Las personas con una enfermedad mental suelen ser a menudo relacionadas con conductas violentas cuando, proporcionalmente, este colectivo comete menos delitos que el resto de la población. Pero no queda ahí el desagravio. Según una revisión de estudios, una de cada cuatro personas con este tipo de trastornos ha sufrido un acto violento, lo que supone que sean cuatro veces más propensas que cualquier otro individuo a padecer un abuso.
En torno a medio millón de personas adultas muere cada año por un acto de violencia. Las personas con discapacidad (que suponen el 15% de los adultos de todo el mundo) parecen tener un mayor riesgo de sufrir un hecho violento por diferentes factores: exclusión de la educación y el empleo, necesidad de recibir asistencia personal en su vida diaria, menor defensa física y emocional, barreras en la comunicación, estigma social y discriminación.
"Comprender la magnitud de la violencia contra estos colectivos es el primer paso en salud pública para prevenir la violencia", señalan los autores de una revisión y metaanálisis de 26 estudios que incluían los datos de 21.500 personas con discapacidad de siete países: Australia, Canadá, Nueva Zelanda, Taiwán, Reino Unido, Estados Unidos y Sudáfrica.
Tal y como explica el principal autor de esta revisión, Mark Bellis, de la Universidad John Moores de Liverpool, "aproximadamente el 3% de las personas con un deterioro no específico [físico, mental o emocional, o problemas de salud que conlleven una restricción de las actividades] habrá sufrido un acto violento en los últimos 12 meses, aumentando a casi una cuarta parte cuando hablamos de personas con una enfermedad mental. El tiempo de exposición a la violencia y la proporción de estas personas que son directamente amenazadas o que viven con el temor de llegar a ser una víctima, son sustancialmente mayores de lo que pensábamos".
En concreto, lo que comprobaron al analizar los datos de este análisis, publicado en la revista 'The Lancet', fue que la prevalencia de cualquier acto violento (físico, sexual o de género) fue mayor tanto en los adultos con una enfermedad mental (24,3%) como en aquellos con un deterioro intelectual -deterioro cognitivo, retraso mental o de aprendizaje- (6,1%).
Otro hecho que denuncian los autores de esta revisión es que, a pesar de las cifras, existen pocos estudios que analicen este tipo de actos violentos desde diferentes puntos de vista y, en muchos de ellos, algunos colectivos de víctimas quedan fuera de su interés: "No encontramos ningún estudio sobre la violencia que sufren las personas con un deterioro cognitivo o de aprendizaje en centros institucionales, a pesar de que se considera a estas personas especialmente vulnerables a la violencia", explican. Por otro lado, también ponen de manifiesto que la calidad de los estudios analizados es moderada y la mayor parte de ellos se realiza en países desarrollados cuando las personas con discapacidad más vulnerables a la violencia están en los países de medios o bajos ingresos.
"Aunque se necesitan claramente más investigaciones sobre este tema, la revisión subraya la gravedad de la violencia contra los adultos con algún tipo de discapacidad y sugiere la importancia de coordinar esfuerzos para identificar y responder frente a estos actos violentos", señala un editorial de la revista 'The Lancet'. "Deberían implementarse métodos para detectar a estas víctimas en los centros de salud, programas para las mujeres que han sufrido abusos, y centros de acogida independientes para albergar a un amplio colectivo de personas con discapacidad que hayan experimentado abusos".
**Publicado en "EL MUNDO"
01 March 2012
Gluten-Free, Casein-Free Diet May Help Some Children With Autism, Research Suggests
A gluten-free, casein-free diet may lead to improvements in behavior and physiological symptoms in some children diagnosed with an autism spectrum disorder (ASD), according to researchers at Penn State. The research is the first to use survey data from parents to document the effectiveness of a gluten-free, casein-free diet on children with ASD.
"Research has shown that children with ASD commonly have GI [gastrointestinal] symptoms," said Christine Pennesi, medical student at Penn State College of Medicine. "Notably, a greater proportion of our study population reported GI and allergy symptoms than what is seen in the general pediatric population. Some experts have suggested that gluten- and casein-derived peptides cause an immune response in children with ASD, and others have proposed that the peptides could trigger GI symptoms and behavioral problems."
