What do sweaty palms and abnormal heart rhythms have in common? Both can be initiated by the nervous system during an adrenaline-driven "flight-or-fight" stress reaction, when the body senses danger. Hyperhidrosis, an abnormal flight-or-fight response of the sympathetic nervous system that causes excessively sweaty palms may also contribute to problems like dangerous irregular rhythms from the lower chambers of the heart, known as ventricular arrhythmias.
UCLA cardiologists have now found that surgery to snip nerves associated with the sympathetic nervous system on both the left and right sides of the chest may be helpful in stopping dangerous, incessant ventricular arrhythmias -- known as an "electrical storm" -- when other treatment methods have failed. This same type of surgery has been used for years to alleviate hyperhidrosis.
The UCLA team's findings are reported in the Dec. 27-Jan. 3 issue of the Journal of the American College of Cardiology. The study is one of the first to assess the impact of bilateral cardiac sympathetic denervation (BCSD), surgery on both sides of the heart, to control arrhythmias. The research builds on previous work at UCLA in which a similar procedure was performed only on the left side. But for some patients to obtain relief, the researchers said, it must be done bilaterally.
Many people suffer from ventricular arrhythmias, one of the leading causes of death in the U.S. (400,000 deaths per year). These arrhythmias can usually be controlled by using medications, an implantable cardioverter defibrillator that automatically shocks the heart back into normal rhythm, or a procedure called catheter ablation, which involves a targeted burn to the tiny area of the heart causing the irregular heart beat.
"When these treatment options fail, especially for a patient experiencing a life-threatening electrical storm, the situation becomes critical," said the study's senior author, Dr. Kalyanam Shivkumar, director of the UCLA Cardiac Arrhythmia Center and co-director of the Oppenheimer Family Center for Neurobiology of Stress at UCLA. "We are always seeking additional options to help patients."
The UCLA findings add to a growing field of research on the sympathetic nervous system's impact on stress and its possible role in disease. Shivkumar noted that this research may provide a unique opportunity; if snipping the cardiac sympathetic nerve proves to effectively alleviate irregular heart rhythms, perhaps the treatment could be initiated early, before the condition manifests itself.
"In the future, we may be able to correct what is wrong with the heart early, like fixing what's broken in an airplane engine before we need a 'parachute,' like an implantable defibrillator," said Shivkumar, who is also a professor of medicine and radiological sciences at the David Geffen School of Medicine at UCLA.
During the procedure, surgeons cut the stellate ganglia, part of the sympathetic nervous system that delivers information to the body about stress and initiates the flight-or-fight response. These ganglia contain thousands of nerve-cell bodies and run along either side of the spinal cord in long chains. From the ganglia, nerves then travel to the heart.
To help control arrhythmias, surgeons snip the stellate ganglion, as well as the three ganglia directly below it, to completely remove the nerves destined for the heart. The procedure can be done on the left, on the right or on both sides of the thorax -- the area of the body between the neck and the abdomen that contains organs such as the heart and lungs.
For the study, researchers reviewed records from patients at UCLA and a collaborating center in France. The patients all presented with electrical storms. Their average age was 60, and all were poor candidates for heart transplants. After other treatments -- including medications, catheter ablation and implantable defibrillators -- had failed, the patients underwent surgery to snip the cardiac sympathetic nerves destined for both sides of the heart.
Researchers found that after the surgery, four of the six patients responded completely, with no more arrhythmias. One patient had a partial response, and one had no response at all.
With their heart rhythms stabilized, three of the responding patients received no more shocks from their defibrillators, which would previously occur when the devices tried to normalize irregular rhythms. One of these patients had been experiencing approximately 11 shocks a day. The patient who partially responded to treatment had a shock reduction of more than 50 percent.
All five responding patients survived until hospital discharge; two died after discharge as a result of health issues not related to arrhythmias. No major operative complications occurred in the patients studied, and typical side-effects related to the procedure, such as alterations in sweating or temperature regulation, were not significant. Researchers noted that such side-effects are usually acceptable to seriously ill patients experiencing an electrical storm, considering that the alternatives include continued arrhythmias, defibrillator shocks or death.
*Source: University of California - Los Angeles Health Sciences
20 December 2011
La neuroimagen y la estimulación cerebral abren nuevas esperanzas contra la depresión
Una de cada seis personas padece depresión clínica al menos una vez en su vida y un 7% de la población sufre esta enfermedad al cabo del año. La extensión de este problema psiquiátrico ha hecho que tenga un impacto sobre la salud pública similar al de enfermedades crónicas como la artritis o la diabetes. Sin embargo, a menudo se pasa por alto o se confunde con una simple y natural tristeza.
