Where there´s a will, there´s a way from Almontgrave on Vimeo.
*Fuente: "EL PERIODICO DE CATALUNYA"
02 March 2012
How Marijuana Impairs Memory
A major downside of the medical use of marijuana is the drug's ill effects on working memory, the ability to transiently hold and process information for reasoning, comprehension and learning. Researchers reporting in the March 2 print issue of the Cell Press journal Cell provide new insight into the source of those memory lapses. The answer comes as quite a surprise: Marijuana's major psychoactive ingredient (THC) impairs memory independently of its direct effects on neurons. The side effects stem instead from the drug's action on astroglia, passive support cells long believed to play second fiddle to active neurons.
The findings offer important new insight into the brain and raise the possibility that marijuana's benefits for the treatment of pain, seizures and other ailments might some day be attained without hurting memory, the researchers say.
With these experiments in mice, "we have found that the starting point for this phenomenon -- the effect of marijuana on working memory -- is the astroglial cells," said Giovanni Marsicano of INSERM in France.
"This is the first direct evidence that astrocytes modulate working memory," added Xia Zhang of the University of Ottawa in Canada.
The new findings aren't the first to suggest astroglia had been given short shrift. Astroglial cells (also known as astrocytes) have been viewed as cells that support, protect and feed neurons for the last 100 to 150 years, Marsicano explained. Over the last decade, evidence has accumulated that these cells play a more active role in forging the connections from one neuron to another.
The researchers didn't set out to discover how marijuana causes its cognitive side effects. Rather, they wanted to learn why receptors that respond to both THC and signals naturally produced in the brain are found on astroglial cells. These cannabinoid type-1 (CB1R) receptors are very abundant in the brain, primarily on neurons of various types.
Zhang and Marsicano now show that mice lacking CB1Rs only on astroglial cells of the brain are protected from the impairments to spatial working memory that usually follow a dose of THC. In contrast, animals lacking CB1Rs in neurons still suffer the usual lapses. Given that different cell types express different variants of CB1Rs, there might be a way to therapeutically activate the receptors on neurons while leaving the astroglial cells out, Marsicano said.
"The study shows that one of the most common effects of cannabinoid intoxication is due to activation of astroglial CB1Rs," the researchers wrote.
The findings further suggest that astrocytes might be playing unexpected roles in other forms of memory in addition to spatial working memory, Zhang said.
The researchers hope to explore the activities of endogenous endocannabinoids, which naturally trigger CB1Rs, on astroglial and other cells. The endocannabinoid system is involved in appetite, pain, mood, memory and many other functions. "Just about any physiological function you can think of in the body, it's likely at some point endocannabinoids are involved," Marsicano said.
And that means an understanding of how those natural signaling molecules act on astroglial and other cells could have a real impact. For instance, Zhang said, "we may find a way to deal with working memory problems in Alzheimer's."
The findings offer important new insight into the brain and raise the possibility that marijuana's benefits for the treatment of pain, seizures and other ailments might some day be attained without hurting memory, the researchers say.
With these experiments in mice, "we have found that the starting point for this phenomenon -- the effect of marijuana on working memory -- is the astroglial cells," said Giovanni Marsicano of INSERM in France.
"This is the first direct evidence that astrocytes modulate working memory," added Xia Zhang of the University of Ottawa in Canada.
The new findings aren't the first to suggest astroglia had been given short shrift. Astroglial cells (also known as astrocytes) have been viewed as cells that support, protect and feed neurons for the last 100 to 150 years, Marsicano explained. Over the last decade, evidence has accumulated that these cells play a more active role in forging the connections from one neuron to another.
The researchers didn't set out to discover how marijuana causes its cognitive side effects. Rather, they wanted to learn why receptors that respond to both THC and signals naturally produced in the brain are found on astroglial cells. These cannabinoid type-1 (CB1R) receptors are very abundant in the brain, primarily on neurons of various types.
Zhang and Marsicano now show that mice lacking CB1Rs only on astroglial cells of the brain are protected from the impairments to spatial working memory that usually follow a dose of THC. In contrast, animals lacking CB1Rs in neurons still suffer the usual lapses. Given that different cell types express different variants of CB1Rs, there might be a way to therapeutically activate the receptors on neurons while leaving the astroglial cells out, Marsicano said.
"The study shows that one of the most common effects of cannabinoid intoxication is due to activation of astroglial CB1Rs," the researchers wrote.
The findings further suggest that astrocytes might be playing unexpected roles in other forms of memory in addition to spatial working memory, Zhang said.
The researchers hope to explore the activities of endogenous endocannabinoids, which naturally trigger CB1Rs, on astroglial and other cells. The endocannabinoid system is involved in appetite, pain, mood, memory and many other functions. "Just about any physiological function you can think of in the body, it's likely at some point endocannabinoids are involved," Marsicano said.
