Journal of Biomedical Science 2009, 16:98doi:10.1186/1423-0127-16-98
Published: 5 November 2009
Yuanbin Liu and David R Schubert
Cellular Neurobiology Laboratory, The Salk Institute for Biological Studies,10010 N. Torrey Pines Road, La Jolla, California 92037-1099 USA
OPEN ACCESS
Abstract (provisional)
Background
Reactive oxygen species (ROS) play an important role in aging and age-related diseases such as Parkinson's disease and Alzheimer's disease. Much of the ROS production under conditions of toxic stress is from mitochondria, and multiple antioxidants prevent ROS accumulation. The aim of this study is to examine the specificity of the interaction between the antioxidants and ROS production in stressed cells.
Methods
Using fluorescent dyes for ROS detection and mitochondrial inhibitors of known specificities, we studied ROS production under three conditions where ROS are produced by mitochondria: oxidative glutamate toxicity, state IV respiration induced by oligomycin, and tumor necrosis factor-induced cell death.
Results
We demonstrated that there are at least four mitochondrial ROS-generating sites in cells, including the flavin mononucleotide (FMN) group of complex I and the three ubiquinone-binding sites in complexes I, II and III. ROS production from these sites is modulated in an insult-specific manner and the sites are differentially accessible to common antioxidants.
Conclusions
The inhibition of ROS accumulation by different antioxidants is specific to the site of ROS generation as well as the antioxidant. This information should be useful for devising new interventions to delay aging or treat ROS-related diseases.
Link to full text: http://www.jbiomedsci.com/content/pdf/1423-0127-16-98.pdf
Friday, November 6, 2009
Thursday, November 5, 2009
Auditory Perception in Individuals with Friedreich's Ataxia
Audiol Neurotol 2010;15:229-240 (DOI: 10.1159/000255341)
Gary Rancea, Louise Corbenb, Elizabeth Barkera, Peter Carewa, Donella Chisaria, Meghan Rogersa, Richard Dowella, Saiful Jamaluddina, Rochelle Brysona, Martin B. Delatyckib
aDepartment of Otolaryngology, The University of Melbourne, and
bMurdoch Children's Research Institute, Parkville, Vic., Australia
Keywords: Friedreich's ataxia, Auditory perception, Temporal processing, Speech perception.
Gary Rancea, Louise Corbenb, Elizabeth Barkera, Peter Carewa, Donella Chisaria, Meghan Rogersa, Richard Dowella, Saiful Jamaluddina, Rochelle Brysona, Martin B. Delatyckib
aDepartment of Otolaryngology, The University of Melbourne, and
bMurdoch Children's Research Institute, Parkville, Vic., Australia
Keywords: Friedreich's ataxia, Auditory perception, Temporal processing, Speech perception.
Wednesday, November 4, 2009
Auditory plasticity and speech motor learning
Sazzad M. Nasira and David J. Ostrya,
Department of Psychology, McGill University, Montreal, QC, Canada H3A 1B1; and Haskins Laboratories, New Haven, CT 06511
Edited by Michael M. Merzenich, University of California, San Francisco, CA, and approved September 24, 2009 (received for review June 28, 2009)
OPEN ACCES
Abstract
Is plasticity in sensory and motor systems linked? Here, in the context of speech motor learning and perception, we test the idea sensory function is modified by motor learning and, in particular, that speech motor learning affects a speaker's auditory map. We assessed speech motor learning by using a robotic device that displaced the jaw and selectively altered somatosensory feedback during speech. We found that with practice speakers progressively corrected for the mechanical perturbation and after motor learning they also showed systematic changes in their perceptual classification of speech sounds. The perceptual shift was tied to motor learning. Individuals that displayed greater amounts of learning also showed greater perceptual change. Perceptual change was not observed in control subjects that produced the same movements, but in the absence of a force field, nor in subjects that experienced the force field but failed to adapt to the mechanical load. The perceptual effects observed here indicate the involvement of the somatosensory system in the neural processing of speech sounds and suggest that speech motor learning results in changes to auditory perceptual function.
