La Universidad de Granada celebra su V Jornada de Spin-Off

La inauguración tendrá lugar el viernes, 11 de octubre, a las 9,30 horas en la Sala de Conferencias del Complejo Administrativo

El próximo viernes, 11 de octubre, a las 9,30 horas en la Sala de Conferencias del Complejo Administrativo Triunfo tendrá lugar la inauguración de la V Jornada de Spin-Off de la Universidad de Granada, en la que participan 33 ‘spin off’ y 15 entidades invitadas.

El acto contará con la presencia de la vicerrectora de Política Científica e Investigación de la Universidad de Granada, Mª Dolores Suárez Ortega; el delegado del rector para la Transferencia, Innovación y Empresa de la UGR, Jesús Chamorro Martínez; el delegado territorial en Granada de la Consejería de Economía, Innovación, Ciencia y Empleo de la Junta de Andalucía, José Antonio Aparicio López, y la concejala de Comercio y Ocupación de la Vía Pública del Ayuntamiento de Granada, María Francés Barrientos.

PROGRAMA

09:30 – Sala de Conferencias del Complejo Administrativo Triunfo

Inauguración de la Jornada por parte de:

  • Vicerrectora de Política Científica e Investigación de la UGR. Mª Dolores Suárez Ortega.
  • Delegado Territorial en Granada de la Consejería de Economía, Innovación, Ciencia y Empleo de la Junta de Andalucía. José Antonio Aparicio López.
  • Concejala de Comercio y Ocupación de la Vía Pública del Excmo. Ayuntamiento de Granada. María Francés Barrientos.
  • Delegado de Transferencia, Innovación y Empresa de la Universidad de Granada. Jesús Chamorro Martínez.

10:00 – Sala de Conferencias del Complejo Administrativo Triunfo

Conferencia Inaugural

  • Responsable Transferencia Tecnológica en FRSTsquare. Francesc Xavier Roca. Título: Nuevas aplicaciones comerciales para tu tecnología/conocimiento.

11:45 – Sala de Conferencias del Complejo Administrativo Triunfo

  • Entrega de premios III Concurso “Emprendimiento Universitario 2013” de la UGR – Modalidad Proyectos Empresariales Spin-Off.

12:00 –Crucero del Hospital Real

Café

14:30 – Crucero del Hospital Real. Clausura de la Jornada

Stands Spin-Off de la Universidad de Granada y Entidades Invitadas:

  • OGE Management Partner
  • InterimGestión
  • Haya Capital
  • Caja Rural de Granada
  • GemacConsultores
  • Servicios Integrales de Congresos
  • Vicerrectorado del Parque Tecnológico Ciencias de la Salud
  • Parque Tecnológico Ciencias de la Salud
  • Agencia de Innovación y Desarrollo de Andalucía
  • Andalucía Emprende. Fundación Pública Andaluza
  • Delegación de Transferencia, Innovación y Empresa (OTRI y FEUGR)
  • Fundación Pública Andaluza para la investigación Biosanitaria de Andalucía Oriental (FIBAO)
  • Asociación de Jóvenes Empresarios de Granada
  • Confederación Granadina de Empresarios
  • Cámara de Comercio

Descargue el díptico con el programa.

CONVOCATORIA:

  • Asunto: Inauguración de la V Jornada de Spin-Off de la Universidad de Granada
  • DÍA: Viernes, 11 de octubre
  • HORA: 9,30 horas
  • LUGAR: Sala de Conferencias del Complejo Administrativo Triunfo

 

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Arranca el ciclo de conferencias “Fronteras de la Física” en la Facultad de Ciencias de la UGR

La primera charla correrá a cargo de Miguel A. Muñoz, catedrático del Departamento de Electromagnetismo y Física de la Materia de la Universidad de Granada

El Instituto Carlos I de Física Teórica y Computacional ha organizado un ciclo de conferencias titulado “Fronteras de la Física”. La primera de ellas tendrá lugar el viernes, 11 de octubre, a las 12:30 horas, y correrá a cargo de Miguel A. Muñoz, catedrático del Departamento de Electromagnetismo y Física de la Materia de la Universidad de Granada, bajo el título “Puntos críticos y la transmisión de información en sistemas biológicos”. El acto se celebrará en el aula F-1 del área de Físicas de la Facultad de Ciencias.

