TRIPOLI (Reuters) ? Libya's interim leader urged NATO on Wednesday to maintain its involvement in the country until the end of the year, though the Western military alliance that helped topple Muammar Gaddafi is keen to wind up its formal mission within days.
With Gaddafi's son and heir-apparent believed still at large and seeking to flee following his father's killing last week, Mustafa Abdel Jalil, chairman of the National Transitional Council (NTC), said he wanted NATO help in stopping Gaddafi loyalists escaping justice.
But at the Brussels headquarters of the alliance, whose air strikes and intelligence backed the motley rebel forces for eight months at substantial financial cost, NATO officials recalled that their U.N. mandate was to protect civilians, not target individuals.
A meeting of NATO ambassadors, postponed from Wednesday to Friday to allow for further discussion with the NTC and United Nations, was still due to endorse a preliminary decision to halt the Libya mission on October 31, a spokeswoman for the bloc said.
Speaking in Qatar, the most active Arab backer of the Western move against Gaddafi, Abdel Jalil told reporters: "We look forward to NATO continuing its operations until the end of the year."
He added: "We seek technical and logistics help from neighboring and friendly countries."
The Libyan war, which saw Gaddafi's power extinguished in late August at a cost of no casualties for NATO forces, has been proclaimed a triumph for Western intervention. But the expense of thousands of air strikes, led by French and British jets with U.S. logistical support, has left NATO governments keen to end it now.
Asked if NATO ambassadors on Friday would stick to the decision to end the mission at the end of the month, spokeswoman Carmen Romero said: "That is the preliminary decision ... The formal decision will be taken this week."
She added that, for the time being, "NATO continues to monitor the situation on the ground, and retains the capability to respond to any threats to civilians."
"NO RISK"
Romero said NATO Secretary-General Anders Fogh Rasmussen was in consultations with the United Nations and the National Transitional Council about plans to conclude the mission.
NATO states took their decision last week based on military recommendations. The commander the Libya mission Lieutenant-General Charles Bouchard said on Monday he saw virtually no risk of forces loyal to Gaddafi mounting successful attacks to regain power and NATO believed NTC forces were able to handle security threats.
NATO states have been keen to see a quick conclusion to a costly effort that has involved more than 26,000 air sorties and round-the-clock naval patrols at a time when defense budgets are under severe strain due to the global economic crisis.
NATO has said it does not intend to keep forces in the Libyan region after concluding its mission and has repeatedly stated that its U.N. mandate is to protect civilians, not to pursue individuals -- although Gaddafi himself was captured after his convoy was hit in a NATO air strike.
On Tuesday, NATO Deputy Assistant Secretary General for Political Affairs and Security Policy James Appathurai said he expected the alliance to confirm its decision to end the mission. "I don't expect that there will be a change to that decision," he said.
NATO has already begun winding down the mission, and diplomats have said the majority of NATO equipment, including warplanes, has already been withdrawn.
A NATO statement on Tuesday said operations in the interim would involve intelligence, surveillance and reconnaissance missions, although NATO would retain the capability to conduct air strikes if they were needed.
SAIF AL-ISLAM
Saif al-Islam Gaddafi, long seen as his father's heir-apparent, was believed to be in the southern desert near Niger and Algeria and was set to flee Libya using a false passport, an NTC official said.
Like his father, he is wanted by both the new Libyan leadership and the International Criminal Court for crimes against humanity.
Military experts stress, however, that even NATO's extensive aerial and satellite power has little chance of detecting fleeing convoys across the expanses of the Sahara, while the remote desert is also out of realistic range for any mission to strike such a group of vehicles, even if NATO's mandate were interpreted to allow it.
(Reporting by Regan Doherty in Doha and David Brunnstrom in Brussels; Writing by Alastair Macdonald)
First of all, yes, okay, pretty much anything can kill you under the right circumstances. But what about marbles, and what about the specific circumstance of pretty little glass marbles, shot by a stainless steel slingshot into ballistic gelatin, by an amusingly t-shirted Eastern European madman? In super-slow motion? More »
CANCUN, Mexico ? Tourists abandoned Cancun and other resorts while Mexican authorities evacuated hundreds of residents from low-lying areas ahead of a weakened Hurricane Rina's pass along Yucatan's Caribbean coast Thursday.
Civil protection officials moved some 2,300 people from Holbox, an island where the Caribbean meets the Gulf of Mexico, and the federal government closed the archaeological sites that dot the coast. NASA cut short an undersea laboratory mission near Key Largo, Florida, bringing the crew back to land.