link to full text: http://www.pnas.org/content/early/2009/10/30/0907032106.full.pdf
Department of Psychology, McGill University, Montreal, QC, Canada H3A 1B1; and Haskins Laboratories, New Haven, CT 06511
Edited by Michael M. Merzenich, University of California, San Francisco, CA, and approved September 24, 2009 (received for review June 28, 2009)
OPEN ACCES
Abstract
Is plasticity in sensory and motor systems linked? Here, in the context of speech motor learning and perception, we test the idea sensory function is modified by motor learning and, in particular, that speech motor learning affects a speaker's auditory map. We assessed speech motor learning by using a robotic device that displaced the jaw and selectively altered somatosensory feedback during speech. We found that with practice speakers progressively corrected for the mechanical perturbation and after motor learning they also showed systematic changes in their perceptual classification of speech sounds. The perceptual shift was tied to motor learning. Individuals that displayed greater amounts of learning also showed greater perceptual change. Perceptual change was not observed in control subjects that produced the same movements, but in the absence of a force field, nor in subjects that experienced the force field but failed to adapt to the mechanical load. The perceptual effects observed here indicate the involvement of the somatosensory system in the neural processing of speech sounds and suggest that speech motor learning results in changes to auditory perceptual function.
link to full text: http://www.pnas.org/content/early/2009/10/30/0907032106.full.pdf
Researchers Unlock The 'Sound Of Learning' By Linking Sensory And Motor Systems
Medicalnewstoday, Article Date: 04 Nov 2009 - 0:00 PST
Learning to talk also changes the way speech sounds are heard, according to a new study published in Proceedings of the National Academy of Sciences by scientists at Haskins Laboratories, a Yale-affiliated research laboratory. The findings could have a major impact on improving speech disorders. (read more)
Learning to talk also changes the way speech sounds are heard, according to a new study published in Proceedings of the National Academy of Sciences by scientists at Haskins Laboratories, a Yale-affiliated research laboratory. The findings could have a major impact on improving speech disorders. (read more)
Frataxin interacts with Isu1 through a conserved tryptophan in its beta-sheet.
Hum Mol Genet. 2009, Nov 2.
Leidgens S, De Smet S, Foury F.
Unité de Biochimie Physiologique, Institut des Sciences de la Vie, Université Catholique de Louvain, Croix du Sud 5-15, 1348 Louvain-la-Neuve, Belgium.
Keywords: Friedreich's ataxia, frataxin, iron-sulfur (Fe/S) clusters, Yfh1, Isu1, beta-sheet platform, Q129A, I130A, W131A(F), R141A, low aconitase activity, Gln-129, Trp-131, Arg-141, aromatic side chain.
Leidgens S, De Smet S, Foury F.
Unité de Biochimie Physiologique, Institut des Sciences de la Vie, Université Catholique de Louvain, Croix du Sud 5-15, 1348 Louvain-la-Neuve, Belgium.
Keywords: Friedreich's ataxia, frataxin, iron-sulfur (Fe/S) clusters, Yfh1, Isu1, beta-sheet platform, Q129A, I130A, W131A(F), R141A, low aconitase activity, Gln-129, Trp-131, Arg-141, aromatic side chain.
Monday, November 2, 2009
Iron Deficiency is the Most Common Deficiency Among People
November 02, 2009
http://www.associatedcontent.com/
Keyword: Dr. Timothy Stemmler, Wayne State University, University of Michigan-Dearborn, iron deficiency, Anemia, Parkinson's, Fredreich's Ataxia, frataxin.
http://www.associatedcontent.com/
Keyword: Dr. Timothy Stemmler, Wayne State University, University of Michigan-Dearborn, iron deficiency, Anemia, Parkinson's, Fredreich's Ataxia, frataxin.
