The trefoil factor 3 (TFF3) protein protects and maintains the integrity of the epithelial surface in the normal breast. New research has found that while TFF3 protein expression is higher in well-differentiated low grade tumors and therefore associated with features of a good prognosis, it has a more sinister role in breast cancer invasion and metastasis. The report is published in the March issue of The American Journal of Pathology. "Our findings suggest that TFF3 is regulated by estrogen and has beneficial properties in breast epithelia," says lead investigator Felicity E.B. May, PhD, of the Northern Institute for Cancer Research and the Department of Pathology at Newcastle University, UK. "We propose that early during breast tumorigenesis, TFF3 retains its association with normal functionality of breast epithelial cells. Subsequently, with the loss of tumor cell differentiation, its function is subverted to promote the development of tumors and infiltration and lymph node metastasis."
To determine the role of TFF3 in breast cancer, researchers measured its level in tissue samples from normal breasts, benign breast lesions, in situ carcinomas, invasive carcinomas, and involved lymph nodes. TFF3 was expressed in the majority of benign and malignant breast lesions studied. Well-differentiated tumor types expressed higher levels of TFF3. There was a positive association between TFF3 protein expression and microvessel density, suggesting that it stimulates angiogenesis in breast tumors.
A striking finding of the study is the strength and consistency of the association between TFF3 expression and a more metastatic phenotype in invasive breast cancer. TFF3 was expressed at higher levels in primary tumors with associated metastasis, and its expression was higher in malignant cells that have metastasized away from those within the primary tumor. There appears to be a switch in the normal polarized secretion of TFF3 in invasive cancer, which allows it to exert invasion-promoting effects.
The study suggests that TFF3 may be one of the genes that mediate the various effects of estrogens in breast cancer. "The paradox remains, however, for both the estrogen receptor and TFF3, that they contribute to the normal physiology of the breast epithelium yet are involved in the progression of cancer," notes Dr. May.
Importantly, the investigators also evaluated the potential of TFF3 as a biomarker of lymphovascular invasion and lymph node metastasis. They found that TFF3 had greater predictive power than other markers analyzed, including tumor grade, age, tumor size and type, and estrogen and progesterone receptor status. "Our study reinforces the view that TFF3 expression merits evaluation as a prognostic biomarker and as a predictive marker of response to therapy," concludes Dr. May. "It is probable that its malign effects will be mitigated by adjuvant endocrine therapy in women with hormone-responsive cancers. However, the usefulness of TFF3 as a marker of hormone responsiveness needs to be evaluated."
**Source: Elsevier Health Sciences
17 February 2012
La OMS analiza los límites a la difusión de estudios sobre la gripe aviar
La Organización Mundial de la Salud (OMS) reúne en Ginebra a científicos que están analizando los recientes estudios sobre el virus de la gripe aviar (H5N1) y discuten si es necesario o deseable publicarlos, dado el eventual peligro de que sean utilizados con fines ajenos a la investigación.
En la reunión participan una veintena de científicos de Australia, EEUU, Francia, Gran Bretaña y Holanda, y de países asiáticos como China, Indonesia, Japón y Vietnam, afectados especialmente por ese virus.
A mediados de diciembre del año pasado se supo que 38 científicos de las universidades Erasmo de Rotterdam (Holanda) y Wisconsin (EEUU), liderados por el virólogo holandés Ron Fouchier, habían descubierto cinco mutaciones genéticas que el virus H5N1 puede sufrir para su contagio entre las personas.
El objetivo del estudio holandés, que ha sido financiado por el Instituto Nacional de Salud estadounidense, perseguía conseguir la información necesaria para evitar una posible pandemia originada por esa variante de la gripe. Para ello, estaban intentando crear la vacuna que protegería contra las nuevas cepas.
Los científicos estaban a punto de publicar sus resultados en las revistas especializadas 'Nature' y 'Science', pero fueron presionados para no hacerlo por las autoridades sanitarias de EEUU, que temían que, si compartían públicamente estos conocimientos, podían eventualmente ser usados por terroristas para crear un arma biológica.
Normalmente, el virus H5N1 se transmite entre aves de corral y su contagio a humanos se produce raramente, por lo que la transmisión entre personas podría ser altamente letal.
