El Instituto Valenciano de Infertilidad y Air Liquide Medicinal han renovado su acuerdo de colaboración centrado en el suministro de gases y en el compromiso de investigación y desarrollo.
Las investigaciones, que comenzaron el año pasado, están encaminadas a la mejora de la calidad y la eficacia de los tratamientos de fertilidad. De hecho, Air Liquide suministra a todos los centros del IVI en España (un total de 14) nitrógeno líquido limpio que se obtiene a través del dispositivo Ceralin, patentado por Air Liquide.
El nitrógeno líquido limpio es utilizado en la criopreservación de muestras biológicas, células o tejidos que posteriormente pueden emplearse en humanos. De ahí la importancia de controlar la carga microbiológica que pueda contener el nitrógeno líquido utilizado para la criopreservación.
"Esta unión entre la experiencia de Air Liquide en aplicación de gases a bajas temperaturas y del IVI, el centro de reproducción asistida de referencia en Europa, nos permitirá seguir trabajando en el desarrollo de tecnologías que mejoren la calidad en los procesos criobiológicos" explica Ángel Bajils, Director General de Air Liquide Medicinal.
Luis Saurat, director general de IVI, comenta: "la utilización del nitrógeno líquido limpio de Air Liquide ha contribuido a que los resultados del banco de óvulos de IVI, el más grande del mundo con más de 10.000 óvulos de donantes almacenados, sean espectaculares ya que el 95% de los óvulos sobreviven al proceso de desvitrificación ofreciendo los mismos resultados reproductivos que los ovocitos frescos".
Además del suministro del nitrógeno líquido utilizado en la congelación y conservación de muestras, se encuentran el oxígeno medicinal para respiración, el óxido nitroso medicinal para anestesia, así como el dióxido de carbono y otras mezclas destinadas a las atmósferas modificadas de las incubadoras y otras aplicaciones.
11 July 2011
La Federación Española de Cáncer de Mama reclama un pacto por la sanidad para la sostenibilidad del sistema
La Junta directiva de la Federación Española de Cáncer de Mama (FECMA), integrada por representantes de 38 asociaciones que suman 35.000 asociadas, pide a los responsables de todas las administraciones sanitarias públicas "responsabilidad, sensibilidad y compromiso para alcanzar un Pacto por la Sanidad que garantice la sostenibilidad del sistema público de salud", subraya su presidenta, Antonia Gimón.
En este sentido, precisa que "sostenibilidad y calidad no son conceptos contrapuestos, sino exigencias complementarias ante el futuro".
La dirección de FECMA ha hecho estas valoraciones en la reunión mantenida en Santander, coincidiendo con la celebración en la Universidad Internacional Menéndez Pelayo del curso 'Políticas de género en el ámbito de la salud', organizado por la Federación y dirigido por el oncólogo José Manuel López Vega.
La resolución de la Junta Directiva aboga por un pacto sanitario "que garantice la sostenibilidad, la cohesión, la equidad y la calidad de nuestro sistema nacional de salud, que es gestionado por diferentes administraciones pero es único es su concepción constitucional como garante del derecho universal a la salud".
"Como pacientes activas, defendemos una medicina integral que reconozca derechos y deberes de los pacientes y de los profesionales, vinculando esa sanidad integral a lo mejor de la tradición del humanismo en la medicina y al reconocimiento de una visión integral de la persona", finaliza Gimón.
En este sentido, precisa que "sostenibilidad y calidad no son conceptos contrapuestos, sino exigencias complementarias ante el futuro".
La dirección de FECMA ha hecho estas valoraciones en la reunión mantenida en Santander, coincidiendo con la celebración en la Universidad Internacional Menéndez Pelayo del curso 'Políticas de género en el ámbito de la salud', organizado por la Federación y dirigido por el oncólogo José Manuel López Vega.
La resolución de la Junta Directiva aboga por un pacto sanitario "que garantice la sostenibilidad, la cohesión, la equidad y la calidad de nuestro sistema nacional de salud, que es gestionado por diferentes administraciones pero es único es su concepción constitucional como garante del derecho universal a la salud".
