Aloka Co., Ltd., Japan, became a 100% subsidiary of Hitachi Medical Corporation, Japan, on 3 March 2011, followed by a corporate name change to Hitachi Aloka Medical, Ltd., on 1 April 2011. With this step, Hitachi Medical Corporation and Hitachi Aloka Medical, Ltd., announced the integration of their strengths in ultrasound, making them one of the largest ultrasound companies in the world.
As a result, Aloka Holding Europe AG, Switzerland, a subsidiary of Hitachi Aloka Medical, is legally integrated into Hitachi Medical Systems Europe Holding AG, Switzerland, a subsidiary of Hitachi Medical Corporation, on 1 December 2011. The two entities will combine their broad experience and knowledge, synergizing the expertise and talents on both sides to offer their customers an even more attractive range of medical ultrasound solutions. Aloka has an exceptional history as an innovator in ultrasound and is renowned for high-quality ultrasound systems and support. Combining both product lines will allow them to broaden the participation and penetration of this large and diverse market. In addition, Hitachi Medical Systems Europe, which - besides ultrasound platforms - also sells a full line of MR and CT systems, will be able to enrich the portfolio and hence offer great synergies to the medical market.
Hitachi Medical Systems Europe will be responsible for the marketing, sales, service and clinical application support of the combined Aloka and Hitachi ultrasound systems' range and will continue with a high level of service quality for their customers.
Hitachi Medical Systems Europe further announces the appointment of Masanobu Tada, former CEO of Aloka Holding Europe to the position of Vice-President of the newly formed organization. "I am pleased to have Mr. Tada on board since Aloka and Hitachi have more than five years' technical cooperation behind them," says Hitoshi Matsuo, President and CEO of Hitachi Medical Systems Europe.
The collective forces of both companies will enable them to increase their presence in all fields of application and to enter new markets by developing and delivering breakthrough technologies that improve healthcare, reduce costs and increase efficiency. But this was only the first step. Following the integration of the two European headquarters, the integration of the respective subsidiaries will follow and is expected to be completed by early 2012.
01 December 2011
Unlocking the genetic and molecular mystery of soft-tissue sarcoma
Scientists at Joslin Diabetes Center in Boston have uncovered important molecular and genetic keys to the development of soft-tissue sarcomas in skeletal muscle, giving researchers and clinicians additional targets to stop the growth of these often deadly tumors. Published in the Proceedings of the National Academy of Sciences, the study identified two major molecular signaling pathways (the Ras and mTOR pathways) that are common in tumor growth and development. These molecular pathways regulate cell growth and division, two cellular properties whose over-activation are hallmarks of cancer biology.
"In humans, some sarcomas respond to chemotherapy, says lead author Amy J. Wagers, PhD, an associate professor of stem cell and regenerative biology at Harvard Medical School and Joslin Diabetes Center, "but many don't. With these findings, we have vetted a list of new candidate targets whose inhibition may lead to regression of these tumors."
Many soft-tissue sarcomas, which develop in certain tissues such as bone and muscle, carry specific genetic mutations or unique gene signatures, which can allow scientists to develop more precise, targeted therapies. Wagers and her colleagues engineered a tumor system in mice by introducing into mouse skeletal muscle a cancer-carrying gene, or oncogene, known to cause tumors in humans. They used this engineered system to identify a small set of genes that are active in sarcoma tumors.
There are many different types of soft-tissue sarcomas, which develop in tissues that connect, support or surround other structures and organs, including muscle, tendons, nerves, fat and blood vessels. If diagnosed early, treatment, primarily through surgical removal of the tumor, radiation therapy or chemotherapy, can be effective. If the tumor has spread, however, the tumor can be controlled only for a period of time, but treatment does not often cure the disease.
By inducing these tumors in mice, Wagers says the scientists knew when the tumors would form in the mice and where in the body they would develop, which helped them better understand the molecular and genetic pathways underlying the disease. With this knowledge, researchers may be able to develop new intervention strategies that interfere with these genetic activities and stop the growth of this type of tumor.
