Induced neural stem cells: a new tool for studying neural development and neurological disorders. Cell Research advance online publication 1 May 2012; doi: 10.1038/cr.2012.73, Guang-Hui Liu, Fei Yi, Keiichiro Suzuki, Jing Qu, Juan Carlos Izpisua Belmonte.
National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing China. Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA. Center for Regenerative Medicine in Barcelona, 08003 Barcelona, Spain.
Recent advances in the generation of multipotent and expandable induced
neural stem cells are exciting. They not only hold great promises for
potential clinical applications but may also open up a new era for
neural stem cell research in the near future.
Tuesday, May 8, 2012
alpha-Tocotrienol quinone modulates oxidative stress response and the biochemistry of aging. Bioorganic & Medicinal Chemistry Letters 21 (2011) 3693–3698, William D. Shrader, Akiko Amagata, Adam Barnes, Gregory M. Enns, Andrew Hinman, Orion Jankowski , Viktoria Kheifets, Ryo Komatsuzaki, Edgar Lee, Paul Mollard, Katsuyuki Murase, Alfredo A. Sadun, Martin Thoolen, Kieron Wesson, Guy Miller.
Keywords: Redox, Antioxidants, Quinone, Aging, Digital Biology, frataxin, Friedreich's Ataxia.
Keywords: Redox, Antioxidants, Quinone, Aging, Digital Biology, frataxin, Friedreich's Ataxia.
Sunday, May 6, 2012
The role of hydration in protein stability: comparison of the cold and heat unfolded states of Yfh1.
The role of hydration in protein stability: comparison of the cold and heat unfolded states of Yfh1. JMol Biol. 2012Apr 13;417(5):413-24. Epub 2012 Feb 14. Adrover M, Martorell G, Martin SR, Urosev D, Konarev PV, Svergun DI, Daura X, Temussi P, Pastore A.
Keywors: Protein unfolding, high- and low-temperature unfolded states, Yfh1, residual secondary structures, protein stability.
Keywors: Protein unfolding, high- and low-temperature unfolded states, Yfh1, residual secondary structures, protein stability.
Friday, May 4, 2012
The State of Gene Therapies: The FDA Perspective
The State of Gene Therapies: The FDA Perspective, Molecular Therapy (2012); 20 5, 877–878. doi:10.1038/mt.2012.51, Daniel Takefman and Wilson Bryan
Full Text.
Keywords: Clinical development of gene therapy, 320 ongoing gene therapy clinical trials, Office of Cellular Tissue and Gene Therapies (OCTGT), Center for Biologics Evaluation and Research of the US Food and Drug Administration (FDA), treatments for specific, well-defined genetic disorders ... Full Text.
Keywords: Clinical development of gene therapy, 320 ongoing gene therapy clinical trials, Office of Cellular Tissue and Gene Therapies (OCTGT), Center for Biologics Evaluation and Research of the US Food and Drug Administration (FDA), treatments for specific, well-defined genetic disorders ... Full Text.
Wednesday, May 2, 2012
Human adipose stem cell-conditioned medium increases survival of Friedreich’s ataxia cells submitted to oxidative stress
Human adipose stem cell-conditioned medium increases survival of Friedreich’s ataxia cells submitted to oxidative stress . Dr. Jonathan Jones, Mrs. Alicia Estirado, Dr. Carolina Redondo, Dr. Carlos Bueno, and Salvador Martinez. Stem Cells and Development. doi:10.1089/scd.2012.0029.
Keywords: Friedreich’s ataxia, progressive gait, ataxia, cardiomyopathy, in vitro, adult stem cells, periodontal ligament cells, oxidative stress, adipose stem cell-conditioned medium, trophic factors, BDNF (brain-derived neurotrophic factor.
Keywords: Friedreich’s ataxia, progressive gait, ataxia, cardiomyopathy, in vitro, adult stem cells, periodontal ligament cells, oxidative stress, adipose stem cell-conditioned medium, trophic factors, BDNF (brain-derived neurotrophic factor.
Tuesday, May 1, 2012
Decreased functional brain activation in Friedreich ataxia using the Simon effect task.
Decreased functional brain activation in Friedreich ataxia using the Simon effect task.Brain Cogn. 2012 Apr 27;79(3):200-208. [Epub ahead of print], Georgiou-Karistianis N, Akhlaghi H, Corben LA, Delatycki MB, Storey E, Bradshaw JL, Egan GF.
Keyword: Simon effect task, functional brain reorganization, Friedreich ataxia (FRDA), magnetic resonance imaging (fMRI).
Keyword: Simon effect task, functional brain reorganization, Friedreich ataxia (FRDA), magnetic resonance imaging (fMRI).
Accelerating progress in iPS cell research for neurological diseases
Accelerating progress in iPS cell research for neurological diseases. Daisuke Ito, Hideyuki Okano and Norihiro Suzuki, Annals of Neurology, Accepted manuscript online: 29 MAR 2012 06:18AM EST | DOI: 10.1002/ana.23596
Keywords: induced pluripotent stem cells (iPSCs), pluripotency, embryonic stem cells (ESCs, personalized replacement therapy, elucidate the pathological processes, neurodegenerative diseases, drug discovery, regenerative medicine.
