César Antón, director del Imserso, a EL PAIS: "“No se atiende igual a personas con la misma dependencia”

César Antón (Palencia, 1957) ha sido cocinero antes que fraile: de su etapa como consejero en Castilla y León conoce el proceder de las comunidades y ahora, como nuevo director del Instituto de Mayores y Servicios Sociales (Imserso), también el del Gobierno. Y en la implantación de la Ley de Dependencia la relación entre ambas Administraciones ha sido un constante tira y afloja. El objetivo del Gobierno, explica, es que, a igual grado de dependencia, dos personas reciban el mismo servicio en cualquier lugar de España. Quiere unificar los criterios para el copago del usuario, fijar indicadores comunes para determinar lo que cuesta la dependencia en cada comunidad y primar la prestación de servicios.
Pregunta. ¿Se prevén recortes en dependencia y servicios sociales?
Respuesta. Las prestaciones sociales seguirán siendo la prioridad del Gobierno.
P. ¿Por qué está paralizada la Ley de Dependencia?
R. Hay ritmos distintos por comunidades, cada una lo ha adaptado a sus circunstancias, pero, con respeto hacia ellas, han dado mejores resultados aquellas que han canalizado el desarrollo de la ley a través del sistema de servicios sociales. Sin embargo, hay diferencias en la aplicación.
P. Esas diferencias permiten que haya ciudadanos de primera y de segunda a la hora de percibir las ayudas. ¿Es tolerable?
R. Los ciudadanos tiene que ser iguales ante la ley. Hay que analizar cómo se ha puesto en marcha la norma y la evaluación de resultados y cómo se reconduce en el futuro. Agua pasada no mueve molinos. Es verdad que hay sitios donde los procedimientos se alargan por causas achacables a las Administraciones. Hay que dar un impulso, reordenar el procedimiento, entre todos.
P. ¿Y cómo se reconduce?
R. Nuestro objetivo es que ante situaciones iguales de dependencia se dé un tratamiento igual en todo el territorio, porque a igual grado no se está atendiendo de la misma forma. Tenemos, también, que acordar cómo se mide la capacidad económica del usuario y unificar su aportación económica, que tampoco es igual.
P. ¿Por qué las comunidades siguen sin dar datos reales de lo que les cuesta la dependencia?
R. No hay una valoración del coste porque no hemos fijado indicadores comunes para calcular esos costes. La ministra ha ofrecido la posibilidad de que se llegue a un acuerdo sobre la forma de medir la capacidad económica del usuario y su aportación al sistema para el conjunto del territorio. Y también para determinar el coste de los servicios. Luego sabremos quién aporta y cuánto. En los Presupuestos Generales del Estado se determina claramente la partida para la dependencia (nivel mínimo y nivel acordado, seguridad social, etcétera). ¿Acaso existe ese detalle en los presupuestos de las comunidades autónomas?

“Hay sitios donde los procedimientos se alargan por las Administraciones”
P. Trascendió la intención del Gobierno de financiar a las comunidades según el coste del servicio al ciudadano, y no de su grado de dependencia, como ahora.
R. El reparto de los créditos de los presupuestos del Estado debiera hacerse primando a las comunidades que prestan servicios frente a las que dan prestaciones económicas, porque es el espíritu de la ley. Hoy, para repartir los recursos se tienen en cuenta otras variables, como la extensión del territorio, pero lo más importante deben ser los servicios que se presten y las personas atendidas. No puede ser que la población pese más en este reparto; en todo caso debe pesar la población dependiente, la forma de atenderla y las personas atendidas.
P. ¿Van a simplificar el baremo, el examen que fija el grado de dependencia de los ciudadanos?
R. No hay nada predeterminado,pero hay que reflexionar sobre su eficacia.
P. ¿Ese baremo permite que entren en el sistema más grandes dependientes de media que los que tienen otros países?
R. En la única estimación que se hizo en España se calculó que habría 205.000 personas con el mayor grado de dependencia y estamos en más de 425.000, más del doble. Las estimaciones nunca aciertan del todo, pero parece que estamos por encima de la media de la UE.
P. En el otro extremo están los dependientes moderados, cuya atención ha sido aplazada un año por el Gobierno. ¿Cree que todos los dependientes moderados deben entrar bajo el paraguas de la dependencia?