And that means an understanding of how those natural signaling molecules act on astroglial and other cells could have a real impact. For instance, Zhang said, "we may find a way to deal with working memory problems in Alzheimer's."
**Source: "SCIENCE DAILY"
Clearer Picture of How Protein Machine Systems Tweak Gene Expression
Indiana University biologists have found that specific types of RNA polymerase enzymes, the molecular machines that convert DNA into RNA, can differ in function based on variation in the parts -- in this case protein subunits -- used to assemble those machines.
The new findings on the synthesis and function of different RNA polymerases (Pols), including two RNA polymerases that lead author Craig Pikaard discovered over a decade ago -- the plant-specific enzymes Pol IV and Pol V -- indicate that subunit composition of the polymerases plays a role in selecting how some genes are silenced while others are not.
All eukaryotes -- a group that includes plants, animals, fungi and all other organisms with nuclei -- contain life-essential Pols I, II and III that are each built from different combinations of 12 to 17 protein subunits, with each of the three enzymes assigned specific, unique tasks in the cell. In 1999 while analyzing the newly sequenced genome of Arabidopsis thaliana, a member of the mustard family considered a model organism for experimentation in plant biology, Pikaard identified Pol IV and Pol V.
Pikaard's work has since shown that while the Pol IV and Pol V enzymes are not essential to life and are actually specialized forms of Pol II (the RNA polymerase responsible for generating RNAs that encode proteins), they play important roles in RNA-directed DNA methylation, a process that silences mobile genetic elements known as retrotransposons that can cause trouble if allowed to spread.
"In fact, most of the 12 protein subunits present in Pols II, IV and V are encoded by the same genes," Pikaard said. "Interestingly, among these common subunits are alternative forms of the ninth subunit, and the two forms of the ninth subunit (9a and 9b) are extremely similar, differing in only 8 of their 114 amino acids."
This high degree of similarity suggested 9a and 9b proteins might be redundant, but the Pikaard lab's new research found this to be only partially true.
"When you remove both proteins, the plants die as embryos; but if they lack just one of the proteins, they still survive, which is evidence that the two alternative forms of the protein are redundant for survival," he said. "But despite this, plants missing either 9a or 9b have different physical characteristics, such as leaf shape, suggesting that Pol II built using 9a does not function exactly the same as Pol II assembled using 9b."
Another unique feature found between the two protein subunits involves the functionality of Pol V and its ability to conduct RNA-directed DNA methylation: The Pol V polymerase built using 9b facilitates methylation, while the 9a-built Pol V does not.
"This is the first evidence showing that different functional subtypes of nuclear RNA polymerases are generated using alternative subunits, and there are multiple subunits for which more than one variant is produced," Pikaard said. "The results also show for the first time that the ninth subunit has a role in RNA-directed DNA methylation."
With new evidence from other research that RNA-directed DNA methylation and transposon silencing also takes place in the sperm-forming cell lineage in mammals, and not just in plants, Pol II transcription is implicated in methylation in both plants and animals.
"Alterations in DNA methylation and gene silencing are involved in multiple genetic disorders and diseases, including cancer," Pikaard said. "Our studies of RNA Pol IV and Pol V may tell us important things about their cousin, Pol II, that may not be possible to know otherwise, including how RNA synthesis can help specify sites of DNA methylation."
Pikaard is the Carlos O. Miller Professor of Plant Growth and Development in the IU Bloomington College of Arts and Sciences' Department of Biology and Department of Molecular and Cellular Biochemistry. Last year he was also named as an investigator of the Howard Hughes Medical Institute and the Gordon and Betty Moore Foundation along with 14 other scientists as part of a $75 million plant science initiative.
The new findings on the synthesis and function of different RNA polymerases (Pols), including two RNA polymerases that lead author Craig Pikaard discovered over a decade ago -- the plant-specific enzymes Pol IV and Pol V -- indicate that subunit composition of the polymerases plays a role in selecting how some genes are silenced while others are not.
All eukaryotes -- a group that includes plants, animals, fungi and all other organisms with nuclei -- contain life-essential Pols I, II and III that are each built from different combinations of 12 to 17 protein subunits, with each of the three enzymes assigned specific, unique tasks in the cell. In 1999 while analyzing the newly sequenced genome of Arabidopsis thaliana, a member of the mustard family considered a model organism for experimentation in plant biology, Pikaard identified Pol IV and Pol V.
Pikaard's work has since shown that while the Pol IV and Pol V enzymes are not essential to life and are actually specialized forms of Pol II (the RNA polymerase responsible for generating RNAs that encode proteins), they play important roles in RNA-directed DNA methylation, a process that silences mobile genetic elements known as retrotransposons that can cause trouble if allowed to spread.