The team -- which included Laura Cousino Klein, associate professor of biobehavioral health and human development and family studies -- asked 387 parents or primary caregivers of children with ASD to complete a 90-item online survey about their children's GI symptoms, food allergy diagnoses, and suspected food sensitivities, as well as their children's degree of adherence to a gluten-free, casein-free diet. The team's results appeared online this month in the journal Nutritional Neuroscience.
Pennesi and Klein and their team found that a gluten-free, casein-free diet was more effective in improving ASD behaviors, physiological symptoms and social behaviors for those children with GI symptoms and with allergy symptoms compared to those without these symptoms. Specifically, parents noted improved GI symptoms in their children as well as increases in their children's social behaviors, such as language production, eye contact, engagement, attention span, requesting behavior and social responsiveness, when they strictly followed a gluten-free, casein-free diet.
According to Klein, autism may be more than a neurological disease -- it may involve the GI tract and the immune system.
"There are strong connections between the immune system and the brain, which are mediated through multiple physiological symptoms," Klein said. "A majority of the pain receptors in the body are located in the gut, so by adhering to a gluten-free, casein-free diet, you're reducing inflammation and discomfort that may alter brain processing, making the body more receptive to ASD therapies."
The team found that parents who eliminated all gluten and casein from their children's diets reported that a greater number of their children's ASD behaviors, physiological symptoms and social behaviors improved after starting the diet compared to children whose parents did not eliminate all gluten and casein. The team also found that parents who implemented the diet for six months or less reported that the diet was less effective in reducing their child's ASD behaviors.
According to the researchers, some of the parents who filled out the surveys had eliminated only gluten or only casein from their children's diets, but survey results suggested that parents who completely eliminated both gluten and casein from their child's diet reported the most benefit.
"While more rigorous research is needed, our findings suggest that a gluten-free, casein-free diet might be beneficial for some children on the autism spectrum," Pennesi said. "It is also possible that there are other proteins, such as soy, that are problematic for these children."
The reason Klein and Pennesi examined gluten and casein is because they are two of the most common "diet offenders."
"Gluten and casein seem to be the most immunoreactive," Klein said. "A child's skin and blood tests for gluten and casein allergies can be negative, but the child still can have a localized immune response in the gut that can lead to behavioral and psychological symptoms. When you add that in with autism you can get an exacerbation of effects."
Klein's advice to parents of children with ASD?
"If parents are going to try a gluten-free, casein-free diet with their children, they really need to stick to it in order to receive the possible benefits," she said. "It might give parents an opportunity to talk with their physicians about starting a gluten-free, casein-free diet with their children with ASD."
**Published in "SCIENCE DAILY"
"Research has shown that children with ASD commonly have GI [gastrointestinal] symptoms," said Christine Pennesi, medical student at Penn State College of Medicine. "Notably, a greater proportion of our study population reported GI and allergy symptoms than what is seen in the general pediatric population. Some experts have suggested that gluten- and casein-derived peptides cause an immune response in children with ASD, and others have proposed that the peptides could trigger GI symptoms and behavioral problems."
The team -- which included Laura Cousino Klein, associate professor of biobehavioral health and human development and family studies -- asked 387 parents or primary caregivers of children with ASD to complete a 90-item online survey about their children's GI symptoms, food allergy diagnoses, and suspected food sensitivities, as well as their children's degree of adherence to a gluten-free, casein-free diet. The team's results appeared online this month in the journal Nutritional Neuroscience.
Pennesi and Klein and their team found that a gluten-free, casein-free diet was more effective in improving ASD behaviors, physiological symptoms and social behaviors for those children with GI symptoms and with allergy symptoms compared to those without these symptoms. Specifically, parents noted improved GI symptoms in their children as well as increases in their children's social behaviors, such as language production, eye contact, engagement, attention span, requesting behavior and social responsiveness, when they strictly followed a gluten-free, casein-free diet.
According to Klein, autism may be more than a neurological disease -- it may involve the GI tract and the immune system.
"There are strong connections between the immune system and the brain, which are mediated through multiple physiological symptoms," Klein said. "A majority of the pain receptors in the body are located in the gut, so by adhering to a gluten-free, casein-free diet, you're reducing inflammation and discomfort that may alter brain processing, making the body more receptive to ASD therapies."
