Biochim Biophys Acta. 2009 Aug 10
Lu C, Schoenfeld R, Shan Y, Tsai C, Hammock B, Cortopassi G.
Department of Molecular Biosciences, University of California, Davis, California, 95616.
Saturday, August 15, 2009
The Interaction of Mitochondrial Iron with Manganese Superoxide Dismutase*
J. Biol. Chem., Vol. 284, Issue 34, 22633-22640, August 21, 2009
Amornrat Naranuntarat
1 , Laran T. Jensen , Samuel Pazicni
, James E. Penner-Hahn , and Valeria C. Culotta2
12 From the From the
Keywords: Superoxide dismutase 2 (SOD2), mitochondrial enzymes, manganese, iron, iron-sulfur cluster biogenesis, Isu proteins.
Related Topic:
"Manganese Is the Link between Frataxin and Iron-Sulfur Deficiency in the Yeast Model of Friedreich Ataxia",
Verónica Irazusta, Elisa Cabiscol, Gemma Reverter-Branchat, ,Joaquim Ros2 , and Jordi Tamarit
"Manganese Is the Link between Frataxin and Iron-Sulfur Deficiency in the Yeast Model of Friedreich Ataxia",
Verónica Irazusta, Elisa Cabiscol, Gemma Reverter-Branchat, ,
From the Grup de Bioquímica de l'Estrés Oxidatiu, Departament de Ciències Mèdiques Bàsiques, Facultat de Medicina, Universitat de Lleida, 25008 Lleida, Spai.
J. Biol. Chem., Vol. 281, Issue 18, 12227-12232, May 5, 2006Thursday, August 13, 2009
FDA Clarifies Access to Investigational Drugs
By Cole Petrochko, Staff Writer, MedPage Today
Published: August 13, 2009
WASHINGTON -- The FDA has issued two final rules expanding access to investigational drugs for seriously ill patients who have no alternatives and regulating drug developers' charges for those medicines.
Published: August 13, 2009
WASHINGTON -- The FDA has issued two final rules expanding access to investigational drugs for seriously ill patients who have no alternatives and regulating drug developers' charges for those medicines.
Wednesday, August 12, 2009
Mitochondrial Dysfunction Leads to Nuclear Genome Instability via an Iron-Sulfur Cluster Defect
Comment: Although in the FA we have not problems with the mtDNA, the genetic information of frataxin is in nDNA, this is a very interesting article.
Cell, Volume 137, Issue 7, 26 June 2009, Pages 1247-1258
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WSN-4WM10D8-J&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=978708264&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=c8d80ad217bf0eefe71a1bba6364c95a
Joshua R. Veatch1, 2, Michael A. McMurray1, 2, 3, Zara W. Nelson1 and Daniel E. Gottschling1, ,
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, WA 98109, USA
2The Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98109, USA
3Present address: Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 94720, USA
Keywords: mitochondrial genome (mtDNA), inestability of the nuclear genome, defect in iron-sulfur cluster (ISC) biogenesis, ISC protein biogenesis.
Cell, Volume 137, Issue 7, 26 June 2009, Pages 1247-1258
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WSN-4WM10D8-J&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=978708264&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=c8d80ad217bf0eefe71a1bba6364c95a
Joshua R. Veatch1, 2, Michael A. McMurray1, 2, 3, Zara W. Nelson1 and Daniel E. Gottschling1, ,
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, WA 98109, USA
2The Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98109, USA
3Present address: Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 94720, USA
Keywords: mitochondrial genome (mtDNA), inestability of the nuclear genome, defect in iron-sulfur cluster (ISC) biogenesis, ISC protein biogenesis.
Saturday, August 8, 2009
Cardiac involvement in Friedreich's ataxia: our experience.
Minerva Cardioangiol. 2009 Apr;57(2):269-70.
Not abstrac
Fazio G., Vitello D., D’Angelo L., Visconti C., Trapani R., Fabiano A., Di Gesaro G., Novo G., Novo S.
