La utilidad pedagógica y terapéutica del ajedrez es tan clara que el Parlamento Europeo debate la conveniencia de aumentar el número de colegios de la UE que ya lo imparten como asignatura o actividad extraescolar. La resolución se aprobará si la respaldan 369 eurodiputados (la mitad más uno) antes del 15 de marzo; hasta hoy se han recogido 259 firmas.
“Sea cual sea la edad del niño, el ajedrez puede mejorar su concentración, paciencia y persistencia; y puede ayudarle a desarrollar el sentido de la creatividad, la intuición, la memoria y las competencias, tanto analíticas como de toma de decisiones; el ajedrez enseña asimismo determinación, motivación y deportividad”, dice la declaración propuesta por los europarlamentarios. Y añade: “El ajedrez es un juego accesible para los niños de cualquier grupo social, podría mejorar la cohesión social y contribuir a los objetivos políticos, tales como la integración, la lucha contra la discriminación, la reducción de las tasas de delincuencia e incluso la lucha contra diferentes adicciones”.
-Su práctica estimula el rendimiento en matemáticas y lectura
La iniciativa partió de la Unión Europea de Ajedrez, presidida por el búlgaro Silvio Danáilov, y apoyada por la fundación del excampeón del mundo Gari Kaspárov. Ambos la presentaron ante el Parlamento Europeo y volverán a Estrasburgo esta semana. “El ajedrez está organizado como un deporte, pero sus aplicaciones pedagógicas y culturales son muy importantes. Ya contamos con el apoyo de la Unesco, y ahora esperamos convencer a los 110 eurodiputados que nos faltan”, explica Danáilov. Si lo consiguen, la recomendación de la UE para que el ajedrez se imparta como asignatura llevará implícita una asignación económica, que debería destinarse a la formación ajedrecística de maestros de escuela.
Así se evitará lo ocurrido en España. En 1995, el Senado, a propuesta de Coalición Canaria y sin votos en contra, “instó al Gobierno” a que recomendara la introducción del ajedrez en los colegios como asignatura optativa o actividad extraescolar por sus virtudes pedagógicas. Los Parlamentos de Andalucía y Extremadura tomaron decisiones similares. Ningún Gobierno, en 17 años, se hizo eco de esa recomendación.
El impulso ciudadano ha sido mucho más rápido que el oficial. España es uno de los países más avanzados del mundo en la utilización del ajedrez como herramienta pedagógica: no son pocos los colegios donde se juega como actividad obligatoria, extraescolar o como asignatura optativa. Y serían más si hubiera maestros preparados para atender la demanda, pero solo la Universidad de Huelva ofrece cursos de posgrado de ajedrez para licenciados.
El índice de satisfacción entre alumnos, padres y profesores es superior al 80%. Eso explica que, por ejemplo, en los colegios Luis Vives (Elche, público) y El Altillo (Jerez de la Frontera, privado) el ajedrez sea obligatorio desde hace 17 y 7 años, respectivamente. Caso llamativo es el del colegio Mirabal, privado, en Pozuelo de Alarcón (Madrid), donde el ajedrez se imparte desde 1995, y ahora es práctica común para todos los alumnos que no eligen música y para casi todos los que no acuden a las clases de religión.
De los eurodiputados españoles solo 18 de los 50 con escaño en Estrasburgo han firmado hasta el momento. De ellos, 12 son del PP (el primero fue el actual ministro de Exteriores, José Manuel García-Margallo) y dos del PSOE. Ignacio Sánchez Amor, diputado por Extremadura en el Congreso, está convencido de que pronto serán muchos más. “En Extremadura se están consiguiendo resultados impresionantes con el ajedrez como herramienta social y pedagógica con personas mayores, desempleados, presos, exdrogadictos, niños hiperactivos...”.
Numerosos estudios científicos realizados desde 1925 demuestran que los niños ajedrecistas desarrollan más la inteligencia y mejoran su rendimiento académico (en un 17%, de media), sobre todo en matemáticas y lectura. La práctica frecuente del ajedrez retrasa el envejecimiento cerebral y podría prevenir el alzhéimer, tesis apoyada en el reciente congreso celebrado en Cádiz. El neurólogo José Félix Martí Massó (Hospital Donostia) remacha: “El ajedrez es un excelente gimnasio para la mente”.