De hecho, cada vez que se refiere al H5N1, la OMS recuerda que el virus es potencialmente muy peligroso porque si bien normalmente no contamina a las personas, cuando lo hace, mata al 60% de los infectados.
Tras la polémica, el pasado 30 de diciembre la OMS alertó del riesgo potencial de hacer investigaciones sobre el virus de gripe si no se aplican las estrictas normas y recomendaciones aprobadas por este organismo, y más de 20 días después, decidió convocar la reunión que se celebra hoy.
Mientras, los científicos no sólo no publicaron los resultados, sino que se impuso una moratoria de 60 días, en los que no continuarán con las investigaciones, a la espera de que la comunidad científica se ponga de acuerdo sobre cómo proceder en el futuro.
**AGENCIAS
En la reunión participan una veintena de científicos de Australia, EEUU, Francia, Gran Bretaña y Holanda, y de países asiáticos como China, Indonesia, Japón y Vietnam, afectados especialmente por ese virus.
A mediados de diciembre del año pasado se supo que 38 científicos de las universidades Erasmo de Rotterdam (Holanda) y Wisconsin (EEUU), liderados por el virólogo holandés Ron Fouchier, habían descubierto cinco mutaciones genéticas que el virus H5N1 puede sufrir para su contagio entre las personas.
El objetivo del estudio holandés, que ha sido financiado por el Instituto Nacional de Salud estadounidense, perseguía conseguir la información necesaria para evitar una posible pandemia originada por esa variante de la gripe. Para ello, estaban intentando crear la vacuna que protegería contra las nuevas cepas.
Los científicos estaban a punto de publicar sus resultados en las revistas especializadas 'Nature' y 'Science', pero fueron presionados para no hacerlo por las autoridades sanitarias de EEUU, que temían que, si compartían públicamente estos conocimientos, podían eventualmente ser usados por terroristas para crear un arma biológica.
Normalmente, el virus H5N1 se transmite entre aves de corral y su contagio a humanos se produce raramente, por lo que la transmisión entre personas podría ser altamente letal.
De hecho, cada vez que se refiere al H5N1, la OMS recuerda que el virus es potencialmente muy peligroso porque si bien normalmente no contamina a las personas, cuando lo hace, mata al 60% de los infectados.
Tras la polémica, el pasado 30 de diciembre la OMS alertó del riesgo potencial de hacer investigaciones sobre el virus de gripe si no se aplican las estrictas normas y recomendaciones aprobadas por este organismo, y más de 20 días después, decidió convocar la reunión que se celebra hoy.
Mientras, los científicos no sólo no publicaron los resultados, sino que se impuso una moratoria de 60 días, en los que no continuarán con las investigaciones, a la espera de que la comunidad científica se ponga de acuerdo sobre cómo proceder en el futuro.
**AGENCIAS
Common flame retardant linked to social, behavioral and learning deficits
Mice genetically engineered to be susceptible to autism-like behaviors that were exposed to a common flame retardant were less fertile and their offspring were smaller, less sociable and demonstrated marked deficits in learning and long-term memory when compared with the offspring of normal unexposed mice, a study by researchers at UC Davis has found. The researchers said the study is the first to link genetics and epigenetics with exposure to a flame retardant chemical. The research was published online February 16 in the journal Human Molecular Genetics. It will be presented during a symposium on Feb. 18, at the annual meeting of the American Association for the Advancement of Science (AAAS) by Janine LaSalle, a professor in the Department of Medical Microbiology and Immunology in the UC Davis School of Medicine and the UC Davis Genome Center.
"This study highlights the interaction between epigenetics and the effects of early exposure to flame retardants," said Janine LaSalle, the study's senior author and a researcher affiliated with the UC Davis MIND Institute. "Our experiments with wild-type and mutant mice indicate that exposure to flame retardants presents an independent risk of neurodevelopmental deficits associated with reduced sociability and learning."
Epigenetics describes the heritable changes in gene expression caused by mechanisms other than those in the DNA sequence. One such mechanism is DNA methylation, in which genes are silenced when their activation no longer is required. DNA methylation is essential for normal development. The researchers chose a mouse that was genetically and epigenetically susceptible to social behavioral deficits in order to understand the potential effect of this environmental pollutant on genetically susceptible humans.