Lundbeck starts clinical phase IIa with Lu AA24493 (cEPO) in Friedreich's ataxia in a study also assessing efficacy via biomarkers
PR-inside.com,
London, November , 02, 2009
Keywords: H. Lundbeck A/S, phase IIa clinical studies, project Lu AA24493, safety and
tolerability, Friedreich's ataxia, carbamoylated form of human erythropoietin (EPO), loss of haematopoietic effects, neuronal damage,
----------------------------------------------------------
Pharmacy Europe,
Latest News, Monday 2nd November 2009
Lundbeck starts clinical phase IIa with Lu AA24493 (cEPO)
---------------------------------------------------------
Reuters.com
Mon Nov 2, 2009 5:10am EST
Lundbeck says expands stroke drug candidate trials
London, November , 02, 2009
Keywords: H. Lundbeck A/S, phase IIa clinical studies, project Lu AA24493, safety and
tolerability, Friedreich's ataxia, carbamoylated form of human erythropoietin (EPO), loss of haematopoietic effects, neuronal damage,
----------------------------------------------------------
Pharmacy Europe,
Latest News, Monday 2nd November 2009
Lundbeck starts clinical phase IIa with Lu AA24493 (cEPO)
---------------------------------------------------------
Reuters.com
Mon Nov 2, 2009 5:10am EST
Lundbeck says expands stroke drug candidate trials
Saturday, October 31, 2009
Whole-body isometric force/torque measurements for functional assessment in neuro-rehabilitation: platform design, development and verification
OPEN ACCESS
Journal of NeuroEngineering and Rehabilitation 2009, 6:38doi:10.1186/1743-0003-6-38
Published: 30 October 2009
Abstract (provisional)
Background
One of the main scientific and technological challenges of rehabilitation bioengineering is the development of innovative methodologies, based on the use of appropriate technological devices, for an objective assessment of patients undergoing a rehabilitation treatment. Such tools should be as fast and cheap to use as clinical scales, which are currently the daily instruments most widely used in the routine clinical practice.
Methods
A human-centered approach was used in the design and development of a mechanical structure equipped with eight force/torque sensors that record quantitative data during the initiation of a predefined set of Activities of Daily Living (ADL) tasks, in isometric conditions.
Results
Preliminary results validated the appropriateness, acceptability and functionality of the proposed platform, that has become now a tool used for clinical research in three clinical centres.
Conclusions
This paper presented the design and development of an innovative platform for whole-body force and torque measurements on human subjects. The platform has been designed to perform accurate quantitative measurements in isometric conditions with the specific aim to address the needs for functional assessment tests of patients undergoing a rehabilitation treatment as a consequence of a stroke. The versatility of the system also enlightens several other interesting possible areas of application for therapy in neurorehabilitation, for research in basic neuroscience, and more.
Link to full text: http://www.jneuroengrehab.com/content/pdf/1743-0003-6-38.pdf
Journal of NeuroEngineering and Rehabilitation 2009, 6:38doi:10.1186/1743-0003-6-38
Published: 30 October 2009
Abstract (provisional)
Background
One of the main scientific and technological challenges of rehabilitation bioengineering is the development of innovative methodologies, based on the use of appropriate technological devices, for an objective assessment of patients undergoing a rehabilitation treatment. Such tools should be as fast and cheap to use as clinical scales, which are currently the daily instruments most widely used in the routine clinical practice.
Methods
A human-centered approach was used in the design and development of a mechanical structure equipped with eight force/torque sensors that record quantitative data during the initiation of a predefined set of Activities of Daily Living (ADL) tasks, in isometric conditions.
Results
Preliminary results validated the appropriateness, acceptability and functionality of the proposed platform, that has become now a tool used for clinical research in three clinical centres.
Conclusions
This paper presented the design and development of an innovative platform for whole-body force and torque measurements on human subjects. The platform has been designed to perform accurate quantitative measurements in isometric conditions with the specific aim to address the needs for functional assessment tests of patients undergoing a rehabilitation treatment as a consequence of a stroke. The versatility of the system also enlightens several other interesting possible areas of application for therapy in neurorehabilitation, for research in basic neuroscience, and more.
