Saturday, July 4, 2009
[Peridural anaesthesia with ropivacaine for a patient with Friedrich's ataxia : Caesarean section after dorsal stabilisation of the spinal column (Th5
Hanusch P, Heyn J, Well H, Weninger E, Hasbargen U, Rehm M.
Klinik für Anästhesiologie und Intensivmedizin, Klinikum der Universität München, Marchioninistr. 15, 81377, München, Deutsc
Keywords: Friedreich's ataxia, increased sensitivity to muscle relaxants, special care during anaesthesia, peridural anaesthesia, ropivacaine, sufentanil, muscle weakness, scoliosis, cardiomyopathy, impaired glucose tolerance.
Novel swing-assist un-motorized exoskeletons for gait training

Kalyan Mankala , Sai Banala
and Sunil Agrawal
Journal of NeuroEngineering and Rehabilitation 2009, 6:24doi:10.1186/1743-0003-6-24
| Published: | 3 July 2009 |
Abstract (provisional)
Robotics is emerging as a promising tool for functional training of human movement. Much of the research in this area over the last decade has focused on upper extremity orthotic devices. Some recent commercial designs proposed for the lower extremity are powered and expensive - hence, these are unaffordable by most clinics. In this paper, we present a novel un-motorized bilateral exoskeleton that can be used to assist in treadmill training of motor-impaired patients, such as with motor-incomplete spinal cord injury. The exoskeleton is designed such that the human leg will have a desirable swing motion, once it is strapped to the exoskeleton. Since this exoskeleton is un-motorized, it can be produced cheaply and also will have the potential to reduce the physical demand on therapists during treadmill training. The salient features of this swing-assist exoskeleton are: (i) The design uses torsional springs at the hip and the knee joints to assist the swing motion. The springs get charged by the treadmill during stance phase of the leg and provide propulsion forces to the leg during swing. (ii) The design of the exoskeleton uses simple dynamic models of sagittal plane walking, which are used to optimize the parameters of the springs so that the foot can clear the ground and have a desirable forward motion during walking. (iii) This design approach was used to construct a bilateral exoskeleton and was tested during treadmill walking for a range of walking speeds between 1.0 mph and 4.0 mph. Joint encoders and interface force-torque sensors mounted on the exoskeleton were used to evaluate the effectiveness of the exoskeleton in terms of the hip and knee joint torques applied by the human during treadmill walking.
Full text: provisional PDF
Thursday, July 2, 2009
Ataxia with vitamin E deficiency in southeast Norway, case report.
Faculty of Medicine, University of Oslo, Oslo, Norway.
Keywords: AVED, Friedreich's ataxia, Frataxin gene, unknown prevalence, Norway, preschool age, neurological examination, re-evaluation, re-examination, neuropathy. Vitamin E, heterozygous mutation, p.A120T, p.R134X, alpha-tocopherol transport protein gene, chromosome 8q13, treatment available,
Tuesday, June 30, 2009
Nitric oxide and frataxin: two players contributing to maintain cellular iron homeostasis.
Ramirez L, Zabaleta EJ, Lamattina L.
Instituto de Investigaciones Biológicas, Facultad de Ciencias Exactas y Naturales, CONICET-Universidad Nacional de Mar del Plata, CC 1245, (7600) Mar del Plata, Argentina.
Keywords: PLANTS, animals, bacteria, Nitric oxide, iron metabolism, Frataxin, mitochondrial iron homeostasis, frataxin knock-down Arabidopsis thaliana mutants.
NITRIC OXIDE IN CELL SURVIVAL: A JANUS MOLECULE.
Calabrese V, Cornelius C, Rizzarelli E, Owen JB, Dinkova-Kostova AT, Butterfield DA.
University of Catania, Department of Chemistry, Catania, Italy; calabres@unict.it.
Keywors: Nitric oxide, nervous system, synaptic activity, neural plasticity, memory function, cysteine residues , neuroinflammation, neurodegeneration, Alzheimer's disease, amyothrophic lateral sclerosis, Parkinson's disease, multiple sclerosis, Friedreich's ataxia, Huntington, glutathione, nitrosative stress, redox signaling.
