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.
BEIRUT (Reuters) ? Syria faced growing economic sanctions and condemnation over "gross human rights violations" on Monday, but President Bashar al-Assad showed no sign of buckling under international pressure to end his military crackdown on popular unrest.
State television broadcast pro-Assad rallies "supporting national unity and rejecting foreign interference," after the Arab League imposed sanctions on Sunday.
The European Union weighed in one day later, further tightening the financial screws on Damascus for its "brutality and unwillingness to change course."
Assad's foreign minister Walid al-Moualem hit back, lambasting the Arab League for "a declaration of economic war" that he said had closed the door to resolving the crisis.
"Sanctions are a two-way street," Moualem told a televised news conference. "I am not warning here, but we will defend the interests of our people ...."
In Geneva, a United Nations commission of inquiry said Syrian military and security forces had committed crimes against humanity including murder, torture and rape, for which Assad and his government bore direct responsibility.
It demanded an end to "gross human rights violations" and the release of those rounded up in mass arrests since March by Syrian forces quashing pro-democracy demonstrations.
Over 3,500 people were killed in 8 months, the UN says.
Syria's close trading partners Lebanon and Iraq rejected the Arab League measures, whose economic impact could be less severe than intended, analysts said.
"We do not agree with these sanctions and we will not go along with them," said Lebanese Foreign Minister Adnan Mansour.
The Arab League meanwhile appealed once more to Damascus, offering "a review of all of the measures" if Syria dropped its opposition to an Arab plan to end the crackdown.
Anti-Assad activists in Syria said on Sunday that security forces had killed at least 24 civilians, many in a town north of Damascus that has become a focus for the protests. Others were killed in raids on towns in the province of Homs, they said.
In an apparent political concession, which protesters have been demanding for months, Moualem said Syria planned to drop a constitutional clause which designates Assad's Baath Party as the leading party.
The revised constitution foresees "multi-party" politics with "no place for discrimination between parties," he said.
FIGHTING BACK
The Arab League sanctions hit banking, finance, investment and official travel but stop short of a full trade embargo.
"The sanctions are still economic but if there is no movement on the part of Syria then we have a responsibility as human beings to stop the killings," said Sheikh Hamad bin Jassim al-Thani of Qatar, the League's point man on Syria.
"Power is not worth anything when a ruler kills his people."
The president of the Union of Arab Banks, a division of the Arab League, said the sanctions would hit Syria's central bank, which has "big deposits" in the region, especially the Gulf.
Moualem said 95 percent of the targeted money had already been withdrawn beyond the reach of sanctions.
Along with peaceful protests, some of Assad's opponents are fighting back. Army defectors are grouped loosely under the banner of a Syrian Free Army and more insurgent attacks on loyalist troops have been reported in the last few weeks.
Arab nations wanted to avert a repeat of what happened in Libya, where a U.N. Security Council resolution led to NATO air strikes. Sheikh Hamad warned fellow Arabs that the West could intervene in Syria if it felt the League was not serious.
British Foreign Secretary William Hague said the Arab League sanctions demonstrate that "the regime's repeated failure to deliver on its promises will not be ignored."
France said it wanted Syria's powerful and critical neighbor Turkey to join an EU foreign ministers' conference to discuss further measures. Paris has proposed a secure humanitarian corridor linking Syria to Turkey.
One Western diplomat said Assad could, for now, count on support from China and Russia at the United Nations. But they may change position if he intensifies the crackdown and if the Arab League campaigns for international intervention.
China and Russia have oil concessions in Syria. Moscow also has a naval repair base on Syria's Mediterranean coast and announced on Monday that it was sending warships there, in an apparent display of determination to defend its interests.
"The sanctions are likely to lose Assad support among those in Syria who have been waiting to see whether he will be able to turn things around, such as merchants who could now see their businesses take more hits," the diplomat said.
Syrian officials blame the violence on armed groups targeting civilians. Government security forces say 1,100 of their members have been killed.
Assad, who inherited power from his father in 2000, said in an interview this month that he would continue the crackdown and blamed the unrest on outside pressure to "subjugate Syria."
(Additional reporting by Laila Bassam in Beirut, Khaled Oweis in Amman, David Brunnstrom and Justyna Pawlak in Brussels and Stephanie Nebehay in Geneva; writing by Douglas Hamilton; editing by Philippa Fletcher)
CAIRO -- With Egypt's first democratic elections since the fall of Hosni Mubarak now less than a day away, voter confusion and the complexity of the process threaten to undermine the balloting -- assuming, that is, that renewed unrest doesn't sideline voting altogether.
For much of the past week, campaigning and party politics were largely set aside, as anti-regime protests and violent clashes with Egyptian security forces commanded most of the country's attention.
