Money to fund researching neurological diseases
The Crimson White, Published: Thursday, July 16, 2009
.../...
While they are researching different topics, both professors are focusing on certain proteins found in the body and their roles in neurological diseases. Busenlehner’s research focuses on a neurodegenerative disease called Friedreich’s ataxia, which is caused by decreased levels of the protein frataxin.
“What we are wanting to know is what is the exact function of this protein, frataxin, in the human body,” Busenlehner said.
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Thursday, July 16, 2009
Wednesday, July 15, 2009
Huntington's: Researchers Gain Insight Into Mechanism Underlying The Disease
Medical News Today , Article Date: 15 Jul 2009 - 0:00 PDT
Researchers at the University of Kentucky Markey Cancer Center and Graduate Center for Toxicology (GCT) have gained new insight into the genetic mechanisms underlying Huntington's disease and other neurodegenerative or neuromuscular disorders caused by trinucleotide repeats (or TNRs) in DNA.
This newspaper article is based on this research: http://friedreichscientificnews.blogspot.com/2009/07/incision-dependent-and-error-free.html
Researchers at the University of Kentucky Markey Cancer Center and Graduate Center for Toxicology (GCT) have gained new insight into the genetic mechanisms underlying Huntington's disease and other neurodegenerative or neuromuscular disorders caused by trinucleotide repeats (or TNRs) in DNA.
This newspaper article is based on this research: http://friedreichscientificnews.blogspot.com/2009/07/incision-dependent-and-error-free.html
Incision-dependent and error-free repair of (CAG)(n)/(CTG)(n) hairpins in human cell extracts
Nat Struct Mol Biol. 2009 Jul 13
Hou C, Chan NL, Gu L, Li GM.
Graduate Center for Toxicology and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, Kentucky, USA.
Keywords: Expansion of CAG/CTG trinucleotide repeats, neurological disorders, Huntington's disease, proliferating cell nuclear antigen (PCNA), endonuclease activities, trinucleotide repeat instability.
Hou C, Chan NL, Gu L, Li GM.
Graduate Center for Toxicology and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, Kentucky, USA.
Keywords: Expansion of CAG/CTG trinucleotide repeats, neurological disorders, Huntington's disease, proliferating cell nuclear antigen (PCNA), endonuclease activities, trinucleotide repeat instability.
[Diseases caused by triplet expansion.]
Rev Neurol. 2009 Jul 16-31;49(2):79-87
[Article in Spanish]
Rosales-Reynoso MA, Ochoa-Hernandez AB, Barros-Nunez P.
Centro de Investigacion Biomedica de Occidente IMSS (CIBO), Guadalajara, Mexico
Keywords: expansion of nucleotide triplets, meiosis, mitosis, CGG/ GCC, CAG/GTC, CTG/GAC, GAA/CTT, bulbospinal muscular atrophy, Huntington's diseas, spinocerebellar ataxias, fragile X syndrome, Friedreich's ataxia, myotonic dystrophy, cis-acting, trans-acting, pre-mutations, dynamic mutation processes.
[Article in Spanish]
Rosales-Reynoso MA, Ochoa-Hernandez AB, Barros-Nunez P.
Centro de Investigacion Biomedica de Occidente IMSS (CIBO), Guadalajara, Mexico
Keywords: expansion of nucleotide triplets, meiosis, mitosis, CGG/ GCC, CAG/GTC, CTG/GAC, GAA/CTT, bulbospinal muscular atrophy, Huntington's diseas, spinocerebellar ataxias, fragile X syndrome, Friedreich's ataxia, myotonic dystrophy, cis-acting, trans-acting, pre-mutations, dynamic mutation processes.