**publicado en "EL PAIS"
13 February 2012
Drug halts organ damage in inflammatory genetic disorder
A new study shows that Kineret (anakinra), a medication approved for the treatment of rheumatoid arthritis, is effective in stopping the progression of organ damage in people with neonatal-onset multisystem inflammatory disease (NOMID). This rare and debilitating genetic disorder causes persistent inflammation and ongoing tissue damage. The research was performed by scientists at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), part of the National Institutes of Health.
NOMID affects numerous organs and body systems, including the skin, joints, eyes, and central nervous system. The first sign of the disease is often a rash that develops within the first weeks of life. Other problems, including fever, meningitis, joint damage, vision and hearing loss, and mental retardation, can follow. Kineret, one of a relatively new class of drugs known as biologic response modifiers or biologics, blocks the activity of interleukin-1 (IL-1), a protein made by cells of the immune system. IL-1 is overproduced in NOMID and a number of other diseases, leading to damaging inflammation. Previous work by the same NIAMS group showed that blocking IL-1 was effective in relieving symptoms of NOMID. However, this is the first study to show that Kineret works over the long-term and, at higher doses, can also control damage that often results in vision and hearing loss, and brain lesions.
"Inflammation prolonged over many years will eventually cause irreversible damage and loss of function," said lead author Dr. Raphaela Goldbach-Mansky of the NIAMS Translational Autoinflammatory Disease Section.
For example, inflammation of the cochlea -- a tiny structure of the inner ear -- was found to be responsible for hearing loss in people with NOMID. Thinning of the optic nerve caused by inflammation-related pressure in the brain has been identified as a cause of vision loss.
"We knew we could effectively block inflammation in the inner ear and in the brain and eyes. The next step was to find out if we could sufficiently prevent the progression of hearing or vision loss," said Goldbach-Mansky.
The group sought the answers to their questions in the study published online in Arthritis & Rheumatism. Study participants, who ranged in age from 10 months to 42 years, were treated with daily doses of Kineret based on body weight -- 1 to 5 milligrams of Kineret per kilogram of body weight (1 to 5 mg/kg/day) -- for at least 36 months and as long as 60 months. Disease activity was monitored with blood tests to measure C-reactive protein, a marker for inflammation in the body, and by daily diaries kept by the patients or their parents. The researchers also used sensitive MRI imaging methods to assess inflammation in the inner ear and brain.
Researchers found the initial Kineret doses used were insufficient to control organ inflammation, but by increasing the dose, they were able to do so. By preventing organ inflammation, scientists were able to preserve organ function in most patients. In addition, the scientists found ways to predict who is at greatest risk of hearing and vision loss.
"The few patients in the study who had hearing loss were also the ones who continued to have inflammation in the inner ear," said the study's first author Dr. Cailin H. Sibley. "We also found that people who had thin optic nerves when we assessed their vision were more likely to lose vision than those who had thick optic nerves, simply because they had already lost fibers due to untreated disease and, therefore, started with a huge disadvantage."
These findings point to the importance of early diagnosis and treatment to keep organ damage from developing. "We are continuing the study with an emphasis on enrolling very young children to prospectively show that we can prevent any organ damage from developing if we start treatment early in life," Goldbach-Mansky said.
*Source: NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
NOMID affects numerous organs and body systems, including the skin, joints, eyes, and central nervous system. The first sign of the disease is often a rash that develops within the first weeks of life. Other problems, including fever, meningitis, joint damage, vision and hearing loss, and mental retardation, can follow. Kineret, one of a relatively new class of drugs known as biologic response modifiers or biologics, blocks the activity of interleukin-1 (IL-1), a protein made by cells of the immune system. IL-1 is overproduced in NOMID and a number of other diseases, leading to damaging inflammation. Previous work by the same NIAMS group showed that blocking IL-1 was effective in relieving symptoms of NOMID. However, this is the first study to show that Kineret works over the long-term and, at higher doses, can also control damage that often results in vision and hearing loss, and brain lesions.
"Inflammation prolonged over many years will eventually cause irreversible damage and loss of function," said lead author Dr. Raphaela Goldbach-Mansky of the NIAMS Translational Autoinflammatory Disease Section.
For example, inflammation of the cochlea -- a tiny structure of the inner ear -- was found to be responsible for hearing loss in people with NOMID. Thinning of the optic nerve caused by inflammation-related pressure in the brain has been identified as a cause of vision loss.
"We knew we could effectively block inflammation in the inner ear and in the brain and eyes. The next step was to find out if we could sufficiently prevent the progression of hearing or vision loss," said Goldbach-Mansky.
