Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, September 14, 2012

Ceria nanoparticles could lessen the damage from ischemic strokes

Start clinical trials now!!!
http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
 When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp
When blood flow to areas of the brain is restricted, reactive oxygen compounds like superoxide radical anions (O2• –), hydrogen peroxide (H2O2), and hydroxyl radicals (HO• –) form and accumulate. These species cause oxidative damage and are responsible for tissue damage and cell death during a stroke. Nerve connections and neurovascular units are destroyed and the function of the brain in these areas stops. Despite various treatments that primarily combat the causes of reduced blood flow, such as thrombosis, there has been no way to protect nerves from oxidative damage after an acute ischemic stroke. Seung-Hoon Lee, Taeghwan Hyeon, and their team at Seoul National University hope that nanoparticles made of ceria may represent a new approach for treatment. Cells contain enzymes that can break down reactive oxygen species: superoxide dismutases, which convert superoxide anions to hydrogen peroxide; and catalase, which splits hydrogen peroxide. Ceria nanoparticles can do both. How does this work? The cerium in ceria crystals is present in the form of Ce4+. However, if the particle size is reduced to a few nanometers in diameter, some spots on the surface are missing oxygen atoms. These places have Ce3+ instead, which can easily be reduced back to Ce4+ and can reversibly bind oxygen. The researchers treated cell cultures with a substance that increases the concentrations of reactive oxygen species, which leads to increased cell death. Treatment with cerium oxide nanoparticles drastically improved the cell survival rate. In animal trials, the researchers induced ischemic strokes in rats. Intravenously administered ceria nanoparticles considerably reduced the stroke volume and nerve damage. An optimized, carefully balanced dose is necessary, however. Interestingly, the concentrations of ceria nanoparticles in the healthy areas of the brain were very low, while those in the ischemic areas were drastically elevated. The researchers speculate that the ceria nanoparticles can barely pass through the intact blood-brain barrier. However, the barrier is damaged in the ischemic areas, allowing the diseased areas of the brain to be reached and oxidative damage to be stopped.

Read more at: http://phys.org/news/2012-09-ceria-nanoparticles-lessen-ischemic.html#jCp

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