"In fact, most of the 12 protein subunits present in Pols II, IV and V are encoded by the same genes," Pikaard said. "Interestingly, among these common subunits are alternative forms of the ninth subunit, and the two forms of the ninth subunit (9a and 9b) are extremely similar, differing in only 8 of their 114 amino acids."
This high degree of similarity suggested 9a and 9b proteins might be redundant, but the Pikaard lab's new research found this to be only partially true.
"When you remove both proteins, the plants die as embryos; but if they lack just one of the proteins, they still survive, which is evidence that the two alternative forms of the protein are redundant for survival," he said. "But despite this, plants missing either 9a or 9b have different physical characteristics, such as leaf shape, suggesting that Pol II built using 9a does not function exactly the same as Pol II assembled using 9b."
Another unique feature found between the two protein subunits involves the functionality of Pol V and its ability to conduct RNA-directed DNA methylation: The Pol V polymerase built using 9b facilitates methylation, while the 9a-built Pol V does not.
"This is the first evidence showing that different functional subtypes of nuclear RNA polymerases are generated using alternative subunits, and there are multiple subunits for which more than one variant is produced," Pikaard said. "The results also show for the first time that the ninth subunit has a role in RNA-directed DNA methylation."
With new evidence from other research that RNA-directed DNA methylation and transposon silencing also takes place in the sperm-forming cell lineage in mammals, and not just in plants, Pol II transcription is implicated in methylation in both plants and animals.
"Alterations in DNA methylation and gene silencing are involved in multiple genetic disorders and diseases, including cancer," Pikaard said. "Our studies of RNA Pol IV and Pol V may tell us important things about their cousin, Pol II, that may not be possible to know otherwise, including how RNA synthesis can help specify sites of DNA methylation."
Pikaard is the Carlos O. Miller Professor of Plant Growth and Development in the IU Bloomington College of Arts and Sciences' Department of Biology and Department of Molecular and Cellular Biochemistry. Last year he was also named as an investigator of the Howard Hughes Medical Institute and the Gordon and Betty Moore Foundation along with 14 other scientists as part of a $75 million plant science initiative.
**Published by "SCIENCE DAILY"
El Senado de EE UU rechaza limitar la cobertura de anticonceptivos
El Senado de Estados Unidos ha rechazado la enmienda presentada por el senador republicano Roy Blunt que abogaba por permitir a los empresarios y a las compañías de seguros rechazar “por cuestiones religiosas y morales” la cobertura de métodos anticonceptivos y otros tratamientos médicos a sus empleadas.
La votación, resuelta por un margen de tres votos -51 en contra y 48 a favor, más estrecho del esperado-, implica un apoyo por parte de la Cámara Alta a la política sanitaria en materia anticonceptiva del presidente Barack Obama. Como estaba previsto, todos los representantes republicanos, salvo una senadora que ya anunció que no apoyaría la enmienda, y tres demócratas, han votado a favor.
El verano pasado Obama presentó su política anticonceptiva que incluía, tal y como establecía la reforma sanitaria de 2010, la cobertura gratuita de los anticonceptivos por parte de los empresarios y las compañías aseguradoras. Durante la sesión de hoy, los defensores de la enmienda han esgrimido argumentos a favor de la libertad religiosa. Los republicanos consideran que la norma de Obama obliga a las instituciones religiosas a ir en contra de sus principios para garantizar a sus empleadas el acceso gratuito a métodos anticonceptivos. “El presidente está pisoteando la libertad religiosa” ha declarado el senador republicano por Nebraska Mike Johanns.
-Los republicanos creen que la norma de Obama obliga a las instituciones religiosas a ir en contra de sus principios
Los demócratas, por su parte, han criticado el riesgo que la enmienda Blunt suponía para los derechos de la mujer y de las minorías, y sostienen que la propuesta solo trataba de minar la reforma sanitaria. La senadora por el Estado de Maryland Barbara A. Mikulski se ha felicitado por el resultado de la votación y ha subrayado que la propuesta forma parte de la “guerra sistemática de los republicanos contra las mujeres”.
Aunque el presidente ya recalcó en verano que todos los empresarios y las compañías de seguros debían cubrir los gastos de los métodos anticonceptivos a sus empleados, fueron las explicaciones de la secretaria de Salud, Kathleen Sebelius, el 20 de enero -recordando que esa obligación incluía a las instituciones católicas-, las que provocaron una dura oposición por parte de la jerarquía católica. Para paliar el malestar de un grupo que tradicionalmente apoya a los demócratas, en pleno año electoral, en febrero Obama modificó la norma para que las empresas religiosas no tuvieran que hacerse cargo del abono de los anticonceptivos cuyo coste correría a cargo de las aseguradoras.