The group sought the answers to their questions in the study published online in Arthritis & Rheumatism. Study participants, who ranged in age from 10 months to 42 years, were treated with daily doses of Kineret based on body weight -- 1 to 5 milligrams of Kineret per kilogram of body weight (1 to 5 mg/kg/day) -- for at least 36 months and as long as 60 months. Disease activity was monitored with blood tests to measure C-reactive protein, a marker for inflammation in the body, and by daily diaries kept by the patients or their parents. The researchers also used sensitive MRI imaging methods to assess inflammation in the inner ear and brain.
Researchers found the initial Kineret doses used were insufficient to control organ inflammation, but by increasing the dose, they were able to do so. By preventing organ inflammation, scientists were able to preserve organ function in most patients. In addition, the scientists found ways to predict who is at greatest risk of hearing and vision loss.
"The few patients in the study who had hearing loss were also the ones who continued to have inflammation in the inner ear," said the study's first author Dr. Cailin H. Sibley. "We also found that people who had thin optic nerves when we assessed their vision were more likely to lose vision than those who had thick optic nerves, simply because they had already lost fibers due to untreated disease and, therefore, started with a huge disadvantage."
These findings point to the importance of early diagnosis and treatment to keep organ damage from developing. "We are continuing the study with an emphasis on enrolling very young children to prospectively show that we can prevent any organ damage from developing if we start treatment early in life," Goldbach-Mansky said.
*Source: NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
Sleep breathing machine shows clear benefits in children with sleep apnea
Children and adolescents with obstructive sleep apnea had substantial improvements in attention, anxiety and quality of life after treatment with positive airway pressure (PAP) -- a nighttime therapy in which a machine delivers a stream of air through a mask into the nose. "The benefits occurred even when children didn't fully adhere to the treatment," said study leader Carole L. Marcus, M.D., a sleep specialist and director of the Sleep Center at The Children's Hospital of Philadelphia. The Sleep Center follows thousands of children and adolescents with sleep problems.
The study appears online ahead of print in the American Journal of Respiratory and Clinical Care Medicine.
Obstructive sleep apnea syndrome (OSAS) is a condition of interrupted breathing caused by a narrowing in the throat or upper airway, related to large tonsils and adenoids, obesity or other medical problems. Using continuous positive airway pressure commonly relieves OSAS in adults, in whom it has been studied extensively. However, there have been few studies of PAP in children with OSAS.
"The vast majority of children with OSAS undergo surgery on their tonsils and adenoids instead of receiving PAP therapy," said Dr. Marcus. "It is difficult to get children to wear the mask used in PAP treatments." However, surgery is not always effective in treating OSAS in children, especially in obese children," said Dr. Marcus. She added that many children who require PAP therapy have underlying chronic illnesses such as Down syndrome, or developmental delays. Furthermore, the rising incidence of obesity among children and adolescents has also increased the rate of OSAS in young people.
The current study followed 52 children and adolescents with OSAS at Children's Hospital. The patients had a mean age of 12 years old, and 10 of them had significant developmental delays. The study team assessed sleepiness, behavioral problems, attention, and quality of life at baseline and after three months of PAP treatment.
The researchers found significant improvements in attention deficits, daytime sleepiness, behaviors such as anxiety and shyness, and quality of life. Both the parents and children reported on quality of life using standardized questionnaires that asked about feelings, daily activities, getting along with other children, and keeping up with schoolwork.
"We found that improvements occurred even when children were only using PAP as little as three hours a night," said Dr. Marcus, who noted that higher compliance would be expected to yield greater benefits. She added that getting children to fully adhere to treatments requires a commitment by parents and family members to a behavioral plan that supports the treatments.
Dr. Marcus said that further pediatric sleep research is warranted, such as blinded studies to compare treatment to a placebo group and further investigations of neurobehavioral outcomes. "This study was the first comprehensive study of PAP use in children, so more research should be performed, but our results have encouraging implications for using this treatment in children with sleep apnea," she concluded.
*Source: Children's Hospital of Philadelphia
The study appears online ahead of print in the American Journal of Respiratory and Clinical Care Medicine.
Obstructive sleep apnea syndrome (OSAS) is a condition of interrupted breathing caused by a narrowing in the throat or upper airway, related to large tonsils and adenoids, obesity or other medical problems. Using continuous positive airway pressure commonly relieves OSAS in adults, in whom it has been studied extensively. However, there have been few studies of PAP in children with OSAS.