LaSalle and her colleagues examined the effects of the chemical BDE-47 (Tetrabromodiphenl ether), a member of the class of flame retardants called polybrominated diphenylethers, or PBDEs. PBDEs have been used in a wide range of products, including electronics, bedding, carpeting and furniture. They have been shown to persist in the environment and accumulate in living organisms, and toxicological testing has found that they may cause liver toxicity, thyroid toxicity and neurodevelopmental toxicity, according to the U.S. Environmental Protection Agency. BDE-47 is the PBDE found at highest concentrations in human blood and breast milk, raising concerns about its potential neurotoxic effects during pregnancy and neonatal development.
The research was conducted in the offspring of mice genetically engineered for the autism phenotype found in Rett syndrome, a disorder that occurs primarily in females and causes regression in expressive language, motor skills and social reciprocity in late infancy. The condition affects about 1 in 10,000 children.
Autism spectrum disorders are a group of neurodevelopmental disabilities that can cause significant social, communication and behavioral deficits. The U.S. Centers for Disease Control and Prevention estimates that an average of 1 in 110 children born in the United States today will be diagnosed with an autism spectrum disorder.
Rett syndrome is causally linked to defects in the methyl-CpG-binding protein 2 gene MECP2 situated on the X chromosome. Mutations in MECP2 result in a nonfunctional MeCP2 protein, which is required for normal brain development. The researchers evaluated the effects of exposure to BDE-47 on mice genetically engineered to have mutations in MECP2 and their offspring, or pups. The genetically engineered Mecp2 mother mice, or dams, were bred with non-mutant wild-type males. The dams were monitored for 10 weeks -- for four weeks prior to conception, three weeks during gestation and three weeks of lactation. They were then compared with a control group of normal, unexposed dams and pups over several generations and hundreds of mice.
The study found that that the weights of the pups of the lactating BDE-47-exposed dams were diminished when compared with the controls, as were their survival rates. To assess the effects of the flame retardant exposure on the pups and their genotypes, the researchers placed them through more than 10 cognitive, social and physical tests.
Female offspring of dams exposed with BDE-47 spent half as much time interacting with another mouse in a 10-minute sociability test compared to controls. The reduced sociability in BDE-47 exposed females corresponded to reduced DNA methylation in females regardless of genotype. In addition, genetic and environmental interaction effects in this study were specifically observed in females.
In a short-term memory test of social novelty, although all mice showed the expected preference for interacting with a novel over a familiar mouse, BDE-47-exposed mutant female mice spent about half as much time interacting with the familiar mouse than their non-mutant littermates. In a long-term memory test of swimming to reach a hidden platform in a cloudy pool, female mice who were both mutant and BDE-47 exposed did not learn to reach the platform faster after fourdays of training. These behavioral changes in social and cognitive learning specifically in the interaction group corresponded to changes in a known epigenetic regulator of DNA methylation in brain, DNA methyltransferase 3a (Dnmt3a).
LaSalle said that the study results are important because better understanding of the epigenetic pathways implicated in social behavior and cognition may lead to improved treatments for autism spectrum disorders.
"While the obvious preventative step is to limit the use and accumulation of PBDEs in our environment, this would likely be a long-term solution," LaSalle said. "These pollutants are going to be hard to get rid of tomorrow. However, one important preventative that all women could do tomorrow is to start taking prenatal vitamins before becoming pregnant, as these may counteract the toxins in our environment through DNA methylation," she said.
**Source: University of California - Davis Health System
"This study highlights the interaction between epigenetics and the effects of early exposure to flame retardants," said Janine LaSalle, the study's senior author and a researcher affiliated with the UC Davis MIND Institute. "Our experiments with wild-type and mutant mice indicate that exposure to flame retardants presents an independent risk of neurodevelopmental deficits associated with reduced sociability and learning."
Epigenetics describes the heritable changes in gene expression caused by mechanisms other than those in the DNA sequence. One such mechanism is DNA methylation, in which genes are silenced when their activation no longer is required. DNA methylation is essential for normal development. The researchers chose a mouse that was genetically and epigenetically susceptible to social behavioral deficits in order to understand the potential effect of this environmental pollutant on genetically susceptible humans.