Los fenómenos críticos en Física aparecen bajo circunstancias muy especiales, tienen un comportamiento muy complejo, y están gobernados por leyes muy peculiares y distintas a las de casi cualquier otro sistema físico. Paradójicamente, sistemas con aspecto “crítico” se observan frecuentemente en la naturaleza en infinidad de ámbitos -geofísica, astrofísica, superconductores, etc.- por lo que debe existir algún mecanismo que organice sistemas reales para ser críticos o cuasi-críticos. En esta charla, el investigador de la UGR revisará brevemente dichos mecanismos, y presentará nuevos descubrimientos y teorías que muestran que ciertos aspectos del cerebro y -más en general, del procesado de información en sistemas biológicos- han sido seleccionados por la evolución para ser críticos.

Más información: http://ic1.ugr.es/ciclo_conferencias/

 

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New mechanism preserving genomic integrity and is abnormal in the rare DiGeorge syndrome

67208 An international team of scientists—including researchers at GENYO, the Centre for Genomics and Oncological Research (Pfizer-University of Granada- Andalusian Regional Government)—has described a molecular mechanism that facilitates the defence of the human genome against «bombarding» by mobile DNA sequences. Abnormalities in the mechanism could be responsible for some symptoms of DiGeorge syndrome, a rare disease. The research could in the future help develop new therapies against the disease, which is caused by the microdeletion of a small part of chromosome 22.

The study, published this week in the prestigious Nature Structural and Molecular Biology journal, describes a sophisticated mechanism that enables all of our cells to control the uncontrolled movement of mobile DNA in our genomes. In patients with DiGeorge syndrome, the cells present abnormalities in the control mechanism. Currently, the research team are trying to generate stem cells that «suffer» from the disease from cells donated by patients who have it—which would enable them to clarify the molecular base of this complex pathology.

DiGeorge syndrome, also known as deletion 22q11.2, is the most common genetic disease caused by a chromosome microdeletion in humans. It has an estimated prevalence of 1 in 4000 births and symptoms vary greatly. Typically, these affect the heart and immune system, as well as presenting as learning difficulties, mental retardation and psychiatric disorders.

The disease is characterized by absence of the «Microprocessor» protein complex, which means these patients lack a ‘vigilante’ gene to watch out for repeated sequences and, therefore, are potentially susceptible to being bombarded by these DNA fragments.

«Microprocessor» is the key

Sara R. Heras—co-author of the study and GENYO researcher—explains that all our cells contain «Microprocessor», a protein complex whose known function at the moment is that of generating small regulatory molecules of ribonucleic acid (RNA), known as microRNAs. «Our study has shown that this complex also acts as ‘vigilante’ and defends the integrity of the human genome. Hence, these proteins are capable of recognizing and fragmenting the repeated DNA sequences that escape previous control mechanisms, thus preventing them from replicating and introducing themselves into the genome».

In Nature Structural and Molecular Biology, Sara R. Heras, Sara Macías and their collaborators have described a new mechanism by which most human cells can avoid being bombarded by these DNA fragments. This study has been conducted in the laboratory headed by Dr. José Luis García Pérez in GENYO (Granada) in collaboration with Dr. Javier Cáceres «Medical Research Council-Human Genetic Unit» in Edinburgh (United Kingdom) and Dr. Eduardo Eyras’ laboratory at the Universidad Pompeu Fabra, Barcelona.