"The vast majority of children with OSAS undergo surgery on their tonsils and adenoids instead of receiving PAP therapy," said Dr. Marcus. "It is difficult to get children to wear the mask used in PAP treatments." However, surgery is not always effective in treating OSAS in children, especially in obese children," said Dr. Marcus. She added that many children who require PAP therapy have underlying chronic illnesses such as Down syndrome, or developmental delays. Furthermore, the rising incidence of obesity among children and adolescents has also increased the rate of OSAS in young people.
The current study followed 52 children and adolescents with OSAS at Children's Hospital. The patients had a mean age of 12 years old, and 10 of them had significant developmental delays. The study team assessed sleepiness, behavioral problems, attention, and quality of life at baseline and after three months of PAP treatment.
The researchers found significant improvements in attention deficits, daytime sleepiness, behaviors such as anxiety and shyness, and quality of life. Both the parents and children reported on quality of life using standardized questionnaires that asked about feelings, daily activities, getting along with other children, and keeping up with schoolwork.
"We found that improvements occurred even when children were only using PAP as little as three hours a night," said Dr. Marcus, who noted that higher compliance would be expected to yield greater benefits. She added that getting children to fully adhere to treatments requires a commitment by parents and family members to a behavioral plan that supports the treatments.
Dr. Marcus said that further pediatric sleep research is warranted, such as blinded studies to compare treatment to a placebo group and further investigations of neurobehavioral outcomes. "This study was the first comprehensive study of PAP use in children, so more research should be performed, but our results have encouraging implications for using this treatment in children with sleep apnea," she concluded.
*Source: Children's Hospital of Philadelphia
Curry spice component may help slow prostate tumor growth
Curcumin, an active component of the Indian curry spice turmeric, may help slow down tumor growth in castration-resistant prostate cancer patients on androgen deprivation therapy (ADT), a study from researchers at Jefferson's Kimmel Cancer Center suggests. Reporting in a recent issue of Cancer Research, Karen Knudsen, Ph.D., a Professor of Cancer Biology, Urology and Radiation Oncology at Thomas Jefferson University, and colleagues observed in a pre-clinical study that curcumin suppresses two known nuclear receptor activators, p300 and CPB (or CREB1-binding protein), which have been shown to work against ADT.
ADT aims to inhibit the androgen receptor -- an important male hormone in the development and progression of prostate cancer -- in patients. But a major mechanism of therapeutic failure and progression to advanced disease is inappropriate reactivation of this receptor. Sophisticated tumor cells, with the help of p300 and CPB, sometimes bypass the therapy.
Thus, development of novel targets that act in concert with the therapy would be of benefit to patients with castration-resistant prostate cancer.
For the study, prostate cancer cells were subjected to hormone deprivation in the presence and absence of curcumin with "physiologically attainable' doses. (Previous studies, which found similar results, included doses that were not realistic.)
Curcumin augments the results of ADT, and reduced cell number compared to ADT alone, the researchers found. Moreover, the spice was found to be a potent inhibitor of both cell cycle and survival in prostate cancer cells.
To help support their findings, the researchers also investigated curcumin in mice, which were castrated to mimic ADT. They were randomized into two cohorts: curcumin and control. Tumor growth and mass were significantly reduced in the mice with curcumin, the researchers report.
These data demonstrate for the first time that curcumin not only hampers the transition of ADT-sensitive disease to castration-resistance, but is also effective in blocking the growth of established castrate-resistant prostate tumors.
"This study sets the stage for further development of curcumin as a novel agent to target androgen receptor signaling," said Dr. Knudsen. "It also has implications beyond prostate cancer since p300 and CBP are important in other malignancies, like breast cancer. In tumors where these play an important function, curcumin may prove to be a promising therapeutic agent."
ADT aims to inhibit the androgen receptor -- an important male hormone in the development and progression of prostate cancer -- in patients. But a major mechanism of therapeutic failure and progression to advanced disease is inappropriate reactivation of this receptor. Sophisticated tumor cells, with the help of p300 and CPB, sometimes bypass the therapy.
Thus, development of novel targets that act in concert with the therapy would be of benefit to patients with castration-resistant prostate cancer.
For the study, prostate cancer cells were subjected to hormone deprivation in the presence and absence of curcumin with "physiologically attainable' doses. (Previous studies, which found similar results, included doses that were not realistic.)
Curcumin augments the results of ADT, and reduced cell number compared to ADT alone, the researchers found. Moreover, the spice was found to be a potent inhibitor of both cell cycle and survival in prostate cancer cells.
To help support their findings, the researchers also investigated curcumin in mice, which were castrated to mimic ADT. They were randomized into two cohorts: curcumin and control. Tumor growth and mass were significantly reduced in the mice with curcumin, the researchers report.
