o
postdoctoral research. Raised with a passion for American comic books, Dr.
Sliskovic says he jumped at the opportunity to come to the U.S.
Two
years later, his research completed, he received a job offer from
Warner-Lambert Co.'s Ann Arbor labs. "Holy cow! I accept," he
remembers saying.
Dr.
Sliskovic was hired as the pharmaceutical business entered a golden era of huge
profits. Its labs churned out drugs for chronic conditions such as heart
disease and depression, while its armies of salesmen promoted them through
aggressive marketing. Warner-Lambert assigned him to a team of three other
chemists investigating a new idea: whether lowering cholesterol -- the soft,
waxy substance that can clog arteries -- would help people avoid heart attacks.
Other companies were at work on similar projects.
Dr.
Sliskovic's new boss, Bruce Roth, had invented a chemical structure that he
thought would work. In the late 1980s, Dr. Sliskovic fine-tuned the compound,
isolating its potent part. An early version of the compound wasn't absorbed
well by the body, so the team brainstormed about how to modify it to get more
of it into the bloodstream. "We sat around the table and said 'You try
this, you try that,' and they said, 'Bob, why don't you look at salt
formation?'" Dr. Sliskovic recalls.
A
calcium salt he tried solved the problem, and Lipitor was born. Though it would
reach the market in 1997 after several rival drugs, Lipitor would turn into a
blockbuster because it was more potent.
Its
runaway success sparked Pfizer's $116 billion hostile takeover of
Warner-Lambert in 2000. Ahead of the takeover, Pfizer suggested one of Warner's
main appeals was its research-and-development force. "We would like to
keep them all," Pfizer's then-research chief, John Niblack, told The Wall
Street Journal in 1999. "You need a big staff to run this strategy.
Warner-Lambert offers us a nice instant fix."
With
the acquisition, New York-based Pfizer inherited the Ann Arbor labs where Dr.
Sliskovic worked and continued to base much of its pharmaceutical research
there. Between 2001 and 2006, it invested $300 million to expand the
facilities.
By
that time, Dr. Sliskovic had moved on to other projects. As Lipitor traveled
down the long road of animal and human testing in the early '90s, he led a
group of chemists developing drugs to prevent cholesterol from being absorbed
by the body and stored in arteries. Lipitor, by contrast, works by reducing the
amount of cholesterol the liver produces.
One
compound, called avasimibe, seemed to work well in animals. Despite skepticism
from higher-ups, Dr. Sliskovic and his team persuaded Warner-Lambert to take it
into human testing. For a while, it looked as though avasimibe could be a
contender to succeed Lipitor. But it failed in an intermediate stage of
clinical testing, and the company abandoned it.
Dr.
Sliskovic had devoted about six years to the drug. He recalls needing pep talks
from his boss about picking up and starting over. He blocked out
disappointment, he says, by throwing himself into the day's science rather than
thinking about the odds of creating a marketable drug. "You've got to
develop the hide of a rhino," he says.
In
the mid-90s, he tried to develop compounds to counter inflammation in the
heart, which some scientists think can cause heart attacks. Those projects also
flopped but got him interested in another area of research, inflammatory
arthritis.
Dr.
Sliskovic took on the challenge of finding a drug that would repair the
cartilage that can break down between bones and cause arthritic pain. But the
several compounds he concocted didn't meet testing requirements. In 1999, Dr.
Sliskovic was promoted to a management role that took him away from the
day-to-day work of drug discovery. He says his new job required him to teach
his scientists how to remain excited in the wake of failure. "It was me
who started telling them, 'Oh well, never mind. What can we do about this other
project?'" he says.
But
over time those failures added up. In December 2006, Pfizer killed torcetrapib,
the cholesterol compound the company had placed its hopes on, because it was
associated with too many deaths in clinical testing. It was a huge setback
because Pfizer didn't have much else in its research pipeline to replace
Lipitor's sales. The company relies on Lipitor for more than a quarter of its
revenues, and the drug could face generic competition as early as 2010.
The
company has had some successes: Pfizer appears to have a rich cancer-drug
pipeline and has come up with two notable new chemical-based hits recently, the
antismoking medicine Chantix and a pain drug, Lyrica, which was discovered in Ann
Arbor. The company's new chief executive, Jeffrey Kindler, has emphasized
biotech after taking over some 16 months ago. In October, Pfizer opened a new
biologics center in San Francisco.
By
January 2007, Mr. Kindler was promising to do something radical to shake the
world's biggest drug maker out of its worsening slump. Rumors of layoffs were
swirling at Pfizer. Few imagined anything as drastic as closing the
half-century-old Ann Arbor labs, where Pfizer was just finishing the $300
million expansion.
Dr.
Sliskovic says he learned of the closure on Jan. 22, in a morning meeting with
the site's top managers. The room went silent, he says.
After
the meeting, Dr. Sliskovic called his wife on her cellphone to tell her the
news. She thought he was kidding. Realizing he was serious, she offered to
increase her hours at her part-time job at a pet-food store. Later, at home
over lunch, his 19-year-old daughter asked whether they would have to sell the
family's three horses.
The
announcement also took Michigan officials by surprise. The state, which has the
country's worst unemployment rate, was already reeling from auto-industry cuts.
Pfizer was also Ann Arbor's largest taxpayer, contributing $14 million a year
into city coffers. At a press conference later in the day, local officials
pledged to fight for scientists to stay in the area. Later, they pledged $8
million in interest-free loans for start-ups run by laid-off scientists or
existing companies that hire them. A state-budget deadlock delayed the money
for months, but it is now being handed out to scientists.
Pfizer
offered about half of the Ann Arbor researchers internal transfers, mostly to
its other big research facility, in Groton, Conn. But a higher proportion of
those offers went to biologists than to chemists, former lab employees say.
Though it is far from abandoning chemistry-based research, Pfizer has been
increasingly outsourcing chemistry work to contract research organizations,
some in India. Pfizer declined to comment on which scientists were offered
transfers.
In
April, about 80 laid-off Pfizer chemists from Ann Arbor traveled to nearby
Detroit to hear a talk by career consultant Lisa Balbes. Ms. Balbes told them
the story of a former chemist who now uses her skills to enhance acoustics in
stereo systems. Her message: Start thinking about different career paths.
As
winter turned into spring, Dr. Sliskovic found himself going to a parade of
goodbye parties for colleagues. Dr. Roth, his former boss, left in April for
Genentech Inc., the biotech pioneer based in South San Francisco. Dr. Sliskovic
organized the send-off. In early May, David Canter, the head of the Ann Arbor
site, threw a dinner party for other departing employees. A band played songs
parodying Pfizer and the executive who symbolized headquarters'
decision-making: John LaMattina, Pfizer's Connecticut-based head of research.
