Researchers at the Swedish medical university Karolinska Institutet have demonstrated that a growth hormone, PDGF-BB, and the blood protein EPO are involved in the development of cancer tumours and that they combine to help the tumours proliferate in the body. These new preclinical findings offer new potential for inhibiting tumour growth and bypassing problems of resistance that exist with many drugs in current use. The results are published in the scientific journal Nature Medicine.
Angiogenesis is the formation of new blood vessels from pre-existing ones, and is one of the most important research fields in the treatment of such diverse conditions as cancer, metastases, obesity, heart disease, stroke, diabetes and chronic inflammation. The process is also important in healthy individuals for wound healing, the menstrual cycle and other normal processes. Professor Yihai Cao and his team are researching into angiogenesis and its links to cancer and other diseases, and in the present study show the significant role played by a growth factor, PDGF-BB.
"It's a member of the PDGF family and significantly contributes to blood vessel development, which is one of the characteristic signs of cancer, says Professor Yihai Cao. Our preclinical findings suggest that PDGF-BB causes systemic effects in the body, which is to say that rather than being active locally it goes into the blood and interferes with the function of several organs so that the entire body is affected."
Their studies are carried out on mice, and in the present study they were able to show that when the growth factor PDGF-BB binds to its receptors, it stimulates the blood protein EPO (Erythropoietin), which, in turn, controls the production of red blood cells, that provide more oxygen for tumor growth and metastasis.
"EPO has several functions," says Professor Yihai Cao. "It produces more blood and stimulates angiogenesis, and we have revealed the underlying mechanism. It also stimulates tumour angiogenesis by directly stimulating the proliferation, migration and growth of endothelial cells and their ability to form the so-called epithelial tube. PDGF-BB promotes the stimulation of extramedullary haematopoiesis, enlargement of the liver and spleen, which increases oxygen perfusion and protection against anaemia." The introduction of PDGF-BB in mice thus boosts erythropoietin production and the haematopoietic parameters. In addition, EPO may directly act on tumor cells to promote their growth and metastasis.
"We believe that the increase in EPO might be responsible for tumoural resistance to anti-angiogenetic drugs, which only target PDGF ligands. The combination of drugs targeted at both PDGF and EPO has potential superior therapeutic benefits and might circumvent today's serious resistance problems," says Professor Yihai Cao, adding that they will continue to study mouse models and explore opportunities for clinical studies on patients.
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Karolinska Institutet: http://info.ki.se/ki
Thanks to Karolinska Institutet for this article.
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Regeneration of specialized cells offers hope for treating chronic kidney diseasePublic release date: 4-Dec-2011 [ | E-mail | Share ]
Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center
STANFORD, Calif. -- Damage to podocytes -- a specialized type of epithelial cell in the kidney -- occurs in more than 90 percent of all chronic kidney disease. Now researchers at the Stanford University School of Medicine have uncovered an unexpected pathway that reveals for the first time how these cells may regenerate and renew themselves during normal kidney function.
This finding is an important step toward one day therapeutically coaxing the cells to divide, which could be used to treat people with chronic kidney disease.
"Researchers have studied these cells for years, but the prevailing view has been that they don't renew themselves," said associate professor of medicine Steven Artandi, MD, PhD. "Now we've found that podocytes can enter and leave the cell cycle in response to certain common signaling pathways."
Artandi is the senior author of the study, which will be published online Dec. 4 in Nature Medicine. The first author of the work is former postdoctoral scholar Marina Shkreli, PhD, who is now at the Laboratory of Biology and Pathology of Genomes at the University of Nice in France.
Podocytes are found only in the kidney and are an integral structural component of its blood-filtering system. They stand shoulder-to-shoulder in a part of the organ called the glomerulus and wrap their long "feet" around the semi-permeable capillaries through which blood flows. Narrow slits between the feet allow small molecules, such as water and salts, to pass while blocking large proteins.