LaSalle and her colleagues examined the effects of the chemical BDE-47 (Tetrabromodiphenl ether), a member of the class of flame retardants called polybrominated diphenylethers, or PBDEs. PBDEs have been used in a wide range of products, including electronics, bedding, carpeting and furniture. They have been shown to persist in the environment and accumulate in living organisms, and toxicological testing has found that they may cause liver toxicity, thyroid toxicity and neurodevelopmental toxicity, according to the U.S. Environmental Protection Agency. BDE-47 is the PBDE found at highest concentrations in human blood and breast milk, raising concerns about its potential neurotoxic effects during pregnancy and neonatal development.
The research was conducted in the offspring of mice genetically engineered for the autism phenotype found in Rett syndrome, a disorder that occurs primarily in females and causes regression in expressive language, motor skills and social reciprocity in late infancy. The condition affects about 1 in 10,000 children.
Autism spectrum disorders are a group of neurodevelopmental disabilities that can cause significant social, communication and behavioral deficits. The U.S. Centers for Disease Control and Prevention estimates that an average of 1 in 110 children born in the United States today will be diagnosed with an autism spectrum disorder.
Rett syndrome is causally linked to defects in the methyl-CpG-binding protein 2 gene MECP2 situated on the X chromosome. Mutations in MECP2 result in a nonfunctional MeCP2 protein, which is required for normal brain development. The researchers evaluated the effects of exposure to BDE-47 on mice genetically engineered to have mutations in MECP2 and their offspring, or pups. The genetically engineered Mecp2 mother mice, or dams, were bred with non-mutant wild-type males. The dams were monitored for 10 weeks -- for four weeks prior to conception, three weeks during gestation and three weeks of lactation. They were then compared with a control group of normal, unexposed dams and pups over several generations and hundreds of mice.
The study found that that the weights of the pups of the lactating BDE-47-exposed dams were diminished when compared with the controls, as were their survival rates. To assess the effects of the flame retardant exposure on the pups and their genotypes, the researchers placed them through more than 10 cognitive, social and physical tests.
Female offspring of dams exposed with BDE-47 spent half as much time interacting with another mouse in a 10-minute sociability test compared to controls. The reduced sociability in BDE-47 exposed females corresponded to reduced DNA methylation in females regardless of genotype. In addition, genetic and environmental interaction effects in this study were specifically observed in females.
In a short-term memory test of social novelty, although all mice showed the expected preference for interacting with a novel over a familiar mouse, BDE-47-exposed mutant female mice spent about half as much time interacting with the familiar mouse than their non-mutant littermates. In a long-term memory test of swimming to reach a hidden platform in a cloudy pool, female mice who were both mutant and BDE-47 exposed did not learn to reach the platform faster after fourdays of training. These behavioral changes in social and cognitive learning specifically in the interaction group corresponded to changes in a known epigenetic regulator of DNA methylation in brain, DNA methyltransferase 3a (Dnmt3a).
LaSalle said that the study results are important because better understanding of the epigenetic pathways implicated in social behavior and cognition may lead to improved treatments for autism spectrum disorders.
"While the obvious preventative step is to limit the use and accumulation of PBDEs in our environment, this would likely be a long-term solution," LaSalle said. "These pollutants are going to be hard to get rid of tomorrow. However, one important preventative that all women could do tomorrow is to start taking prenatal vitamins before becoming pregnant, as these may counteract the toxins in our environment through DNA methylation," she said.
**Source: University of California - Davis Health System
Successful human tests for first wirelessly controlled drug-delivery chip
About 15 years ago, MIT professors Robert Langer and Michael Cima had the idea to develop a programmable, wirelessly controlled microchip that would deliver drugs after implantation in a patient's body. This week, the MIT researchers and scientists from MicroCHIPS Inc. reported that they have successfully used such a chip to administer daily doses of an osteoporosis drug normally given by injection. The results, published in the Feb. 16 online edition of Science Translational Medicine, represent the first successful test of such a device and could help usher in a new era of telemedicine -- delivering health care over a distance, Langer says.
"You could literally have a pharmacy on a chip," says Langer, the David H. Koch Institute Professor at MIT. "You can do remote control delivery, you can do pulsatile drug delivery, and you can deliver multiple drugs."