Thursday, April 26, 2012
Scoliosis in patients with Friedreich's ataxia.
Scoliosis in patients with Friedreich's ataxia., J Bone Joint Surg Br. 2012 May;94(5):684-9. Tsirikos AI, Smith G. Scottish National Spine Deformity Centre, Royal Hospital for Sick Children, Sciennes Road, Edinburgh EH9 1LF, UK. doi: 10.1302/0301-620X.94B5.28391
Keywords: Friedreich's ataxia, scoliosis, thoracic curvatures, thoracolumbar, double thoracic/lumbar, pelvic obliquity, hyperkyphosis.
Tuesday, April 24, 2012
DESIGN OF HYPOXIA STRATEGY AS A TREATMENT OF FRIEDREICH’S ATAXIA
DESIGN OF HYPOXIA STRATEGY AS A TREATMENT OF FRIEDREICH’S ATAXIA, Unpublished paper, José Luis García Giménez, Abstract "Premi Científico-Tècnic Ciutat d’Algemessí.", 2012
Friedreich’s ataxia is an inherited disease that causes progressive damage to the nervous system resulting in symptoms ranging from muscle weakness, speech problems to heart disease. There is currently no effective treatment for Friedreich’s ataxia. However, many of the symptoms accompanying complications can be treated to help patients maintain optimal functioning as long as possible. There are possible treatments for the different symptoms. For example, diuretic and antiarrhythmic drugs to treat the cardiomyophaty can be used.
Drugs such as recombinant human erythropoietin (rHuEPO) have shown the capability to increase frataxin levels in primary fibroblasts cell cultures derived from Friedreich’s ataxia patients (Acquaviva F. et al. 2008). Clinical pilot trials using rHuEPO in FRDA patients indicate that frataxin levels increase, while indicators of oxidative stress decreased significantly (Boeschs S., et al. 2008). But the use of rHuEPO could have various contraindications depending on the nature of each individual. Specially, rHuEPO is a prohibitively expensive treatment, restrictive for FRDA patients and very expensive for public administrations.
We propose a novel method set in the hypoxia as a "non-invasive" and “easy to use” treatment for Friedreich's ataxia. This protocol should cover different fronts of the disease. It may stimulate the expression of endogenous erythropoietin and consequently the expression of frataxin, the molecular cause of the FRDA.
Therefore, hypoxia is presented as a therapeutic tool that can improve the physiopathological features of the disease because it can stimulate the expression of endogenous EPO, a glycoprotein hormone that it has shown beneficial effects in Friedreich’s ataxia.
Friedreich’s ataxia is an inherited disease that causes progressive damage to the nervous system resulting in symptoms ranging from muscle weakness, speech problems to heart disease. There is currently no effective treatment for Friedreich’s ataxia. However, many of the symptoms accompanying complications can be treated to help patients maintain optimal functioning as long as possible. There are possible treatments for the different symptoms. For example, diuretic and antiarrhythmic drugs to treat the cardiomyophaty can be used.
Drugs such as recombinant human erythropoietin (rHuEPO) have shown the capability to increase frataxin levels in primary fibroblasts cell cultures derived from Friedreich’s ataxia patients (Acquaviva F. et al. 2008). Clinical pilot trials using rHuEPO in FRDA patients indicate that frataxin levels increase, while indicators of oxidative stress decreased significantly (Boeschs S., et al. 2008). But the use of rHuEPO could have various contraindications depending on the nature of each individual. Specially, rHuEPO is a prohibitively expensive treatment, restrictive for FRDA patients and very expensive for public administrations.
We propose a novel method set in the hypoxia as a "non-invasive" and “easy to use” treatment for Friedreich's ataxia. This protocol should cover different fronts of the disease. It may stimulate the expression of endogenous erythropoietin and consequently the expression of frataxin, the molecular cause of the FRDA.
Therefore, hypoxia is presented as a therapeutic tool that can improve the physiopathological features of the disease because it can stimulate the expression of endogenous EPO, a glycoprotein hormone that it has shown beneficial effects in Friedreich’s ataxia.
Monday, April 23, 2012
Coming into view: Eukaryotic iron chaperones and intracellular iron delivery.
Coming into view: Eukaryotic iron chaperones and intracellular iron delivery. Caroline C. Philpott. April 20, 2012 The Journal of Biological Chemistry, 287, 13518-13523. doi: 10.1074/jbc.R111.326876
Keywords: Iron Metabolism, Iron-Sulfur Protein, Metalloenzymes, Metalloproteins, Protein-Metal Ion Interaction, Frataxin, Glutaredoxin, Iron Chaperone, Poly(rC)-binding Protein.
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Keywords: Iron Metabolism, Iron-Sulfur Protein, Metalloenzymes, Metalloproteins, Protein-Metal Ion Interaction, Frataxin, Glutaredoxin, Iron Chaperone, Poly(rC)-binding Protein.
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