September 29, 2004: At 8:13 this morning PDT, SpaceShipOne (SS1) coasted above the 100 km altitude point and successfully completed the first of two X-Prize flights. The peak altitude reached was 337,500 ft. The motor was shut down when the pilot, Mike Melvill, noted that his altitude predictor exceeded the required 100 km mark. The motor burn lasted 77 seconds – 1 second longer than on the June 21st flight. Melvill was prepared to burn the motor up to 89 seconds, which indicates significant additional performance remains in SS1.
The second X-Prize flight is tentatively scheduled for Monday, October 4.
Click through on that previous link to links for videos and photos.
Note that Burt Rutan is considering trying for a second flight on October 3 since that is the 47th anniversary of the launch of Sputnik.
MOJAVE, CALIFORNIA – The frightening spin of SpaceShipOne during its trip into space Wednesday was caused by a known deficiency and at no time led to an out-of-control situation, officials said today.
The unofficial altitude reached by SpaceShipOne yesterday, based on radar tracking, was 337,500 feet -- about 64 miles.
The Ansari X-Prize was modelled on the $25,000 prize that Charles Lindbergh won in his Spirit of St Louis for the first solo Transatlantic flight between New York and Paris in 1927.
The success of the X Prize competition argues for more and larger such prizes to achieve other goals in aerospace exploration and development. A portion of NASA's budget ought to be set aside for prize awards. Imagine much larger prizes for private spacecraft flight records, private orbital space station habitation for some period of tim, trips around the moon, manned landings on the moon with successful return, and successful construction an underground (because the moon is outside of the Van Allen Belt and radiation levels there are much higher) moon base with, say, 90 day continuous occupancy. A billion dollars a year accumulating in some fund would provide incentive for all sorts of highly cost-effective private aerospace development efforts.
The new service will be called Virgin Galactic and expects to fly 3,000 new astronauts in its first five years. Fares will start at $208,000 for a suborbital flight, including three days’ training.
Designs for the Virgin Galactic craft are progressing on a weekly basis at Rutan's base in Mojave, California and by early 2005 the final design for the maiden Virgin Galactic ship, the VSS (Virgin SpaceShip) Enterprise, should be signed-off.
What will follow will be a concerted Research and Development programme to earn the craft their qualification to carry some of the world's first scheduled space tourists. Safety is paramount. It is planned to have multiple levels of redundancy on key systems in order to achieve a very robust system in every phase of flight.
Virgin's experience in aviation, adventure, luxury travel and cutting-edge design will be vital in contributing to the design of the spaceship, the smooth operation of the spaceline and creating an unforgettable experience unlike any other available to mankind.
"We've always had a dream of developing a space tourism business and Paul Allen's vision, combined with Burt Rutan's technological brilliance, have brought that dream a step closer to reality. The deal with Mojave Aerospace Ventures is just the start of what we believe will be a new era in the history of mankind, one day making the affordable exploration of space by human beings a real possibility." Richard Branson
One argument for putting NASA into a prize-granting role is that some of its existing missions could be taken over by private efforts anyway. NASA ought to put up an award for building a space hotel. The hotel could be used by scientists as well as by tourists. A hotel built for prize money would not cost the government as much as the International Space Station because the prize amount would be some fixed lower amount.
The Methuselah Foundation has announced that their Methuselah Mouse Prize award offered to scientists who break records in lab mouse longevity has reached the half million dollar mark in funding.
Lorton, VA. September 1, 2004. The Methuselah Foundation, creators of the Methuselah Mouse Prize, the world's first scientific prize for research on extending longevity, today announced that it has secured $500,000 in funding commitments and a long term support commitment from an anonymous supporter making his donation in the name of the X PRIZE Foundation, the multi-million-dollar bounty which has successfully encouraged the development of private passenger space travel.
"We've seen how prizes such as the X PRIZE and the Methuselah Mouse Prize can dramatically increase competition and innovation, and create interest for the public," said Dr. Peter H. Diamandis, Founder and Executive Producer of the X PRIZE. "With this contribution, we're signaling our belief that Prizes can not only take us into space, but help bring about breakthroughs in the way we live and age."
"We're thrilled to have the support of the X PRIZE, said David Gobel, Director of the Methuselah Foundation and the Methuselah Mouse Prize. "This landmark contribution will further swell the size of the Prize, and encourage scientific research teams around the world to develop breakthrough techniques for extending the healthy human lifespan. It will create a needed impetus and focus for the development of new rejuvenation therapies."
The Methuselah Mouse Prize is being offered to scientific research teams who develop the longest living Mus musculus, the breed of mouse most commonly used in scientific research. This is a critical precursor to the development of human anti-aging techniques. Currently, six teams around the world are vying for the prize, and this new contribution is expected to swell that number.
"By encouraging the development of technologies that enable sustainable human rejuvenation, the Methuselah Foundation is the first and most developed organization directly promoting the development of human "Projuvenation" technology." Said the Methuselah Foundation's Chief Science Officer - Dr. Aubrey de Grey. "The focus of the Methuselah Foundation is not simply extending human life; it is discovering ways to limit and eventually eliminate the destructive effects of human aging, promoting not only longer life but freedom from the effects of aging-related conditions and diseases."
Your support of the Methuselah Mouse Prize is the best and most effective way that you can help ensure that human biological rejuvenation technologies are developed and widely available as quickly as possible. The future return on your investment is a longer, healthier, and ultimately better quality of life for yourself and your loved ones."
There is an obvious parallel here with the $10 million X Prize for private groups to launch humans into space. The X Prize has been very successful in attracting private groups to make a serious effort to build craft that can fly into orbit. In the latest turn in that fierce competition the Scaled Composites SpaceShipOne may have a leg up over the da Vinci Project due to a parts shortage affecting the latter.
I understand the appeal of building rockets to get into space. It is great to watch the unfolding of the competition to build private space launch vehicles. But priorities seem out of whack when the Ansari X Prize has $10 million now available to the winners whereas the Methuselah Mouse Prize has a mere half million. Look at it this way: Once we can achieve an indefinite state of youth (basically until we die by accident, murder, or suicide) using Strategies for Engineered Negligible Senescence (SENS) we will have centuries to migrate into space.
Of course, what is far more out of whack is that NASA has billions of dollars to spend per year while the Ansari X Prize is achieving far more per dollar spent with their prize offering. Similarly, many individual diseases get funding per year of hundreds of millions or even billions of dollars whereas eternal youth research advances with literally orders of magnitude less money spent on it.
Gordon G. Gallup, Jr., Susan M. Hughes and Franco Dispenza have found that people with sexy voices get more sex and have more symmetrical body shapes.
In "Ratings of voice attractiveness predict sexual behavior and body configuration," published in the September issue of Evolution and Human Behavior, published by Elsevier, Susan Hughes, Franco Dispenza, and Gordon Gallup of the University's department of psychology tested 149 men and women by having them listen to recorded, neutral voices counting from 1 to 10. They were then asked to rate the anonymous voices on a scale from "very unattractive" to "very attractive." The results were compared to surveys and morphological measurements taken among the speakers. Researchers discovered that people whose voices are judged to be attractive tend to have sexual intercourse at an earlier age, have more sexual partners than those with voices rated less attractive, and are more prone to sexual infidelity. They also have more sex partners among people involved in other relationships.
"In short," Gallup said, "ratings of voice attractiveness are correlated with promiscuity in both men and women."
The fact that people with more symmetrical bodies have sexier voices is especially interesting. This suggests that the quality of development of a fetus translates into not just a more attractive symmetrical appearance but also into a throat shape that creates more pleasing vocal sounds.
The full paper is on-line.(PDF format)
We investigated the relationship between ratings of voice attractiveness and sexually dimorphic differences in shoulder-to-hip ratios (SHR) and waist-to-hip ratios (WHR), as well as different features of sexual behavior. Opposite-sex voice attractiveness ratings were positively correlated with SHR in males and negatively correlated with WHR in females. For both sexes, ratings of opposite-sex voice attractiveness also predicted reported age of first sexual intercourse, number of sexual partners, number of extra-pair copulation (EPC) partners, and number of partners that they had intercourse with that were involved in another relationship (i.e., were themselves chosen as an EPC partner). Coupled with previous findings showing a relationship between voice attractiveness and bilateral symmetry, these results provide additional evidence that the sound of a person’s voice may serve as an important multidimensional fitness indicator.
A sexy voice might be more important for a female than a male. Males might be better off with bigger shoulders.
It is interesting that voice attractiveness was a better predictor of sexual behavior in females than WHR was. The best predictor of promiscuity (as measured by number of sexual partners) in males was SHR, whereas in females, it was voice attractiveness. As shown in Table 2, the correlations between opposite-sex ratings of voice attractiveness and sexual behavior in females were consistently higher than those found for WHR and sexual behavior. However, just the opposite was true for males (see Table 1). Among males, SHR was a better predictor of sexual behavior than voice was. For example, whereas opposite-sex voice attractiveness accounted for 13% of the variance in promiscuity among males, SHR accounted for 28% of the variance in male promiscuity. The same sex differences held for the relationship between voice and body configuration. Male SHR accounted for more variance (25%) in opposite sex ratings of voice attractiveness than did female WHR (14%).
Perhaps people with unsexy voices should avoid talking much in bars.
Stanford researchers have shown in a preliminary non-double blind trial that the anti-depressant Selective Serotonin Uptake Inhibitor (SSRI) escitalopram (Lexapro) reduces the severity of kleptomania.