La polémica en torno a la enmienda Blunt no ha enfrentado únicamente a republicanos y demócratas. También se ha colado en la lucha por las primarias de los conservadores. Las posturas de cada uno de los candidatos sobre política anticonceptiva han centrado buena parte de los debates y del contenido de sus comparecencias. Ayer Mitt Romney, durante una entrevista en una televisión de Ohio, dijo estar en contra de la enmienda Blunt. Horas después tuvo que rectificar en un programa de radio excusándose en que había entendido mal la pregunta del periodista. Un desliz al que ha aludido su principal oponente en la lucha por la candidatura republicana a la Casa Blanca, Rick Santorum, durante una comparecencia en Fargo para destacar sus valores republicanos frente a los de Romney: “Si a mí me hubieran hecho esa pregunta, mi reacción inmediata hubiera sido: ‘Hay que defender la Primera Enmienda; hay que defender la libertad religiosa”.
**Publicado en "EL PAIS"
La votación, resuelta por un margen de tres votos -51 en contra y 48 a favor, más estrecho del esperado-, implica un apoyo por parte de la Cámara Alta a la política sanitaria en materia anticonceptiva del presidente Barack Obama. Como estaba previsto, todos los representantes republicanos, salvo una senadora que ya anunció que no apoyaría la enmienda, y tres demócratas, han votado a favor.
El verano pasado Obama presentó su política anticonceptiva que incluía, tal y como establecía la reforma sanitaria de 2010, la cobertura gratuita de los anticonceptivos por parte de los empresarios y las compañías aseguradoras. Durante la sesión de hoy, los defensores de la enmienda han esgrimido argumentos a favor de la libertad religiosa. Los republicanos consideran que la norma de Obama obliga a las instituciones religiosas a ir en contra de sus principios para garantizar a sus empleadas el acceso gratuito a métodos anticonceptivos. “El presidente está pisoteando la libertad religiosa” ha declarado el senador republicano por Nebraska Mike Johanns.
-Los republicanos creen que la norma de Obama obliga a las instituciones religiosas a ir en contra de sus principios
Los demócratas, por su parte, han criticado el riesgo que la enmienda Blunt suponía para los derechos de la mujer y de las minorías, y sostienen que la propuesta solo trataba de minar la reforma sanitaria. La senadora por el Estado de Maryland Barbara A. Mikulski se ha felicitado por el resultado de la votación y ha subrayado que la propuesta forma parte de la “guerra sistemática de los republicanos contra las mujeres”.
Aunque el presidente ya recalcó en verano que todos los empresarios y las compañías de seguros debían cubrir los gastos de los métodos anticonceptivos a sus empleados, fueron las explicaciones de la secretaria de Salud, Kathleen Sebelius, el 20 de enero -recordando que esa obligación incluía a las instituciones católicas-, las que provocaron una dura oposición por parte de la jerarquía católica. Para paliar el malestar de un grupo que tradicionalmente apoya a los demócratas, en pleno año electoral, en febrero Obama modificó la norma para que las empresas religiosas no tuvieran que hacerse cargo del abono de los anticonceptivos cuyo coste correría a cargo de las aseguradoras.
La polémica en torno a la enmienda Blunt no ha enfrentado únicamente a republicanos y demócratas. También se ha colado en la lucha por las primarias de los conservadores. Las posturas de cada uno de los candidatos sobre política anticonceptiva han centrado buena parte de los debates y del contenido de sus comparecencias. Ayer Mitt Romney, durante una entrevista en una televisión de Ohio, dijo estar en contra de la enmienda Blunt. Horas después tuvo que rectificar en un programa de radio excusándose en que había entendido mal la pregunta del periodista. Un desliz al que ha aludido su principal oponente en la lucha por la candidatura republicana a la Casa Blanca, Rick Santorum, durante una comparecencia en Fargo para destacar sus valores republicanos frente a los de Romney: “Si a mí me hubieran hecho esa pregunta, mi reacción inmediata hubiera sido: ‘Hay que defender la Primera Enmienda; hay que defender la libertad religiosa”.
**Publicado en "EL PAIS"
Planarian Genes That Control Stem Cell Biology Identified
Despite their unassuming appearance, the planarian flatworms in Whitehead Institute Member Peter Reddien's lab are revealing powerful new insights into the biology of stem cells -- insights that may eventually help such cells deliver on a promising role in regenerative medicine.
In this week's issue of the journal Cell Stem Cell, Reddien and scientists in his lab report on their development of a novel approach to identify and study the genes that control stem cell behavior in planarians. Intriguingly, at least one class of these genes has a counterpart in human embryonic stem cells.
