Adding nuts to the diet can help to lower blood cholesterol levels.
“Folate decreases arterial aging, decreases blood pressure and decreases cancer rate,” Dr. Roizen says. On labels, look for the words “folate” or “folic,” he says.
Oranges can be part of a healthy diet
NEW YORK (Reuters) — Testosterone supplements may make aging men feel and look better, but the results of a study conducted in rats suggest that it could lead to kidney damage and worsen high blood pressure (hypertension).
By David Stipp, Fortune
The mysterious disappearance of millions of bees is fueling fears of an agricultural disaster, writes Fortune’s David Stipp.
Pennsylvania apiarist Dennis vanEngelsdorp helped form a group trying to crack the case of the vanishing insects.
A frame removed from a hive afflicted by colony collapse disorder (CCD). The ‘smoker’ on top is used to sedate the bees.
David Hackenberg sounded the alarm about collapsing colonies.
(Fortune Magazine) — It’s a sweet time for honeybees in the rolling hills of eastern Pennsylvania, and the ones humming around Dennis vanEngelsdorp seem too preoccupied by the blooming knapweed nearby to sting him as he carefully lifts the top off their hive. VanEngelsdorp, Pennsylvania’s state apiarist, spots signs of plenty within: honeycomb stocked with yellow pollen, neat rows of wax hexagons housing larval bees, and a fertile queen churning out eggs.
But something has gone terribly wrong in this little utopia in a box. “There should be a lot more workers than there are,” he says. “This colony is in trouble.”
That pattern — worker bees playing Amelia Earhart — has become dismayingly familiar to the nation’s beekeepers over the past year, as well as to growers whose crops are pollinated by honeybees. A third of our food, from apples to zucchinis, begins with floral sex acts abetted by honeybees trucked around the country on 18-wheelers.
The mysterious deaths of the honeybees
We wouldn’t starve if the mysterious disappearance of bees, dubbed colony collapse disorder, or CCD, decimated hives worldwide. For one thing, wheat, corn, and other grains don’t depend on insect pollination.
But in a honeybee-less world, almonds, blueberries, melons, cranberries, peaches, pumpkins, onions, squash, cucumbers, and scores of other fruits and vegetables would become as pricey as sumptuous old wine. Honeybees also pollinate alfalfa used to feed livestock, so meat and milk would get dearer as well. Ditto for farmed catfish, which are fed alfalfa too.
And jars of honey, of course, would become golden heirlooms to pass along to the grandkids. (Used for millennia as a wound dressing, honey contains potent antimicrobial compounds that enable it to last for decades in sealed containers.)
In late June, U.S. Agriculture Secretary Mike Johanns starkly warned that “if left unchecked, CCD has the potential to cause a $15 billion direct loss of crop production and $75 billion in indirect losses.”
$9.3 billion worth of endangered crops
Late last year vanEngelsdorp, a strapping, 37-year-old Netherlands native with a thatch of blond hair and a close-cropped goatee, helped organize a group of bee experts to identify the killer. In recent months he’s acted as the team’s gumshoe, driving thousands of miles to collect bees and honeycomb samples from CCD-afflicted hives to analyze for clues.
Meanwhile, Pennsylvania State University entomologist Diana Cox-Foster has scoured bees from collapsed colonies for signs of disease-causing microbes. She’s shown that the insects are chock-full of them, as if their immune systems are suppressed.
Now the entomologists, aided by Ian Lipkin, a Columbia University scientist known for cracking the case of the West Nile virus (he identified the mosquito-transmitted killer of birds and sometimes people), are closing in on possible culprits and reportedly have submitted a study identifying a virus associated with CCD to a scientific journal. The bug may have been introduced into the U.S. via imported bees or bee-related products, say researchers familiar with the study.
“If I were a betting man,” says Dewey Caron, a University of Delaware entomologist who co-authored a recent report on CCD’s toll, “I’d bet it’s a virus that’s fairly new or one that’s mutated to become more virulent.” Other pathogens, such as fungi, may have combined forces with the virus, he adds.
But merely showing that germs selectively turn up in cases of CCD, he cautions, won’t necessarily nail the culprit, for it will leave a key question unanswered: Are such microbes the main killers, or has something else stomped bees’ immune systems, making them vulnerable to the infections?
After all, the first report on AIDS focused on a strange outbreak of rare fungal pneumonia, “opportunistic” infections whose root cause was later identified as HIV, the human immunodeficiency virus.
A fight about fish farms
Fortunately, a bee apocalypse seems unlikely at this point. Beekeepers have recovered from CCD-like hits in the past — major bee die-offs seem to occur about once a decade. Most beekeepers recently contacted by Fortune say hives generally appear normal of late.
Still, ominous reports of worker-scarce hives like the one vanEngelsdorp recently examined suggest that whatever causes CCD is still in circulation and may well decimate hives again when bees’ floral support system drops away this fall.
If that happens, “it will be a lot worse than the first time, because [commercial beekeepers] have already spent a lot of their money” replacing lost bees, says Richard Adee, head of the country’s largest beekeeping operation, Adee Honey Farms of Bruce, S.D., which, despite its name, is largely a pollination business.