Una completa revisión de los estudios publicados entre 2005 y 2010, recién publicada en la revista 'The Lancet', ha determinado que se han producido "avances claros" en este tiempo a nivel de investigación, aunque sigue sin haber tratamientos "completamente satisfactorios para la depresión mayor".
El problema es que, aunque esta enfermedad puede curarse, la mayoría de los pacientes requieren probar sucesivos tratamientos y combinar terapias hasta encontrar una clara mejoría. Uno de los trabajos que se revisan -llamado STAR*D y definido como "el mayor estudio sobre depresión jamás realizado fuera de la industria farmacéutica"- arrojó resultados reveladores.
"El objetivo era la remisión [de la enfermedad] y no sólo la respuesta. Las tasas de remisión en pasos del primero al cuarto fueron desalentadoras (...), con una remisión acumulada del 67% tras los cuatro pasos", indican el investigador David J. Kupfer, del Centro Médico de la Universidad de Pittsburgh (EEUU) y sus coautores.
No obstante, la revisión confirma que tanto los fármacos como la psicoterapia son "efectivos" contra la depresión clínica, "solos o en combinación". "La depresión, con un tratamiento adecuado, se cura, y los pacientes pueden llevar una vida absolutamente normal", resuelve el doctor José Luis Carrasco, jefe de la unidad de Trastornos de la Personalidad en el Hospital Clínico San Carlos de Madrid.
Sin embargo, esta enfermedad psiquiátrica corre el riesgo de pasar inadvertida, sobre todo si se produce en combinación con una dolencia física de gravedad. Así lo resalta la mencionada revisión: "Una implicación crucial es que los servicios de Atención Primaria no deberían ignorar la presencia de depresión en pacientes que tienen un desorden físico crónico ", insisten Kupfer y sus colegas.
"Es habitual que en enfermedades crónicas el porcentaje de depresión clínica esté entre el 30% y el 40%", detalla Carrasco. "No es que tengan una reacción de tristeza, que sería normal, sino que están deseando que todo se acabe y morirse. Esto dificulta el tratamiento, empeora sus hábitos, induce al consumo de tóxicos como el alcohol y empeora el pronóstico de la enfermedad", añade.
-Áreas de vanguardia
La revisión de 'The Lancet' también menciona áreas de vanguardia en el estudio y el tratamiento de la depresión mayor. Entre ellas destacan varias investigaciones en el campo de la neurobiología, como la búsqueda de genes asociados a esta enfermedad -o a la respuesta del paciente a los fármacos- y las técnicas de neuromiagen, que han detectado áreas del cerebro relacionadas con los estados de depresión clínica. "Sin embargo, el grado en que los hallazgos de estudios neurobiológicos pueden ayudar a mejorar la respuesta clínica y funcional de las personas con esta enfermedad es todavía incierto", admiten los autores.
Destacan, sin embargo, la estimulación cerebral profunda como una importante esperanza en el tratamiento de la depresión. El doctor Carrasco se muestra de acuerdo con esta afirmación, aunque matiza que la técnica aún "está verde, en el sentido de que no se sabe bien dónde y cuándo estimular. Es prometedora pero hay que afinarla".
Los autores de la revisión también se han topado con diversas publicaciones en torno al supuesto riesgo de suicidio derivado de los inhibidores de la recaptación de serotonina, un tratamiento habitual contra la depresión cuya seguridad han puesto en duda algunos estudios. Estiman, sin embargo, que no existen datos concluyentes sobre este efecto. Más contundente se muestra el doctor Carrasco: "Los psiquiatras tenemos muy claro que los inhibidores reducen los suicidios. Es al revés, los pacientes se suicidan si no les das medicación ".
Este experto matiza, en todo caso, que las dos primeras semanas de tratamiento -cuando el paciente "aún no tiene el efecto antidepresivo y se siente más agitado"- requieren un seguimiento exhaustivo, sobre todo con adolescentes. "Pero esto se ha sabido siempre", asegura.
**Publicado en "EL MUNDO"
Una completa revisión de los estudios publicados entre 2005 y 2010, recién publicada en la revista 'The Lancet', ha determinado que se han producido "avances claros" en este tiempo a nivel de investigación, aunque sigue sin haber tratamientos "completamente satisfactorios para la depresión mayor".