STANFORD, Calif. – Researchers at Stanford University School of Medicine are reporting promising early results in a study of a medication to treat kleptomania. More volunteers are needed for the confidential 24-week trial that, the researchers say, has curbed the urge to steal in the majority of patients who have entered the study so far.
“The preliminary results from the first patients to go through the study are even better than we expected,” said Elias Aboujaoude, MD, a clinical instructor in the Department of Psychiatry and Behavioral Sciences and one of the study investigators. “What we have seen so far is very impressive, with 78 percent of the patients responding to the drug in the open-label phase.” The open-label phase is when trial participants are aware that they are taking a particular drug and not a placebo.
Kleptomania, the guilt-ridden, impulsive stealing of inexpensive and unneeded items, often goes untreated as many who suffer from the disorder hesitate to seek help out of fear of being turned in for their illegal activities. More than 1.2 million people in the United States are thought to suffer from kleptomania. The condition differs from shoplifting, in which the action is usually planned, guilt-free and motivated by need or monetary gain. Kleptomania appears to affect more women than men, and the age of onset often dates back to childhood or adolescence.
Although the cause of kleptomania remains unknown, some researchers believe it involves disruptions of the brain neurotransmitter, serotonin. Earlier studies have suggested that a class of medications known as selective serotonin reuptake inhibitors, or SSRIs, can be effective in treating disorders with similar aspects, such as compulsive skin picking or compulsive shopping.
Lorrin Koran, MD, the professor of psychiatry and behavioral sciences who is leading the study, said it is the first double-blind, placebo-controlled test of a medication to treat kleptomania: in this instance, the study is researching the effect of the SSRI escitalopram, which is marketed as Lexapro and has been approved by the Food and Drug Administration for treating major depressive disorder.
SSRIs are being tried for a number of other obsessive compulsive disorders. For example, Stanford researchers have previous shown that the anti-depressant SSRI citalopram reduces the severity of obsessive compulsive shopping disorder.
Since so many people are taking SSRIs (e.g. Prozac, Zoloft, Paxil, Luvox, Celexa) it is quite possible that the incidence of obsessive compulsive disorders has dropped as a side effect of treating millions of people for depression.
BTW, if you are interested in taking SSRIs check out this table of SSRI side effect rates. There is no one SSRI that is best on all side effects for all people. Many depressed people have to try out a few SSRIs before finding one that works best.
Quite a large body of research literature is building in support of the idea that chronic inflammation is a major cause of many degenerative diseases. One of the causes of chronic inflammation is obesity.
In research published in the Sept 21 issue of Circulation, the researchers show for the first time that circulating mononuclear cells -- the body's monocytes (the largest type of white blood cell) and lymphocytes -- exist in a proinflammatory state in obese persons known to be at increased risk of developing diabetes, heart disease or both.
"These cells are creating a lot of nuisance in the obese," said Paresh Dandona, M.D., Ph.D., head of UB's Division of Endocrinology, Diabetes and Metabolism and senior author on the study. "They enter the artery and set up atherosclerosis. They activate fat cells to produce more proinflammatory factors. They interfere with insulin signaling, causing insulin resistance. They even enter the brain."
Husam Ghanim, Ph.D., research associate, is first author on the study.
The good news, said Dandona, is that, based on these findings, the status of mononuclear cells from one blood sample could serve as an easy early-warning system for the risk of developing insulin resistance and circulatory problems.
The research was conducted using fasting blood samples from 16 normal-weight subjects with an average body mass index (BMI) of 22.6 and from 16 obese subjects with an average BMI of 40. All participants had similar glucose levels and were taking no anti-inflammatory medication. The research was conducted at the Diabetes-Endocrinology Center of Western New York located in Kaleida Health's Milliard Fillmore-Gates Hospital.
Mononuclear cells were isolated, and proinflammatory and anti-inflammatory factors within the nucleus and the cell were assayed. The researchers also calculated an insulin-resistance index for each participant, using a standard formula.
Results showed that measures of proinflammatory factors were significantly higher in blood samples from obese subjects than the average weight subjects, while levels of factors that normally inhibit inflammation were significantly lower.
"This proinflammatory state may contribute to insulin resistance," said Dandona, "because the cytokines produced may interfere with insulin action." The index of insulin resistance in the obese subjects was nearly three times higher, on average, than that of the normal subjects, findings showed.
Lose excess weight to lower your level of body-wide inflammation and you will live longer as a result.
The randomized trial was conducted from June 2001 to January 2004 at a university hospital in Italy among 180 patients (99 men and 81 women) with the metabolic syndrome. Patients in the intervention group (n=90) were instructed to follow a Mediterranean-style diet and received detailed advice about how to increase daily consumption of whole grains, fruits, vegetables, nuts, and olive oil; patients in the control group (n=90) followed a prudent diet (carbohydrates, 50 percent-60 percent; proteins, 15 percent-20 percent; total fat, less than 30 percent).
The researchers found that after 2 years, patients in the Mediterranean diet intervention group had significant decreases in body weight, blood pressure, levels of glucose, insulin, total cholesterol, and triglycerides and a significant increase in levels of high-density lipoprotein cholesterol, all of which were greater than those recorded in the control group. Serum concentrations of interleukins 6 (IL-6), 7 (IL-7), and 18 (IL-18) and high-sensitivity C-reactive protein (hs-CRP) were significantly reduced in patients in the intervention group compared with those in the control group. Endothelial function score improved in the intervention group but remained stable in the control group. Forty patients consuming the intervention diet still had features of the metabolic syndrome, compared with 78 patients consuming the control diet. Participants who followed the intervention diet showed a reduction in the number of the components of the syndrome such that the overall prevalence of the metabolic syndrome was reduced by approximately one half.
You can also read the abstract of the Journal of the American Medical Association paper of the previous report.
Elevatation of inflammation marker high-sensitivity C Reactive Protein (hs-CRP) correlates with greater arterial plaque build-up and therefore greater risk of heart disease and other circulatory ailments.
The study of 386 Olmsted County, Minn., residents used transesophageal echocardiography (TEE) to obtain high-quality images of the lining of the aorta, the main artery through which the heart pumps blood to the body. TEE images are clearer than traditional echocardiograms because they come from an ultrasound probe inserted down the throat. This enables imaging of the heart and major blood vessels without interference from the ribs and chest wall.
The researchers found partial blockages, called atherosclerotic plaques, in the aortas of 69 percent of the study subjects, whose median age was 66. The level of high-sensitivity C-reactive protein (hs-CRP), a marker in the bloodstream that indicates inflammation, was the single factor most closely associated with the presence of plaques and their severity.
Emotional states have a large influence on blood levels of C Reactive Protein and the risk of circulatory and heart-related ailments. Anger and depression increase the risks of heart disease .
In earlier studies, Suarez has shown that people who are prone to anger, hostility and depressive symptoms respond to stress with increased production of the stress hormone norepinephrine. Scientific evidence suggests that an increase in this stress hormone activates the inflammatory arm of the immune system and triggers the expression of genes that cause chronic, low-grade inflammation. This inflammation is characterized by high levels of CRP, he said.
"Individuals with these psychological attributes may evaluate their environment in a cynically hostile manner, and thus respond with greater anger, which is often accompanied by mild to moderate symptoms of depression," said Suarez. "These psychological attributes tend to cluster within the same individual, and the clustering of attributes may produce even greater risk than any single trait alone."
Suarez said the levels of depressive symptoms and angry/hostile moods necessary to raise CRP do not constitute psychiatric conditions. "That is, you don't have to be clinically depressed or have extreme and frequent bouts of anger to show higher levels of CRP," he said.
In the Duke study, 121 healthy men and women were asked to complete standard personality questionnaires in which they described their psychological attributes, including anger, hostility and depression. The volunteers did not have any pre-existing conditions -- such as smoking, high blood pressure, diabetes or heart disease -- that would predispose them to having high CRP levels. High-sensitivity blood tests were then conducted to measure CRP levels.Respondents who were prone to anger, had high hostility levels, and showed mild to moderate symptoms of depression had two to three times higher CRP levels than their calmer counterparts. The more pronounced their negative moods, the higher CRP levels they had, the study showed.
The highest levels of CRP were in the range of 1.7 mg/L to 3.0 mg/L. While these levels are still considered relatively low – fever, an active infection, or physical trauma is associated with CRP levels above 10.0/mg/L –CRP levels in this range are associated with a moderate to high risk of heart attacks and strokes, said Suarez.
Stay skinny. Eat great food. Also, be careful with your thoughts since they have a lot of impact upon your body. Avoid anger and depression. Plus, since exercise lowers inflammation markers and brightens the mood working out is good for your mental and physical health.
LOS ALAMOS, N.M., Sept. 16, 2004 -- A University of California scientist working at Los Alamos National Laboratory and researchers from Northrop Grumman Space Technology have developed a novel method for generating electrical power for deep-space travel using sound waves. The traveling-wave thermoacoustic electric generator has the potential to power space probes to the furthest reaches of the Universe.
In research reported in a recent issue of the journal Applied Physics Letters, Laboratory scientist Scott Backhaus and his Northrop Grumman colleagues, Emanuel Tward and Mike Petach, describe the design of a thermoacoustic system for the generation of electricity aboard spacecraft. The traveling-wave engine/linear alternator system is similar to the current thermoelectric generators in that it uses heat from the decay of a radioactive fuel to generate electricity, but is more than twice as efficient.