The team found that parents who eliminated all gluten and casein from their children's diets reported that a greater number of their children's ASD behaviors, physiological symptoms and social behaviors improved after starting the diet compared to children whose parents did not eliminate all gluten and casein. The team also found that parents who implemented the diet for six months or less reported that the diet was less effective in reducing their child's ASD behaviors.
According to the researchers, some of the parents who filled out the surveys had eliminated only gluten or only casein from their children's diets, but survey results suggested that parents who completely eliminated both gluten and casein from their child's diet reported the most benefit.
"While more rigorous research is needed, our findings suggest that a gluten-free, casein-free diet might be beneficial for some children on the autism spectrum," Pennesi said. "It is also possible that there are other proteins, such as soy, that are problematic for these children."
The reason Klein and Pennesi examined gluten and casein is because they are two of the most common "diet offenders."
"Gluten and casein seem to be the most immunoreactive," Klein said. "A child's skin and blood tests for gluten and casein allergies can be negative, but the child still can have a localized immune response in the gut that can lead to behavioral and psychological symptoms. When you add that in with autism you can get an exacerbation of effects."
Klein's advice to parents of children with ASD?
"If parents are going to try a gluten-free, casein-free diet with their children, they really need to stick to it in order to receive the possible benefits," she said. "It might give parents an opportunity to talk with their physicians about starting a gluten-free, casein-free diet with their children with ASD."
**Published in "SCIENCE DAILY"
Genetically Altered Bird Flu Virus Not as Dangerous as Believed, Its Maker Asserts
His new revelations have prompted the United States government to ask that the experiments be re-evaluated by a government advisory panel that recommended in December that certain details of the work be kept secret and not published, for fear that terrorists could use them to make bioweapons. Critics of the work had also warned that the virus might leak out of the lab accidentally and start a pandemic.
“We heard many times that this virus would spread like wildfire if it would come out of our facility,” said Ron Fouchier, the leader of the team that genetically altered the flu virus, at Erasmus Medical Center in Rotterdam, the Netherlands. “We do not think this is the case.”
Dr. Anthony Fauci, head of the National Institute for Allergy and Infectious Diseases, said he also thought that the danger might have been overstated. “There is a gross, pervasive misunderstanding out there,” he said, adding that he had recommended that the data be examined again by the National Science Advisory Board for Biosecurity, overseen by the National Institutes of Health. He said the board would probably reconvene in March.
The experiments involve a type of bird flu virus known as H5N1. It does not often infect people, but appears unusually deadly when it does. Of about 600 known cases since 1997, more than half have been fatal. The exact death rate is not known because some deaths and mild cases may go uncounted. But most researchers think the virus is more deadly than other flu viruses, even the notorious 1918 flu, which killed as many as 50 million people worldwide. But the 1918 flu was highly contagious; so far, bird flu has rarely spread from person to person. People who fall ill have nearly always caught it from poultry.
Dr. Fouchier’s experiments involved ferrets, which are considered a good model for flu research because they react to the virus in much the same way that people do. Researchers can infect ferrets with H5N1 by squirting the virus into their noses or lungs, but then the animals normally do not infect one another. Dr. Fouchier’s team altered the virus genetically so that it could become airborne, and spread from one ferret to another by coughing and sneezing.
Until recently, Dr. Fouchier had not revealed much about what happened to the infected ferrets, in part because he had agreed to keep the details secret until decisions could be made about how much of it to make public. But on Wednesday, at a meeting in Washington of the American Society for Microbiology, he said that when healthy ferrets were exposed to the coughs and sneezes of infected ones, not all became infected. Those that did become infected did not get very sick or die. In addition, he said, if the ferrets were previously exposed to a run-of-the-mill seasonal flu, they were immune to the bird flu.
Most adult humans have had some type of flu, and therefore, Dr. Fouchier said, they may also have some natural protection against bird flu.
But Michael Osterholm, a member of the biosecurity board, warned that ferrets were not a perfect model for what would happen in humans, and that it was impossible to tell how virulent or contagious the new virus would be in people. He said that the board would review any new information with great care and caution.
A version of this article appeared in print on March 1, 2012, on page A6 of the New York edition with the headline: Genetically Altered Bird Flu Virus Not as Dangerous as Believed, Its Maker Asserts.
