Tecnología de F1 para diseñar prótesis

Dos jóvenes ingenieros, uno de ellos antiguo becario del equipo del piloto Fernando Alonso, han comenzado a aplicar la avanzada tecnología de la Fórmula 1 en el desarrollo de prótesis de diseño personalizado. Son los impulsores de BRECA Health Care, una empresa almeriense que ha introducido la biomecánica en la medicina.

Con estas técnicas pueden reproducir 'prototipos' de cualquier parte del cuerpo para que el cirujano pueda estudiarla con sus manos y realizar un tratamiento mucho más individualizado. Este sistema reduce el tiempo de operación y de recuperación.

**publicado en "CON SALUD"

invendo medical anuncia el permiso 510(k) de la FDA para el sistema de colonoscopía de avance asistido y un solo uso

invendo medical ha anunciado hoy que la compañía ha recibido el permiso 510(k) de la Administración de Fármacos y Alimentos de Estados Unidos para el nuevo sistema de colonoscopía de la compañía C20(TM), incluyendo el colonoscopio de un solo uso SC20(TM).
invendoscope(TM) SC20 cuenta con varias características que son nuevas dentro del campo de la colonoscopía:

- Se trata de un colonoscopio de un solo uso con canal funcional
- No se avanza ni se empuja, sino que utiliza una tecnología de impulse ayudada por ordenador
- Todas las funciones colonoscópicas se realizan usando un instrumento de mano y
- Reduce las fuerzas en la pared del colon

Un ensayo clínico realizado con el colonoscopio de la compañía ha proporcionado unos resultados convincentes, con una tasa de intubación cecal de un >98% y lesiones detectadas en el 41% de los pacientes controlados. No se observador efectos secundarios relacionados con el instrumento durante el ensayo.
El sistema de colonoscopio C20(TM) ya ha recibido la Marca CE en Europa.
"Estamos muy orgullosos de haber conseguido el logro más destacado en la historia de nuestra compañía hasta el momento", explicó Berthold Hackl, consejero delegado de invendo medical. "Estamos tremendamente ilusionados de llevar este nuevo sistema de colonoscopía al mercado de Estados Unidos. Creemos que el sistema de invendo reduce la carga asociada a los actuales sistemas convencionales, y esto podría ayudar a mejorar las tasas de compatibilidad de colonoscopía, uno de los principales factores que afectan a la incidencia futura del cáncer colorectal".

**Acerca de invendo medical - http://www.invendo-medical.com
Con sede en Nueva York, Estados Unidos, y Kissing (cerca de Munich), Alemania, invendo medical es un destacado desarrollador de productos de endoscopía desechables en el campo de la gastroenterología que son higiénicamente seguros y que emplean tecnología avanzada ayudada por ordenador "sin empuje manual".

The Astellas European Foundation Winner of Urology 2012 Grant Announced

The Astellas European Foundation is delighted to announce the winner of the 2012 Urology Grant:
Dr Gommert Van Koeveringe from
Maastricht University Medical Center, the Netherlands
The team including Dr Daisy Vrijens from Maastricht University and Professor Matthias Oelke from the University of Hannover, Germany received the grant of US$ 300,000 to support work on their project entitled 'Detrusor Underactivity: development of an algorithm for detection, diagnosis and assessment' at the Astellas European Foundation Grant Event, last night.
Dr Ayad Abdulahad, Astellas European Foundation Trustee and Vice President of Medical Affairs and Health Economics for Astellas Pharma Europe Ltd. commented, "We received 54 entries from across Europe and as always, the standard of these entries was extremely high, covering a broad range of topics in urology. It was very difficult for the Judging Faculty to choose one winner, but Dr Van Koeveringe's research will contribute considerably to the understanding of detrusor underactivity and could have a significant clinical impact for patients." He continued "the Foundation would especially like to acknowledge all those who submitted their research proposals."
The Astellas European Foundation is a registered charity. It was set up in 2005 with the long-term goal of providing support for programmes and activities that advance our understanding of medicine and health. The Astellas European Foundation Urology Grant supports basic medical and related scientific programmes which contribute to advancements in urology. The winner of the grant was chosen by a Judging Faculty that includes independent European thought leaders.
At the Awards Presentation Event in Paris, France, the Astellas European Foundation emphasised their continued and long term commitment to research and development.
Dr Van Koeveringe said "We are delighted to have received this grant from the Astellas European Foundation in support of our collaborative research project in this relatively new area. We are sure that this grant will enable us to improve knowledge of this underestimated and underdiagnosed condition and encourage further research for new treatment options. We look forward to reporting our findings in the future."