The new design is an improvement over current thermoelectric devices used for the generation of electricity aboard spacecraft. Such devices convert only 7 percent of the heat source energy into electricity. The traveling-wave engine converts 18 percent of the heat source energy into electricity. Since the only moving component in the device besides the helium gas itself is an ambient temperature piston, the device possesses the kind of high-reliability required of deep space probes.
The traveling-wave engine is a modern-day adaptation of the 19th century thermodynamic invention of Robert Stirling -- the Stirling engine -- which is similar to a steam engine, but uses heated air instead of steam to drive a piston. The traveling-wave engine works by sending helium gas through a stack of 322 stainless-steel wire-mesh discs called a regenerator. The regenerator is connected to a heat source and a heat sink that causes the helium to expand and contract. This expansion and contraction creates powerful sound waves -- in much the same way that lightning in the atmosphere causes the thermal expansion that produces thunder. These oscillating sound waves in the traveling-wave engine drive the piston of a linear alternator that generates electricity.
Note that they are not making any claims for this device as a propulsion system. Nuclear propulsion holds a lot of promise for space both manned and unmanned exploration. But even a more compact power source would allow space probes to either carry more sensors or beam back information at a higher speed or have fancier on-board computers for more complex decision-making.
Antibodies injected into a small number of Alzheimer's Disease (AD) patients appear to have stopped the progression of Alzheimer's by attacking the plaques assocated with the disease.
Immunoglobulins which are already being used to treat multiple sclerosis may also be able to help patients with Alzheimer's. This, at least, is the finding of a pilot study on five patients at the University of Bonn. The results are set out in the forthcoming edition of the Journal of Neurology, Neurosurgery and Psychiatry (vol. 75, pp. 1472-1474), which also devotes its editorial to this discovery.
Immunoglobulins contain, among other things, anti-bodies against a protein which is the 'main suspect' thought to trigger off Alzheimer's. After six months of immuno-globulin doses the concentration of this protein in the patients' cerebrospinal fluid was reduced by one third. The patients' cognitive abilities improved slightly.
Even if the treatment is effective it is not surprising there was not a bigger improvement in cognitive function. AD kills neurons. A halt of the disease progression is still going to leave current AD patients with a lot of brain damage. Even if replacement neurons can eventually be grown a large portion of who an AD sufferer was originally is irretrievably lost.
However, the medical team involved emphasise that their findings are still very tentative. They are now planning a large-scale double-blind clinical trial with about sixty patients so as to further confirm the positive effect of the immunoglobulins.
The cerebral cortex of Alzheimer's patients regularly contains large protein aggregates, what are known as Alzheimer's glands. They predominantly consist of beta-amyloid peptide, a small protein. This peptide collects in the brain of Alzheimer's patients and forms protein deposits which can damage and even destroy the sensitive nerve cells.
A promising approach in combating the disease seems to be the treatment with anti-bodies which are specifically effective against beta-amyloid. Thus, in animal experiments the injection of beta-amyloid anti-bodies led to a reduction in the protein deposits and an improvement in the behavioural deficits in these animals. Another study recently showed that immunising was not only able to reduce amyloid plaques, it also prevented the formation of the abnormal tau protein.
Recently the team led by the Bonn lecturer Dr. Richard Dodel was able to show that every person's blood contains anti-bodies against beta-amyloid, but that the concentration in Alzheimer's patients is markedly lower. Their findings have been confirmed by two US teams. 'There are already anti-body blood preparations which are used for particular diseases of the nervous system such as multiple sclerosis, which are known as immunoglobulins,' Dr. Dodel explains. 'We have now investigated whether these preparations contain anti-bodies against beta-amyloid and if these can be used to fight Alzheimer's.' His team did in fact find anti-bodies in one type of immunoglobulin medication which are very effective specifically against beta-amyloid. In a pilot study carried out on five Alzheimer's patients the team then studied the effect of the immunoglobulins on the progress of the disease. This involved giving the patients an immunoglobulin injection intravenously every four weeks throughout the six-month study. Before beginning and on completing the therapy the researchers determined the beta-amyloid content in the blood and the CSF fluid – the latter being the liquid which is present in the brain and spinal cord. 'On average the beta-amyloid concentration in the fluid decreased in the course of the study by over 30 per cent, while the concentration in the blood rose 2.3 times,' Dr. Dodel says. 'The immunoglobulins therefore seem to have the effect of flushing out the beta-amyloid from the brain' – how exactly this occurs is as yet unclear.
At the same time the team carried out various tests which enabled them to check the cerebral performance of dementia patients. After six months four of the five patients did slightly better than before in what is known as the ADAS-cog test (Alzheimer's Disease Assessment Scale, cognitive subscale). In the MMSE (Mini-Mental State Examination) test three patients improved. 'What is even more remarkable is that none of our test persons deteriorated,' Dr. Dodel explains. 'Without treatment Alzheimer's patients on average score seven to eleven points worse in the ADAS-cog test one year later, and even patients on medication score four to six points worse. In our study they improved on average by 3.7 points.'
These researchers still need to follow up with a larger and double-blind study that they are planning. But if ths treatment could work it would save the minds of tens of millions of people (4.5 million Americans currently suffer from AD) while saving the families of those sufferers enormous amounts of work, money, and a tremendous stress and burden.
This result is not surprising. In a previous study with a vaccine called AN-1792 many of the patients experienced a slowing or stopping of Alzheimer's Disease progression. Unfortunately, 17 out of the 300 patients in that study developed an encephalitis probably caused by an auto-immune response. But if I was an Alzheimer's Disease patient who was just diagnosed (i.e. if I still could reason well enough to make choices) I'd jump at those odds and take the risk of the encephalitis. However, governments do not let us take risks even when we are in the process of losing our minds to a fatal disease.
Another Alzheimer's vaccine appears to work in rhesus monkeys. Also, drugs are under development to block beta amyloid plaque formation.
With the baby-boom generation aging and life expectancy continuing to increase, Alzheimer's disease has become a ticking time bomb. The fastest-growing segment of the population is 85 and older. In Mr. Dillon's age group, 65 to 74, 3 percent have Alzheimer's; in the 85-and-over group, it is a staggering 47 percent, according to the National Institutes of Health.
Absent an effective treatment the number of AD cases is expected to triple by the middle of the 21st century. However, AD is a much more approachable problem as compared to cancer. The proteins that form into plaques that appear to play a vital role in AD development are turning out to be removable via immune system approaches. So I expect that within 20 or 30 years we will have effective treatments to stop AD progress. However, once we can stop the disease that will still leave millions with the brain damaged they suffered before a cure was developed. Also, while effective treatments are probably going to happen in the next couple of decades this is not reason for complacency. We ought to be trying even harder to achieve a cure. Money spent on AD research will pay itself back many times over.
If you want to reduce your risk of AD then my advice is to get lots of omega 3 fatty acids to slow disease progess and plenty of folic acid and vitamin B12 to keep down blood homocysteine which is an AD risk factor. If you are curious to review the literature on AD risk factors check out this list of summaries of AD risk factor studies. Even if some of the controllable factors listed there do not help reduce the risk of AD a diet aimed at those factors will certainly lower the risk of heart disease and stroke. Exercise helps lower Alzheimer's Disease risk too.
The city of Chicago is going to take the video feeds from 2000 existing cameras and 250 new cameras and send the streaming video through image processing software that will be able to recognize a large assortment of potential security and crime threats as well as identify people who need help for a variety of reasons. (same article here)
Sophisticated new computer programs will immediately alert the police whenever anyone viewed by any of the cameras placed at buildings and other structures considered terrorist targets wanders aimlessly in circles, lingers outside a public building, pulls a car onto the shoulder of a highway, or leaves a package and walks away from it. Images of those people will be highlighted in color at the city's central monitoring station, allowing dispatchers to send police officers to the scene immediately.
Of course this report provides no indication of how well this software works in each of the scenarios cited above. How many false positives and false negatives will it generate in each case? Anyone reading this have any first hand knowledge of how well this stuff works in practice? It doesn't have to be perfect to be useful. Even with a substantial error rate the software is likely to increase the productivity of the people who are employed watching video feeds from cameras located around the city of Chicago.
If the software picked up suspicious behavior, a staff member in the city's Office of Emergency Management would be alerted and could then notify police, medical personnel or a tow truck - whatever the situation called for.
With time the software will no doubt get better while cameras, computers, and fiber optic networks get cheaper. The function of watching the video feeds which is now done by humans and is probably the most expensive part of any monitoring system (anyone know for sure?). Therefore, as the threat and problem recognition software becomes more sophisticated that will drive down costs and enable much wider spread use of monitoring cameras. Now, you may be biterly opposed to the spread of such cameras. But my guess is that as automation lowers costs their use will grow by leaps and bounds. So far there just has not been much significant public opposition.
Officials estimate the first phase of the project will be completed by spring 2006.The $5.1 million project will be funded through a federal homeland security grant and will be the city's first initiative to integrate intelligent video surveillance under one roof.
My prediction: Use of video cameras for monitoring public places will grow by orders of magnitude.
Men and women differed in their participation in reproduction, the researchers report. More men than women get squeezed out of the mating game. As a result, twice as many women as men passed their genes to the next generation.
"It is a pattern that's built up over time. The norm through human evolution is for more women to have children than men," said Jason Wilder, a postdoctoral fellow in UA's Arizona Research Laboratories and lead author on the research articles. "There are men around who aren't able to have children, because they are being outcompeted by more successful males."