The losses weren’t insured, he adds: Because of all the unpredictable things that can kill bees, from mites to droughts, insurers have long refused to cover them. “We’ll see a lot of guys just hang it up.”
So that’s the thing to worry about: While CCD isn’t likely to obliterate honeybees, it may wipe out enough migratory beekeepers to precipitate a pollination crisis.
They’re already thin on the ground — a rare breed of truck drivers who also happen to be applied entomologists, amateur botanists, skilled nursemaids of cussed old machines, traveling salesmen, and Job-like nurturers of finicky, stinging insects that, when they’re not mysteriously dying off, can suddenly swarm on you like something out of Hitchcock.
Commercial beekeepers make up only about 1% of the 135,000 owners of hives in the U.S., but they manage over 80% of the nation’s 2.4 million honeybee colonies. If the waning number of hives in the U.S. is any indication, commercial beekeeping was already in a long-term decline before CCD struck — in 1960 there were about five million hives, more than twice as many as there are today.
Meanwhile, demand for pollination services is growing, largely because of our love affair with the almond — it’s increasingly seen as a health food, and the FDA acknowledged in 2004 that there are data “suggesting” a daily dose of 1.5 ounces of almonds or other nuts, along with a low-fat diet, may lower the risk of heart disease. By 2012 nearly 90% of the hives now estimated to exist in the U.S. will be needed to pollinate California’s almond groves each spring, according to the Almond Board of California.
10 crops most at risk
Commercial beekeeping has a lot in common with the disappearing family farm. The typical bee rancher is a salt-of-the-earth, 50-something, strong-armed guy who often sweats through the night forklifting hives filled with seriously annoyed bees onto a flatbed semi in order to rush them to his next customer’s field 500 miles away, which just may be near a crop sprayed with insecticides that will kill 15% of his livestock as they wing around the area.
Cheap honey imported from China and Argentina has clobbered his profits, forcing him to work his bees ever harder as migratory pollinators. He loses lots of bees to “vampire” mites, hive-busting bears, human vandals, and sometimes to beekeepers gone bad, who steal hives by night and pollinate by day. His kids can see that there are much easier ways to make a living.
But for all that, he’s never lost the sense of wonder that came over him the first time he heard the piping of a queen — a kind of battle cry that newly emerged honeybee queens make before fighting to the death for hive supremacy. From outside a hive, it sounds like a child wistfully tooting a toy trumpet in a distant room.
If CCD flares up again, one of the casualties may be the Paul Revere of colony collapse, a lanky, 58-year-old beekeeper named David Hackenberg. The story of the disappearing bees began one afternoon last October when he and his son Davey pulled into one of their “bee yards” near Tampa to check on 400 hives they had placed there three weeks earlier.
The Hackenbergs’ main center of operations is a farm near Lewisburg, Pa., but like most migratory beekeepers, they move their bees south each winter for a few months of R&R (rest and reproduction) before the rigors of spring pollination.
Hackenberg, a gregarious raconteur with a Walter Brennan voice, says the first sign of trouble was that “there were hardly any bees flying around the hives. It was kind of a weird sensation, no bees in the air. We got out our smokers” — bellows grafted to tin cans that beekeepers use to waft bee-sedating smoke into hives before opening them – “and smoked a few hives, and suddenly I thought, ‘Wait a minute, what are we smoking?’
“Next thing, I started jerking covers off hives … It was like somebody took a sweeper and swept the bees right out of the boxes. I set there a minute scratching my head, then I literally got down on my hands and knees and started looking for dead bees. But there weren’t any.”
Attack of the mutant rice
Hackenberg spread the word about his vanished bees. Within days other beekeepers began reporting similar cases. Penn State’s Cox-Foster, vanEngelsdorp, and other bee experts launched an investigation. After turning up more than a dozen cases of collapsing colonies across the country, the team issued a report in mid-December telling of beekeepers who’d lost up to 90% of their bees.
The “unprecedented losses,” according to the report, had many keepers “openly wondering if the industry can survive.”
By late spring CCD had made headlines around the world. Assorted phobia purveyors vied to adopt the die-off as a poster child for everything from cellphone emanations to God’s Just Wrath. Internet bloggers thrilled themselves silly bandying about a sentence from Albert Einstein, which the great physicist apparently tossed off about 40 years after his death to the public-relations department of a French beekeeping group: “If the bee disappears from the surface of the earth, man will have no more than four years to live.”
A survey sponsored by Bee Alert Technology, a Missoula, Mont., firm that sells hive-tracking devices and other bee wares, turned up reports of CCD in 35 states and Puerto Rico by early June.
Despite the widespread impression that CCD started with Hackenberg’s losses last October in Florida, says Bee Alert CEO Jerry Bromenshenk, “our survey shows that it probably first began to show up the previous spring in Michigan, Wisconsin, and Iowa. By midsummer [last year] it was moving through the heartland,” hitting hives in the Dakotas, then appearing widely a few months later in the South and on both coasts.