"With the engineered system we developed, we can find new fragile points in the tumor to target," says first author Simone Hettmer, MD, a pediatric oncologist at the Dana-Farber/Children's Hospital Cancer Center, who treats children with these tumors. In addition, she adds, the system allows scientists to look at the genetic changes in sarcomas and how they interact with the development of tumors and can be applied to sarcomas in tissues other than skeletal muscle.
Surprisingly, says Wagers, the researchers found they could induce tumors using several different 'beginning' cells. The scientists generated tumor cells using stem cell-like cells that go on to make either muscle or other connective tissues. Tumors that develop from muscle cells were rhabdomyosarcomas, the most common form of soft-tissue sarcoma seen in children, while tumors that developed from non-muscle cells represented other types of sarcoma.
Wagers and her colleagues are now working on establishing a similar engineered model using human cells to test the effectiveness of anti-sarcoma medications. These preclinical experiments are designed to identify the most promising candidates for the treatment of soft-tissue sarcoma that ultimately will be pursued in human clinical trials. Early studies have identified several chemical compounds that, in cell cultures at least, appear to slow the growth of sarcoma cells.
"In humans, some sarcomas respond to chemotherapy, says lead author Amy J. Wagers, PhD, an associate professor of stem cell and regenerative biology at Harvard Medical School and Joslin Diabetes Center, "but many don't. With these findings, we have vetted a list of new candidate targets whose inhibition may lead to regression of these tumors."
Many soft-tissue sarcomas, which develop in certain tissues such as bone and muscle, carry specific genetic mutations or unique gene signatures, which can allow scientists to develop more precise, targeted therapies. Wagers and her colleagues engineered a tumor system in mice by introducing into mouse skeletal muscle a cancer-carrying gene, or oncogene, known to cause tumors in humans. They used this engineered system to identify a small set of genes that are active in sarcoma tumors.
There are many different types of soft-tissue sarcomas, which develop in tissues that connect, support or surround other structures and organs, including muscle, tendons, nerves, fat and blood vessels. If diagnosed early, treatment, primarily through surgical removal of the tumor, radiation therapy or chemotherapy, can be effective. If the tumor has spread, however, the tumor can be controlled only for a period of time, but treatment does not often cure the disease.
By inducing these tumors in mice, Wagers says the scientists knew when the tumors would form in the mice and where in the body they would develop, which helped them better understand the molecular and genetic pathways underlying the disease. With this knowledge, researchers may be able to develop new intervention strategies that interfere with these genetic activities and stop the growth of this type of tumor.
"With the engineered system we developed, we can find new fragile points in the tumor to target," says first author Simone Hettmer, MD, a pediatric oncologist at the Dana-Farber/Children's Hospital Cancer Center, who treats children with these tumors. In addition, she adds, the system allows scientists to look at the genetic changes in sarcomas and how they interact with the development of tumors and can be applied to sarcomas in tissues other than skeletal muscle.
Surprisingly, says Wagers, the researchers found they could induce tumors using several different 'beginning' cells. The scientists generated tumor cells using stem cell-like cells that go on to make either muscle or other connective tissues. Tumors that develop from muscle cells were rhabdomyosarcomas, the most common form of soft-tissue sarcoma seen in children, while tumors that developed from non-muscle cells represented other types of sarcoma.
Wagers and her colleagues are now working on establishing a similar engineered model using human cells to test the effectiveness of anti-sarcoma medications. These preclinical experiments are designed to identify the most promising candidates for the treatment of soft-tissue sarcoma that ultimately will be pursued in human clinical trials. Early studies have identified several chemical compounds that, in cell cultures at least, appear to slow the growth of sarcoma cells.
**Source: Joslin Diabetes Center
Engineered botulism toxins could have broader role in medicine
The most poisonous substance on Earth -- already used medically in small doses to treat certain nerve disorders and facial wrinkles -- could be re-engineered for an expanded role in helping millions of people with rheumatoid arthritis, asthma, psoriasis and other diseases, scientists are reporting. Their study appears in ACS' journal Biochemistry. Edwin Chapman and colleagues explain that toxins, or poisons, produced by Clostridium botulinum bacteria, cause of a rare but severe form of food poisoning, are the most powerful toxins known to science. Doctors can inject small doses, however, to block the release of the neurotransmitters, or chemical messengers, that transmit signals from one nerve cell to another. The toxins break down a protein in nerve cells that mediates the release of neurotransmitters, disrupting nerve signals that cause pain, muscle spasms and other symptoms in certain diseases. That protein exists not just in nerve cells, but in other cells in the human body. However, these non-nerve cells lack the receptors needed for the botulinum toxins to enter and work. Chapman's group sought to expand the potential use of the botulinum toxins by hooking it to a molecule that can attach to receptors on other cells.