"This is a huge step forward in establishing planarians as an in vivo system for which the roles of stem cell regulators can be dissected," says Reddien, who is also an associate professor of biology at MIT and a Howard Hughes Medical Institute (HHMI) Early Career Scientist. "In the grand scheme of things for understanding stem cell biology, I think this is a beginning foray into seeking general principles that all animals utilize. I'd say we're at the beginning of that process."
Planarians (Schmidtea mediterranea) are tiny freshwater flatworms with the ability to reproduce through fission. After literally tearing themselves in half, the worms use stem cells, called cNeoblasts, to regrow any missing tissues and organs, ultimately forming two complete planarians in about a week.
Unlike muscle, nerve, or skin cells that are fully differentiated, certain stem cells, such as cNeoblasts and embryonic stem cells are pluripotent, having the ability to become almost cell type in the body. Researchers have long been interested in harnessing this capability to regrow damaged, diseased, or missing tissues in humans, such as insulin-producing cells for diabetics or nerve cells for patients with spinal cord injuries.
Several problems currently confound the therapeutic use of stem cells, including getting the stem cells to differentiate into the desired cell type in the appropriate location and having such cells successfully integrate with surrounding tissues, all without forming tumors. To solve these issues, researchers need a better understanding of how stem cells tick at the molecular level, particularly within the environment of a living organism. To date, a considerable amount of embryonic stem cell research has been conducted in the highly artificial environment of the Petri dish.
With its renowned powers of regeneration and more than half of its genes having human homologs, the planarian seems like a logical choice for this line of research. Yet, until now, scientists have been unable to efficiently find the genes that regulate the planarian stem cell system.
Postdoctoral researcher Dan Wagner, first author of the Cell Stem Cell paper, and Reddien devised a clever method to identify potential genetic regulators and then determine if those genes affect the two main functions of stem cells: differentiation and renewal of the stem cell population.
After identifying genes active in cNeoblasts, Wagner irradiated the planarians, leaving a single surviving cNeoblast in each planarian. Left alone, each cNeoblast can form colonies of new cells at very specific rates of differentiation and stem cell renewal.
The researchers knocked down each of the active genes, one per planarian, and observed how the surviving cNeoblasts responded. By comparing the rate of differentiation and stem cell renewal to that of normal cNeoblasts, they could determine the role of each gene. Thus, if a colony containing a certain knocked down gene were observed to have fewer stem cells than the controls, it could be concluded that gene in question plays a role in the process of stem cell renewal. And if the colony had fewer differentiated cells than normal, the knocked down gene could be associated with differentiation.
"Because it's a quantitative method, we can now precisely measure the role of each gene in different aspects of stem cell function," says Wagner. "Being able to measure stem cell activity with a colony is a great improvement over methods that existed before, which were much more indirect."
In total, Wagner identified 10 genes impacting cNeoblast renewal, and two genes with roles in both renewal and differentiation. According to Wagner, three of the stem cell renewal genes are particularly intriguing because they code for proteins that are similar to components of Polycomb Repressive Complex 2 (PRC2), known to regulate stem cell biology in mammalian embryonic stem cells and in other stem cell systems.
"It's interesting because it suggests a parallel between how stem cells operate in planarians and in mammals. For example, there might be similarities between how cNeoblasts and embryonic stem cells function and maintain stemness at the molecular level," he says.
In this week's issue of the journal Cell Stem Cell, Reddien and scientists in his lab report on their development of a novel approach to identify and study the genes that control stem cell behavior in planarians. Intriguingly, at least one class of these genes has a counterpart in human embryonic stem cells.
"This is a huge step forward in establishing planarians as an in vivo system for which the roles of stem cell regulators can be dissected," says Reddien, who is also an associate professor of biology at MIT and a Howard Hughes Medical Institute (HHMI) Early Career Scientist. "In the grand scheme of things for understanding stem cell biology, I think this is a beginning foray into seeking general principles that all animals utilize. I'd say we're at the beginning of that process."
Planarians (Schmidtea mediterranea) are tiny freshwater flatworms with the ability to reproduce through fission. After literally tearing themselves in half, the worms use stem cells, called cNeoblasts, to regrow any missing tissues and organs, ultimately forming two complete planarians in about a week.
Unlike muscle, nerve, or skin cells that are fully differentiated, certain stem cells, such as cNeoblasts and embryonic stem cells are pluripotent, having the ability to become almost cell type in the body. Researchers have long been interested in harnessing this capability to regrow damaged, diseased, or missing tissues in humans, such as insulin-producing cells for diabetics or nerve cells for patients with spinal cord injuries.