Lines snaked from ticket counters in Cancun's crowded airport Wednesday as jumbo airliners heading to Canada and Europe waited in pouring rain. Many travelers said they were already scheduled to leave on Wednesday. But Janet Gallo, 41, of New York City decided to cut short her five-day trip to the town of Playa del Carmen.
"At the hotel, they told us they would make a decision whether to evacuate later today, but we didn't want to wait. We would rather be home when it hits," Gallo said.
Ports closed to navigation for recreational, fishing and small boats in the state of Quintana Roo, home to Cancun, and neighboring Yucatan state, while the island of Cozumel was closed to larger vessels, including the ferry that connects the island and Playa del Carmen.
Rina was forecast to remain a hurricane as it swept along Mexico's most popular tourist destinations of Cancun, Cozumel and the Riviera Maya, though forecasters predicted it would continue to weaken.
Rina's maximum sustained winds were clocked at 85 mph (135 kph) late Wednesday, down from 110 mph (175 kph) earlier in the day. It was about 140 miles (225 kilometers) south of the island of Cozumel and was moving northwest at about 6 mph (9 kph).
About 275 people living in the fishing town of Punta Allen, south of Tulum, were moved to emergency shelters and a smaller group was evacuated from the atoll of Banco Chinchorro.
Luh McDevitt, 56, a furniture and interior designer in Cozumel, said her family was fitting hurricane shutters to the house and securing furniture.
"I am not really scared," said the Cincinnati, Ohio, native who has lived in Cozumel since 2000. "Hurricane Andrew in 1992 was a Category 5. The worst part of the hurricane is after. We didn't have electricity in our house for three weeks."
Mexico's government said it was sending nearly 2,400 electrical workers plus cranes, vehicles and generators to repair and maintain services as quickly as possible after the storm.
Jorge Arturo Cruz, spokesman for Quintana Roo's education department, said schools were ordered closed in communities along the coast and on Cozumel in anticipation of the storm.
The coastal area around Tulum is dotted with Mayan ruins and farther north is Playa del Carmen, another popular spot for international tourists and the departure point for ferries serving Cozumel.
State Tourism Director Juan Carlos Gonzalez Hernandez said there had been about 83,000 tourists in the state, with about 28,000 of them in Cancun and 45,000 more on the stretch of coast south of Cancun that includes Tulum and Playa de Carmen.
He estimated 10,000 tourists had left by Wednesday night. There were only about 1,719 tourists on Cozumel, and many of them had left, he said.
At least eight cruise ships were changing itineraries away from the storm's path, said a spokesman for Carnival Cruise Lines, Vance Gulliksen.
The area was badly damaged by Hurricane Wilma in 2005, when Cancun's white-sand beaches were largely washed away. Insurance officials estimated total damage at $3 billion.
A hurricane warning was in effect for the east coast of the Yucatan Peninsula from north of Punta Gruesa to Cancun.
The projected track showed Rina curving east toward Cuba and the Straits of Florida after crossing the eastern tip of Yucatan, though the U.S. National Hurricane Center cautioned "there is great uncertainty as to where Rina will be located by the weekend."
___
Associated Press writer Adriana Gomez Licon in Mexico City contributed to this story.
Windows XP first went on sale ten years ago today. In that span, it has become the desktop OS of choice with a worldwide install base of as much as 80 percent. Here's looking at you XP. More »
Jon Heder and daughter Evan Jane, 4?, hang with the Yo Gabba Gabba! gang at the Vans x Yo Gabba Gabba shoe launch, held Thursday at Kitson Kids in Los Angeles.
Geoscientists find key to why some patients get infections from cardiac implantsPublic release date: 25-Oct-2011 [ | E-mail | Share ]
Contact: Cheryl Dybas cdybas@nsf.gov 703-292-7734 National Science Foundation
Bacterial cells have gene mutations that allow them to 'stick' to the devices
New research suggests that some patients develop a potentially deadly blood infection from their implanted cardiac devices because bacterial cells in their bodies have gene mutations that allow them to stick to the devices.
Geoscientists were the major contributors to the finding.
Proceedings of the National Academy of Sciences published the study results online this week.
"Geobiologists, key to these results, use atomic force microscopy to study the forces with which bacteria adhere to mineral surfaces," said Enriqueta Barrera, program director in the National Science Foundation's Division of Earth Sciences, which funded the research.
"These scientists have adapted this approach, along with molecular dynamics simulations, to gain a better understanding of the strength with which the proteins of infectious bacteria adhere to cardiac implants," said Barrera. "Such results might have implications for the development of medication to treat this type of infection."
Patients with implants can develop infections because of a biofilm of persistent bacteria on the surfaces of their devices.