To the tune from Evita, they sang, "Don't Cry for Me, LaMattina."
A
few weeks later, Dr. LaMattina himself announced his retirement, as part of Mr.
Kindler's broad reorganization of top company executives.Martin Mackay, who
succeeded Dr. LaMattina as research chief and played a major role in the
research restructuring, says the company was "very aware" of its
impact on the community. "We made this decision after very careful and
thorough review of all possible alternatives," Mr. Mackay said in a
statement.
Scott
Larsen, one of the chemists who attended the going-away party, came to Pfizer
four years ago when the company merged with his former employer, Pharmacia
Corp. He applied for a transfer to Groton but didn't get an offer. He tells his
two sons, who are both in college and love science, not to go work for a drug
company.
In
August, Dr. Sliskovic's team stopped doing research and began transferring
projects to other Pfizer sites. The labs are now being cleaned, inspected and
sealed off. The 177-acre campus is a ghost town of empty rooms and boxed-up
equipment.
Dr.
Sliskovic didn't seek an internal transfer. He felt that moving would be too
hard on his family.
As
acting head of chemistry at the Ann Arbor labs, Dr. Sliskovic earned far above
the $112,000 a year paid to the average chemist of his experience level. Dr.
Sliskovic says he will receive severance pay for between 18 months and two
years. With two children in college and another in high school, he says, two
years is the longest he could afford to forgo a paycheck.
Dr.
Sliskovic has already repainted the family kitchen and living room. Now he is
festooning the house and yard with holiday lights. Worried about their
financial future, his wife, Cindy, took a second part-time job at the barn
where they keep their horses. The irony that the drug her husband helped
discover will bring in nearly $13 billion for Pfizer this year hasn't been lost
on her. As a staff scientist, Dr. Sliskovic earned no bonus or royalties for
his work on Lipitor.
Former
Pfizer scientists have founded 23 companies in the area. Dr. Sliskovic says he
would prefer to do the creative work of discovering drugs instead of the rote
chemistry some such companies do for drug makers.
Instead,
he dreams of being involved in another blockbuster. Sometimes, he says, he lies
in bed at night wondering if it will happen. "If the best thing I did was
Lipitor in 1988, it's like being the high-school athlete who was on the
football team and that was that," he says.
22222222222222
Louis J
Sheehan Major Jackson
attended
these gatherings with unfailing regularity, but soon after
his
arrival he drew the line at dancing, and musical parties became
the
limit of his dissipation. He was anything but a convivial
companion.
He never smoked, he was a strict teetotaller, and he never
touched a
card. http://Louis-J-Sheehan.us
His
diet, for reasons of health, was of a most
sparing
kind; nothing could tempt him to partake of food between his
regular
hours, and for many years he abstained from both tea and
coffee.
In those peaceful times, moreover, there was nothing either
commanding
or captivating about the Professor of Artillery. His
little
romance in Mexico had given him no taste for trivial
pleasures;
and his somewhat formal manner was not redeemed by any
special
charm of feature.
It took
some time for his subordinates to develop a deep and abiding respect for
General Jackson, but after he lead them to numerous victories against superior
forces the bond was established that lasted until his untimely death. One of
the great contradictions in Jackson's life was his steadfast Christian beliefs
contrasted with his unrelenting will to destroy the enemy on the battlefield.
For example, http://louis-j-sheehan.us/Blog/blog.aspx
Tate
mentions an exchange between Jackson and his chief surgeon when the surgeon
inquired, "How shall we ever cope with the overwhelming numbers of the
enemy?" http://louis-j-sheehan.us/page1.aspx
After a
long pause Jackson replied, "Kill them, sir! Kill every man." It was
that strength of will that helped make Jackson the hero that he was and is.
Stonewall
Jackson usually thought only in terms of attack. This attitude was exemplified
on December 14, 1862, at Fredericksburg, Virginia. Vastly outnumbered by the
Federals, Jackson was asked by a staff member, ⌠How shall we ever cope with the
overwhelming numbers of the enemy ?■ Jackson▓s reply was to the point, ⌠Kill
them, sir, kill every man!■
General
Jackson.."Kill them, kill them all, sir!"
http://louis-j-sheehan.us/Blog/blog.aspx
888888
December 9, 2007
Your Child’s Disorder May Be
Yours, Too
BY age 2 it was clear that the boy had a
sensibility all his own, affectionate and distant at the same time, often more
focused on patterns and objects than the people around him.
He was neither naturally social like his mother,
nor an early and gifted reader like his father. Quirky, curious, exuberant, he
would leap up and dance across the floor after solving a problem or winning a
game, duck walking like an N.F.L. receiver posing for a highlight film.
Yet after Phil and Susan Schwarz received a
diagnosis for their son, Jeremy, of high functioning autism, they began to think carefully about
their own behaviors and histories.
Mr. Schwarz, a software developer in Framingham,
Mass., found in his son’s diagnosis a new language to understand his own life.
His sensitivities when growing up to loud noises and bright light, his own
diffidence through school, his parents’ and grandparents’ special intellectual
skills — all echoed through his and Jeremy’s behavior, like some ancient
rhythm.
His son’s diagnosis, Mr. Schwarz said, “provided a
frame in which a whole bunch of seemingly unrelated aspects of my own life
growing up fit together for the first time.”
Researchers have long known that many psychiatric
disorders and developmental problems run in families. Children born to parents
with bipolar disorder, in which moods cycle between
euphoria and depression, run about eight times the normal
risk for developing a mood problem. Those born to parents with depression run
three times the usual risk. Attention and developmental disorders like autism
also have a genetic component.
AS more youngsters than ever receive diagnoses of
disorders — the number has tripled since the early 1990s, to more than six
million — many parents have come to recognize that their own behavior is
symptomatic of those disorders, sometimes in a major, but more commonly, in a minor
way. In effect, the diagnosis may spread from the child to other family
members, forcing each to confront family frustrations and idiosyncrasies that
they might prefer to have left unacknowledged.
“It happens very frequently, with all sorts of
disorders, from attention-deficit difficulties to mood problems like bipolar
disorder,” said Dr. Gregory Fritz, a child psychiatrist and academic director
of Bradley Hospital in Providence, R.I., the largest child-psychiatry hospital in the country. “Sometimes
it’s a real surprise, because the child is the first one in the family ever to
get a thorough evaluation and history. The parents are there, and they begin to
see the pattern.”
But diagnosing an adult through his or her child
has its risks, psychiatrists say. In an act of solidarity,
parents may exaggerate similarities between their thinking and behavior and
their son’s or daughter’s. Families desperate to find a diagnosis for a
troubled child are also prone to adopt a vague label — bipolar disorder, say,
which is not well understood in young children — and attribute all variety of
difficulties to it, when the real source may be elsewhere.