Their laboratory experiments showed that these engineered botulinum toxins do work in non-nerve cells, blocking the release of a protein from immune cells linked to inflammation, which is the underlying driving force behind a range of diseases. Such botulinum toxin therapy holds potential in a range of chronic inflammatory diseases and perhaps other conditions, which could expand the role of these materials in medicine.
**Source: American Chemical Society
Their laboratory experiments showed that these engineered botulinum toxins do work in non-nerve cells, blocking the release of a protein from immune cells linked to inflammation, which is the underlying driving force behind a range of diseases. Such botulinum toxin therapy holds potential in a range of chronic inflammatory diseases and perhaps other conditions, which could expand the role of these materials in medicine.
**Source: American Chemical Society
Early sign of Alzheimer's reversed in lab
One of the earliest known impairments caused by Alzheimer's disease -- loss of sense of smell -- can be restored by removing a plaque-forming protein in a mouse model of the disease, a study led by a Case Western Reserve University School of Medicine researcher finds. The study confirms that the protein, called amyloid beta, causes the loss.
"The evidence indicates we can use the sense of smell to determine if someone may get Alzheimer's disease, and use changes in sense of smell to begin treatments, instead of waiting until someone has issues learning and remembering," said Daniel Wesson, assistant professor of neuroscience at Case Western Reserve and lead investigator. "We can also use smell to see if therapies are working."
A description of the research is published in the Nov. 2 issue of The Journal of Neuroscience.
Smell loss can be caused by a number of ailments, exposures and injuries; but since the 1970s, it has been identified as an early sign of this disease. The new research shows how and where in the brain this happens, and that the impairment it can be treated.
"Understanding smell loss, we think, will hold some clues about how to slow down this disease," Wesson said.
There is currently no effective treatment or cure for the disease, marked by eroding senses, cognition and coordination, leading to death. Currently 5.3 million Americans suffer from Alzheimer's and the number is expected to triple to 16 million by 2050, according to the Alzheimer's Association.
Wesson worked with Anne H. Borkowski, a researcher at the Nathan S. Kline Institute in Orangeburg, N.Y., Gary E. Landreth, professor of neuroscience at Case Western Reserve School of Medicine, and Ralph A. Nixon, Efrat Levy and Donald A. Wilson, of the New York University School of Medicine.
They found that just a tiny amount of amyloid beta -- too little to be seen on today's brain scans -- causes smell loss in mouse models.
Amyloid beta plaque accumulated first in parts of the brain associated with smell, well before accumulating in areas associated with cognition and coordination.
Early on, the olfactory bulb, where odor information from the nose is processed, became hyperactive.
Over time, however, the level of amyloid beta increased in the olfactory bulb and the bulb became hypoactive. Despite spending more time sniffing, the mice failed to remember smells and became incapable of telling the difference between odors.
The same pattern is seen in people with the disease. They become unresponsive to smells as they age.
While losses in the olfactory system occurred, the rest of the mouse model brain, including the hippocampus, which is a center for memory, continued to act normally early in the disease stage.
"This shows the unique vulnerability of the olfactory system to the pathogenesis of Alzheimer's disease," Wesson said.
The team then sought to reverse the effects. Mice were given a synthetic liver x-receptor agonist, a drug that clears amyloid beta from the brain. After two weeks on the drug, the mice could process smells normally.
After withdrawal of the drug for one week, impairments returned.
Wesson and his team are now following-up on these discoveries to determine how amyloid spreads throughout the brain, to learn methods to slow disease progression.
**Source: Case Western Reserve University
"The evidence indicates we can use the sense of smell to determine if someone may get Alzheimer's disease, and use changes in sense of smell to begin treatments, instead of waiting until someone has issues learning and remembering," said Daniel Wesson, assistant professor of neuroscience at Case Western Reserve and lead investigator. "We can also use smell to see if therapies are working."