In the new study, funded and overseen by MicroCHIPS, scientists used the programmable implants to deliver an osteoporosis drug called teriparatide to seven women aged 65 to 70. The study found that the device delivered dosages comparable to injections, and there were no adverse side effects.
These programmable chips could dramatically change treatment not only for osteoporosis, but also for many other diseases, including cancer and multiple sclerosis. "Patients with chronic diseases, regular pain-management needs or other conditions that require frequent or daily injections could benefit from this technology," says Robert Farra, president and chief operating officer at MicroCHIPS and lead author of the paper.
"Compliance is very important in a lot of drug regimens, and it can be very difficult to get patients to accept a drug regimen where they have to give themselves injections," says Cima, the David H. Koch Professor of Engineering at MIT. "This avoids the compliance issue completely, and points to a future where you have fully automated drug regimens."
Achieving precision
The MIT research team started working on the implantable chip in the mid-1990s. John Santini, then a University of Michigan undergraduate visiting MIT, took it on as a summer project under the direction of Cima and Langer. Santini, who later returned to MIT as a graduate student to continue the project, is also an author of the new paper.
In 1999, the MIT team published its initial findings in Nature, and MicroCHIPS was founded and licensed the microchip technology from MIT. The company refined the chips, including adding a hermetic seal and a release system that works reliably in living tissue. Teriparatide is a polypeptide and therefore much less chemically stable than small-molecule drugs, so sealing it hermetically to preserve it was an important achievement, Langer says.
The human clinical trial began in Denmark in January 2011. Chips were implanted during a 30-minute procedure at a doctor's office using local anesthetic, and remained in the patients for four months. The implants proved safe, and patients reported they often forgot they even had the implant, Cima says.
Chips used in the study stored 20 doses of teriparatide, individually sealed in tiny reservoirs about the size of a pinprick. The reservoirs are capped with a thin layer of platinum and titanium that melts when a small electrical current is applied, releasing the drug inside. MicroCHIPS is now working on developing implants that can carry hundreds of drug doses per chip.
Because the chips are programmable, dosages can be scheduled in advance or triggered remotely by radio communication over a special frequency called Medical Implant Communication Service (MICS). Current versions work over a distance of a few inches, but researchers plan to extend that range.
Consistent results
In the Science Translational Medicine study, the researchers measured bone formation in osteoporosis patients with the implants, and found that it was similar to that seen in patients receiving daily injections of teriparatide. Another notable result is that the dosages given by implant had less variation than those given by injection.
Henry Brem, professor of neurosurgery, ophthalmology, oncology and biological engineering at Johns Hopkins University School of Medicine, called the results "stunning."
**Source: Massachusetts Institute of Technology
"You could literally have a pharmacy on a chip," says Langer, the David H. Koch Institute Professor at MIT. "You can do remote control delivery, you can do pulsatile drug delivery, and you can deliver multiple drugs."
In the new study, funded and overseen by MicroCHIPS, scientists used the programmable implants to deliver an osteoporosis drug called teriparatide to seven women aged 65 to 70. The study found that the device delivered dosages comparable to injections, and there were no adverse side effects.
These programmable chips could dramatically change treatment not only for osteoporosis, but also for many other diseases, including cancer and multiple sclerosis. "Patients with chronic diseases, regular pain-management needs or other conditions that require frequent or daily injections could benefit from this technology," says Robert Farra, president and chief operating officer at MicroCHIPS and lead author of the paper.
"Compliance is very important in a lot of drug regimens, and it can be very difficult to get patients to accept a drug regimen where they have to give themselves injections," says Cima, the David H. Koch Professor of Engineering at MIT. "This avoids the compliance issue completely, and points to a future where you have fully automated drug regimens."
Achieving precision
The MIT research team started working on the implantable chip in the mid-1990s. John Santini, then a University of Michigan undergraduate visiting MIT, took it on as a summer project under the direction of Cima and Langer. Santini, who later returned to MIT as a graduate student to continue the project, is also an author of the new paper.