Erythropoietin overrides the triggering effect of DNA platination products in a mouse model of Cisplatin-induced neuropathy
OPEN ACCES
Min-Suk Yoon , Zaza Katsarava , Mark Obermann , Maria Schaefers , Bernd Liedert , Anna Dzagnidze , Andreas Kribben , Rupert Egensperger , Volker Limmroth , Hans Christoph-Diener and Juergen Thomale
BMC Neuroscience 2009, 10:77doi:10.1186/1471-2202-10-77
Published:
15 July 2009
Abstract (provisional)
Background
Cisplatin mediates its antineoplastic activity by formation of distinct DNA intrastrand cross links. The clinical efficacy and desirable dose escalations of cisplatin are restricted by the accumulation of DNA lesions in dorsal root ganglion (DRG) cells leading to sensory polyneuropathy (PNP). We investigated in a mouse model by which mechanism recombinant erythropoietin (rhEPO) protects the peripheral nervous system from structural and functional damage caused by cisplatin treatment with special emphasis on DNA damage burden.
Results
A cumulative dose of 16 mg cisplatin/kg resulted in clear electrophysiological signs of neuropathy, which were significantly attenuated by concomitant erythropoietin (cisplatin 32,48 m/s +/- 1,68 m/s; cisplatin + rhEPO 49,66 m/s +/- 1,26 m/s; control 55,01 m/s +/- 1,88 m/s; p < 0,001). The co-application of rhEPO, however, did not alter the level of unrepaired cisplatin-DNA lesions accumulating in DRG target cells. Micro-morphological analyses of the sciatic nerve from cisplatin-exposed mice showed damaged myelin sheaths and mitochondria. Co-administered rhEPO inhibited myelin sheaths from structural injuries and resulted in an increased number of intact mitochondria.
Conclusion
The protective effect of recombinant erythropoietin is not mediated by reducing the burden of DNA platination in the target cells, but it is likely to be due to a higher resistance of the target cells to the adverse effect of DNA damage. The increased frequency of intact mitochondria might also contribute to this protective role.
Full text: http://www.biomedcentral.com/content/pdf/1471-2202-10-77.pdf
Min-Suk Yoon , Zaza Katsarava , Mark Obermann , Maria Schaefers , Bernd Liedert , Anna Dzagnidze , Andreas Kribben , Rupert Egensperger , Volker Limmroth , Hans Christoph-Diener and Juergen Thomale
BMC Neuroscience 2009, 10:77doi:10.1186/1471-2202-10-77
Published:
15 July 2009
Abstract (provisional)
Background
Cisplatin mediates its antineoplastic activity by formation of distinct DNA intrastrand cross links. The clinical efficacy and desirable dose escalations of cisplatin are restricted by the accumulation of DNA lesions in dorsal root ganglion (DRG) cells leading to sensory polyneuropathy (PNP). We investigated in a mouse model by which mechanism recombinant erythropoietin (rhEPO) protects the peripheral nervous system from structural and functional damage caused by cisplatin treatment with special emphasis on DNA damage burden.
Results
A cumulative dose of 16 mg cisplatin/kg resulted in clear electrophysiological signs of neuropathy, which were significantly attenuated by concomitant erythropoietin (cisplatin 32,48 m/s +/- 1,68 m/s; cisplatin + rhEPO 49,66 m/s +/- 1,26 m/s; control 55,01 m/s +/- 1,88 m/s; p < 0,001). The co-application of rhEPO, however, did not alter the level of unrepaired cisplatin-DNA lesions accumulating in DRG target cells. Micro-morphological analyses of the sciatic nerve from cisplatin-exposed mice showed damaged myelin sheaths and mitochondria. Co-administered rhEPO inhibited myelin sheaths from structural injuries and resulted in an increased number of intact mitochondria.
Conclusion
The protective effect of recombinant erythropoietin is not mediated by reducing the burden of DNA platination in the target cells, but it is likely to be due to a higher resistance of the target cells to the adverse effect of DNA damage. The increased frequency of intact mitochondria might also contribute to this protective role.