But psychological experts say traces of a disorder
in the family tree are very often real, and the stickier issue is what to do
once they surface.
Depending on the family, for instance, one parent
may not want to shoulder the responsibility for having “passed on” the behavior
problem, they say. “The adult may have spent a lifetime compensating for the
problem, as well, and is still struggling with it and would rather not be
identified that way,” said Dania Jekel, executive director of the Asperger’s
Association of New England.
Openness can nonetheless have its benefits, say
parents who have chosen to accept their contribution to a child’s diagnosis.
Self-examination, for instance, may lead to an appropriate diagnosis for the
adult.
Norine Eaton, 51, of Williamsville, N.Y., reared
two boys who were diagnosed with attention deficit disorders. “The younger one
was literally climbing out second-floor windows, climbing bookcases, onto
counters,” she said. “Nothing was safe in the house. It was insanity.”
After the boy and his brother each received a
diagnosis of attention deficit disorder, Ms. Eaton sought treatment at the
Center for Children and Families at the State University at Buffalo, where she
now works. She soon began thinking about her own behavior, past and present.
She had long had difficulty focusing on even simple jobs, like paying bills on
time and remembering and keeping appointments.
She decided to have one of her sons’ psychologists evaluate her for attention
problems. The symptoms of attention deficit disorder, which some scientists now
see as a temporary delay in the maturing of the brain, can last through
adulthood, but it almost always shows up first in childhood. To make a proper
diagnosis, doctors like to see some evidence of a problem in childhood —
evidence that can be hard to come by.
“In my case, I went to school here in Buffalo, and
I dug through some boxes and found reports going back to elementary school,”
Ms. Eaton said. “Sure enough, they said things like, ‘Disorganized,’ and ‘Has
trouble paying attention.’”
She now takes a stimulant medication, she said,
that helps her focus enough to compensate for the problem, by making calendars,
notes to herself, and responding to invitations and messages on time. Once it’s
out in the open, knowledge of a parent’s diagnosis or behavioral tendencies can
ease strained relations in a family, especially if the previously unappreciated
disability contributed to the rupture.
John Halpern, 76, a retired physicist living in
Massachusetts, began to review his own life not long after hearing a radio
interview with an expert on Asperger’s syndrome. He immediately recognized
himself as a textbook case, he said, and decided to call his daughter, whom he
hadn’t spoken to in 10 years. He wanted to apologize, he said, “for my
inadequacy as both a father and a husband to her mother.”
But as soon as he started explaining, he said, his
daughter cut him off. “That’s Asperger’s,” she told him. “She knew,” he said.
“She had been looking into it herself, wondering if in fact I had it.”
Mr. Halpern said that over several calls they
shared feelings and agreed “to work on our new relationship and see how far we
can take it.” The two now talk regularly, at least once a week, he said.
Children made miserable by a psychiatric or
developmental disorder may not always want company; but they often long for
evidence that they aren’t the only ones putting a burden on the family, some
psychiatrists say. Having a parent with the same quirks who can talk about it
eases the guilt a child may feel. The child has a fellow traveler, and in some
families maybe more.
“When we got reports that our son was not
interacting in school, that he was very quiet, slouching, unusual — we said,
‘Well, that’s us; our family is like that,’” said Susan Shanfield, 54, a social
worker living in Newton, Mass.
AFTER her son’s difficulties were diagnosed as a
learning deficit, a neuro-lingual disorder, she quickly identified some of the
same traits in herself. “It was very therapeutic for me,” she said. “I had
known I was different from an early age, and now I had a definition that could
at least explain some of that. I also told my father, a man now in his 80s, and
he was very moved by it.” He has since talked openly about painful memories
from growing up, and during his time raising his own family, that were all but
off-limits before, she said, and become more tolerant of his own past mistakes
and others’.
It can alter the present, too, if parent and child
have enough common ground. Mr. Schwarz, the software developer in Framingham,
said he became in some ways like a translator for his son, who’s now 16.
“I think there are a lot of parents of kids with
these diagnoses who have at least a little bit of the traits their kids have,”
Mr. Schwarz said. “But because of the stigma this society places on anything associated
with disability, they’re inhibited from embracing that part of themselves and
fully leveraging it to help their kids.”
Astronomers are radically reshaping our picture of the Milky Way’s
neighbors. Our corner of the cosmos, known as the Local
Group, includes two giant spiral galaxies—the Milky Way and
Andromeda—and smaller satellite galaxies orbiting them. The Milky Way was
thought to have about 10 satellites, but within the last year or so,
that number has nearly doubled. “Most astronomers, myself included, thought we
at least knew the members of the Local Group,” says Daniel Zucker of Cambridge
University, whose team found the new batch of eight galaxies. “I don’t think
anyone expected us to find a significant population of these things. They’re
fainter than anybody thought a galaxy could be—even smaller and less luminous
than what are typically considered dwarf galaxies,” he adds, so they became
“hobbit galaxies.” One, Leo T, still has gas associated with it, providing the
raw material for stellar births. “It’s arguably the smallest star-forming
galaxy known,” Zucker says. The survey that found the satellite galaxies
scanned only a fifth of the sky, so there could be dozens more waiting to be
found.
In another surprise,
Harvard University astrophysicist Nitya Kallivayalil recently announced that
two of our largest satellite galaxies probably aren’t satellites at all.
Kallivayalil found that the Large and Small Magellanic
clouds are shooting by us at around 200 miles per second, faster
than a satellite would. With that kind of speed, she says, they are likely to
be travelers speeding through the region. The only scenario in which the clouds
could remain satellites enthralled in the gravitational pull of the Milky Way
requires that the galaxy have twice its currently estimated mass.
Astronomers are also resizing our largest neighboring galaxy, Andromeda, finding that its radius is up to
five times larger than anyone thought. Observations revealed a halo of stars
half a million light-years from the galaxy’s center but still bound to it.
“Much of the space between the Milky Way and Andromeda is filled with stars
that belong to those galaxies,” says University of California at Santa Cruz
astronomer Raja Guhathakurta, whose team discovered the halo. “They practically
overlap. It really challenges the notion of galaxies as groups of stars with
empty space between them.”
Future astronomers will
become intimately acquainted with Andromeda as it screams toward us on a collision course with the Milky Way. A new
simulation indicates that the first pass of galactic jousting will
occur in 2 billion years, and the galaxies will fuse within 5 billion years. As
the universe expands, all other galaxies will fade from sight. Harvard
astrophysicist Avi Loeb, who developed the simulation, says astronomers should
appreciate that we live at a special time in cosmic history: “Now when we look
up, we see many galaxies. In the distant future, this will become a lonely
place, with nothing to look at. If we want to learn about the universe at
large, we’d better do it while we still can.”