El problema es que, aunque esta enfermedad puede curarse, la mayoría de los pacientes requieren probar sucesivos tratamientos y combinar terapias hasta encontrar una clara mejoría. Uno de los trabajos que se revisan -llamado STAR*D y definido como "el mayor estudio sobre depresión jamás realizado fuera de la industria farmacéutica"- arrojó resultados reveladores.
"El objetivo era la remisión [de la enfermedad] y no sólo la respuesta. Las tasas de remisión en pasos del primero al cuarto fueron desalentadoras (...), con una remisión acumulada del 67% tras los cuatro pasos", indican el investigador David J. Kupfer, del Centro Médico de la Universidad de Pittsburgh (EEUU) y sus coautores.
No obstante, la revisión confirma que tanto los fármacos como la psicoterapia son "efectivos" contra la depresión clínica, "solos o en combinación". "La depresión, con un tratamiento adecuado, se cura, y los pacientes pueden llevar una vida absolutamente normal", resuelve el doctor José Luis Carrasco, jefe de la unidad de Trastornos de la Personalidad en el Hospital Clínico San Carlos de Madrid.
Sin embargo, esta enfermedad psiquiátrica corre el riesgo de pasar inadvertida, sobre todo si se produce en combinación con una dolencia física de gravedad. Así lo resalta la mencionada revisión: "Una implicación crucial es que los servicios de Atención Primaria no deberían ignorar la presencia de depresión en pacientes que tienen un desorden físico crónico ", insisten Kupfer y sus colegas.
"Es habitual que en enfermedades crónicas el porcentaje de depresión clínica esté entre el 30% y el 40%", detalla Carrasco. "No es que tengan una reacción de tristeza, que sería normal, sino que están deseando que todo se acabe y morirse. Esto dificulta el tratamiento, empeora sus hábitos, induce al consumo de tóxicos como el alcohol y empeora el pronóstico de la enfermedad", añade.
-Áreas de vanguardia
La revisión de 'The Lancet' también menciona áreas de vanguardia en el estudio y el tratamiento de la depresión mayor. Entre ellas destacan varias investigaciones en el campo de la neurobiología, como la búsqueda de genes asociados a esta enfermedad -o a la respuesta del paciente a los fármacos- y las técnicas de neuromiagen, que han detectado áreas del cerebro relacionadas con los estados de depresión clínica. "Sin embargo, el grado en que los hallazgos de estudios neurobiológicos pueden ayudar a mejorar la respuesta clínica y funcional de las personas con esta enfermedad es todavía incierto", admiten los autores.
Destacan, sin embargo, la estimulación cerebral profunda como una importante esperanza en el tratamiento de la depresión. El doctor Carrasco se muestra de acuerdo con esta afirmación, aunque matiza que la técnica aún "está verde, en el sentido de que no se sabe bien dónde y cuándo estimular. Es prometedora pero hay que afinarla".
Los autores de la revisión también se han topado con diversas publicaciones en torno al supuesto riesgo de suicidio derivado de los inhibidores de la recaptación de serotonina, un tratamiento habitual contra la depresión cuya seguridad han puesto en duda algunos estudios. Estiman, sin embargo, que no existen datos concluyentes sobre este efecto. Más contundente se muestra el doctor Carrasco: "Los psiquiatras tenemos muy claro que los inhibidores reducen los suicidios. Es al revés, los pacientes se suicidan si no les das medicación ".
Este experto matiza, en todo caso, que las dos primeras semanas de tratamiento -cuando el paciente "aún no tiene el efecto antidepresivo y se siente más agitado"- requieren un seguimiento exhaustivo, sobre todo con adolescentes. "Pero esto se ha sabido siempre", asegura.
**Publicado en "EL MUNDO"
Salk discovery may lead to safer treatments for asthma, allergies and arthritis
Scientists have discovered a missing link between the body's biological clock and sugar metabolism system, a finding that may help avoid the serious side effects of drugs used for treating asthma, allergies and arthritis. In a paper published last week in Nature, scientists at the Salk Institute for Biological Studies report finding that proteins that control the body's biological rhythms, known as cryptochromes, also interact with metabolic switches that are targeted by certain anti-inflammatory drugs.
The finding suggests that side effects of current drugs might be avoided by considering patients' biological rhythms when administering drugs, or by developing new drugs that target the cryptochromes.