This filtering process is the first step to forming urine, and it is critically important -- even one missing cell can leave a gap that would allow unwanted molecules through the barrier. (Imagine wrapping your hands around a length of leaky garden hose so that the water seeps out between your fingers. Lift up one finger and you're liable to get sprayed in the face.)
This may be why previous researchers searching for signs of self-renewal in podocytes were unsuccessful, because any such renewal or replacement would likely need to be carefully orchestrated to avoid compromising the filtration system. As a result, scientists have been forced to conclude that the podocytes rarely, if ever, divided.
"It used to be thought that you were born with podocytes, and you died with the same podocytes -- you don't make any more during your lifetime," said Artandi. The only exception was certain rare types of kidney disease in which the podocytes abandon their blood-filtration duties en masse to de-differentiate into less-specialized, dividing cells that little resemble their predecessors. As a result, the glomerulus collapses and the patients' kidneys begin to fail. One such disease is HIV-associated nephropathy, or HIVAN.
The problem was, such a scenario doesn't make a lot of evolutionary sense -- particularly when other epithelial cells routinely regenerate themselves. "Podocytes are vitally important, and are also under enormous physical stress," said Artandi. "It's hard to understand why we would have such a vulnerable blood-filtration system."
To understand more about kidney biology, Artandi and Shkreli investigated the role of a protein component of the telomerase complex called TERT. Although telomerase is best known as an enzyme involved in cell aging, recent research in Artandi's lab and others have shown that TERT also plays a role in many types of cellular regeneration.
The researchers found that temporarily increasing the expression of TERT in adult, otherwise healthy laboratory mice caused the formerly stolid podocytes to abruptly de-differentiate and begin dividing. As a result, the glomerulus collapsed in a way that resembles what happens in humans with HIVAN. Conversely, ceasing the overexpression allowed the cells to stop dividing, re-specialize and resume their normal functions.
When Artandi and Shkreli looked closely at the glomeruli in humans with HIVAN, they found that TERT expression was increased. Equally important, the Wnt signaling pathway, which is important in embryonic development and in the self-renewal of stem cells, was also activated. (Previous research in the Artandi lab has linked telomerase activity to the Wnt pathway.) Blocking Wnt signaling in a mouse model of HIVAN also stopped the podocytes from dividing and improved their function.
"The implication is that podocytes may utilize recognized pathways of regeneration to renew themselves throughout life," said Artandi. People suffering from chronic kidney disease may simply have worn out or outpaced their podocytes' capacity for renewal, he believes.
Now that the researchers know podocytes have the ability regenerate in response to common cellular signals, their next step is to learn whether this regeneration occurs in healthy animals and people. "If we can harness this regeneration," Artandi said, "we may one day be able to treat people with chronic kidney disease."
In addition to Artandi and Shkreli, other Stanford researchers involved in the study include medical resident Kavita Sarin, MD, PhD; graduate students Matthew Pech and Peggie Cheung; medical student Woody Chang; lab manager Stephanie Brockman; former research assistant Eunice Lee; research associate Frank Kuhnert, PhD; and associate professor of medicine Calvin Kuo, MD, PhD.
The research was funded by the National Institutes of Health, the Stanford School of Medicine, the Stanford Center on Longevity and the Glenn Laboratories for the Biology of Aging at Stanford. Information about Stanford's Department of Medicine, which also supported the work, is available at http://medicine.stanford.edu.
# # #
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine
STANFORD, Calif. -- Damage to podocytes -- a specialized type of epithelial cell in the kidney -- occurs in more than 90 percent of all chronic kidney disease. Now researchers at the Stanford University School of Medicine have uncovered an unexpected pathway that reveals for the first time how these cells may regenerate and renew themselves during normal kidney function.
This finding is an important step toward one day therapeutically coaxing the cells to divide, which could be used to treat people with chronic kidney disease.