Muons
Meet the Maya
At its
most glamorous, the life of an experimental high-energy physicist consists of
smashing obscure subatomic particles with futuristic-sounding names into each
other to uncover truths about the universe—using science's biggest, most
expensive toys in exciting locations such as Switzerland or Illinois. But it
takes a decade or two to plan and build multibillion-dollar atom smashers.
While waiting, what's a thrill-seeking physicist to do?
How about using some
of the perfectly good, and completely free, subatomic particles that rain down
on Earth from space every day to peek inside something really big and
mysterious, like, say, a Mayan pyramid? That's exactly what physicist Roy
Schwitters of the University of Texas at Austin is preparing to do.
High-energy particles
known as muons, which are born of cosmic radiation, have ideal features for
creating images of very large or dense objects. Muons easily handle situations
that hinder other imaging techniques. Ground-penetrating radar, for instance,
can reach only 30 meters below the surface under ideal conditions. And seismic
reflection, another method, doesn't fare well in a complex medium. With muons,
all you need is a way to capture them and analyze their trajectories.
Besides probing
pyramids in Belize and Mexico, physicists are applying the muon method to
studying active volcanoes and detecting nuclear materials. The concept sounds
out of this world, but it's really quite simple. When cosmic rays hit the
Earth's atmosphere, collisions with the nuclei of air atoms spawn subatomic
particles called pions that quickly decay into muons that continue along the
same path. Many of the muons survive long enough to penetrate the Earth's
surface. Because of their high energy, the particles can easily pass through
great volumes of rock or metal or whatever else they encounter. However, they
are deflected from their path by atoms in the material, and the denser the
material, the greater the deflection.
Schwitters wants to
exploit this deflection to see if there are any rooms or chambers inside a
Mayan pyramid in Belize, he told science journalists in Spokane, Wash., at a
recent meeting sponsored by the Council for the Advancement of Science Writing.
His team is building several muon detectors that would be buried in shallow
holes around the base of the pyramid to create an image of what's inside by
measuring the trajectories of the muons that pass through it.
"What you see is
very much like an X ray," he says. "If you see a spot with more
muons, it means there's a space there. If you see fewer muons, it means there's
something extra-dense there."
Schwitters won't be
the first to marry physics and archaeology in this way. In 1967, Nobel
prize–winning physicist Luis Alvarez of the University of California, Berkeley
placed a muon detector in a chamber beneath the pyramid of Khafra in Egypt to
see if it was hiding any burial chambers like those discovered in the larger
pyramid of Khufu. He found none, but the experiment showed that the method
worked.
As the director of the
Superconducting Supercollider laboratory in Texas until 1993, when Congress
gave the project the axe, Schwitters is no stranger to waiting for the next big
thing. And he has always been intrigued by the possibility of applying the
tools of the high-energy physics trade elsewhere, so a chance conversation with
one of Alvarez' former colleagues, combined with a little spare time, got
Schwitters wondering what other enigmatic ancient structures were waiting to be
probed.
Archaeologist Fred
Valdez, director of the Mesoamerican Archaeological Research Laboratory at UT
Austin, had the answer: an enormous pyramid in the third-largest Mayan city in
Belize. The city is in an area in northwestern Belize known as La Milpa, which
was home to one of the densest populations of Maya from as early as 1000 B.C.
until around A.D. 850. The area was packed with four large cities, each with
20,000 or more residents, that were only around 8 to 12 kilometers apart with
60 or more towns, villages, and hamlets in between. Valdez believes there is much
to be learned from the society that existed there.
"The amazing part
is how close how many of these large cities are to each other," he said.
"The Maya were clearly expert at adapting to their environment and
exploiting their environment, clearly making better use of things than we are
today, just to support the populations that were there."
Because there isn't a
chamber below the La Milpa pyramid, Schwitters plans to harness muons with four
or five smaller detectors spaced around the structure to get a
three-dimensional view inside. Each detector will be a cylinder wrapped with
strips of polystyrene, which emits light when hit by a muon. The bursts of
light as each particle passes through both sides of the detector will be
recorded by photo detectors at the end of the cylinder and used to reconstruct
the muon trajectories.
Dense matter will
deflect muons away from their paths, so fewer muons will hit the detectors from
that area while more particles will pass through empty spaces to reach the
detectors. A computer program will translate the information into an image that
can be read like a CT scan or an X ray with bright spots indicating voids and
dark areas correlating to more dense matter. Because muons hit the Earth at the
rate of about 1 per square centimeter per minute, it will take several months
to get a good image of the guts of the pyramid. Schwitters hopes he'll be able
to resolve chambers as small as a cubic meter.
Knowing exactly where
to dig to find potential tombs or other chambers could save precious time when
dealing with very large structures like the pyramid in Belize. It could also
save artifacts that need special treatment, sometimes within hours, to keep
them from deteriorating from exposure. Dust in a tomb that is normally trampled
during excavation could contain valuable information about diseases that
affected the Maya, or about the plants and herbs they used.
"Ideally, the
results would give us a look into the building without having to do the
destructive process of excavation," Valdez said.
He envisions being
able to drill a small auger hole into a chamber and send a fiber-optic camera
down to take a look. That way he can study the chambers exactly as they were
left, and the appropriate experts and equipment can be on hand to deal with the
contents as they are exposed by coating them with resin, immersing them in
water, or sealing them in an airtight case.
"That's
tremendous information," he said. "It's almost like 20/20
hindsight."
With funding from
Sandia National Laboratory in Albuquerque, N.M., and support from UT and
National Instruments, Schwitters' team has already built and successfully
tested one detector at UT that weighs in around a ton, at 4.5 m long with a 1.5
m diameter. The detectors that will go to Belize will be much smaller, around
the size of water heaters and weighing about 200 pounds. Depending on funding,
the detectors could be ready for showtime in 2009.
Another team of
scientists may be just months away from using muons to image the Pyramid of the
Sun in Teotihuacán, Mexico, in a quest to learn why the pyramid was built. And
if burial chambers such as those found in the nearby Pyramid of the Moon are
discovered, they could reveal whether the society was ruled by a single person
or a government of several leaders.
Led by physicist
Arturo Menchaca-Rocha of the National Autonomous University of Mexico, the team
is currently working out some kinks in its detector having to do with wires
cracking from temperature changes. Once that hurdle is cleared, which will
likely be sometime after January, their single detector will be placed in a
tunnel discovered under the pyramid in 1971, much like Alvarez' experiment in
Egypt.
"We are quite
delayed," Menchaca-Rocha said in an e-mail from a meeting in Veracruz.
"But the pyramid has been sitting there for 2,000 years, so it can wait
for us to be perfectly happy about the detector."