In 1999, the MIT team published its initial findings in Nature, and MicroCHIPS was founded and licensed the microchip technology from MIT. The company refined the chips, including adding a hermetic seal and a release system that works reliably in living tissue. Teriparatide is a polypeptide and therefore much less chemically stable than small-molecule drugs, so sealing it hermetically to preserve it was an important achievement, Langer says.
The human clinical trial began in Denmark in January 2011. Chips were implanted during a 30-minute procedure at a doctor's office using local anesthetic, and remained in the patients for four months. The implants proved safe, and patients reported they often forgot they even had the implant, Cima says.
Chips used in the study stored 20 doses of teriparatide, individually sealed in tiny reservoirs about the size of a pinprick. The reservoirs are capped with a thin layer of platinum and titanium that melts when a small electrical current is applied, releasing the drug inside. MicroCHIPS is now working on developing implants that can carry hundreds of drug doses per chip.
Because the chips are programmable, dosages can be scheduled in advance or triggered remotely by radio communication over a special frequency called Medical Implant Communication Service (MICS). Current versions work over a distance of a few inches, but researchers plan to extend that range.
Consistent results
In the Science Translational Medicine study, the researchers measured bone formation in osteoporosis patients with the implants, and found that it was similar to that seen in patients receiving daily injections of teriparatide. Another notable result is that the dosages given by implant had less variation than those given by injection.
Henry Brem, professor of neurosurgery, ophthalmology, oncology and biological engineering at Johns Hopkins University School of Medicine, called the results "stunning."
**Source: Massachusetts Institute of Technology
Prueban con éxito un dispositivo implantable, a prueba de olvidos, que controla la osteoporosis sin tener que tomar pastillas ni inyecciones
En las próximas décadas los enfermos crónicos probablemente no tengan que estar pendientes de su medicación diaria ni de los ajustes en el tratamiento. Habrá sistemas a prueba de olvidos. Bastará, entonces, con que el médico haga una llamada desde un teléfono móvil o envíe la orden desde un ordenador para que un dispositivo implantado en el organismo libere la dosis necesaria de medicamento. El primer paso para que esto sea una realidad lo acaba de dar un equipo de investigadores estadounidenses al diseñar un microchip que libera un fármaco (teripatida), utilizado contra la osteoporosis más grave. El tratamiento, probado con éxito en un grupo reducido de siete mujeres danesas, se acaba de publicar en la revista «Science Translational Medicine» y se ha presentado en el congreso que la Sociedad Americana para el Avance de la Ciencia.
Es la primera vez que un dispositivo de estas características se prueba con éxito y abre una nueva vía de tratamiento, no solo para la osteoporosis sino para otras enfermedades crónicas como el cáncer, la esclerosis múltiple o las enfermedades cardiovasculares. «Podemos tener una farmacia en un chip», explicó Robert Langer, uno de los científicos del Instituto de Tecnología de Massachusetts (MIT) que ha desarrollado el ingenio. La fórmula no solo es más eficaz y cómoda sino que además podría ser más económica.
El microchip se implanta bajo la piel con anestesia local. El ingenio contiene celdas diminutas donde se aloja el fármaco y solo se abren cuando reciben una señal por control remoto. A las siete mujeres que participaron en el estudio se les colocó en la cintura. Allí estuvo alojado durante cuatro meses, sin causar ninguna molestia. Todas tenían una forma severa de osteoporosis que les obligaba a seguir un tratamiento inyectable diario para combatir la debilidad de sus huesos. El dispositivo liberaba el mismo fármaco que se les inyectaba, un formador de hueso que reduce el riesgo de fracturas. Al final del estudio los resultados de seguridad y eficacia fueron los mismos que los proporcionados con la versión inyectable. Aunque con una ventaja: el tratamiento llegaba siempre a la misma hora, sin riesgo de variación en la medicación por olvido o problemas de los pacientes.
Es la primera vez que un dispositivo de estas características se prueba con éxito y abre una nueva vía de tratamiento, no solo para la osteoporosis sino para otras enfermedades crónicas como el cáncer, la esclerosis múltiple o las enfermedades cardiovasculares. «Podemos tener una farmacia en un chip», explicó Robert Langer, uno de los científicos del Instituto de Tecnología de Massachusetts (MIT) que ha desarrollado el ingenio. La fórmula no solo es más eficaz y cómoda sino que además podría ser más económica.