**Published in "THE NEW YORK TIMES"
“We heard many times that this virus would spread like wildfire if it would come out of our facility,” said Ron Fouchier, the leader of the team that genetically altered the flu virus, at Erasmus Medical Center in Rotterdam, the Netherlands. “We do not think this is the case.”
Dr. Anthony Fauci, head of the National Institute for Allergy and Infectious Diseases, said he also thought that the danger might have been overstated. “There is a gross, pervasive misunderstanding out there,” he said, adding that he had recommended that the data be examined again by the National Science Advisory Board for Biosecurity, overseen by the National Institutes of Health. He said the board would probably reconvene in March.
The experiments involve a type of bird flu virus known as H5N1. It does not often infect people, but appears unusually deadly when it does. Of about 600 known cases since 1997, more than half have been fatal. The exact death rate is not known because some deaths and mild cases may go uncounted. But most researchers think the virus is more deadly than other flu viruses, even the notorious 1918 flu, which killed as many as 50 million people worldwide. But the 1918 flu was highly contagious; so far, bird flu has rarely spread from person to person. People who fall ill have nearly always caught it from poultry.
Dr. Fouchier’s experiments involved ferrets, which are considered a good model for flu research because they react to the virus in much the same way that people do. Researchers can infect ferrets with H5N1 by squirting the virus into their noses or lungs, but then the animals normally do not infect one another. Dr. Fouchier’s team altered the virus genetically so that it could become airborne, and spread from one ferret to another by coughing and sneezing.
Until recently, Dr. Fouchier had not revealed much about what happened to the infected ferrets, in part because he had agreed to keep the details secret until decisions could be made about how much of it to make public. But on Wednesday, at a meeting in Washington of the American Society for Microbiology, he said that when healthy ferrets were exposed to the coughs and sneezes of infected ones, not all became infected. Those that did become infected did not get very sick or die. In addition, he said, if the ferrets were previously exposed to a run-of-the-mill seasonal flu, they were immune to the bird flu.
Most adult humans have had some type of flu, and therefore, Dr. Fouchier said, they may also have some natural protection against bird flu.
But Michael Osterholm, a member of the biosecurity board, warned that ferrets were not a perfect model for what would happen in humans, and that it was impossible to tell how virulent or contagious the new virus would be in people. He said that the board would review any new information with great care and caution.
A version of this article appeared in print on March 1, 2012, on page A6 of the New York edition with the headline: Genetically Altered Bird Flu Virus Not as Dangerous as Believed, Its Maker Asserts.
**Published in "THE NEW YORK TIMES"
Los disruptores endocrinos son unas sustancias tóxicas que hacen que nuestro cuerpo acumule grasa y no músculo
Un estudio ha alertado de que la contaminación no solo provoca enfermedades respiratorias que cada año causan 370.000 muertes en todo el mundo, 16.000 de ellas en España, sino que además propicia la obesidad.
Así lo ha determinado un trabajo del Centro de Investigación Biomédica en Red-Fisiopatológica de la Obesidad y la Nutrición (CIBERobn) tras analizar los disruptores endocrinos (EDCs), unas sustancias tóxicas que hacen que nuestro cuerpo acumule grasa y no músculo, y que están presentes en los alimentos y en multitud de productos de uso cotidiano como champús, perfumes, plásticos y cosméticos que alteran nuestro sistema endocrino.
La mayoría de estos compuestos químicos, que se acumulan en las grasas con facilidad, pertenecen al grupo de contaminantes orgánicos persistentes, unos compuestos químicos (sobre todo pesticidas e insecticidas) poco biodegradables que se mantienen durante décadas en el ambiente y se introducen en la cadena alimenticia.
Buen ejemplo de ello es el DDT, un pesticida prohibido en 1975 y que todavía hoy está presente en el 88 por ciento de la población española, explica el investigador del CIBERobn y presidente de la Sociedad Española de Endocrinología y Nutrición, Javier Salvador.
Como consecuencia de la producción agrícola y la pesca -a través de los vertidos de aguas residuales-, la exposición de los seres vivos a los disruptores endocrinos es universal y se acumulan en la grasa humana de una generación a otra, ya que la madre los pasa al bebé en la gestación y la lactancia.