Sunday, June 28, 2009
FEDER presenta la Primera Guía Psicológica de Afectados por ER
La organización y gracias al apoyo de Merck Serono ha desarrollado esta publicación que tiene por objetivo ofrecer herramientas de intervención con familias y afectados
Saturday, June 27, 2009
Comparison of three clinical rating scales in Friedreich ataxia (FRDA)
Katrin Bürk, MD 1 2 *, Ulrike Mälzig, MD 1, Stefanie Wolf, PhD 1, Suzette Heck, MD 3, Konstantinos Dimitriadis, MD 3, Tanja Schmitz-Hübsch, MD 4, Sascha Hering, MD 5, Tobias M. Lindig, MD 6, Verena Haug, MD 7, Dagmar Timmann, MD 8, Ingrid Degen, MD 9, Bernd Kruse, MD 10, Jan-Markus Dörr, MD 11, Susanne Ratzka, MD 1, Anja Ivo, MD 4, Ludger Schöls, MD 6, Sylvia Boesch, MD 5, Thomas Klockgether, MD 4, Thomas Klopstock, MD 3, Jörg B. Schulz, MD 1 |
| 1Department of Neurodegeneration and Restorative Research, Centers of Molecular Physiology of the Brain and Neurological Medicine, University of Göttingen, Göttingen, Germany 2Department of Neurology, University of Marburg, Marburg, Germany 3Department of Neurology, University of Munich, Munich, Germany 4Department of Neurology, University of Bonn, Bonn, Germany 5Department of Neurology, University of Innsbruck, Innsbruck, Austria 6Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany 7Department of Neuropediatrics, University of Freiburg, Freiburg, Germany 8Department of Neurology, University of Essen, Essen, Germany 9Department of Neuropediatrics, Sankt Elisabeth Krankenhaus, Neuwied, Germany 10Department of Neuropediatrics, University of Hamburg, Hamburg, Germany 11Department of Neurology, Helios-Klinikum, Berlin, Germany |
| email: Katrin Bürk (buerk@ngi.de) |
*Correspondence to Katrin Bürk, Department of Neurodegeneration and Restorative Research, Center of Molecular Physiology of the Brain and Center of Neurological Medicine, University of Göttingen, Waldweg 33, Göttingen D-37073, Germany
Keywords: Friedreich ataxia • clinical rating scales • validation • SARA • ICARS • FARS
Development of a brief ataxia rating scale (BARS) based on a modified form of the ICARS
Jeremy D. Schmahmann, MD *, Raquel Gardner, MD, Jason MacMore, BA, Mark G. Vangel, PhD |
| Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA |
| email: Jeremy D. Schmahmann (jschmahmann@partners.org) |
*Correspondence to Jeremy D. Schmahmann, Department of Neurology, Massachusetts General Hospital, Suite 340, Charles River Plaza South, 55 Fruit Street, Boston, Massachusetts 02114
| Keywords |
Friday, June 26, 2009
PGC-1[alpha] AND PGC-1[beta] regulate mitochondrial density in neurons.
Przemyslaw W, Vaarmann A, Choubey V, Safiulina D, Liiv J, Kuum M, Kaasik A.
Department of Pharmacology, University of Tartu, Estonia.
Link to full text: http://www.jbc.org/cgi/reprint/M109.018911v1?view=long&pmid=19542216
Keywords: PGC-1[alpha], PGC-1[beta, peroxisome-proliferator-activated receptor gamma coactivator-1a, mitochondrial biogenesis , cellular energy metabolism , muscle, liver, neurons, activates transcriptional activity of PGC-1[alpha] in neurons, compensate neuronal mitochondrial loss , treating neurodegenerative diseases , mitochondrial dysfunction , oxidative damage.
Antidepressant directly stimulates brain growth factor receptors
The widely used antidepressant and pain medication amitriptyline--but not other closely related drugs -- can impersonate the brain's own growth factors, researchers at Emory University School of Medicine have shown.
Other sources:
http://www.sciencedaily.com/releases/2009/06/090625133059.htm
http://www.eurekalert.org/pub_releases/2009-06/eu-ads062209.php