Not abstrac
Friday, August 7, 2009
Nitrative and Oxidative Stress in Toxicology and Disease
OPEN ACCESS
ToxSci Advance Access published online on August 5, 2009 Toxicological Sciences, doi:10.1093/toxsci/kfp179
Ruth A. Roberts1, Debra L. Laskin2, Charles V. Smith3, Fredika M. Robertson4, Erin M.G. Allen5, Jonathan A. Doorn5 and William Slikker6
1 AstraZeneca R&D Safety Assessment, Alderley Park, UK 2 Department of Pharmacology and Toxicology, Rutgers University, Piscataway, NJ 3 Center for Developmental Therapeutics, Seattle Children's Research Institute, Seattle, WA 4 Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, TX 5 College of Pharmacy, University of Iowa, Iowa City, IA 6 NCTR, USFDA, Jefferson, AR
ruth.roberts@astrazeneca.com
Received June 15, 2009; revision received July 22, 2009; accepted July 24, 2009
Abstract
Persistent inflammation and the generation of reactive oxygen and nitrogen species play pivotal roles in tissue injury during disease pathogenesis and as a reaction to toxicant exposures. The associated oxidative and nitrative stress promote diverse pathologic reactions including neurodegenerative disorders, atherosclerosis, chronic inflammation, cancer, and premature labor and stillbirth. These effects occur via sustained inflammation, cellular proliferation and cytotoxicity and via induction of a proangiogenic environment. For example, exposure to the ubiquitous air pollutant ozone leads to generation of reactive oxygen and nitrogen species in lung macrophages that play a key role in subsequent tissue damage. Similarly, studies indicate that genes involved in regulating oxidative stress are altered by anesthetic treatment resulting in brain injury, most notable during development. In addition to a role in tissue injury in the brain, inflammation and oxidative stress are implicated in Parkinson's disease, a neurodegenerative disease characterized by the loss of dopamine neurons. Recent data suggest a mechanistic link between oxidative stress and elevated levels of DOPAL, a neurotoxin endogenous to dopamine neurons. These findings have significant implications for development of therapeutics and identification of novel biomarkers for PD pathogenesis. Oxidative and nitrative stress is also thought to play a role in creating the pro-inflammatory microenvironment associated with the aggressive phenotype of inflammatory breast cancer. An understanding of fundamental concepts of oxidative and nitrative stress can underpin a rational plan of treatment for diseases and toxicities associated with excessive production of reactive oxygen and nitrogen species.
© The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.orgThe online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.
Full text: http://toxsci.oxfordjournals.org/cgi/reprint/kfp179v1
ToxSci Advance Access published online on August 5, 2009 Toxicological Sciences, doi:10.1093/toxsci/kfp179
Ruth A. Roberts1, Debra L. Laskin2, Charles V. Smith3, Fredika M. Robertson4, Erin M.G. Allen5, Jonathan A. Doorn5 and William Slikker6
1 AstraZeneca R&D Safety Assessment, Alderley Park, UK 2 Department of Pharmacology and Toxicology, Rutgers University, Piscataway, NJ 3 Center for Developmental Therapeutics, Seattle Children's Research Institute, Seattle, WA 4 Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, TX 5 College of Pharmacy, University of Iowa, Iowa City, IA 6 NCTR, USFDA, Jefferson, AR
ruth.roberts@astrazeneca.com
Received June 15, 2009; revision received July 22, 2009; accepted July 24, 2009
Abstract
Persistent inflammation and the generation of reactive oxygen and nitrogen species play pivotal roles in tissue injury during disease pathogenesis and as a reaction to toxicant exposures. The associated oxidative and nitrative stress promote diverse pathologic reactions including neurodegenerative disorders, atherosclerosis, chronic inflammation, cancer, and premature labor and stillbirth. These effects occur via sustained inflammation, cellular proliferation and cytotoxicity and via induction of a proangiogenic environment. For example, exposure to the ubiquitous air pollutant ozone leads to generation of reactive oxygen and nitrogen species in lung macrophages that play a key role in subsequent tissue damage. Similarly, studies indicate that genes involved in regulating oxidative stress are altered by anesthetic treatment resulting in brain injury, most notable during development. In addition to a role in tissue injury in the brain, inflammation and oxidative stress are implicated in Parkinson's disease, a neurodegenerative disease characterized by the loss of dopamine neurons. Recent data suggest a mechanistic link between oxidative stress and elevated levels of DOPAL, a neurotoxin endogenous to dopamine neurons. These findings have significant implications for development of therapeutics and identification of novel biomarkers for PD pathogenesis. Oxidative and nitrative stress is also thought to play a role in creating the pro-inflammatory microenvironment associated with the aggressive phenotype of inflammatory breast cancer. An understanding of fundamental concepts of oxidative and nitrative stress can underpin a rational plan of treatment for diseases and toxicities associated with excessive production of reactive oxygen and nitrogen species.