A description of the research is published in the Nov. 2 issue of The Journal of Neuroscience.
Smell loss can be caused by a number of ailments, exposures and injuries; but since the 1970s, it has been identified as an early sign of this disease. The new research shows how and where in the brain this happens, and that the impairment it can be treated.
"Understanding smell loss, we think, will hold some clues about how to slow down this disease," Wesson said.
There is currently no effective treatment or cure for the disease, marked by eroding senses, cognition and coordination, leading to death. Currently 5.3 million Americans suffer from Alzheimer's and the number is expected to triple to 16 million by 2050, according to the Alzheimer's Association.
Wesson worked with Anne H. Borkowski, a researcher at the Nathan S. Kline Institute in Orangeburg, N.Y., Gary E. Landreth, professor of neuroscience at Case Western Reserve School of Medicine, and Ralph A. Nixon, Efrat Levy and Donald A. Wilson, of the New York University School of Medicine.
They found that just a tiny amount of amyloid beta -- too little to be seen on today's brain scans -- causes smell loss in mouse models.
Amyloid beta plaque accumulated first in parts of the brain associated with smell, well before accumulating in areas associated with cognition and coordination.
Early on, the olfactory bulb, where odor information from the nose is processed, became hyperactive.
Over time, however, the level of amyloid beta increased in the olfactory bulb and the bulb became hypoactive. Despite spending more time sniffing, the mice failed to remember smells and became incapable of telling the difference between odors.
The same pattern is seen in people with the disease. They become unresponsive to smells as they age.
While losses in the olfactory system occurred, the rest of the mouse model brain, including the hippocampus, which is a center for memory, continued to act normally early in the disease stage.
"This shows the unique vulnerability of the olfactory system to the pathogenesis of Alzheimer's disease," Wesson said.
The team then sought to reverse the effects. Mice were given a synthetic liver x-receptor agonist, a drug that clears amyloid beta from the brain. After two weeks on the drug, the mice could process smells normally.
After withdrawal of the drug for one week, impairments returned.
Wesson and his team are now following-up on these discoveries to determine how amyloid spreads throughout the brain, to learn methods to slow disease progression.
**Source: Case Western Reserve University
El momento clave de la enfermedad celiaca
Los especialistas calculan que el 1% de la población española padece enfermedad celiaca. Estas personas tienen una intolerancia permanente al gluten, que es una proteína presente en cereales como el trigo, el centeno o la cebada, entre otros, por lo que deben eliminar estos productos de su dieta para evitar complicaciones. Sin embargo, la gran mayoría de los enfermos desconoce que lo son.
"Sólo uno de cada seis o siete pacientes se diagnostica adecuadamente, por lo que muchos se pierden", ha explicado a ELMUNDO.es Eduardo Arranz, presidente de la Sociedad Española de Enfermedad Celiaca durante el simposio 'Soluciones emergentes para la Celiaquía' que ha organizado esta semana en Madrid la Fundación Ramón Areces y el Colegio Oficial de Químicos de Madrid.
Este encuentro, que ha reunido a los principales especialistas en la materia, ha servido de altavoz al Proyecto PACE (Proyecto de Ayuda a los Celiacos Españoles), una iniciativa que reclama esfuerzos para abordar la problemática de la enfermedad celiaca desde un punto de vista multidisciplinar, es decir, tanto desde la óptica de salud pública, y la mejora de la detección y los tratamientos, como desde la industria de fabricación de alimentos sin gluten, la detección de la proteína o la formación del profesorado escolar.
Uno de los principales mensajes que se han lanzado en el simposio hace hincapié en los importantes logros que en los últimos años se han logrado sobre el conocimiento de la enfermedad y las técnicas de diagnóstico disponibles. Sin embargo, expertos como Amado Salvador Peña, profesor emérito de la Universidad Medisch Centrum de Amsterdam (Holanda), también han subrayado la importancia de que estos logros se traduzcan pronto "en una mejor identificación de los casos" y en una uniformidad de los criterios empleados para la detección.
