Kathie and Graeme's Christmas Party 2010

Baby aspirin cuts risk for prostate cancer mortality

According to a new report in The Lancet, just published on line, a daily aspirin regimen reduces deaths due to several common cancers — including those caused by prostate cancer.

The report by Rothwell et al., in this week’s issue of The Lancet, is based on data from eight randomized trials (including 25,570 patients and 674 cancer deaths). These trials were originally designed to evaluate the impact of aspirin therapy on risk for cardiovascular events.

We can summarize the data from these trials as follows:

• When data from all eight trials are considered), patinets randomized to aspirin therapy had a statistically signifciant reduction in risk of death due to any form of cancer (odds ratio [OR] = 0.79).
• When individual patient data — available from seven of the eight trials (23 535 patients, 657 cancer deaths) — were analyzed , benefit was apparent only after 5 years’ follow-up.
  • For all cancers, the hazard ratio [HR] was 0.66.
  • For gastrointestinal cancers, the hazard ratio was 0·46.
• The 20-year risk of cancer death (based on 1,634 deaths in 12,659 patients in three trials) remained lower in the aspirin groups than in the control groups.
  • For all solid tumors, HR = 0·80.
  • For gastrointestinal cancers, HR = 0·65
• The time to evidence of an effect on deaths (the “latent period”) was about 5 years for oesophageal, pancreatic, brain, and lung cancers, but was longer for stomach, colorectal, and prostate cancers.
• The overall effect on 20-year risk of cancer death was greatest for adenocarcinomas (HR = 0·66), and the vast majority of prostate cancers areadenocarcinomas.
• The benefit of aspirin therapy was unrelated to aspirin dose (75 mg upwards), sex, or smoking, but increased with age.
• The absolute reduction in 20-year risk of cancer death was 7·08 percent (range, 2·42 to 11·74 percent) at age 65 years and older.

Now we should be clear that daily aspirin therapy — even with a “baby” dose of aspirion each day of 75 mg — is not risk-free. Long term aspirin therapy is associated with such side effects as gastrointestinal bleeding and with strokes. Men who wish to consider daily aspirin therapy as a means to lower their risk for cardiovascular disorders and cancer should always consult with their physician prior to initiating such a regimen.

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Tooth decay to be a thing of the past? Enzyme responsible for dental plaque sticking to teeth deciphered

ScienceDaily (Dec. 4, 2010) — The Groningen professors Bauke Dijkstra and Lubbert Dijkhuizen have deciphered the structure and functional mechanism of the glucansucrase enzyme that is responsible for dental plaque sticking to teeth. This knowledge will stimulate the identification of substances that inhibit the enzyme. Just add that substance to toothpaste, or even sweets, and caries will be a thing of the past. The results of the research have been published this week in the journal Proceedings of the National Academy of Sciences (PNAS).

The University of Groningen researchers analysed glucansucrase from the lactic acid bacteriumLactobacillus reuteri, which is present in the human mouth and digestive tract. The bacteria use the glucansucrase enzyme to convert sugar from food into long, sticky sugar chains. They use this glue to attach themselves to tooth enamel. The main cause of tooth decay, the bacterium Streptococcus mutans, also uses this enzyme. Once attached to tooth enamel, these bacteria ferment sugars releasing acids that dissolve the calcium in teeth. This is how caries develops.

Three dimensional structure

Using protein crystallography, the researchers were able to elucidate the three dimensional (3D) structure of the enzyme. The Groningen researchers are the first to succeed in crystallizing glucansucrase. The crystal structure has revealed that the folding mechanism of the protein is unique. The various domains of the enzyme are not formed from a single, linear amino acid chain but from two parts that assemble via a U-shaped structure of the chain; this is the first report on such a folding mechanism in the literature.