Co-author Michael Hammer, a research scientist in UA's Arizona Research Laboratories, said, "We may think of ourselves as a monogamous species, but we're coming from an evolutionary history that's probably slightly polygamous. If we're shifting toward monogamy, it's so recent it hasn't left an imprint on our genome."
Or the same reproductive behavior is continuing, but in a culturally accepted fashion, Wilder said. "The modern version that we generally don't find offensive is that men tend to remarry and have more children much more often than women do."
The team's research also overturns the long-accepted idea that, on average, women's genes traveled farther from their birthplace than did men's. That idea was based on a common marriage practice called patrilocality, wherein women tended to move from their natal village to their husbands' village.
If anything, men and their genes moved farther overall, the new research indicates.
To sort out how far men and women's genes traveled, the UA researchers used DNA from the Y chromosome, which is passed from father to son. Women's lineages were traced using mitochondrial DNA, which passes from mother to daughter.
The researchers report their findings in two related articles, one in the online early edition of the October issue of Nature Genetics and one in an upcoming edition of Molecular Biology and Evolution. The research was funded by the National Institutes of Health.
Scientists have puzzled over the fact that men's common ancestor, dubbed Y-chromosome Adam, seems to have lived around 100 thousand years ago, whereas women's common ancestor, known as mitochondrial Eve, lived almost 200 thousand years ago.
Worldwide, the DNA from the Y chromosome has much less genetic variability than does mitochondrial DNA.
"We wanted to know what shapes the patterns of Y-chromosome and mitochondrial DNA variation," said Wilder. "What can we learn about human behavior?"
To find out, Wilder, Hammer and Zahra Mobasher, a research specialist at UA's Arizona Research Laboratories, tested Y-chromosome DNA and mitochondrial DNA from three far-flung populations of humans: the Khoisan of southern Africa, Mongolian Khalks and highland Papua New Guineans. For each group, DNA from 24 or 25 people was tested.
Previously, researchers assumed equal numbers of men and women procreated. Based on that assumption, scientists explained the relative youth and low variability of the Y chromosome by suggesting that a beneficial mutation on the Y had swept through the whole world. However, the genetic patterns the UA researchers found contradicts those ideas.
If a beneficial mutation had swept through the males, men's common paternal ancestor would be the same age no matter where the UA researchers looked. Instead, the age of men's common ancestor differs between the southern African, Mongolian and Papua New Guinean populations studied. The finding tends to rule out some global beneficial mutation as the reason Y-chromosome DNA is less variable than mitochondrial DNA.
"Because we don't think the pattern we see was caused by an event that swept across the globe, we had to re-examine our assumptions about whether equal numbers of men and women are mating," Wilder said.
The team thinks the genetic patterns are all about sex.
Or lack thereof. Lots more men than women are childless, and it has ever been thus, the researchers say.
My guess is that the legalization and increasing use of divorce has increased the gap between what percentage of women and what percentage of men manage to reproduce in each generation. The most sucessful men have a legally sanctioned way to have a series of wives while the least successful men become street people. Nature is harsh. Why we refer to such an unforgiving and brutal reality as mother nature is beyond me. What is loving and kind about natural selection and evolution in action? Nothing that I can see.
In the longer run people will genetically engineer their offspring. So they will voluntarily reduce the amount of their genetic sequences that they pass along to their offspring. Also, some will clone themselves as a way to increase the amount of their own DNA that they pass along.
Update: Greater female reproductive success is likely to accelerate for another reason. Selective abortion of female fetuses is creating a shortage of female births and adult women in China, in Taiwan, and in India. This trend will probably spread to additional countries as well. A shortage of females will very likely select for genes carried by males who become more successful. Genetic variations that select for intelligence, drive, and a certain degree of masculine aggressiveness will likely be selected for. Physical attractiveness will be selected for more strongly as well. Out-going personalities might also be getting selected for.
Once non-genetic factors such as age, illness, or smoking were removed, a subset of the group seemed to have a blood-oxygen concentration that was 10% higher than normal. This trait was inherited in a way that suggested the difference was due to a single gene.
The researchers also found that the children of women with this putative gene are much more likely to survive to the age of 15, when they are old enough to have children of their own. In the low-oxygen group, each woman had on average 2.5 children that died during childhood. In the high-oxygen group, that average was just 0.4.
The fact that this genetic variation (which has not yet been identified) is under such active selection suggests that it is a variation of fairly recent vintage. A successful adaptation that has been around for a long time in some ecological niche will tend to be present in all organisms of the species which are in that niche unless they have only recently entered that niche. Of course, human conquest where one group wipes out most of another group in some niche could bring the invader group into the niche that the conquered group is already adapted to (even if the conquered group was not well enough adapted to warfare). So the adaptation could have been around for a long time and yet still happen to be getting rapidly selected for in the present time.
Human populations in less developed areas are not the only human groups still undergoing changes in frequencies of genetic variations due to natural selective pressures. All humans are still subject to selective pressures. Darwinian natural selection has not stopped in industrialized countries. What has changed is what is being selected for or against (e.g. intelligence is currently being selected against unfortunately).
The three major human population groups living at high altitudes in Ethiopia, the Himalayas, and the Andes have developed three different sets of adaptations to high altitude living. One reason that their sets of adaptations are different is likely just plain chance. But another reason is that they have not all been living at high altitudes for the same length of time. Initial genetic adaptations are usually not as ideal as adaptations that arise over longer periods of time.
The Andeans, whose lowland ancestors migrated from Asia perhaps 16,000 years ago, adjust to altitude essentially the same way as any lowlander would today -- and it is not a perfect solution.
"Creating more red cells is a pathological response," said Temple University anthropologist Charles Weitz. "If you have too many red cells, the blood's too thick, and it's like pumping oil. Eventually you have to move downhill."
By this same argument athletes who use erythropoietin (EPO) to boost their red blood cell counts are like evolutionary primitives. In the future better understanding of genetic variations for high altitude living will allow athletes to become more like Ethiopians or Himalyan Tibetans.
All of the Tibetans had significantly higher levels of a free radical-fighting enzyme, or antioxidant, called glutathione-S-transferase, and another enzyme, enoyl coenzyme A hydratase, that improves cellular energy production. Tibetans also possessed fewer mitochondria, which are the power manufacturers of cells.
Anthropologist Cynthia Beall of Case Western Reserve University said that Tibetans breathe more per minute than people who live at sea level. Andes residents are able to hold more oxygen in their blood.
Healthy sea-level dwellers have saturations of oxygen in their bloods that vary from 92-100 percent. In the Amabaras sample, the oxygen saturation averaged 95 percent, which surprised Beall, because the oxygen saturation in the Andean and Tibetan highlanders at similar altitudes was in the mid to high 80s.
Of course, once gene therapies and stem cell therapies become feasible then people will be able to have their choice of the best Himalayan and Ethiopian high altitude genetic enhancements. Some will use these enhancements for distance running. Others will enhance in order to do mountaineering. Expect to see extreme mountaineers use genetic engineering to so enhance their oxygen processing capacity that they will be able to easily climb Mount Everest without using supplemental oxygen and without suffering oxygen deprivation symptoms.
In a study published September 10, 2004, in the online edition of the Annals of Neurology, scientists describe a patient who lost all dreaming, and very little else, following a stroke in one distinct region of the brain, suggesting that this area is crucial for the generation of dreams.
"How dreams are generated, and what purpose they might serve, are completely open questions at this point. These results describe for the first time in detail the extent of lesion necessary to produce loss of dreaming in the absence of other neurological deficits. As such, they offer a target for further study of the localization of dreaming," said author Claudio L. Bassetti, M.D., of the Department of Neurology at the University Hospital of Zurich in Switzerland.
These unique scientific observations began with an unfortunate event: a stroke suffered by a 73-year-old woman. When blood flow was disrupted to a relatively small area deep in the back part of her brain, she lost a number of brain functions.
Most of these disabilities were related to vision, which was not unexpected, since one of the brain functions localized to this area of the brain is the processing of visual information.
Fortunately, within a few days of the stroke, the visual problems had gone away. But a new symptom emerged: The patient stopped dreaming.
Such loss of dreaming--along with visual disturbances--following damage to a specific part of the brain goes by the name Charcot-Wilbrand syndrome, named for the eminent neurologists Jean-Martin Charcot and Hermann Wilbrand, who first described it in the 1880s.
The syndrome is quite rare, especially cases that lack symptoms other than dream loss. Bassetti, then at the University of Bern, and his colleague Matthias Bischof, M.D, realized that this woman's misfortune might provide valuable answers to the localization of dreaming in the brain.
For six weeks following the stroke, the researchers studied the patient's brain waves as she slept. They found no disruptions in her sleep cycle. The fact that REM sleep continued normally was significant, because dreaming and REM sleep occur together, though research has pointed to different brain systems underlying the two. These results appear to confirm that dreaming and REM sleep are driven by independent brain systems.
Before the stroke, the patient recalled, she had experienced dreams three to four times a week. She now reported no dreams, even when awakened during REM sleep.
With time, some dreaming function did return. A year after the stroke, she experienced occasional dreams, but no more than one per week. The dreams were of a reduced vividness and intensity compared to before the stroke.With MRI scans, Bischof and Bassetti determined that the stroke had damaged areas located deep in the back half of the brain. Recent research has shown that some of this region is involved in the visual processing of faces and landmarks, as well as the processing of emotions and visual memories, a logical set of functions for a brain area that would generate or control dreams.