"Researchers have studied these cells for years, but the prevailing view has been that they don't renew themselves," said associate professor of medicine Steven Artandi, MD, PhD. "Now we've found that podocytes can enter and leave the cell cycle in response to certain common signaling pathways."
Artandi is the senior author of the study, which will be published online Dec. 4 in Nature Medicine. The first author of the work is former postdoctoral scholar Marina Shkreli, PhD, who is now at the Laboratory of Biology and Pathology of Genomes at the University of Nice in France.
Podocytes are found only in the kidney and are an integral structural component of its blood-filtering system. They stand shoulder-to-shoulder in a part of the organ called the glomerulus and wrap their long "feet" around the semi-permeable capillaries through which blood flows. Narrow slits between the feet allow small molecules, such as water and salts, to pass while blocking large proteins.
This filtering process is the first step to forming urine, and it is critically important -- even one missing cell can leave a gap that would allow unwanted molecules through the barrier. (Imagine wrapping your hands around a length of leaky garden hose so that the water seeps out between your fingers. Lift up one finger and you're liable to get sprayed in the face.)
This may be why previous researchers searching for signs of self-renewal in podocytes were unsuccessful, because any such renewal or replacement would likely need to be carefully orchestrated to avoid compromising the filtration system. As a result, scientists have been forced to conclude that the podocytes rarely, if ever, divided.
"It used to be thought that you were born with podocytes, and you died with the same podocytes -- you don't make any more during your lifetime," said Artandi. The only exception was certain rare types of kidney disease in which the podocytes abandon their blood-filtration duties en masse to de-differentiate into less-specialized, dividing cells that little resemble their predecessors. As a result, the glomerulus collapses and the patients' kidneys begin to fail. One such disease is HIV-associated nephropathy, or HIVAN.
The problem was, such a scenario doesn't make a lot of evolutionary sense -- particularly when other epithelial cells routinely regenerate themselves. "Podocytes are vitally important, and are also under enormous physical stress," said Artandi. "It's hard to understand why we would have such a vulnerable blood-filtration system."
To understand more about kidney biology, Artandi and Shkreli investigated the role of a protein component of the telomerase complex called TERT. Although telomerase is best known as an enzyme involved in cell aging, recent research in Artandi's lab and others have shown that TERT also plays a role in many types of cellular regeneration.
The researchers found that temporarily increasing the expression of TERT in adult, otherwise healthy laboratory mice caused the formerly stolid podocytes to abruptly de-differentiate and begin dividing. As a result, the glomerulus collapsed in a way that resembles what happens in humans with HIVAN. Conversely, ceasing the overexpression allowed the cells to stop dividing, re-specialize and resume their normal functions.
When Artandi and Shkreli looked closely at the glomeruli in humans with HIVAN, they found that TERT expression was increased. Equally important, the Wnt signaling pathway, which is important in embryonic development and in the self-renewal of stem cells, was also activated. (Previous research in the Artandi lab has linked telomerase activity to the Wnt pathway.) Blocking Wnt signaling in a mouse model of HIVAN also stopped the podocytes from dividing and improved their function.
"The implication is that podocytes may utilize recognized pathways of regeneration to renew themselves throughout life," said Artandi. People suffering from chronic kidney disease may simply have worn out or outpaced their podocytes' capacity for renewal, he believes.
Now that the researchers know podocytes have the ability regenerate in response to common cellular signals, their next step is to learn whether this regeneration occurs in healthy animals and people. "If we can harness this regeneration," Artandi said, "we may one day be able to treat people with chronic kidney disease."
###
In addition to Artandi and Shkreli, other Stanford researchers involved in the study include medical resident Kavita Sarin, MD, PhD; graduate students Matthew Pech and Peggie Cheung; medical student Woody Chang; lab manager Stephanie Brockman; former research assistant Eunice Lee; research associate Frank Kuhnert, PhD; and associate professor of medicine Calvin Kuo, MD, PhD.
