| Deaf (22) |  |
| Deafness (52) | |
| Hearing loss (35) | |
| Deaf (22) | |
| Deafness (52) | |
| Hearing loss (35) | |
The technical advances from the Healthy Aims project allows one to envision a future without deafness,
which was funded by the National Institute on Deafness and Other Communication Disorders the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Hearing Health Foundation.
the National Institute on Deafness and Other Communication Disorders, and the Seton Healthcare Family supported the research.
causing a wide range of problems that include extreme fatigue, dementia, stunted growth, deafness, blindness, multi-organ failure, and even death.
and Blood Institute, National Institute of Allergy and Infectious diseases Extramural Activities and the National Institute on Deafness and other Communication Disorders s
Eye and Ear clinicians and scientists are driven by a mission to find cures for blindness, deafness and diseases of the head and neck.
#Have scientists found a cure for deafness? Gene therapy that restores hearing in mice could be used on humans in just five years By Ellie Zolfagharifard For Dailymail. com and Reuters Published:
01:22 GMT, 9 july 2015 Gene therapy to treat hereditary human deafness could be available within five years.
Scientists say the mice mutated genes are similar to those responsible for some hereditary human deafness
In the case of deafness, this involves injecting a gene-carrying engineered virus into the inner ear.
but at least half of deafness that occurs before a baby learns to speak is caused by defects in one of more than 70 individual genes.
which is a common cause of human genetic deafness, accounting for 4 to 8 percent of cases.
Scientists say other forms of hereditary deafness could also be fixed using the same strategy. Work at Novartis is advanced more,
'There are a big range of deafness types needing different approaches, 'said Moser
#Behold the PENTAQUARK! Large hadron collider discovers new particle that has eluded scientists since the 1960s A new particle called the pentaquark has been discovered by scientists at the Large hadron collider (LHC).
The paper was authored by former doctoral student Alexander X. Cartagena-Rivera, now a postdoctoral fellow at the National institutes of health's National Institute on Deafness and Other Communication Disorders (NIDCD;
researchers at Boston Children's Hospital and Harvard Medical school have restored hearing in mice with a genetic form of deafness.
Charles Askew More than 70 different genes are known to cause deafness when mutated. Holt, with first author Charles Askew and colleagues at École Polytechnique Fédérale de Lausanne in Switzerland, focused on a gene called TMC1.
because it is a common cause of genetic deafness, accounting for 4 to 8 percent of cases,
--and is a good model for the dominant form of TMC1-related deafness. In this form, less common than the recessive form, a single copy of the mutation causes children to gradually go deaf beginning around the age of 10 to 15 years.
In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to sound--producing a measurable electrical current--and also restored activity in the auditory portion of the brainstem.
In the dominant deafness model, gene therapy with a related gene, TMC2, was successful at the cellular and brain level,
"Holt believes that other forms of genetic deafness may also be amenable to the same gene therapy strategy.
"I can envision patients with deafness having their genome sequenced and a tailored, precision medicine treatment injected into their ears to restore hearing,
a mutation in the TMC1 gene is sufficient to cause deafness. However, Holt's study also showed that gene therapy with TMC2 could compensate for loss of a functional TMC1 gene,
restoring hearing in the recessive deafness model and partial hearing in the dominant deafness model."
and can ultimately challenge, the burden of deafness in humans. The results are testament to the immense dedication of the research team
researchers at Boston Children's Hospital and Harvard Medical school have restored hearing in mice with a genetic form of deafness.
More than 70 different genes are known to cause deafness when mutated. Holt, with first author Charles Askew and colleagues at École Polytechnique Fédérale de Lausanne in Switzerland
because it is a common cause of genetic deafness, accounting for 4 to 8 percent of cases,
--and is a good model for the dominant form of TMC1-related deafness. In this form, less common than the recessive form, a single copy of the mutation causes children to gradually go deaf beginning around the age of 10 to 15 years.
In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to sound--producing a measurable electrical current--and also restored activity in the auditory portion of the brainstem.
In the dominant deafness model, gene therapy with a related gene, TMC2, was successful at the cellular and brain level,
"Holt believes that other forms of genetic deafness may also be amenable to the same gene therapy strategy.
"I can envision patients with deafness having their genome sequenced and a tailored, precision medicine treatment injected into their ears to restore hearing,
a mutation in the TMC1 gene is sufficient to cause deafness. However, Holt's study also showed that gene therapy with TMC2 could compensate for loss of a functional TMC1 gene,
restoring hearing in the recessive deafness model and partial hearing in the dominant deafness model."
and can ultimately challenge, the burden of deafness in humans. The results are testament to the immense dedication of the research team
of which are similar to human genes involved in deafness. Hearing is one of the other interests of Dr. Burgess lab.)This produced mutations in 82 of the 83 genes.
researchers at Boston Children Hospital and Harvard Medical school have restored hearing in mice with a genetic form of deafness.
More than 70 different genes are known to cause deafness when mutated. Holt, with first author Charles Askew and colleagues at École Polytechnique Fédérale de Lausanne in Switzerland, focused on a gene called TMC1.
because it is a common cause of genetic deafness, accounting for 4 to 8 percent of cases,
The other type of mouse, called Beethoven, has a specific TMC1 mutation change in a single amino acidnd is a good model for the dominant form of TMC1-related deafness.
In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to soundroducing a measurable electrical currentnd also restored activity in the auditory portion of the brainstem.
In the dominant deafness model, gene therapy with a related gene, TMC2, was successful at the cellular and brain level,
Holt believes that other forms of genetic deafness may also be amenable to the same gene therapy strategy.
000 live births. can envision patients with deafness having their genome sequenced and a tailored, precision medicine treatment injected into their ears to restore hearing,
a mutation in the TMC1 gene is sufficient to cause deafness. However, Holt study also showed that gene therapy with TMC2 could compensate for loss of a functional TMC1 gene,
restoring hearing in the recessive deafness model and partial hearing in the dominant deafness model. his is a great example of how the basic science can lead to clinical therapies,
and can ultimately challenge, the burden of deafness in humans. The results are testament to the immense dedication of the research team
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