A survey led by vanEngelsdorp and Florida apiary inspector Jerry Hayes suggests that a quarter of U.S. beekeepers were struck by CCD between September 2006 and March 2007. Those hit by mysterious die-offs lost, on average, 45% of their hives.
The surveys failed to show patterns suggesting CCD’s cause. But they provided alibis for some prime suspects, such as beekeeper enemy No. 1: blood-sucking Varroa destructor mites. (Picture a tick as big as a Frisbee glommed onto your back — that’s what Varroa is like for a bee.) Varroa both transmits harmful viruses to bees and suppresses their immune systems.
But CCD has been reported in many hives without significant mite problems, says Jeff Pettis, an entomologist at the U.S. Department of Agriculture’s Bee Research Laboratory in Beltsville, Md.
Sugar cane ethanol’s not-so-sweet future
Another leading suspect — stress on bees due to migratory pollination — hasn’t gotten off the hook so easily. Low honey prices coupled with rising pollination fees for certain crops have prompted migratory beekeepers to put their bees on the road more than ever during the past few years.
Some now truck hives coast to coast, beginning in February with California almonds, then moving on to crops in the East, such as Maine blueberries. That potentially exposes bees to ever more diseases and insecticides. And many of the crops, such as cranberries, don’t provide adequate bee nutrition.
The insects aren’t very good travelers either. When a truck carrying bees gets caught in a summer traffic jam, for instance, hives quickly overheat, despite the fact that the millions of workers inside them furiously fan their wings in an attempt to prevent it, says Wes Card, a beekeeper whose Merrimack Valley Apiaries in Billerica, Mass., pollinates crops from California to Maine.
“Then every minute counts,” he adds, for unless the driver can quickly find a way to pull off the road and hose down the hives with cooling water, desperately hot queens emerge from their inner sanctums and typically wind up venturing into nearby colonies on the truck, where they are perceived as alien invaders and promptly killed. (Ironically, worker bees typically execute a condemned monarch by clustering around her and vibrating their wing muscles to generate heat, fatally raising her temperature — beekeepers call it “balling the queen” because the executioners form a ball of bees.) A hot day can turn a load of hives into a costly mess within minutes.
Stress probably isn’t the main culprit, though. In fact, the biggest commercial beekeepers — those with over 500 hives, most of whom are migratory pollinators — lost a smaller percentage of their hives when hit by CCD last winter than did hobbyist beekeepers, according to the survey co-authored by vanEngelsdorp.
Further, there’s some evidence that CCD may antedate the modern stresses put on bees. Large numbers of honeybees have mysteriously vanished a number of times since the mid-19th century, suggesting that CCD may be just the latest episode in a “cycle of disappearance” caused by a mystery disease that periodically flares up like a deadly worldwide flu epidemic.
Still, entomologists who have personally observed the effects of CCD insist that it is unlike any bee die-off they’ve seen. The University of Delaware’s Caron, one of the bee world’s biggest names, says he was stunned when 11 of 12 hives in the school’s apiary collapsed last winter, apparently because of CCD.
“Never in 40 years had I witnessed the symptoms I was seeing,” he says.
Winning in the wine biz
One of CCD’s strangest symptoms, say bee experts, is a phenomenon that might be called the madness of the nurses. Nurse bees are workers that nurture a hive’s preadult bees, called brood. Workers begin their adult lives as nurses, and only during the final third or so of their six-week lives do they become foragers, venturing outside the hive to collect nectar and pollen.
Researchers have discovered that the young nurses are maintained in a kind of immature, thickheaded state by chemical signals emanating from the queen. Nurses aren’t supposed to leave the hive. They’re not ready to cope with the big outside world, which requires a mature bee’s smarts. Besides, with nurses on leave, the all-important brood would wither.
Yet empty hives struck by CCD are often found with intact brood, which means nurses were on the job shortly before all the bees flew off forever. Beekeepers find this gross dereliction of duty much weirder than the disappearance of foragers, which essentially work themselves to death and often die outside the hive.
Says Hackenberg: “Basically, I’ve never seen bees go off and leave brood. That’s the real kicker.”
To explain the psychotic behavior, some beekeepers, including Hackenberg, point the finger at an increasingly popular class of insecticides called neonicotinoids. The chemicals are widely used by farmers on fruits and vegetables that bees pollinate, as well as on corn and other crops often grown nearby.
Soon after Bayer (Charts), the German drug and chemicals concern, first put the products on the market in the early 1990s, they were implicated in a bee die-off in France, where their use was then sharply restricted. Since 2000, studies by French and Italian researchers have suggested that low, “sublethal” doses of the chemicals — which bees might get from lingering traces of the insecticides in fields — can mess up the insects’ memories and navigational abilities, potentially making them get lost. Bayer has countered with its own studies, which it asserts demonstrate that the products, when properly used, don’t pose significant risks.
Honeybees’ exposure to trace amounts of neonicotinoids can’t be ruled out, says Chris Mullin, a Penn State University entomologist investigating whether pesticides are involved in CCD.