Now, several revolutionary activists insist that unless the ruling military regime that has governed Egypt since February promises to turn over power to a civilian president, the vote for a parliament shouldn't go forward at all. Many of them have once again taken to Tahrir Square, the site of the original revolution earlier this year, and pledged to stay there until the military yields.
But with a voting process that was invented entirely by the military regime this spring, and which at times seems designed to confound, many observers say there could be trouble ahead even without a spike in violence on election day or a dedicated boycott movement.
"Even without Tahrir, there are a million ways this could be a disaster," one Western election observer said this weekend, after being briefed on the intricacies of the process.
International election observers, who arrived in Cairo in droves over the weekend, say the system for electing a parliament from nearly 7,000 candidates is needlessly complex and time-consuming. The vote will take place over two days, plus a third run-off period, a process that will be repeated twice more in different regions of the country over the course of a month and a half.
Once in the booth, voters will have to select a party list, as well as two independent candidates. If they do not choose two independents, their entire vote will be invalidated, a technicality that few voters seem to be aware of.
Many essential decisions about the process have not yet been announced by the state. Details such as how the votes will be counted, how ballots will be stored overnight, and what portion of the results will be made publicly available before the entire process is complete remain unclear.
Other decisions, observers note, appear to have been made on the fly without much consideration. Until very recently, it wasn't clear how votes that were filed from abroad would be collected and tallied, and what districts they would be apportioned to. Observers say the government has suggested that they would let voters abroad self-indicate which district their votes would go to, and trust them to be honest.
Even the decision to expand voting in each locality to two days only was announced, with little explanation, on the election commission's Facebook page this Friday. Between the first and second day of voting, ballot boxes will be stored overnight in polling stations. They will be secured with locks and wax seals, but not security tape or numbered plastic ties, which are far preferred.
"It's not good," another Western election observer said. "What little 'system' there is is complicated, contradictory and non-transparent. The larger problem is that many procedures for the actual conduct of the voting remain undefined and could be interpreted and implemented differently in every polling center."
Meanwhile, political parties have been largely kept in the dark. In one particularly inept move, the government distributed information on registered voters to the campaigns, but ended up only including their names, and not any specific data about their locations or voting districts. "It was useless," a third observer said.
International election experts, from groups like NDI, the International Republican Institute and the Carter Center, have expressed concern, shared by many in Egypt, that their participation might offer false legitimacy to an inherently flawed process.
"Believe me, I've thought about it a lot; it's something that's on our minds," said Les Campbell, the Middle East and North Africa director for the National Democratic Institute (NDI), who is in Cairo as an election witness. "But the way I see it is, I'll let the Egyptians define what is legitimate or not. What we can do is amplify whatever that decision is. If the politicians are willing to compete, we should be willing to observe. But we will not pull punches on what we see."
"If we had to do it over again, I think it would be better if the rules weren't changing every day -- even up to today," Campbell said.
Among the voters themselves, confusion and lack of information about the process run rampant.
During a canvassing session last week, before violence erupted in Tahrir Square, a candidate repeatedly found himself being forced to explain the voting mechanisms and locations to the potential voters he encountered, rather than talk about his policy positions.
CNN's Ben Wedeman, who spent much of Sunday tweeting pictures of campaign flyers strewn across Cairo and the simplified hieroglyphs associated with the candidates -- bananas, blenders, carrots, missiles -- also sent out a diagram printed in a local newspaper of the convoluted party and bloc alignments (for a clearer map, see here).
"Simple, isn't it?" he wrote in jest.
Meanwhile, international observers' input seems to have been largely disregarded by the military regime. None of the observers interviewed by The Huffington Post in recent days seemed able to explain how the regime had settled on its formulas for the vote.
Late on Sunday, as a soft drizzle fell on Cairo, most of the city -- even the hundred or so revolutionary diehards left in Tahrir Square -- seemed resigned to the reality that the vote was one just one night away. Egypt's first democratic election was coming, ready or not.
Below, see a list of some of the main parties in this year's election. For more information on Egypt's election process, visit the Carnegie Endowment For International Peace's elections guide, Al Ahram's guide, or the analysis by the International Foundation For Electoral Systems.
Al-Hurriya Wa Al-Adala
1?of?20
* Freedom And Justice Party
* Muslim Brotherhood party
* Dominant Islamist party
* Established Democratic Alliance
* Freedom And Justice Party
* Muslim Brotherhood party
* Dominant Islamist party
* Established Democratic Alliance
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Al-Hurriya Wa Al-Adala
* Freedom And Justice Party
* Muslim Brotherhood party
* Dominant Islamist party
* Established Democratic Alliance
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Public release date: 4-Dec-2011
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