"Como pacientes activas, defendemos una medicina integral que reconozca derechos y deberes de los pacientes y de los profesionales, vinculando esa sanidad integral a lo mejor de la tradición del humanismo en la medicina y al reconocimiento de una visión integral de la persona", finaliza Gimón.
Anoréxicos sexuales por culpa del porno
Con el distintivo «Parental advisory: Explicit Content», se podría, al parecer, poner un semáforo rojo a los menores que ven porno en Youtube. Es, para la Asociación de Industria Discográfica de Estados Unidos (RIIA por sus siglas en inglés), una forma de advertir a los progenitores de que sus hijos consumen este material. Porque hay estudios que revelan que esto puede hacer que los muchachos se cansen del sexo antes siquiera de empezar, si lo ven en exceso. La falta de interés la ha observado Carlo Foresta, director de la Sociedad de Medicina Sexual y de Andrología Italiana (SIAM).
«La sexualidad por internet es agresiva. Estas experiencias desvían la maduración gradual e instintiva sexual y llevan a considerar menos interesantes las prácticas normales», dice a este semanario.En el estudio realizado por Foresta y su equipo con casi 3.000 hombres, la mayoría afirmó haber comenzado a ver este tipo de cine con 14 años, y mostraron los primeros síntomas de anorexia sexual alrededor de los 25. Foresta matiza que «no va acorde al desarrollo psicológico e intelectual del joven. Su cerebro no está lo suficientemente desarrollado y estas películas representan una sexualidad cruel y muy fuerte, alejada de la afectividad y el erotismo».
Según los especialistas, la pérdida de deseo sobreviene por la repetición y la pasividad. «En la vida real, las experiencias de las películas son difíciles de alcanzar, y eso es lo que determina un deseo cada vez más pobre». ErecciónPero a esta práctica le han colgado el San Benito de ser, además de perniciosa, potenciadora de problemas fisiológicos relacionados con la erección. No obstante, Foresta aclara que «la disfunción eréctil no está relacionada con este tipo de práctica».
En contraposición, Irving Biederman, psicólogo y profesor de neurociencia en la Universidad del Sur de California, afirma que no existen tales efectos nocivos. «Hace algunos años la llamada “Meese Commission” (bajo el antiguo ministro de Justicia estadounidense Meese) buscó evidencias de que la pornografía era dañina. Pero, a pesar de la tendencia antiporno extrema, fueron incapaces de encontrar pruebas». La conclusión general (más bien que lo que algunos ideólogos de la derecha desearon concluir) era que los hombres usaban la pornografía para su despertar sexual y esto tenía un efecto beneficioso sobre su experiencia sin conducir a los crímenes de violación o atentados contra el pudor».
**Publicado en "LA RAZON"
Advances in research into Alzheimer's disease
Advances in research into Alzheimer's disease: transporter proteins at the blood CSF barrier and vitamin D may help prevent amyloid β build up in the brain Advancing age is a major risk factor for Alzheimer's disease and is associated with build- up of the peptide amyloid β in the brain. New research published in BioMed Central's open access journal Fluids and Barriers of the CNS shows that removal of amyloid β from the brain depends on vitamin D and also on an age-related alteration in the production of transporter proteins which move amyloid β in and out of the brain.
Low levels of vitamin D are thought to be involved in age-related decline in memory and cognition and are also associated with Alzheimer's disease. Researchers from Tohoku University, Japan, looked at the mechanism behind this and found that vitamin D injections improved the removal of amyloid β from the brain of mice.
Prof Tetsuya Terasaki said, "Vitamin D appears increase transport of amyloid β across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway. These results lead the way towards new therapeutic targets in the search for prevention of Alzheimer's disease."
The transport of amyloid β across the BBB is known to be orchestrated by transporter proteins such as LRP-1 and P-gp, which move amyloid β out of the brain, and RAGE, which controls influx. Looking at the transport of amyloid β from blood to cerebrospinal fluid (CSF), and from CSF to blood, researchers from Rhode Island Hospital and The Warren Alpert Medical School, found that LRP-1 and P-gp at the blood-cerebrospinal fluid barrier (BCSFB), increased with age so increasing removal of amyloid β from the CSF and brain.