But he and other CCD investigators doubt that neonicotinoids will turn out to be the primary culprits. For one thing, many other chemicals to which bees are exposed are nerve toxins that can make them act strange at low doses. And it’s hard to reconcile the rapid, widespread appearance of CCD last year with the fact that numerous such chemicals have long been widely used.
Could infectious microbes induce the nurses’ insanity?
The great corn gold rush
Maybe. Young workers with a disease caused by “sacbrood” virus tend to start foraging abnormally early in life, when their healthy peers are still nursing. And as if discombobulated in their new roles, they fail to collect pollen.
Although sacbrood virus has been detected in bees from some hives with CCD symptoms, as have a number of other viruses, it doesn’t appear to be closely associated with the disorder. But its ability to warp young bees’ behavior suggests that viruses may well induce nurses to do the unthinkable.
Another explanation may make more sense, though: Perhaps the nurses aren’t really acting crazy when they fly away. Instead, their strange behavior may represent a perfectly natural attempt by doomed workers to protect their sisters from killer microbes.
After all, a hive’s workers represent a famously close-knit sorority, geared by evolution to act strictly in the best interests of their colonies. (Male “drones” don’t work, by the way. They loaf about the hive most of their lives, zip out about noon every day in hopes of mating on the wing with young queens, then immediately die after copulating, presumably happy.) Beekeepers have long known that sick bees generally leave the hive to die, minimizing the risk that they will infect others.
In his seminal 1879 tome The A B C of Bee Culture, Amos Ives Root, an early giant of U.S. beekeeping, marveled that “when a bee is crippled or diseased from any cause, he [sic] crawls away … out of the hive, and rids the community of his presence as speedily as possible. If bees could reason, we would call this a lesson of heroic self-sacrifice for the good of the community.”
Might a fast-spreading, immune-suppressing disease be making nurses so sick that their urge to stay put is overruled by the altruistic impetus to depart?
The organic milk price war
The effort to answer such questions has entered a new phase with the recent linking of specific infectious agents to CCD (the ones whose identities are expected to be disclosed soon in a scientific journal). Now Cox-Foster says she and colleagues are trying to reproduce CCD’s effects on bee colonies by seeding healthy hives with the agents — the biomedical equivalent of getting a killer to confess.
Meanwhile, scattered reports over the summer of hives with abnormally few workers and little stored honey have many bee people worried. A few beekeepers, frazzled by earlier heavy losses and worried that truly ruinous ones are on the way, have already bailed out.
CCD 2 would probably be a lot uglier for growers — and for us fruit and veggie eaters — than version one was. In fact, we got lucky the first time it hit: “A lot of the bees brought to California this year were total junk,” their hives sparsely populated because of CCD and other problems, says Lyle Johnston, a Rocky Ford, Colo., beekeeper who arranges the placement of 50,000 hives owned by other keepers in almond groves each spring. “But we had the most perfect weather during the almond bloom that I can recall. It saved our butts,” by enabling bees to take to the air more often than they usually do.
“We dodged the bullet with fruit, too, this year,” says the University of Delaware’s Caron. “We had weak bees, but the weather was exceptional during the apple, blueberry, and cranberry blooms.”
Unfortunately, Caron and others note, by keeping crop prices low, the good weather may have actually discouraged legislators from funding studies on CCD. To beekeepers’ dismay, the farm bill recently passed by the U.S. House of Representatives, which calls for $286 billion to be spent over the next five years on everything from school snacks to biofuels, earmarked no funds specifically for CCD research.
And the lucky run of weather probably won’t last much longer. Extraordinarily dry weather through spring and early summer in California and the Southeast has stressed bees in those regions, potentially setting up many hives for collapse later in the year.
Despite making some progress, cash-strapped scientists looking into CCD aren’t likely to identify what causes it — and ways to fend it off — before the high-risk season for bee die-offs arrives with the onset of cold weather.
So what to do in light of this new, unsolved, and probably ongoing threat to our food supply? Don’t panic. But do take time to slowly savor your next sweet, spicy slice of cantaloupe, watermelon, apple, peach, or pear.
The pure pleasure of it may get a lot rarer.
Credit: Originally published by Howard Hughes Medical Institute
A new red fluorescent protein—derived from a brilliant red sea anemone purchased in a Moscow pet shop—can reveal body tissues more vividly than other fluorescent proteins in use today. The Russian researchers who developed the new protein said it can render cancers and other target tissues easily visible in living animals, making them glow like Christmas bulbs.
The development of the red fluorescent protein, which the researchers call Katushka, was reported by Howard Hughes Medical Institute international research scholars Andrey Zaraisky, Sergey A. Lukyanov, and their colleagues August 26, 2007, in the online version of Nature Methods. Principal development of Katushka was carried out by Dmitry Chudakov and colleagues in Lukyanov’s laboratory at the Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry in Moscow. Zaraisky and his colleagues are also at the institute.