In the meantime,
physicists at Los Alamos National Laboratory in New Mexico are looking to muons
to help detect special nuclear materials such as plutonium and uranium at the
country's borders. Current nuclear-detection capability relies on identifying
the gamma-ray radiation emitted by the materials, but that doesn't always work.
"If someone wants
to bring in nuclear material to build a bomb, they need to shield it with
something dense like lead to stop the gamma rays," says Los Alamos
physicist Chris Morris.
So Morris is working
on a detector that would use muons to root out both nuclear materials and
shielding. Lead is dense enough to perturb a muon's path, and it is even easier
to spot the muon fingerprint of things like plutonium and uranium because their
high density and big atomic charge scatter the particles more than anything
else.
Los Alamos lab has
partnered with Decision Sciences Corporation of San Diego to build a prototype
four-sided muon detector that resembles a carport before the end of the year.
Vehicles would drive into the device like entering a car wash and wait while
detectors on all four sides of the tunnel record muon trajectories. A single
muon would be recorded by multiple detectors, revealing any changes in its
path.
"It measures the
track of every muon going through the vehicle," Morris says. "In 20
seconds you can detect whether or not they have a chunk of metal that's 4
inches by 4 inches by 4 inches. If you went a little longer, you can see
something smaller."
But the real strength
of muon imaging is tackling very large structures, such as volcanoes, that defy
other methods. Scientists led by Hiroyuki Tanaka of the University of Tokyo
installed a single muon detector 1 kilometer from the summit of Mount Asama on
the main island of Japan. By measuring muons traveling nearly horizontally
through the volcano, the detector successfully imaged a lava mound that was
created a few hundred meters below the crater floor during a 2004 eruption and
a conduit below it.
"The cosmic-ray
muon imaging technique has much higher resolving power than conventional
geophysical techniques, with resolutions up to several meters allowing it to
see smaller objects and greater detail in volcanoes," Tanaka wrote in a
report on the results of the Mount Asama study in the Nov. 15 Earth and Planetary Science Letters.
Tanaka's team has also
used muon detection to image a lava dome that has been smoking since 1945 on
the flank of Usu volcano in Hokkaido, Japan. Both of Tanaka's current studies
involved single detectors. But adding more detectors would give a
three-dimensional view and help untangle the effect of higher-density materials
on the muons from that of a longer distance traveled through somewhat
less-dense material.
"This technique
might provide a way to forecast a volcanic eruption by monitoring changes in
the density of the magma channel inside the summit region of a volcano,"
Tanaka writes in a study on the lava dome in the Nov. 16 Geophysical Research Letters.
Even more promising is
a real-time digital muon camera that Tanaka is working on that could capture
real-time images of an active volcano. He hopes to have one installed with a
view of Mt. Asama from 1.5 km away by May 2008, and a second one sometime
thereafter that could provide a 3-D picture of Asama's next eruption.
"With this
device, I think that the technique would be more practical for use in
forecasting eruptions," he wrote in an e-mail from Japan.
Schwitters envisions
other geologic studies that could benefit from muon detection, such as gauging
the size and location of underground aquifers or assessing the stability of the
geology around nuclear-waste depositories. But for now he is content to focus
on the pyramids buried under dirt, trees, and vines in the forest in Belize.
"There
is good reason to believe they contain rooms and chambers that have not been
disturbed since the Maya left, and that's what makes them so exciting," he
says.
Jim Hammond is an elite athlete. He works out two hours a day with a
trainer, pushing himself through sprints, runs, and strength-building
exercises. His resting heart rate is below 50. He’s won three gold medals and
one silver in amateur competitions this year alone, running races from 100 to
800 meters. In his division, he’s broken four national racing records. But
perhaps the most elite thing about Hammond is his age.
He is 93. And really, there’s nothing much wrong with him, aside from
the fact that he doesn’t see very well. He takes no drugs and has no
complaints, although his hair long ago turned white and his skin is no longer
taut.
His secret? He doesn’t
have one. Hammond never took exceptional measures during his long life to
preserve his health. He did not exercise regularly until his fifties and didn’t
get serious about it until his eighties, when he began training for the Georgia
Golden Olympics. “I love nothing better than winning,” he says. “It’s been a
wonderful thing for me.” Hammond is aging, certainly, but somehow he isn’t
getting old—at least, not in the way we usually think about it.
They say aging is one of the only certain things in life. But it turns
out they were wrong. In recent years, gerontologists have overturned much of
the conventional wisdom about getting old. Aging is not the simple result of
the passage of time. According to a provocative new view, it is actually
something our own bodies create, a side effect of the essential inflammatory
system that protects us against infectious disease. As we fight off invaders,
we inflict massive collateral damage on ourselves, poisoning our own organs and
breaking down our own tissues. We are our own worst enemy.
This paradox is transforming the way we understand aging. It is also
changing our understanding of what diseases are and where they come from.
Inflammation seems to underlie not just senescence but all the chronic
illnesses that often come along with it: diabetes, atherosclerosis, Alzheimer’s,
heart attack. “Inflammatory factors predict virtually all bad outcomes in
humans,” says Russell Tracy, a professor of pathology and biochemistry at the
University of Vermont College of Medicine, whose pioneering research helped demonstrate the
role of inflammation in heart disease. “It predicts having heart attacks,
having heart failure, becoming diabetic; predicts becoming fragile in old age;
predicts cognitive function decline, even cancer to a certain extent.”
The idea that chronic diseases might be caused by persistent
inflammation has been kicking around since the 19th century. Only in the past
few years, though, have modern biochemistry and the emerging field of systems
biology made it possible to grasp the convoluted chemical interactions involved
in bodywide responses like inflammation. Over a lifetime, this essential set of
defensive mechanisms runs out of bounds and gradually damages
organs throughout the body.
When you start to think about aging as a consequence of inflammation,
as Tracy and many prominent gerontologists now do, you start to see old age in
a different, much more hopeful light. If decrepitude is driven by an overactive
immune system, then it is treatable. And if many chronic diseases share this
underlying cause, they might all be remedied in a similar way. The right
anti-inflammatory drug could be a panacea, treating diabetes, dementia, heart
disease, and even cancer. Such a wonder drug might allow us to live longer, but
more to the point, it would almost surely allow us to live better, increasing
the odds that we could all spend our old age feeling like Jim Hammond: healthy,
vibrant, and vital. And unlike science fiction visions of an immortality pill,
a successful anti-inflammatory treatment could actually happen within our
lifetime.
For the last century and a half, the average life span in wealthy
countries has increased steadily, climbing from about 45 to more than 80 years.
There is no good reason to think this increase will suddenly stop. But longer
life today often simply means taking longer to die—slowly, expensively, and
with more disease and disability. “If you talk to many old people, what they
are really desperate about is not the fact that they’re going to die but that
they are going to be sick, dependent, have to rely on others,” says Luigi
Ferrucci, chief of the longitudinal studies section at the National Institute
on Aging and director of the Baltimore Longitudinal Study of Aging, the
nation’s longest-running study of old age.