The research was funded by the National Institutes of Health, the Stanford School of Medicine, the Stanford Center on Longevity and the Glenn Laboratories for the Biology of Aging at Stanford. Information about Stanford's Department of Medicine, which also supported the work, is available at http://medicine.stanford.edu.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
###
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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.
Regeneration of specialized cells offers hope for treating chronic kidney diseasePublic release date: 4-Dec-2011 [ | E-mail | Share ]
Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center
STANFORD, Calif. -- Damage to podocytes -- a specialized type of epithelial cell in the kidney -- occurs in more than 90 percent of all chronic kidney disease. Now researchers at the Stanford University School of Medicine have uncovered an unexpected pathway that reveals for the first time how these cells may regenerate and renew themselves during normal kidney function.
This finding is an important step toward one day therapeutically coaxing the cells to divide, which could be used to treat people with chronic kidney disease.
"Researchers have studied these cells for years, but the prevailing view has been that they don't renew themselves," said associate professor of medicine Steven Artandi, MD, PhD. "Now we've found that podocytes can enter and leave the cell cycle in response to certain common signaling pathways."
Artandi is the senior author of the study, which will be published online Dec. 4 in Nature Medicine. The first author of the work is former postdoctoral scholar Marina Shkreli, PhD, who is now at the Laboratory of Biology and Pathology of Genomes at the University of Nice in France.
Podocytes are found only in the kidney and are an integral structural component of its blood-filtering system. They stand shoulder-to-shoulder in a part of the organ called the glomerulus and wrap their long "feet" around the semi-permeable capillaries through which blood flows. Narrow slits between the feet allow small molecules, such as water and salts, to pass while blocking large proteins.
This filtering process is the first step to forming urine, and it is critically important -- even one missing cell can leave a gap that would allow unwanted molecules through the barrier. (Imagine wrapping your hands around a length of leaky garden hose so that the water seeps out between your fingers. Lift up one finger and you're liable to get sprayed in the face.)
This may be why previous researchers searching for signs of self-renewal in podocytes were unsuccessful, because any such renewal or replacement would likely need to be carefully orchestrated to avoid compromising the filtration system. As a result, scientists have been forced to conclude that the podocytes rarely, if ever, divided.
"It used to be thought that you were born with podocytes, and you died with the same podocytes -- you don't make any more during your lifetime," said Artandi. The only exception was certain rare types of kidney disease in which the podocytes abandon their blood-filtration duties en masse to de-differentiate into less-specialized, dividing cells that little resemble their predecessors. As a result, the glomerulus collapses and the patients' kidneys begin to fail. One such disease is HIV-associated nephropathy, or HIVAN.
The problem was, such a scenario doesn't make a lot of evolutionary sense -- particularly when other epithelial cells routinely regenerate themselves. "Podocytes are vitally important, and are also under enormous physical stress," said Artandi. "It's hard to understand why we would have such a vulnerable blood-filtration system."
To understand more about kidney biology, Artandi and Shkreli investigated the role of a protein component of the telomerase complex called TERT. Although telomerase is best known as an enzyme involved in cell aging, recent research in Artandi's lab and others have shown that TERT also plays a role in many types of cellular regeneration.
The researchers found that temporarily increasing the expression of TERT in adult, otherwise healthy laboratory mice caused the formerly stolid podocytes to abruptly de-differentiate and begin dividing. As a result, the glomerulus collapsed in a way that resembles what happens in humans with HIVAN. Conversely, ceasing the overexpression allowed the cells to stop dividing, re-specialize and resume their normal functions.
When Artandi and Shkreli looked closely at the glomeruli in humans with HIVAN, they found that TERT expression was increased. Equally important, the Wnt signaling pathway, which is important in embryonic development and in the self-renewal of stem cells, was also activated. (Previous research in the Artandi lab has linked telomerase activity to the Wnt pathway.) Blocking Wnt signaling in a mouse model of HIVAN also stopped the podocytes from dividing and improved their function.