These data demonstrate for the first time that curcumin not only hampers the transition of ADT-sensitive disease to castration-resistance, but is also effective in blocking the growth of established castrate-resistant prostate tumors.
"This study sets the stage for further development of curcumin as a novel agent to target androgen receptor signaling," said Dr. Knudsen. "It also has implications beyond prostate cancer since p300 and CBP are important in other malignancies, like breast cancer. In tumors where these play an important function, curcumin may prove to be a promising therapeutic agent."
**Source: Thomas Jefferson University
Arthritic knees, but not hips, have robust repair response
Researchers at Duke University Medical Center used new tools they developed to analyze knees and hips and discovered that osteoarthritic knee joints are in a constant state of repair, while hip joints are not. "This suggests the knee has capacity for repair we didn't know about and the main treatment strategy probably would need to focus on turning off the breakdown of knee tissue," said Virginia Kraus, MD, PhD, professor of Rheumatology and Immunology at Duke. "I was hugely surprised to find this."
This suggests that knee and hip osteoarthritis may need different treatment approaches, Kraus said.
Perhaps the natural repair response would be sufficient to lead to a reversal or halting of the disease process in the knee if the joint breakdown could be halted, Kraus said.
"At least with the knee you've got an ongoing repair response that we didn't appreciate until now," Kraus said. "If you could capitalize on that and turn off the degradative (breakdown) processing you might have some good effects."
The findings, published in the Journal of Biological Chemistry on Feb. 10, suggest that for hips, however, halting the degenerative process might not be enough. The hips would need a treatment to both stop degeneration as well as stimulate factors that could help to begin repair.
The knee is very accessible for injections, so it would make sense to inject the knee with agents that could turn off the degradative processes, and these could be delivered periodically with close monitoring, Kraus said. "That seems like a very viable strategy."
A number of treatment strategies are being tested in clinical trials to switch off the joint breakdown processes, and Kraus is hopeful that this approach will lead to treatment breakthroughs for osteoarthritis.
A cocktail of drugs might be needed for the hip, however, both to halt the degradation and to stimulate the right type of reparative elements.
"I am speculating that a single agent would work for the knee," Kraus said.
The findings about the knee were shocking to her, because the literature for years had compared the knee and ankle. Scientists knew the ankle was resistant to osteoarthritis, but the knee was very susceptible.
The thinking was that the ankle joint bones fit together well, like a ball in a socket, so the joint cartilage is less likely to degrade, while the knee joint bones fit less well together and require tissue, like the meniscus, to create a better fit -- so knee cartilage is more likely to degrade.
"What we found is startling, because the hip joint also has a ball-in-socket structure yet it degrades and fails to mount a strong repair response," Kraus said. "We think this means that joint congruency alone cannot explain the difference in the repair response of joints, so there is more to learn."
Kraus and her team discovered a biomarker that is a measure of an altered (deaminated) protein, called D-COMP. In the circulation it signals hip degeneration and in cartilage it provides insight into the repair response of joint tissues. Kraus said this is the first biomarker specific to a particular joint site, and may be developed into a monitoring tool for hip-joint breakdown.
The next step is to understand the reasons for the difference between knees and hips and also to use the new tools to analyze the ankle for its level of repair response.
"Why is the ankle less susceptible than the knee to osteoarthritis?" Kraus asked. "Can we develop other tools to be specific indicators of joint health for other joints in the body?"
**Source: Duke University Medical Center
This suggests that knee and hip osteoarthritis may need different treatment approaches, Kraus said.
Perhaps the natural repair response would be sufficient to lead to a reversal or halting of the disease process in the knee if the joint breakdown could be halted, Kraus said.
"At least with the knee you've got an ongoing repair response that we didn't appreciate until now," Kraus said. "If you could capitalize on that and turn off the degradative (breakdown) processing you might have some good effects."
The findings, published in the Journal of Biological Chemistry on Feb. 10, suggest that for hips, however, halting the degenerative process might not be enough. The hips would need a treatment to both stop degeneration as well as stimulate factors that could help to begin repair.
The knee is very accessible for injections, so it would make sense to inject the knee with agents that could turn off the degradative processes, and these could be delivered periodically with close monitoring, Kraus said. "That seems like a very viable strategy."
A number of treatment strategies are being tested in clinical trials to switch off the joint breakdown processes, and Kraus is hopeful that this approach will lead to treatment breakthroughs for osteoarthritis.