Los efectos sobre la salud humana de la exposición continua a los EDCs han sido objeto de estudio desde hace décadas, pero ahora el CIBERobn ha avanzado en esta investigación y concluye que contaminación y obesidad están relacionados.
En concreto, estos tóxicos aumentan el riesgo de dos trastornos muy relacionados con la diabetes: el síndrome metabólico y la resistencia a la insulina. Según el doctor Salvador, "la obesidad visceral promueve la liberación de ácidos grasos libres que llegan al hígado y contribuyen a generar resistencia a la insulina, lo que favorece la diabetes".
**AGENCIAS
Así lo ha determinado un trabajo del Centro de Investigación Biomédica en Red-Fisiopatológica de la Obesidad y la Nutrición (CIBERobn) tras analizar los disruptores endocrinos (EDCs), unas sustancias tóxicas que hacen que nuestro cuerpo acumule grasa y no músculo, y que están presentes en los alimentos y en multitud de productos de uso cotidiano como champús, perfumes, plásticos y cosméticos que alteran nuestro sistema endocrino.
La mayoría de estos compuestos químicos, que se acumulan en las grasas con facilidad, pertenecen al grupo de contaminantes orgánicos persistentes, unos compuestos químicos (sobre todo pesticidas e insecticidas) poco biodegradables que se mantienen durante décadas en el ambiente y se introducen en la cadena alimenticia.
Buen ejemplo de ello es el DDT, un pesticida prohibido en 1975 y que todavía hoy está presente en el 88 por ciento de la población española, explica el investigador del CIBERobn y presidente de la Sociedad Española de Endocrinología y Nutrición, Javier Salvador.
Como consecuencia de la producción agrícola y la pesca -a través de los vertidos de aguas residuales-, la exposición de los seres vivos a los disruptores endocrinos es universal y se acumulan en la grasa humana de una generación a otra, ya que la madre los pasa al bebé en la gestación y la lactancia.
Los efectos sobre la salud humana de la exposición continua a los EDCs han sido objeto de estudio desde hace décadas, pero ahora el CIBERobn ha avanzado en esta investigación y concluye que contaminación y obesidad están relacionados.
En concreto, estos tóxicos aumentan el riesgo de dos trastornos muy relacionados con la diabetes: el síndrome metabólico y la resistencia a la insulina. Según el doctor Salvador, "la obesidad visceral promueve la liberación de ácidos grasos libres que llegan al hígado y contribuyen a generar resistencia a la insulina, lo que favorece la diabetes".
**AGENCIAS
Blockade of learning and memory genes may occur early in Alzheimer's disease
A repression of gene activity in the brain appears to be an early event affecting people with Alzheimer's disease, researchers funded by the National Institutes of Health have found. In mouse models of Alzheimer's disease, this epigenetic blockade and its effects on memory were treatable. "These findings provide a glimpse of the brain shutting down the ability to form new memories gene by gene in Alzheimer's disease, and offer hope that we may be able to counteract this process," said Roderick Corriveau, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research.
The study was led by Li-Huei Tsai, Ph.D., who is director of The Picower Institute for Learning and Memory at the Massachusetts Institute of Technology and an investigator at the Howard Hughes Medical Institute. It was published online February 29 in Nature.
Dr. Tsai and her team found that a protein called histone deacetylase 2 (HDAC2) accumulates in the brain early in the course of Alzheimer's disease in mouse models and in people with the disease. HDAC2 is known to tighten up spools of DNA, effectively locking down the genes within and reducing their activity, or expression.
In the mice, the increase in HDAC2 appears to produce a blockade of genes involved in learning and memory. Preventing the build-up of HDAC2 protected the mice from memory loss.
Dr. Tsai and her team examined two mouse models of Alzheimer's around the time that the mice begin to show signs of brain cell degeneration. They found that the mice had higher levels of HDAC2, but not other related HDAC proteins, specifically in the parts of the brain involved in learning and memory. This increase in HDAC2 was associated with a decrease in the expression of neuronal genes that HDAC2 is known to regulate.
Use of a gene therapy approach to reduce the levels of HDAC2 prevented the blockade of gene expression. The treatment also prevented learning and memory impairments in the mice. It did not prevent neuronal death, but it did enhance neuroplasticity -- the ability of neurons to form new connections.
