locally or globally?
For example, suppose a big warming took place. Would you favor cloud seeding over Greenland to increase snow build-up as a way to reduce melting of the Greenland ice pack? Or would you prefer to see much of Bangladesh and south Florida submerged under rising ocean waters?
Or suppose we were hit by a half percent decrease in solar energy output similar to that which happened during the Maunder Minimum of 1645 to 1715 where the decrease in sun spot activity reduced solar output and deepened an existing cooler period. Suppose at the same time we were hit by a massive volcanic eruption or even a few of them and the sulfur in the atmosphere helped cause an even deeper cooling with snow falling in New England during June and July. I'm describing a period of history that happened just a few hundred years ago. So such a scenario is not far-fetched or improbable.
Given a big cooling would you oppose or support making all buildings and roads black so that they absorbed more light energy? Or if this happens 50 years from now and we have cheap space launch at that point would you oppose or support the launching of a satellite system of reflectors to aim more light at some part of the Earth to warm it up?
My take on the climate is that it is not as stable as is widely believed. We ought to expect change just from natural processes. Throw in our own increasing effects on the atmosphere and we ought to have an even greater expectation of change. This view makes me think we need better tools for adapting to climate changes. Certainly we need more rapid development of better technologies for energy production and energy conservation. We also need better agricultural technologies that would allow us to more rapidly change crop mixes to fit with climate changes and to develop crop strains that are more resistant to whatever weather might throw at them. If climate changes become big enough at some point we'll even need climate modification technologies.
While decay of myelin due to auto-immune damage is suspected as a cause of multiple sclerosis some UCLA researchers see a much wider role for insufficient myelination as a cause of a large assortment of mental and behavioral disorders.
New evidence points to production of myelin, a fatty insulation coating the brain's internal wiring, as a neural Achilles' heel early in life.
An upcoming application of a novel model of human brain development and degeneration pioneered by a UCLA neuroscientist identifies disruption of myelination as a key neurobiological component behind childhood developmental disorders and addictive behaviors.
Detailed in an article in press with the upcoming annual peer-reviewed publication Adolescent Psychiatry (Hillsdale, N.J.; The Analytic Press Inc.; 2005) the analysis suggests that many factors can disrupt myelination and contribute to or worsen disorders such as autism, attention deficit/hyperactivity disorder and schizophrenia.
Note above that problems with myelination may contribute to addictive behaviors and ADHD.
There's a vicious cycle aspect to this report. Due to insufficient myelination a kid could be more prone to use of addictive drugs. But then the use of the drugs could prevent the myelination process from proceeding. This reminds me of people I know who used a lot of drugs while teenagers who never seem to have grown up since then. Did their drug and alcohol use block their own brain's maturation?
In addition, the analysis suggests that alcohol and other drugs of abuse have toxic effects on the myelination process in some adolescents, contributing to poor treatment outcomes and exacerbating co-existing psychiatric disorders.
Author Dr. George Bartzokis, a professor of neurology at UCLA's David Geffen School of Medicine, concludes that the high incidence of impulsive behaviors that characterize the teen years as well as many psychiatric disorders that occur in the teens and 20s are related to incomplete myelination of inhibitory "stop" brain circuits, while the "go" circuits become fully functional earlier in development. These inhibitory circuits are not on line to quickly interrupt high-risk behaviors that are so prevalent in teens and young adults.
If memory serves the development of the inhibitory circuits does not complete until about age 25. As a consequence of blocked myelin formation are heavy adolescent drug users more prone to impulsive, self-destructive, and violent behaviors even as adults?
There's an aging angle to myelination and demyelination.
"Myelination, a process uniquely elaborated in humans, arguably is the most important and most vulnerable process of brain development as we mature and age," said Bartzokis, who directs the UCLA Memory Disorders and Alzheimer's Disease Clinic and the Clinical Core of the UCLA Alzheimer's Disease Research Center.
"Environmental toxins, genetic predispositions and even diet appear to influence and sometimes disrupt this process," he added. "By shifting our research focus to medications that act on brain metabolism and development, as opposed to brain neurotransmitter chemistry, neuroscientists will likely find a wealth of novel opportunities for addressing the cause of brain disease rather than simply the symptoms."
Myelin is a sheet of lipid, or fat, with very high cholesterol content — the highest of any brain tissue. The high cholesterol content allows myelin to wrap tightly around axons, speeding messages through the brain by insulating these neural "wire" connections.
Bartzokis' analysis of magnetic resonance images and post-mortem tissue data suggests that the production of myelin is a key component of brain development through childhood and well into middle age, when development peaks and deterioration begins (Neurobiology of Aging, January 2004). He also identifies the midlife breakdown of myelin as a key to onset of Alzheimer's disease later in life (Archives of Neurology, March 2003; Neurobiology of Aging, August 2004).
We need rejuvenation therapies that will repair and replace aging myelin sheaths in the brain. Sign me up. I want rejuvenated myelin. Myelin rejuvenation no doubt will be part of the Strategies for Engineered Negligible Senescence (SENS) treatments.
Imagine a future two or three decades hence where parents take their kids in for cell therapies and gene therapies to make their myelin sheaths grow over their inhibitory circuitry more rapidly. Such therapies would reduce adolescent deaths from car accidents and from murder. Plus, the therapies would also reduce adolescent use of destructive drugs.
Adolescent rashness might have been selected for so that males in particular would compete more aggressively for mates. The slow myelination of inhibitory brain circuits might be an obsolete and maladaptive left-over consequence of evolution by natural selection.
In two Stanford studies, researchers demonstrated that people with musical experience found it easier than non-musicians to detect small differences in word syllables. They also discovered that musical training helps the brain work more efficiently in distinguishing split-second differences between rapidly changing sounds that are essential to processing language.Nadine Gaab, a former Stanford postdoctoral fellow, will present the findings at 9:30 a.m. Nov. 16 at the Society for Neuroscience's annual meeting in Washington, D.C. "These results have important potential implications for improving speech processing in children struggling with language and reading skills," she said. They also could help "seniors experiencing a decline in their ability to pick up rapid changes in the pitch and timing of sounds, as well as speech perception and verbal memory skills, and even for people learning a second language."
But does musical training really help language skills development all that much? The problem with this study (and with most social science for that matter) is that it compares people at a snapshot point. All sorts of selection effects could be responsible for this result.
Adults with and without musical training were compared in their ability to recognize syllable sequences.
In the first study, researchers took 28 adults, divided into musicians and non-musicians, who were matched for age, gender, intelligence and general language ability. Musicians in the study were required to have started playing an instrument before the age of 7, to have never stopped playing and to have continued to play several hours a week. When musicians play, Gaab said, they must actively distinguish between sounds and their order, and adjust as necessary.
Suppose a large cohort of 7 year olds were tested for general intelligence and language skills and then some proceeded to learn music an others did not. Would the music learners be better at understanding and speaking language 20 years later? I'm skeptical.
Non-musicians in the study had to be native English speakers with minimal experience studying non-tonal foreign languages such as Spanish. People who had studied a tonal language such as Mandarin were not included.
During the experiment, participants listened to pairs of syllables such as ba-da, ba-wa and ga-ka, and noted if each syllable in the pair sounded the same or different. Depending on how they performed, the scientists made the task increasingly difficult by using syllables that sounded more and more alike. Musicians outperformed their non-musician peers in how quickly and accurately they perceived these rapid changes, Gaab said.
In the second experiment, researchers used functional magnetic resonance imaging (fMRI) to find out whether musical training changes the way the brain processes sound. The fMRI scanning machines, which look like beds that slide into tubes, normally are used to check for brain injuries or tumors. With slightly different software they can be used to measure which regions of the brain are active by looking for changes in blood oxygenation, a process that occurs in parts of the brain where the neurons are active.