Full text: http://www.biomedcentral.com/content/pdf/1471-2202-10-77.pdf
Sunday, July 12, 2009
Abnormal Left Atrial Contraction in Friedreich Ataxia—Relation with Both Alleles of the FXN Gene
Heart, Lung and Circulation
Volume 18, Supplement 3, 2009, Page S15
Abstracts for the Cardiac Society of Australia and New Zealand Annual Scientific Meeting and the International Society for Heart Research, Australasian Section, Annual Scientific Meeting
Volume 18, Supplement 3, 2009, Page S15
Abstracts for the Cardiac Society of Australia and New Zealand Annual Scientific Meeting and the International Society for Heart Research, Australasian Section, Annual Scientific Meeting
R.E. Peverill1, 
The role of PGC-1{alpha} on mitochondrial function and apoptotic susceptibility in muscle
1School of Kinesiology and Health Science, 2Department of Biology, and 3The Muscle Health Research Centre, York University, Toronto, Ontario, Canada; 4Copenhagen Muscle Research Centre and Centre of Inflammation and Metabolism, Department of Biology, University of Copenhagen, Denmark, and 5Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Autonomous University of Barcelona, Barcelona, Spain
Submitted 12 February 2009 ; accepted in final form 5 May 2009
Keywords: endurance training; exercise; mitochondrial biogenesis; reactive oxygen species, cytochrome-c oxidase activity, brain, liver, pancreas.
Friday, July 10, 2009
Mitochondrial Dysfunction Leads to Nuclear Genome Instability via an Iron-Sulfur Cluster Defect
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
Received 14 September 2008; revised 30 January 2009; accepted 1 April 2009. Published: June 25, 2009. Available online 25 June 2009
Keywords; nuclear genome, genome instability, mitochondrial membrane potential, iron-sulfur cluster. a
Friedreich's Ataxia - Frataxin
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
Received 14 September 2008; revised 30 January 2009; accepted 1 April 2009. Published: June 25, 2009. Available online 25 June 2009
Keywords; nuclear genome, genome instability, mitochondrial membrane potential, iron-sulfur cluster. a
Friedreich's Ataxia - Frataxin
Thursday, July 9, 2009
Large-Scale Expansions of Friedreich's Ataxia GAA Repeats in Yeast
MolecularCell, Volume 35, Issue 1, 10 July 2009, Pages 82-92
Alexander A. Shishkin1, Irina Voineagu1, Robert Matera1, Nicole Cherng1, Brook T. Chernet1, Maria M. Krasilnikova2, Vidhya Narayanan3, Kirill S. Lobachev3 and Sergei M. Mirkin1, ,
1Department of Biology, Tufts University, Medford, MA 02155, USA
2Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA
3School of Biology and Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332
Received 22 August 2008; revised 7 January 2009; accepted 18 June 2009. Published: July 9, 2009. Available online 9 July 2009.
Keywords: DNA repeats , GAA repeats, Friedreich's ataxia, chimeric URA3 gene, rates of expansions of GAA repeats.
Alexander A. Shishkin1, Irina Voineagu1, Robert Matera1, Nicole Cherng1, Brook T. Chernet1, Maria M. Krasilnikova2, Vidhya Narayanan3, Kirill S. Lobachev3 and Sergei M. Mirkin1, ,
1Department of Biology, Tufts University, Medford, MA 02155, USA
2Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA
3School of Biology and Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332
Received 22 August 2008; revised 7 January 2009; accepted 18 June 2009. Published: July 9, 2009. Available online 9 July 2009.
Keywords: DNA repeats , GAA repeats, Friedreich's ataxia, chimeric URA3 gene, rates of expansions of GAA repeats.
Of yeast and men: Unraveling the molecular mechanisms of Friedreich's ataxia
Public release date: 9-Jul-2009
EurekAlert¡
This news is in reference to this work: Large-Scale Expansions of Friedreich's Ataxia GAA Repeats in Yeast
EurekAlert¡
This news is in reference to this work: Large-Scale Expansions of Friedreich's Ataxia GAA Repeats in Yeast
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