But more interesting than the location is the fact that everything else about the woman seemed to be normal. She showed no signs of any problems with memory, attention or any other mental abilities, and beyond a few visual disturbances in the first few days, normal vision. “She has no other cognitive problems after a full clinical assessment,” says Bassetti. “She has a normal visual imagination.”
But did this woman really not lose any cognitive function other than the ability to dream? Can she form long term visual memories as well now as she could before the stroke? Since her cognitive abilities were not measured in detail before the stroke we can't be certain that she didn't lose any cognitive abilities.
At present, the functions of REM sleep are as elusive as those of dreaming. Adults spend a quarter of their nightly slumber in REM sleep, scattered throughout the night. The remaining time is spent deeper in unconsciousness. So REM may simply bring the brain back from deep sleep periodically to help us wake up if we need to, says Horne.
So then do people who don't experience REM sleep wake up more slowly than those who have REM episodes in sleep?
The images obtained from the astronomy test station at Dome C, 75° south and 3260 metres above sea level, were up to three times sharper and six times brighter than those from the best mid-latitude observatories, including those in Hawaii and Chile. On some nights, the images were almost as good as those from the Hubble Space Telescope.
Some astronomers would like to build a very large telescope at this site. Others would like to build a pair of infrared telescopes at the site and use them to search for planets.
Space is a very expensive place to do anything. Even a land-based telescope in Antarctica could be reached for a small fraction of the cost of a maintenance trip to Hubble. Buidling telescopes at this Antarctic site sounds like a great idea.
UCLA neuroscientists have shown for the first time that a diet high in the omega-3 fatty acid DHA helps protect the brain against the memory loss and cell damage caused by Alzheimer's disease. The new research suggests that a DHA-rich diet may lower one's risk of Alzheimer's disease and help slow progression of the disorder in its later stages. The journal Neuron reported the findings on Sept. 2.
"This is the first proof that our diets affect how our brain cells communicate with each other under the duress of Alzheimer's disease," said Greg Cole, senior author and a professor of neurology at the David Geffen School of Medicine at UCLA. "We saw that a diet rich in DHA, or docosahexaenoic acid, dramatically reduces the impact of the Alzheimer's gene.
"Consuming more DHA is something the average person can easily control," added Cole, associate director of the UCLA Alzheimer's Disease Research Center. "Anyone can buy DHA in its purified form, fish-oil capsules, high-fat fish or DHA-supplemented eggs."
Cole and his colleagues focused on Alzheimer's damage to synapses — the chemical connections between brain cells that enable memory and learning.
By using mice bred with genetic mutations that cause the brain lesions linked to advanced Alzheimer's disease, the UCLA researchers created a mouse model to test environmental risk factors for the disorder. When the mice developed the lesions, but showed minimal memory loss or synaptic brain damage, however, the scientists took a closer look at the animals' diet.
"We discovered that the mice lived on a nutritious diet of soy and fish — two ingredients chock-full of omega-3 fatty acids," said Sally Frautschy, co-author and an associate professor of neurology at the school.
"Because earlier studies suggest that omega-3 fatty acids may prevent Alzheimer's disease, we realized that the mice's diet could be countering the very thing we were trying to accomplish — showing the progression of the Alzheimer's-related brain damage," she said.
The UCLA team swapped safflower oil for the soy and fish to create an unhealthful diet depleted of omega-3 fatty acids. They divided the animals into two sets of older mice, which already showed brain lesions but displayed no major loss of brain-cell activity. The researchers placed both groups on the new diet, but fed the second group DHA supplements from algae.
After five months, the researchers compared each set of mice to a control group that consumed the same diet but did not carry the Alzheimer's genes. The results surprised them.
"We found high amounts of synaptic damage in the brains of the Alzheimer's-diseased mice that ate the DHA-depleted diet," Frautschy said. "These changes closely resembled those we see in the brains of people with Alzheimer's disease."
Although the mice on the DHA-supplemented diet also carried the Alzheimer's genes, they still performed much better in memory testing than the mice in the first group.
"After adjusting for all possible variables, DHA was the only factor remaining that protected the mice against the synaptic damage and memory loss that should have resulted from their Alzheimer's genes," Cole said. "We concluded that the DHA-enriched diet was holding their genetic disease at bay."
The present results provide, for the first time, evidence that the combination of genetic (mutant human APP) and environmental risk factors (dietary essential fatty acids) for AD can act synergistically to quantitatively reduce synaptic proteins, specifically, dendritic scaffold proteins, that are critical for cognition as evidenced by memory deficits observed in the Morris water maze paradigm," wrote the researchers.
"The results show a dramatic impact of diet on the expression of the AD-related postsynaptic marker phenotype and provide new insight into how essential fatty acid intake may modulate the expression of neurodegenerative diseases, including AD," they wrote.
The researchers also wrote that their findings "suggest that patients bearing a genetic risk of AD may be more vulnerable to a lack of essential fatty acids," which tend to be reduced in the brain both in normal aging and AD. They concluded that their findings "support the idea that increased DHA intake should be considered as a potential neuroprotective strategy for AD."
Omega 3 fatty acids are not the only nutrients that have been found to slow Alzheimer's Disease progression in mice genetically engineered to develop the disease. Dr. James Joseph, associate professor of nutrition and chief of the Neuroscience Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts Univesity has found that blueberries help maintain normal cognitive function in mice genetically engineered to develop Alzheimer's.
Joseph continues to research the benefits of blueberries, which, among other things, have been found to improve memory. Collaborating with researchers at the University of Florida, Joseph is working worked with double-transgenic mice that have been genetically programmed to have Alzheimer's disease. When fed a diet of blueberries for 11 months, the mice's Y-maze performance was normal, and he recorded in them a higher level of expression of enzymes associated with signal transduction than in the control group.
"Either directly or working as an antioxidant, the diet appears to have an effect on synaptic plasticityÑthe signal transduction or communication between neurons," says Joseph.
The challenge, then, is to find a way to make a blueberry fish dish. I personally find that pineapple works mixed in as a flavoring with salmon. Haven't tried blueberries and salmon yet.
DALLAS – Sept. 14, 2004 – Prolonged and sustained endurance training prevents stiffening of the heart, a condition associated with the onset of heart failure, according to researchers at UT Southwestern Medical Center at Dallas.
The researchers also report that a sedentary lifestyle, in addition to aging, puts older people at risk for heart failure, the leading cause of hospitalizations for patients over 65 and a condition that affects eight out of every 1,000 people older than 70.
Their findings are available online and will be published in the Sept. 28 print edition of Circulation.
"It appears that lifelong exercise training completely prevented the stiffening of the heart muscle that has been thought to be an inevitable consequence of aging. We found that it is aging in addition to being sedentary," said Dr. Benjamin Levine, professor of internal medicine and senior author of the study.
"If people can train and sustain it, a huge impact will be made on one of the biggest scourges of the elderly, which is heart failure with a normal ejection fraction, also called 'diastolic heart failure'. The overall health of the population would radically improve if a larger number of people would make exercise a part of their daily life."
About 40 percent of all hospitalizations for heart failure in patients 65 and older are due to diastolic heart failure, a condition in which the heart appears to pump normally. It appears to occur as a result of stiffening of the heart muscle, causing excess fluid to accumulate in the lungs, feet, ankles and legs.
The researchers measured the function and compliance of the left ventricle (the heart's main pumping chamber) in the study participants. Twelve healthy but sedentary seniors (all about 70 years old), 12 Masters athletes (average age of 68) and 14 young, sedentary controls, (average age of 29) were tested. Six of the Masters athletes, who participate in events from swimming to track, were nationally ranked competitors and six were regional champions. Sedentary participants had not engaged in regular endurance exercise throughout their life.
The researchers tested whether left ventricular compliance decreased with aging alone, or if physical inactivity contributed equally to this process.
"We found that the older, sedentary individuals' hearts were 50 percent stiffer than the Masters athletes, which we expected," said Dr. Levine, medical director of the Institute for Exercise and Environmental Medicine, a collaboration between UT Southwestern and Presbyterian Hospital of Dallas. "But what we didn't expect was that the hearts of these senior athletes were indistinguishable from those of the healthy younger participants.
"That specific finding led us to conclude that a sedentary lifestyle is associated with a decline of ventricular compliance and prolonged, sustained endurance training preserves ventricular compliance and may reduce the high incidence of heart failure in the elderly."
Exercise will provide a large benefit even if started later in life.
Dr. Levine and his collaborators have already designed an endurance-training program for several of the elderly, sedentary study participants, which has already yielded dramatic results.
"About two-thirds of the sedentary, elderly participants have trained for a year and there is already improvement in their cardiac compliance. Their hearts are more muscular and more flexible," Dr. Levine said.
A sedentary lifestyle is detrimental to one's health, but starting and sticking with an endurance-training program plays a major role in reversing the damage done to the heart, even if that program is initiated later in life, he added. Most of the Masters athletes were not elite athletes when they were younger, Dr. Levine pointed out. In fact, most of them did not start training until they were in their 30s.
Exercise also raises blood HDL cholesterol levels. So you can also reduce your risk of artery clogging by exercising. My advice: Get a dog that likes to run and obey his daily entreaties to get out there and run like a dog.
Well, as Gilda Radner playing Roseann Roseannadanna used to say "its always something". The Christian Science Monitor has an article on the dangers posed to marine organisms by rising levels of carbonic acid formed by carbon dioxide dissolving into the oceans.