Forty people, evenly divided into musicians and non-musicians, listened to three-tone sequences made from different combinations of low and high pitches. Participants had to reproduce the order of the tones they heard by manually pressing buttons on a panel.
Musicians once again beat the non-musicians with this task. "We were surprised that musicians could do it almost perfectly," Gaab said. Musicians got the fastest tone sequences right at least 85 percent of the time, compared to non-musicians who hit a 50-percent average. They also could replicate the sequences a lot faster. "Non-musicians needed to make a lot more effort—their brains were not as finely attuned."
According to Gaab, musical training appears to alter the ability of the brain's language areas to process pitch and timing changes that are common to perceiving both words and music. "The brain becomes more efficient and can process more subtle auditory cues that occur simultaneously," she said.
I see these results as analogous to how a doctor or nurse has a fingertip that is very good at measuring a pulse. The ability measured is fairly narrow. A person who learns music might be better able to distinguish syllables and words which are mumbled or spoken quietly or spoken with an acccent or under noisy conditions. The effect would be equivalent to simply having better hearing. But the benefit might be limited to just an enhanced ability to signal process sounds and may not carry over at all into enhanced ability to parse sentences and understand, say, written language.
I've long wondered how much the learning of particular skills enhance or interfere with the ability to learn other skills. For example, learning math enables the learning of physics, engineering, andd sciences because it provides a conceptual toolbox needed to understand many other subjects. But does, say, learning foreign languages use up neuons that then are unavailable for learning other subjects? Or if a person is born blind does that person have more mental resources available to learn, say, spoken languages because their mind is not cluttered by visual image information? Do parts of their brain which otherwise would have been recruited for processing images instead get recruited for better processing of sounds?
The New Scientist reports that government-engineered demand for biofuels is destroying rainforests.
THE drive for "green energy" in the developed world is having the perverse effect of encouraging the destruction of tropical rainforests. From the orang-utan reserves of Borneo to the Brazilian Amazon, virgin forest is being razed to grow palm oil and soybeans to fuel cars and power stations in Europe and North America. And surging prices are likely to accelerate the destruction.
The rush to make energy from vegetable oils is being driven in part by European Union laws requiring conventional fuels to be blended with biofuels, and by subsidies equivalent to 20 pence a litre. Last week, the British government announced a target for biofuels to make up 5 per cent of transport fuels by 2010. The aim is to help meet Kyoto protocol targets for reducing greenhouse-gas emissions.
Hey, I've repeatedly said that biomass crops are mostly a bad idea. Why increase the demand for crop land in the tropics? High efficiency photovoltaics will use less land area than biomass and most photovoltaics could be placed on existing human structures. Greenies who want immediate reductions in fossil fuels consumption ought to look at better insulation and building designs. For the medium and long term we should be accelerating nuclear and photovoltaics research and development. Better battery technology is the way to reduce the need for liquid fuels. With higher energy density and cheaper batteries we can get transportation energy from nuclear, wind, and photovoltaics.
Crucial to making the link between social behavior and hormones was the work of co-author Toni Ziegler, an endocrinologist at the UW-Madison National Primate Research Center, who developed a technique that enables researchers to track vasopressin and oxytocin levels through the analysis of urine. The procedure is far less invasive than the existing method of analyzing blood or cerebrospinal fluid, and may one day find applications in several areas of child research such as the field of autism, Ziegler says.
The UW-Madison scientists worked with 18 four-year-old children who had lived in Russian and Romanian orphanages before being adopted into homes in the Milwaukee area. Despite the fact that the children now live in stable homes - for over three years, in some cases - they might still display some of the telltale behaviors that researchers have come to associate with early neglect. The abnormal willingness of a child to seek comfort from unfamiliar adults, even in the presence of the adopted parent, is one common instance of such behavior, says Wismer Fries.
Before starting her experiment, Wismer Fries collected urine samples from the young subjects to track baseline levels of vasopressin and oxytocin. Immediately, the scientists noticed that the children who experienced early neglect had markedly lower levels of vasopressin than the control group of non-adopted children. Researchers believe that vasopressin is essential for recognizing individuals in a familiar social environment. Lower levels of the hormone, Pollak says, may point to the social deprivation these children endured early on.
During the experiment, study subjects sat on the laps of either their mother or an unfamiliar woman and participated in an animated interactive computer game. The 30-minute game directed the children to engage in various types of physical contact with the adult they were sitting with, such as whispering or tickling each other, and patting each other on the head. When the game ended, Wismer Fries collected another urine sample from each child.
The UW-Madison researchers expected to see a hormonal response in the children following the physical contact with their mothers. And predictably, oxytocin levels rose in family-reared subjects. Yet, levels stayed the same among the previously neglected group. That result may help explain the difficulties many of these children have in forming secure relationships, the UW-Madison scientists say.
An obvious long term question needs answering: Do oxytocin and vasopressin levels of neglected kids eventually converge with levels found in normal kids of the neglected kids are adopted into stable homes? What happens after 10 or 15 years? Are these kids permanently tweaked?
The New York Times has an interesting article on the appropriateness of sleep aid drugs for adolescents.
Because teenagers are more likely to have trouble falling asleep than staying asleep all night, shorter-acting drugs, like Sonata and Ambien, may be more appropriate for them than Lunesta, which is longer-lasting, the specialists say.
Rozerem, an insomnia medication just approved by the F.D.A. in July for use in adults, may have an even more selective effect on the brain.
It is directed at receptors in the suprachiasmatic nucleus, which sets the body's internal clock.
And because this clock is thought to shift adolescents' sleep patterns, some doctors suspect that Rozerem may be useful in treating their sleep problems.
Since adolescents tend to stay up later and get up later why not just shift schools to later hours to make school hours fit the natural body rhythms of adolescents? To say that adolescents have sleep problems implies a medical condition like an illness. But we do not know why so many adolescents operate on later sleep cycles. Their behavior might be the result of Darwinian natural selection for effective mating strategies. Or their minds might respond more to light stimuli and artificial lighting might be shifting their melatonin production to make them stay out later. Or perhaps adolescent brains develop better if they can spend part of their days in lower light conditions and hence natural selection produced this behavior to improve brain development.
I'm speculating. But my point is that we do not know what causes adolescent sleeping patterns. Therefore efforts to pharmaceutically interfere with natural sleep cycles in order to make adolescents fit in better in institutions shaped for adult convenience seem ill advised. Such interference might produce unforeseeable and harmful consequences on brain development or other aspects of the body's growth.
Perhaps the use of high intensity lights to shift adolescent sleep patterns would be a less risky alternative. If the adolescent brain's sleep regulating mechanism can be fooled into thinking the day starts earlier and ends earlier then it might be able to function just fine on earlier real clock times.
But, again, why not just shift school schedules a couple of hours? Start schools at 10 AM or 11 AM. The kids sitting like zombies in classes at 8 AM aren't learning as much as they could learn at later hours in the day. Teachers could handle teaching till 5 PM rather than 3 PM in the afternoon. Institutions should be molded around human biology rather than the other way around. Or instead of listening to so many hours of live lectures in the morning when so many kids are half asleep the kids could watch more high resolution recorded lectures in the evenings when their minds are sharp. We can use technology to adjust institutions to humans. Why not do it?
One way proposed for exploration to other solar systems is to have a space ship built that is so large, long lasting, and technologically advanced that it could travel for hundreds of years. The proponents of this approach argue for families to travel via such space ships so that they can give birth to children who will replace them as crew when the original generation gets old and dies. The idea is that the original generation would not live to step foot on some distant planet but their descendants many generations removed would some day colonize a planet orbiting a star many light years from Earth.
