BEIJING (Reuters) - China's Foreign Ministry said it would continue to take "necessary measures" to safeguard its sovereignty over a number of disputed islands in the East China Sea after Japan said it was considering a plan to "buy" them from private landowners. The uninhabited islands, known as Senkaku in Japan and Diaoyu in China, have long been the centre of maritime territorial disputes ...
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1:00 AM
By Steve Mistler smistler@pressherald.com Staff Writer
Gov. Paul LePage used his weekly radio address Saturday to blast President Barack Obama's health care law and described the Internal Revenue Service as the "new Gestapo."
The IRS description was a reference to a provision in the Affordable Care Act that requires most Americans to buy health insurance or pay an annual penalty when filing their tax returns. The provision, known more broadly as the individual mandate, was the subject of a multi-state lawsuit but was recently upheld by the U.S. Supreme Court.
LePage said the court decision has "made America less free."
"We the people have been told there is no choice," he said. "You must buy health insurance or pay the new Gestapo -- the IRS."
Maine Democratic Party Chairman Ben Grant, responding to LePage's remarks, said, "We've come to expect a bunch of nonsense from Gov. LePage, but this is a step too far. There appears now to be no limit to the extreme language he will use to misinform, degrade and insult people. Somebody needs to explain to him that he's the governor of a state, and not a talk radio host. I demand a full apology on behalf of all those who suffered at the hands of the real Gestapo."
"There is nothing that degrades politics more than purported leaders who so cavalierly invoke the worst in human history when they can't get their way in legitimate, modern policy disagreements," Grant said.
The debate about the mandate has become a political flash point since the health law was enacted. Republicans maintain that the requirement is an unfair tax. Democrats say the mandate was originally a Republican idea born from the conservative Heritage Foundation, which introduced the measure in 1989 as a counterpoint to calls for a single-payer health care system.
The Gestapo was Nazi Germany's official secret police under Adolf Hitler. It imprisoned and murdered thousands of people without cause.
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In theory, the U.S. Supreme Court's decision to uphold President Barack Obama's health care law would appear to be a clear win for the president's re-election chances in Virginia and for Democrats in general.
But turning a legal victory into political capital in the commonwealth is not a guarantee.
Working off vehement disapproval of the law among the GOP's more conservative wing, Republicans are cashing in on the high court's ruling and attempting to build momentum in Virginia's key races.
Democrats, meanwhile, are rallying around the court victory, claiming the decisive vote from conservative Chief Justice John Roberts gives the law new credibility in the eyes of independents and moderates.
And the decision has been a fundraising boon for both parties.
In the 24 hours after the decision broke, Romney's campaign raised $4.6 million from more than 47,000 donors nationwide, according to campaign officials. In Virginia, nearly 2,000 donors more than 60 percent of whom had never donated to the Romney campaign before contributed close to $200,000.
The Democratic Congressional Campaign Committee, meanwhile, says it raised more than $2.3 million since the ruling, with Saturday being the biggest grass-roots fundraising day in its history. The amount raised in Virginia since the ruling was not available.
Two days after the June 28 ruling, the coordinated Victory 2012 effort between the Romney camp and the Republican Party of Virginia opened several offices across the state and also gained 1,500 new volunteers.
"I've been around politics and campaigns for 20 years, and I've never seen an uptick or surge like we've experienced since the decision," said Pete Snyder, chairman of the Victory 2012 effort.
"If our troops were at an eight or a nine on an intensity scale, they're at a 15 now," Snyder added, saying that while he was disappointed in the ruling, it was "liquid gold for the campaign."
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Democrats, Republicans using health care ruling to raise funds
1:00 AM
BY STEPHEN OHLEMACHER, Associated Press
WASHINGTON -- The Supreme Court's decision to uphold most of President Barack Obama's health care law will come home to roost for most taxpayers in about 2 1/2 years, when they'll have to start providing proof on their tax returns that they have health insurance.
That scenario puts the Internal Revenue Service at the center of the debate, renewing questions about whether the agency is capable of policing the health care decisions of millions of people in the United States while also collecting the taxes needed to run the federal government.
Under the law, the IRS will provide tax breaks and incentives to help pay for health insurance and impose penalties on some people who don't buy coverage and on some businesses that don't offer it to employees.
The changes will require new regulations, forms and publications, new computer programs and a big new outreach program to explain it all to taxpayers and tax professionals. Businesses that don't claim an exemption will have to prove they offer health insurance to employees.