Several problems currently confound the therapeutic use of stem cells, including getting the stem cells to differentiate into the desired cell type in the appropriate location and having such cells successfully integrate with surrounding tissues, all without forming tumors. To solve these issues, researchers need a better understanding of how stem cells tick at the molecular level, particularly within the environment of a living organism. To date, a considerable amount of embryonic stem cell research has been conducted in the highly artificial environment of the Petri dish.
With its renowned powers of regeneration and more than half of its genes having human homologs, the planarian seems like a logical choice for this line of research. Yet, until now, scientists have been unable to efficiently find the genes that regulate the planarian stem cell system.
Postdoctoral researcher Dan Wagner, first author of the Cell Stem Cell paper, and Reddien devised a clever method to identify potential genetic regulators and then determine if those genes affect the two main functions of stem cells: differentiation and renewal of the stem cell population.
After identifying genes active in cNeoblasts, Wagner irradiated the planarians, leaving a single surviving cNeoblast in each planarian. Left alone, each cNeoblast can form colonies of new cells at very specific rates of differentiation and stem cell renewal.
The researchers knocked down each of the active genes, one per planarian, and observed how the surviving cNeoblasts responded. By comparing the rate of differentiation and stem cell renewal to that of normal cNeoblasts, they could determine the role of each gene. Thus, if a colony containing a certain knocked down gene were observed to have fewer stem cells than the controls, it could be concluded that gene in question plays a role in the process of stem cell renewal. And if the colony had fewer differentiated cells than normal, the knocked down gene could be associated with differentiation.
"Because it's a quantitative method, we can now precisely measure the role of each gene in different aspects of stem cell function," says Wagner. "Being able to measure stem cell activity with a colony is a great improvement over methods that existed before, which were much more indirect."
In total, Wagner identified 10 genes impacting cNeoblast renewal, and two genes with roles in both renewal and differentiation. According to Wagner, three of the stem cell renewal genes are particularly intriguing because they code for proteins that are similar to components of Polycomb Repressive Complex 2 (PRC2), known to regulate stem cell biology in mammalian embryonic stem cells and in other stem cell systems.
"It's interesting because it suggests a parallel between how stem cells operate in planarians and in mammals. For example, there might be similarities between how cNeoblasts and embryonic stem cells function and maintain stemness at the molecular level," he says.
*Source: "SCIENCE DAILY"
Las herramientas web pueden ser útiles como vehículo terapéutico y educativo
Internet ha cambiado el mundo y está cambiando también la medicina. Además de facilitar el acceso a los conocimientos y la innovación, la 'world wide web' ofrece un espacio en el que los pacientes pueden encontrar herramientas para mejorar su día a día e, incluso, a través de las cuales recibir un tratamiento eficaz. Dos estudios analizan algunas de estas alternativas.
El síndrome de fatiga crónica es un trastorno de origen desconocido que se suela tratar mediante terapia conductual cognitiva y los pacientes mejoran sustancialmente, en comparación con aquellos que no reciben ningún tratamiento. Pero la dificultad en el acceso a ella, por la escasez de especialistas, "supone un acceso desigual".
Para saltar esta barrera, un grupo de expertos del Wihelmina Children's Hospital (Holanda) decidió explorar el poder de esta terapia cuando se ofrece a través de internet. Sesenta y ocho adolescentes que sufrían este síndrome siguieron este tratamiento virtual durante seis meses y la mejora fue notable.
El 85% ya no sufría fatiga grave y el 78% tenía una función motora normal, comparado con el 27% y el 20%, respectivamente, de aquellos que siguieron con la terapia presencial. El programa, llamado FITNET, también logró que el 75% de los pacientes asistiera al colegio, frente al 16% del grupo control.
Las fortalezas de este tratamiento, que podrían explicar su éxito, son que "está disponible en cualquier momento, evita las barreras del cara a cara (retrasos debido a las dificultades de acceso, problemas con las citas, ausencia en el colegio o el trabajo, desplazamientos hasta la consulta) y reduce los tiempos de terapia y los costes", señalan los autores en las páginas de 'The Lancet'.
-Formando 'pacientes activos'
Además de ser una herramienta terapéutica, también puede ser una plataforma educativa para dotar al enfermo de mayor autonomía. El concepto de 'paciente activo' se refiere a aquél capaz de manejar su enfermedad día a día, aquél que puede tomar decisiones cuando se presentan las complicaciones normales de la enfermedad que padece y que tiene confianza en sus habilidades para hacer todo esto. Los programas 'on-line' pueden fomentar estas capacidades, especialmente en los enfermos crónicos, para reducir así la carga que suponen para el sistema sanitario.
"El cuidado de los pacientes con enfermedades crónicas consume el 78% del coste total de gasto sanitario de EEUU" y esta cifra, debido al envejecimiento de la población y al aumento de algunas patologías, va en aumento. Por eso, "un objetivo crucial del sistema sanitario es proporcionarles las herramientas necesarias para que tomen decisiones informadas sobre los cuidados que necesitan y para resolver los problemas que se encuentran día a día", señala un trabajo publicado en 'Journal of Medical Internet Research'.