According to the researchers, Katushka solves a major problem in the field of fluorescent reporter proteins. Fluorescent proteins have become invaluable research tools for labeling specific genes and tissues. This labeling permits researchers to follow gene activity visually or to track cellular development. However, there is no tracer that glows brightly in a particular “window” of the far-infrared spectrum favorable for maximally penetrating living tissues. Thus, such proteins were not practical for optically imaging tagged genes, cells or tissues in whole animals.
The development of Katushka might never have happened had it not been for the shrewd bargaining of Lukyanov. Visiting a Moscow pet shop, Lukyanov saw a brilliant red sea anemone among the denizens of the store’s aquarium. Sensing that the vivid red coloring in the anemone might provide the blueprint for a new biological tracer, he tried to buy the anemone. He was told by the shopkeeper that it had already been sold, and the buyer was expected shortly. Unfazed, Lukyanov persistently outbid the buyer and procured the creature.
Back in Lukyanov’s laboratory, Chudakov and his coworkers isolated the red protein from the anemone and then developed an enhanced version, which they named turbo red fluorescent protein (TurboRFP). The protein comprised a string of identical protein subunits, so the researchers also developed a single-unit monomeric version, which they called TagRFP.
Although TurboRFP was twice as bright as a comparable red protein, DsRed2, the researcher set out to improve its brightness in the infrared window. They created about 100,000 variants of the gene for TurboRFP, screening the resulting proteins for high brightness in the far-infrared. This screening yielded a highly bright variant protein, which they further optimized by randomly mutating the gene and selecting the brightest protein. They named this protein Katushka, a Russian diminutive for the name Ekaterina—after co-author Ekaterina Merzlyak, in recognition of her work developing TurboRFP and TagRFP. Katushka proved to be up to 10-fold brighter in the far-infrared, compared to the spectrally close fluorescent proteins HcRed and mPlum. mPlum was developed in 2004 by HHMI investigator Roger Y. Tsien at the University of California, San Diego, a leader in the study of fluorescent proteins for cell biology research. The researchers also generated a monomeric version of Katushka, called mKate, which is useful for molecular labeling of proteins.
Zaraisky and his colleagues tested Katushka’s properties as a tracer by introducing it into living cells in culture, as well as into the muscle cells of the African clawed frog Xenopus laevis, widely used in research. They found the protein to be highly visible and nontoxic.
“The key feature of Katushka that makes it valuable as a fluorescent marker is the unique combination of high brightness, far-red emission and fast rate of the chromophore maturation,” said Zaraisky. “As far as I know, none of the known fluorescent proteins demonstrates this combination of properties.”
Early appearance of the Katushka protein in tissues is particularly important, said Zaraisky. “It’s desirable to detect transgenic expression at the earliest stage of embryonic development to be able to investigate early events of embryogenesis,” he said. “This means that you need to use the fastest-maturing and brightest fluorescent protein as a reporter. At the same time, since frog embryos are not transparent at early stages, your fluorescent reporter should emit as far in the infrared as possible, because the longer wavelength can more easily pass through living tissues.”
As an added benefit, the researchers found that the Katushka protein persisted in labeled tissues as the frogs reached adulthood. “We hoped that Katushka could be visible in adult frogs, but it was a surprise that it has appeared so bright,” Zaraisky said.
Zaraisky sees broad uses for Katushka in research. “We believe that Katushka has a big potential in cancer research, because it could significantly simplify some experiments that should be done only at the whole-body level. It would be possible, for example, to generate model lines of mice that would specifically express the Katushka transgene in cells of different types of cancer. Then, these lines of mice could be used to test influence of different drugs on progression of cancer metastases.
“Also, Katushka is an excellent choice as a living reporter for experiments in developmental biology, especially for such semi-transparent models as frog and early mouse embryos,” he said. For example, Zaraisky and his colleagues plan to use the frog embryos generated in their analysis of Katushka’s properties to study muscle cell differentiation.
According to Chudakov, further improvements in Katushka are likely. “The palette of basic fluorescent proteins is currently almost complete, the only gap remaining in the very far-red part of the visible spectrum,” he said. “We hope that further development of Katushka and mKate will finally fill the gap.”
Galactic Suite, Space hotel sees 2012 opening
* Story Highlights
* Three-bedroom, $3 billion “Galactic Suite” set to open in 2012
* Boutique hotel will cost $4 million for a three-day stay
* Guests would orbit the Earth in 80 minutes and see 15 sunrises a day
BARCELONA (Reuters) — “Galactic Suite”, the first hotel planned in space, expects to open for business in 2012 and would allow guests to travel around the world in 80 minutes.
An artist’s impression of the Galactic Suite, where guests would enjoy views of the Earth during their three-day stay
Its Barcelona-based architects say the space hotel will be the most expensive in the galaxy, costing $4 million for a three-day stay.
During that time guests would see the sun rise 15 times a day and use Velcro suits to crawl around their pod rooms by sticking themselves to the walls like Spiderman.