Dr. Tsai and her team also examined HDAC2 levels in autopsied brain tissue from 19 people with Alzheimer's at different stages of the disease, and from seven unaffected individuals. Even in its earliest stages, the disease was associated with higher HDAC2 levels in the learning and memory regions of the brain
"We think that the blockade of gene expression plays a very important role in the cognitive decline associated with Alzheimer's disease," said Dr. Tsai. "The good news is that the blockade is potentially reversible."
Alzheimer's disease is the most common cause of dementia in older adults, and affects as many as 5.1 million Americans. In the most common type of Alzheimer's disease, symptoms usually appear after age 65. A hallmark of the disease is the accumulation of a toxic protein fragment called beta-amyloid in brain cells, which is widely believed to be the initial trigger for neurodegeneration.
Dr. Tsai theorizes that HDAC2 is brought into play by beta-amyloid. Indeed, she and her team found that exposing mouse neurons to beta-amyloid caused them to produce more HDAC2.
"We think beta-amyloid triggers a cascade of damaging reactions. Once of these is to activate HDAC2, which in turn blocks the expression of genes needed for brain plasticity. Once this blockade is in place, it may have a more systemic, chronic effect on the brain," she said.
Vaccines and other therapies aimed at reducing beta-amyloid are in clinical trials. Efforts to reduce HDAC2 may provide a complementary approach to treating Alzheimer's, Dr. Tsai said. She has previously reported that HDAC inhibitor compounds can protect against signs of Alzheimer's disease in mice. A problem with such compounds is that they inhibit not only HDAC2 but related HDAC proteins, leading to broad and potentially toxic effects. The new study supports the possibility of developing drugs more specifically targeted to HDAC2 and the pathology of Alzheimer's disease, Dr. Tsai said. Her team is working to identify HDAC2-specific inhibitors that could be developed into drugs and moved into trials.
The study was led by Li-Huei Tsai, Ph.D., who is director of The Picower Institute for Learning and Memory at the Massachusetts Institute of Technology and an investigator at the Howard Hughes Medical Institute. It was published online February 29 in Nature.
Dr. Tsai and her team found that a protein called histone deacetylase 2 (HDAC2) accumulates in the brain early in the course of Alzheimer's disease in mouse models and in people with the disease. HDAC2 is known to tighten up spools of DNA, effectively locking down the genes within and reducing their activity, or expression.
In the mice, the increase in HDAC2 appears to produce a blockade of genes involved in learning and memory. Preventing the build-up of HDAC2 protected the mice from memory loss.
Dr. Tsai and her team examined two mouse models of Alzheimer's around the time that the mice begin to show signs of brain cell degeneration. They found that the mice had higher levels of HDAC2, but not other related HDAC proteins, specifically in the parts of the brain involved in learning and memory. This increase in HDAC2 was associated with a decrease in the expression of neuronal genes that HDAC2 is known to regulate.
Use of a gene therapy approach to reduce the levels of HDAC2 prevented the blockade of gene expression. The treatment also prevented learning and memory impairments in the mice. It did not prevent neuronal death, but it did enhance neuroplasticity -- the ability of neurons to form new connections.
Dr. Tsai and her team also examined HDAC2 levels in autopsied brain tissue from 19 people with Alzheimer's at different stages of the disease, and from seven unaffected individuals. Even in its earliest stages, the disease was associated with higher HDAC2 levels in the learning and memory regions of the brain
"We think that the blockade of gene expression plays a very important role in the cognitive decline associated with Alzheimer's disease," said Dr. Tsai. "The good news is that the blockade is potentially reversible."
Alzheimer's disease is the most common cause of dementia in older adults, and affects as many as 5.1 million Americans. In the most common type of Alzheimer's disease, symptoms usually appear after age 65. A hallmark of the disease is the accumulation of a toxic protein fragment called beta-amyloid in brain cells, which is widely believed to be the initial trigger for neurodegeneration.
Dr. Tsai theorizes that HDAC2 is brought into play by beta-amyloid. Indeed, she and her team found that exposing mouse neurons to beta-amyloid caused them to produce more HDAC2.