A cocktail of drugs might be needed for the hip, however, both to halt the degradation and to stimulate the right type of reparative elements.
"I am speculating that a single agent would work for the knee," Kraus said.
The findings about the knee were shocking to her, because the literature for years had compared the knee and ankle. Scientists knew the ankle was resistant to osteoarthritis, but the knee was very susceptible.
The thinking was that the ankle joint bones fit together well, like a ball in a socket, so the joint cartilage is less likely to degrade, while the knee joint bones fit less well together and require tissue, like the meniscus, to create a better fit -- so knee cartilage is more likely to degrade.
"What we found is startling, because the hip joint also has a ball-in-socket structure yet it degrades and fails to mount a strong repair response," Kraus said. "We think this means that joint congruency alone cannot explain the difference in the repair response of joints, so there is more to learn."
Kraus and her team discovered a biomarker that is a measure of an altered (deaminated) protein, called D-COMP. In the circulation it signals hip degeneration and in cartilage it provides insight into the repair response of joint tissues. Kraus said this is the first biomarker specific to a particular joint site, and may be developed into a monitoring tool for hip-joint breakdown.
The next step is to understand the reasons for the difference between knees and hips and also to use the new tools to analyze the ankle for its level of repair response.
"Why is the ankle less susceptible than the knee to osteoarthritis?" Kraus asked. "Can we develop other tools to be specific indicators of joint health for other joints in the body?"
**Source: Duke University Medical Center
La ESA ensaya un sistema 3D para cuidar la salud de los astronautas
Un sistema basado en la realidad aumentada, difundido por la Agencia Espacial Europea (ESA), ayudará a los astronautas a cuidar de su salud en el espacio y les permitirá realizar intervenciones quirúrgicas de forma autónoma.
El proyecto, que se encuentra en fase de prototipo y ha sido impulsado por dos centros de investigación alemanes y un consorcio de aplicaciones espaciales con sede en Bélgica, lleva el nombre de Sistema de Diagnosis Médica y Cirugía Asistida por Ordenador (CAMDASS).
El dispositivo requiere primero registrar el cuerpo del paciente con una cámara tras haberle colocado unas marcas de referencia, y luego superpone sobre el campo de visión del usuario unos gráficos en tres dimensiones generados por ordenador que proporcionan información en tiempo real sobre lo que tiene ante sí y cómo actuar.
Esta técnica de visualización se ha comenzado a experimentar con los exámenes por ultrasonidos, porque la ESA dispone ya de los equipos necesarios para realizarlos, pero es una tecnología que según la agencia podría aplicarse a cualquier procedimiento médico.
El proyecto, que se encuentra en fase de prototipo y ha sido impulsado por dos centros de investigación alemanes y un consorcio de aplicaciones espaciales con sede en Bélgica, lleva el nombre de Sistema de Diagnosis Médica y Cirugía Asistida por Ordenador (CAMDASS).
El dispositivo requiere primero registrar el cuerpo del paciente con una cámara tras haberle colocado unas marcas de referencia, y luego superpone sobre el campo de visión del usuario unos gráficos en tres dimensiones generados por ordenador que proporcionan información en tiempo real sobre lo que tiene ante sí y cómo actuar.
Esta técnica de visualización se ha comenzado a experimentar con los exámenes por ultrasonidos, porque la ESA dispone ya de los equipos necesarios para realizarlos, pero es una tecnología que según la agencia podría aplicarse a cualquier procedimiento médico.
-Ensayos en un hospital
Los ensayos realizados en un hospital en Bruselas demostraron que usuarios sin experiencia pudieron llevar a cabo procedimientos relativamente difíciles gracias a las indicaciones del CAMDASS.
El dispositivo muestra a los usuarios cómo colocar y mover de forma adecuada el transductor de ultrasonidos para examinar el área de interés, y presenta además una serie de imágenes con indicaciones sobre lo que se pueden encontrar.
Con este avance, según indicó la ESA, se pretende conseguir que los astronautas puedan solucionar los problemas médicos por su cuenta, porque a medida que se alejen más de la Tierra en futuras misiones del Sistema Solar se incrementa la posibilidad de que haya interferencias en las comunicaciones con la base.
Pero el CAMDASS, añadió la ESA, también podría utilizarse como un sistema de "telemedicina por vía satélite", para "prestar primeros auxilios en países en vías de desarrollo o en la Antártida", o igualmente como herramienta para prestar primeros auxilios.
Los ensayos realizados en un hospital en Bruselas demostraron que usuarios sin experiencia pudieron llevar a cabo procedimientos relativamente difíciles gracias a las indicaciones del CAMDASS.