Internet ofrece una oportunidad única para fomentar este autocuidado y varias herramientas dispuestas en la 'www' han probado suerte con el fin de crear 'pacientes activos'. MyHealth Online, de Carolinas Healthcare System, es una de ellas. Durante 12 semanas, 100 pacientes que padecen asma, diabetes o hipertensión siguieron un programa con las aplicaciones interactivas que ofrece este portal. Otros 100 pacientes, el grupo de control, sólo accedieron a los contenidos educativos.
El diseño de los ejercicios, específico para cada patología, mejoró la activación de los pacientes, que ganaron capacidad y confianza en el manejo de su enfermedad. Este efecto fue más evidente sobre aquellos participantes que partían desde niveles más bajos de activación, según el estudio.
Herramientas como esta, "contribuyen a ampliar la población de pacientes que son capaces de manejan activamente sus patologías", señalan los autores. Además de tener el potencial para fomentar el autocuidado -y de liberar así al sistema sanitario- "los pacientes activos son más propensos a seguir las recomendaciones de los médicos lo que implica una mejor salud", subrayan.
**Publicado en "EL MUNDO"
El síndrome de fatiga crónica es un trastorno de origen desconocido que se suela tratar mediante terapia conductual cognitiva y los pacientes mejoran sustancialmente, en comparación con aquellos que no reciben ningún tratamiento. Pero la dificultad en el acceso a ella, por la escasez de especialistas, "supone un acceso desigual".
Para saltar esta barrera, un grupo de expertos del Wihelmina Children's Hospital (Holanda) decidió explorar el poder de esta terapia cuando se ofrece a través de internet. Sesenta y ocho adolescentes que sufrían este síndrome siguieron este tratamiento virtual durante seis meses y la mejora fue notable.
El 85% ya no sufría fatiga grave y el 78% tenía una función motora normal, comparado con el 27% y el 20%, respectivamente, de aquellos que siguieron con la terapia presencial. El programa, llamado FITNET, también logró que el 75% de los pacientes asistiera al colegio, frente al 16% del grupo control.
Las fortalezas de este tratamiento, que podrían explicar su éxito, son que "está disponible en cualquier momento, evita las barreras del cara a cara (retrasos debido a las dificultades de acceso, problemas con las citas, ausencia en el colegio o el trabajo, desplazamientos hasta la consulta) y reduce los tiempos de terapia y los costes", señalan los autores en las páginas de 'The Lancet'.
-Formando 'pacientes activos'
Además de ser una herramienta terapéutica, también puede ser una plataforma educativa para dotar al enfermo de mayor autonomía. El concepto de 'paciente activo' se refiere a aquél capaz de manejar su enfermedad día a día, aquél que puede tomar decisiones cuando se presentan las complicaciones normales de la enfermedad que padece y que tiene confianza en sus habilidades para hacer todo esto. Los programas 'on-line' pueden fomentar estas capacidades, especialmente en los enfermos crónicos, para reducir así la carga que suponen para el sistema sanitario.
"El cuidado de los pacientes con enfermedades crónicas consume el 78% del coste total de gasto sanitario de EEUU" y esta cifra, debido al envejecimiento de la población y al aumento de algunas patologías, va en aumento. Por eso, "un objetivo crucial del sistema sanitario es proporcionarles las herramientas necesarias para que tomen decisiones informadas sobre los cuidados que necesitan y para resolver los problemas que se encuentran día a día", señala un trabajo publicado en 'Journal of Medical Internet Research'.
Internet ofrece una oportunidad única para fomentar este autocuidado y varias herramientas dispuestas en la 'www' han probado suerte con el fin de crear 'pacientes activos'. MyHealth Online, de Carolinas Healthcare System, es una de ellas. Durante 12 semanas, 100 pacientes que padecen asma, diabetes o hipertensión siguieron un programa con las aplicaciones interactivas que ofrece este portal. Otros 100 pacientes, el grupo de control, sólo accedieron a los contenidos educativos.
El diseño de los ejercicios, específico para cada patología, mejoró la activación de los pacientes, que ganaron capacidad y confianza en el manejo de su enfermedad. Este efecto fue más evidente sobre aquellos participantes que partían desde niveles más bajos de activación, según el estudio.
Herramientas como esta, "contribuyen a ampliar la población de pacientes que son capaces de manejan activamente sus patologías", señalan los autores. Además de tener el potencial para fomentar el autocuidado -y de liberar así al sistema sanitario- "los pacientes activos son más propensos a seguir las recomendaciones de los médicos lo que implica una mejor salud", subrayan.