"We knew that our sleep and wake cycle are tied to when our bodies process nutrients, but how this happened at the genetic and molecular level was a complete mystery," says Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, who led the research team. "Now we've found the link between these two important systems, which could serve as a model for how other cellular processes are linked and could hold promise for better therapies."
Glucocorticoids are steroid hormones that occur naturally in the body and help control the amount of sugar in a person's blood, so that nutrient levels rise in the morning to fuel daily activities and fall again at night. They function in cells by interacting with glucocorticoid receptors, molecular switches on the outside of the nucleus, which Evans first discovered in 1985.
Glucocorticoids also play a role in regulating inflammation and are used as anti-inflammatory drugs for diseases caused by an overactive immune system, such as allergies, asthma and rheumatoid arthritis. They are also used to treat inflammation in cancer patients.
However, because of their role in sugar metabolism, the steroids can disrupt a person's normal metabolism, resulting in dangerous side effects, including excessively high blood sugar levels, insulin resistance and diabetic complications.
The Salk researchers may have found a way around these side effects by discovering a new function for cryptochromes 1 and 2, proteins that were previously known for their function in the biological clock.
The cryptochromes serve as breaks to slow the clock's activity, signaling our biological systems to wind down each evening. In the morning, they stop inhibiting the clock's activity, helping our physiology ramp up for the coming day.
In their new study on mouse cells, Evans and his colleagues made the surprising discovery that cryptochromes also interact with glucocorticoid receptors, helping to regulate how the body stores and uses sugar.
"We found that not only are the crytopchromes essential to the functioning of the circadian clock, they regulate glucocorticoid action, and thus are central to how the clock interacts with our daily metabolism of nutrients," says Katja A. Lamia, an assistant professor at The Scripps Research Institute and former post-doctoral researcher in Evan's laboratory at Salk.
Mouse cells function much like human cells, so the findings could have important implications for treatment of autoimmune diseases and cancer. By taking into account the daily rise and fall of cryptochrome levels, the scientists say, doctors might be able to better time administration of glucocorticoid drugs to avoid certain side effects related to sugar metabolism.
The discovery also raises the possibility of developing new anti-inflammatory drugs that avoid some side effects by targeting cryptochromes instead of directly targeting the glucocorticoid switches.
More broadly, Evans says, the study may help explain the connection between sleep and nutrient metabolism in our bodies, including why people with jobs that require night work or erratic hours are at higher risk for obesity and diabetes.
"Disrupting the normal day-night cycle of activity may prevent a person's biological clock from synchronizing correctly with their daily patterns of nutrient metabolism," Evans says. "As a result, the body might not store and process sugar normally, leading to metabolic disease."
The finding suggests that side effects of current drugs might be avoided by considering patients' biological rhythms when administering drugs, or by developing new drugs that target the cryptochromes.
"We knew that our sleep and wake cycle are tied to when our bodies process nutrients, but how this happened at the genetic and molecular level was a complete mystery," says Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, who led the research team. "Now we've found the link between these two important systems, which could serve as a model for how other cellular processes are linked and could hold promise for better therapies."
Glucocorticoids are steroid hormones that occur naturally in the body and help control the amount of sugar in a person's blood, so that nutrient levels rise in the morning to fuel daily activities and fall again at night. They function in cells by interacting with glucocorticoid receptors, molecular switches on the outside of the nucleus, which Evans first discovered in 1985.
Glucocorticoids also play a role in regulating inflammation and are used as anti-inflammatory drugs for diseases caused by an overactive immune system, such as allergies, asthma and rheumatoid arthritis. They are also used to treat inflammation in cancer patients.
However, because of their role in sugar metabolism, the steroids can disrupt a person's normal metabolism, resulting in dangerous side effects, including excessively high blood sugar levels, insulin resistance and diabetic complications.
The Salk researchers may have found a way around these side effects by discovering a new function for cryptochromes 1 and 2, proteins that were previously known for their function in the biological clock.
The cryptochromes serve as breaks to slow the clock's activity, signaling our biological systems to wind down each evening. In the morning, they stop inhibiting the clock's activity, helping our physiology ramp up for the coming day.
In their new study on mouse cells, Evans and his colleagues made the surprising discovery that cryptochromes also interact with glucocorticoid receptors, helping to regulate how the body stores and uses sugar.
