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OWN PRESENTATION: My name is ISAAC AMELA ABELLAN and I’m 28 years old.

Second INFOBIOMED Training Challenge. OWN PRESENTATION: My name is ISAAC AMELA ABELLAN and I’m 28 years old. I live in Cabrils, a village near Barcelona, here in Spain.

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OWN PRESENTATION: My name is ISAAC AMELA ABELLAN and I’m 28 years old.

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  1. Second INFOBIOMED Training Challenge • OWN PRESENTATION: • My name is ISAAC AMELA ABELLAN and I’m 28 years old. • I live in Cabrils, a village near Barcelona, here in Spain. • I'm affected by a neurodegenerative disease called FRIEDREICH ATAXIA that limits my mobility. Curiously this disease is the main issue of my Ph.D. project. • I like very much every type of sports, nature and science especially. • Moreover, I have practiced many sports while I have been able and I now continue practicing those that my physical condition allows me (for example skiing).

  2. Second INFOBIOMED Training Challenge • PRESENT POSITION AND EDUCATION: • PhD Student [ 2005 to 2008 pre-doctoral scholarship granted by the Autonomous University of Barcelona (UAB) ] • Laboratory of Bioinformatics • Institute of Biotechnology and Biomedicine (IBB) • Autonomous University of Barcelona (UAB) • 08193 Bellaterra, Barcelona. Spain. • Phone: 34-93-5812807 • e-mail: iamela@bioinf.uab.es • 1996-2000 University of Girona (UdG), degree in Biology. • 2000-2004 Autonomous University of Barcelona (UAB), degree in Biotechnology.

  3. Second INFOBIOMED Training Challenge • RESEARCH AREA: • Protein sequence, structure and function analysis. • Molecular modelling of protein interaction mechanisms involved in some human diseases. • DNA microarray analysis of relevant data available about some human diseases. • Sequence analysis of probably autoimmune reactive proteins in several bacterial pathogens.

  4. Second INFOBIOMED Training Challenge • FRIEDREICH ATAXIA: • Friedreich Ataxia is a neurological, progressive and hereditary disease which concerns the balance and the coordination of movements basically. • It is the most common autosomal recessive ataxia and it is associated with a pronounced lack of a conserved mitochondrial inner membrane protein of not fully understood function called frataxin. • A large expansion of a triplet GAA in the first intron of the gene FRDA/X25 involve an aberrant structure of the DNA helix complicating the pass of RNA polymerase enzyme during the transcription of the gene. This event causes a reduced expression of frataxin encoded by the FRDA gene. • Frataxin has been associated with iron accumulation in the mitochondria and increased sensitivity to oxidative stress.

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