The most obvious objection to such a proposal is that why would anyone want to get on a spaceship and tavel to some place they will never see? Such explorers would be very unlike the human explorers of the last few hundred years who at least got to see amazing scenery even if, say, they didn't make it to the root of the Nile or the South Pole. But "explorers" embarking on a multi-generational trip between planets would have no such experiences. They'd step foot onto a rotating spaceship probably built in Earth's orbit and as the Earth receded from view they would have no new places to look at and investigate. They'd have a detailed understanding of their spaceship before even setting foot on it. They'd have stars to look at that would be little different than what they'd see from Earth's orbit.
But my biggest objection to a multi-generational spaceship colony is ethical: How dare some bunch of idealistic nut space explorers set out on a voyage that will condemn all their descendants for many generations to be born, live, and die in a relatively small confined area deep in space! The people who would be born, live, and die in such a vessel would be cut off from any planet, from scientific advances, technological advances, new cultural products, and from significant relationships with the bulk of humanity.
The act of the original generation of explorers would be incredibly selfish. Consider that the original generation of explorers would have direct experience of Earth societies and of travelling around and living in a variety of places on Earth. But the original generation would condemn many subsequent generations to a far narrower range of experiences and would deny the subsequent generations of the choice of whether to live in space or on Earth.
The subsequent generations born on the ship wouldn't be explorers in any meaningful sense. They'd be born on and live their lives out on a spaceship where there'd be nothing to explore. Their sole purpose would be to raise children so that those children would raise children so that some generation would some day see another planet.
Possibly the spaceship would be able to receive a laser beam transmission of information from Earth for at least part of the voyage. But this hardly makes up for the many losses that people would experience as a result of being born on a spaceship deep in space.
Worse yet, the whole sacrifice might turn out to be totally worthless in the end. The spaceship could suffer a catastrophic failure with the loss of all hands. Or an advance in propulsion made a few decades after the ship left orbit might allow much more rapid movement between planets.
But there is a very likely future change in circumstance where many decades or centuries long trips between the stars will become easier to justify both ethically and in terms of the satisfaction of the original explorers: The development of technologies which implement Aubrey de Grey's Strategies for Engineered Negligible Senescence (SENS) will allow the original explorers to live in a state of youthfulness for the entire length of a trip to another solar system. Long space trips would therefore no longer involve one generation deciding a very dismal fate of many future generations.
If you want to become a space explorer then your best chance of fulfilling that desire is to politically support the development of SENS technologies. Advocate for increased spending to accelerate the development of rejuvenating biotechnologies such as stem cells, growth of replacement organs, gene therapy, and techniques for getting rid of accumulated intracellular and extracellular junk. Rejuvenation with SENS would allow you to live long enough to be alive and young when interstellar travel technologies get developed and become cheap enough to be accessible to many people. Plus, the SENS technologies would make it possible for you to live long enough to survive the trip and actually set foot on another world. Alternatively, you could stay on Earth longer and wait for the development of faster than light technologies assuming FTL travel will ever be possible.
If you want to travel between the stars you might also want to advocate the development of technologies for hibernation and cryogenic freezing and restoration. A couple hundred years in a space ship would get awfully boring. However, once SENS is developed we'll have plenty of time to develop hibernation technologies.
The news reports about H5N1 avian flu have filtered up to corporate board rooms. BusinessWeek reports that some large corporations are taking pandemic preparedness seriously.
POSSIBLE SCENARIOS. Increasingly, though, the threat of a global pandemic is beginning to creep into executive suites. "It's a giant leap from a year ago, when it wasn't on the business community's radar screen," says Dorothy Teeter, director of public health for Seattle & King County, Wash. DuPont formed a 20-person pandemic team in May. With avian flu spreading, the team stepped up its pace in October and now meets every week.
French construction-materials company Lafarge, which lost 200 employees in Indonesia during last December's killer tsunami, has launched an avian flu intranet site to send information to distant operations. Pitney Bowes (PBI ) in Stamford, Conn., is ensuring that large numbers of employees can work from home. And 17 U.S. airports have or are setting up quarantine programs. The lesson from past megadisasters is that "you have to think the unthinkable," says Christian Crews, director of futures strategy at Pitney Bowes.
Businesses could reduce the disruption and risk from a highly lethal pandemic by what I call "workplace cocooning". Basically, some workplaces could be converted into live-in quarantine areas where groups worked together but isolated from the outside world. For more on this see my previous post "Economic Collapse Avoidable During An Influenza Pandemic". Even short of a full quarantine one step businesses could take during a pandemic would be to partition people up into workgroups that rarely come into contact with other workgroups. Instead of putting people into large rooms full of cubicles put them in smaller rooms with just the people they need to work with. Also, stagger hours so that fewer people are in a building at the same time. The general goal should be to reduce the number of times people have to come into contact with other people and reduce number of different people from different groups that each person needs to come into contact with.
Businesses could do many other things to reduce disease transmission risk during a pandemic. Many of those changes could be made in advance of a pandemic with the added benefit of reducing the rate of infectious illness spread in workplaces. First off, encourage sick people to stay at home. Far too many people bring diseases to work and reduce the productivity of others who then get the diseases. Second, make physical changes in workplaces to reduce the amount to which workers have to touch common work surfaces which can transmit viruses. For example, make doors openable without the use of hands to turn door knobs. Also, make water at sinks controllable without the use of hands to touch knobs.
Workplaces could also be structured to reduce the distance that cough droplets can travel. Raise up cubicle walls all the way to the ceiling for example. Make it easier for individual workers to isolate themselves from people who they do not have business needs to come into contact with. When workers do come in coughing either suggest they go home or hand them face masks.
How about offering free flu vaccines in workplaces? Just get up from your desk and get a shot in 5 minutes instead of having to make a doctor's appointment or having to hunt down a clinic offering shots. Businesses also ought to lobby for the development of vaccines against rhinoviruses and other causes of the common cold. Costs are there to be eliminated. We need to treat diseases as costs that are in urgent need of elimination.
Normal colds and flus are costly enough and unpleasant enough that businesses ought to change their practices to reduce the incidence of infectious diseases even before considering the potential threat from avian flu.
"The medications and interventional therapies available so far are intended only to limit further damage to the heart," said Andreas Zeiher, professor at J.W. Goethe University in Frankfurt, Germany, and a senior author of the study.
"In contrast, progenitor cell therapy has the potential not only to limit further damage, but to regenerate heart function," he said.
The improvement was small.
But patients who received the bone marrow cell infusion saw an improvement in their left ventricular ejection fraction -- a measure of heart efficiency -- on average, of 5.5 percent. Those getting placebo saw a 3 percent improvement.
The hearts of treated patients also swelled less and had better blood supply.
More than 200 individuals who had had a heart attack were enrolled in the trial. Half of the participants received infusions of their own bone marrow progenitor cells into their hearts while the other half received placebo infusions.
Both groups had similar left ventricular function (LVEF), a surrogate predictor of a patient's prognosis after a heart attack, at the beginning of the trial: 47 percent in the placebo group and 48 percent in the bone marrow cell group.
What we really need: Therapies that can prevent heart attacks in the first place. In most cases such therapies will involve clearing arterial plaque, prevention of plaque formation, and growth of new blood vessels. You can do some of that now with better diet and statin drugs to lower cholesterol.
Using data from the Framingham Heart Study which follows several thousand people in Framingham Massachusetts Dutch researchers found that running 30 minutes a day 5 days a week will add 3.5 to 3.7 years to one's life.
"This shows that physical activity really does make a difference -- not only for how long you live but for how long you live a healthy life," said Oscar H. Franco of the Erasmus M.C. University Medical Center in Rotterdam, who led the study, published yesterday in the Archives of Internal Medicine. "Being more physically active can give you more time."