"We think beta-amyloid triggers a cascade of damaging reactions. Once of these is to activate HDAC2, which in turn blocks the expression of genes needed for brain plasticity. Once this blockade is in place, it may have a more systemic, chronic effect on the brain," she said.
Vaccines and other therapies aimed at reducing beta-amyloid are in clinical trials. Efforts to reduce HDAC2 may provide a complementary approach to treating Alzheimer's, Dr. Tsai said. She has previously reported that HDAC inhibitor compounds can protect against signs of Alzheimer's disease in mice. A problem with such compounds is that they inhibit not only HDAC2 but related HDAC proteins, leading to broad and potentially toxic effects. The new study supports the possibility of developing drugs more specifically targeted to HDAC2 and the pathology of Alzheimer's disease, Dr. Tsai said. Her team is working to identify HDAC2-specific inhibitors that could be developed into drugs and moved into trials.
Las múltiples formas de los espermatozoides
De todos los tipos de células en el reino animal, las más diversas son los espermatozoides, que pueden estar adornados con colas, pelos, cerdas y muchos más «accesorios» a cada cual más curioso. Esta variedad de formas de las células germinales masculinas -su increíble aspecto puede verse en las imágenes- se debe a las distintas estrategias reproductivas adoptadas por las especies con reproducción sexual. No todas las especies copulan igual, así que, por lo tanto, los espermatozoides de sus machos se adaptan a la situación.
El equipo dirigido por Lukas Schärer, de la Universidad de Basilea en Suiza, observó con un microscopio la cópula de 16 especies de gusanos hermafrodita (macrostomum), que tienen una variedad de formas de espermatozoides. Después del sexo, algunas especies succionaban el semen, posiblemente como una forma de seleccionar los espermatozoides que son aceptados en última instancia.
Los investigadores, según publicaba Nature, encontraron que las especies que presentan este comportamiento de succión tienen espermatozoides adornados con características tales como un par de largas cerdas que emergen en la mitad y una cola parecida a un pincel. Estos apéndices pueden quedar atrapados en el orificio de las hembras después de la cópula, evitando que los espermatozoides sean absorbidos. Las especies que no retiran los espermatozoides los desarrollan en formas más simples. Tienden a ser más pequeños, sin pelos ni cerdas.
El equipo dirigido por Lukas Schärer, de la Universidad de Basilea en Suiza, observó con un microscopio la cópula de 16 especies de gusanos hermafrodita (macrostomum), que tienen una variedad de formas de espermatozoides. Después del sexo, algunas especies succionaban el semen, posiblemente como una forma de seleccionar los espermatozoides que son aceptados en última instancia.
Los investigadores, según publicaba Nature, encontraron que las especies que presentan este comportamiento de succión tienen espermatozoides adornados con características tales como un par de largas cerdas que emergen en la mitad y una cola parecida a un pincel. Estos apéndices pueden quedar atrapados en el orificio de las hembras después de la cópula, evitando que los espermatozoides sean absorbidos. Las especies que no retiran los espermatozoides los desarrollan en formas más simples. Tienden a ser más pequeños, sin pelos ni cerdas.
**NATURE
New infant formula ingredients boost babies' immunity by feeding their gut bacteria
Adding prebiotic ingredients to infant formula helps colonize the newborn's gut with a stable population of beneficial bacteria, and probiotics enhance immunity in formula-fed infants, two University of Illinois studies report. "The beneficial bacteria that live in a baby's intestine are all-important to an infant's health, growth, and ability to fight off infections," said Kelly Tappenden, a U of I professor of nutrition and gastrointestinal physiology. "Breast-fed babies acquire this protection naturally. Formula-fed infants get sick more easily because the bacteria in their gut are always changing."
The idea is to make formula more like breast milk by promoting the sorts of intestinal bacteria that live in breast-fed babies' intestines, she added.
Prebiotics are carbohydrates that resist digestion by human enzymes and stimulate the growth and activity of beneficial bacteria in the gastrointestinal tract.
-Probiotics are actual live bacteria that are beneficial to intestinal health, she said.
Infants have a special need for stimulation of their gut microbiota because they are born with a sterile intestine, Tappenden said.
"A strong, robust population of microbes in the gut provides colonization resistance, and pathogens can't invade and infect an infant who has that resistance as easily," she added.