-“No hay valoración del coste porque faltan indicadores para calcularlo”
R. Debiéramos hacer un análisis entre todos para ver si muchas de esas personas no están siendo atendidas ya de forma muy similar por los servicios sociales, porque antes de la ley ya se atendían esas necesidades.
P. Si se les saca de la ley, su atención quedará al arbitrio de las comunidades autónomas, porque una ayuda de los servicios sociales no se adquiere por derecho, ya que están sujetas a la disponibilidad presupuestaria.
R. Yo no conozco que se haya dejado de atender a alguien que haya entrado a ser atendido en los servicios sociales. Las nuevas leyes de servicios sociales de las comunidades también garantizan esa atención por derecho.
P. Pero apenas hay tres comunidades con esas nuevas leyes.
R. Yo creo que cuatro o más.
P. Pero se trata del acceso a las ayudas. ¿Cómo se va a garantizar que tengan prestaciones en los servicios sociales cuando en algunos casos no se garantizan ni las ayudas que se conceden por la Ley de Dependencia?
R. No es solo el acceso, y siguen accediendo personas a los servicios sociales, sino también las que ya están atendidas. En España hay 451.366 usuarios de ayuda a domicilio, 165.294 plazas públicas de residencia de un total de 344.000. Aunque ha habido recortes presupuestarios, las comunidades y los Ayuntamientos han priorizado sus servicios sociales.
P. Un informe encargado por el Gobierno anterior determinó que el Imserso servía de poco tal cual estaba. ¿Para qué sirve?
R. Ha sido siempre un referente en política social y de mayores. Está totalmente justificado para dar cohesión, como ocurre en sanidad
P. Pero la cohesión sanitaria existe sin un Imserso.
R. Porque se hizo una ley para ello... Pero el Imserso, entre otras cosas, se hace cargo de las pensiones no contributivas, por ejemplo. Es el responsable de garantizar que todos los meses se cobren esas pensiones.

**Publicado en "EL PAIS"

Genetic Variation in East Asians Found to Explain Resistance to Cancer Drugs

A multinational research team led by scientists at Duke-NUS Graduate Medical School has identified the reason why some patients fail to respond to some of the most successful cancer drugs.

Tyrosine kinase inhibitor drugs (TKI) work effectively in most patients to fight certain blood cell cancers, such as chronic myelogenous leukemia (CML), and non-small-cell lung cancers (NSCLC) with mutations in the EGFR gene.
These precisely targeted drugs shut down molecular pathways that keep these cancers flourishing and include TKIs for treating CML, and the form of NSCLC with EGFR genetic mutations.
Now the team at Duke-NUS Graduate Medical School in Singapore, working with the Genome Institute of Singapore (GIS), Singapore General Hospital, and the National Cancer Centre Singapore, has discovered that there is a common variation in the BIM gene in people of East Asian descent that contributes to some patients' failure to benefit from these tyrosine kinase inhibitor drugs.
"Because we could determine in cells how the BIM gene variant caused TKI resistance, we were able to devise a strategy to overcome it," said S. Tiong Ong, MBBCh, senior author of the study and associate professor in the Cancer and Stem Cell Biology Signature Research Programme at Duke-NUS and Division of Medical Oncology, Department of Medicine, at Duke University Medical Center.
"A novel class of drugs called the BH3-mimetics provided the answer," Ong said. "When the BH3 drugs were added to the TKI therapy in experiments conducted on cancer cells with the BIM gene variant, we were able to overcome the resistance conferred by the gene. Our next step will be to bring this to clinical trials with patients."
Said Yijun Ruan, PhD, a co-senior author of this study and associate director for Genome Technology and Biology at GIS: "We used a genome-wide sequencing approach to specifically look for structural changes in the DNA of patient samples. This helped in the discovery of the East Asian BIM gene variant. What's more gratifying is that this collaboration validates the use of basic genomic technology to make clinically important discoveries."
The study was published online in Nature Medicine on March 18.
If the drug combination does override TKI resistance in people, this will be good news for those with the BIM gene variant, which occurs in about 15 percent of the typical East Asian population. By contrast, no people of European or African ancestry were found to have this gene variant.
"While it's interesting to learn about this ethnic difference for the mutation, the greater significance of the finding is that the same principle may apply for other populations," said Patrick Casey, PhD, senior vice dean for research at Duke-NUS and James B. Duke Professor of Pharmacology and Cancer Biology.
"There may well be other, yet to be discovered gene variations that account for drug resistance in different world populations. These findings underscore the importance of learning all we can about cancer pathways, mutations, and treatments that work for different types of individuals. This is how we can personalize cancer treatment and, ultimately, control cancer."
"We estimate that about 14,000 newly diagnosed East Asian CML and EGFR non-small-cell lung cancer patients per year will carry the gene variant," Ong said. "Notably, EGFR NSCLC is much more common in East Asia, and accounts for about 50 percent of all non-small-cell lung cancers in East Asia, compared to only 10 percent in the West."
The researchers found that drug resistance occurred because of impaired production of BH3-containing forms of the BIM protein. They confirmed that restoring BIM gene function with the BH3 drugs worked to overcome TKI resistance in both types of cancer.
"BH3-mimetic drugs are already being studied in clinical trials in combination with chemotherapy, and we are hopeful that BH3 drugs in combination with TKIs can actually overcome this form of TKI resistance in patients with CML and EGFR non-small-cell lung cancer," Ong said. "We are working closely with GIS and the commercialization arm of the Agency for Science, Technology & Research (A*STAR), to develop a clinical test for the BIM gene variant, so that we can take our discovery quickly to the patient."