"The implication is that podocytes may utilize recognized pathways of regeneration to renew themselves throughout life," said Artandi. People suffering from chronic kidney disease may simply have worn out or outpaced their podocytes' capacity for renewal, he believes.
Now that the researchers know podocytes have the ability regenerate in response to common cellular signals, their next step is to learn whether this regeneration occurs in healthy animals and people. "If we can harness this regeneration," Artandi said, "we may one day be able to treat people with chronic kidney disease."
In addition to Artandi and Shkreli, other Stanford researchers involved in the study include medical resident Kavita Sarin, MD, PhD; graduate students Matthew Pech and Peggie Cheung; medical student Woody Chang; lab manager Stephanie Brockman; former research assistant Eunice Lee; research associate Frank Kuhnert, PhD; and associate professor of medicine Calvin Kuo, MD, PhD.
The research was funded by the National Institutes of Health, the Stanford School of Medicine, the Stanford Center on Longevity and the Glenn Laboratories for the Biology of Aging at Stanford. Information about Stanford's Department of Medicine, which also supported the work, is available at http://medicine.stanford.edu.
# # #
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine
STANFORD, Calif. -- Damage to podocytes -- a specialized type of epithelial cell in the kidney -- occurs in more than 90 percent of all chronic kidney disease. Now researchers at the Stanford University School of Medicine have uncovered an unexpected pathway that reveals for the first time how these cells may regenerate and renew themselves during normal kidney function.
This finding is an important step toward one day therapeutically coaxing the cells to divide, which could be used to treat people with chronic kidney disease.
"Researchers have studied these cells for years, but the prevailing view has been that they don't renew themselves," said associate professor of medicine Steven Artandi, MD, PhD. "Now we've found that podocytes can enter and leave the cell cycle in response to certain common signaling pathways."
Artandi is the senior author of the study, which will be published online Dec. 4 in Nature Medicine. The first author of the work is former postdoctoral scholar Marina Shkreli, PhD, who is now at the Laboratory of Biology and Pathology of Genomes at the University of Nice in France.
Podocytes are found only in the kidney and are an integral structural component of its blood-filtering system. They stand shoulder-to-shoulder in a part of the organ called the glomerulus and wrap their long "feet" around the semi-permeable capillaries through which blood flows. Narrow slits between the feet allow small molecules, such as water and salts, to pass while blocking large proteins.
This filtering process is the first step to forming urine, and it is critically important -- even one missing cell can leave a gap that would allow unwanted molecules through the barrier. (Imagine wrapping your hands around a length of leaky garden hose so that the water seeps out between your fingers. Lift up one finger and you're liable to get sprayed in the face.)
This may be why previous researchers searching for signs of self-renewal in podocytes were unsuccessful, because any such renewal or replacement would likely need to be carefully orchestrated to avoid compromising the filtration system. As a result, scientists have been forced to conclude that the podocytes rarely, if ever, divided.
"It used to be thought that you were born with podocytes, and you died with the same podocytes -- you don't make any more during your lifetime," said Artandi. The only exception was certain rare types of kidney disease in which the podocytes abandon their blood-filtration duties en masse to de-differentiate into less-specialized, dividing cells that little resemble their predecessors. As a result, the glomerulus collapses and the patients' kidneys begin to fail. One such disease is HIV-associated nephropathy, or HIVAN.
The problem was, such a scenario doesn't make a lot of evolutionary sense -- particularly when other epithelial cells routinely regenerate themselves. "Podocytes are vitally important, and are also under enormous physical stress," said Artandi. "It's hard to understand why we would have such a vulnerable blood-filtration system."
To understand more about kidney biology, Artandi and Shkreli investigated the role of a protein component of the telomerase complex called TERT. Although telomerase is best known as an enzyme involved in cell aging, recent research in Artandi's lab and others have shown that TERT also plays a role in many types of cellular regeneration.