"Estamos en una encrucijada en cuanto que tenemos que saber cómo aunar todas las herramientas de las que disponemos para diagnosticar de una forma más eficaz", ha coincidido Arranz.
"Hay que valorar muy bien y hacer estudios que valoren el coste y la eficacia para encontrar esos pacientes que se escapan y cuya falta de diagnóstico está acarreando también gastos al sistema sanitario", ya que una enfermedad celiaca no detectada puede acarrear trastornos tan dispares como infertilidad, ataxias o depresión.
El gluten será sin, duda, un elemento clave a investigar en el futuro ya que, según ha explicado Arranz, cada vez hay más evidencias científicas de que esta proteína también puede causar síntomas gastrointestinales a personas que, en puridad, no son celiacos.
"En pruebas diagnósticas, como la serología, dan negativo y muchos tampoco tienen lesiones intestinales, pero vemos que cuando retiramos el gluten de su dieta experimentan una importante mejoría", señala. "Tenemos que estudiar a fondo esa sensibilidad y ver cómo debe ser el abordaje de estos pacientes", añade.
Según su punto de vista, para el futuro es fundamental seguir apuntalando la colaboración entre especialistas en la práctica clínica, genetistas, inmunólogos y tecnólogos de los alimentos, entre otros expertos.
**publicado en "EL MUNDO"
"Sólo uno de cada seis o siete pacientes se diagnostica adecuadamente, por lo que muchos se pierden", ha explicado a ELMUNDO.es Eduardo Arranz, presidente de la Sociedad Española de Enfermedad Celiaca durante el simposio 'Soluciones emergentes para la Celiaquía' que ha organizado esta semana en Madrid la Fundación Ramón Areces y el Colegio Oficial de Químicos de Madrid.
Este encuentro, que ha reunido a los principales especialistas en la materia, ha servido de altavoz al Proyecto PACE (Proyecto de Ayuda a los Celiacos Españoles), una iniciativa que reclama esfuerzos para abordar la problemática de la enfermedad celiaca desde un punto de vista multidisciplinar, es decir, tanto desde la óptica de salud pública, y la mejora de la detección y los tratamientos, como desde la industria de fabricación de alimentos sin gluten, la detección de la proteína o la formación del profesorado escolar.
Uno de los principales mensajes que se han lanzado en el simposio hace hincapié en los importantes logros que en los últimos años se han logrado sobre el conocimiento de la enfermedad y las técnicas de diagnóstico disponibles. Sin embargo, expertos como Amado Salvador Peña, profesor emérito de la Universidad Medisch Centrum de Amsterdam (Holanda), también han subrayado la importancia de que estos logros se traduzcan pronto "en una mejor identificación de los casos" y en una uniformidad de los criterios empleados para la detección.
"Estamos en una encrucijada en cuanto que tenemos que saber cómo aunar todas las herramientas de las que disponemos para diagnosticar de una forma más eficaz", ha coincidido Arranz.
"Hay que valorar muy bien y hacer estudios que valoren el coste y la eficacia para encontrar esos pacientes que se escapan y cuya falta de diagnóstico está acarreando también gastos al sistema sanitario", ya que una enfermedad celiaca no detectada puede acarrear trastornos tan dispares como infertilidad, ataxias o depresión.
El gluten será sin, duda, un elemento clave a investigar en el futuro ya que, según ha explicado Arranz, cada vez hay más evidencias científicas de que esta proteína también puede causar síntomas gastrointestinales a personas que, en puridad, no son celiacos.
"En pruebas diagnósticas, como la serología, dan negativo y muchos tampoco tienen lesiones intestinales, pero vemos que cuando retiramos el gluten de su dieta experimentan una importante mejoría", señala. "Tenemos que estudiar a fondo esa sensibilidad y ver cómo debe ser el abordaje de estos pacientes", añade.
Según su punto de vista, para el futuro es fundamental seguir apuntalando la colaboración entre especialistas en la práctica clínica, genetistas, inmunólogos y tecnólogos de los alimentos, entre otros expertos.