By the middle of the next century, for example, coral reefs in shallow waters could lose up to 30 percent of the calcium carbonate they need to build their structures, calculates an international research group led by Joan Kleypas, a marine biologist at the National Center for Atmospheric Research in Boulder, Colo. That could lead to stunted growth or other effects, which could make them more vulnerable to erosion or storm damage.
Also, increased CO2 levels caused key plankton species to create badly formed or incomplete calcium carbonate shells, according to a team led by Ulf Riebesell with the Alfred Wegener Institute for Polar and Marine Research in Bremerhaven, Germany. In lab experiments the ratio of shell to the rest of the organism dropped by as much as 52 percent.
Here is yet another report claiming yet another harm caused by carbon dioxide emissions produced by burning fossil fuels. What to do about it? Suppose atmospheric carbon dioxide build-up is going to cause even a quarter as many problems as the alarmists claim then isn't the most sensible and cost-effective response to spend money on basic research into energy technologies that will reduce or stop the emissions of carbon dioxide or even remove it from the atmosphere? Cheaper and cleaner energy technologies would displace fossil fuels without any regulatory interventions. No international treaties or international disputes about emissions would be needed.
There are historical parallels for cheaper cleaner technologies displacing more expensive and dirtier technologies. The displacement of coal for heating by oil and natural gas was driven by cost and convenience. No one wanted to wake up and shovel coal into their house heater in the morning or to clean out the accumulated ash or pay for chimney sweeps.
A regulatory response to the problem of carbon dioxide emissions would be incredibly expensive with total costs running into the hundreds of trillions of dollars. Contrast with this an alternative approach: spend major research bucks (Nobelist Richard Smalley argues for $10 billion a year which is a huge sum for basic research) to develop energy technologies that will be cheaper than fossil fuels and far less polluting.
Over on the Crumb Trail blog back40 argues that Richard Smalley may be advocating premature choosing of potential technological winners in energy technologies. However, I do not see Smalley's approach to energy funding through grants to basic researchers as likely to suffer from that problem. Obviously large major categories of research have to be chosen. But that is the case with, for example, NSF and NIH funding where the agencies have many subcategories of research in which researchers can apply for grants. It is easy to imagine, say, a category for photovoltaic thin films and another for photovoltaic nanotubes. Similarly, one can imagine a few subcategories for batteries and fuel cells. At a $10 billion a year funding level broken out across many categories it seems unlikely any major area of promising research would be neglected.
Even if the scale of the carbon dioxide accumulation problem is exaggerated that is not an argument against obsolescing fossil fuels. The displacement of fossil fuels through new energy technologies would provide a number of other benefits including lowering costs of energy, a reduction of a variety of pollutants that really do cause harm (e.g. particulates, mercury, sulfur oxides, and ground level ozone), and a reduction in the flow of money into Middle Eastern countries where it funds terrorism and the spread of Wahabbi and Salafist Islam. A regulatory approach to carbon dioxide emissions reduction would provide much less of each of these other benefits.
Imperial College of London psychologist John Gruzelier used hypnosis on 12 patients resistant to hypnosis and 12 susceptible to hypnosis while watching their brains with functional Magnetic Resonance Imaging (fMRI) and gave them orders to follow. The hypnotically suspectible showed a difference in brain activity in the anterior cingulate gyrus and in the left prefrontal cortex of the brain.
But under hypnosis, Gruzelier found that the highly susceptible subjects showed significantly more brain activity in the anterior cingulate gyrus than the weakly susceptible subjects. This area of the brain has been shown to respond to errors and evaluate emotional outcomes.
The highly susceptible group also showed much greater brain activity on the left side of the prefrontal cortex than the weakly susceptible group. This is an area involved with higher level cognitive processing and behaviour.
Gruzelier also suspects that hypnotism may interfere with subjects' evaluation of future emotions such as embarrassment. A region in the brain's medio-frontal cortex, close to the anterior cingulate, governs our perception of how we will feel if we take a certain course of action, he says. If connections between the two regions are impaired, stage volunteers might happily act without thinking.
Professor John Gruzelier, from Imperial College London, said: “We have a magnificent therapeutic tool which is being ignored because there’s no evidence of the mechanism involved. Now we’re getting evidence of the mechanism and we hope people will take it more seriously.”
Last year, Stanford University psychiatric researcher David Spiegel used positron emission tomography (PET) scans to watch changes in brain function in volunteers who were highly hypnotizable.
The hypnotized volunteers were told to see colour. Then, regardless of whether or not the researchers showed them colour, the areas of the visual cortex that registers colour would fire. When the researchers told them to see "grey" objects, the volunteers had less activity in the colour zones of the brain.
Of course the development of greater understanding the mechanisms underlying hypnosis will inevitably lead to the development of more powerful and reliable techniques for invoking hypnotic states even in people who can not now be hypnotized. That, in turn, will inevitably lead to abuses of the techniques. Imagine a police state that brings in its citizens, invokes hypnotic states, and then feeds them with all sorts of suggestions about what they should believe and do. Imagine brain implants that can be used to remotely trigger a hypnotic state. Technology enhances the ability to carry out both good and evil acts.
Dr. Leonid A. Gavrilov and Dr. Natalia S. Gavrilova have a new article out in the IEEE Spectrum on their reliability engineering approach to understanding aging.
If only we could maintain our body functions as they are at age 10, we could expect to live about 5000 years on average. Unfortunately, from age 11 on, it's all downhill!
The problem is that our bodies deteriorate with age. For most of our lives, the risk of death is increasing exponentially, doubling every eight years. So, why do we fall apart, and what can we do about it?
They go on to explain how engineering reliability theory can be applied to understanding how humans age and die. One of their conclusions is the same position argued for by rejuvenation advocates: we need to develop the ability to grow replacement parts and to do more kinds of repairs.
Their point that we start increasing our risk of dying of aging from about age 11 is demonstrated by a recent study led by Dr Faisal Khan of the University of Dundee in the UK. Dundee and colleagues found that children as young as 11 years old already show signs of endothelial cell dysfunction that will contribute to the development of heart disease and other circulatory diseases.
“This is the stage of life where changes to a person’s body are potentially reversible,” says lead researcher Faisal Khan at the University of Dundee, UK. “If you leave it until their 30s or 40s, it is much harder.”
Khan and his colleagues studied the lining of tiny blood vessels, or endothelium, in 158 Scottish children, aged 11 to 14. Within this group, 20% of children showed impaired endothelial activity.
In some children capillaries failed to expand in response to drug exposure.
The researchers rubbed a drug through their skin to make their blood vessels expand. The vessels were then monitored using a laser.
In about 20 per cent of children, the tiny capillaries and arteries failed to expand, suggesting that the cells lining the vessels, a layer called the endothelium, was damaged. Endothelial cells control a vessel's ability to contract and dilate.
Problems in the cells that make up endothelium can lead to progressive hardening and narrowing of blood vessels, called atherosclerosis, which can ultimately lead to cardiovascular diseases.
The rate of malfunction of epithelial cells is higher in obese kids. Even in youth bad diets begin the process of accumulation of aging damage. It is never too soon to start eating a healthful diet.
How many defects we are born with determines how much redundancy we have to start out with in all our bodiy systems. We all start out with a different total number of microscopic errors in our bodies at birth. From that point on the rates at which we accumulate more damage varies from person to person and under different living conditions. There is some amount of randomness as to where the damage occurs.
We are actually better off if the damage accumulation is more evenly spread. If the damage accumulation is concentrated in a sinlge essential component then that component will fail sooner and kill us sooner.
We need better ways to slow damage accumulation. But even more so we need techniques for doing repair and replacement. Cell therapy, growth of replacement organs, and techniques for getting rid of accumulated junk are just a few of the several Strategies of Engineered Negligible Senescence that could fix our accumulated damage and restore redundancy to our aging body parts.
Psychologists Elaine Duncan of the Glasgow Caledonian University and David Sheffield of Staffordshire University compared a group of people who kept regular diaries to a group that did not and found that diarists are more socially awkward, have more headaches, digestive problems, and other problems.
Statistically, the diarists scored much worse on health measures than the non-diarists. And worst affected of all were those who had written about trauma. “They were most susceptible to headaches and the like,” says Duncan.
Are those who decide to write diaries more prone to mental and physical unhealthiness in the first place? The fact that diarists who have written about trauma do worse than those who haven't suggests that it is the diary writing that is causing the health effects.
This result reminds me of the controversy over the question of whether post-trauma debriefing by counselors is beneficial for trauma victims. The results of a number of studies have been mixed. At best debriefing where victims are made to think through and discuss traumatic events probably has no value for most victims. At worst it may be causing the painful memories to have an even greater harmful effect upon mental health.
Malachy Corrigan, the director of the Counseling Service Unit of the New York City Fire Department, was once a proponent of debriefing—but months before the September 11th attacks he decided that it was generally not a beneficial technique. “Sometimes when we put people in a group and debriefed them, we gave them memories that they didn’t have,” he told me. “We didn’t push them to psychosis or anything, but, because these guys were so close and they were all at the fire, they eventually convinced themselves that they did see something or did smell something when in fact they didn’t.” For the workers in the pit at Ground Zero, Corrigan enlisted other firefighters to be “peer counsellors” and to provide moral support and educational information about the possible mental-health impact of sustained trauma.