El dispositivo muestra a los usuarios cómo colocar y mover de forma adecuada el transductor de ultrasonidos para examinar el área de interés, y presenta además una serie de imágenes con indicaciones sobre lo que se pueden encontrar.
Con este avance, según indicó la ESA, se pretende conseguir que los astronautas puedan solucionar los problemas médicos por su cuenta, porque a medida que se alejen más de la Tierra en futuras misiones del Sistema Solar se incrementa la posibilidad de que haya interferencias en las comunicaciones con la base.
Pero el CAMDASS, añadió la ESA, también podría utilizarse como un sistema de "telemedicina por vía satélite", para "prestar primeros auxilios en países en vías de desarrollo o en la Antártida", o igualmente como herramienta para prestar primeros auxilios.
*AGENCIAS
Starve a virus, feed a cure?
A protein that protects some of our immune cells from the most common and virulent form of HIV works by starving the virus of the molecular building blocks that it needs to replicate, according to research published online in Nature Immunology. The finding comes from an international team of researchers including scientists from the University of Rochester Medical Center, NYU Langone Medical Center, several institutions in France -- and a graduate student who who is a political refugee from Africa and is now at work in a Rochester laboratory, intent on helping his people who have been devastated by the HIV epidemic.
While researchers hope the work will one day lead to a way to make anti-HIV drugs more effective by increasing their potency against the virus, they're also excited about its implications for our knowledge of other pathogens, such as herpes viruses, which use the same machinery within our cells that HIV does to replicate.
"The findings may explain why certain anti-HIV drugs used today are more effective under some circumstances and not others," said Baek Kim, Ph.D., professor of Microbiology and Immunology at the University of Rochester Medical Center and one of three corresponding authors of the paper. "It also provides new insights on how many other viruses that afflict people operate in the body."
The work centers on a protein known as SAMHD1, which is found in white blood cells known as macrophages and related cells known as dendritic cells. Last year scientists discovered that the molecule makes it difficult for HIV-1 to infect macrophages -- cells that specialize in gobbling up and destroying invaders like viruses.
Now researchers have discovered that the molecule cuts off the supply line of the raw material that HIV needs to create DNA and replicate. That raw material, dNTP, comprises the building blocks of DNA, and without it, HIV can't recreate its DNA in our cells.
The team found that SAMHD1 destroys most of these building blocks, making it nearly impossible for HIV-1 to replicate itself where SAMHD1 resides -- the macrophages. Instead, HIV-1 uses the macrophage as a safe haven, surviving in patients for years as it dodges the immune system as well as the drugs designed to kill it. It's thanks largely to its ability to hide out in the body that HIV is able to survive for decades and ultimately win out against the body's relentless immune assault.
The team also discovered how a protein in the other common type of HIV -- HIV-2, which is found mainly in Africa -- knocks out SAMHD1. They found that the protein Vpx destroys SAMHD1, clearing the way for HIV-2 to infect macrophages. While scientists have known that HIV-2 needs Vpx to infect macrophages, they hadn't known precisely why.
Interestingly, while one might think that a virus that is able to replicate itself in crucial cells like macrophages might be more dangerous than one that cannot, that's not the case with HIV. HIV-2 is actually less virulent than HIV-1.
"We don't know precisely how SAMHD1 and Vpx affect the virulence of HIV-1 and HIV-2, but it's something we're actively exploring," said Kim. "In this case, the ability of HIV-2 to replicate more quickly in macrophages does not help it become more virulent."
One possibility is that, like a starving man who becomes more and more desperate for food, the virus -- when faced with a shortage of raw materials -- puts its mutation gear into overdrive, creating more mutations in an effort to circumvent the pathway blocked by SAMHD1. Such constant mutations are one feature of HIV that makes it so challenging to treat patients.
"It makes sense that a mechanism like this is active in macrophages," said Kim. "Macrophages literally eat up dangerous organisms, and you don't want those organisms to have available the cellular machinery needed to replicate. And macrophages themselves don't need it, because they don't replicate. So macrophages have SAMHD1 to get rid of the raw material those organisms need to copy themselves. It's a great host defense.
"The work suggests new ways to target virus replication in macrophages, a critically important cell population that serves as a key reservoir of virus infection and a contributor to HIV-induced disease," added Kim.