**publicado en "EL MUNDO"
Eating fish reduces risk of Alzheimer's disease
People who eat baked or broiled fish on a weekly basis may be improving their brain health and reducing their risk of developing mild cognitive impairment (MCI) and Alzheimer's disease, according to a study presented November 30 at the annual meeting of the Radiological Society of North America (RSNA). "This is the first study to establish a direct relationship between fish consumption, brain structure and Alzheimer's risk," said Cyrus Raji, M.D., Ph.D., from the University of Pittsburgh Medical Center and the University of Pittsburgh School of Medicine. "The results showed that people who consumed baked or broiled fish at least one time per week had better preservation of gray matter volume on MRI in brain areas at risk for Alzheimer's disease."
Alzheimer's disease is an incurable, progressive brain disease that slowly destroys memory and cognitive skills. According to the National Institute on Aging, as many as 5.1 million Americans may have Alzheimer's disease. In MCI, memory loss is present but to a lesser extent than in Alzheimer's disease. People with MCI often go on to develop Alzheimer's disease.
For the study, 260 cognitively normal individuals were selected from the Cardiovascular Health Study. Information on fish consumption was gathered using the National Cancer Institute Food Frequency Questionnaire. There were 163 patients who consumed fish on a weekly basis, and the majority ate fish one to four times per week. Each patient underwent 3-D volumetric MRI of the brain. Voxel-based morphometry, a brain mapping technique that measures gray matter volume, was used to model the relationship between weekly fish consumption at baseline and brain structure 10 years later. The data were then analyzed to determine if gray matter volume preservation associated with fish consumption reduced risk for Alzheimer's disease. The study controlled for age, gender, education, race, obesity, physical activity, and the presence or absence of apolipoprotein E4 (ApoE4), a gene that increases the risk of developing Alzheimer's.
Gray matter volume is crucial to brain health. When it remains higher, brain health is being maintained. Decreases in gray matter volume indicate that brain cells are shrinking.
The findings showed that consumption of baked or broiled fish on a weekly basis was positively associated with gray matter volumes in several areas of the brain. Greater hippocampal, posterior cingulate and orbital frontal cortex volumes in relation to fish consumption reduced the risk for five-year decline to MCI or Alzheimer's by almost five-fold.
"Consuming baked or broiled fish promotes stronger neurons in the brain's gray matter by making them larger and healthier," Dr. Raji said. "This simple lifestyle choice increases the brain's resistance to Alzheimer's disease and lowers risk for the disorder."
The results also demonstrated increased levels of cognition in people who ate baked or broiled fish.
"Working memory, which allows people to focus on tasks and commit information to short-term memory, is one of the most important cognitive domains," Dr. Raji said. "Working memory is destroyed by Alzheimer's disease. We found higher levels of working memory in people who ate baked or broiled fish on a weekly basis, even when accounting for other factors, such as education, age, gender and physical activity."
Eating fried fish, on the other hand, was not shown to increase brain volume or protect against cognitive decline.
**Source: Radiological Society of North America
Alzheimer's disease is an incurable, progressive brain disease that slowly destroys memory and cognitive skills. According to the National Institute on Aging, as many as 5.1 million Americans may have Alzheimer's disease. In MCI, memory loss is present but to a lesser extent than in Alzheimer's disease. People with MCI often go on to develop Alzheimer's disease.
For the study, 260 cognitively normal individuals were selected from the Cardiovascular Health Study. Information on fish consumption was gathered using the National Cancer Institute Food Frequency Questionnaire. There were 163 patients who consumed fish on a weekly basis, and the majority ate fish one to four times per week. Each patient underwent 3-D volumetric MRI of the brain. Voxel-based morphometry, a brain mapping technique that measures gray matter volume, was used to model the relationship between weekly fish consumption at baseline and brain structure 10 years later. The data were then analyzed to determine if gray matter volume preservation associated with fish consumption reduced risk for Alzheimer's disease. The study controlled for age, gender, education, race, obesity, physical activity, and the presence or absence of apolipoprotein E4 (ApoE4), a gene that increases the risk of developing Alzheimer's.
Gray matter volume is crucial to brain health. When it remains higher, brain health is being maintained. Decreases in gray matter volume indicate that brain cells are shrinking.
The findings showed that consumption of baked or broiled fish on a weekly basis was positively associated with gray matter volumes in several areas of the brain. Greater hippocampal, posterior cingulate and orbital frontal cortex volumes in relation to fish consumption reduced the risk for five-year decline to MCI or Alzheimer's by almost five-fold.