"We found that not only are the crytopchromes essential to the functioning of the circadian clock, they regulate glucocorticoid action, and thus are central to how the clock interacts with our daily metabolism of nutrients," says Katja A. Lamia, an assistant professor at The Scripps Research Institute and former post-doctoral researcher in Evan's laboratory at Salk.
Mouse cells function much like human cells, so the findings could have important implications for treatment of autoimmune diseases and cancer. By taking into account the daily rise and fall of cryptochrome levels, the scientists say, doctors might be able to better time administration of glucocorticoid drugs to avoid certain side effects related to sugar metabolism.
The discovery also raises the possibility of developing new anti-inflammatory drugs that avoid some side effects by targeting cryptochromes instead of directly targeting the glucocorticoid switches.
More broadly, Evans says, the study may help explain the connection between sleep and nutrient metabolism in our bodies, including why people with jobs that require night work or erratic hours are at higher risk for obesity and diabetes.
"Disrupting the normal day-night cycle of activity may prevent a person's biological clock from synchronizing correctly with their daily patterns of nutrient metabolism," Evans says. "As a result, the body might not store and process sugar normally, leading to metabolic disease."
**Source: Salk Institute
Deporte de élite y riesgo de osteoporosis
Los hombres que son deportistas de élite y que juegan al fútbol, rugby o hockey sobre hielo, tienen más riesgo de desarrollar osteoporosis de cadera y de rodilla que aquellos que realizan poco o nada de ejercicio, según revela un estudio publicado en el American Journal of Sports Medicine.
«La osteoporosis de cadera o de rodilla (...) se encuentra con más frecuencia en exdeportistas de élite», ha aseverado uno de los artífices del estudio, Magnus Tveit, de la Universidad Lund de Suecia. Así, los observadores reconocen que existe el doble de riesgo de padecer esta dolencia en aquellos que practican fútbol y balonmano, y el triple en los que juegan hockey sobre hielo.
En el estudio participaron 700 deportistas suecos retirados ya del mundo profesional y en edades comprendidas entre los 50 y 93 años y cerca de 1.4000 hombres que practicaban poco o nada de ejercicio. De esta manera, los resultados señalaron que el riesgo de padecer una osteoporosis de cadera o de rodilla era más alto (en un 85%) en deportistas profesionales. Mientras que el riesgo era menor (19%) en los que habían hecho poco o nada de deporte.
En este sentido, un experto en Medicina de la Universidad de Iowa (EE.UU.), Joseph Buckwalter, ha reconocido que, a pesar de que «el ejercicio físico es importante para la salud y para encontrarse bien», existen prácticas deportivas que pueden suponer «riesgo de sufrir daños». De este modo, expertos apuntan a deportes como natación, ciclismo y yoga como alternativa.
*AGENCIAS
«La osteoporosis de cadera o de rodilla (...) se encuentra con más frecuencia en exdeportistas de élite», ha aseverado uno de los artífices del estudio, Magnus Tveit, de la Universidad Lund de Suecia. Así, los observadores reconocen que existe el doble de riesgo de padecer esta dolencia en aquellos que practican fútbol y balonmano, y el triple en los que juegan hockey sobre hielo.
En el estudio participaron 700 deportistas suecos retirados ya del mundo profesional y en edades comprendidas entre los 50 y 93 años y cerca de 1.4000 hombres que practicaban poco o nada de ejercicio. De esta manera, los resultados señalaron que el riesgo de padecer una osteoporosis de cadera o de rodilla era más alto (en un 85%) en deportistas profesionales. Mientras que el riesgo era menor (19%) en los que habían hecho poco o nada de deporte.
En este sentido, un experto en Medicina de la Universidad de Iowa (EE.UU.), Joseph Buckwalter, ha reconocido que, a pesar de que «el ejercicio físico es importante para la salud y para encontrarse bien», existen prácticas deportivas que pueden suponer «riesgo de sufrir daños». De este modo, expertos apuntan a deportes como natación, ciclismo y yoga como alternativa.