Embryonic model

In these new studies, the authors are using an embryonic model of induced pluripotent stem cells (iPSCs). That is, from cells donated by patients with DiGeorge syndrome, stem cells with the disease are generated. This is an ideal model to determine the impact of the repeated sequences from which the deletion that causes this pathology are generated: in other words, the embryonic stage. It is foreseen that these studies will clarify the molecular base for this highly complex disease, as well as permit the long-term development of new therapies for its treatment.

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New mechanism preserving genomic integrity and is abnormal in the rare DiGeorge syndrome

67208 An international team of scientists — including researchers at GENYO, the Centre for Genomics and Oncological Research (Pfizer-University of Granada- Andalusian Regional Government) — has described a molecular mechanism that facilitates the defence of the human genome against «bombarding» by mobile DNA sequences. Abnormalities in the mechanism could be responsible for some symptoms of DiGeorge syndrome, a rare disease. The research could in the future help develop new therapies against the disease, which is caused by the microdeletion of a small part of chromosome 22. The study, published this week in the journal Nature Structural and Molecular Biology describes a sophisticated mechanism that enables all of our cells to control the uncontrolled movement of mobile DNA in our genomes. In patients with DiGeorge syndrome, the cells present abnormalities in the control mechanism. Currently, the research team are trying to generate stem cells that «suffer» from the disease from cells donated by patients who have it — which would enable them to clarify the molecular base of this complex pathology.

DiGeorge syndrome, also known as deletion 22q11.2, is the most common genetic disease caused by a chromosome microdeletion in humans. It has an estimated prevalence of 1 in 4000 births and symptoms vary greatly. Typically, these affect the heart and immune system, as well as presenting as learning difficulties, mental retardation and psychiatric disorders.

The disease is characterized by absence of the «Microprocessor» protein complex, which means these patients lack a ‘vigilante’ gene to watch out for repeated sequences and, therefore, are potentially susceptible to being bombarded by these DNA fragments.

«Microprocessor» is the key

Sara R. Heras — co-author of the study and GENYO researcher — explains that all our cells contain «Microprocessor,» a protein complex whose known function at the moment is that of generating small regulatory molecules of ribonucleic acid (RNA), known as microRNAs. «Our study has shown that this complex also acts as ‘vigilante’ and defends the integrity of the human genome. Hence, these proteins are capable of recognizing and fragmenting the repeated DNA sequences that escape previous control mechanisms, thus preventing them from replicating and introducing themselves into the genome.»

In Nature Structural and Molecular Biology, Sara R. Heras, Sara Macías and their collaborators have described a new mechanism by which most human cells can avoid being bombarded by these DNA fragments. This study has been conducted in the laboratory headed by Dr. José Luis García Pérez in GENYO (Granada) in collaboration with Dr. Javier Cáceres «Medical Research Council-Human Genetic Unit» in Edinburgh (United Kingdom) and Dr. Eduardo Eyras’ laboratory at the Universidad Pompeu Fabra, Barcelona.

Embryonic model

In these new studies, the authors are using an embryonic model of induced pluripotent stem cells (iPSCs). That is, from cells donated by patients with DiGeorge syndrome, stem cells with the disease are generated. This is an ideal model to determine the impact of the repeated sequences from which the deletion that causes this pathology are generated: in other words, the embryonic stage. It is foreseen that these studies will clarify the molecular base for this highly complex disease, as well as permit the long-term development of new therapies for its treatment.

Descargar


Mechanism preserving genome integrity help develop new therapies against DiGeorge syndrome

67208 An international team of scientists-including researchers at GENYO, the Centre for Genomics and Oncological Research (Pfizer-University of Granada- Andalusian Regional Government)-has described a molecular mechanism that facilitates the defence of the human genome against «bombarding» by mobile DNA sequences. Abnormalities in the mechanism could be responsible for some symptoms of DiGeorge syndrome, a rare disease. The research could in the future help develop new therapies against the disease, which is caused by the microdeletion of a small part of chromosome 22.