A biofilm is a community of bacterial cells that lives on the surface of a solid substrate. Biofilms are the most common mode of life for all bacteria, whether they reside in the environment or in the human body.
The scientific principles governing the formation of bacterial biofilms on cardiac devices are strongly linked with those of biofilm formation on mineral surfaces, hence the connection with geobiology.
Scientists found that some strains of the bacteria, Staphylococcus aureus, have just a few genetic variants in the proteins on their surfaces that make them more likely to form these biofilms.
The research seeks to get to the heart of a medical paradox: devices such as pacemakers, defibrillators and prosthetic cardiac valves save lives, but they cause infections in about 4 percent of the estimated 1 million patients receiving implants each year in the United States.
Because biofilms resist antibiotics, the only treatment is surgery to remove the contaminated device and implant a new one. This adds up to thousands of surgeries and more than $1 billion in health care costs every year.
A team led by scientists at Ohio State University and Duke University Medical Center used atomic force microscopy and powerful computer simulations to determine how Staph bacteria bond to the devices in the process of forming these biofilms.
The findings offer clues about potential techniques that could be employed to prevent infections in patients who need these devices to stay alive.
"We're probing the initial step to that biofilm formation," said Steven Lower, scientist at Ohio State and lead author of the paper reporting the study's results.
"Can you shut that down somehow? If that bacterium never sticks, there's no biofilm. It's that simple. But it's not quite that simple in practice."
Using Staph cells collected from patients--some with cardiac device-related infections--the researchers examined how these bacteria adhere to implants to create a biofilm.
The bond forms when a protein on the bacterial cell surface connects with a common human blood protein coating an implanted device.
But an estimated half of all Americans have Staph bacteria living in their noses, and not every cardiac implant patient develops an infection.
So why do some strains of these bacteria cause infection while others remain dormant?
The researchers discovered that Staph surface proteins containing three genetic variants, or single-nucleotide polymorphisms, formed stronger bonds with the human proteins than did Staph proteins without those variants.
The presence of these genetic variants was associated with the strains of bacteria that had infected implanted cardiac devices.
The finding is a first step toward preventing the bacteria from bonding to the devices.
"It will be useful to explore this in more detail and see if we can understand the basic science behind how these bonds form, and why they form," Lower said. "Perhaps then we can exploit some fundamental force law.
Lower, a scientist with a background in geology, physics and biology, collaborated for a decade with Vance Fowler, a scientist at Duke's Medical Center and the study's co-lead author.
Lower specializes in atomic force microscopy and molecular dynamics simulations to explore molecular-level relationships between inanimate surfaces and living microorganisms.
Fowler, who specializes in infectious diseases, assembled a rare library of hundreds of Staphylococcus aureus isolates collected from patients.
Fowler hopes his samples might help answer a broader question related to varied patient responses to the blood infection bacteremia.
"I believe that our research is a critical first step towards understanding, and eventually preventing, cardiac device infections caused by Staphylococcus aureus," Fowler said.
The researchers used 80 Staph isolates from three different groups: patients with a blood infection and a confirmed cardiac device infection, patients with a blood infection and an uninfected cardiac device, and Staph from the noses of healthy subjects living in the same area.
Single-cell studies of bacteria are complicated by their tiny size, one millionth of a meter, so an atomic-force microscope is required to visualize their behavior.
Co-author and Ohio State researcher Nadia Casillas-Ituarte performed these experiments, connecting single Staph bacteria to a protein-coated probe to allow bonds to form, and then rupturing the bonds to measure the strength of each connection.
Casillas-Ituarte simulated the human heartbeat, allowing bonds to form over the course of a second and then pulling the probe away.
By doing this at least 100 times on each cell and verifying the work on hundreds of additional cells, she generated more than a quarter-million force curve measurements for the analysis.
"The first step is to determine how a bacterium 'feels' a surface," she said. "You can't stop that process until you first understand how it happens."
The researchers coated the probe with fibronectin, a common human blood protein found on the surface of implanted devices.
Staph bacteria can create a biofilm by forming bonds with this protein through a protein on their own surface called fibronectin-binding protein A.
To learn more about the bacterial protein, the scientists then sequenced the amino acids that make up fibronectin-binding protein A in each isolate they studied.
This is where they found the single-nucleotide polymorphisms (SNPs, pronounced "snips"), which were more common in the isolates collected from patients with infections related to their heart implants.
To further test the effects of these SNPs, the team used a supercomputer to simulate the formation of the bond between the bacterial and human proteins.
When they plugged standard amino acid sequences from each protein into the supercomputer, the molecules maintained a distance from each other.