The researchers calculated the effects of low, moderate or high levels of physical activity on life span, accounting for the possible effects of factors such as age, sex, education, and whether they smoked or had serious health problems.
People who engaged in moderate activity -- the equivalent of walking for 30 minutes a day for five days a week -- lived about 1.3 to 1.5 years longer than those who were less active. Those who took on more intense exercise -- the equivalent of running half an hour a day five days every week -- extended their lives by about 3.5 to 3.7 years, the researchers found.
This result strikes me as an argument for getting a dog that is big enough to run as fast as you can. Those little pint-sized dogs just can't keep up to a human running at full gait. Dogs are great personal trainers, coming to you every day trying to get you to take them for a walk or run.
The scientific understanding of the mechanisms of appetite control in the last few years has been making some pretty big leaps. This trend continues. Stanford researchers have discovered an appetite suppressing hormone which they have named obestatin,
STANFORD, Calif. — When the appetite-enhancing hormone ghrelin was discovered a few years ago, researchers thought they had found the last of the major genes that regulate weight.
They were wrong.
Introducing: obestatin, a newly discovered hormone that suppresses appetite.
The finding, published in the Nov. 11 issue of Science, offers a key to researchers developing treatments for obesity. In a nation that desperately needs to slim down—the U.S. Centers for Disease Control and Prevention estimates 65 percent of Americans over the age of 20 are either overweight or obese—obestatin is likely to generate interest from scientists and drugmakers alike.
The financial incentives for appetite suppressant drug development are huge because so many people are, er, huge.
The research was sponsored by Johnson & Johnson Pharmaceutical Research & Development, LLC, which has certain license rights to the discovery.
Researchers at the Stanford University School of Medicine uncovered obestatin by using the principles of evolution to pick clues from data held in the Human Genome Project, as well as the genome sequencing projects for many other organisms, among them, yeast, fruit flies and mice.
Charles Darwin is everywhere. He's like Elvis.
"Darwin led us to this new hormone," said senior author Aaron Hsueh, PhD, an endocrinologist and professor of obstetrics and gynecology. Jian V. Zhang, PhD, a postdoctoral scholar in Hsueh's laboratory, is the lead author.
Drugmakers could use new insights into weight regulation. The discovery of the appetite-suppressing hormone leptin in 1994 and the appetite-boosting hormone ghrelin in 1999 offered high hopes of more effective drugs. And in the past few years, the influence of melanocortin hormones on regulating leptin has become clearer. But these insights have yet to yield a treatment for obesity.
"There are several known pathways that regulate body weight: ghrelin, leptin and melanocortin," explained Greg Barsh, MD, PhD, a Stanford professor of genetics who studies melanocortin, and was not involved in the obestatin project. "This work is notable because it represents a completely new pathway."
The new finding could clear up some confusion over how appetite-regulation hormones work. Since the ghrelin protein increases appetite, scientists had expected that animal experiments deleting the protein's gene would turn appetite off.
But when they tested this theory, they found that deleting the gene linked to ghrelin had almost no effect on growth or appetite. The likely reason? Hsueh's finding shows that deleting the gene for ghrelin also takes out obestatin.
It's rare for more than one protein to come from a single gene sequence. What makes this case even more unusual is that two proteins from the same sequence have such opposite effects: Obestatin behaves in some ways as the "anti-ghrelin."
"That was a big surprise," said Hsueh.
The identification of obestatin occurred as part of the researchers' study of a specific category of hormones-relatively small protein molecules called peptide hormones. These are of particular interest to drug developers because they bind to a type of receptor molecule known as a G-protein-coupled receptor, or GPCR. "These receptors represent targets for almost 50 percent of the drugs in the market," said Hsueh.
GPCRs activated by small-peptide hormones are especially promising. That's because small peptides, unlike larger ones, tend to be easier to synthesize and deliver to patients.
So why does Darwin's theory deserve some credit? Hsueh explained that before he and his colleagues started the project, they used the genome projects' information to create a database of GPCRs that grouped them according to their evolutionary relatedness.
From the 300 GPCRs found in the human genome, the researchers selected about 100 that had no known hormone partner. They then chose those 30 that seemed most likely to interact with a peptide hormone, basing this choice on evolutionary analyses.
"These sequences stood out because they each have evolutionarily close 'sister genes' known to bind peptide hormones," said Hsueh.
Next, they focused on identifying the unknown hormone partners. Darwin again lent a hand. Hsueh and colleagues narrowed the search by focusing on sequences that have been conserved during hundreds of millions of years of evolution-in organisms as diverse as fish and humans-because these are likely to be of greatest biological importance. They zeroed in on several sequences, including the one known to make ghrelin, the appetite-enhancing hormone. That sequence appears in humans and at least 10 other mammals.
Analysis of the ghrelin pre-hormone sequence revealed an additional protein tacked on at the end. The researchers promptly set out to synthesize and learn more about this protein, which they later named obestatin.
"There are no set rules for identifying bioactivity but most of the known peptide hormones are brain/gut hormones," said Hsueh. So the researchers set out to discover whether obestatin is present in rat stomach tissues and brain. It is.
After identifying a peptide candidate hormone they injected the peptide into rat brains and found it cut appetite in half.
Encouraged, they investigated obestatin's effects on laboratory animals. They found that injecting it into rats' abdomens and brains decreased food intake and suppressed weight gain. Rats given obestatin injections ate about half as much as those given no obestatin. Obestatin treatment also slowed the movement of digested food from the stomach into the intestines.
All that remained for the researchers to do was to match this newly discovered hormone to the right receptor.
Once again, evolutionary conservation made their work a little easier. Instead of testing each of the 30 previously identified GPCRs, they started with what the evolutionary record told them was the most likely candidate. Their hunch was that the receptor for obestatin would be closely related to the receptor for ghrelin. A whirl through their database showed them that GPR39 was closely related to the receptor for ghrelin.
Sure enough, later experiments showed them that GPR39 was in fact a receptor for ghrelin's antithesis, obestatin.
Evolutionary theory has become a lot more useful for medical research because of the declining cost of DNA sequencing technologies. Cheap DNA sequencing leads to large quantities of genetic data and that data gets analyzed with computer software written with insights gleaned from theoriizing about natural selection. Evolutionary theorizing therefore increasingly get used by clinical researchers. This is all taking place against the backdrop of political fights over whether kids should even be taught to take the theory of evolution by natural selection. seriously Well, the theory of evolution by natural selection is incredibly useful and medical science would be advancing more slowly without it.
The idea that aberrations in the number or structure of chromosomes can spur tumor formation is more than a century old. Such aberrations--known collectively as "aneuploidy"--arise in two principal ways: as a consequence of abnormal cell division, or as a result of cell fusion. By either mechanism, the resulting aneuploid cells no longer have the proper genetic makeup and frequently die. But researchers now know that tumor cells are often aneuploid--and very much alive. Whether aneuploidy is a cause or a consequence of a cancerous cellular state is the crux of a current debate.
In a recent study, Dr. Yuri Lazebnik and his colleagues at Cold Spring Harbor Laboratory observed, fortuitously, that normal cultured human cells are fused by the action of the Mason-Pfizer Monkey Virus (MPMV), but that the resulting hybrid cells do indeed fail to proliferate. However, the researchers discovered that if one of the fusion partners carried a particular "predisposing" gene mutation (in the oncogenes E1A or Myc, or in the tumor suppressor gene p53), then a significant proportion of the resulting hybrid cells were highly proliferative and thus potentially cancerous.
The missing piece of the puzzle is the question of whether this phenomenon happens in vivo in human bodies.
Whether such proliferating hybrid cells are produced by viruses in the human body, whether they can lead to cancer, and which of the many known and candidate human fusogenic viruses (for example, endogenous retroviruses, whose DNA sequences comprise at least 8 percent of the human genome) might contribute to cancer remain to be determined.