*AGENCIAS
MU researchers find pet kidney injuries are similar to human kidney injuries
When evaluating early kidney injuries in people, doctors monitor blood level increases of creatinine, a waste product of muscle breakdown, to understand the severity of the injury. Creatinine is filtered by the kidneys, and small increases are an indication of early damage to vital kidney function. For pets suffering critical illness or injury, University of Missouri researchers have found that even tiny increases of creatinine in blood also could indicate acute kidney damage. Using human blood measurement guidelines for acute kidney injuries, the researchers believe they can now help pet owners better know the severity of their animals' illness. "The concept of monitoring creatinine for kidney disease in dogs is not new to veterinary medicine," said Marie Kerl, associate teaching professor in the department of veterinary medicine and surgery in the MU College of Veterinary Medicine. "Dog kidneys and human kidneys function the same way; there are only slight structural differences. In people hospitalized with any critical illness, acute kidney injury can develop even if kidney function was normal at admission. Doctors can determine whether kidney injury is occurring by seeing even very small increases in creatinine previously thought to be insignificant. We undertook a study to determine if critically ill dogs showed a similar risk of early kidney injury. If a pet is hit by a car or attacked by a larger animal causing multiple injuries, the kidneys are very susceptible to damage since 25 percent of an animal's blood passes through the kidneys with every heartbeat."
Kerl and her colleagues performed a retrospective study of creatinine change in 164 injured dogs admitted to the intensive care unit at the University of Missouri Veterinary Medical Teaching Hospital. Researchers compared the animal medical records and creatinine levels to criteria used to evaluate human acute kidney injury. The researchers then developed a veterinary acute kidney injury staging system, which would indicate to veterinarians how increases of creatinine correspond to the animal's risk of death.
"One difference between human and animal medicine is that pet owners may have a different tolerance for how far they want to go with treatment," Kerl said. "Cost is always a concern, and while some animals can get better, many animals with multiple injuries will not. This kidney evaluation staging system would be another way for veterinarians to share recommendations based on the probable outcomes."
Kerl's paper, "Characterization of acute kidney injury in hospitalized dogs and evaluation of a veterinary acute kidney injury staging system," was published in the Journal of Veterinary Emergency and Critical Care. Co-authors include Meredith Thoen, who completed residency training in the MU Department of Veterinary Medicine and Surgery.
The research reported in the published paper is part of Mizzou Advantage, the five unique areas that set MU apart from other universities. The project contributes to the "One Health/One Medicine: The Convergence of Human and Animal Health," which expands on MU's pioneering work in the convergence of human and animal health and connects it with research and instruction in health care delivery, health policy, medical ethics, health care business models and the culture of healthy living.
Kerl and her colleagues performed a retrospective study of creatinine change in 164 injured dogs admitted to the intensive care unit at the University of Missouri Veterinary Medical Teaching Hospital. Researchers compared the animal medical records and creatinine levels to criteria used to evaluate human acute kidney injury. The researchers then developed a veterinary acute kidney injury staging system, which would indicate to veterinarians how increases of creatinine correspond to the animal's risk of death.
"One difference between human and animal medicine is that pet owners may have a different tolerance for how far they want to go with treatment," Kerl said. "Cost is always a concern, and while some animals can get better, many animals with multiple injuries will not. This kidney evaluation staging system would be another way for veterinarians to share recommendations based on the probable outcomes."
Kerl's paper, "Characterization of acute kidney injury in hospitalized dogs and evaluation of a veterinary acute kidney injury staging system," was published in the Journal of Veterinary Emergency and Critical Care. Co-authors include Meredith Thoen, who completed residency training in the MU Department of Veterinary Medicine and Surgery.
The research reported in the published paper is part of Mizzou Advantage, the five unique areas that set MU apart from other universities. The project contributes to the "One Health/One Medicine: The Convergence of Human and Animal Health," which expands on MU's pioneering work in the convergence of human and animal health and connects it with research and instruction in health care delivery, health policy, medical ethics, health care business models and the culture of healthy living.
**Source: University of Missouri-Columbia
Un estudio hecho en Italia afirma que comer poco mantiene joven el cerebro
Desde hace tiempo, distintas investigaciones científicas han coincidido en que, para mantenerse joven y conservar el cerebro en plena forma, no hay fórmula más eficaz que comer menos. Sin embargo, el mecanismo molecular preciso que hay detrás de los efectos positivos de una dieta hipocalórica seguía siendo un misterio. Ahora, un grupo de investigadores italianos de la Universidad Católica del Sagrado Corazón en Roma ha descubierto en el cerebro de los ratones una molécula, llamada CREB1, provocada por la restricción calórica, que activa los genes relacionados con la longevidad y el funcionamiento apropiado del cerebro. La investigación, que aparece publicada en la revista Proceedings de la Academia Nacional de Ciencias de EE.UU., podría dar lugar a nuevos fármacos que permitieran activar esta molécula «mágica» sin necesidad de pasar hambre.