Prof Gerald Silverberg said, "While increased production of transporter proteins at the blood CSF barrier may help amyloid β removal from the older brain, production of these proteins eventually fails. This failure may be an important event in brain function as we age and for people with Alzheimer's disease."
**Source: BioMed Central
Low levels of vitamin D are thought to be involved in age-related decline in memory and cognition and are also associated with Alzheimer's disease. Researchers from Tohoku University, Japan, looked at the mechanism behind this and found that vitamin D injections improved the removal of amyloid β from the brain of mice.
Prof Tetsuya Terasaki said, "Vitamin D appears increase transport of amyloid β across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway. These results lead the way towards new therapeutic targets in the search for prevention of Alzheimer's disease."
The transport of amyloid β across the BBB is known to be orchestrated by transporter proteins such as LRP-1 and P-gp, which move amyloid β out of the brain, and RAGE, which controls influx. Looking at the transport of amyloid β from blood to cerebrospinal fluid (CSF), and from CSF to blood, researchers from Rhode Island Hospital and The Warren Alpert Medical School, found that LRP-1 and P-gp at the blood-cerebrospinal fluid barrier (BCSFB), increased with age so increasing removal of amyloid β from the CSF and brain.
Prof Gerald Silverberg said, "While increased production of transporter proteins at the blood CSF barrier may help amyloid β removal from the older brain, production of these proteins eventually fails. This failure may be an important event in brain function as we age and for people with Alzheimer's disease."
**Source: BioMed Central
High-resolution imaging technology reveals cellular details of coronary arteries
Researchers at the Wellman Center for Photomedicine at Massachusetts General Hospital (MGH) have developed a one-micrometer-resolution version of the intravascular imaging technology optical coherence tomography (OCT) that can reveal cellular and subcellular features of coronary artery disease. In a Nature Medicine paper receiving advance online publication, the investigators describe how microOCT – which provides 10 times greater resolution than standard OCT – was able to show individual arterial and inflammatory cells, including features that may identify vulnerable plaques, within coronary artery samples. "MicroOCT has the contrast and resolution required to investigate the cellular and subcellular components underlying coronary atherosclerosis, the disease that precipitates heart attack," says Gary Tearney, MD, PhD, of the Wellman Center and the MGH Pathology Department, who led the study. "This high level of performance opens up the future possibility of observing these microscopic features in human patients, which has implications for improving the understanding, diagnosis and therapeutic monitoring of coronary artery disease."
A catheter-based technology, OCT uses reflected near-infrared light to create detailed images of the internal surfaces of blood vessels. Although the technology is already being used to identify arterial plaques that are likely to rupture, standard OCT can clearly image only structures larger than 10 micrometers (millionths of a meter). Using new types of lenses and advanced imaging components, microOCT is able to image structures as small as one micrometer, revealing in intact tissue the detailed information provided by the prepared tissue slides of traditional pathology much faster and in three dimensions.
The researchers describe how using microOCT to study human and animal coronary artery tissue revealed detailed images of:
endothelial cells that line coronary arteries,
inflammatory cells that contribute to the formation of coronary plaques,
smooth muscle cells that produce collagen in response to inflammation,
fibrin proteins and platelets that are involved in the formation of clots
MicroOCT also produced detailed images of stents placed within coronary arteries, clearly distinguishing bare-metal stents from those covered with a drug-releasing polymer and revealing defects in the polymer coating.
"When we are able to implement microOCT in humans – probably in three to five years – the 10 times greater resolution will allow us to observe cells in the coronary arteries of living patients," says Tearney, a professor of Pathology at Harvard Medical School. "The ability to track and follow cells in three dimensions could help us prove or disprove many theories about coronary artery disease and better understand how clots form on a microscopic level. Improved definitions of high-risk plaques will lead to greater accuracy in identifying those that may go on to rupture and block the coronary artery, and the ability to monitor healing around implanted devices like stents could reduce the number of patients who must be on anticlotting medications, which are expensive and have side effects."