Company director Xavier Claramunt says the three-bedroom boutique hotel’s joined-up pod structure, which makes it look like a model of molecules, was dictated by the fact that each pod room had to fit inside a rocket to be taken into space.
“It’s the bathrooms in zero gravity that are the biggest challenge,” says Claramunt. “How to accommodate the more intimate activities of the guests is not easy.”
But they may have solved the issue of how to take a shower in weightlessness — the guests will enter a spa room in which bubbles of water will float around.
When guests are not admiring the view from their portholes they will take part in scientific experiments on space travel.
Galactic Suite began as a hobby for former aerospace engineer Claramunt, until a space enthusiast decided to make the science fiction fantasy a reality by fronting most of the $3 billion needed to build the hotel.
An American company intent on colonizing Mars, which sees Galaxy Suite as a first step, has since come on board, and private investors from Japan, the United States and the United Arab Emirates are in talks.
Plenty rich enough
If Claramunt is secretive about the identity of his generous backer, he is more forthcoming about the customors he can expect.
“We have calculated that there are 40,000 people in the world who could afford to stay at the hotel. Whether they will want to spend money on going into space, we just don’t know.”
Four million dollars might be a lot to spend on a holiday, but those in the nascent space tourism industry say hoteliers have been slow on the uptake because no one thought the cost of space travel would come down as quickly as it has.
Galactic Suite said the price included not only three nights in space. Guests also get eight weeks of intensive training at a James Bond-style space camp on a tropical island.
“There is fear associated with going into space,” said Claramunt. “That’s why the shuttle rocket will remain fixed to the space hotel for the duration of the guests’ stay, so they know they can get home again.”
In an era of concern over climate change, Galaxy Suite has no plans so far to offset the pollution implications of sending a rocket to carry just six guests at a time into space.
“But,” says Claramunt, “I’m hopeful that the impact of seeing the earth from a distance will stimulate the guests’ urge to value and protect our planet.”
Xavier Claramunt says the three-bedroom boutique hotel’s joined-up pod structure will look oddly molecular; each pod room had to fit inside a rocket to be taken into space. (Maybe they should go inflatable – see the CSS Skywalker – inflatable orbital resort.)
Sci-Fi fans recall the spacious lounge in the orbiting space station in 2001: A Space Odyssey; note the low curving ceiling (this space station was spun on its axis to provide artificial gravity for the guests).
Lounge From Space Station in film, 2001 A Space Odyssey
by Patrick Barry
Aug 11, 2007, ScienceNews.org, If your blood glucose is out of whack, the problem may be in your bones. New research in mice shows that bone cells exert a surprising influence on how the body regulates sugar, energy, and fat.
THE ARM BONE’S CONNECTED. A bone-cell protein called osteocalcin influences energy metabolism through its effects on pancreatic and fat cells.
N. Heim/Columbia Univ. Med. Center
The discovery could lead to new ways to treat type 2 diabetes, a disease involving poor regulation of blood glucose. It also means that skeletons act as endocrine organs, which affect other body tissues by releasing hormones into the bloodstream.
“I’m already changing my teaching slides” about the functions of bones, comments Jennifer Westendorf, an associate professor of orthopedic surgery at the Mayo Clinic in Rochester, Minn. “Now we can add that [the skeleton] affects energy metabolism as well,” she says. “It’s certainly an exciting breakthrough.”
The team announcing the finding, led by Gerard Karsenty of Columbia University, had previously found that fat cells secrete a hormone that influences bone-forming cells called osteoblasts. Because hormone regulation between two cell types is often reciprocal, Karsenty and his team reasoned that osteoblasts might also be emitting hormones that control fat tissue. Osteoblasts make bone throughout a healthy person’s lifetime, while cells called osteoclasts tear down bone—processes that constantly remodel the skeleton.
Osteocalcin, a somewhat enigmatic protein produced only by osteoblasts, seemed like a good hormone candidate, Karsenty says. “[It] has been the flagship molecule of the [bone-research] field for 30 years, but nobody knew what it was doing.”
Karsenty’s team fed a normal diet to mice engineered to lack the gene for osteocalcin. The mice became obese and had low blood concentrations of insulin, a key hormone for controlling blood glucose. The animals also had poor sensitivity to insulin, a hallmark of people with diabetes.
Another group of mice, which had been engineered to have extra osteocalcin, stayed thin despite being fed a high-calorie diet. These animals also maintained higher insulin concentrations and better sensitivity to insulin than the mice lacking osteocalcin did, the team reports in the Aug. 10 Cell.
Further tests on mice showed that osteocalcin causes the insulin-making cells in the pancreas to proliferate and ramp up insulin production. The bone protein also causes fat cells to store less fat and to secrete a hormone called adiponectin. In people as well as in mice, this substance improves cells’ sensitivity to insulin.
Previous research has shown that many people with type 2 diabetes have low blood concentrations of osteocalcin.
“Osteocalcin, if everything goes well, could be a treatment for type 2 diabetes. That’s where the excitement is,” Karsenty says. Columbia University holds a patent on the idea, and Karsenty says that he’s helping form a company to commercialize the treatment.