The health care law "includes the largest set of tax law changes in more than 20 years," according to the Treasury inspector general who oversees the IRS. The agency will have to hire thousands of workers to manage it, requiring significant budget increases that already are being targeted by congressional Republicans determined to dismantle the president's signature initiative.
"Knowing the complexity of the health law, there's no question that the IRS is going to struggle with this," said Rep. Charles Boustany Jr., R-La., chairman of the House Ways and Means oversight subcommittee. "The IRS wants more resources. Well, we need to start digging down into what are they doing with the resources and personnel."
Treasury spokeswoman Sabrina Siddiqui said, "The overwhelming majority of funds used by the agency to implement the Affordable Care Act go to administer the premium tax credits, which will be a tax cut averaging about $4,000 for more than 20 million middle-class people and families."
The Supreme Court, in its 5-4 ruling, upheld the mandate that most Americans get health insurance. The majority said Congress has the power to enforce the mandate under its taxing authority. The decision labeled the penalties a tax, noting that they will be collected by the IRS.
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AP file photoHouse Ways and Means Committee Chairman David Camp, R-Mich., walks to his office on Capitol Hill in Washington. The Supreme Courts decision to uphold most of President Barack Obamas health care law puts the Internal Revenue Service at the center of the debate, renewing questions about whether the agency is capable of policing the health care decisions of millions of Americans while also collecting the taxes needed to fund the federal government.
WASHINGTON The Supreme Courts decision to uphold most of President Barack Obamas health care law will come home to roost for most taxpayers in about two years, when theyll have to start providing proof on their tax returns that they have health insurance.
That scenario puts the Internal Revenue Service at the center of the debate, renewing questions about whether the agency is capable of policing the health care decisions of millions of people in the United States while also collecting the taxes needed to run the federal government.
Under the law, the IRS will provide tax breaks and incentives to help pay for health insurance and impose penalties on some people who dont buy coverage and on some businesses that dont offer it to employees.
The changes will require new regulations, forms and publications, new computer programs and a big new outreach program to explain it all to taxpayers and tax professionals. Businesses that dont claim an exemption will have to prove they offer health insurance to employees.
The health care law includes the largest set of tax law changes in more than 20 years, according to the Treasury inspector general who oversees the IRS. The agency will have to hire thousands of workers to manage it, requiring significant budget increases that already are being targeted by congressional Republicans determined to dismantle the presidents signature initiative.
Knowing the complexity of the health law, theres no question that the IRS is going to struggle with this, said Rep. Charles Boustany Jr., R-La., chairman of the House Ways and Means oversight subcommittee. The IRS wants more resources. Well, we need to start digging down into what are they doing with the resources and personnel.
Treasury spokeswoman Sabrina Siddiqui said, The overwhelming majority of funds used by the agency to implement the Affordable Care Act go to administer the premium tax credits, which will be a tax cut averaging about $4,000 for more than 20 million middle-class people and families.
The Supreme Court, in its 5-4 ruling, upheld the mandate that most Americans get health insurance. The majority said Congress has the power to enforce the mandate under its taxing authority. The decision labeled the penalties a tax, noting that they will be collected by the IRS.
Those who dont get qualified health insurance will be required to pay the penalty or tax starting for the 2014 tax year, unless they are exempt because of low income, religious beliefs, or because they are members of American Indian tribes.
Link:
July 7, 2012 - Frontier League (FL) Florence Freedom FLORENCE,KY- The Evansville Otters scored four runs in the first inning against Freedom starter Daniel DeSimone(2-5) and held off a late Freedom threat for a 7-6 victory. DeSimone was dealt the loss, pitching four innings allowing seven hits, and six earned runs.
Going into the third inning, the Freedom trailed 4-0, but they stormed back to take the lead. Peter Fatse had an RBI single in the inning, as David Harris was able to score on a bases loaded passed ball by catcher Billy Killian, and Drew Rundle hit a three run homerun, his fourth of the year. The Rundle homerun gave the Freedom a 5-4 lead.
The Freedom trailed yet again in this ballgame, but took advantage of some sloppy Evansville defense to get back in the game. With two outs in the seventh inning, and a runner on first base, Fatse hit a fly ball down the left line that appeared to be the final out of the inning, but was dropped by Luis Uribe to extend the inning. After Eddie Rodriguez was hit by a pitch which loaded the bases, Rundle hit a hard grounder to second base which Taylor Black couldn't handle. That error led to the Freedom cutting the deficit to 7-6.