A catheter-based technology, OCT uses reflected near-infrared light to create detailed images of the internal surfaces of blood vessels. Although the technology is already being used to identify arterial plaques that are likely to rupture, standard OCT can clearly image only structures larger than 10 micrometers (millionths of a meter). Using new types of lenses and advanced imaging components, microOCT is able to image structures as small as one micrometer, revealing in intact tissue the detailed information provided by the prepared tissue slides of traditional pathology much faster and in three dimensions.
The researchers describe how using microOCT to study human and animal coronary artery tissue revealed detailed images of:
endothelial cells that line coronary arteries,
inflammatory cells that contribute to the formation of coronary plaques,
smooth muscle cells that produce collagen in response to inflammation,
fibrin proteins and platelets that are involved in the formation of clots
MicroOCT also produced detailed images of stents placed within coronary arteries, clearly distinguishing bare-metal stents from those covered with a drug-releasing polymer and revealing defects in the polymer coating.
"When we are able to implement microOCT in humans – probably in three to five years – the 10 times greater resolution will allow us to observe cells in the coronary arteries of living patients," says Tearney, a professor of Pathology at Harvard Medical School. "The ability to track and follow cells in three dimensions could help us prove or disprove many theories about coronary artery disease and better understand how clots form on a microscopic level. Improved definitions of high-risk plaques will lead to greater accuracy in identifying those that may go on to rupture and block the coronary artery, and the ability to monitor healing around implanted devices like stents could reduce the number of patients who must be on anticlotting medications, which are expensive and have side effects."
**Source: Massachusetts General Hospital
Genetic study sheds new light on auto-immune arthritis
The team of researchers from the Universities of Bristol, Queensland (Australia), Oxford, Texas and Toronto, used a technique called genome-wide association where millions of genetic markers are measured in thousands of people that have the disease and thousands of healthy individuals. Markers which are more frequent in individuals with the disease are more likely to be involved in the condition.
Using this approach the investigators found an additional seven genes likely to be involved in the condition, bringing the total number of genes known to predispose to AS to thirteen. Many of the new genes are already known to be involved in inflammatory and immune processes, providing researchers with further clues about how the disease arises. Two of the new genes are also known to predispose to other auto-immune conditions including Crohn's disease (a form of inflammatory bowel disease) and Celiac disease (an auto-immune intestinal disease).
Researchers were also able to demonstrate an interaction between a genetic mutation called HLA-B27 and a mutation in a gene called ERAP1. Specifically, the ERAP1 mutation only predisposed to disease in those individuals who tested positive for the HLA-B27 mutation.
Dr David Evans from the University of Bristol said: "This finding is important in a number of ways. First of all it's one of the first convincing examples we have of one mutation influencing the effect of another mutation in the development of a relatively common disease. This is exciting because it implies that there may be other examples of this phenomenon in other common diseases that we don't know about yet.
"Second, the interaction itself tells us something very fundamental about how AS is caused. Prior to this study there were a number of competing theories about how the disease was caused. Our study suggests very strongly which one of these competing hypotheses is likely to be correct."
Finally, the researchers also identified a single genetic marker which could be used to assist in diagnosis of Ankylosing Spondylitis.
"AS is notoriously difficult to diagnose in its early stages which can lead to costly delays in its treatment," said Dr Evans. "Typically diagnosis consists of a combination of X-rays, patient symptoms and expensive immunological assays in the laboratory. This genetic marker could easily take the place of an expensive immunological assay. What would normally cost £40-£50 could be done easily for a fraction of the price."
*Source: University of Bristol
Using this approach the investigators found an additional seven genes likely to be involved in the condition, bringing the total number of genes known to predispose to AS to thirteen. Many of the new genes are already known to be involved in inflammatory and immune processes, providing researchers with further clues about how the disease arises. Two of the new genes are also known to predispose to other auto-immune conditions including Crohn's disease (a form of inflammatory bowel disease) and Celiac disease (an auto-immune intestinal disease).
Researchers were also able to demonstrate an interaction between a genetic mutation called HLA-B27 and a mutation in a gene called ERAP1. Specifically, the ERAP1 mutation only predisposed to disease in those individuals who tested positive for the HLA-B27 mutation.