“This could also have important ramifications for cardiovascular disease because of the effect on metabolic syndrome,” a condition related to diabetes, comments Dana T. Graves of Boston University. “The fact that bone cells regulate energy metabolism, and that they do it through osteocalcin, is a major finding,” he says.
by Fred Pearce, New Scientist.com, August 16, 2007, SOME climate tipping points may already have been passed, and others may be closer than we thought, it emerged this week. Runaway loss of Arctic sea ice may now be inevitable. Even more worrying, and very likely, is the collapse of the giant Greenland ice sheet. So said Tim Lenton of the University of East Anglia, UK, speaking on Monday at a meeting on complexity in nature, organised by the British Antarctic Survey in Cambridge.
Lenton warned the meeting that global warming might trigger tipping points that could cause runaway warming or catastrophic sea-level rise. The risks are far greater than suggested in the current IPCC report, he says.
Yet climate modellers are in a quandary. As models get better and forecasts more alarming, their confidence in the detail of their predictions is evaporating.
The IPCC says the Greenland ice sheet will take at least 1000 years to melt. But Lenton’s group – whose members include John Schellnhuber, the chief scientist on climate change at the recent G8 meeting in Germany – says the sheet could break up within 300 years, raising sea levels by 7 metres. This would flood hundreds of millions of people or more out of their homes. “We are close to being committed to a collapse of the Greenland ice sheet,” Lenton says. “But we don’t think we have passed the tipping point yet.” The calculations show the Greenland collapse could be triggered by temperatures 1 °C warmer than today’s, of which 0.7 °C is already “in the pipeline”, held up by time lags in the system.
Lenton’s study has identified eight dangerous tipping points that could be passed this century. Several could have a cascade effect, with each triggering the next, he says.
The tipping points include a collapse of a global ocean circulation system known as the thermohaline circulation. Besides shutting down the Gulf Stream, this could also “switch off” the Asian monsoon and warm the Southern Ocean, perhaps destabilising the West Antarctica ice sheet. This would cause a further 7-metre rise in sea levels. Likewise, warming may cause a near-permanent El Niño in the Pacific, which would hasten a runaway burning of the Amazon rainforest and its disappearance by mid-century.
The existence of potential climate-change tipping points should dramatically alter economists’ assessments of how much climate change we should prevent, said Lenton. The trouble is, the discovery of tipping points has also unmasked growing uncertainty about the reliability of conventional climate models.
At the Cambridge meeting Lenny Smith, a statistician at the London School of Economics, warned about the “naive realism” of current climate modelling. “Our models are being over-interpreted and misinterpreted,” he said. “They are getting better; I don’t want to trash them per se. But as we change our predictions, how do we maintain the credibility of the science?” Over-interpretation of models is already leading to poor financial decision-making, Smith says. “We need to drop the pretence that they are nearly perfect.”
He singled out for criticism the British government’s UK Climate Impacts Programme and Met Office. He accused both of making detailed climate projections for regions of the UK when global climate models disagree strongly about how climate change will affect the British Isles.
Smith is co-author, with Dave Stainforth of the Tyndall Centre for Climate Change Research in Oxford, of a paper published this week on confidence and uncertainty in climate predictions (Philosophical Transactions of the Royal Society A, DOI: 10.1098/rsta.2007.2074). It is one of several papers on the shortfalls of current climate models.
Some authors say modellers should drop single predictions and instead offer probabilities of different climate futures. But Smith and Stainforth say this approach could be “misleading to the users of climate science in wider society”. Borrowing a phrase from former US defence secretary Donald Rumsfeld, Smith told his Cambridge audience that there were “too many unknown unknowns” for such probabilities to be useful.
Policy-makers, he said, “think we know much more than we actually know. We need to be more open about our uncertainties.” Meanwhile, the tipping points loom.
DEAD EYE. White specks are dying nerve cells in retinas of rats with glaucoma. The retina at bottom was treated with three drugs that inhibit amyloid-beta production. Black lines are blood vessels.
L. Guo, Cordeiro
by Nathan Seppa
Aug 11, 2007, ScienceNews.org – A protein fragment that litters the brains of people with Alzheimer’s disease may also bear responsibility for some of the vision loss in glaucoma, a new study in rats shows.
Glaucoma patients typically have abnormal fluid pressure within the eye, but it remains unknown how this stress kills the nerve cells at the back of the retina. While there is no cure for glaucoma, easing eye pressure with drugs or surgery helps prevent vision loss in many patients.
Some glaucoma patients, however, experience vision loss even with normal eye pressure, indicating that other factors are sometimes involved.
The new research suggests that one hidden assailant is amyloid-beta, the same protein fragment that accumulates in the brains of Alzheimer’s patients. An earlier rodent study of glaucoma had found the substance in the animals’ eyes, but other evidence of amyloid-beta in glaucoma is scarce.
In the new study, ophthalmologist M. Francesca Cordeiro of University College London and her colleagues induced glaucoma in 60 rats by injecting saline into the animals’ eyes. Within weeks, amyloid-beta deposits showed up in dying retinal-nerve cells.