We are probably better off letting traumatic memories fade. If the memories are clear we can recall them and relive them and suffer pain from thinking about them.
These results bring up an interesting possibility: Will future biotechnologies that enhance memory formation increase the incidence of mental health problems as people become more able to recall painful experiences? Of course, if that turns out to be the case then there is an obvious counter: selective memory erasure. While I argue that for practical reasons we can't be allowed to have an unlimited right to memory erasure there could be considerable therapeutic benefit from the erasure of particularly traumatic memories. Some scientists argue that after initial memory consolidation takes place it may be possible to recall memories and then interfere with their reconsolidation as a way to erase recalled memories. Until we develop that capability it is probably wisest to avoid dwelling excessively on painful memories. Perhaps diaries should only be written to on happier days. Also, live in ways that reduce your odds of having traumatic or otherwise unhappy experiences so that bad memories don't need to be forgotten in the first place. Don't worry. Be happy.
The naturally occurring mineral serpentine sequesters carbon dioxide very slowly over eons. Some Penn State researchers have found that by dissolving serpentine in sulfuric acid they can produce compounds that will very rapidly bind to carbon dioxide.
The metamorphic mineral serpentine -- or magnesium silicate hydroxide -- is composed of magnesium, silicon and oxygen and is plentiful. He researchers used material from the Cedar Hills quarry on the Pennsylvania/ Maryland border for this study, but the mineral is available in large quantities in many places. The U.S. deposits of the minerals that can be used for this process – serpentine and ovivine – can sequester all the carbon dioxide emissions produced from fossil fuels.
"Previous researchers investigating serpentine for use in sequestering carbon dioxide have crushed serpentine very finely, to sizes smaller than beach sand, but, even at these small sizes, it takes high temperatures to speed up the reaction, "says Maroto-Valer. "With our method, we do not need to crush it that fine and we do not need high temperatures. In fact, the reaction gives off heat. Our method is much less energy expensive."
They aren't done developing this method to the point of being practically useful. Also, there is no big push in the United States at this point to reduce carbon dioxide emissions. Still, this could turn out to be a useful technique if global warming is eventually proven to be a serious problem.
They crush serpentine, dissolve it in sulfuric acid, treat part of it with sodium hydroxide, and the result will react with carbon dioxide to produce magnesium carbonate or magnasite.
The researchers, who also include John M. Andresen, director of the Consortium for Premium Carbon Products from Coal (CPCPC), the Energy Institute; Yinzhi Zhang, post doctoral fellow, the Energy Institute; Matthew E. Kuchta, graduate student in geo-environmental engineering, all at Penn State; and Dan J. Fauth, U.S. Department of Energy's National Energy Laboratory in Pittsburgh, dissolved the crushed serpentine in sulfuric acid.
When serpentine dissolves in sulfuric acid, the silicon in the mineral becomes silicon dioxide, or sand, and falls to the bottom, while the magnesium becomes magnesium sulfate. Treating some of this magnesium sulfate with sodium hydroxide also creates some magnesium hydroxide. The researchers were able to convert large amounts of the serpentine's magnesium to these chemicals providing large surface areas for reactions to occur in solution at room temperature.
Carbon dioxide passed through the solution of magnesium sulfate and magnesium hydroxide converts both to magnesium carbonate or magnesite, which becomes a solid and falls to the bottom. This solid can be used to manufacture construction blocks and there is also a small market for hydrated magnesium carbonate in the cosmetics industry. The silicon dioxide can be used to remove sulfur dioxide from the flue gases, which can subsequently be converted to sulfuric acid to use in the first part of the process.
"The high surface area of the silicon dioxide makes it a natural sorbent for capturing more carbon dioxide and sulfur dioxide," says Maroto-Valer.
Suppose coal can be made to burn extremely cleanly without even generating carbon dioxide emissions. Add in future advances in battery technology that make batteries light enough and cheap enough to be used in electric cars. Then at some point we might burn coal to supply electricity to charge batteries in electric cars.
Psychologist Alan Slater of Exeter University showed pictures rated by adults as being more or less attractive to babies which were, on average, 2 and a half days old and found that babies invariably stared longer at faces which adults had rated as more attractive.
Babies are born with an eye for beauty. Infants only hours old will choose to stare at an attractive face rather than an unattractive one - and they also prefer to listen to Vivaldi straight, rather than Vivaldi backwards.
According to Alan Slater, a developmental psychologist at the University of Exeter, humans may have a biologically ingrained preference for beauty.
As Steven Pinker has argued we are not blank slates! Here's yet another report that is a nail in the coffin of the blank slate myth. Attraction to beauty is an instinctive trait that is present from birth.
Dr Alan Slater, a psychologist at Exeter University, said this proved that attraction to better-looking people was an instinctive human trait, something we are all born with.
"It used to be thought that new-born babies came into the world as a totally blank sheet of paper on which experience will then write," he said yesterday. "But what we are finding more and more is that babies are born with a number of in-built mechanisms that help them to organise and make sense of their newly-perceived world - and one of these is that they display an attractiveness effect."
Another preference present from birth is the ability to appreciate Vivaldi played forward. But then why is it that I didn't come to recognize and appreciate his Seasons until I was well into adulthood?
In a baby's mind, these beautiful faces may represent the stereotypical human face, says Slater, which they have evolved to recognise. Such built-in information helps babies learn quickly including the ability to pair faces with sounds like voices.
"Attractiveness is not simply in the eye of the beholder, it is in the brain of the newborn infant right from the moment of birth and possibly prior to birth," the University of Exeter researcher said.
In spite of the huge number of nails now splintering the Blank Slate coffin into toothpicks some diehard defenders keep soldiering on fighting for the myth that humans are only products of their social environments. See Godless Capitalist's most recent encounter with one of these intellectual dinosaurs in GC's post In which a Lewontinite is introduced to the 21st century. Secular faiths can be just as strongly held as religious ones.
Reka Albert, an assistant professor of physics at Penn State, has led a team examining the national electrical grid in the United States to look for vulnerabilities and her team has found that failures in a fairly small portion of the network can lead to a major disruption. (same article here)
"Our analysis indicates that major disruption can result from loss of as few as two percent of the grid's substations," says Albert, whose research team includes Istvan Albert, research associate in the Bioinformatics Consulting Center at Penn State, and Gary L Nakarado at the National Renewable Energy Laboratory. One implication of the research is that identification of strategic points in the grid system can enhance defense against interruptions, whether by equipment failure, natural disasters, or human activity. Major blackouts caused by failures in the grid, such as the one that affected the northeastern part of the country during the summer of 2003, incur tremendous economic, public-health, and security risks.
The study, titled "Structural Vulnerability of the North American Power Grid," was published in a recent issue of the journal Physical Review E. The researchers constructed a model of the entire transmission grid with over 14,000 "nodes," including generators, transmission substations, and distribution substations, and over 19,000 "edges," corresponding to the high-voltage transmission lines that carry power between the nodes. They measured the importance of each substation node based on its "load," or the number of shortest paths between other nodes that pass through it. "While 40 percent of the nodes had a load below one thousand, the analysis identified 1 percent of the nodes--approximately 140--that have a load higher than one million," Albert says.
However, the grid quickly becomes disconnected when the high-load transmission substations are selectively removed from the system--if the nodes that have the highest load are removed first, followed progressively by the nodes with successively lower loads. According to the model, a loss of only 4 percent of the 10,287 transmission substations results in a 60 percent loss of connectivity. During a cascading failure, in which the high-load substations fail in sequence, the model shows that the loss of only 2 percent of the nodes causes a catastrophic failure of the entire system.
Whether regulation can be changed to allow market forces to bring about changes to make the electric grid less prone to massive failure is a question that Lynne Kiesling addresses on her blog. My guess is that the costs from failures hasn't gotten large enough to overcome the status quo bias problem that Lynne has discussed recently. Also see her post Network Reliability As A Public Good And What To Do About It.
Advances in technologies such fuel cells, cheaper batteries, and Vehicle to Grid will likely lead to much more capacity for local generation of electric power in the longer run. So grid reliability will become relatively less important than it is today.
RIVERSIDE, Calif. (www.ucr.edu) -- A team of biochemists from UC Riverside published a paper in the June 11 issue of the Journal of Molecular Biology that gives one explanation for why humans and primates are so closely related genetically, but so clearly different biologically and intellectually.
It is an established fact that 98 percent of the DNA, or the code of life, is exactly the same between humans and chimpanzees. So the key to what it means to be human resides in that other 2 percent.
According to Achilles Dugaiczyk, professor of Biochemistry at UCR, one important factor resides in something called Alu DNA repeats, sometimes called "junk DNA." These little understood sections of DNA are volatile, and prone to sudden mutations, or genomic rearrangements. At times the results are beneficial in that they give rise to new proteins or an altered gene regulation. Sometimes the mutations result in the growth of a cancer tumor, or some other genetic defect.
The team, which also included Rosaleen Gibbons, Lars J. Dugaiczyk, Thomas Girke, Brian Duistermars and Rita Zielinski, identified over 2,200 new human specific Alu DNA repeats that are absent from the chimpanzee and most likely other primates.
"The explosive expansion of the DNA repeats and the resulting restructuring of our genetic code may be the clue to what makes us human," Dugaiczyk said. “During the same amount of time, humans accumulated more genetic novelties than chimpanzees, making the human/chimpanzee genetic distance larger than that between the chimpanzee and gorilla.”