Elusive Platelet Count and Limb Development Gene Discovered

Researchers have identified an elusive gene responsible for Thrombocytopenia with Absent Radii (TAR), a rare inherited blood and skeletal disorder. As a result, this research is now being transformed into a medical test that allows prenatal diagnosis and genetic counselling in affected families.
The team used genetic sequencing to discover that TAR results from low levels of the protein called Y14. They found that the syndrome occurs by a unique inherited mechanism.
Platelets are the second most abundant cell in the blood. Their main task is to survey the blood vessel wall for damage and to plug and repair it where required. Some people are born with low numbers of platelets and these rare conditions are thought to be inherited. TAR syndrome combines the unique features of low platelet count and prominent bleeding, especially in infancy, and skeletal abnormalities affecting the upper limb ranging from absence of the radial bone in the forearm to virtually total absence of upper limb. The genetic basis of TAR syndrome has eluded researchers for 50 years.
"Without the use of modern genomics technologies, the discovery of this unexpected mechanism of disease inheritance would have been much more difficult," said Dr Cornelis Albers, from the Sanger Institute and the University of Cambridge. "To achieve our latest findings, we deciphered about 40 million letters of genetic code in five patients."
Many people with TAR were known to have a deletion in one copy of chromosome 1, but this was thought not to be the whole story because parents who carry the same deletion do not suffer from TAR: other variants had to be involved. The team sequenced the genomes of people affected by the disorder who also carried the deletion and discovered that the vast majority of them had one of two variants of a gene called RBM8A. They found that when the genetic deletion and one of the variants are co-inherited by a child, TAR results.
RBM8A controls the production of the protein Y14. They found that the combination of the genetic deletion of one copy of the RBM8A gene and the variants on the other copy greatly reduces the level of Y14. The team concluded that it is low levels of Y14 that affect platelet formation and cause TAR disorder.
"The lack of production of adequate amounts of the protein Y14 in TAR patients only seems to affect the formation of platelets but not of other blood cells." said Dr Cedric Ghevaert from the University of Cambridge. "We have shed some light on how some inherited disorders can present with such striking features associating seemingly unconnected characteristics such as skeletal and blood defects"
This is the first human disorder identified to be caused by a presumed defect of the Exon Junction Complex, part of the cellular machinery that contributes to producing messages that direct protein production. This study opens the path that could lead to the identification of the genetic basis of other similar inherited syndromes, which will help improvements in diagnosis, genetic counselling and patient care in the NHS and beyond.
"The discovery of the gene for TAR will make it simpler to diagnose more accurately future cases with a simple DNA test. This new test is currently being developed for the NHS as part of the international ThromboGenomics initiative led by Professor Ouwehand" commented Dr Ruth Newbury-Ecob, Honorary Reader in Medical Genetics and Consultant in Clinical Genetics at the University of Bristol Hospitals.

**Published in "SCIENCE DAILY"

Un estudio español explica por qué dejar de fumar engorda

El 70% de los exfumadores engorda y, de hecho, esa es a menudo una de las razones que muchos esgrimen para no dejar de fumar. Ahí esta el vaso medio vacío. El medio lleno es que el tabaco adelgaza. La pregunta es: ¿cómo lo hace? Si se descubriera, ¿se podría crear un fármaco que copiara su efecto, obviamente sin los efectos negativos del tabaco? El trabajo que publicará Miguel López, de la Universidad de Santiago de Compostela, en la revista Diabetes, ya publicado electrónicamente, supone un paso en esa dirección.
“El arsenal terapéutico actual para tratar la obesidad es muy limitado”, escriben los autores del trabajo. “Aparte de las intervenciones en la dieta, el ejercicio y los cambios de comportamiento, los tratamientos farmacológicos escasean. Por ello, y dada la urgencia del problema, decidimos concentrarnos en aquello para lo que hay evidencias de que hace perder peso, como fumar. Numerosos estudios epidemiológicos han revelado una estrecha relación entre el tabaquismo y el peso corporal; [está establecido] que los no fumadores pesan más que los fumadores”.
López se ha concentrado en la nicotina, el principal componente adictivo del tabaco y del que se sabe que inhibe el apetito y produce pérdida de peso. Ha estudiado su efecto sobre los mecanismos cerebrales que regulan las ganas de comer y el gasto energético del organismo.
En concreto, los investigadores han apuntado a una enzima llamada AMPK, que es clave en el metabolismo de la grasa y que actúa en las áreas del hipotálamo relacionadas con la obesidad inhibiendo el gasto energético y estimulando la ingesta.