Functional mechanism

The unravelling of the 3D structure provided the researchers with detailed insight into the functional mechanism of the enzyme. The enzyme splits sucrose into fructose and glucose and then adds the glucose molecule to a growing sugar chain. Thus far the scientific community assumed that both processes were performed by different parts of the enzyme. However, the model created by the Groningen researchers has revealed that both activities occur in the same active site of the enzyme.

Inhibitors

Dijkhuizen expects that specific inhibitors for the glucansucrase enzyme may help to prevent attachment of the bacteria to the tooth enamel. Information about the structure and functional mechanism of the enzyme is crucial for developing such inhibitors. Thus far, such research has not been successful, states Dijkhuizen: 'The various inhibitors studied not only blocked the glucansucrase, but also the digestive enzyme amylase in our saliva, which is needed to degrade starch.'

Evolution

The crystal structure also provides an explanation for this double inhibition. The data published by the Groningen scientists shows that glucansucrase proteins most likely evolved from amylase enzymes that degrade starch. 'We already knew that the two enzymes were similar', says Dijkhuizen, 'but the crystal structure revealed that the active sites are virtually identical. Future inhibitors thus need to be directed towards very specific targets because both enzymes are evolutionary closely related.'

Toothpaste and sweets

Dijkhuizen points out that in future glucansucrase inhibitors may be added to toothpaste and mouthwash. 'But it may even be possible to add them to sweets', he suggests. 'An inhibitor might prevent that sugars released in the mouth cause damage.' However, Dijkhuizen doesn't expect that toothbrushes have had their day: 'it will always be necessary to clean your teeth.'

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Groningen.

Dim Stars Triple the Universe’s Stellar Tally

Dim Stars Triple the Universe’s Stellar Tally: "


There are more dim bulbs in the universe than even the most hardened pessimist might have imagined.

Astronomers who examined eight relatively nearby galaxies have found evidence of a surprisingly high abundance of faint, low-mass stars — each has about 10 times as many as the Milky Way. Those elderly galaxies are so chock-full of faint stars that the researchers extrapolate that the heavens contain up to three times the total number of stars previously estimated.

The profusion of stars also suggests that the early history of the cosmos may need a rewrite, perhaps doubling previous estimates of the total mass of stars in many of the universe’s first, massive galaxies. If so, those early galaxies would have forged stars at a much more prodigious rate, says Pieter van Dokkum of Yale University. He and Charlie Conroy of the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass., describe their study in a paper appearing online in Nature on December 1.

Van Dokkum and Conroy set out to determine whether spiral galaxies like the Milky Way have a different mix of low-mass and high-mass stars than is found in elliptical galaxies, which tend to have an older stellar population. Such differences had long been suspected but never proven.



Because even the sharpest telescopes can’t resolve individual faint stars in galaxies millions of light-years beyond the Milky Way, the team examined light from the central portion of each of eight massive elliptical galaxies — four in the Coma cluster and four in the Virgo cluster. Such galaxies are thought to account for one-third of the stellar mass in the universe. Massive galaxies that existed during the first billion or so years of cosmic history are believed to be the early ancestors of these ellipticals.

Spectra of light from the galaxies revealed two chemical fingerprints, absorption by sodium atoms and by iron hydride, which are unusually strong in faint red dwarf stars that have less than one-third the sun’s mass. The strength of the absorption features indicates that red dwarfs account for 80 percent of the number of stars in elliptical galaxies and 60 percent of the total stellar mass in those galaxies.

“Extrapolating from the central regions of these eight galaxies to the entire universe is somewhat hazardous, but if the galaxies are typical examples of their class it may well lead to a tripling” of the total number of stars in the cosmos, van Dokkum says.

One caveat, says Richard Ellis of Caltech, is that the researchers assumed that red dwarfs in the elliptical galaxies have the same chemical composition as red dwarfs in the Milky Way. It’s possible, he notes, that the strong absorption signals don’t indicate a very large population of the dwarfs. Instead, those measurements might be explained by a smaller population of red dwarfs that happen to be richer in sodium and iron hydride than red dwarfs in the Milky Way.