If this result is demonstrated to happen in the body then that will suggest a much larger role for viruses in cancer development.
I'm increasingly convinced we underestimate the size of the benefits that would flow from the development of a wider range of vaccines against viruses and bacteria that rarely kill people. First off, of course getting cold or flu or a stomach virus is unpleasant and also costs time. But also, both the infections and the body's reactions to infections are probably accelerating the aging process. We could reduce the rate of aging by reducing our total lifetime disease load. We might also reduce our risks of cancer.
Scientists might have identified one of the reasons why the bird flu virus H5N1 is so deadly to humans. A study published today in the open access journal Respiratory Research reveals that, in human cells, the virus can trigger levels of inflammatory proteins more than 10 times higher than the common human flu virus H1N1. This might contribute to the unusual severity of the disease caused by H5N1 in humans, which can escalate into life-threatening pneumonia and acute respiratory distress.
Michael Chan and colleagues from the University of Hong Kong and collaborators in Vietnam, studied the levels of a subset of the pro-inflammatory proteins called 'cytokines' and 'chemokines', induced by the virus H5N1 in human lung cells, in vitro. The authors compared protein levels induced by strains of the H5N1 virus that had appeared in Hong Kong in 1997 (H5N1/97) and Vietnam in 2004 (H5N1/04), with levels induced by the human flu virus H1N1.
Their results show that H5N1 is a much more potent inducer of pro-inflammatory proteins than H1N1. Twenty-four hours after infection with H5N1/04, the levels of the chemokine IP-10 in bronchial epithelial cells reach 2200 pg/ml, whereas in cells infected with H1N1 they only reach 200pg/ml. In H5N1/97-infected cells, IP-10 levels reach 1750 pg/ml. Similar results were found for other chemokines and cytokines.
High levels of cytokines cause excessive levels of inflammation and that can help to kill you.
Chemokines and cytokines are the "messengers of the immune system" and are critical in coordinating and regulating the immune response. Altering this balance is likely to lead to an uncontrolled inflammatory response in the lung and probably explains, at least in part, the severe lung inflammation associated with avian flu virus H5N1.
Michael Osterholm, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, says cytokine storm caused excessive immune response in 1918 pandemic victims and this caused organ damage and high fatality rates.
Today we are very concerned that the H5N1 virus circulating in wild and domesticated birds in Asia is moving genetically towards a human-to-human transmitted agent and could result in a 1918-like pandemic. If this happens, we expect that the illnesses that we see among those infected with H5N1 virus will be similar to those individuals who were infected in 1918 and the limited number of humans who have been infected with H5N1 to date. Many of the deaths that occurred in these populations resulted from the explosive growth of the virus in humans and a subsequent cytokine storm. A cytokine storm is the release of a chemical in the body that stimulates the human immune system to respond to the virus infection. In these serious illnesses and deaths, it's actually been an over vigorous immune response elicited by this infection that result in the organ damage and ultimately the death of the individual. Ironically this means that those with the strongest immune systems may be at highest risk for a serious outcome if infected with the H5N1 virus.
Also see the Flu Wikie Cytokine Storm entry for more discussion on how a cytokine storm can kill you. Adults between the ages 18 and 40 suffered most of the deaths from the 1918 strain probably because their immune systems were stronger than those of older people. Hence their immune systems were better able to overreact to the cytokines which the 1918 flu caused to be made.
As Mr. Mackey might say, "Cytokine storms are bad, mmmmkay?" and so we need ways to stop cytokine storms, mmmmkay? Well, back in 2003 an Imperial College London team showed that a molecule named OX40:Ig that blocks the effect of OX40
Until now, treatments to eliminate the cytokine storm have focused on inhibiting all T cells. But this leaves the patient unable to clear the virus and susceptible to other infections. Dr Hussell's team have developed a way of down regulating a molecule known as OX40 that only targets T cells that have recently been alerted to the presence of the flu virus.
"OX40 sends out a 'survival signal' instructing activated T cells to remain in the lungs for longer to help fight the infection. However, because new cells are arriving all the time this prolonged presence is not needed," explains lead researcher Ian Humphreys of Imperial's Centre for Molecular Microbiology and Infection.
"Inhibiting this signal therefore allows T cells to vacate the lungs earlier whilst leaving behind a sufficient immune presence."
Using a fusion protein OX40:Ig supplied by the pharmaceutical company Xenova Research, the scientists were able to demonstrate that OX40:Ig blocks active T cells.
Results show six days after infection with flu, mice treated with OX40:Ig were indistinguishable from uninfected control mice. But infected mice that had not been treated lost 25 per cent of their body weight, appeared hunched, withdrawn and lost their appetite - all characteristic symptoms of flu.
When treatment with OX40:Ig was delayed for several days after infection, until the mice had lost 20 per cent of their body weight and OX40:Ig was administered, symptoms were reversed.
Re-infection also indicated that the ability of mice to respond to a second infection was not affected by the reduced T cell immunity during the initial infection.
Parenthetically, OX40 is also known as CD134.
Sounds hopeful, right? That was 2003. Xenova was supposed to begin human testing in 2004.
Hussell believes the drug could potentially treat any illness with an excessive inflammatory response, including asthma and possibly SARS. The researchers are testing the fusion protein as an asthma treatment in mice. They hope to test OX40:Ig in adult humans in a phase one trial in 2004.
Near as I can tell no such human trial took place in 2004. Poking around Xenova's web site I found indications that Xenova probably has not moved on to human trials.
OX40 is a platform technology capable of producing multiple drug candidates targeting cancer, autoimmune and other diseases where the immune system is involved. Xenova is developing the OX40 technology for the up-regulation of the immune system, for the development of novel treatments for cancer and infectious diseases. Xenova's rights to down-regulate the immune system have been the subject of development and licence agreements entered into with Celltech and Genentech (April 2002).
Xenova’s rights to the OX40 technology include rights relating to the up-regulation of the immune system which may be used for the development of novel treatments for cancer and infectious disease. Xenova’s rights to down-regulate the immune system have been the subject of development and licence agreements entered into with Celltech and Genentech.
Here's an August 2004 press release which states more clearly that Xenova has sold the rights for OX40 development to down-regulate against, for example, a cytokine storm caused by an influenza infection.
Xenova retains all rights for the use of OX40 in up-regulation whilst Genentech Inc and Celltech Group plc have the rights for down-regulation.
While neuraminidase inhibitors like Tamiflu can be used against all manner of flu types and hence have a market even when there is no pandemic the OX40 blockers probably do not have much utility against influenza under normal conditions. So OX40 blocker development probably isn't going to get much funding against flu unless governments step in (and my guess is governments are probably not smart enough and prudent enough to do that).
I haven't been able to find indications that Celltech and Genentech are pursuing OX40 development for flu treatment. Rapid development and production of OX40:Ig during an H5N1 pandemic might save millions of lives. Would any governments show sufficient regulatory flexibility to allow rapid introduction of a prototype drug during a pandemic?
So what to do about the cytokine storm threat come a pandemic? Statin drugs such as Lipitor and Crestor (widely used to lower cholesterol) probably will lower the risk of death of those infected by an influenza strain that causes a cytokine storm. If you have high cholesterol and haven't done anything about it go get a statin drug prescription and it might just save your life two different ways: Avoid a heart attack and avoid death in an influenza pandemic.
HONOLULU, October 31, 2005 -- A new study suggests that changes in gastric physiology perform better than standard polygraph methods in distinguishing between lying and telling the truth. The University of Texas study, released today at the 70th Annual Scientific Meeting of the American College of Gastroenterology, demonstrates a clear link between the act of lying and a significant increase in gastric arrhythmia.