When they altered the sequence of three amino acids in the bacterial surface protein and entered that data, hydrogen bonds formed between the bacterial and human proteins.
"We changed the amino acids to resemble the SNPs found in the Staph that came from cardiac device-infected patients," Lower said. "So the SNPs seem to have a relationship to whether a bond forms or not."
Fibronectin-binding protein A is one of about 10 of these types of molecules on the Staph surface that can form bonds with proteins on host cells, Lower noted.
It's also possible that fibronectin, the human protein on the other side of the bond studied so far, might contain genetic variants that contribute to the problem.
What the scientists do know is that bacteria will do all they can to survive, so it won't be easy to outsmart them.
"Bacteria obey Charles Darwin's law of natural selection and can evolve genetic capabilities to allow them to live in the presence of antibiotics," Lower said.
"Most physicists would tell you there are certain laws of physics that dictate what happens and when it happens, and you can't evade or evolve ways around those.
"If you understand the basic physics of it, can you exploit a fundamental force law that bacteria can't evade or evolve a mechanism around?"
###
This work was also supported by grants from the National Institutes of Health, the Brazilian National Council for Scientific and Technological Development/Brazilian National Science and Technology Institute, and the Swiss National Science Foundation/Swiss Medical Association.
Additional co-authors include Supaporn Lamlertthon and L. Barth Reller of Duke; Roberto Lins of the Universidade Federal de Pernambuco, Recipfe, in Brazil; Ruchirej Yongsunthon, Eric Taylor, Alex DiBartola and Brian Lower of Ohio State; Catherine Edmonson and Lauren McIntyre of the University of Florida; Yok-Ai Que of the University of Lausanne in Switzerland; and Robert Ros of Arizona State University.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Geoscientists find key to why some patients get infections from cardiac implantsPublic release date: 25-Oct-2011 [ | E-mail | Share ]
Contact: Cheryl Dybas cdybas@nsf.gov 703-292-7734 National Science Foundation
Bacterial cells have gene mutations that allow them to 'stick' to the devices
New research suggests that some patients develop a potentially deadly blood infection from their implanted cardiac devices because bacterial cells in their bodies have gene mutations that allow them to stick to the devices.
Geoscientists were the major contributors to the finding.
Proceedings of the National Academy of Sciences published the study results online this week.
"Geobiologists, key to these results, use atomic force microscopy to study the forces with which bacteria adhere to mineral surfaces," said Enriqueta Barrera, program director in the National Science Foundation's Division of Earth Sciences, which funded the research.
"These scientists have adapted this approach, along with molecular dynamics simulations, to gain a better understanding of the strength with which the proteins of infectious bacteria adhere to cardiac implants," said Barrera. "Such results might have implications for the development of medication to treat this type of infection."
Patients with implants can develop infections because of a biofilm of persistent bacteria on the surfaces of their devices.
A biofilm is a community of bacterial cells that lives on the surface of a solid substrate. Biofilms are the most common mode of life for all bacteria, whether they reside in the environment or in the human body.
The scientific principles governing the formation of bacterial biofilms on cardiac devices are strongly linked with those of biofilm formation on mineral surfaces, hence the connection with geobiology.
Scientists found that some strains of the bacteria, Staphylococcus aureus, have just a few genetic variants in the proteins on their surfaces that make them more likely to form these biofilms.
The research seeks to get to the heart of a medical paradox: devices such as pacemakers, defibrillators and prosthetic cardiac valves save lives, but they cause infections in about 4 percent of the estimated 1 million patients receiving implants each year in the United States.
Because biofilms resist antibiotics, the only treatment is surgery to remove the contaminated device and implant a new one. This adds up to thousands of surgeries and more than $1 billion in health care costs every year.
A team led by scientists at Ohio State University and Duke University Medical Center used atomic force microscopy and powerful computer simulations to determine how Staph bacteria bond to the devices in the process of forming these biofilms.
The findings offer clues about potential techniques that could be employed to prevent infections in patients who need these devices to stay alive.
"We're probing the initial step to that biofilm formation," said Steven Lower, scientist at Ohio State and lead author of the paper reporting the study's results.
"Can you shut that down somehow? If that bacterium never sticks, there's no biofilm. It's that simple. But it's not quite that simple in practice."
Using Staph cells collected from patients--some with cardiac device-related infections--the researchers examined how these bacteria adhere to implants to create a biofilm.
The bond forms when a protein on the bacterial cell surface connects with a common human blood protein coating an implanted device.
But an estimated half of all Americans have Staph bacteria living in their noses, and not every cardiac implant patient develops an infection.
So why do some strains of these bacteria cause infection while others remain dormant?