Los ratones que participan en los experimentos y están sometidos a restricción calórica solo pueden comer hasta un 70% de los alimentos que consumen normalmente, una manera conocida -al menos de forma experimental- de prolongar la vida. Por lo general, si comen poco, los ratones no se convierten en obesos ni desarrollan diabetes, además de mostrar un mayor rendimiento cognitivo, más memoria y ser menos agresivos. Además, no desarrollan -y si lo hacen, sucede mucho más tarde-, la enfermedad de Alzheimer.
-Futuras terapias
El equipo italiano descubrió que la molécula CREB1, que regula importantes funciones cerebrales como la memoria, el aprendizaje y el control de la ansiedad, se activa por la restricción calórica y provoca beneficios en el cerebro al «encender» a su vez otro grupo de moléculas relacionadas con la longevidad, las sirtuinas. Por otra parte, los investigadores se dieron cuenta de que la acción de CREB1 puede aumentar drásticamente por la mera reducción de la ingesta calórica y que la molécula es esencial para que ésta «funcione» en el cerebro. Es decir, los ratones que carecen de esta molécula no se ven premiados por los beneficios de comer menos y muestran las mismas discapacidades que sus compañeros viejos o sobrealimentados.
«Este descubrimiento tiene importantes implicaciones para desarrollar futuras terapias para mantener el cerebro joven y prevenir su degeneración y el proceso de envejecimiento», concluye Giovambattista Pani, responsable del estudio.
**Publicado en "ABC"
Los ratones que participan en los experimentos y están sometidos a restricción calórica solo pueden comer hasta un 70% de los alimentos que consumen normalmente, una manera conocida -al menos de forma experimental- de prolongar la vida. Por lo general, si comen poco, los ratones no se convierten en obesos ni desarrollan diabetes, además de mostrar un mayor rendimiento cognitivo, más memoria y ser menos agresivos. Además, no desarrollan -y si lo hacen, sucede mucho más tarde-, la enfermedad de Alzheimer.
-Futuras terapias
El equipo italiano descubrió que la molécula CREB1, que regula importantes funciones cerebrales como la memoria, el aprendizaje y el control de la ansiedad, se activa por la restricción calórica y provoca beneficios en el cerebro al «encender» a su vez otro grupo de moléculas relacionadas con la longevidad, las sirtuinas. Por otra parte, los investigadores se dieron cuenta de que la acción de CREB1 puede aumentar drásticamente por la mera reducción de la ingesta calórica y que la molécula es esencial para que ésta «funcione» en el cerebro. Es decir, los ratones que carecen de esta molécula no se ven premiados por los beneficios de comer menos y muestran las mismas discapacidades que sus compañeros viejos o sobrealimentados.
«Este descubrimiento tiene importantes implicaciones para desarrollar futuras terapias para mantener el cerebro joven y prevenir su degeneración y el proceso de envejecimiento», concluye Giovambattista Pani, responsable del estudio.
**Publicado en "ABC"
Hospitals invest heavily in new heart attack care programs but fail to improve access
In a new study, researchers have found a 44 percent increase since 2001 in the number of hospitals that offer definitive emergency care to patients with heart attack, but only a 1 percent increase in access to that care. The study, led by Thomas W. Concannon, PhD, Assistant Professor Tufts Medical Center and Tufts University School of Medicine, will be published January 1, 2012 in Circulation: Cardiovascular Quality and Outcomes, a journal of the American Heart Association. Patients with heart attacks caused by arterial blockages require emergency care to restore normal blood flow to the heart. Timely percutaneous coronary intervention (PCI), a surgical procedure that can manually remove blockages with a balloon and stent-tipped catheter, has been shown to save lives compared to fibrinolytic therapy, a non-surgical procedure that can dissolve some blockages with the injection of a "clot-busting" drug.However, PCI is available only in about one in three U.S. hospitals. When symptoms of a heart attack begin, those patients who are within a 60-minute drive time of these hospitals have the best chance of PCI enabling them to avoid or reduce the damage of a heart attack.
The number of hospitals with a PCI program grew by 519 during the study period, from 1,176 in 2001 to 1,695 in 2006, an increase of 44 percent. Despite this widespread investment in new programs, the percent of the U.S. population with timely access to PCI only grew from 79.0 to 79.9 percent, an increase of 1 percent. In addition, the increase did not substantially reduce typical drive times for those patients who already had access to the procedure. Median projected drive time to the closest PCI-equipped hospital fell from 11.3 to 10.5 minutes nationally, a drop of only 48 seconds.
