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Speed1
Warmer Future Oceans Could Cause Phytoplankton to Thrive Near Poles, Shrink in Tropics
ScienceDaily (Oct. 25, 2012) — In the future, warmer waters could significantly change ocean distribution of populations of phytoplankton, tiny organisms that could have a major effect on climate change.
Reporting in this week's online journal Science Express, researchers show that by the end of the 21st century, warmer oceans will cause populations of these marine microorganisms to thrive near the poles and shrink in equatorial waters.
"In the tropical oceans, we are predicting a 40 percent drop in potential diversity, the number of strains of phytoplankton," says Mridul Thomas, a biologist at Michigan State University (MSU) and co-author of the journal paper."If the oceans continue to warm as predicted," says Thomas, "there will be a sharp decline in the diversity of phytoplankton in tropical waters and a poleward shift in species' thermal niches--if they don't adapt."Thomas co-authored the paper with scientists Colin Kremer, Elena Litchman and Christopher Klausmeier, all of MSU.
"The research is an important contribution to predicting plankton productivity and community structure in the oceans of the future," says David Garrison, program director in the National Science Foundation's (NSF) Division of Ocean Sciences, which funded the research along with NSF's Division of Environmental Biology."The work addresses how phytoplankton species are affected by a changing environment," says Garrison, "and the really difficult question of whether adaptation to these changes is possible."
The MSU scientists say that since phytoplankton play a key role in regulating atmospheric carbon dioxide levels, and therefore global climate, the shift could in turn cause further climate change.
Phytoplankton and Earth's climate are inextricably intertwined. [263]
Speed2 "These results will allow scientists to make predictions about how global warming will shift phytoplankton species distribution and diversity in the oceans," says Alan Tessier, program director in NSF's Division of Environmental Biology."They illustrate the value of combining ecology and evolution in predicting species' responses."
The microorganisms use light, carbon dioxide and nutrients to grow. Although phytoplankton are small, they flourish in every ocean, consuming about half of the carbon dioxide emitted into the atmosphere.When they die, some sink to the ocean bottom, depositing their carbon in the sediment, where it can be trapped for long periods of time.
Water temperatures strongly influence their growth rates.Phytoplankton in warmer equatorial waters grow much faster than their cold-water cousins.
With worldwide temperatures predicted to increase over the next century, it's important to gauge the reactions of phytoplankton species, say the scientists.They were able to show that phytoplankton have adapted to local temperatures.Based on projections of ocean temperatures in the future, however, many phytoplankton may not adapt quickly enough.Since they can't regulate their temperatures or migrate, if they don't adapt, they could be hard hit, Kremer says."We've shown that a critical group of the world's organisms has evolved to do well under the temperatures to which they're accustomed," he says.
But warming oceans may significantly limit their growth and diversity, with far-reaching implications for the global carbon cycle."Future models that incorporate genetic variability within species will allow us to determine whether particular species can adapt," says Klausmeier, "or whether they will face extinction." [258]
Speed3
Violent birth proposed for Saturn’s moon mishmash
Simulation suggests collisions created Titan and smaller satellites
Saturn’s skies sparkle with the faces of its many moons — some frosted and bright, others darker, honeycombed, or hiding beneath haze. How nature built these worlds from the same set of materials is a conundrum that has eluded scientists for years.
Now, a team suggests that violence early in the solar system’s history produced the many strange moons that rise over Saturn’s ringed horizons.
Giant collisions between an extinct population of much larger Saturnian moons could have ultimately produced Titan — the largest of Saturn’s satellites — and spat out a half-dozen midsize moons, says planetary scientist Erik Asphaug of the University of California, Santa Cruz. He presented the theory October 19 at the American Astronomical Society’s Division for Planetary Sciences meeting in Reno, Nev.
“Explaining this diverse grab bag of satellites that presumably had a common origin around Saturn is very challenging,” Asphaug says. ”Collisions are a great way of explaining heterogeneity in the system.”
Saturn’s moons — 62 confirmed so far — come in a variety of sizes, ranging from tiny moonlets that live inside the planet’s iconic rings, to Titan, which holds 96 percent of Saturn’s moon mass. Between those extremes is a smattering of midsized, icy moons. The family includes some of the system’s most photogenic members, such as two-toned Iapetus, saltwater-spitting Enceladus and honeycombed Hyperion.
Some of these middleweight worlds are mostly rocky, others mostly icy. Some, like Enceladus, are geologically active. Others, like Rhea and Iapetus, even show evidence for once having rings or subsatellites of their own. [265]
Speed4 Saturn’s larger neighbor Jupiter doesn’t have such midsized moons. Instead, four large satellites (Ganymede, Callisto, Io and Europa) dominate the Jovian system, which is otherwise full of tiny moons less than 100 kilometers across. Asphaug and his collaborator, Andreas Reufer of the University of Bern in Switzerland, simulated an early version of Saturn with an orbiting menagerie that looked more like present-day Jupiter’s. Instead of a Titan, several large moons spun around the young planet.