Nonetheless, the study provides “the most convincing observational test” that the mix of stars — heavyweights and lightweights — varies dramatically from one type of galaxy to another, says Ellis. Instead of using the assortment of high- and low-mass stars in the Milky Way as a standard template, such differences need to be taken into account when astronomers estimate the stellar mass and star-formation rates of galaxies from the early universe, van Dokkum and Conroy note.



Images: 1) The elliptical galaxy ESO 325-G004, which may harbor 10 times as many dim stars as the Milky Way. Credit: NASA, ESA, and The Hubble Heritage Team (STScI/AURA) 2) Astronomers examined the chemical signature of small, dim stars called red dwarfs (right) in eight elliptical galaxies and found that they are much more numerous than red dwarfs in the Milky Way (left). The finding suggests that the total number of stars in the universe could be up to three times higher than previously thought. Credit: Yale University

See Also:

• Calling All Amateur Astronomers: Help Solve a Mystery
• Odds of Finding Earth-Size Exoplanets Are 1-in-4
• Early Galaxies Formed Stars Fast Because They Had More Gas
• Sharpest Image Yet of Massive Galaxy Collision
• Milky Way May Fizzle Out Sooner Than Expected
• Galaxies Discovered in Their Awkward Teen Phase

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Could This Be How Stonehenge Was Actually Built?

Could This Be How Stonehenge Was Actually Built?: "

One of the most puzzling mysteries is how Stonehenge, the prehistoric circle of stones in England, came to be. We know it was built around 4500 years ago, and the stones came from Wales, some 250km away… but how?

Of course, back then, it wasn’t so easy to transport stuff around the country – especially not 60 bluestones which are said to weigh between two and four tons each. Several theories have been bandied about over the years of how the stones were transported, including sledges; rafts along the rivers; and that Merlin himself used his magic to gather the stones there.

This week, an engineer and former BBC TV presenter, Garry Lavin, tested his theory that wicker baskets made from willows were used to roll the stones all 250kms from the quarry in Preseli Hills, Wales, to Salisbury, in Wiltshire, England. He built one himself, using willow and alder saplings, and enlisted several friends to help roll a one-ton boulder along the ground.

He thinks oxen might’ve helped roll the baskets in some parts, and that rivers could have floated them downstream. But it’s the baskets which Lavin is sure had a huge part in the formation of Stonehenge – and as he’s currently building a maxi-basket to move a five ton stone, we may soon find out the answer. Unless aliens decide to show up and show us otherwise, of course. [Daily Mail]

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Your Next Computer Chip Revolution Unveiled by IBM: Sexy Blend of Lasers, Electrons

IBM's just unveiled a new breakthrough chip tech: CMOS Integrated Silicon Nanophotonics. Confused? It's actually pretty astonishing, promising chip-sized supercomputer power in the near future. Now you're interested....
We've known for a while that optical technology is going to be the next big revolution in computing--it's simply faster than pure electronics, and means you can get even greater performance with lower power demands from similar-sized devices. The trick is about blending optical technology at a nanoscopic scale with existing silicon electronics--and this is where CMOS ISN has achieved a breakthrough. It means thanks to research at IBM's research facility, it's now possible to integrate optical computing technology and conventional electronics onto a single slice of silicon.
Optical signals can carry more information more swiftly than electronics can manage--it's why Intel's fiber-optic Light Peak connection cables may quickly supersede newcomer USB3--and the associated electronics can eat less power than normal silicon tech. This means when you mix the systems together on chips, you can get up to ten times more integration density than is possible with current chip fabrication tech. Putting a bunch of them together results in a computer that shoots data around at rates that would seem incredible compared to current designs.
IBM's trick requires no particularly hefty refits of existing CMOS production plants, and means all the nanoscopic optical equipment like modulators and photodetectors can be built right in to a more conventional chip--meaning there's no need to add in extra-special chips to access the benefits of optical tech when you're building an integrated optical computer.
Still confused? The upshot: Chips can be significantly faster, and still consume less electrical power. Enough that IBM thinks the chips could build an exascale supercomputer, roughly 1,000 times faster than the fastest machine that exists. The side effect of this, of course, will be consumer-level systems that could be as powerful as today's research supercomputers. Your laptop in several years may be driven by chips packed with frikking laser beams, people.
To read more news on this, and similar stuff, keep up with my updates by following me, Kit Eaton, on Twitter.