**Published in "SCIENCE DAILY"

First-ever integrative 'Omics' profile lets Stanford scientist discover, track his diabetes onset

Geneticist Michael Snyder, PhD, has almost no privacy. For more than two years, he and his lab members at the Stanford University School of Medicine pored over his body's most intimate secrets: the sequence of his DNA, the RNA and proteins produced by his cells, the metabolites and signaling molecules wafting through his blood. They spied on his immune system as it battled viral infections. Finally, to his shock, they discovered that he was predisposed to type-2 diabetes and then watched his blood sugar shoot upward as he developed the condition during the study. It's the first eyewitness account -- viewed on a molecular level -- of the birth of a disease that affects millions of Americans. It's also an important milestone in the realization of the promise of truly personalized medicine, or tailoring health care to each individual's unique circumstances.
The researchers call the unprecedented analysis, which relies on collecting and analyzing billions of individual bits of data, an integrative Personal "Omics" Profile, or iPOP. The word "omics" indicates the study of a body of information, such as the genome (which is all DNA in a cell), or the proteome (which is all the proteins). Snyder's iPOP also included his metabolome (metabolites), his transcriptome (RNA transcripts) and autoantibody profiles, among other things.
The researchers say that Snyder's diabetes is but one of myriad problems the iPOP can identify and predict, and that such dynamic monitoring will soon become commonplace. "This is the first time that anyone has used such detailed information to proactively manage their own health," said Snyder. "It's a level of understanding of health at the molecular level that has never before been achieved."
The research was published in the March 16 issue of Cell. Snyder, who chairs the Department of Genetics, is the senior author. Postdoctoral scholars Rui Chen, PhD, George Mias, PhD, Jennifer Li-Pook-Than, PhD, and research associate Lihua Jiang, PhD, are co-first authors of the study, which involved a large team of investigators.
The study provides a glimpse into the future of medicine -- peppered with untold data-management hurdles and fraught with a degree of self-examination and awareness few of us have ever imagined. And, despite the challenges, the potential payoff is great.
"I was not aware of any type-2 diabetes in my family and had no significant risk factors," said Snyder, "but we learned through genomic sequencing that I have a genetic predisposition to the condition. Therefore, we measured my blood glucose levels and were able to watch them shoot up after a nasty viral infection during the course of the study."
As a result, he was able to immediately modify his diet and exercise to gradually bring his levels back into the normal range and prevent the ongoing tissue damage that would have occurred had the disease gone undiagnosed.
Snyder provided about 20 blood samples (about once every two months while healthy, and more frequently during periods of illness) for analysis over the course of the study. Each was analyzed with a variety of assays for tens of thousands of biological variables, generating a staggering amount of information.
The exercise was in stark contrast to the cursory workup most of us receive when we go to the doctor for our regular physical exam. "Currently, we routinely measure fewer than 20 variables in a standard laboratory blood test," said Snyder, who is also the Stanford W. Ascherman, MD, FACS, Professor in Genetics. "We could, and should, be measuring many, many thousands."