The Freedom in the ninth inning, loaded the bases once more, this time against Otter closer Eric Massingham. The right-hander proved why he will be pitching in next week's all-star game as he pitched out of a one out bases loaded jam. With one out, he got Jim Jacquot to hit a ground ball to third baseman Stephen Marino who threw to home plate to get the force out. Then on a 0-2 pitch, John Malloy flew out to right field for the final out. With the loss, the Freedom saw their four game winning streak come to an end.
The Freedom and Otters will wrap up their series and the first of their season with a night game tomorrow. The game can be heard with Steve Jarnicki starting at 5:50 pm on Real Talk 1160 and realtalk1160.com.
Discuss this story on the Frontier League message board... Digg this story Add to Del.icio.us
The opinions expressed in this release are those of the organization issuing it, and do not necessarily reflect the thoughts or opinions of OurSports Central or its staff.
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"Human freedom increasingly depends on who controls what we know and therefore how we understand our world. It depends on what information we are able to create and disseminate: what we can share; how we can share it; and with whom we can share it."
- Rebecca MacKinnon, "Consent of the Networked: The Worldwide Struggle for Internet Freedom."
It's a pivotal moment for online freedom.
In the wake of the Arab Spring, the Internet's power to transform societies and institutions has never been more apparent. But so too are the parallel risks to authoritarian regimes and other entrenched interests. And they're putting up a fight, flexing their muscle to preserve their power at the cost of citizens' digital rights.
The good news is that heavyweight organizations and observers have taken public stands for online freedom in recent days.
On Thursday, the U.N. Human Rights Council adopted a landmark resolution recognizing the right to freedom of expression online and calling on states to promote Internet access. It was at least an important symbolic step, particularly given the lineup of backers, which included nations frequently on the wrong side of this issue, like Egypt, India and Tunisia.
"It doesn't automatically mean that governments around the world will start doing the right thing at all times," said Rebecca MacKinnon, a senior fellow at the New America Foundation and author of "Consent of the Networked." "But it's a very useful tool for citizens around the world to say to their government, 'You signed onto this, you have to live up to it.' "
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Since the season started, lifeguards say the beaches have been closed more days than they have been open. The good news is that all area beaches were open for swimming Saturday, and despite the wet weather in the morning, beach-goers took advantage of the rare opportunity.
"We do have to call in the morning to check if it's closed or not, and there is some disappointment in our house when it is closed," said Tara Simms of Irondequoit.
It was a good day for the Simms family. Swimming was open at Ontario Beach Park after being closed Friday. It's a problem that is not only frustrating for families who use the lake to cool off but also lifeguards.
"This season, we have had high bacteria counts which have kept the water closed, we had a lot of algae wash ashore early on, more than we had seen at least last year," said James Meier, Captain of the Lifeguards.
The high bacteria levels in water can be dangerous for swimmers and make them sick. Meier says the problem hasn't stopped people from showing up.
"We have actually had some pretty good sized crowds considering that we have been closed a lot, during the week especially, we still have folks coming down enjoying the park and trying to enjoy the sand," said Meier.
Since swimming is open less this year, Meier says everyone should take advantage when the water is safe for swimming.
"Come on down and enjoy being here. It's a great beach and when the water is open, it's a wonderful afternoon," said Meier.
"My husband loves coming to the beach, and we have a 3-year-old, so we would be down here every weekend," said Simms.
The health department has a hotline you can call to find out if your favorite beach is open for swimming. That number is 753-5887.
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Southern Arizona's dark skies established the region as an international hub for astronomy in the 1960s. Observatories and other sky-gazing research facilities have brought prestige and millions of dollars to the state.
Today, riches on the ground or, more specifically, below it also have the potential to enrich the state, resulting in an odd collision between mining and astronomy.
Since 2007, when Rosemont Copper, which is owned by Canada's Augusta Resource Co., announced its plans to build a mine in the desert just south of Tucson, the environmental community has warned that the project will devastate the desert landscape.
But when the mine released its draft environmental impact statement in 2009 and revealed its lighting plan for the mine, another group joined the fray: the International Dark-Sky Assn. and the numerous astronomers whose research and livelihoods depend on the desert's dark skies.
"The [mine's] impact on astronomy is potentially very, very significant," said Scott Kardel, public affairs director of the association, a Tucson-based nonprofit that has worked to preserve and protect the darkness of night skies since 1988.
Because the mine would operate 24 hours a day, seven days a week, nighttime floodlights required by federal safety requirements could create significant light pollution that would interfere with astronomy.