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A Healthy Brain Needs a Healthy Heart

When the National Institutes of Health convened a panel of independent experts this past April on how to prevent Alzhei­mer’s disease, the conclusions were pretty grim. The panel determined that “no evidence of even moderate scientific quality” links anything--from herbal or nutritional supplements to prescription medications to social, economic or environmental conditions--with the slightest decrease in the risk of developing Alzheimer’s. Furthermore, the committee argued, there is little credible evidence that you can do anything to delay the kinds of memory problems that are often associated with aging. The researchers’ conclusions made headlines around the world and struck a blow at the many purveyors of “brain boosters,” “memory enhancers” and “cognitive-training software” that advertise their wares on the Web and on television. One of the panel experts later told reporters in a conference call that the group wanted to “dissuade folks from spending extraordinary amounts of money on stuff that doesn’t work.”
But did the panel overstate its case? Some memory and cognition researchers privately grumbled that the conclusions were too negative--particularly with respect to the potential benefits of not smoking, treating high blood pressure and engaging in physical activity. In late September the British Journal of Sports Medicine published a few of these criticisms. As a longtime science journalist, I suspected that this is the kind of instructive controversy--with top-level people taking opposing positions--that often occurs at the leading edge of research. As I spoke with various researchers, I realized that the disagreements signaled newly emerging views of how the brain ages. Investigators are exploring whether they need to look beyond the brain to the heart to understand what happens to nerve cells over the course of decades. In the process, they are uncovering new roles for the cardiovascular system, including ones that go beyond supplying the brain with plenty of oxygen-rich blood. The findings could suggest useful avenues for delaying dementia or less severe memory problems.

Dementia, of course, is a complex biological phenomenon. Although Alzheimer’s is the most common cause of dementia in older adults, it is not the only cause. Other conditions can contribute to dementia as well, says Eric B. Larson, executive director of the Group Health Research Institute in Seattle. For example, physicians have long known that suffering a stroke, in which blood flow to the brain has been interrupted by a clot or a hemorrhage, can lead to dementia. But research over the past few years has documented the importance of very tiny strokes—strokes so small they can be detected only under a microscope after death—as another possible cause for dementia. Studies at autopsy of people who had dementia have detected many of these so-called microvascular infarcts either by themselves or along with the plaques and tangles more typical of Alzheimer’s in the brains of people with dementia. These findings suggest that most dementias, even those caused by Alzheimer’s, are triggered by multiple pathological processes and will require more than one treatment.

Proving that cardiovascular treatment is one of those approaches will take some doing. Just because microinfarcts may make dementia worse does not mean that preventing them will delay the brain’s overall deterioration. Maybe severe dementia makes people more vulnerable to microinfarcts. And just because better control of high blood pressure and increased physical activity seem to decrease a person’s risk of stroke, that does not necessarily mean they are less likely to suffer microinfarcts. Correlation, after all, does not necessarily imply causation. That scientific truism was the problem that kept bothering the panel of outside experts put together by the NIH. Thus, the expert panel concluded, with one exception, that “all existing evidence suggests that antihypertensive treatment results in no cognitive benefit.” Data showing the benefits of boosting physical activity in folks with confirmed memory problems were “preliminary.”