For Snyder, one set of measurements was particularly telling. On day 301, about 12 days after a viral infection, his glucose regulation appeared to be abnormal. Shortly thereafter his glucose levels became elevated, prompting him to visit his primary care physician. On day 369, he was diagnosed with type-2 diabetes.
"We are all responsible for our own health," said Snyder, who is also the director of the Stanford Center for Genomics and Personalized Medicine. "Normally, I go for a physical exam about once every two or three years. So, under normal circumstances, my diabetes wouldn't have been diagnosed for one or two years. But with this real-time information, I was able to make diet and exercise changes that brought my blood sugar down and allowed me to avoid diabetes medication."
Snyder started his study in the months after arriving at Stanford in 2009, when whole-genome sequencing of individuals was just becoming a reality. Stephen Quake, PhD, who is Stanford's Lee Otterson Professor of Bioengineering, had recently completed the complete sequencing of his own genome and was working to use the information to predict his risk for dozens of diseases.
But while the predictive power in genomic information is due in part to its static nature -- because it doesn't change over time, a one-time analysis can hint at future events -- our bodies are dynamic. They use our DNA blueprints to churn out RNA and protein molecules in varying amounts and types precisely calibrated to respond to the changing conditions in which we live. The result is an exquisitely crafted machine that turns on a dime to metabolize food, flex our muscles, breathe air, fight off infections and make all the other little adjustments that keep us healthy. A misstep can lead to disease or illness.
To generate Snyder's iPOP, he first had his complete genome sequenced at a level of accuracy that has not been achieved previously. Then, with each sample, the researchers took dozens of molecular snapshots, using a variety of different techniques, of thousands of variables and then compared them over time. The composite result was a dynamic picture of how his body responded to illness and disease -- and it was a number of molecular cues that led to the discovery of his diabetes.
A number of molecular cues led to the discovery of Snyder's diabetes. His genomic sequence suggested he had an increased risk for high cholesterol, coronary artery disease (which he knew already), as well as basal cell carcinoma and type-2 diabetes, which was unexpected. Conversely, the sequence predicts his risk for hypertension, obesity and prostate cancer is lower than that of other men his age (54 when the study started). A check of his triglyceride levels at the start of the study confirmed that they were high: 321 mg/dL. Snyder took the cholesterol-lowering drug simvastatin, and his levels dropped dramatically to 81-116 mg/dL. Based on the type-2 diabetes prediction, the team decided to also monitor Snyder's blood sugar levels, which were normal when the study began.
Snyder, who has two small children, experienced two viral infections during the course of the study: one with rhinovirus (at day 0), and one with respiratory syncytial virus (beginning at day 289). Each time, his immune system reacted by increasing the blood levels of pro-inflammatory cytokines -- secreted proteins that cells use to communicate and coordinate their responses to external events such as an infection. Snyder also exhibited increased levels of auto-antibodies, or antibodies that reacted with his own proteins, after viral infection. Although auto-antibody production can be a normal, temporary reaction to illness, the researchers were interested to note that one in particular targeted an insulin receptor binding protein.