The study, published this week in the prestigious Nature Structural and Molecular Biology journal, describes a sophisticated mechanism that enables all of our cells to control the uncontrolled movement of mobile DNA in our genomes. In patients with DiGeorge syndrome, the cells present abnormalities in the control mechanism. Currently, the research team are trying to generate stem cells that «suffer» from the disease from cells donated by patients who have it-which would enable them to clarify the molecular base of this complex pathology.

DiGeorge syndrome, also known as deletion 22q11.2, is the most common genetic disease caused by a chromosome microdeletion in humans. It has an estimated prevalence of 1 in 4000 births and symptoms vary greatly. Typically, these affect the heart and immune system, as well as presenting as learning difficulties, mental retardation and psychiatric disorders.

The disease is characterized by absence of the «Microprocessor» protein complex, which means these patients lack a ‘vigilante’ gene to watch out for repeated sequences and, therefore, are potentially susceptible to being bombarded by these DNA fragments.

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Detallan cómo la arquitectura cerebral controla la actividad neuronal

68047 Científicos españoles han descrito de manera minuciosa cómo la arquitectura de conexiones del cerebro humano controla la actividad de las neuronas, demostrando que en este órgano se producen continuamente pequeñas y variadas ‘avalanchas’ o ‘terremotos’ de actividad. El estudio, que publica Nature Communication, ayudará a entender mejor la conexión entre estructura y dinámica del cerebro.
Más información sobre:conexiones cerebro neuronas
UGRdivulga | 09 octubre 2013 13:15

1 / 1Mapa de alta resolución de conexiones cerebrales obtenido por el Human Connectome Project. P. Hagmann P et al.-PLoS Biol
Paolo Moretti y Miguel Ángel Muñoz, investigadores del Instituto Carlos I de Física Teórica y Computacional y del grupo de investigación en Física Estadística y de los Sistemas Complejos de la Universidad de Granada (UGR) aportan nuevo datos sobre el enigma científico de cómo la estructura del cerebro –es decir los detalles del enmarañado tejido de sus interconexiones– condiciona y afecta la actividad de las neuronas a nivel global, influenciando así los procesos sensoriales y cognitivos. El estudio se publica en Nature Communications.

En los últimos años, diversas investigaciones han permitido obtener gran cantidad de información sobre cómo es el diseño de la intrincadísima red de conexiones neuronales del cerebro y de cuáles son los mapas de actividad neuronal en sus distintas regiones, a distintas escalas y durante la realización de tareas. Estos mapas se han logrado con mediciones de distinta naturaleza (magnetoencelografía, resonancia magnética funcional o potenciales de campos locales, por ejemplo).

Como explica Muñoz, catedrático de Física Teórica y Computacional de la UGR, «utilizando una sencilla analogía es como si tuviéramos a nuestra disposición, por un lado, un detallado atlas de carreteras, y por otro, un mapa del tráfico en distintos y determinados momentos del día».

Los científicos granadinos han empleado el mapa de las conexiones cerebrales más preciso elaborado hasta la fecha, llevado a cabo por el profesor Sporns, de la Universidad de Indiana (EE UU). Usando como soporte la arquitectura de dicha red de interconexiones (la red de carreteras), los investigadores del Instituto Carlos I utilizaron modelos matemático-computacionales relativamente sencillos para analizar cómo la actividad neuronal se propaga por la red (ver como fluye en distintas condiciones).

Avalanchas de actividad neuronal

Los modelos analizados en la UGR dan lugar de forma natural a la presencia de avalanchas de actividad. «Estos episodios de actividad o ‘avalanchas’ no podemos compararlos con el ejemplo del tráfico, porque para ello debería ocurrir que los coches, en un punto, pudiesen desdoblarse en varios y multiplicarse o evaporarse», explica Muñoz.

«Por el contrario –añade–, se parecen a los terremotos o episodios de actividad sísmica que, a mayor o menor escala, continuamente perturban la superficie de la tierra, y que en un proceso de cascada desencadenan avalanchas sísmicas de gran variabilidad. Los episodios de actividad neuronal constituyen un mecanismo para entender cómo la información codificada en las neuronas viaja de un lugar a otro del cerebro, haciendo así posible la integración de toda la información, dando coherencia al sistema».