To test their hypothesis that the gastrointestinal tract is uniquely sensitive to mental stress because of the communication between the central nervous system and the enteric nervous system, researchers at the University of Texas Medical Branch recruited sixteen healthy volunteers to undergo simultaneous electrogastrogram (EGG) and electrocardiogram (EKG) recordings for three periods.
The researchers found that both lying and truth telling affected cardiac symptoms, while the act of lying was also associated with gastric symptoms. The EGG showed a significant decrease in the percentage of normal gastric slow waves when the subject was lying that corresponded to a significant increase in the average heart rate during the same situation.
"We concluded that the addition of the EGG to standard polygraph methods has clear value in improving the accuracy of current lie detectors," said Pankaj Pasricha, MD, University of Texas Medical Branch. "The communication between the big brain and the little brain in the stomach can be complex and merits further study."
Pasricha emphasises that the test will be an addition, not a replacement, for today’s polygraph devices – and only after further research involving hundreds more test subjects.
The initial study only included 16 subjects because it began as Pasricha’s daughter’s high school science fair project in May 2005 – she won second prize.
Pasricha says he needs funding to use a large enough number of subjects to test out the reliability of this approach and he's hoping for a corporate sponsor. The FBI and CIA ought to take notice. The value of lie detection is high for criminal investigations and national security.
In the long run I we'll see the development of technologies that can make the body act like you are not lying. Imagine a drug, for example, that would stimulate gastric slow waves to mimic truth-telling. The problem with such a drug is that a subject of interrogation could be instructed to tell lies in response to certain questions and the monitoring equipment could detect that the gastric slow waves did not decrease. What's needed is an implant that would not be detected in an x-ray that would allow a person to dynamically adjust the stomach's response. Perhaps a person could control the response by wiggling a toe or moving a finger that has nanosensors embedded in it.
Count on capitalists to find ways to satisfy increased demand. Tamiflu production capacity will be an order of magnitude greater in 2006 than it was in 2003.
"There's a shortage right now," said William M. Burns, head of Roche's pharmaceutical division. But he quickly added that the company plans to raise annual production capacity to 300 million courses of treatment by this time next year: a drastic increase from 55 million this year and more than 10 times the output capacity in 2003.
"This is a capacity significantly larger than the cumulative number of orders we have," Mr. Burns said.
If H5N1 avian flu does not mutate into a human pandemic strain the next year then anyone wanting to stockpile Tamiflu will have a much easier time doing so next summer.
But if you take the flu pandemic threat seriously then the best preparations that you can take in advance are measures that would decrease your odds of getting exposed to influenza in the first place. Stockpile high quality face masks. Take a job or adjust your job in ways that will allow you to reduce your exposure to other people. Save money ahead of time so that you can live off that money rather than go to an office every day that has lots of people in it.
The pandemic preparation option I'd most like to have that is technically possible but not now available: Get vaccinated against current H5N1 strains in order to build partial immunity against a pandemic strain.
STANFORD, Calif. – Researchers at the Stanford University School of Medicine have shown for the first time that a sample of children who either have or are at high risk for bipolar disorder score higher on a creativity index than healthy children. The findings add to existing evidence that a link exists between mood disorders and creativity.
The small study, published in the November issue of the Journal of Psychiatric Research, compared creativity test scores of children of healthy parents with the scores of children of bipolar parents. Children with the bipolar parents—even those who were not bipolar themselves—scored higher than the healthy children.
“I think it’s fascinating,” said Kiki Chang, MD, assistant professor of psychiatry and behavioral sciences and co-author of the paper. “There is a reason that many people who have bipolar disorder become very successful, and these findings address the positive aspects of having this illness.”
Obviously genetics plays an important role in creativity, ADHD, and bipolar disorder.
Artists have higher rates of mental illness.
Many scientists believe that a relationship exists between creativity and bipolar disorder, which was formerly called manic-depressive illness and is marked by dramatic shifts in a person’s mood, energy and ability to function. Numerous studies have examined this link; several have shown that artists and writers may have two to three times more incidences of psychosis, mood disorders or suicide when compared with people in less creative professions.
Terence Ketter, MD, professor of psychiatry and behavioral sciences and a study co-author, said he became interested in the link between mental illness and creativity after noticing that patients who came through the bipolar clinic, despite having problems, were extraordinarily bright, motivated people who “tended to lead interesting lives.” He began a scholarly pursuit of this link and in 2002 published a study that showed healthy artists were more similar in personality to individuals with bipolar disorder (the majority of whom were on medication) than to healthy people in the general population.
Some people with higher intellectual capabilities might be able to handle their bipolar and ADHD and still manage to be productive. But less bright people are probably more likely to be overwhelmed by their mental illness and unable to harness their creativity for productive purposes. But do the genetic variations that contribute to causing bipolar also raise IQ?
People who use their negative emotions to initiate searches for solutions to problems tend to be more creative.
Some researchers believe that bipolar disorder or mania, a defining symptom of the disease, causes creative activity. Ketter said he believes that bipolar patients’ creativity stems from their mobilizing energy that results from negative emotion to initiate some sort of solution to their problems. “In this case, discontent is the mother of invention,” he said.
The children of parents with bipolar disorder were themselves either bipolar or had ADHD (attention deficit hyperactivity disorder).
During the study, the researchers looked at creative characteristics in 40 bipolar patients and 40 offspring, comparing them with 18 healthy adults and 18 healthy offspring. The children in the study ranged in age from 10 to 18. Half of the children of bipolar patients also had bipolar disorder; the other half had attention deficit hyperactivity disorder or ADHD, which appears to be an early sign of bipolar disorder in offspring of parents with the condition. The majority of participants with bipolar or ADHD were on medication.
The researchers included children with ADHD so they could study creativity before the onset of full bipolar disorder. “We wanted to see whether having a manic episode is necessary for this sort of creativity,” said Chang, who also directs the Pediatric Bipolar Disorders Program at Lucile Packard Children’s Hospital.
Study participants were given psychiatric evaluations and then completed the Barron-Welsh Art Scale, or BWAS, a test that seeks to provide an objective measure of creativity. The scoring is based on “like” and “dislike” responses to figures of varying complexity and symmetry; past studies suggest that creative people tend to dislike the simple and symmetric symbols.
The researchers found that the bipolar parents had 120 percent higher BWAS “dislike” scores than the healthy parents. The children with bipolar and the children with ADHD had, respectively, 107 and 91 percent higher BWAS dislike scores than the healthy children.
“The results of this study support an association between bipolar disease and creativity and contribute to a better understanding of possible mechanisms of transmission of creativity in families with genetic susceptibility for bipolar disease,” the researchers wrote in their paper.
On the bright side, the bipolar mania stage is not needed to cause creativity. The presence of ADHD alone boosts creativity. The problem, though, is that people with ADHD might be full of ideas. But many lack the patience needed to translate their ideas into implementations. If you can't stand to focus long enough to write down the melody or story line you see in your head or to draw a mechanical design that you've thought of your creativity doesn't do you or the world much good.
The researchers had hypothesized that the scores of children with ADHD would differ significantly from the scores of bipolar children so they were surprised when the scores did not. Chang said this indicates that mania is not what is fueling the creativity. “The kids with ADHD who hadn’t been manic yet still had very high levels of creativity,” he said.
Being mentally ill for a longer time erodes the BWAS dislike score. Mentally ill people burn out and cease to be creative.
The researchers also found a link between the length of a bipolar child’s illness and creativity: the longer a child was sick or manic, the lower the BWAS dislike score. It makes sense, Chang said, that this illness could, over time, erode one’s creativity. “After awhile you aren’t able to function and you can’t access your creativity,” he explained.
We all get less creative with age.
