Brain (2011) first published online October 27, 2011 doi:10.1093/brain/awr266
Anna M. Tedesco, Francesca R. Chiricozzi, Silvia Clausi, Michela Lupo, Marco Molinari, and Maria G. Leggio
Keywords: cerebellar role in non-motor functions, cerebellar cognitive affective syndrome, cerebellar damage, ataxia, cerebellum, cognition.
Friday, October 28, 2011
Pioglitazone and bladder cancer
In France, is currently running Friedreich's Ataxia clinical trial with Pioglitazone
The Lancet, Volume 378, Issue 9802, Pages 1543 - 1544, 29 October 2011
Dominique Hillaire-Buys a bEmail Address, Jean-Luc Faillie b c, Jean-Louis Montastruc d e
a CHRU Montpellier, Department of Medical Pharmacology and Toxicology, Lapeyronie Hospital, 34295 Montpellier, France
b Faculty of Medicine, University of Montpellier 1, Montpellier, France
c CHU Nîmes, Department of Epidemiology and Clinical Research, Nîmes University Hospital, Nîmes, France
d CHRU Toulouse, Department of Clinical Pharmacology, Toulouse University Hospital, Toulouse, France
e Department of Pharmacoepidemiology INSERM U1027, Faculty of Medicine, University of Toulouse, Toulouse, France
Keywords: Pioglitazone, peroxisome-proliferator-activated receptor (PPAR)agonist, oral hypoglycaemic drug, bladder cancer, US Food and Drug Administration (FDA), FDA Adverse Event Reporting System, European Medicines Agency.
Pioglitazone and bladder cancer
The Lancet, Volume 378, Issue 9802, Page 1544, 29 October 2011, doi:10.1016/S0140-6736(11)61663-2
Robert Elford Ryder
Department of Diabetes and Endocrinology, City Hospital, Birmingham B18 7QH, UK
Keywords: French and German regulatory bodies, risk of bladder cancer, European Medicines Agency (EMA), increased fractures, heart failure, type 2 diabetes, cardiovascular benefit.
"Despite the EMA's conclusion over bladder cancer risk, the overall risk—benefit balance remains strongly in favour of continued use of pioglitazone, especially in patients with ischaemic heart disease (but without heart failure) or stroke"
Pioglitazone and bladder cancer — Authors' reply
Erland Erdmann a, John A Dormandy b, Massimo Massi-Benedetti c, Robert Spanheimer
Monday, October 24, 2011
Saturday, October 22, 2011
Hidden Administration of Drugs
Clinical Pharmacology & Therapeutics 90, 651-661 (November 2011) | doi:10.1038/clpt.2011.206
F Benedetti, E Carlino and A Pollo
Keywords: placebo-controlled trials, dummy treatment (placebo), psychological component, psychology and pharmacodynamics.
F Benedetti, E Carlino and A Pollo
Keywords: placebo-controlled trials, dummy treatment (placebo), psychological component, psychology and pharmacodynamics.
An unusual atrial tachycardia in a patient with Friedreich ataxia
Europace (2011) 13 (11): 1660-1661. doi: 10.1093/europace/eur156
Justin M.S. Lee1,*, Ian Turner1, Ajit Agarwal2 and Simon P. Fynn1
1Department of Cardiology, Papworth Hospital, Cambridge CB23 3RE, UK
2Department of Cardiology, West Suffolk Hospital, Bury St Edmunds, IP33 2QZ, UK
Keywords: atrial tachycardia, Friedreich ataxia, arrhythmi, linear ablation.
Justin M.S. Lee1,*, Ian Turner1, Ajit Agarwal2 and Simon P. Fynn1
1Department of Cardiology, Papworth Hospital, Cambridge CB23 3RE, UK
2Department of Cardiology, West Suffolk Hospital, Bury St Edmunds, IP33 2QZ, UK
Keywords: atrial tachycardia, Friedreich ataxia, arrhythmi, linear ablation.
Anaesthesia for a patient with Friedreich's ataxia.
Indian J Anaesth. 2011 Jul;55(4):418-20.
Ganesan I.
Department of Anaesthesiology, SRM Medical College Hospital and Research Centre, Chennai, Tamil Nadu, India.
NO ABSTRAC
Ganesan I.
Department of Anaesthesiology, SRM Medical College Hospital and Research Centre, Chennai, Tamil Nadu, India.
NO ABSTRAC
Thursday, October 20, 2011
Inactivation of mitochondrial aspartate aminotransferase contributes to the respiratory deficit of yeast frataxin-deficient cells
Biochem. J. (2011) Immediate Publication, doi:10.1042/BJ20111574
Dominika Sliwa, Julien Dairou, Jean-Michel Camadro and Renata Santos
Institut Jacques Monod, Paris, France
Keywords: Friedreich ataxia, frataxin, iron homeostasis, hypersensitivity to oxidants, NAD+ and NADH, malate-aspartate NADH shuttle, mitochondrial aspartate aminotransferase (Aat1), mitochondrial acetylated proteins, post-translational modification.
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Dominika Sliwa, Julien Dairou, Jean-Michel Camadro and Renata Santos
Institut Jacques Monod, Paris, France
Keywords: Friedreich ataxia, frataxin, iron homeostasis, hypersensitivity to oxidants, NAD+ and NADH, malate-aspartate NADH shuttle, mitochondrial aspartate aminotransferase (Aat1), mitochondrial acetylated proteins, post-translational modification.