Dr David Evans from the University of Bristol said: "This finding is important in a number of ways. First of all it's one of the first convincing examples we have of one mutation influencing the effect of another mutation in the development of a relatively common disease. This is exciting because it implies that there may be other examples of this phenomenon in other common diseases that we don't know about yet.
"Second, the interaction itself tells us something very fundamental about how AS is caused. Prior to this study there were a number of competing theories about how the disease was caused. Our study suggests very strongly which one of these competing hypotheses is likely to be correct."
Finally, the researchers also identified a single genetic marker which could be used to assist in diagnosis of Ankylosing Spondylitis.
"AS is notoriously difficult to diagnose in its early stages which can lead to costly delays in its treatment," said Dr Evans. "Typically diagnosis consists of a combination of X-rays, patient symptoms and expensive immunological assays in the laboratory. This genetic marker could easily take the place of an expensive immunological assay. What would normally cost £40-£50 could be done easily for a fraction of the price."
*Source: University of Bristol
New genetic clues for schizophrenia
De novo mutations – genetic errors that are present in patients but not in their parents – are more frequent in schizophrenic patients than in normal individuals, according to an international group of scientists led by Dr. Guy A. Rouleau of the University of Montreal and CHU Sainte-Justine Hospital. The discovery, published today in Nature Genetics, may enable researchers to define how the disease results from these mutations and eventually develop new treatments for it. "The occurrence of de novo mutations, as observed in this study, may in part explain the high worldwide incidence of schizophrenia," says Dr. Rouleau, who is also Director of the CHU Sainte-Justine Research Center and researcher at the University of Montreal Hospital Research Centre. "Because the mutations are located in many different genes, we can now start to establish genetic networks that would define how these gene mutations predispose to schizophrenia," adds Simon Girard, the student who performed the key experiments that led to this discovery. "Most of the genes identified in this study have not been previously linked to schizophrenia, thereby providing new potential therapeutic targets."
Schizophrenia is a major mental disorder characterized by a wide spectrum of symptoms, including delusions, hallucinations, disturbances in thinking, and deterioration of social behaviours. According to the World Health Organization, as many as 24 million individuals worldwide suffer from schizophrenia and over half of them are not receiving appropriate care to relieve their symptoms.
Dr. Rouleau's team used modern DNA sequencing technologies to identify genetic changes in patients with schizophrenia whose parents showed no signs of the disease. To identify genetic mutations associated with schizophrenia, Dr. Rouleau and his team analysed approximately 20,000 genes from each participant in the study. The research team was especially interested in "de novo" mutations, meaning those that are present in patients but absent in their parents.
"Our results not only open the door to a better understanding of schizophrenia," adds Dr. Rouleau. "They also give us valuable information about the molecular mechanisms involved in human brain development and function."
The identification of de novo mutations in schizophrenia supports the hypothesis proposed by Dr. Rouleau in 2006, that this type of mutation plays a role in several diseases affecting brain development such as autism, schizophrenia and mental retardation.
**Source: University of Montreal
Schizophrenia is a major mental disorder characterized by a wide spectrum of symptoms, including delusions, hallucinations, disturbances in thinking, and deterioration of social behaviours. According to the World Health Organization, as many as 24 million individuals worldwide suffer from schizophrenia and over half of them are not receiving appropriate care to relieve their symptoms.
Dr. Rouleau's team used modern DNA sequencing technologies to identify genetic changes in patients with schizophrenia whose parents showed no signs of the disease. To identify genetic mutations associated with schizophrenia, Dr. Rouleau and his team analysed approximately 20,000 genes from each participant in the study. The research team was especially interested in "de novo" mutations, meaning those that are present in patients but absent in their parents.
"Our results not only open the door to a better understanding of schizophrenia," adds Dr. Rouleau. "They also give us valuable information about the molecular mechanisms involved in human brain development and function."
The identification of de novo mutations in schizophrenia supports the hypothesis proposed by Dr. Rouleau in 2006, that this type of mutation plays a role in several diseases affecting brain development such as autism, schizophrenia and mental retardation.
**Source: University of Montreal
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