At Rochester, Kim was joined in the research by graduate student Waaqo Daddacha, one of two first authors of the paper. A native of the Oromia region of Ethiopia, Daddacha came as a political refugee to the United States. He started out as a computer programmer, then decided to pursue HIV research as a way to help his homeland, where the rate of HIV is one of the highest in the world. As an undergraduate in Minnesota, he visited several laboratories around the nation that focus on HIV, eventually settling on the Kim lab, which he joined four years ago.
"Back home, many people are infected with HIV, and many people are dying because of it. I wanted to contribute to help solve the problem, and that's why I decided to pursue HIV research," said Daddacha, who still has family in Oromia. In Kim's lab he is focusing on understanding drug resistance among HIV patients and on finding ways to limit resistance to make the drugs more effective in patients.
**Source: University of Rochester Medical Center
While researchers hope the work will one day lead to a way to make anti-HIV drugs more effective by increasing their potency against the virus, they're also excited about its implications for our knowledge of other pathogens, such as herpes viruses, which use the same machinery within our cells that HIV does to replicate.
"The findings may explain why certain anti-HIV drugs used today are more effective under some circumstances and not others," said Baek Kim, Ph.D., professor of Microbiology and Immunology at the University of Rochester Medical Center and one of three corresponding authors of the paper. "It also provides new insights on how many other viruses that afflict people operate in the body."
The work centers on a protein known as SAMHD1, which is found in white blood cells known as macrophages and related cells known as dendritic cells. Last year scientists discovered that the molecule makes it difficult for HIV-1 to infect macrophages -- cells that specialize in gobbling up and destroying invaders like viruses.
Now researchers have discovered that the molecule cuts off the supply line of the raw material that HIV needs to create DNA and replicate. That raw material, dNTP, comprises the building blocks of DNA, and without it, HIV can't recreate its DNA in our cells.
The team found that SAMHD1 destroys most of these building blocks, making it nearly impossible for HIV-1 to replicate itself where SAMHD1 resides -- the macrophages. Instead, HIV-1 uses the macrophage as a safe haven, surviving in patients for years as it dodges the immune system as well as the drugs designed to kill it. It's thanks largely to its ability to hide out in the body that HIV is able to survive for decades and ultimately win out against the body's relentless immune assault.
The team also discovered how a protein in the other common type of HIV -- HIV-2, which is found mainly in Africa -- knocks out SAMHD1. They found that the protein Vpx destroys SAMHD1, clearing the way for HIV-2 to infect macrophages. While scientists have known that HIV-2 needs Vpx to infect macrophages, they hadn't known precisely why.
Interestingly, while one might think that a virus that is able to replicate itself in crucial cells like macrophages might be more dangerous than one that cannot, that's not the case with HIV. HIV-2 is actually less virulent than HIV-1.
"We don't know precisely how SAMHD1 and Vpx affect the virulence of HIV-1 and HIV-2, but it's something we're actively exploring," said Kim. "In this case, the ability of HIV-2 to replicate more quickly in macrophages does not help it become more virulent."
One possibility is that, like a starving man who becomes more and more desperate for food, the virus -- when faced with a shortage of raw materials -- puts its mutation gear into overdrive, creating more mutations in an effort to circumvent the pathway blocked by SAMHD1. Such constant mutations are one feature of HIV that makes it so challenging to treat patients.
"It makes sense that a mechanism like this is active in macrophages," said Kim. "Macrophages literally eat up dangerous organisms, and you don't want those organisms to have available the cellular machinery needed to replicate. And macrophages themselves don't need it, because they don't replicate. So macrophages have SAMHD1 to get rid of the raw material those organisms need to copy themselves. It's a great host defense.
"The work suggests new ways to target virus replication in macrophages, a critically important cell population that serves as a key reservoir of virus infection and a contributor to HIV-induced disease," added Kim.
At Rochester, Kim was joined in the research by graduate student Waaqo Daddacha, one of two first authors of the paper. A native of the Oromia region of Ethiopia, Daddacha came as a political refugee to the United States. He started out as a computer programmer, then decided to pursue HIV research as a way to help his homeland, where the rate of HIV is one of the highest in the world. As an undergraduate in Minnesota, he visited several laboratories around the nation that focus on HIV, eventually settling on the Kim lab, which he joined four years ago.
"Back home, many people are infected with HIV, and many people are dying because of it. I wanted to contribute to help solve the problem, and that's why I decided to pursue HIV research," said Daddacha, who still has family in Oromia. In Kim's lab he is focusing on understanding drug resistance among HIV patients and on finding ways to limit resistance to make the drugs more effective in patients.
**Source: University of Rochester Medical Center
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