The controversy boils down to semantics, says Martha L. Daviglus, chair of the consensus panel and a preventive cardiology researcher at Northwestern University’s School of Medicine. “Obviously, smoking and hypertension are risk factors for cardiovascular disease,” she says. “And they may turn out to be risk factors for Alzheimer’s disease as well,” she says. But after reviewing all the evidence, Daviglus and her fellow panelists concluded that it “failed to provide convincing evidence” of the link, whereas other researchers see “some evidence” of a link.

Getting better data may be a problem, however. One of the best ways scientists have to prove cause and effect in medicine is to conduct a randomized controlled trial, in which study subjects are randomly assigned to two groups. One group—the so-called control group—receives the usual standard of care. The other group—the so-called experimental group—gets whichever intervention is being tested. The simplest way to prove that treating high blood pressure helps to delay the onset of dementia would be to treat one group for hypertension and leave the other group deliberately untreated for the sake of the experiment. No ethical physician would participate in such a study.

One way out of this dilemma, Daviglus notes, is to design a study in which patients suffering from hypertension get treatment, and doctors analyze the results based on how well the patients’ blood pressure was controlled. If the amount by which blood pressure dropped closely paralleled the decrease in dementia risk, that would be powerful evidence of a beneficial link. Such a so-called dose-response study has not been done yet—it is a complex and expensive undertaking—but there is reason to believe it could be worth the investment.

Observational studies, which follow people as they get older without directly intervening in their treatment, have uncovered some suggestive trends. Larson and others have shown that people who have good control of their blood pressure from age 65 to 80 are less likely to develop dementia. After age 85, controlling blood pressure does not have much effect on dementia risk. That doesn’t mean anyone older than 85 should stop taking blood pressure medication. Lowering high blood pressure still prevents congestive heart failure and promotes kidney health. But these studies suggest that doctors do not have to take aggressive measures when treating patients older than 85 for hypertension.

As for physical activity, the best evidence in favor of its benefits for the brain comes from Australia. Two years ago researchers there published the results of a randomized controlled trial of physical activity in 170 older adults who had started showing greater memory problems than their peers and were thus at increased risk of developing dementia. Study participants averaged an extra 20 minutes a day of physical activity over six months. The study was so rigorously designed that individuals undertook the extra exercise by themselves at home to preclude the possibility that the true benefit had come from socializing with other people during group activities. The benefits of extra exercise were obvious and lasted—albeit at a diminishing level—­for 12 months after the exercise program ended. Not only did the experimental group score better on tests of their cognition compared with the control group, but the improvement was twice as great as the one that had previously been shown for the antidementia drug donepezil (brand name Aricept). This was the first time that anyone had proved in a randomized controlled trial that exercise could improve mental functioning in people with some cognitive problems.

No one understands on a biochemical level why physical activity might help the brain. The best explanation so far, says Henrietta van Praag, a neurobiologist at the National Institute on Aging, is that exercising the heart somehow stimulates growth factors to produce new nerve cells in the brain. In 1999 van Praag showed that more new nerves formed in the hippocampus—­one of the key centers in the brain for memory and learning—in physically active mice than in inactive ones. (She was working at the time as a postdoctoral researcher in Fred Gage’s laboratory at the Salk Institute.) She has since shown that the new cell growth is associated with a marked improvement in learning and memory. The new nerves also show qualitative differences from their older counterparts. The younger cells are better at establishing new connections with other cells. The effect is somewhat temporary. After a couple of months, the new cells start acting like the older cells, although they do not die off.

Maybe 10 or 15 years in the future, we will know for sure whether quitting smokingand exercising regularly help to delay dementia. That leaves the rest of us—who may have seen the devastating effects of dementia on older family and friends and cannot afford to wait for a definitive scientific answer on how we might avoid a similar fate—in an uncomfortable state of ignorance. Even if these steps never end up helping your brain, however, they will do your heart a world of good. 

Editor's note: This article was published in the print issue with the title, "The Heart-Brain Connection".