Las avalanchas de actividad aparecen en el cerebro con gran variedad de formas óptimas
En el artículo se demuestra, mediante cálculos matemáticos y el uso extensivo de simulaciones computacionales en el superordenador PROTEUS del Instituto Carlos I, que las avalanchas de actividad aparecen en el cerebro con una variabilidad enorme de tamaños y formas óptimas, ni exclusivamente pequeñas, ni sistemáticamente grandes.

«Si las avalanchas fuesen demasiado breves, la información codificada en ellas no podría viajar de una parte a otra del cerebro y no habría una coherencia suficiente para las operaciones cognitivas. Por otro lado, si las avalanchas fuesen siempre demasiado intensas, el cerebro estaría en un estado perpetuo de terremoto devastador, o dicho con algo más de precisión, en un estado de perpetua actividad epiléptica. Ambas posibilidades serían nefastas para el correcto funcionamiento del cerebro y ambas se pueden relacionar con patologías mentales», apuntan los autores.

A la luz de los resultados de este trabajo, la dinámica de las redes neuronales sanas parece operar justo en un punto crítico, en el límite entre los dos estados anteriores: la actividad se propaga de forma marginal, pudiendo llegar a todas partes pero sin sobresaturar el sistema, con un delicado balance de avalanchas pequeñas y grandes, de todas las escalas posibles.

Moretti y Muñoz han demostrado que la arquitectura del cerebro a gran escala, que tiene una estructura organizada en distintas capas en modo jerárquico, es tal que hace que sea mucho más sencillo alcanzar este estado de avalanchas críticas de lo que se pensaba hasta el momento. El trabajo ha sido financiado por la Junta de Andalucía mediante un Proyecto de Excelencia y está auspiciado por el Campus de Excelencia Internacional (CEI) Biotic de la UGR.

Referencia bibliográfica:

Paolo Moretti y Miguel A. Muñoz. «Griffiths phases and the stretching of criticality in brain networks». Nature Communications 4:2521, 2013.DOI: 10.1038/ncomms3521.

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Scientists discover new mechanism that preserves genomic integrity and is abnormal in the rare DiGeorge syndrome

67208 An international team including GENYO centre researchers has described a molecular mechanism that defends human genome integrity against «bombarding» by mobile DNA sequences. Alterations in the mechanism could be responsible for symptoms causing this syndrome

Their research—an important step forward in the field of genetics—is published this week in the prestigious Nature Structural and Molecular Biology journal

This scientific advance could in the future help develop new therapies against the disease, caused by microdeletion of a small part of chromosome 22

An international team of scientists—including researchers at GENYO, the Centre for Genomics and Oncological Research (Pfizer-University of Granada- Andalusian Regional Government)—has described a molecular mechanism that facilitates the defence of the human genome against «bombarding» by mobile DNA sequences. Abnormalities in the mechanism could be responsible for some symptoms of DiGeorge syndrome, a rare disease. The research could in the future help develop new therapies against the disease, which is caused by the microdeletion of a small part of chromosome 22.

The study, published this week in the prestigious Nature Structural and Molecular Biologyjournal, describes a sophisticated mechanism that enables all of our cells to control the uncontrolled movement of mobile DNA in our genomes. In patients with DiGeorge syndrome, the cells present abnormalities in the control mechanism. Currently, the research team are trying to generate stem cells that «suffer» from the disease from cells donated by patients who have it—which would enable them to clarify the molecular base of this complex pathology.

DiGeorge syndrome, also known as deletion 22q11.2, is the most common genetic disease caused by a chromosome microdeletion in humans. It has an estimated prevalence of 1 in 4000 births and symptoms vary greatly. Typically, these affect the heart and immune system, as well as presenting as learning difficulties, mental retardation and psychiatric disorders.