The site of the proposed Rosemont Copper Mine is 12 miles northeast of the Fred Lawrence Whipple Observatory, known for its Multiple Mirror Telescope and work in ground-based gamma-ray astronomy.
"The initial lighting estimate of the [mine's] light output was very bad," said Emilio Falco, project director at the Whipple Observatory, which is part of the Harvard-Smithsonian Center for Astrophysics.
According to that initial estimate, the mine's lumen output the measure of the amount of visible light emitted by a source would be 21.7 million lumens, or the equivalent of about 12,000 houses.
The scientific community and the industries that cater to the astronomers were alarmed. In 2007, a study conducted by the University of Arizona estimated that astronomy contributed $250 million annually to the state's economy.
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MINNEAPOLIS, MN July 5, 2012 Donaldson Company, Inc. (NYSE: DCI), the leading provider of filtration solutions for aerospace and defense, industrial and heavy manufacturing applications, will display many of its most innovative products for a global audience July 9-13 at the Farnborough International Airshow 2012. The company will exhibit products and meet visitors at Booth C16, Hall 1.
Donaldson Aerospace & Defense Group offers a comprehensive line of filtration applications for commercial and military aircraft and ground vehicles. The Farnborough exhibit will showcase hydraulic manifolds that provide smooth operation of essential flight systems; propellant surface tension devices for reliable fuel flow; fuel filters to eliminate particulates that can foul engines; and inlet barrier filters to ensure clean air flow into turbine engine intakes. The Donaldson Air Purification System (APS) will also be featured.
Donaldson executives and technical experts will be available to discuss these and other systems throughout the event. Customers can schedule appointments by contacting Jessica Sammeter at 661-705-3850 or email jessica.sammeter@donaldson.com.
Donaldson product excellence and dedicated technical and support teams have made us a valued partner for aerospace companies and governments and military forces around the world, said Mike Trevino, Director of Sales, Donaldson Aerospace & Defense Group. We are delighted to attend Farnborough and demonstrate the unmatched capabilities of our advanced filtration systems and expand our worldwide customer base.
About Donaldson's Aerospace & Defense Group
Donaldson's Aerospace & Defense group is a leading worldwide provider of filtration systems for the aerospace and defense industry. Our filtration solutions protect fixed wing aircraft, rotorcraft, military ground vehicles, electronic equipment, space vehicles, missiles, military shipboard systems and amphibious vehicles. We are committed to advancing filtration technology, providing quality products and prompt customer service. Our group serves customers from sales, engineering and manufacturing locations around the world.
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Donaldson Showcases Filtration Systems for Global Aerospace Industry at Farnborough 2012
July 6, 2012 How Parkinsons Disease starts and spreads
Anonymous Science Daily The Daily Item Fri Jul 06, 2012, 02:00 PM EDT
PHILADELPHIA
Injection of a small amount of clumped protein triggers a cascade of events leading to a Parkinsons-like disease in mice, according to an article published in the Journal of Experimental Medicine and reported by Science Daily.
Progressive accumulation of clumps of the protein alpha-synuclein in the brains of patients with Parkinsons disease coincides with the onset of motor dysfunction. However, whether these clumps are sufficient to trigger neurodegeneration, and how these clumps spread throughout the brain, remained unclear.
To answer these questions, a team led by Virginia M.Y. Lee at the University of Pennsylvania School of Medicine studied mice expressing a mutated form of alpha-synuclein found in patients with Parkinsons disease. These mice show symptoms of disease around one year of age but not earlier.
Lee and colleagues found that injecting preformed clumps of human alpha-synuclein into the brains of young mice accelerated disease onset and severity. These clumps seemed to act as seeds that recruited even the mouse version of alpha-synuclein into new clumps, which then spread throughout the brain. The pattern of spreading from neuron to neuron suggests that the clumps may hijack the highway traveled by normal brain signals.
These findings suggest that Parkinsons disease, like other neurodegenerative diseases including Alzheimers, may start and progress due to abnormal aggregation and accumulation of proteins within the brain. What gets these clumps going in the first place remains unclear.
Continued here:
How Parkinson’s Disease starts and spreads
NIH-funded study shows cells from different patients have unique drug responses
Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.
The researchers collected skin cells from patients with genetically inherited forms of Parkinsons and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
The results were published in Science Translational Medicine.
"These findings suggest new opportunities for clinical trials of Parkinsons disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
A consortium of researchers conducted the study with primary funding from NINDS. The consortium is led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston.
The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.
Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.
Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.
Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.
View original post here:
Patient-Derived Stem Cells Could Improve Drug Research For Parkinson's
NIH-funded study shows cells from different patients have unique drug responses
Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.