The researchers also found substantial regional variation in timely access to PCI. Access was highest in the Northeast (87.8 percent of the population) and lowest in the South (75.7 percent). Better than 90 percent of the population in seven states had timely access to the interventions (California, 90.9 percent Connecticut, 93.6 percent, Delaware, 91.7 percent, Florida, 91.2 percent, Massachusetts, 94.6 percent, New Jersey, 96.5 percent, Rhode Island, 96.1 percent and the District of Columbia, 100 percent).However, less than 50 percent of the population of seven other states lived within a 60-minute drive of a PCI-equipped hospital (North Dakota, 48.9 percent, South Dakota, 40.3 percent, Vermont, 38.3 percent, West Virginia, 45.6 percent, Alaska, 40.0 percent, Montana, 45.3 percent and Wyoming, 30.5 percent).
"New hospital PCI programs after 2001 have largely failed to improve patient access or reduce delays to treatment," said Concannon. "For regions that wish to boost access to PCI, the focus should be on enhanced ambulance services and on well-positioned PCI programs, rather than on the sheer number of PCI programs. A shift in priorities could make a significant impact and it could save lives."
The study, "A Percutaneous Coronary Intervention Lab in Every Hospital?" was funded by the Agency for Healthcare Research and Quality and by the Tufts Medical Center Research Fund. The Tufts Medical Center Clinical and Translational Science Institute (CTSI) provided statistical support. Data sources included the 2006 American Hospital Association (AHA) Annual Survey Database of all 50 states and the District of Columbia, the 2006 Health Care Cost and Utilization Project's (HCUP) State Inpatient Databases from 21 states, and the 2000 US Census. To satisfy inclusion criteria for the study, hospitals were required to perform at least four PCI interventions per calendar year and provide PCI care to U.S. adults aged 18 years or older.
**Source: Tufts Medical Center
The number of hospitals with a PCI program grew by 519 during the study period, from 1,176 in 2001 to 1,695 in 2006, an increase of 44 percent. Despite this widespread investment in new programs, the percent of the U.S. population with timely access to PCI only grew from 79.0 to 79.9 percent, an increase of 1 percent. In addition, the increase did not substantially reduce typical drive times for those patients who already had access to the procedure. Median projected drive time to the closest PCI-equipped hospital fell from 11.3 to 10.5 minutes nationally, a drop of only 48 seconds.
The researchers also found substantial regional variation in timely access to PCI. Access was highest in the Northeast (87.8 percent of the population) and lowest in the South (75.7 percent). Better than 90 percent of the population in seven states had timely access to the interventions (California, 90.9 percent Connecticut, 93.6 percent, Delaware, 91.7 percent, Florida, 91.2 percent, Massachusetts, 94.6 percent, New Jersey, 96.5 percent, Rhode Island, 96.1 percent and the District of Columbia, 100 percent).However, less than 50 percent of the population of seven other states lived within a 60-minute drive of a PCI-equipped hospital (North Dakota, 48.9 percent, South Dakota, 40.3 percent, Vermont, 38.3 percent, West Virginia, 45.6 percent, Alaska, 40.0 percent, Montana, 45.3 percent and Wyoming, 30.5 percent).
"New hospital PCI programs after 2001 have largely failed to improve patient access or reduce delays to treatment," said Concannon. "For regions that wish to boost access to PCI, the focus should be on enhanced ambulance services and on well-positioned PCI programs, rather than on the sheer number of PCI programs. A shift in priorities could make a significant impact and it could save lives."
The study, "A Percutaneous Coronary Intervention Lab in Every Hospital?" was funded by the Agency for Healthcare Research and Quality and by the Tufts Medical Center Research Fund. The Tufts Medical Center Clinical and Translational Science Institute (CTSI) provided statistical support. Data sources included the 2006 American Hospital Association (AHA) Annual Survey Database of all 50 states and the District of Columbia, the 2006 Health Care Cost and Utilization Project's (HCUP) State Inpatient Databases from 21 states, and the 2000 US Census. To satisfy inclusion criteria for the study, hospitals were required to perform at least four PCI interventions per calendar year and provide PCI care to U.S. adults aged 18 years or older.
**Source: Tufts Medical Center
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