The disease is characterized by absence of the «Microprocessor» protein complex, which means these patients lack a ‘vigilante’ gene to watch out for repeated sequences and, therefore, are potentially susceptible to being bombarded by these DNA fragments.

«Microprocessor» is the key

Sara R. Heras—co-author of the study and GENYO researcher—explains that all our cells contain «Microprocessor», a protein complex whose known function at the moment is that of generating small regulatory molecules of ribonucleic acid (RNA), known as microRNAs. «Our study has shown that this complex also acts as ‘vigilante’ and defends the integrity of the human genome. Hence, these proteins are capable of recognizing and fragmenting the repeated DNA sequences that escape previous control mechanisms, thus preventing them from replicating and introducing themselves into the genome».

In Nature Structural and Molecular Biology, Sara R. Heras, Sara Macías and their collaborators have described a new mechanism by which most human cells can avoid being bombarded by these DNA fragments. This study has been conducted in the laboratory headed by Dr. José Luis García Pérez in GENYO (Granada) in collaboration with Dr. Javier Cáceres «Medical Research Council-Human Genetic Unit» in Edinburgh (United Kingdom) and Dr. Eduardo Eyras’ laboratory at the Universidad Pompeu Fabra, Barcelona.

Embryonic model

In these new studies, the authors are using an embryonic model of induced pluripotent stem cells (iPSCs). That is, from cells donated by patients with DiGeorge syndrome, stem cells with the disease are generated. This is an ideal model to determine the impact of the repeated sequences from which the deletion that causes this pathology are generated: in other words, the embryonic stage. It is foreseen that these studies will clarify the molecular base for this highly complex disease, as well as permit the long-term development of new therapies for its treatment.

The study published in Nature Structural and Molecular Biology and current research into DiGeorge syndrome, has been and is today part-financed by the 7th Marie Curie European Framework Program CIG-Grant (PCIG-GA-2011-303812). Moreover, these and other studies in Dr. Garcia-Perez’s laboratory in GENYO are financed by the Spanish Ministry of Health (FIS-FEDER-PI11/01489), the Andalusian Regional Government Departments of Innovation and Science (CICE-FEDER-P09-CTS-4980) and Health (PeS-FEDER-PI-002), by the prestigious US «Howard Hughes Medical Institute» (IECS-55007420), and by the European Research Council (ERC-Starting-2012-LS1-EPIPLURIRETRO-339064).

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El Pueblo de Ceuta

Pág. 10: La Facultad de Educación celebra la «Jornada de acogida al estudiante de nuevo ingreso»

Descarga por URL: http://sl.ugr.es/04XF

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El Telegrama de Melilla

Pág. 18: «Melilla Acoge» muestra a los universitarios la dura realidad de los inmigrantes

Descarga por URL: http://sl.ugr.es/04XE

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Melilla Hoy

Pág. 22: Esta tarde, presentación de un libro sobre diversidad cultural

Convocatoria de subvenciones de la Delegación de Estudiantes de la UGR

Decarga por URL: http://sl.ugr.es/04XD

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El Faro de Melilla

Pág. 12: SATE-STEs y la UGR presentan un libro sobre diversidad cultural

Descarga por URL: http://sl.ugr.es/04XC

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Granada Hoy

Pág. 3: Universidad. Posible pérdida de 250 profesores en la UGR

Pág. 12: Las becas de colaboración del Ministerio caen un 55% en cinco años

Demuestran pequeños «terremotos» en la actividad cerebral

Pág. 13: Publicidad. Plan Propio de becas y ayudas al estudio de la UGR

Pág. 18: Conferencia: Lorca, Falla, Lanz y las experiencias titiriteras granadinas

Pág. 19: Cine forum en la Casa de Porras: «Fuga sin fin»

Págs. 36-37: La noche en que la cultura NO DUERME

Descarga por URL: http://sl.ugr.es/04XB

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