**Source: Stanford University Medical Center

White rice increases risk of Type 2 diabetes

The risk of type 2 diabetes is significantly increased if white rice is eaten regularly, claims a new study. The authors from the Harvard School of Public Health look at previous studies and evidence of the association between eating white rice and the risk of type 2 diabetes. Their study seeks to determine whether this risk is dependent on the amount of rice consumed and if the association is stronger for the Asian population, who tend to eat more white rice than the Western world.
The authors analysed the results of four studies: two in Asian countries (China and Japan) and two in Western countries (USA and Australia). All participants were diabetes free at study baseline.
White rice is the predominant type of rice eaten worldwide and has high GI values. High GI diets are associated with an increased risk of developing type 2 diabetes. The average amount of rice eaten varies widely between Western and Asian countries, with the Chinese population eating an average of four portions a day while those in the Western world eat less than five portions a week.
A significant trend was found in both Asian and Western countries with a stronger association found amongst women than men. The results also show that the more white rice eaten, the higher the risk of type 2 diabetes: the authors estimate that the risk of type 2 diabetes is increased by 10% with each increased serving of white rice (assuming 158g per serving).
White rice has a lower content of nutrients than brown rice including fibre, magnesium and vitamins, some of which are associated with a lower risk of type 2 diabetes. The authors report, therefore, that a high consumption of white rice may lead to increased risk because of the low intake of these nutrients.
In conclusion, the authors state that "higher white rice intake is associated with a significantly elevated risk of type 2 diabetes." This applies for both Asian and Western cultures, although due to findings suggesting that the more rice eaten the higher the risk, it is thought that Asian countries are at a higher risk. The authors recommend eating whole grains instead of refined carbohydrates such as white rice, which they hope will help slow down the global diabetes epidemic.
In an accompanying editorial, Dr Bruce Neal from the University of Sydney suggests that more, bigger studies are needed to substantiate the research hypothesis that white rice increases the chances of getting type 2 diabetes.

**Source: BMJ-British Medical Journal

ABC Salud premia la excelencia sanitaria con 10 galardones

El Premio ABC Salud, que reconoce la labor más destacada de profesionales, instituciones y compañías del mundo sanitario, ya tiene los galardones de su segunda edición. El jurado, presidido por Pilar Farjas, número dos del Ministerio de Sanidad, tuvo en cuenta las iniciativas y trayectorias que más han contribuido a generar conocimiento en el campo de la salud en 2011. La entrega tendrá lugar el 22 de marzo en la Casa de ABC.
Luis Fernández-Vega, uno de los oftalmólogos de mayor prestigio europeo, se alzó con el premio al «Médico del Año». Preside la Sociedad Española de Oftalmología y dirige desde Oviedo uno de los centros oftalmológicos más potentes de Europa que ha invertido grandes esfuerzos en investigación. Se ha caracterizado por llevar con rapidez los últimos avances a la consulta. Los últimos han sido las técnicas que hacen más sencilla y segura las operaciones de cataratas.
Al hospital La Paz de Madrid, un centro de referencia nacional, se le reconoce su labor diaria en casos como el del pequeño Ibai, el niño vizcaíno al que se le trasplantaron cinco órganos. Pero también la creación de unidades que mejoran la calidad de vida de los pacientes, como el hospital del Dolor.
Como hospital privado, el premio recae en la Fundación Jiménez Díaz de Madrid por la rapidez en la atención a pacientes con alerta clínica y por ser un ejemplo de una asistencia mixta que combina la actividad privada con la pública.
En la categoría de laboratorios, como compañía del año, el galardón ha ido para Lilly. Se reconoce así su esfuerzo por mantener su apuesta por la investigación y la innovación así como sus plantas en España, en una época de crisis. La empresa Medtronic recibe el premio por una de sus últimas tecnologías estrella, la denervación renal para el tratamiento de la hipertensión.
Dos laboratorios, Janssen y MSD, reciben «ex aequo» el premio al Medicamento del Año por sus fármacos «victrelis» e «incivo», que abren nuevas líneas de tratamiento para la hepatits C.
En esfuerzo en I+D+i, el premio es para la clínica de la Universidad de Navarra por su laboratorio de Medicina Nuclear, el de mayor producción de radiofármacos de España para el diagnóstico del cáncer, alzhéimer o párkinson. En responsabilidad social corporativa, se reconoce la labor de la Real Academia de Medicina por su Diccionario de términos médicos.
Los premios ABC Salud no olvidan a las asociaciones de pacientes. En esta segunda edición, se ha elegido a Alcer por su trabajo en el apoyo y educación de los enfermos renales. Por las iniciativas de las oficinas de farmacia, se ha premiado de forma conjunta al Consejo de Colegios de Farmacéuticos por el proyecto Azuaga y al Colegio de Sevilla por su apoyo a las enfermedades raras. Y, por último, el mejor proyecto de Enfermería ha sido el de José Luis Lázaro de la Clínica Universitaria de Podología de la Universidad Complutense por haber puesto en marcha nuevas técnicas para tratar las úlceras de presión.