BWAS dislike scores tend to decrease with age even in healthy individuals, so more research is needed, Ketter said. Further studies are also needed to assess the role of genetic and environmental factors in creativity and bipolar, he added. The team plans to next examine whether the degree of creativity in parents correlates with the degree of creativity in their children.
If the mental illness eventually leads to declining creatvitiy by causeing neuronal cell death then perhaps the development of treatments based on Strategies for Engineered Negligible Senescence (SENS) will provide ways to preserve neurons and creativity as the years and decades go by.
Maybe one cause of hyperactivity is a low threshold for noticing external stimuli. See my previous post "Low Latent Inhibition Plus High Intelligence Leads To High Creativity?"
They agreed to spend $450 million in 2006 on Yucca Mountain, the planned underground repository for 77,000 tons of the nation's most radioactive nuclear waste.
The project's budget was $577 million in each of the past two years, and Bush asked for $650 million for the dump in his 2006 budget request.
The nuclear waste that will eventually to go Yucca Moutain (assuming Yucca Mountain goes into operation in 2012 or some later date) sits at nuclear plant sites around the United States. Each state Congressional delegation doesn't want a nuclear waste disposal site in their jurisdiction. So Nevada's delegation predictably tries to slow Yucca's development. But I do not expect the Nevada delegation to stop it entirely.
Note that the money that is not getting spent here is money that has already been paid by the United States nuclear power plant operators. The nuclear power industry pays a tax to fund the construction of a nuclear waste storage site. The nuclear power industry has paid much more in taxes than has been spent to date preparing Yucca Mountain.
Development of a plant to convert plutonium from old nuclear weapons into useful nuclear power plant fuel has also been slowed.
Spends $220 million to build a plant at the federal Savannah River complex in South Carolina where weapons-grade plutonium would be processed into a mixed-oxide (MOX) fuel — a less dangerous fuel for commercial power reactors. That figure is $118 million lower than Bush's request.
Congress ought to be greatly accelerating the development of nuclear power, not slowing it. Similarly, Congress ought to greatly accelerating research into photovoltaics and into electrochemistry for next generation batteries. We can't phase out fossil fuels without first developing technologies for producing and storing energy from non-fossil fuel energy sources.
The United States Congress seems entirely unserious about energy policy. The growth of China will boost greenhouse gas emissions 50% by 2030 if current trends continue.
Yesterday the International Energy Agency warned that the growing appetite of China - added to the huge demand in the US and Europe - had created an unsustainable trend. Energy demand and greenhouse gas emissions will soar by more than 50% by 2030 if consumers keep burning oil unchecked, the agency warned.
Most thinkers have just not factored in what the growth of China means. China won't magically stop growing once 2030 hits. Each year will bring further growth and therefore further economic growth in energy demand. See my posts "Planned Coal Plants Reverse 5 Times CO2 Impact Of Kyoto Protocol" and "Carbon Dioxide Emissions Continue Rapid Increase". China produced nearly half the carbon dioxide emissions rise in 2004. China's fraction of the total increase will probably rise much higher in future decades.
If we melt the ice on Greenland the world sea levels will rise about 20 feet. Lots of valuable real estate will be lost. It is very imprudent to simply hope a large increase in atmospheric CO2 won't lead to a climate change large enough to melt the Greenland ice pack. It is especially imprudent because the steps we could take to prevent such a drastic result are probably not very expensive.
I'm not arguing for slowing economic growth or imposing heavy taxes to prevent that outcome. We just need to greatly accelerate the rate of advance of non-fossil fuels energy technologies. The recently deceased Nobel laureate Richard Smalley (felled by cancer at age 62 - what a terrible waste) argued for $10 billion a year to fund research into a wide range of energy technologies. Smalley was right. Acceleration of the rate of technological advanes is the right solution. $10 billion per year is less than one tenth of one percent of the US economy. It is quite affordable. The technologies developed by such an effort would eventually be cheaper than fossil fuels and would displace fossil fuels just by market decisions to go with the lower cost energy sourcse. So why aren't we already making the big push to develop new energy technologies? Our current course seems like a reckless gamble.
The volunteers , donors , and members of The Three Hundred became even more certain of the Mprize's eventual success when the prize to reverse the decay and debilitation of aging benefited from the addition of a ONE MILLION DOLLAR cashier's check from an anonymous donor (and - yes - the check cleared :-). This donation makes the second major anonymous donation within the last few weeks - these donors let us know that they didn't want to become the "elephant in the room" instead preferring to direct attention to the power of prizes and the Mprize in particular to achieve the nigh unto impossible and to encourage others by their example. We would like to publicly thank those who have supported the Mprize from the beginning whether as volunteer, donor or member of The Three Hundred. It is without doubt your tireless devotion and generosity that is breathing life into this mission thus bringing us to a better place for all tomorrow. Let's make it happen sooner. Add your pebble to the landslide that will bury the suffering of aging and http://www.mprize.org/join us.
The Methuselah Mouse Prize is the premiere effort of The Methuselah Foundation™; a scientific competition designed to draw attention to the ability of new technologies to slow and even reverse the damage of the aging process, preserving health and wisdom in a world that sorely needs it. Read More...
The Methuselah Mouse Prize (or Mprize) is a series of cash awards to scientists who develop ways to make a common lab mice live longer. The goal of the prize is to encourage scientists to develop biotechnologies that will demonstrate the practicality of life extension and that will also extend the lives of humans.
Consider what you spend money on. If you have a lot of discretionary income then ask yourself whether you'll get the most value it of it by such choices as spending on immediate desires or leaving it to your estate. Wouldn't it be better to spend it in a way that increases the odds you can become young again and live a longer, healthier, and youthful life? You can't take it with you when you die. Spend some to accelerate research to reverse aging and you'll be able to spend the rest in a very long future of youth.
To the delight of the volunteers at the Methuselah Foundation, an anonymous donor has given $1 million to the Methuselah Mouse Prize, or Mprize for Rejuvenation, the scientific research prize aimed at bringing an end to the degenerations and indignities of aging. Volunteers for the Mprize couldn't believe it when they saw the size of the latest check: topping previous and exceedingly generous five- and six-figure donations, this was a check for $1 million out of the blue!
We stand within reach of a cure for human aging according to trailblazing biomedical gerontologist Aubrey de Grey of Cambridge University, Chairman and Chief Science Officer of the Methuselah Foundation. Like de Grey, more and more are convinced of the power prizes have shown to make a difference to the future of healthy and longevity – and are putting their money where their hopes are!
Over the past several years, a growing band of enthusiasts - regular folk from all corners of the world have donated to the Mprize, a scientific research prize modeled on the extraordinarily successful prizes such as the Longitude Prize and the X Prize. The Mprize, or Methuselah Mouse Prize, rewards scientists who increase the maximum healthy lifespan by rejuvenating mice that are already in late middle age.
In early 2005, the Mprize hit its first million-dollar mark in pledges, entirely made up of small donations from people in more than 18 countries around the world. Today's anonymous donation will push the Mprize fund to nearly 3 million dollars.
The anonymous $1 million donor cited an initial skepticism – and then a growing understanding of the real possibility of curing aging in our lifetimes as his reason for making such a tremendous investment. He first learned about de Grey's work from the popular press. The donor then learned more by following the Fight Aging! blog (http://www.fightaging.org) and the online newsletter Longevity Meme (http://www.longevitymeme.org). Both sites explore the coming reality of life extension and how we are likely to achieve it. These blogs advocate de Grey's work and the Mprize in particular. In the Mprize, this donor saw a popular movement in the making, where every dollar in the prize fund represents a powerful voice, calling for the scientific community to take audacious yet practical steps towards real, working anti-aging medicine.