But not for long.
Soon after the system’s birth — perhaps due to a marauding ice giant planet, or migration of the satellites themselves — the infant moons spasmed in their orbits, veered off course and collided with one another. The collisions simultaneously stripped the impacting bodies of their icy, rocky outer layers, leaving their cores to merge. Eventually, those cores became Titan. Material flung from the collisions coalesced into the midsize moons, a simple way to explain the diversity observed today. The story also explains Titan’s elongated orbit, another conundrum that has puzzled scientists.
Asphaug points out that there are still some important unresolved issues, including how the midsize moons would survive being swept up during Titan's accretion.
Another issue, says planetary scientist William McKinnon of Washington University in St. Louis, is how to get the moons where they are. Some, like Iapetus, are very, very far from Saturn.
McKinnon notes that there are several other theories describing early Saturnian, moon-making dramas. One involves a second large, young satellite, an unfortunate infant that wandered too close to Saturn and was shredded, leaving behind bits of material that then clumped into midsize moons. Another suggests the medium moons grew from the planet’s rings themselves — though no one has really been able to make that one work. [289]
Speed5 The clues come from the moons themselves.
“If we can figure out what icy satellites are made out of, that places strong constraints on how they formed,” says Joseph O’Rourke of Caltech.
Recently, O’Rourke considered how Titan may be put together. Gravity data returned from NASA’s Cassini spacecraft suggest that Titan is only partially differentiated — it lacks discrete core, mantle and crust layers. But heat circulating inside Titan would make an undifferentiated ice-and-rock interior unstable over billions of years, O’Rourke and planetary scientist David Stevenson of Caltech, report in a paper posted online October 21 at arXiv.org. Such an ice-rock mix, O’Rourke says, requires formation from a cool, slowly coalescing mix of gas and dust — not a chaotic, collision-riddled environment. If Titan is differentiated, as O’Rourke’s calculations suggest, then its interior may not be a salt-and-pepper mix of rock and ice.
“Once things get too warm for the rock and ice to stay together, the rock will begin to sink toward the center,” says planetary scientist Jonathan Lunine of Cornell University. In 2010, Lunine proposed a different type of interior consisting of a large amount of puffy, hydrated silicate near the moon’s center. Building Titan with that type of material would occur more favorably if the satellite formed quickly in a warmer environment where ice could melt and hydrate the silicates. “If we had X-ray vision and could see [Titan] was not completely separated, we would know something very profound about how hot it got when it was young,” McKinnon says. “If it’s completely separated, all we know is that at some time during the last 4.5 billion years, it got hot enough to separate.” [275]
越 障
Diagnosing cancer Difference Engine: Blissful ignorance
MEN in America, Europe and other developed regions of the world have a 16% chance of being diagnosed with prostate cancer at some point during their lives—and yet they have only a 3% chance of dying from the disease. Despite the statistics, an industry has grown up around treating prostate cancer which, in most cases, would be best left well alone. The problem is finding the few instances where the cancer is aggressive enough to spread. Unfortunately, lacking better diagnostics, 48 men have to be needlessly treated—at considerable discomfort and possible change in lifestyle for the worse—so that one man's life may be spared.
Three out of four men in America aged 50 or older have had a PSA test, often unbeknown to themselves during a routine check-up. The test measures the amount of prostate-specific antigen floating around in the blood. PSA is a protein made in the prostate gland to help sperm do its job. The test, which has nothing directly to do with a man's reproductive capacity, is carried out solely to screen for prostate cancer.
So, what is wrong with that? For a start, while elevated levels of PSA in the blood can indicate the presence of cancer cells in the prostate, higher levels than normal can also be caused by an enlarged prostate (common in older men), infection, inflammation, irritation, head-ache pills like ibuprofen, and whether the person concerned recently had sex. Even a doctor's digital rectal examination (“thumb up the bum”) can raise a patient's PSA level.
The widely used PSA test has been criticised for giving too many false-positive results, which, in turn, lead to over-treatment of cancers that might never have caused harm. Among men with PSA levels in the warning zone (between four and ten nanograms of PSA per millilitre of blood), biopsies show that over two-thirds of them had no trace of prostate cancer. Meanwhile, one in six men with PSAs in the normal zone (below 4ng/mL) were subsequently found to have been harbouring cancer cells in their prostate glands.
Usually a family doctor will refer a patient to a urologist if his PSA level is above 4ng/mL—or if the level rises by more than 0.35ng/mL over the course of a year. Because of the vagaries of the PSA blood test, many urologists confronted with borderline cases have started using a biomarker in the urine that focuses on a gene called PCA3. Comparing the activity level of the PCA3 gene with that of the PSA gene can be twice as accurate as relying on a PSA test alone. Based on such findings, the urologist may recommend a biopsy.