"Consuming baked or broiled fish promotes stronger neurons in the brain's gray matter by making them larger and healthier," Dr. Raji said. "This simple lifestyle choice increases the brain's resistance to Alzheimer's disease and lowers risk for the disorder."
The results also demonstrated increased levels of cognition in people who ate baked or broiled fish.
"Working memory, which allows people to focus on tasks and commit information to short-term memory, is one of the most important cognitive domains," Dr. Raji said. "Working memory is destroyed by Alzheimer's disease. We found higher levels of working memory in people who ate baked or broiled fish on a weekly basis, even when accounting for other factors, such as education, age, gender and physical activity."
Eating fried fish, on the other hand, was not shown to increase brain volume or protect against cognitive decline.
**Source: Radiological Society of North America
Ha muerto Winstone Zulu, la cara más conocida del sida en África
Un día Wistone Zulu se presentó en el programa 'Buenos días Zambia' que emitía la televisión nacional. Se sentó en un sillón del estudio y cuando las cámaras le enfocaron dijo que tenía el VIH. Era 1990 y él la primera persona en África que admitía públicamente su condición de seropositivo. Desde entonces y hasta el pasado mes de octubre, cuando falleció por causas relacionadas con el sida, fue puerta por puerta y congreso tras congreso defendiendo los derechos de los pacientes con VIH. Su activismo lo convirtió en la cara más conocida del sida en el continente africano.
Su lucha por mejorar las cosas para los demás transcurrió de forma paralela a su lucha personal. No le fue fácil aceptar que había contraído el virus. Se enteró cuando ya tenía todo preparado para salir de su Zambia natal para ir a estudiar a Rusia. Lo único que le faltaba era un análisis médico, requisito que le pedían para viajar. Se lo hizo confiado, sin saber que con la sangre que le estaban sacando, le estaban quitando también su sueño.
Cuando le dieron el diagnóstico se hundió. Pensó que iba morir, como dos de sus hermanos, que ya habían fallecido por tuberculosis -una complicación recurrente de la infección por VIH-. Pero pensar en ellos le dio la fuerza necesaria para dar un paso al frente. ¿Y si hubieran estado también infectados sin saberlo? Cayó en la cuenta de que mucha gente estaba pasando por lo mismo que él pero nadie hablaba de eso. "Sentí que no tenía nada de lo que avergonzarme. Ser seropositivo no es lo mismo que ser un criminal y sólo ellos ocultan lo que han hecho. Yo no era un criminal, así que no tenía por qué esconderme", reconoció luego, según recuerda la revista 'The Lancet', que le rinde tributo.
Así que se plantó en la televisión y, a partir de ahí, en todos los lugares en los que quisieron escucharle. Reclamaba un mayor acceso al tratamiento antirretroviral pero también al tratamiento para la tuberculosis. Combatía la homofobia y defendía el derecho de los seropositivos a ser padres, algo que él llevó a cabo (tuvo cuatro hijos sanos, gracias a que su mujer tomó la nevirapina durante el embarazo y no amamantó a los bebés). Y para aumentar la conciencia sobre esta enfermedad fundó la organización 'Positive and Living Squad' (PALS).
"Era un hombre brillante, educado e increíblemente valiente a la hora de hablar de su situación cuando nadie más lo hacía por aquel entonces", recuerda en la revista médica Peter Godfrey-Fausset, profesor de la Escuela de Medicina Tropical de Londres.
El acceso a los fármacos era un tema que le preocupaba mucho. "Tengo amigos, matrimonios, que ambos tienen el virus y que solamente pueden conseguir tratamiento para uno de ellos. Así que tienen que componérselas para ver cuál se toma la medicación. ¿Se quedarán sus hijos sin padre o sin madre? ¿Qué clase de elección es ésa?", contaba indignado en el libro '28 historias de sida en África', de Stephanie Nolen.
