Your doctor should know if they solved the problem between the sexes.
Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury
The new study here;
http://medicalxpress.com/news/2013-02-chemical-reaction-stroke-damaged-brain.html
"In this study, we've
uncovered new clues as to how natural chemical reactions in the brain
can contribute to brain damage—loss of memory and cognitive function—in a
number of diseases," said Stuart A. Lipton, M.D., Ph.D., director of
Sanford-Burnham's Del E. Webb Neuroscience, Aging, and Stem Cell
Research Center and a clinical neurologist.
Lipton led the study, along with Sanford-Burnham's Tomohiro Nakamura,
Ph.D., who added that these new molecular clues are important because
"we might be able to develop a new strategy for treating stroke and
other disorders if we can find a way to reverse nitric oxide's effect on
a particular enzyme in nerve cells."
Nitric oxide inhibits the neuroprotective ERK1/2 signaling pathway
Learning and memory are in part controlled by NMDA-type glutamate
receptors in the brain. These receptors are linked to pores in the nerve
cell membrane that regulate the flow of calcium and sodium in and out
of the nerve cells. When these NMDA receptors get over-activated, they
trigger the production of nitric oxide. In turn, nitric oxide attaches
to other proteins via a reaction called S-nitrosylation, which was first
discovered by Lipton and colleagues. When those S-nitrosylated proteins
are involved in cell survival and lifespan, nitric oxide can cause
brain cells to die prematurely—a hallmark of neurodegenerative disease.
In their latest study, Lipton, Nakamura and colleagues used cultured
neurons as well as a living mouse model of stroke to explore nitric
oxide's relationship with proteins that help repair neuronal damage.
They found that nitric oxide reacts with the enzyme SHP-2 to inhibit a
protective cascade of molecular events known as the ERK1/2 signaling
pathway. Thus, nitric oxide not only damages neurons, it also blocks the
brain's ability to self-repair.
Journal reference: Proceedings of the National Academy of Sciences
search and more info website
Read more at: http://medicalxpress.com/news/2013-02-chemical-reaction-stroke-damaged-brain.html#jCp
"In this study, we've uncovered new clues as to how natural chemical reactions in the brain can contribute to brain damage—loss of memory and cognitive function—in a number of diseases," said Stuart A. Lipton, M.D., Ph.D., director of Sanford-Burnham's Del E. Webb Neuroscience, Aging, and Stem Cell Research Center and a clinical neurologist. Lipton led the study, along with Sanford-Burnham's Tomohiro Nakamura, Ph.D., who added that these new molecular clues are important because "we might be able to develop a new strategy for treating stroke and other disorders if we can find a way to reverse nitric oxide's effect on a particular enzyme in nerve cells." Nitric oxide inhibits the neuroprotective ERK1/2 signaling pathway Learning and memory are in part controlled by NMDA-type glutamate receptors in the brain. These receptors are linked to pores in the nerve cell membrane that regulate the flow of calcium and sodium in and out of the nerve cells. When these NMDA receptors get over-activated, they trigger the production of nitric oxide. In turn, nitric oxide attaches to other proteins via a reaction called S-nitrosylation, which was first discovered by Lipton and colleagues. When those S-nitrosylated proteins are involved in cell survival and lifespan, nitric oxide can cause brain cells to die prematurely—a hallmark of neurodegenerative disease. In their latest study, Lipton, Nakamura and colleagues used cultured neurons as well as a living mouse model of stroke to explore nitric oxide's relationship with proteins that help repair neuronal damage. They found that nitric oxide reacts with the enzyme SHP-2 to inhibit a protective cascade of molecular events known as the ERK1/2 signaling pathway. Thus, nitric oxide not only damages neurons, it also blocks the brain's ability to self-repair. Journal reference: Proceedings of the National Academy of Sciences search and more info websiteRead more at: http://medicalxpress.com/news/2013-02-chemical-reaction-stroke-damaged-brain.html#jCp
"In this study, we've
uncovered new clues as to how natural chemical reactions in the brain
can contribute to brain damage—loss of memory and cognitive function—in a
number of diseases," said Stuart A. Lipton, M.D., Ph.D., director of
Sanford-Burnham's Del E. Webb Neuroscience, Aging, and Stem Cell
Research Center and a clinical neurologist.