© The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.orgThe online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.
Full text: http://toxsci.oxfordjournals.org/cgi/reprint/kfp179v1
Vision based interface system for hands free control of an intelligent wheelchair
Open Access
Jin Sun Ju , Yunhee Shin and Eun Yi Kim
Journal of NeuroEngineering and Rehabilitation 2009, 6:33doi:10.1186/1743-0003-6-33
Published: 6 August 2009
Abstract (provisional)
Due to the shift of the age structure in today's populations, the necessities for developing the devices or technologies to support them have been increasing. Traditionally, the wheelchair, including powered and manual ones, is the most popular and important rehabilitation assistive device for the disabled and the elderly. However, it is still highly restricted especially for severely disabled. As a solution to this, the Intelligent Wheelchairs have received considerable attention as mobility aids. The purpose of this work is to develop the IW interface for providing more convenient and efficient interface to the people the disability in their limbs. This paper proposes an intelligent wheelchair control system for the people with various disabilities. To facilitate a wide variety of user abilities, the proposed system involves the use of face-inclination and mouth-shape information, where the direction of an IW is determined by the inclination of the user's face, while proceeding and stopping are determined by the shapes of the user's mouth. Our system is composed of electric powered wheelchair, data acquisition board, ultrasonic infra-red sensors, a PC camera, and vision system. Then the vision system to analyze user's gestures is performed by three stages: detector, recognizer, and converter. In the detector, the facial region of the intended user is first obtained using Adaboost, thereafter the mouth region is detected based on edge information. The extracted features are sent to the recognizer, which recognizes the face inclination and mouth shape using statistical analysis and K-means clustering, respectively. These recognition results are then delivered to the converter to control the wheelchair. The advantages of the proposed system include 1) accurate recognition of user's intention with minimal user motion and 2) robustness to a cluttered background and the time-varying illumination. To prove these advantages, the proposed system was tested with 34 users in indoor and outdoor environments and the results were compared with those of other systems, then the results showed that the proposed system has superior performance to other systems in terms of speed and accuracy. Therefore, it is proved that proposed system provided a friendly and convenient interface to the severely disabled peo
Full text: http://www.jneuroengrehab.com/content/pdf/1743-0003-6-33.pdf
Jin Sun Ju , Yunhee Shin and Eun Yi Kim
Journal of NeuroEngineering and Rehabilitation 2009, 6:33doi:10.1186/1743-0003-6-33
Published: 6 August 2009
Abstract (provisional)
Due to the shift of the age structure in today's populations, the necessities for developing the devices or technologies to support them have been increasing. Traditionally, the wheelchair, including powered and manual ones, is the most popular and important rehabilitation assistive device for the disabled and the elderly. However, it is still highly restricted especially for severely disabled. As a solution to this, the Intelligent Wheelchairs have received considerable attention as mobility aids. The purpose of this work is to develop the IW interface for providing more convenient and efficient interface to the people the disability in their limbs. This paper proposes an intelligent wheelchair control system for the people with various disabilities. To facilitate a wide variety of user abilities, the proposed system involves the use of face-inclination and mouth-shape information, where the direction of an IW is determined by the inclination of the user's face, while proceeding and stopping are determined by the shapes of the user's mouth. Our system is composed of electric powered wheelchair, data acquisition board, ultrasonic infra-red sensors, a PC camera, and vision system. Then the vision system to analyze user's gestures is performed by three stages: detector, recognizer, and converter. In the detector, the facial region of the intended user is first obtained using Adaboost, thereafter the mouth region is detected based on edge information. The extracted features are sent to the recognizer, which recognizes the face inclination and mouth shape using statistical analysis and K-means clustering, respectively. These recognition results are then delivered to the converter to control the wheelchair. The advantages of the proposed system include 1) accurate recognition of user's intention with minimal user motion and 2) robustness to a cluttered background and the time-varying illumination. To prove these advantages, the proposed system was tested with 34 users in indoor and outdoor environments and the results were compared with those of other systems, then the results showed that the proposed system has superior performance to other systems in terms of speed and accuracy. Therefore, it is proved that proposed system provided a friendly and convenient interface to the severely disabled peo
Full text: http://www.jneuroengrehab.com/content/pdf/1743-0003-6-33.pdf
Wednesday, August 5, 2009
Ataxias with autosomal, X-chromosomal or maternal inheritance.