FULL TEXT PDF
Monday, October 17, 2011
Physiological oxygen level is critical for modeling neuronal metabolism in vitro
Zhu, J., Aja, S., Kim, E.-K., Park, M. J., Ramamurthy, S., Jia, J., Hu, X., Geng, P. and Ronnett, G. V. (2011), Journal of Neuroscience Research. doi: 10.1002/jnr.22765
KEYWORDS: In vitro models, nonphysiological conditions, ambient (21%) oxygen levels, physiological oxygen level (5% O2), glucose uptake, glycolysis, glucose oxidation , fatty acid oxidation, AMPK activity, intracellular ATP level,
"Oxygen level is an important parameter to consider when modeling neuronal responses to stress in vitro".
KEYWORDS: In vitro models, nonphysiological conditions, ambient (21%) oxygen levels, physiological oxygen level (5% O2), glucose uptake, glycolysis, glucose oxidation , fatty acid oxidation, AMPK activity, intracellular ATP level,
"Oxygen level is an important parameter to consider when modeling neuronal responses to stress in vitro".
Friday, October 14, 2011
Un score pour évaluer la stabilité au cours de la marche : méthodologie et validation chez le patient atteint d’ataxie de Friedreich
A. Gouelle a, ⁎, F. Mégrot b, A. Yelnik c, G.-F. Penneçot d
a Plate-forme d’analyse du mouvement, hôpital Robert-Debré, AP–HP, 48, boulevard Sérurier, 75019 Paris, France
b Unité clinique d’analyse de la marche et du mouvement, CMPRE Bois-Larris, Lamorlaye, France
c Service de médecine physique et de réadaptation, hôpital Fernand-Widal, Paris, France
d Service de chirurgie orthopédique, hôpital Robert-Debré, Paris, France
KEYWORDS : Score, Marche, Stabilité dynamique, Paramètres spatiotemporels
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a Plate-forme d’analyse du mouvement, hôpital Robert-Debré, AP–HP, 48, boulevard Sérurier, 75019 Paris, France
b Unité clinique d’analyse de la marche et du mouvement, CMPRE Bois-Larris, Lamorlaye, France
c Service de médecine physique et de réadaptation, hôpital Fernand-Widal, Paris, France
d Service de chirurgie orthopédique, hôpital Robert-Debré, Paris, France
KEYWORDS : Score, Marche, Stabilité dynamique, Paramètres spatiotemporels
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Tuesday, October 11, 2011
Friedreich ataxia: The vicious circle hypothesis revisited
BMC Medicine 2011, 9:112doi:10.1186/1741-7015-9-112, Published: 11 October 2011
Aurelien Bayot, Renata Santos, Jean-Michel Camadro and Pierre Rustin
OPEN ACCES
Abstract (provisional)
Friedreich ataxia, the most frequent progressive autosomal recessive disorder involving the central and peripheral nervous system, is mostly associated with an unstable expansion of GAA trinucleotide repeats in the first intron of the FXN gene which encodes the mitochondrial frataxin protein. Since FXN was shown to be involved in Friedreich ataxia in the late 1990s, the consequence of frataxin loss of function has been generating vigorous debate. Very early on, we suggested a unifying hypothesis according to which frataxin deficiency leads to a vicious circle of faulty iron handling, impaired iron-sulfur cluster synthesis, and increased oxygen radical production. However, data from cell and animal models now indicate that iron accumulation is an inconsistent and late event and that frataxin deficiency does not always impair the activity of iron-sulfur cluster-containing proteins. In contrast, frataxin deficiency appears consistently associated with increased sensitivity to reactive oxygen species, as opposed to increased oxygen radical production. Compiling findings from fundamental researches to clinical observations, we defend here the opinion that the very first consequence of frataxin depletion is indeed an abnormal oxidative status which initiates the pathogenic mechanism underlying Friedreich ataxia.
FULL TEXT PDF
Aurelien Bayot, Renata Santos, Jean-Michel Camadro and Pierre Rustin
OPEN ACCES
Abstract (provisional)
Friedreich ataxia, the most frequent progressive autosomal recessive disorder involving the central and peripheral nervous system, is mostly associated with an unstable expansion of GAA trinucleotide repeats in the first intron of the FXN gene which encodes the mitochondrial frataxin protein. Since FXN was shown to be involved in Friedreich ataxia in the late 1990s, the consequence of frataxin loss of function has been generating vigorous debate. Very early on, we suggested a unifying hypothesis according to which frataxin deficiency leads to a vicious circle of faulty iron handling, impaired iron-sulfur cluster synthesis, and increased oxygen radical production. However, data from cell and animal models now indicate that iron accumulation is an inconsistent and late event and that frataxin deficiency does not always impair the activity of iron-sulfur cluster-containing proteins. In contrast, frataxin deficiency appears consistently associated with increased sensitivity to reactive oxygen species, as opposed to increased oxygen radical production. Compiling findings from fundamental researches to clinical observations, we defend here the opinion that the very first consequence of frataxin depletion is indeed an abnormal oxidative status which initiates the pathogenic mechanism underlying Friedreich ataxia.
FULL TEXT PDF
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