Why didn't he tell us his name? Like many who have donated, including the originator of a $125,000 grant donated earlier this year, he didn't want to become the news story. He wanted to make sure that the message was: End aging as we know it? A million times - Yes! The Mprize is an all-volunteer effort. All donations go directly into the Prize fund -- there is no overhead. This December, Mprize Three Hundred Members, the group of donors who commit to giving $1000 per year for 25 years, plan to celebrate the recent growth of the prize with a Three Hundred member dinner where the speakers will be Aubrey de Grey and Mprize donor Ray Kurzweil, author of The Singularity is Near
Predictors for exceptional human longevity may include birth order, place of birth and early-life living conditions, according to a recent Society of Actuaries (SOA) study that suggests there are several factors linked to one’s longevity. The data indicates that first-born daughters are three times more likely to survive to age 100 compared to later-born daughters. The chances for exceptional longevity are minimal for sons having a birth order of four to six compared to those born earlier or later.
The research, developed by the SOA in partnership with researchers at the Center on Aging and the National Opinion Research Center at the University of Chicago, evaluated detailed family data for nearly 1,000 centenarians born in the U.S. between 1875-1899. Drs. Natalia Gavrilova and Leonid Gavrilov collected data from publicly available computerized genealogies of 75 million individuals identified in previous studies and validated ages and birth dates by linking records to the Social Security Administration Death Master File and reviewing U.S. censuses for years 1900, 1910 and 1920.
“The study supports the idea that early childhood conditions might be important for survival to advanced ages,” said Dr. Natalia Gavrilova. “Limited access to parental care, including attention and supervision, may result in less attention being paid to the health and safety of later-born children, resulting in a higher risk of infections and malnutrition during early childhood.”
The data further suggests that children born to parents who are farmers and childhood residence in the Western region of the U.S. may be indicators for subsequent survival to age 100. The study determined that children of farming parents who lived in the Mountain Pacific and West Pacific regions of the U.S. have a greater chance of surviving to age 100 than those from the Midwest and Northeast areas of the country.
“Without the type of food processing that’s currently available, living on a farm 100 years ago meant fresher food with more nutrient value,” said Thomas Edwalds, Fellow of the SOA and chairman of the project oversight committee. “This very well might correlate to prenatal and perinatal nutrition as factors of exceptional longevity.”
People living to age 100 and beyond represent one of the fastest-growing age groups of the American population, increasing at a rate of about 4.1 percent each year.
“Actuaries are skilled at measuring risks, and this research helps us better understand the predictors of longevity and quantify the implications on society and business,” continued Edwalds. “This research also illustrates that studies on human longevity could be modernized and advanced further by using new computerized data resources such as genealogies.”
Can one use this information in any way? Without knowing the mechanism which cause these effects it is hard to say. Some possible causes of this phenomenon could be managed for better results. For example, one could imagine ways that a woman's body could treat an earlier pregnancy differently than a later pregnancy. During a first pregnancy a woman could have a larger store of minerals and vitamins to give to a fetus. So a woman could compensate with vitamin supplements. But alternatively the immune system of a woman's body could could respond to a succession of pregnancies differently and become poorer at avoiding immune responses to a pregnancy. That'd be harder to do something about.
Infection is also hard to manage. A first born child typically grows up in a home with fewer children than a later born child. So the first born does not have the later children as vectors to give the first born infections. But the later born children have the older earlier born children as sources of pathogens. When the 5 or 6 year old goes off to school, gets infected, and then brings home the infectious pathogen to infect the 1 and 2 year olds then the younger later birth children end up getting hit by more infections which each exact their toll. How to compensate for this? One could imagine that home schooling might reduce the infectious disease risk posed by older children to younger children in the same family. If the kids do not go to school to get dosed with pathogens by other kids then the kids won't bring those diseases home to infect their siblings.
Suppose a big factor in causing the above results is frequency of infections. Let me take this as an opportunity to pitch for one of my favorite public health ideas: Vaccines should be developed for more diseases including the many rhinoviruses (which cause some cases of the common cold). Development of technologies that allow much larger numbers of pathogens to be targetted by vaccines could reduce the frequency of infection during early childhood and later in life and reduce the aging caused by infection. It'd also eliminate many miserable days of being sick.
Sex appeal comes from a hormone. More estrogen makes a woman's face prettier.
Women with high levels of the sex hormone oestrogen have prettier faces, research suggests.
The findings make evolutionary sense - men are attracted to the most fertile women, the University of St Andrews team told a Royal Society journal.
Miriam Law Smith and colleagues photographed 59 women, aged between 18 and 25, every week for six weeks. On each occasion, they provided a urine sample for hormone analysis and gave information on where they were in their menstrual cycle. None of the women wore make-up, nor were they taking the contraceptive pill.
The researchers then selected the photograph of each woman that had been taken at the time of her highest urine-oestrogen level. As expected, this correlated to the point of ovulation in the women’s menstrual cycles. These photographs were rated by 14 men and 15 women, also aged 18 to 25, for attractiveness, health and femininity.
Women with higher levels of oestrogen were rated as more attractive, healthy and feminine looking. Interestingly, no relationship between appearance and oestrogen was found in women wearing make-up. The researchers believe that while make-up improves facial appearance it may be masking cues normally seen in the face.
That men should be attracted to more fertile women makes sense from an evolutionary perspective. Also, the relationship between hormone levels, shapely bodies, and fertility is well-established. Women with higher levels of estradiol are about 3 times more likely to get pregnant. See my post "Women With Hourglass Bodies Have More Reproductive Hormones".
Eventually stem cell therapy and gene therapy will be widely used by women to enhance their feminine appearance. The average level of attractiveness of both men and women will be far higher in the future. Once Strategies for Engineered Negligible Senescence (SENS) become available everyone will look young and highly attractive.
Last week, Joe Howton, medical director at the Adventist Medical Center in Portland, Oregon, suggested a way to double supplies, after browsing basic safety data from Roche for a talk on avian flu.
The technique was invented during the Second World War to extend precious penicillin supplies. Scientists found that a simple benzoic acid derivative called probenecid stops many drugs, including antibiotics, being removed from the blood by the kidneys. Probenecid is readily available and is still widely used alongside antibiotics to treat gonorrhoea and syphilis, and in emergency rooms, where doctors need their patients to have high, sustained levels of antibiotics in their blood.
Howton believes that Tamiflu doses could be cut in half when taken with Probenecid. This would effectively double the amount of Tamiflu available should a pandemic occur. To make this work Probenecid would need to be made in sufficient quantity. But quite possibly other existing drugs could be found that also interfere with Tamiflu excretion.
Drugs that may adversely interact with Tamiflu are the drugs containing Probenecid. Combining Tamiflu and drugs containing Probenecid may result in higher blood levels for patients.
Coadministration of probenecid results in an approximate 2-fold increase in exposure to the active metabolite due to a decrease in active anionic tubular secretion in the kidney. Other drugs excreted via anionic tubular secretion have not been evaluated.
If you haven't already stockpiled your own Tamiflu supply your odds of getting Tamiflu during a pandemic are rather slim even if Probenecid works to stretch Tamiflu supplies. The key to surviving a highly lethal influenza pandemic would be to greatly reduce your exposure to other people who might be influenza carriers. My favorite proposal for reducing the risk of getting a pandemic virus while simultaneously reducing the economic disruption of a pandemic is "workplace cocooning".
I also think we should have large crash programs for the development of cellular methods for growing flu vaccine and for the development of DNA vaccines as well. Plus, I'd gladly take a shot of a vaccine against existing H5N1 avian flu strains as a way to get partial immunity against an eventual possible human pandemic strain of H5N1.
Update: Do not casusally go taking probenecid to avoid the flu. First off, it does no good unless taken in combination with Tamiflu. Second, probenecid has potentially dangerous side effects and should not be taken casually. Do not take extra doses. You could kill yourself if you do.