But that has problems, too. Tissue cores are taken from various parts of the prostate using an instrument with a dozen hollow needles that is inserted via the rectum. The sampling covers only a minuscule part of the prostate, making it easy to miss regions where cancerous cells may lurk. The procedure is not painless and can cause infection, fever, bleeding, problems with urination, and other conditions requiring hospitalisation. In the laboratory, a pathologist slices the cylindrical biopsy samples taken from the patient's prostate and examines them under a microscope. A grade is assigned, first, to the most common tumour pattern and, second, to the next most common pattern. The two grades, each with ranges 1 to 5, are added together to give what is called a Gleason score ranging from 2 to 10. For a Gleason score of 7, the combination 4+3 denotes a more aggressive cancer than 3+4.
With a Gleason score of 6 or less, the urologist may advise active surveillance rather than surgery or radiation. “Watchful waiting” involves tracking the PSA level every three months or so and having an annual biopsy. That may be the best advice the patient will ever receive. But it does require that the person is content to live with the knowledge that he has cancer and has chosen not to have it treated. Most men find that daunting—and opt for treatment, even though medically it may not be warranted.
Even in cases where a biopsy proves positive, the majority of cancer cells found are likely to be localised and to grow so slowly as never to cause even the symptoms of prostate cancer, let alone death. The condition has been likened to a handful of tortoises crawling around the bottom of a well. In the vast majority of instances, they remain trapped at the bottom. But, once in a while, a tortoise manages to crawl up the side and escape into the surroundings.
In the majority of cases, men who do nothing about cancer cells found in their prostates will most likely die in old age of something else—heart attack, stroke, lung cancer, pneumonia or whatever—long before they would have succumbed to prostate cancer. In other words, they will die with the disease, not from it. The same goes for the vast majority of men who live in blissful ignorance, having never had a PSA test. Autopsies show that three out of four men who reached the age of 85 had prostate cancer but died of other causes. Yet, the urgency to treat any detected cancer—whether aggressive or not—can be immense. The pressure to do so can come as much from the patient himself (“Get that thing out of me!”) as from a medical professional (“To be on the safe side, we advise surgery or radiation.”). Such screening can cause serious stress and anxiety. Researchers at Harvard and Brigham & Women's Hospital in Boston have found that just being diagnosed with prostate cancer doubles the risk of dying from heart attack or suicide.
If over-detection resulting from PSA screening and biopsies has its risks, over-treatment involves even bigger ones. None of the treatments—and there are half a dozen or so different ones to chose from—is benign.
Among men who opt to have their prostates removed—often to treat cancers that would never have harmed them—0.5% die within a month due to complications from the surgery. Up to 7% have serious problems but survive. And between 20% and 30% of those treated with surgery or radiation finish up with erectile dysfunction, urinary incontinence and other disabilities. Of those who use chemotherapy to suppress the hormones that feed cancerous cells in the prostate, 40% become impotent.
If truth be told, the PSA test can cause more grief than relief. There is no evidence that the test provides any advantages, even to men who turn out to have the fast-growing version of the disease. The first sign of the invasive form of prostate cancer occurs too late for it to be treated successfully. No amount of screening will prevent those destined to develop the deadly, untreatable form of the disease from doing so. In the final analysis, PSA screening has allowed more prostate cancers to be detected, but it has not lowered the death rate from the disease. [1164] 剩余部分 Even the scientist who discovered PSA over 40 years ago has argued vociferously for routine testing of prostate-specific antigen levels to be abandoned. Richard Ablin, professor of immunobiology and pathology at the University of Arizona, has called the test based on his work “a public health disaster” that is little better than the toss of a coin. So why is it still used? “Because drug companies continue peddling the tests and advocacy groups [encourage] men to get screened,” Dr Ablin wrote in the New York Times.
Two years ago, the United States Preventive Services Task Force, an independent panel of medical experts empowered to evaluate cancer testing, recommended against PSA screening for men over 75 years of age. Being older and frailer, such men were viewed as unlikely to benefit from having surgery, radiation and other treatments that were unlikely to prolong their lives, but could well cause incontinence and impotence. At the time, the panel made no change in its recommendation for younger men.
Having reviewed the findings of leading studies in Europe and America, the Task Force has now downgraded its previous recommendation on prostate-cancer screening for younger men. In an announcement on October 7th, the panel noted that for men 50 to 69 years old the reduction in death caused by prostate cancer ten years after screening “is small to none”. In other words, the PSA test does not save lives, and is not needed by healthy men showing no symptoms of the disease. The risks it causes outweigh any benefits it may bestow.
But even Dr Ablin admits PSA testing has a place. “After treatment for prostate cancer, for instance, a rapidly rising [PSA] score indicates a return of the disease,” he wrote in his Op-Ed piece last year. And men with a family history of prostate cancer should probably get a regular PSA test. At present, PCA3 screening looks a better bet, but it could turn out eventually to have similar drawbacks as PSA.
The real problem with prostate-cancer screening—whatever the test employed—is the over-treatment that ensues. If that could be eliminated, even the PSA test might do more good than harm. Ultimately, what is needed, of course, is a way of identifying the odd tortoise that escapes from the well, while ignoring all the other critters that will never do any harm. That is something science has yet to deliver [398]
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