Biologists have known for a while that inflammation increases with
age, but until recently, given everything else that slumps, spikes, or goes off
the rails as we get old, it didn’t seem especially important. Some researchers
on aging still think that way.
But a big clue linking inflammation with aging came in the late 1990s,
when Tracy and his colleagues showed that C-reactive protein (CRP), an
inflammatory protein, is an amazingly accurate predictor of a future heart attack—as
good as or better than high blood pressure or high cholesterol. At least in
heart disease, inflammation isn’t just a bystander. What’s more, we could do
something to decrease it. Aspirin, which was already known to help people with
heart disease, seems to work primarily by reducing inflammation.
So why should our own
immune system rely on such an apparently dangerous mechanism? The answer lies
in the fact that infectious disease has historically been the number one killer
of human beings, and responding to this threat has profoundly shaped our
biology. Possessing a fierce and ferocious immune response primed to keep us
alive long enough to reproduce was an evolutionary no-brainer.
Inflammation is what gives us that response. It serves as all-purpose
protection against invaders and traumatic damage. To take a simple scenario,
suppose you are bitten by a cat. First, coagulation factors promote clotting in
order to stanch bleeding and prevent germs from spreading from the wound site.
A menagerie of phagocytes, which swallow and destroy pathogens, surge out of
the bloodstream and squeeze into the affected tissue, engulfing bacteria and
secreting cytokines—messenger proteins that send out the call for more
responders. The phagocytes also generate reactive oxygen species, unstable compounds
that chew up bacteria as well as damaged human tissue.
At the same time, other switches get flipped throughout the body,
modifying everything from metabolism to cell growth, via other cytokines, such
as IL-6 and tumor necrosis factor–a, and things like CRP, which mark bacteria
for destruction. The specialized adaptive immune response eliminates any
remaining germs.
So far, so good. But the
inflammation response can kick in even when there’s no invader. Atherosclerosis, or hardening of the arteries,
is a classic example. In response to fatty deposits on the walls of the
arteries, a type of phagocyte called a macrophage identifies the growing
lesions as trouble spots and infiltrates them, swelling and destabilizing the
deposits. Those lesions can then break open, resulting in the formation of a
blood clot that can clog blood vessels and cause heart attacks. The more active
the macrophages are, the more CRP is in the bloodstream, and the more likely
the lesions will break open, block your arteries, and kill you.
The evidence that inflammation is behind other diseases is indirect,
but it is mounting. Researchers have long known that in patients with
Alzheimer’s, the areas of the human brain clogged with senility-associated
plaques also bristle with inflammatory cells and cytokines.
Modern research has found that cytokines block memory formation in mice. In
diabetes, inflammation and insulin resistance apparently track together, and
drugs that effectively restore insulin sensitivity also appear to reduce
inflammatory factors like IL-6 and CRP. Inflammation is also being investigated
by a group at Leiden University in the Netherlands as a culprit in declining
lung function, in osteoporosis, and in old-age depression. Even the weakness of
old age may have an inflammatory cause: Ferrucci has found that inflammatory
activity breaks down skeletal muscle, leading to the
loss of lean muscle mass. Being fat makes all these diseases strike earlier, and that
seems to be at least in part because fat cells spur more inflammation.
These findings have provided researchers with a totally new
appreciation of how subtly inflammation can work and how wildly awry it can go
over time. It’s not about “a massive infection or a welt the size of an egg
because you got hit in the head with a two-by-four,” Tracy says. “Inflammation
also goes on at a much lower level.” As it simmers in the background, over
years and decades, collateral damage accumulates—in the heart, in the brain,
everywhere. Harvey Jay Cohen, chairman of the department of medicine and
director of the Center for the Study of Aging at Duke University Medical
Center, likens inflammation to “little waves lapping on the shore. It’s a relatively
low level of activity, one that sustained over time wears away at the beach and
stimulates other bad events.”
Evolution has designed into us a cruel trade-off: What saves us in the
short term kills us over the long haul. As we get older, acute episodes of
inflammation tend to turn into chronic ones, perhaps because the regulation of
the immune system becomes less efficient. Inflammatory factors in the blood can
increase two- to fourfold. Chronic infections may be partly to blame. Although
we usually don’t know it, nearly all adults are infected with the Epstein-Barr
virus, and at least 60 percent of us with cytomegalovirus. These two pathogens
can stay in our bodies in a latent state, hiding out in our cells. But Ronald
Glaser, a viral immunologist at Ohio State University Medical Center and his
research partner (and wife), psychologist Janice Kiecolt-Glaser, think that
these viruses are not fully dormant. They’ve found evidence
(pdf) that with age, antibodies to these viruses increase, indicating a
reawakened virus and an active immune response.
Early experiences may also influence the way that inflammation affects
an individual’s aging, says Caleb Finch, a neurobiologist and gerontologist at
the University of Southern California. Analyzing historical birth and death
records from 19th-century Europe, he and Eileen Crimmins, a gerontologist and
sociologist at the University of Southern California, found that longevity is directly
related to exposure to childhood disease. Children born during years
of high neonatal mortality who survived to adulthood didn’t live as long as
those born in healthier years. The reason, he says, is inflammation: A high
infectious burden in childhood results in a high inflammatory burden in
adulthood, which results in a shorter, sicker life. Conversely, Finch believes
that people in affluent countries now live so long because their childhoods are
free from diseases like measles, typhoid, malaria, whooping cough, and worms.
Without these diseases, people grow bigger and stronger—and live much longer.
Looking beyond provocative findings like those in Finch’s study, Tracy
and other researchers on aging say that it may be too simplistic to think of
inflammation in terms of straightforward cause and effect. Instead we must
think of human biology as a group of interdependent systems. “Is inflammation a
response to aging, or is it causing aging or disease?” Tracy asks. “My answer
is: Yep, yep, yep. It does all those things. There’s no other way to think
about it—it’s both cause and response to what’s going on.”
Inflammation is not
uncontested as a theory of aging. There are many competing hypotheses. Yet
inflammation reinforces some more than others, potentially establishing a
plausible constellation of mechanisms responsible for aging.
For example, according to the “free radical” hypothesis of aging, we
get older because of constant cellular damage caused by reactive oxygen compounds
that are a natural product of metabolism. Inflammation can partly explain how
this might work. Macrophages, as part of the inflammatory response, produce
reactive oxygen species in order to attack bacteria. Oxidative stress and
inflammation clearly egg each other on, and calming one can inhibit the other.