The researchers then gave another round of eye injections to some of the rats. In one eye, the animals received a synthetic antibody that absorbs amyloid-beta. The other eye got a placebo.
After 3 weeks, the medicated eyes showed only one-fourth as much retinal-cell death as did the untreated eyes, the researchers report in an upcoming Proceedings of the National Academy of Sciences. The effect remained 13 weeks later.
Next, the scientists repeated the experiment on other rats with glaucoma, this time using a cocktail that included the antibody and two other drugs with anti–amyloid-beta effects: a dye called Congo red and an enzyme deactivator called beta-secretase inhibitor. The triple combination worked even better than the antibody alone, reducing cell death by 84 percent.
“This offers a novel hypothesis and very intriguing results with the potential for therapeutic impact on a devastating, blinding disease,” says psychiatrist Lee E. Goldstein of Harvard Medical School and the Brigham and Women’s Hospital in Boston. It remains unclear, though, whether amyloid-beta is similarly involved in human glaucoma and, if so, whether it’s a perpetrator of the disease or a bystander. “The jury is still out,” says Goldstein.
Researchers are currently testing an amyloid-beta antibody as a drug in a large trial of Alzheimer’s patients, but Congo red and beta-secretase inhibitor haven’t entered that stage of Alzheimer’s testing, Cordeiro says. She says she’s hopeful that scientists will assess the triple combination in glaucoma patients within 2 or 3 years.
“One of the problems I have as a glaucoma doctor is that there are no other real treatments out there, other than reducing pressure in the eye,” she says.
U.S. News put 5,462 medical centers through progressively finer screens to create the 16 specialties rankings in the 2007 edition of America’s Best Hospitals. Just 173 hospitals made it into the rankings, and of those, a mere 18 displayed the marked breadth of expertise, with high scores in at least six specialties, that qualified them for the Honor Roll. They are ordered by total points—a hospital got 2 points if it ranked at or close to the top in a specialties and 1 point if it ranked slightly lower (View 2007 Methodology).
CHICAGO, Aug. 6, 2007—Adults with attention-deficit/hyperactivity disorder (ADHD) show a blunted response to the drug methylphenidate (Ritalin), which increases brain dopamine levels, according to a report in the August issue of
Archives of General Psychiatry, one of the JAMA/Archives journals. This suggests that dopamine dysfunction may be involved with ADHD symptoms and may contribute to substance abuse that often occurs simultaneously.
ADHD is the most prevalent psychiatric disorder among children, according to background information in the article. “Despite decades of research, the specific neurobiological mechanisms underlying this disorder still remain unclear,” the authors write. “Genetic, clinical and imaging studies point to a disruption of the brain dopamine system, which is corroborated by the clinical effectiveness of stimulant drugs (methylphenidate hydrochloride and amphetamine), which increase extracellular dopamine in the brain.”
Nora D. Volkow, M.D., of the National Institute on Drug Abuse, Bethesda, Md., and colleagues studied 19 adults with ADHD (average age 32) who had never received medication and 24 healthy controls (average age 30). Brain scans were performed using positron emission tomography (PET) and a drug known as raclopride labeled with carbon 11 ([11C]raclopride), which binds with dopamine receptors. Scans were performed twice, after injections of placebo and of methylphenidate; the participants did not know which drug they had received. Participants also were asked to report the severity of their ADHD symptoms, whether they could detect the drug, if they liked or disliked it, and if it made them feel “high,” tired, alert, anxious or restless.
In individuals with ADHD, methylphenidate caused less of a decrease in the amount of [11C]raclopride that bound to dopamine receptors in areas of the brain associated with attention than it did in those without ADHD. Since levels of methylphenidate in the blood were the same in both groups, this suggests that those with ADHD released less dopamine in response to the drug than controls. This blunted response was associated with symptoms of inattention. Exploratory analyses also found evidence of reduced [11C]raclopride binding in the hippocampus and amygdala in those with ADHD. These areas of the brain are part of the limbic system, involved in emotional responses as well as consolidating and retrieving memories.
“The findings of reduced dopamine release in subjects with ADHD are consistent with the notion that the ability of stimulant medications to enhance extracellular dopamine underlies their therapeutic effects in ADHD,” the authors write.
Individuals with ADHD also reported liking methylphenidate more than individuals without ADHD, the authors note. “The reinforcing responses to methylphenidate were negatively correlated with the dopamine increases, suggesting that decreased dopaminergic activity may also be involved in modulating the magnitude of the reinforcing effects of methylphenidate,” they continue. “This suggests that dopamine dysfunction is involved with symptoms of inattention but may also contribute to substance abuse comorbidity in ADHD.”
(Arch Gen Psychiatry. 2007;64(8):932-940. Available to the media pre-embargo at www.jamamedia.org).
Note: This research was supported in part by the Intramural Research Program of the National Institutes of Health, a contract from the Department of Energy, and by a grant from the National Institute of Mental Health. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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