The researchers collected skin cells from patients with genetically inherited forms of Parkinsons and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
The results were published in Science Translational Medicine.
"These findings suggest new opportunities for clinical trials of Parkinsons disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
A consortium of researchers conducted the study with primary funding from NINDS. The consortium is led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston.
The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.
Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.
Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.
Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.
View original post here:
Patient-Derived Stem Cells Could Improve Drug Research For Parkinson's
Washington, July 5 : Researchers have taken a major step in drug research for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments.
The researchers collected skin cells from patients with genetically inherited forms of Parkinson's and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability - in particular, abnormalities in the cellular energy factories known as mitochondria.
At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
"These findings suggest new opportunities for clinical trials of Parkinson's disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
The study was conducted by a consortium of researchers led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston with primary funding from NINDS.
The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.
Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.
Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.
Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.
Because prior studies have suggested that Parkinson's disease involves a breakdown of mitochondrial function, the researchers looked for signs of impaired mitochondria in patient-derived neurons. Mitochondria turn oxygen and glucose into cellular energy.
Link:
Patient-derived stem cells may improve treatments for Parkinson's
Washington, July 5 : Researchers have taken a major step in drug research for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments.
The researchers collected skin cells from patients with genetically inherited forms of Parkinson's and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability - in particular, abnormalities in the cellular energy factories known as mitochondria.
At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
"These findings suggest new opportunities for clinical trials of Parkinson's disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
The study was conducted by a consortium of researchers led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston with primary funding from NINDS.
The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.
Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.
Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.
Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.
Because prior studies have suggested that Parkinson's disease involves a breakdown of mitochondrial function, the researchers looked for signs of impaired mitochondria in patient-derived neurons. Mitochondria turn oxygen and glucose into cellular energy.
Link:
Patient-derived stem cells may improve treatments for Parkinson's
Washington, D.C. - infoZine - Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.
The researchers collected skin cells from patients with genetically inherited forms of Parkinson's and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability -- in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
The results were published in Science Translational Medicine.
"These findings suggest new opportunities for clinical trials of Parkinson's disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
A consortium of researchers conducted the study with primary funding from NINDS. The consortium is led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston.
The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.
Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.
Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.
Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.
Because prior studies have suggested that Parkinson's disease involves a breakdown of mitochondrial function, the researchers looked for signs of impaired mitochondria in patient-derived neurons. Mitochondria turn oxygen and glucose into cellular energy. The researchers found that oxygen consumption rates were lower in patient cells with LRRK2 mutations, and higher in cells with the PINK1 mutation. In PINK1 mutant cells, the researchers also found increased vulnerability to oxidative stress, a damaging process that in theory can be counteracted with antioxidants.
Read the original:
Personalized Medicine for Parkinson's Disease
Washington, D.C. - infoZine - Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.
The researchers collected skin cells from patients with genetically inherited forms of Parkinson's and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability -- in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
The results were published in Science Translational Medicine.
"These findings suggest new opportunities for clinical trials of Parkinson's disease, in which cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention," said Margaret Sutherland, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
A consortium of researchers conducted the study with primary funding from NINDS. The consortium is led by Ole Isacson, M.D., Ph.D., a professor of neurology at McLean Hospital and Harvard Medical School in Boston.
The NINDS consortium's first goal was to transform the patients' skin cells into induced pluripotent stem (iPS) cells, which are adult cells that have been reprogrammed to behave like embryonic stem cells. The consortium researchers then used a combination of growth conditions and growth-stimulating molecules to coax these iPS cells into becoming neurons, including the type that die in Parkinson's disease.
Parkinson's disease affects a number of brain regions, including a motor control area of the brain called the substantia nigra. There, it destroys neurons that produce the chemical dopamine. Loss of these neurons leads to involuntary shaking, slowed movements, muscle stiffness and other symptoms. Medications can help manage the symptoms, but there is no treatment to slow or stop the disease.
Most cases of Parkinson's are sporadic, meaning that the cause is unknown. However, genetics plays a strong role. There are 17 regions of the genome with common variations that affect the risk of developing Parkinson's disease. Researchers have also identified nine genes that, when mutated, can cause the disease.
Dr. Isacson and his collaborators derived iPS cells from five people with genetic forms of Parkinson's disease. By focusing on genetic cases, rather than sporadic cases, they hoped they would have a better chance of seeing patterns in the disease process and in treatment responses. Three of the individuals had mutations in a gene called LRRK2, and two others were siblings who had mutations in the gene PINK1. The researchers also derived iPS cells from two of the siblings' family members who did not have Parkinson's or any known mutations linked to it.