Metaphorically speaking, Dugaiczyk said, “Humans and primates march to the rhythm of a drum that looks identical; the same size, shape and sound. But, the human drum beats faster.”
This chemical analysis of DNA structures also showed something else. The spread of the Alu DNA repeats was written into the chemistry of human chromosomes. The process was not random, Dugaiczyk said, and it was not subject to an environmental "natural selection," separating winners and losers as theorized by Darwin.
I question Dugaiczyk's assertion that the spread of Alu repeats was not selected for. Perhaps each repeat's appearance was not selected for. But possibly a mechanism that increased the rate at which Alu repeats accumulated was selected for. Another possibility is that they were selected for in order to move genes around to make certain genes easier to get to for transcription. If the ancestors of humans were under heavier selective pressure once they broke off from chimps then that may have selected for more large scale rearrangements of the 3-D shape of chromosomes in order to allow changes in frequencies of expression of various genes.
Perhaps what the meaning that Dugaiczyk is trying getting to across is being lost by the short length of the press release. Does he think these Alu repeats are having no effect on phenotype and that they represent a spreading of parasitical DNA sequences? It is not clear.
"We are not contending that natural selection does not exist, but that in this instance it is a chemical process within human chromosomes that explains why humans have an explosive expansion of DNA repeats, and primates do not," Dugaiczyk said.
A chemical process? Mediated by enzymes perhaps? What caused those enzymes to start causing more Alu repeats? Did a genetic mutation make Alu repeats more likely to be generated in the germ line? Or did humans come under other selective pressures that by accident were at odds with selecting against accumulation of junk repeat sequences?
Determining the genetic differences between humans and primates is important for several reasons, Dugaiczyk said, including advancing knowledge about how life developed and evolved on earth. Other benefits include making it easier to identifying human predisposition to genetic disease, by comparing humans with other primate species. A third possible benefit is to underline the importance of protecting endangered primate species.
Another advantage to doing comparisons of genetic differences both between and within species is that we can discover the advantages and disadvantages of each variation for the purpose of future genetic engineering. Replace some of one's own parts with better parts. Or create offspring with a collection of advantages that no single human possesses today.
I question whether we really know enough about how many genetic differences there are between species or which ones are most important. Just within the human species the recent discovery of lots of large copy variations (LCVs) effectively more than doubled the previous estimate of how many genetic variations there are between individual humans.
TORONTO -- Scientists at The Hospital for Sick Children (Sick Kids), Brigham and Women's Hospital (BWH) and Harvard Medical School (HMS) have made the unexpected discovery that significant differences can exist in the overall content of DNA and genes contained in individual genomes. These findings, which point to possible new explanations for individual uniqueness as well as why disease develops, are published in the September 2004 issue of the scientific journal Nature Genetics (available online August 1, 2004).
"Using new genome scanning technologies, we serendipitously found stretches of DNA sometimes hundreds of thousands of chemical bases (nucleotides) long that were present or absent in the genomes of healthy individuals. These large-scale copy variations, or LCVs, frequently overlap with genes and could explain why people are different," said Dr. Stephen Scherer, co-principal investigator of the study, a Sick Kids senior scientist, and an associate professor in the Department of Molecular and Medical Genetics at the University of Toronto.
"At first we were astonished and didn't believe our results because for years we had been taught that most variation in DNA was limited to very small changes. Then we heard the Harvard group was making similar observations and ultimately we combined our data and came to the same conclusion," added Dr. Scherer.
Early information from the Human Genome Project indicated that the DNA in the genome of any two individuals is 99.9 per cent identical with the 0.1 per cent variation arising primarily from some three million single nucleotide changes scattered amongst the chromosomes. The new data from the Sick Kids and Harvard groups revealed 255 regions (comprising more than 0.1 per cent) of the genome where large chunks of DNA are present in different copy numbers between individuals. Over 50 per cent of these alterations lead to changes in gene numbers and at least 14 regions overlapped with known sites associated with human disease.
Since discoveries of genetic differences between humans of this order of magnitude are being found at this stage in the game any estimates about which genetic variations are most responsible for making us different from other primates should be seen as tentative guesses at this point. Those estimates may be based on false assumptions about how many and what kinds of genetic variations any two species have. There may be yet more genetic variations waiting to be discovered and some of the regions now thought to contain junk DNA may be serving some as-yet-undiscovered regulatory purposes.
Master cells nestled within hair follicles of the skin retain the ability to form new hairs as well as skin, new research reported in the September 3 issue of Cell confirms. While earlier work had suggested the presence of stem cells in skin, the new study by Howard Hughes Medical Institute investigators at Rockefeller University in New York provides the first direct evidence that cells extracted from the hair follicles of mice exhibit all of the defining features of true stem cells. The skin stem cells offer potential new methods to reverse baldness and boost wound healing in burn victims and those suffering from other skin injuries, the researchers said.
The putative skin stem cells reproduce themselves seemingly indefinitely in the laboratory, the study found. When engrafted onto the backs of hairless mice, the cells also formed stretches of skin, tufts of hair, and sebaceous glands, which secrete an oily substance known as sebum that lubricates skin and hair.
"We've identified cells within skin that bear all the characteristics of true stem cells--the ability for self renewal and the multipotency required to differentiate into all lineages of epidermis and hair," said Elaine Fuchs, cell biologist at Rockefeller University and senior author of the study. "The results demonstrate for the first time that individual cells isolated from hair follicles can be cultured in the laboratory and retain a capacity to make multiple cell types when grafted."
“An important aspect of this paper was that we found we could isolate and characterize these cells by taking advantage of the cell-surface markers that we had previously identified from molecular profiling experiments,” said Fuchs. “We can now utilize similar methods to begin to compare mouse and human skin stem cells.”
The scientists' analyses of the biochemical characteristics of the isolated mouse stem cells revealed that the bulge contained two distinct populations of stem cells. One type, called “basal” cells, is active during early development. In contrast the “suprabasal” cells appear only after the first hair generation cycle. This distinction offers biologists an opportunity to compare the two groups of cells, in terms of the control that the bulge exerts over their proliferation and differentiation.
The two stem cell types appear at different stages of development.
According to Fuchs, previous studies in her laboratory and others suggested that a structure called the bulge, which is located within each hair follicle, might contain stem cells. Those studies hinted that the stem cells might provide the source of both new skin and hair follicles.
The scientists' analyses of the biochemical characteristics of the isolated mouse stem cells revealed that the bulge contained two distinct populations of stem cells. One type, called “basal” cells, is active during early development. In contrast the “suprabasal” cells appear only after the first hair generation cycle. This distinction offers biologists an opportunity to compare the two groups of cells, in terms of the control that the bulge exerts over their proliferation and differentiation.
Both isolated stem cell types can be used to grow hair.
Despite the fact that the stem cells expressed many different genes, both populations were capable of self-renewal when grown in culture, said Fuchs. The researchers also found that both types of cells — even after being cultured — produced hair follicles when grafted onto the skin of a strain of hairless mice.
“I think clinicians will be interested in the fact that both of these populations can produce hair follicles after culture,” said Fuchs. “Previously, researchers have done similar transplant experiments with dissected parts of the hair follicle. And, while they've had evidence that hair follicle structures were forming, they didn't see generation of hair.
“In contrast, in our experiments, we saw quite a density of hairs, in some cases at a density that's very similar to that of normal mouse fur,” said Fuchs. “While we are not yet able to achieve such density a hundred percent of the time, the fact that we do get such density in some cases tells us that the system is working well. We just need to tweak it to the point where we can get such results consistently,” she said.
Imagine this process repeated using human hair follicles to isolate human follicle stem cells. Those stem cells could be grown up and used to get hair growing again on bald scalps. One can also imagine a modified variation of this approach being used to develop cells that can restore hair color in aged hair follicles.
This is not the first result along these lines. See: Transplanted Stem Cells Grow Hair In Mice. However, the latest result goes further in locating, categorizing, and characterizing the stem cells found in hair follicles.
Li-Hai Tan Ph.D. (who apparently is both Director, Joint Laboratories for Language and Cognitive Neuroscience at the University of Hong Kong, China and working currently at the US National Institute of Mental Health) and colleagues found that dyslexia is caused by malfunctions in a different part of the brain in Chinese readers than in Western language readers.
There is no one cause for dyslexia: rather, the causes vary between languages. So conclude researchers who have found that Chinese children with reading difficulties have different brain anomalies to their Western counterparts1.
Instead of letter-to-sound conversion problems, Chinese dyslexics have difficulties extrapolating from a symbol's shape to its sound and meaning.
Most dyslexia research has focused on letter-based languages such as English or Italian. These studies suggest the condition is tied to the left temporoparietal region of the brain.
Functional Magnetic Resonanace Imaging (fMRI) on dyslexic Chinese children showed that in readers of Chinese characters the brain problem with dyslexia can be traced to the left middle frontal gyrus (LMFG).
The researchers used sophisticated imaging technology to study the brain activity of 16 Chinese dyslexic children as they performed various language-based tasks.
Their study suggests that for these children, the problem lies in another area of the brain - the left middle frontal gyrus (LMFG).
Do different languages cause humans to categorize the world in different ways? Do different symbol systems for written and spoken language take up different amounts of the brain's resources leaving differing amounts of the brain available to perform other tasks? It seems highly plausible, even probable, that the answer to these questions is "yes".
Different symbol encoding systems place different cognitive demands upon the brain. Also see my previous post Mandarin Language Uses More Of The Brain Than English.