El microchip se implanta bajo la piel con anestesia local. El ingenio contiene celdas diminutas donde se aloja el fármaco y solo se abren cuando reciben una señal por control remoto. A las siete mujeres que participaron en el estudio se les colocó en la cintura. Allí estuvo alojado durante cuatro meses, sin causar ninguna molestia. Todas tenían una forma severa de osteoporosis que les obligaba a seguir un tratamiento inyectable diario para combatir la debilidad de sus huesos. El dispositivo liberaba el mismo fármaco que se les inyectaba, un formador de hueso que reduce el riesgo de fracturas. Al final del estudio los resultados de seguridad y eficacia fueron los mismos que los proporcionados con la versión inyectable. Aunque con una ventaja: el tratamiento llegaba siempre a la misma hora, sin riesgo de variación en la medicación por olvido o problemas de los pacientes.
-Centenares de dosis
El implante liberaba el medicamento en el momento deseado, accionado con control remoto. Pero además el fármaco llegaba al torrente sanguíneo con la misma rapidez y eficacia que si se pusiera una inyección. Las mujeres tratadas, de entre 65 y 70 años, estaban dispuestas a repetir la experiencia y aseguraron que durante el tiempo que duró el ensayo prácticamente se olvidaron de que lo llevaban bajo la piel.
Los microchips utilizados estaban preparados para alojar 20 dosis del medicamento, aunque se trabaja en nuevos ingenios que podrían almacenar centenares de dosis en celdas diminutas. Cada una de estas celdas está recubierta con una ligera capa de platino y titanio. Cuando se envía una señal a distancia, el microchip libera una pequeña corriente que funde la cobertura de platino para dejar salir al medicamento.
El implante liberaba el medicamento en el momento deseado, accionado con control remoto. Pero además el fármaco llegaba al torrente sanguíneo con la misma rapidez y eficacia que si se pusiera una inyección. Las mujeres tratadas, de entre 65 y 70 años, estaban dispuestas a repetir la experiencia y aseguraron que durante el tiempo que duró el ensayo prácticamente se olvidaron de que lo llevaban bajo la piel.
Los microchips utilizados estaban preparados para alojar 20 dosis del medicamento, aunque se trabaja en nuevos ingenios que podrían almacenar centenares de dosis en celdas diminutas. Cada una de estas celdas está recubierta con una ligera capa de platino y titanio. Cuando se envía una señal a distancia, el microchip libera una pequeña corriente que funde la cobertura de platino para dejar salir al medicamento.
**Publicado en "ABC"
Mejor no usar antibióticos para las sinusitis según un estudio
Los antibióticos no ayudan a combatir la mayoría de las infecciones sinusales, aunque los médicos los prescriben habitualmente para ese fin, según un estudio realizado en EE.UU. y publicado en Journal of the American Medical Association (JAMA). Los investigadores han visto que los antibióticos no alivian los síntomas de los pacientes o que éstos se reincorporen al trabajo antes que un placebo.
El abuso o mal uso de antibióticos es un problema de salud pública, debido a las resistencias antimicrobianas. Pero, en la sinusitis, es difícil saber si la enfermedad está causada por bacterias o por un virus, en el que los antibióticos no sirven para nada.
«En lugar de administrar a todos un antibiótico, nuestros hallazgos sugieren que es mejor abstenerse y observar la evolución» señaló a Reuters Health Jane Garbutt de Washington University School of Medicine en St. Louis, quien dirigió el estudio. Esto implica controlar a los pacientes para ver si mejoran, y usar sólo analgésicos.
Las personas con sinusitis aguda tienen unos síntomas parecidos al resfriado, como goteo nasal y dolor alrededor de los ojos, la nariz o la frente. «Es la quinta razón más común por la que se recetan antibióticos para adulto», advirtió Garbutt.
Sin diferencias
El equipo de Garbutt asignó aleatoriamente a 166 adultos a recibir placebo o un tratamiento de 10 días con el antibiótico amoxicilina. Al finalizar el estudio, los investigadores encontraron poca diferencia entre los dos grupos de pacientes.