--Los premiados:
-Médico del Año. El oftalmólogo Luis Fernández-Vega.
-Compañía del Año. Lilly
-Medicamento de venta por receta. Otorgado “ex aequo” a Victrelis (MSD) e Incivo (Janssen)
-Medicamento para el Autocuidado de la Salud. Desierto
-Esfuerzo en I+D+i. Clínica de la Universidad de Navarra.
-Responsabilidad Social Corporativa. Real Academia Nacional de Medicina
-Hospital Privado del Año. Fundación Jiménez Díaz
-Hospital Público del Año. Hospital Universitario La Paz
-Empresa de Tecnología Sanitaria. Medtronic
-Oficina de Farmacia. Colegio de Farmacéuticos de Sevilla y Consejo General de Colegios de Farmacéuticos
-Enfermería. José Luis Lázaro de la Clínica de Podología de la Universidad Complutense

Researchers uncover molecular pathway through which common yeast becomes fungal pathogen

Scientists at the University of Toronto have found a molecular mechanism that plays a key role in the transition of Candida albicans yeast into disease-causing fungus -- one of the leading causes of hospital-acquired infection. The finding highlights the importance of heat in fungal growth, and provides a new target for drug therapies to counter Candida albicans infection. Candida albicans is a normally harmless yeast that is present in all humans. It becomes infectious in various genetic and environmental conditions, with temperature as a key determinant. It can produce infections that are mild -- persistent vaginal or gut infections, for example -- or severe, such as systemic, potentially fatal bloodstream infections in patients with AIDS or those who have undergone chemotherapy (or even a simple round of antibiotics).
The molecular workings of Candida albicans were mapped for the first time in 2009 by Professor Leah Cowen of the University of Toronto's Department of Molecular Genetics, whose lab showed that growth of the fungus is tied to the function of a "molecular chaperone" called heat- shock protein 90 (Hsp90). In a study that will appear in the March 20 edition of the journal Current Biology, Prof. Cowen and her colleagues detail a mechanism that controls response to elevated temperature through a protein named Hms1 in conjunction with a cyclin (another type of protein) and its partner protein called a cyclin-dependent kinase.
"This circuitry fundamentally influences how Candida albicans senses temperature, which is crucial for Candida's ability to cause disease," said Prof. Cowen, who holds the Canada Research Chair in Microbial Genomics and Infectious Disease -- a prestigious five-year award for which she was renewed this week.
"We were looking for a transcription factor at the end of a pathway we previously showed was key to the change in shape of the fungus that accompanies elevated temperature or compromise of Hsp90 function, and instead we found an entirely new pathway, with components that haven't been characterized in Candida, so it was very surprising," said Prof. Cowen.
The researchers also showed that deletion of Hms1 inhibits Candida albicans infection, pointing toward a possible clinical therapy. "We observed those weaker disease phenotypes in an insect model system, but the results suggest it may also work in more complicated systems," said Prof. Cowen.
The source of pesky vaginal and gut infections, Candida albicans is a burgeoning problem on implanted medical devices -- it's fatal in roughly one-third of device-associated infections -- and is the fourth-leading cause of hospital-acquired infection. The number of acquired fungal bloodstream infections has increased by more than 200% over the last twenty years, owing in part to growing numbers of AIDS and cancer survivors whose treatments have compromised their immune function.
On finding that the Hms1 pathway affects the growth and development of Candida albicans, and knowing of other key regulators through which Hsp90 operates and suspecting many more exist, Prof. Cowen and her lab examined other pathways and proteins that interact with Hsp90 in another study.
In collaboration with Professor Gary Bader at U of T's Donnelly Centre for Cellular and Biomolecular Research, Prof. Cowen's group mapped a much larger portion of the chaperone network with which Hsp90 interacts through a "chemical genomics" approach that had never been applied to Candida albicans. "If we want to have a more global understanding of what Hsp90 is doing during the transition of this fungus between distinct morphological states with different disease causing properties, we need to take global approaches to determine what its interacting with," said Prof. Cowen.
Their results, published online today in the journal PLoS Genetics, showed 226 genetic interactors with Hsp90 in various conditions, such as different temperatures and during exposure to anti-fungal drugs. Of those interactions, 224 were previously unknown. "That's a lot," said Prof. Cowen. "We now have a myriad of new targets through which Hsp90 could be regulating morphogenesis and drug resistance in Candida."
As well, the researchers drew several predictive rules from their study that govern the Hsp90 chaperone network. Some interactors were only important in a small subset of stress conditions, and these are likely to function "downstream" of Hsp90 regulating specialized cellular processes. Other interactors were important in many stress conditions, and so are likely to work "upstream" of Hsp90 regulating its function.
"Hsp90 stabilizes many proteins, but previously nobody could predict what made an Hsp90 client. That we can make such predictions from the chaperone network is pretty cool and unanticipated, so we're further ahead than we expected," said Prof. Cowen.