The researchers found that temporarily increasing the expression of TERT in adult, otherwise healthy laboratory mice caused the formerly stolid podocytes to abruptly de-differentiate and begin dividing. As a result, the glomerulus collapsed in a way that resembles what happens in humans with HIVAN. Conversely, ceasing the overexpression allowed the cells to stop dividing, re-specialize and resume their normal functions.
When Artandi and Shkreli looked closely at the glomeruli in humans with HIVAN, they found that TERT expression was increased. Equally important, the Wnt signaling pathway, which is important in embryonic development and in the self-renewal of stem cells, was also activated. (Previous research in the Artandi lab has linked telomerase activity to the Wnt pathway.) Blocking Wnt signaling in a mouse model of HIVAN also stopped the podocytes from dividing and improved their function.
"The implication is that podocytes may utilize recognized pathways of regeneration to renew themselves throughout life," said Artandi. People suffering from chronic kidney disease may simply have worn out or outpaced their podocytes' capacity for renewal, he believes.
Now that the researchers know podocytes have the ability regenerate in response to common cellular signals, their next step is to learn whether this regeneration occurs in healthy animals and people. "If we can harness this regeneration," Artandi said, "we may one day be able to treat people with chronic kidney disease."
###
In addition to Artandi and Shkreli, other Stanford researchers involved in the study include medical resident Kavita Sarin, MD, PhD; graduate students Matthew Pech and Peggie Cheung; medical student Woody Chang; lab manager Stephanie Brockman; former research assistant Eunice Lee; research associate Frank Kuhnert, PhD; and associate professor of medicine Calvin Kuo, MD, PhD.
The research was funded by the National Institutes of Health, the Stanford School of Medicine, the Stanford Center on Longevity and the Glenn Laboratories for the Biology of Aging at Stanford. Information about Stanford's Department of Medicine, which also supported the work, is available at http://medicine.stanford.edu.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
###
[ | E-mail | Share ]
?
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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BRUSSELS ? EU foreign ministers failed Thursday to reach an agreement to impose an oil embargo against Iran ? a measure that some argued would have choked off funding for Iran's alleged program to develop nuclear weapons.
But the ministers, incensed by the attack Tuesday by an angry mob on the British embassy in Tehran, did impose a new round of sanctions targeting dozens of people, groups and businesses in the country.
The ministers also imposed new sanctions on Syrian individuals and businesses in hope of pressuring the regime there to halt its deadly crackdown on anti-government protests.
British Foreign Secretary William Hague said the two issues are related, accusing Iran of supporting the violence in Syria. The U.N. High Commissioner for Human Rights estimates Sryian President Bashar Assad's regime has killed more than 4,000 people over the past several months.
"There is a link between what is happening in Iran and what is happening in Syria," Hague said.
In Iran, EU sanctions were imposed on 37 people and 143 "entities" ? companies or organizations. The sanctions include a freeze on assets held in the European Union and a ban on traveling to EU countries.
The full list of names of those targeted will not be known until they are published in the official journal of the EU on Friday. But the official conclusions of the meeting said they include the Islamic Republic of Iran Shipping Line and members of, and entities controlled by, the Islamic Revolutionary Guards Corps.
French Foreign Minister Alain Juppe said that Greece, which relies on Iranian oil, had objected to a ban on buying it. But he said work toward an embargo would continue.
"Greece has put forward a number of reservations," Juppe said. "We have to take that into account. We have to see with our partners that the cuts can be compensated by the increase of production in other countries. It is very possible."
Iran has denied it is pursuing nuclear weapons. The attack on the British embassy is believed to have begun as a state-approved protest over Western sanctions linked to the country's nuclear program.
Britain pulled its diplomats out of Iran after its embassy was stormed. Germany, France and the Netherlands have recalled their ambassadors in solidarity.
With regard to Syria, the EU foreign ministers imposed sanctions on 12 people and 11 entities, adding to the list of those previously sanctioned by the EU. The bloc is working with the Arab League to halt the violence, and the league's chief, Nabil Elaraby, attended Thursday's meeting.