Pero durante la conferencia sobre el sida de Ginebra (1998), Winstone cambió de opinión respecto a su enfermedad. Conoció a un grupo de los llamados "disidentes del sida", que pregonaban que el VIH no existía y que había sido un invento de las farmacéuticas. El activista se dejó seducir por ellos y abandonó sus cargos en todas las organizaciones de sida de las que formaba parte. Y, lo que es peor, dejó de tomar los antirretrovirales. Estuvo así dos años, hasta que cayó muy enfermo y retomó su medicación, fue consciente de que había cometido un error y volvió a sus ideas anteriores.
"Fue un luchador incansable por los derechos y la dignidad de los seropositivos. Gracias a él hoy 400.000 zambianos reciben antirretrovirales gratis. Su ejemplo dio la vuelta al mundo". Con estas palabras le despidió el presidente de Zambia, Michael Sala. Winstone se despidió con su sonrisa, siempre dispuesta pese a las dificultades.
Su lucha por mejorar las cosas para los demás transcurrió de forma paralela a su lucha personal. No le fue fácil aceptar que había contraído el virus. Se enteró cuando ya tenía todo preparado para salir de su Zambia natal para ir a estudiar a Rusia. Lo único que le faltaba era un análisis médico, requisito que le pedían para viajar. Se lo hizo confiado, sin saber que con la sangre que le estaban sacando, le estaban quitando también su sueño.
Cuando le dieron el diagnóstico se hundió. Pensó que iba morir, como dos de sus hermanos, que ya habían fallecido por tuberculosis -una complicación recurrente de la infección por VIH-. Pero pensar en ellos le dio la fuerza necesaria para dar un paso al frente. ¿Y si hubieran estado también infectados sin saberlo? Cayó en la cuenta de que mucha gente estaba pasando por lo mismo que él pero nadie hablaba de eso. "Sentí que no tenía nada de lo que avergonzarme. Ser seropositivo no es lo mismo que ser un criminal y sólo ellos ocultan lo que han hecho. Yo no era un criminal, así que no tenía por qué esconderme", reconoció luego, según recuerda la revista 'The Lancet', que le rinde tributo.
Así que se plantó en la televisión y, a partir de ahí, en todos los lugares en los que quisieron escucharle. Reclamaba un mayor acceso al tratamiento antirretroviral pero también al tratamiento para la tuberculosis. Combatía la homofobia y defendía el derecho de los seropositivos a ser padres, algo que él llevó a cabo (tuvo cuatro hijos sanos, gracias a que su mujer tomó la nevirapina durante el embarazo y no amamantó a los bebés). Y para aumentar la conciencia sobre esta enfermedad fundó la organización 'Positive and Living Squad' (PALS).
"Era un hombre brillante, educado e increíblemente valiente a la hora de hablar de su situación cuando nadie más lo hacía por aquel entonces", recuerda en la revista médica Peter Godfrey-Fausset, profesor de la Escuela de Medicina Tropical de Londres.
El acceso a los fármacos era un tema que le preocupaba mucho. "Tengo amigos, matrimonios, que ambos tienen el virus y que solamente pueden conseguir tratamiento para uno de ellos. Así que tienen que componérselas para ver cuál se toma la medicación. ¿Se quedarán sus hijos sin padre o sin madre? ¿Qué clase de elección es ésa?", contaba indignado en el libro '28 historias de sida en África', de Stephanie Nolen.
Pero durante la conferencia sobre el sida de Ginebra (1998), Winstone cambió de opinión respecto a su enfermedad. Conoció a un grupo de los llamados "disidentes del sida", que pregonaban que el VIH no existía y que había sido un invento de las farmacéuticas. El activista se dejó seducir por ellos y abandonó sus cargos en todas las organizaciones de sida de las que formaba parte. Y, lo que es peor, dejó de tomar los antirretrovirales. Estuvo así dos años, hasta que cayó muy enfermo y retomó su medicación, fue consciente de que había cometido un error y volvió a sus ideas anteriores.
"Fue un luchador incansable por los derechos y la dignidad de los seropositivos. Gracias a él hoy 400.000 zambianos reciben antirretrovirales gratis. Su ejemplo dio la vuelta al mundo". Con estas palabras le despidió el presidente de Zambia, Michael Sala. Winstone se despidió con su sonrisa, siempre dispuesta pese a las dificultades.
**Publicado en "EL MUNDO"
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