The researchers compared the effects of feeding pre- and probiotics with infants fed breast milk and control formulas. They also compared the enhanced formulas' effects in both vaginally and Caesarean-delivered babies.
"The probiotic formula significantly enhanced immunity in formula-fed infants," Tappenden said.
Also, babies delivered by C-section had an especially improved immune response, an important finding because C-section babies are a more vulnerable group, she said.
Why? "Babies delivered naturally are exposed to the mother's bacteria as they travel through the birth canal, and they develop a healthier population of gut bacteria as a result. Babies delivered by C-section enter a sterile environment, and their gut microbiota is quite different," Tappenden noted.
In the probiotics study, scientists at five sites divided 172 healthy six-week-old infants into two formula-fed groups and a breast-fed group. Beginning at six weeks of age, the formula-fed groups received either a control formula or a formula that contained the beneficial bacteria Bifidobacterium animalis subspecies lactis (Bb12) for a six-week period. The infants receiving the probiotic formula had increased concentrations of secretory, anti-rotavirus, and anti-poliovirus-specific immunoglobulin A (IgA).
Fecal samples from babies receiving the probiotic formula revealed significantly heightened immunity, especially among Caesarian-delivered infants, Tappenden said.
Infants who consumed the formula containing the prebiotic ingredients also benefited. In that study, 139 healthy babies were divided into three groups. Breast-fed infants were compared with babies fed either a control formula or a formula supplemented with galacto- and fructo-oligosaccharides for six weeks.
Oligosaccharides, found in breast milk, contribute to the healthy population of bacteria found in the guts of breast-fed infants.
When fecal samples were tested, babies fed the prebiotic formula showed modest improvement in the number of beneficial bacteria and decreases in the types of bacteria that are often associated with illness.
**Source: University of Illinois College of Agricultural, Consumer and Environmental Sciences
The idea is to make formula more like breast milk by promoting the sorts of intestinal bacteria that live in breast-fed babies' intestines, she added.
Prebiotics are carbohydrates that resist digestion by human enzymes and stimulate the growth and activity of beneficial bacteria in the gastrointestinal tract.
-Probiotics are actual live bacteria that are beneficial to intestinal health, she said.
Infants have a special need for stimulation of their gut microbiota because they are born with a sterile intestine, Tappenden said.
"A strong, robust population of microbes in the gut provides colonization resistance, and pathogens can't invade and infect an infant who has that resistance as easily," she added.
The researchers compared the effects of feeding pre- and probiotics with infants fed breast milk and control formulas. They also compared the enhanced formulas' effects in both vaginally and Caesarean-delivered babies.
"The probiotic formula significantly enhanced immunity in formula-fed infants," Tappenden said.
Also, babies delivered by C-section had an especially improved immune response, an important finding because C-section babies are a more vulnerable group, she said.
Why? "Babies delivered naturally are exposed to the mother's bacteria as they travel through the birth canal, and they develop a healthier population of gut bacteria as a result. Babies delivered by C-section enter a sterile environment, and their gut microbiota is quite different," Tappenden noted.
In the probiotics study, scientists at five sites divided 172 healthy six-week-old infants into two formula-fed groups and a breast-fed group. Beginning at six weeks of age, the formula-fed groups received either a control formula or a formula that contained the beneficial bacteria Bifidobacterium animalis subspecies lactis (Bb12) for a six-week period. The infants receiving the probiotic formula had increased concentrations of secretory, anti-rotavirus, and anti-poliovirus-specific immunoglobulin A (IgA).
Fecal samples from babies receiving the probiotic formula revealed significantly heightened immunity, especially among Caesarian-delivered infants, Tappenden said.
Infants who consumed the formula containing the prebiotic ingredients also benefited. In that study, 139 healthy babies were divided into three groups. Breast-fed infants were compared with babies fed either a control formula or a formula supplemented with galacto- and fructo-oligosaccharides for six weeks.
Oligosaccharides, found in breast milk, contribute to the healthy population of bacteria found in the guts of breast-fed infants.
When fecal samples were tested, babies fed the prebiotic formula showed modest improvement in the number of beneficial bacteria and decreases in the types of bacteria that are often associated with illness.
**Source: University of Illinois College of Agricultural, Consumer and Environmental Sciences
Subscribe to:
Comments (Atom)