Link to full text: http://www.jneuroengrehab.com/content/pdf/1743-0003-6-38.pdf
Friday, October 30, 2009
Progressive GAA·TTC Repeat Expansion in Human Cell Lines
OPEN ACCESS
Scott Ditch, Mimi C. Sammarco, Ayan Banerjee, Ed Grabczyk*
Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States of America
Abstract
Trinucleotide repeat expansion is the genetic basis for a sizeable group of inherited neurological and neuromuscular disorders. Friedreich ataxia (FRDA) is a relentlessly progressive neurodegenerative disorder caused by GAA·TTC repeat expansion in the first intron of the FXN gene. The expanded repeat reduces FXN mRNA expression and the length of the repeat tract is proportional to disease severity. Somatic expansion of the GAA·TTC repeat sequence in disease-relevant tissues is thought to contribute to the progression of disease severity during patient aging. Previous models of GAA·TTC instability have not been able to produce substantial levels of expansion within an experimentally useful time frame, which has limited our understanding of the molecular basis for this expansion. Here, we present a novel model for studying GAA·TTC expansion in human cells. In our model system, uninterrupted GAA·TTC repeat sequences display high levels of genomic instability, with an overall tendency towards progressive expansion. Using this model, we characterize the relationship between repeat length and expansion. We identify the interval between 88 and 176 repeats as being an important length threshold where expansion rates dramatically increase. We show that expansion levels are affected by both the purity and orientation of the repeat tract within the genomic context. We further demonstrate that GAA·TTC expansion in our model is independent of cell division. Using unique reporter constructs, we identify transcription through the repeat tract as a major contributor to GAA·TTC expansion. Our findings provide novel insight into the mechanisms responsible for GAA·TTC expansion in human cells.
Link to full text: http://www.plosgenetics.org/article/fetchObjectAttachment.action;jsessionid=1C3EDADDCEC7DDCE3438B379DC71EE00?uri=info%3Adoi%2F10.1371%2Fjournal.pgen.1000704&representation=PDF
Scott Ditch, Mimi C. Sammarco, Ayan Banerjee, Ed Grabczyk*
Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States of America
Abstract
Trinucleotide repeat expansion is the genetic basis for a sizeable group of inherited neurological and neuromuscular disorders. Friedreich ataxia (FRDA) is a relentlessly progressive neurodegenerative disorder caused by GAA·TTC repeat expansion in the first intron of the FXN gene. The expanded repeat reduces FXN mRNA expression and the length of the repeat tract is proportional to disease severity. Somatic expansion of the GAA·TTC repeat sequence in disease-relevant tissues is thought to contribute to the progression of disease severity during patient aging. Previous models of GAA·TTC instability have not been able to produce substantial levels of expansion within an experimentally useful time frame, which has limited our understanding of the molecular basis for this expansion. Here, we present a novel model for studying GAA·TTC expansion in human cells. In our model system, uninterrupted GAA·TTC repeat sequences display high levels of genomic instability, with an overall tendency towards progressive expansion. Using this model, we characterize the relationship between repeat length and expansion. We identify the interval between 88 and 176 repeats as being an important length threshold where expansion rates dramatically increase. We show that expansion levels are affected by both the purity and orientation of the repeat tract within the genomic context. We further demonstrate that GAA·TTC expansion in our model is independent of cell division. Using unique reporter constructs, we identify transcription through the repeat tract as a major contributor to GAA·TTC expansion. Our findings provide novel insight into the mechanisms responsible for GAA·TTC expansion in human cells.
Link to full text: http://www.plosgenetics.org/article/fetchObjectAttachment.action;jsessionid=1C3EDADDCEC7DDCE3438B379DC71EE00?uri=info%3Adoi%2F10.1371%2Fjournal.pgen.1000704&representation=PDF
Thursday, October 29, 2009
Researchers Find Brain Cell Transplants Help Repair Neural Damage
ScienceDaily (Oct. 29, 2009) — A Swiss research team has found that using an animal's own brain cells (autologous transplant) to replace degenerated neurons in select brain areas of donor primates with simulated but asymptomatic Parkinson's disease and previously in a motor cortex lesion model, provides a degree of brain protection and may be useful in repairing brain lesions and restoring function. (read more)
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