Lipton led the study, along with Sanford-Burnham's Tomohiro Nakamura,
Ph.D., who added that these new molecular clues are important because
"we might be able to develop a new strategy for treating stroke and
other disorders if we can find a way to reverse nitric oxide's effect on
a particular enzyme in nerve cells."
Nitric oxide inhibits the neuroprotective ERK1/2 signaling pathway
Learning and memory are in part controlled by NMDA-type glutamate
receptors in the brain. These receptors are linked to pores in the nerve
cell membrane that regulate the flow of calcium and sodium in and out
of the nerve cells. When these NMDA receptors get over-activated, they
trigger the production of nitric oxide. In turn, nitric oxide attaches
to other proteins via a reaction called S-nitrosylation, which was first
discovered by Lipton and colleagues. When those S-nitrosylated proteins
are involved in cell survival and lifespan, nitric oxide can cause
brain cells to die prematurely—a hallmark of neurodegenerative disease.
In their latest study, Lipton, Nakamura and colleagues used cultured
neurons as well as a living mouse model of stroke to explore nitric
oxide's relationship with proteins that help repair neuronal damage.
They found that nitric oxide reacts with the enzyme SHP-2 to inhibit a
protective cascade of molecular events known as the ERK1/2 signaling
pathway. Thus, nitric oxide not only damages neurons, it also blocks the
brain's ability to self-repair.
Journal reference: Proceedings of the National Academy of Sciences
search and more info website
Read more at: http://medicalxpress.com/news/2013-02-chemical-reaction-stroke-damaged-brain.html#jCp
Read more at: http://medicalxpress.com/news/2013-02-chemical-reaction-stroke-damaged-brain.html#jCp
"In this study, we've
uncovered new clues as to how natural chemical reactions in the brain
can contribute to brain damage—loss of memory and cognitive function—in a
number of diseases," said Stuart A. Lipton, M.D., Ph.D., director of
Sanford-Burnham's Del E. Webb Neuroscience, Aging, and Stem Cell
Research Center and a clinical neurologist.
Lipton led the study, along with Sanford-Burnham's Tomohiro Nakamura,
Ph.D., who added that these new molecular clues are important because
"we might be able to develop a new strategy for treating stroke and
other disorders if we can find a way to reverse nitric oxide's effect on
a particular enzyme in nerve cells."
Nitric oxide inhibits the neuroprotective ERK1/2 signaling pathway
Learning and memory are in part controlled by NMDA-type glutamate
receptors in the brain. These receptors are linked to pores in the nerve
cell membrane that regulate the flow of calcium and sodium in and out
of the nerve cells. When these NMDA receptors get over-activated, they
trigger the production of nitric oxide. In turn, nitric oxide attaches
to other proteins via a reaction called S-nitrosylation, which was first
discovered by Lipton and colleagues. When those S-nitrosylated proteins
are involved in cell survival and lifespan, nitric oxide can cause
brain cells to die prematurely—a hallmark of neurodegenerative disease.
In their latest study, Lipton, Nakamura and colleagues used cultured
neurons as well as a living mouse model of stroke to explore nitric
oxide's relationship with proteins that help repair neuronal damage.
They found that nitric oxide reacts with the enzyme SHP-2 to inhibit a
protective cascade of molecular events known as the ERK1/2 signaling
pathway. Thus, nitric oxide not only damages neurons, it also blocks the
brain's ability to self-repair.
Journal reference: Proceedings of the National Academy of Sciences
search and more info website
Read more at: http://medicalxpress.com/news/2013-02-chemical-reaction-stroke-damaged-brain.html#jCp
Read more at: http://medicalxpress.com/news/2013-02-chemical-reaction-stroke-damaged-brain.html#jCp
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