Después de siete días, hubo signos de beneficios de los antibióticos, pero el efecto fue pequeño y se había desvanecido otros tres días más tarde. A los 10 días, el 78 por ciento de las personas tratadas antibióticos y el 80 por ciento de los tratados con placebo dijeron que se sentían mucho mejor y ya no tenía síntomas.
Menos del dos por ciento de las infecciones sinusales son bacterianas. La mayoría de los casos son víricos, y la gran mayoría no requieren antibióticos. En este sentido, la Sociedad Americana de Enfermedades Infecciosas ha elaborado directrices que recomiendan tratar sólo a pacientes cuyos síntomas duran por lo menos 10 días, aquellos que están gravemente enfermos con fiebre alta y otros síntomas, o que mejoran para después empeorar.
**Publicado en "ABC SALUD"
El abuso o mal uso de antibióticos es un problema de salud pública, debido a las resistencias antimicrobianas. Pero, en la sinusitis, es difícil saber si la enfermedad está causada por bacterias o por un virus, en el que los antibióticos no sirven para nada.
«En lugar de administrar a todos un antibiótico, nuestros hallazgos sugieren que es mejor abstenerse y observar la evolución» señaló a Reuters Health Jane Garbutt de Washington University School of Medicine en St. Louis, quien dirigió el estudio. Esto implica controlar a los pacientes para ver si mejoran, y usar sólo analgésicos.
Las personas con sinusitis aguda tienen unos síntomas parecidos al resfriado, como goteo nasal y dolor alrededor de los ojos, la nariz o la frente. «Es la quinta razón más común por la que se recetan antibióticos para adulto», advirtió Garbutt.
Sin diferencias
El equipo de Garbutt asignó aleatoriamente a 166 adultos a recibir placebo o un tratamiento de 10 días con el antibiótico amoxicilina. Al finalizar el estudio, los investigadores encontraron poca diferencia entre los dos grupos de pacientes.
Después de siete días, hubo signos de beneficios de los antibióticos, pero el efecto fue pequeño y se había desvanecido otros tres días más tarde. A los 10 días, el 78 por ciento de las personas tratadas antibióticos y el 80 por ciento de los tratados con placebo dijeron que se sentían mucho mejor y ya no tenía síntomas.
Menos del dos por ciento de las infecciones sinusales son bacterianas. La mayoría de los casos son víricos, y la gran mayoría no requieren antibióticos. En este sentido, la Sociedad Americana de Enfermedades Infecciosas ha elaborado directrices que recomiendan tratar sólo a pacientes cuyos síntomas duran por lo menos 10 días, aquellos que están gravemente enfermos con fiebre alta y otros síntomas, o que mejoran para después empeorar.
**Publicado en "ABC SALUD"
16 February 2012
Fundación Josep Carreras contra la Leucemia: Experimento Valora la vida
Barcelona. Mes de enero de 2012. Tres personas de diferentes edades quieren lanzar un mensaje a la sociedad: que estamos en crisis, sí, pero que en lugar de ser negativos, tenemos que dar gracias por lo que tenemos, la salud, ser solidarios y valorar la vida.
Virginia, Yolanda y Victor tienen 32, 24 y 57 años respectivamente. A primera vista nada tienen en común pero resulta que comparten una misma historia. Hace alrededor de 2 años y medio los tres padecían una enfermedad hematológica maligna: Virginia tuvo leucemia, Yolanda y Victor un linfoma. Les hemos propuesto un reto: salir a la calle y transmitir a la sociedad que a pesar de la época difícil que estamos viviendo, sonrían y se den cuenta que la vida es maravillosa. Las personas que se han cruzado con ellos no sabían quiénes eran, sólo recibieron un papel que les llegó al corazón...
Virginia, Yolanda y Victor tienen 32, 24 y 57 años respectivamente. A primera vista nada tienen en común pero resulta que comparten una misma historia. Hace alrededor de 2 años y medio los tres padecían una enfermedad hematológica maligna: Virginia tuvo leucemia, Yolanda y Victor un linfoma. Les hemos propuesto un reto: salir a la calle y transmitir a la sociedad que a pesar de la época difícil que estamos viviendo, sonrían y se den cuenta que la vida es maravillosa. Las personas que se han cruzado con ellos no sabían quiénes eran, sólo recibieron un papel que les llegó al corazón...
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