**Source: University of Toronto

Lanzan un cómic sin complejos sobre el Síndrome de Down

Las anécdotas y ocurrencias de Pablo, un hombre con Síndrome de Down, supusieron el mejor aliciente para que su sobrino, Noel Lang, se decidiera junto con su cuñado e ilustrador, Rodrigo García a plasmar el día a día de las personas con esta enfermedad en forma de cómic. El objetivo de «Downtown» no es otro que «contribuir, mediante la creación de un personaje de cómic con esta patología, a la normalización de un colectivo que todavía es desconocido para muchas personas.

Además, la obra es la única de estas características que, en la actualidad, existe en el mercado», explica Lang. Hablar sin tapujos de una patología que, en la actualidad, engloba en España a 34.000 personas, contribuye a que «a través de este formato la gente pueda reírse y divertirse con los protagonistas sin complejos ni tabúes. Las diferencias cognitivas que tiene este colectivo se traducen en respuestas ingeniosas razonadas desde el pensamiento lateral que, en el mundo de la creatividad, significa que hacen gracia. Creemos que Blo, el protagonista, tiene el mismo derecho a hacer reír que Mafalda o Charlie Brown», añade el guionista.

El título de la obra coincide, además, con el disco de Vinilo que Blo lleva consigo a cualquier parte del mundo y que sólo deja a sus amigos de confianza. Según Lang, «Todos los personajes tienen una personalidad muy marcada. Bibi es la novia de Blo; Ruth la coqueta del grupo; Benjamín, calvo por la tricotilomanía y autista y Miguelote, de aspecto grande y perezoso».

La obra cuenta, además, con el prólogo de Vicente del Bosque, seleccionador Nacional de Fútbol y embajador de la Fundación Síndrome de Down Madrid. «Coincidimos con Del Bosque en Alicante y cuando le comentamos el proyecto aceptó encantado escribir el prólogo», añade el guionista. El cómic, que ha tenido una gran acogida en el mercado, «lleva dos semanas a la venta, este mismo año se lanzará en Estados Unidos y en países de Sudamérica como Argentina y México nos han pedido que lo publiquemos». Iniciativas como ésta coinciden, además, con la celebración el próximo miércoles del día Mundial del Síndrome de Down. Todas las asociaciones que agrupan a estas personas organizarán diversas actividades para dar a conocer la enfermedad al público general.

Desde la Fundación Síndrome de Down Madrid abordarán, en colaboración con el Hospital de la Princesa de Madrid, una jornada científica abierta al público sobre la enfermedad que reunirá a los mejores expertos en discapacidad intelectual del país; el domingo 25 de marzo celebrarán la I carrera de bicis «Todo sobre ruedas» en Pozuelo de Alarcón (Madrid), así como la inauguración del Centro 3 Olivos para la Atención Integral para adultos cuyo objetivo es proporcionar una atención integral a las necesidades de este colectivo.

-De interés para los afectados: FUNDACIÓN SÍNDROME DE DOWN MADRID Dirección: C/ Caídos de la División Azul, 21

Teléfono: 91 310 53 64

Web: http://www.downmadrid.org/

**Publicado en "LA RAZON"