A statement from the foreign ministers said the crackdown by the Syrian government "risks taking Syria down a very dangerous path of violence, sectarian clashes and militarization."
The statement also said the EU is extremely worried about the deteriorating living conditions of the Syrian people in areas affected by the unrest, especially in the region of Homs. The EU urged the Syrian government to allow humanitarian organizations immediate access.
The White House welcomed the sanctions on both Iran and Syria, saying in a statement that it applauded "the EU's determination to pressure these regimes to end their unacceptable actions, as well as its readiness to consider further steps going forward."
"We look forward to continued coordination with both the European Union and other concerned governments to increase the pressure on both Syria and Iran to ensure that their flagrant violations of international norms comes to an end," it said.
Also discussed at the meeting was the situation in Camp Ashraf, an enclave in eastern Iraq that houses about 3,400 Iranian exiles, many of whom are dedicated to overthrowing the government of Iran.
Iraq, whose government has close ties with Iran, has said Camp Ashraf must be closed by the end of this year. Struan Stevenson, a prominent member of the European Parliament, said Wednesday that Iraq's government is "continuously working on its plan to attack Ashraf and massacre the residents."
The U.N. says at least 34 people were killed when Iraqi security forces raided the camp in April.
EU foreign policy chief Catherine Ashton said after the meeting that she is "in discussion and dialogue" with EU member states, the U.N., the U.S. and the Iraqi government to assure the safety of those now living in Camp Ashraf.
_______________
Don Melvin can be reached at http://twitter.com/Don_Melvin
Yesterday's rampage by Iranian 'students' are just the latest example of how Iranian domestic anger gets focused on diplomats.
With troops pulling out of Iraq and drawing down in Afghanistan, the global war on terror appears to be all but finished. But the reverberations from that war may be felt for some time.
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Earlier this week, US-Pakistani relations took a dive because of a NATO bombing raid on a Pakistani border post that killed 24 Pakistani soldiers. Yesterday, Iranian students and members of an elite volunteer militia called the ?Basij? ? apparently not held back by Iranian police ? jumped the fence and raided the British Embassy in Tehran, prompting London to pull back most of its diplomats there. Foreign Secretary William Hague warned that there would be ?serious consequences.?
America?s and Britain?s relations with Iran ? which appeared to be moving toward rapprochement in the early days following Sept. 11 attacks ? have since taken a nosedive after Bush administration officials increasingly attempted to draw links between Iran?s security services and Al Qaeda as well as concerns about a covert Iranian nuclear weapons program. In that context, yesterday?s protests by Iranian students make sense, but what would get them so angry to raid the British embassy is a bit hard to explain. The Guardian?s Riazat Butt does write, in his penultimate paragraph, this explanation.
The storming of the embassy was triggered by the UK's decision to sever ties to the Iranian banking system and parliament, the Majlis, after the International Atomic Energy Agency published a report citing "credible" evidence that Iranian scientists had experimented with a nuclear warhead design and could be continuing to do so.
Frequent readers of the Monitor ? you know who you are ? will have read Scott Peterson?s excellent piece on Nov. 8 detailing the IAEA report on Iran?s nuclear program. Relying on intelligence reports and Iranian official information smuggled out of the country in a pilfered laptop, the IAEA concluded that Iran had continued to study ways to enrich uranium beyond the normal uses of civilian power-generation, and also continued to study ways to deliver a nuclear payload aboard Iran?s long-range Shahab-3 missiles. Iran has hotly denied that its nuclear program is for anything other than peaceful purposes, and calls the IAEA report ?politically motivated.?