The researchers discovered that Staph surface proteins containing three genetic variants, or single-nucleotide polymorphisms, formed stronger bonds with the human proteins than did Staph proteins without those variants.
The presence of these genetic variants was associated with the strains of bacteria that had infected implanted cardiac devices.
The finding is a first step toward preventing the bacteria from bonding to the devices.
"It will be useful to explore this in more detail and see if we can understand the basic science behind how these bonds form, and why they form," Lower said. "Perhaps then we can exploit some fundamental force law.
Lower, a scientist with a background in geology, physics and biology, collaborated for a decade with Vance Fowler, a scientist at Duke's Medical Center and the study's co-lead author.
Lower specializes in atomic force microscopy and molecular dynamics simulations to explore molecular-level relationships between inanimate surfaces and living microorganisms.
Fowler, who specializes in infectious diseases, assembled a rare library of hundreds of Staphylococcus aureus isolates collected from patients.
Fowler hopes his samples might help answer a broader question related to varied patient responses to the blood infection bacteremia.
"I believe that our research is a critical first step towards understanding, and eventually preventing, cardiac device infections caused by Staphylococcus aureus," Fowler said.
The researchers used 80 Staph isolates from three different groups: patients with a blood infection and a confirmed cardiac device infection, patients with a blood infection and an uninfected cardiac device, and Staph from the noses of healthy subjects living in the same area.
Single-cell studies of bacteria are complicated by their tiny size, one millionth of a meter, so an atomic-force microscope is required to visualize their behavior.
Co-author and Ohio State researcher Nadia Casillas-Ituarte performed these experiments, connecting single Staph bacteria to a protein-coated probe to allow bonds to form, and then rupturing the bonds to measure the strength of each connection.
Casillas-Ituarte simulated the human heartbeat, allowing bonds to form over the course of a second and then pulling the probe away.
By doing this at least 100 times on each cell and verifying the work on hundreds of additional cells, she generated more than a quarter-million force curve measurements for the analysis.
"The first step is to determine how a bacterium 'feels' a surface," she said. "You can't stop that process until you first understand how it happens."
The researchers coated the probe with fibronectin, a common human blood protein found on the surface of implanted devices.
Staph bacteria can create a biofilm by forming bonds with this protein through a protein on their own surface called fibronectin-binding protein A.
To learn more about the bacterial protein, the scientists then sequenced the amino acids that make up fibronectin-binding protein A in each isolate they studied.
This is where they found the single-nucleotide polymorphisms (SNPs, pronounced "snips"), which were more common in the isolates collected from patients with infections related to their heart implants.
To further test the effects of these SNPs, the team used a supercomputer to simulate the formation of the bond between the bacterial and human proteins.
When they plugged standard amino acid sequences from each protein into the supercomputer, the molecules maintained a distance from each other.
When they altered the sequence of three amino acids in the bacterial surface protein and entered that data, hydrogen bonds formed between the bacterial and human proteins.
"We changed the amino acids to resemble the SNPs found in the Staph that came from cardiac device-infected patients," Lower said. "So the SNPs seem to have a relationship to whether a bond forms or not."
Fibronectin-binding protein A is one of about 10 of these types of molecules on the Staph surface that can form bonds with proteins on host cells, Lower noted.
It's also possible that fibronectin, the human protein on the other side of the bond studied so far, might contain genetic variants that contribute to the problem.
What the scientists do know is that bacteria will do all they can to survive, so it won't be easy to outsmart them.
"Bacteria obey Charles Darwin's law of natural selection and can evolve genetic capabilities to allow them to live in the presence of antibiotics," Lower said.
"Most physicists would tell you there are certain laws of physics that dictate what happens and when it happens, and you can't evade or evolve ways around those.
"If you understand the basic physics of it, can you exploit a fundamental force law that bacteria can't evade or evolve a mechanism around?"
###
This work was also supported by grants from the National Institutes of Health, the Brazilian National Council for Scientific and Technological Development/Brazilian National Science and Technology Institute, and the Swiss National Science Foundation/Swiss Medical Association.
Additional co-authors include Supaporn Lamlertthon and L. Barth Reller of Duke; Roberto Lins of the Universidade Federal de Pernambuco, Recipfe, in Brazil; Ruchirej Yongsunthon, Eric Taylor, Alex DiBartola and Brian Lower of Ohio State; Catherine Edmonson and Lauren McIntyre of the University of Florida; Yok-Ai Que of the University of Lausanne in Switzerland; and Robert Ros of Arizona State University.
[ | E-mail | Share ]
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
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Public release date: 25-Oct-2011
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