To take another prominent example, a low-calorie diet is known to increase the life spans of
creatures ranging from flatworms to rats, but no one knows why,
or whether it will help humans live longer. Inflammation provides a clue:
Dietary restriction sharply inhibits the inflammatory response, and that may be
part of why it promotes longevity at the same time that it reduces insulin
resistance and slows dementia. Yet another widely discussed theory of why we
age blames the shortening of telomeres, chromosomal structures that, in most
cells, dwindle with each division and may ultimately limit the number of times
any cell can divide. It is possible that inflammation could play a role here,
too, because it prompts the faster turnover of cells in the immune system and
other tissues.
Still, nobody thinks
that there is a single root cause of aging—different species may age in
different ways, and multiple mechanisms are probably at work. “I think it would
be a mistake to suggest that inflammation is the cause of aging, or that all
theories of aging must be tied to it,” Cohen says. Then again it may not
ultimately matter whether inflammation is the most significant cause of our
decay. More important is that inflammation offers an unparalleled opportunity
to do something about it.
Some ways to reduce inflammation are elementary. It is impossible to
know exactly what is going on in Jim Hammond’s body, but all the aspects of his
regimen—healthy food, exercise, and a good attitude—reduce systemic
inflammation. Those of us without his tenacity can turn to drug companies,
which are exploring new anti-inflammatory drugs like flavonoids. Researchers
are also looking at new uses for old drugs—trying to prevent Alzheimer’s using
ibuprofen, for example. “The research is really to prevent the chronic
debilitating diseases of aging,” says Nir Barzilai, a molecular geneticist and
director of the Institute for Aging Research at the Albert Einstein College of
Medicine in New York. “But if I develop a drug, it will have a side effect,
which is that you will live longer.”
Some of this research stretches the boundaries of what we know. Rudi
Westendorp, head of the department of gerontology and geriatrics at the Leiden
University Medical Center, is trying to treat old-age depression with drugs that are
currently used for autoimmune conditions like rheumatoid arthritis. Harvard
University researchers are considering a vaccine against atherosclerosis, which
may provoke a reaction that suppresses inflammation.
The caveat with these experiments is that by modifying inflammation,
we are playing with fire. After all, fighting off infection is an absolutely
essential bodily function. “The danger of monkeying around in a system like
that is that you may do more harm than good,” Cohen says. But humans appear
willing to renegotiate the ancient evolutionary bargain that traded robust
reproductive health for frail old age.
Think of Jim Hammond if
you have any doubts. In his blog, he describes running the 800-meter race in
the 2007 National Senior Olympics games. “I won in a photo finish, and I broke
the national record,” he wrote. The crowd went nuts. At the age of 93, Hammond
had the most exhilarating experience of his entire life.
December 4, 2007
NEWS ANALYSIS
An Assessment Jars a Foreign
Policy Debate About Iran
WASHINGTON, Dec. 3 — Rarely, if ever, has a single
intelligence report so completely, so suddenly, and so surprisingly altered a
foreign policy debate here.
An administration that had cited Iran’s pursuit of nuclear weapons as the
rationale for an aggressive foreign policy — as an attempt to head off World
War III, as President Bush himself put it only weeks ago — now has in its hands
a classified document that undercuts much of the foundation for that approach.
The impact of the National Intelligence Estimate’s
conclusion — that Iran had halted a military program in 2003, though it
continues to enrich uranium, ostensibly for peaceful uses — will be felt in
endless ways at home and abroad.
It will certainly weaken international support for
tougher sanctions against Iran, as a senior administration official grudgingly
acknowledged. And it will raise questions, again, about the integrity of
America’s beleaguered intelligence agencies, including whether what are now
acknowledged to have been overstatements about Iran’s intentions in a 2005
assessment reflected poor tradecraft or political pressure.
Seldom do those agencies vindicate irascible
foreign leaders like President Vladimir V. Putin of Russia, who several weeks
ago said there was “no evidence” that Iran was building a nuclear weapon,
dismissing the American claims as exaggerated.
The biggest change, though, could be its effect on
President Bush’s last year in office, as well as on the campaign to replace
him. Until Monday, 2008 seemed to be a year destined to be consumed, at least
when it comes to foreign policy, by the prospects of confrontation with Iran.
There are still hawks in the administration, Vice
President Dick Cheney chief among them, who view Iran
with deep suspicion. But for now at least, the main argument for a military
conflict with Iran — widely rumored and feared, judging by antiwar protesters
that often greet Mr. Bush during his travels — is off the table for the
foreseeable future.
As Senator Chuck Hagel, Republican of Nebraska, put it,
the intelligence finding removes, “if nothing else, the urgency that we have to
attack Iran, or knock out facilities.” He added: “I don’t think you can
overstate the importance of this.”
The White House struggled to portray the estimate
as a validation of Mr. Bush’s strategy, a contention that required swimming
against the tide of Mr. Bush’s and Mr. Cheney’s occasionally apocalyptic
language.
The national security adviser, Stephen J. Hadley, said the estimate showed
that suspicions about Iran’s intentions were warranted, given that it had a
weapons program in the first place.
“On balance, the estimate is good news,” Mr. Hadley
said, appearing at the White House. “On one hand, it confirms that we were
right to be worried about Iran seeking to develop nuclear weapons. On the other
hand, it tells us that we have made some progress in trying to ensure that that
does not happen. But it also tells us that the risk of Iran acquiring a nuclear
weapon remains a very serious problem.”
Mr. Hadley insisted, as he and others have, that
the administration had hoped and still hoped to resolve the outstanding
questions about Iran’s nuclear programs using diplomacy, not force. But the
nuances of his on-this-hand-on-the-other argument will probably make it much harder
to persuade American allies to accept the administration’s harder line.
One official pointed out that the chief American
diplomat on the Iran question, Under Secretary of State R. Nicholas Burns, had
just met with counterparts from Europe, Russia and China, and had seemed to
make some headway on winning support for a third round of sanctions by the United Nations Security Council. The official
said Mr. Burns could not divulge the intelligence findings at that meeting on
Friday because Congress had not been briefed.
The immediate task for Mr. Burns and other
administration officials is to untangle the confusion caused by its own statements
and findings and to persuade skeptics that this time, the United States has it
right about what Iran was doing before 2003 and what that means for what it
might do in the future.
“The way this will play is that the intelligence
community has admitted it was wrong,” said Jon B. Alterman of the Center for
Strategic and International Studies. “So why should we believe them now?”
Mr. Hadley said the drastic reversal in the
intelligence agencies’ knowledge about Iran’s weapons programs was based “on
new intelligence, some of which has been received in the last few months.”
He also said that he and other senior officials,
including Mr. Cheney, Secretary of State Condoleezza Rice and Secretary of Defense Robert M. Gates, had reviewed it and debated
it two weeks ago.