The Iranian rampage has all the elements of us-versus-them that characterizes so much about international politics these days, but the Washington Post?s Thomas Erdbrink and Joby Warrick note that there are signs of dissension within the Iranian regime about whether the student raid on the British embassy was appropriate behavior. Students raiding the embassy pledged loyalty to Iran?s supreme leader, Ayatollah Ali Khamanei, the Post wrote, while a spokesman for Iranian President Mahmoud Ahmadinejad called the rampage ?unacceptable.?
The winds reached 97 mph at one mountain peak. More than 380,000 homes lost power. Thousands of trees snapped, blocking roads and damaging property. Scores of schools were closed, as was Griffith Park. And motorists battled gridlock caused by broken traffic signals and blowing debris.
The storm, which produced some of the strongest wind gusts in more than a decade, was caused by a highly unusual weather system that even had experts marveling at its power.
While Santa Ana winds are common this time of year, this storm was anything but.
PHOTOS: Sana Ana wind damage
The winds were produced by two separate weather systems that channeled cold air from the north into the Los Angeles area.
A clockwise high-pressure system was parked over Northern California and the Great Basin as a counter-clockwise low-pressure system hovered over Arizona.
Like two massive gears spinning in opposite directions, the systems funneled the winds.
"In some places we've seen gusts over hurricane force, which for the Southwest part of the country is not something that usually happens," said Brian Edwards, a meteorologist for AccuWeather.com. "This is a one-every-10-years kind of thing."
Indeed, the blustery conditions extended across the Southwest, including Utah, Nevada, Wyoming, Arizona and New Mexico. In some places, including Utah, wind gusts topped 100 mph.
Experts said one reason for the extensive damage was that the winds were remarkably choppy and unpredictable.
In some places, winds suddenly shifted from 10 mph or 20 mph to more than 80 mph. The shift made trees as well as roofs and power lines vulnerable.
"Everything lined up perfectly," said Bill Patzert, a climatologist for Jet Propulsion Laboratory in La Ca?ada-Flintridge.
Trees were no match for the winds, especially those with heavy canopies. Patzert noted that trees in urban Southern California neighborhoods don't have the strong root systems found in more natural environments.
"L.A. trees don't have deep roots. The urban forest is artificial and is primarily watered by lawn sprinklers," Patzert said. "So what keeps our urban forest alive is people watering their lawns, which are not natural, so you don't have deep root systems. So our trees are very vulnerable to Santa Ana events."
Walter Warriner, a Santa Monica arborist and community forester, agreed, adding that the large canopies of many local trees lack strong foundations.
"When you look at a tree above ground there's a ratio of 20 to 1 compared to below ground, so there's not that many roots holding our big trees in place," he said.
While damage was reported across the Southland, communities in the western San Gabriel Valley were particularly hard-hit, including Pasadena, South Pasadena, San Marino, Altadena and La Ca?ada-Flintridge.
National Weather Service meteorologist Eric Boldt said this, too, was unusual.
Typically, the San Fernando Valley and Ventura County get the brunt of such windstorms.
Amid a flurry of salacious allegations, GOP Presidential candidate Herman Cain is thinking seriously about becoming former GOP Presidential candidate Herman Cain.
All before a single vote has been cast in the race, no less.
The Georgia businessman told his staff this morning that he's "reassessing" his bid for the White House after yet another female accuser - Ginger White - came forward with accusations against him, specifically that they had a 13-YEAR affair.
The Iowa caucuses are scheduled for January 3. While he no longer has frontrunner status, polling indicates Cain could still be competitive in Iowa.
Cain has denied the affair allegations in public and did so again during the conference call, but told his staff, "Obviously, this is cause for reassessment."
Before Ginger White, four other women accused Cain of sexual harassment during his tenure as head of the National Restaurant Association in the '90s.
He refuted those claims as well, but acknowledged that with White, he says, "we have to reassess whether or not this is going to create too much of a cloud, in some people’s minds, as to whether or not they would be able to support us going forth."
Cain admits he knows White, but had only been trying to help her out financially ... as a friend. No word if Gloria Cain will back him up on that one.
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Public release date: 4-Dec-2011
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