Can J Neurol Sci. 2009 Jul;36(4):409-28.
Finsterer J.
Krankenanstalt Rudolfstiftung, Vienna, Austria, Europe.
Keywors: Heredoataxias, genetic disorders, cerebellar syndrome, inheritance, autosomal dominant, autosomal recessive, X-linked, and maternally inherited heredoataxias, Friedreich ataxia.
Finsterer J.
Krankenanstalt Rudolfstiftung, Vienna, Austria, Europe.
Keywors: Heredoataxias, genetic disorders, cerebellar syndrome, inheritance, autosomal dominant, autosomal recessive, X-linked, and maternally inherited heredoataxias, Friedreich ataxia.
New clues about vitamin D functions in the nervous system
by: E. Garcion, N. Wionbarbot, C. Monteromenei, F. Berger, D. Wion
Trends in Endocrinology and Metabolism, Vol. 13, No. 3. (01 April 2002), pp. 100-105.
Keywords: 1α,25 dihydroxyvitamin D 3 [1,25-(OH) 2 D 3 ], brain function, nuclear receptor, neurons, glial cells, neurotrophic factors, neurotransmitter synthesis, nitric oxide synthase, increase glutathione levels, brain detoxification pathways, neuroprotective, immunomodulatory effects, neurodegenerative diseases, neuroimmune diseases, glioma cell death, brain tumors.
Other link: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T3K-45BCJ53-7&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=36fe7df09fbacd4b33fe816072a1793d
Trends in Endocrinology and Metabolism, Vol. 13, No. 3. (01 April 2002), pp. 100-105.
Keywords: 1α,25 dihydroxyvitamin D 3 [1,25-(OH) 2 D 3 ], brain function, nuclear receptor, neurons, glial cells, neurotrophic factors, neurotransmitter synthesis, nitric oxide synthase, increase glutathione levels, brain detoxification pathways, neuroprotective, immunomodulatory effects, neurodegenerative diseases, neuroimmune diseases, glioma cell death, brain tumors.
Other link: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T3K-45BCJ53-7&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=36fe7df09fbacd4b33fe816072a1793d
Abnormal Brain Circuits May Prevent Movement Disorder
ScienceDaily (Aug. 4, 2009)
.../...
Standaert says that although dystonia is a relatively rare disorder, the study has implications for other neurological illnesses, such as Parkinson's, Alzheimer's, and Huntington's diseases; ataxia and muscular dystrophies; and even forms of migraine.
.../...
Source: The Journal of Neuroscience, August 5, 2009, 29(31):9740-9747; doi:10.1523/JNEUROSCI.2300-09.2009
Cerebellothalamocortical Connectivity Regulates Penetrance in Dystonia
.../...
Standaert says that although dystonia is a relatively rare disorder, the study has implications for other neurological illnesses, such as Parkinson's, Alzheimer's, and Huntington's diseases; ataxia and muscular dystrophies; and even forms of migraine.
.../...
Source: The Journal of Neuroscience, August 5, 2009, 29(31):9740-9747; doi:10.1523/JNEUROSCI.2300-09.2009
Cerebellothalamocortical Connectivity Regulates Penetrance in Dystonia
1Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York 11030, Departments of 2Neurology and 3Medicine, North Shore University Hospital and New York University School of Medicine, Manhasset, New York 11030, 4Department of Radiology, Weill Cornell Medical College, New York, New York 10065, and 5Mirken Department of Neurology, Beth Israel Medical Center, New York, New York 10003
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