Because prior studies have suggested that Parkinson's disease involves a breakdown of mitochondrial function, the researchers looked for signs of impaired mitochondria in patient-derived neurons. Mitochondria turn oxygen and glucose into cellular energy. The researchers found that oxygen consumption rates were lower in patient cells with LRRK2 mutations, and higher in cells with the PINK1 mutation. In PINK1 mutant cells, the researchers also found increased vulnerability to oxidative stress, a damaging process that in theory can be counteracted with antioxidants.
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Personalized Medicine for Parkinson's Disease
Author Gabriel Garcia Marquez, from his Facebook page.
CARTAGENA, Colombia, July 7 (UPI) -- Colombian author and Nobel literature laureate Gabriel Garcia Marquez is suffering from dementia and has been forced to stop writing, his brother announced.
The 84-year-old author, best known for the novel "One Hundred Years of Solitude," which has sold more than 30 million copies, is currently in the middle of writing his autobiography, The Daily Telegraph reported Saturday. Brother Jaime Garcia Marquez told students at a lecture in Cartagena his brother no longer has the mental faculties to complete the book, "Living to Tell the Tale."
"He is doing well physically, but he has been suffering from dementia for a long time," he said. "From a physical standpoint he's doing well, although he now has some memory lapses" that have been made worse by a battle with lymphatic cancer in 1999.
"Dementia runs in our family and he's now suffering the ravages prematurely due to the cancer that put him almost on the verge of death," he said.
Garcia Marquez, who lives in Mexico, was a pioneer of the literary school of magical realism, producing the novels "Love in the Time of Cholera," "Chronicle of a Death Foretold" and "The General in His Labyrinth."
"He still has the humor, joy and enthusiasm that he has always had," his brother told his students.
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Author Gabriel Garcia Marquez has dementia
irishtimes.com - Last Updated: Saturday, July 7, 2012, 16:02
The celebrated Nobel prize winning author Gabriel Garcia Marquez is suffering from dementia and is no longer able to write, his family have announced.
The brother of the Colombian author who won the Noble prize in 1982 said the family had tried to keep the secret, not because there is anything people should not know "but because it's his life and he's always tried to protect it."
"The fact is there are lots of comments. Some are true but they're always filled with morbid (details). Sometimes you get the sense they'd rather he were dead, as if his death were some great news," Jaime Garcia Marquez said.
Addressing students at a lecture in Cartagena he said his 84-year-old brother frequently phones him to ask simple questions.
"He has problems with his memory. Sometimes I cry because I feel like I'm losing him," he said, adding that he had now stopped writing altogether.
Jaime Garcia Marquez, his younger brother, is the first family member to speak publicly about it. "He is doing well physically, but he has been suffering from dementia for a long time," he said. "From a physical standpoint he's doing well, although he now has some memory lapse.
"But he still has the humour, joy and enthusiasm that he has always had."
Best known for One Hundred Years of Solitude, which has sold more than 30 million copies, Marquez lives in Mexico. His novels include Love in the Time of Cholera, Chronicle of a Death Foretold and The General in His Labyrinth.
He has not published anything since the novel, Memoirs of My Melancholy Whores, which was published five years ago to mixed reviews.
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Garcia Marquez has dementia, brother says
Queensland scientists have moved a step closer to new treatments for a rare degenerative brain disease.
Ataxia telangiectasia is an inherited disease causing severe disability, a weakened immune system, susceptibility to infection and an increased risk of cancer.
It affects between one in 100,000 and one in 300,000 people and is ultimately fatal.
Patients are frequently confined to a wheelchair by their early teenage years and generally die by their 20s.
People with the disease can develop cancer and brain degeneration because a gene that recognises and repairs DNA damage is defective.
Researchers from the University of Queensland's Australian Institute for Bioengineering and Nanotechnology have found a way to develop brain cells to study in the lab from the skin cells of children.
By reprogramming the skin cells into stem cells, then brain cells, researchers hope to be able to correct the genetic mutations and demonstrate that they can replace the defective cells that cause the problems in the disease.
Replacing the defective cells with corrected cells, or developing new drugs using the cells in the study, could help treat the disease.
The researchers could start screening medicines in one to two years, but testing in animals would have to be completed before they could be used in humans.
The skin cell reprogramming research has been published in the journal Stem Cells Translational Medicine.
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Rare disease treatment hope