With some of the administration’s most prominent
hawks having departed and not taking part in the review of findings like these,
it is possible that the zeal for another military conflict has diminished.
After all, the first two wars on Mr. Bush’s watch remain unresolved at best.
Senator Hagel said he hoped that the administration
might in its final year in office show the kind of diplomatic flexibility it
did with North Korea over its nuclear weapons or with the conference in
Annapolis, Md., last week on the Israeli-Palestinian conflict. He has
previously called for the United States to open direct and unconditional talks
with Iran to end the state of enmity that has existed since 1979.
He said Iran’s halt of weapons activity had created
an opening for such talks, indicating, as the assessment does, that Iran’s
government may be more rational than the one that Mr. Bush said in August had
threatened to put the entire region “under the shadow of a nuclear holocaust.”
“If we’re wise here, if we’re careful, I think we
have some opportunities,” Mr. Hagel said.
The findings, though, remain open for
interpretation, as they always do, even in documents meant to reflect the
consensus of the intelligence community. When it comes to Iran, at odds with
the United States on many fronts beyond the nuclear question, hawks remain.
“Those who are suspicious of diplomacy are well dug
in in this administration,” said Kurt M. Campbell, chief executive officer of
the Center for a New American Security.
John R. Bolton, the former ambassador to the United Nations, who recently left the
administration and began to criticize it, sounded very much like Mr. Hadley on
Monday, saying the assessment underscored the need for American toughness. He
said Iran’s intentions would always remain a concern as long as it continued to
enrich uranium.
“The decision to weaponize and at what point is a
judgment in the hands of the Iranians,” he said. He added that the finding that
Iran halted a weapons program could just mean that it was better hidden now.
JAKARTA (Reuters) - Many of Indonesia's islands may
be swallowed up by the sea if world leaders fail to find a way to halt rising
sea levels at this week's climate change conference on the resort island of
Bali.
Doomsters take this dire warning by Indonesian
scientists a step further and predict that by 2035, the Indonesian capital's
airport will be flooded by sea water and rendered useless; and by 2080, the
tide will be lapping at the steps of Jakarta's imposing Dutch-era Presidential
palace which sits 10 km inland (about 6 miles).
The Bali conference is aimed at finding a successor
to the Kyoto Protocol, which expires in 2012, on cutting climate warming carbon
emissions. With over 17,000 islands, many at risk of being washed away,
Indonesians are anxious to see an agreement reached and quickly implemented
that will keep rising seas at bay.
Just last week, tides burst through sea walls,
cutting a key road to Jakarta's international airport until officials were able
to reinforce coastal barricades.
"Island states are very vulnerable to sea
level rise and very vulnerable to storms. Indonesia ... is particularly
vulnerable," Nicholas Stern, author of an acclaimed report on climate
change, said on a visit to Jakarta earlier this year.
Even large islands are at risk as global warming
might shrink their land mass, forcing coastal communities out of their homes
and depriving millions of a livelihood.
The island worst hit would be Java, which accounts
for more than half of Indonesia's 226 million people. Here rising sea levels
would swamp three of the island's biggest cities near the coast -- Jakarta,
Surabaya and Semarang -- destroying industrial plants and infrastructure.
"Tens of millions of people would have to move
out of their homes. There is no way this will happen without conflict,"
Environment Minister Rachmat Witoelar said recently.
"The cost would be very high. Imagine, it's
not just about building better infrastructure, but we'd have to relocate people
and change the way people live," added Witoelar, who has said that
Indonesia could lose 2,000 of its islands by 2030 if sea levels continue to
rise.
CRUNCH TIME AT BALI
Environmentalists say this week's climate change
meeting in Bali will be crunch time for threatened coastlines and islands as
delegates from nearly 190 countries meet to hammer out a new treaty on global
warming.
Several small island nations including Singapore,
Fiji, Kiribati, Tuvalu and Caribbean countries have raised the alarm over
rising sea levels which could wipe them off the map.
The Maldives, a cluster of 1,200 islands renowned
for its luxury resorts, has asked the international community to address
climate change so it does not sink into a watery grave.
According to a U.N. climate report, temperatures
are likely to rise by between 1.1 and 6.4 degrees Celsius (2.0 and 11.5 degrees
Fahrenheit) and sea levels by between 18 cm and 59 cm (seven and 23 inches)
this century.
Under current greenhouse gas emission levels,
Indonesia could lose about 400,000 sq km of land mass by 2080, including about
10 percent of Papua, and 5 percent of both Java and Sumatra on the northern
coastlines, Armi Susandi, a meteorologist at the Bandung Institute of
Technology, told Reuters.
Indonesia, the world's fourth-most populous
country, has faced intense pressure over agricultural land for decades.
Susandi, who has researched the impact of climate
change on Indonesia, estimated sea levels would rise by an average of 0.5 cm a
year until 2080, while the submersion rate in Jakarta, which lies just above
sea level, would be higher at 0.87 cm a year.
A study by the UK-based International Institute for
Economy and Development (IIED) said at least 8 out of 92 of the outermost small
islands that make up the country's borders are vulnerable.
TOO MANY ISLANDS TO COUNT
Less than half of Indonesia's islands are inhabited
and many are not even named. Now, the authorities are hastily counting the
coral-fringed islands that span a distance of 5,000 km, the equivalent of going
from Ireland to Iran, before it is too late.
Disappearing islands and coastlines would not only
change the Indonesian map, but could also restrict access to mineral resources
situated in the most vulnerable spots, Susandi said.
He estimates that land loss alone would cost
Indonesia 5 percent of its GDP without taking into account the loss of property
and livelihood as millions migrate from low-lying coastlines to cities and
towns on higher ground.
There are 42 million people in Indonesia living in
areas less than 10 meters above the average sea level, who could be acutely
affected by rising sea levels, the IIED study showed.
A separate study by the United Nations Environment
Programme in 1992 showed in two districts in Java alone, rising waters could
deprive more than 81,000 farmers of their rice fields or prawn and fish ponds,
while 43,000 farm laborers would lose their job.
One solution is to cover Indonesia's fragile
beaches with mangroves, the first line of defense against sea level rise, which
can break big waves and hold back soil and silt that damage coral reefs.
A more expensive alternative is to erect multiple
concrete walls on the coastlines, as the United States has done to break the
tropical storms that hit its coast, Susandi said.
Some areas, including the northern shores of
Jakarta, are already fitted with concrete sea barriers, but they are often
damaged or too low to block rising waters and big waves such as the ones that
hit Jakarta in November.
"It will be like permanent flooding,"
Susandi said. "By 2050, about 24 percent of Jakarta will disappear,"
possibly even forcing the capital to move to Bandung, a hill city 180 km east
of Jakarta.
(Editing
by Megan Goldin)
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