**Publicado en "EL MUNDO"
A Supercharged Protein Reduces Damage from Heart Attack
Researchers from the University of North Carolina at Chapel Hill reduced damage from a heart attack by 50 percent by enhancing a protective protein found in mice and humans. The study, in which mice were bred to make a supercharged version of the protein focal adhesion kinase, or FAK, appeared March 1 in the online edition of the journal Arteriosclerosis, Thrombosis and Vascular Biology.
"This study shows that we can enhance existing cell survival pathways to protect heart cells during a heart attack," said Joan Taylor, PhD, associate professor in UNC's department of pathology and laboratory medicine. Taylor added that the findings could lead to new treatment approaches for heart attacks and may have broad implications for scientists seeking to manipulate the body's natural defensive systems.
During a heart attack, oxygen-deprived heart cells emit signals that activate the usually inert protein FAK, like the cry of a damsel in distress awakening her sleeping knight. If the gallant FAK arrives in time, it can save the cell and reduce permanent damage to the heart.
Taylor and her colleagues were intrigued by FAK's protective abilities. "We thought if we could activate FAK to a greater extent, then we could better protect those heart cells," said Taylor. Based on their previous studies that defined the signals induced by FAK in heart cells, they reasoned that expression of FAK set to an "always-on" position would eventually suffer uncontrolled inflammation and heart failure. "Simply having more of a good thing isn't always better," said Taylor. "The dynamics of the protein's activities are important to appropriately transmitting those survival signals."
The researchers then adjusted their formula to create a new protein they called "SuperFAK." To enhance its protective abilities without the harmful side effects, SuperFAK was primed for activation -- ready to rush to the scene at the slightest provocation from stressed heart cells -- but remained under the control of the mice's natural feedback systems that would shut it off when the crisis passed.
Mice with SuperFAK showed a much stronger FAK response during a heart attack than mice with the natural protein, and three days later had about 50 percent less heart damage. Critically, SuperFAK deactivated at the appropriate time, so the eight-week follow-up revealed no detrimental effects.
The findings offer evidence that, rather than simply activating or de-activating key proteins, researchers can benefit from a more nuanced approach that taps into the body's natural feedback loops. "I think folks could use this idea to exploit mutations in other molecules -- by thinking about how to modify the protein so that it can be under natural controls," said Taylor. "Negative feedback loops are important because they 'reset' the system."
The findings also may help researchers augment FAK in patients undergoing chemotherapy. Some chemotherapy drugs are known to break down FAK, leaving patients' hearts more vulnerable to damage.
**Source: "SCIENCE DAILY"
"This study shows that we can enhance existing cell survival pathways to protect heart cells during a heart attack," said Joan Taylor, PhD, associate professor in UNC's department of pathology and laboratory medicine. Taylor added that the findings could lead to new treatment approaches for heart attacks and may have broad implications for scientists seeking to manipulate the body's natural defensive systems.
During a heart attack, oxygen-deprived heart cells emit signals that activate the usually inert protein FAK, like the cry of a damsel in distress awakening her sleeping knight. If the gallant FAK arrives in time, it can save the cell and reduce permanent damage to the heart.
Taylor and her colleagues were intrigued by FAK's protective abilities. "We thought if we could activate FAK to a greater extent, then we could better protect those heart cells," said Taylor. Based on their previous studies that defined the signals induced by FAK in heart cells, they reasoned that expression of FAK set to an "always-on" position would eventually suffer uncontrolled inflammation and heart failure. "Simply having more of a good thing isn't always better," said Taylor. "The dynamics of the protein's activities are important to appropriately transmitting those survival signals."
The researchers then adjusted their formula to create a new protein they called "SuperFAK." To enhance its protective abilities without the harmful side effects, SuperFAK was primed for activation -- ready to rush to the scene at the slightest provocation from stressed heart cells -- but remained under the control of the mice's natural feedback systems that would shut it off when the crisis passed.
Mice with SuperFAK showed a much stronger FAK response during a heart attack than mice with the natural protein, and three days later had about 50 percent less heart damage. Critically, SuperFAK deactivated at the appropriate time, so the eight-week follow-up revealed no detrimental effects.
The findings offer evidence that, rather than simply activating or de-activating key proteins, researchers can benefit from a more nuanced approach that taps into the body's natural feedback loops. "I think folks could use this idea to exploit mutations in other molecules -- by thinking about how to modify the protein so that it can be under natural controls," said Taylor. "Negative feedback loops are important because they 'reset' the system."
The findings also may help researchers augment FAK in patients undergoing chemotherapy. Some chemotherapy drugs are known to break down FAK, leaving patients' hearts more vulnerable to damage.
**Source: "SCIENCE DAILY"
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