-El descubrimiento abre una nueva vía en la investigación de tratamientos contra la obesidad
Este grupo de científicos es uno de los pioneros en la identificación de la enzima AMPK como una de las claves de la obesidad. Actuando sobre esta y otras moléculas que intervienen en el metabolismo de las grasas en el cerebro, en los últimos años estos investigadores han conseguido alterar sustancialmente la masa corporal de animales de experimentación: han conseguido que animales que comen poco engorden y, al contrario, que otros con una ingesta desmedida pierdan mucho peso.
Los investigadores pensaron en la relación entre la nicotina y la AMPK por experimentos previos que indicaban que ambas sustancias debían tener efecto tanto sobre la ingesta como sobre el gasto energético, es decir, los dos términos de la ecuación de la obesidad.
Lo que ha hallado el grupo de López en ratas es que la nicotina adelgaza porque inactiva la acción de esta proteína en una determinada región cerebral. Y cuando esto ocurre se come menos y se gasta más, porque se moviliza la llamada grasa parda —que al ser consumida aumenta la temperatura del organismo— y se acelera el metabolismo de las grasas en general. Por el contrario, cuando la nicotina deja de actuar sobre la AMPK, o cuando los investigadores activan esta enzima a propósito en las regiones cerebrales adecuadas, los animales engordan de nuevo.
“Nosotros no decimos que se trate la obesidad con nicotina o fumando”, señala López, “pero el efecto está ahí: hemos identificado una diana farmacológica que puede ser muy interesante, porque modula tanto la ingesta como el gasto energético, lo que la hace incluso más atractiva”. La mayoría de los tratamientos actuales para perder peso inciden bien sobre la ingesta o bien sobre el gasto energético, pero no sobre ambos. Y está, además, la nueva diana ahora identificada, que podría servir no solo para tratar la obesidad, sino también para dejar de fumar.

**publicado en "EL PAIS"

Researchers test sugary solution to Alzheimer’s

Slowing or preventing the development of Alzheimer’s disease, a fatal brain condition expected to hit one in 85 people globally by 2050, may be as simple as ensuring a brain protein’s sugar levels are maintained.
That’s the conclusion seven researchers, including David Vocadlo, a Simon Fraser University chemistry professor and Canada Research Chair in Chemical Glycobiology, make in the latest issue of Nature Chemical Biology.
The journal has published the researchers’ latest paper Increasing O-GlcNAc slows neurodegeneration and stabilizes tau against aggregation.
Vocadlo and his colleagues describe how they’ve used an inhibitor they’ve chemically created — Thiamet-G — to stop O-GlcNAcase, a naturally occurring enzyme, from depleting the protein Tau of sugar molecules.
“The general thinking in science,” says Vocadlo, “is that Tau stabilizes structures in the brain called microtubules. They are kind of like highways inside cells that allow cells to move things around.”
Previous research has shown that the linkage of these sugar molecules to proteins, like Tau, in cells is essential. In fact, says Vocadlo, researchers have tried but failed to rear mice that don’t have these sugar molecules attached to proteins.
Vocadlo, an accomplished chess player in his spare time, is having great success checkmating troublesome enzymes with inhibitors he and his students are creating in the SFU chemistry department’s Laboratory of Chemical Glycobiology.
Research prior to Vocadlo’s has shown that clumps of Tau from an Alzheimer brain have almost none of this sugar attached to them, and O-GlcNAcase is the enzyme that is robbing them.
Such clumping is an early event in the development of Alzheimer’s and the number of clumps correlate with the disease’s severity.
Scott Yuzwa and Xiaoyang Shan, grad students in Vocadlo’s lab, found that Thiamet-G blocks O-GlcNAcase from removing sugars off Tau in mice that drank water with a daily dose of the inhibitor. Yuzwa and Shan are co-first authors on this paper.
The research team found that mice given the inhibitor had fewer clumps of Tau and maintained healthier brains.
“This work shows targeting the enzyme O-GlcNAcase with inhibitors is a new potential approach to treating Alzheimer’s,” says Vocadlo. “This is vital since to date there are no treatments to slow its progression.
“A lot of effort is needed to tackle this disease and different approaches should be pursued to maximize the chance of successfully fighting it. In the short term, we need to develop better inhibitors of the enzyme and test them in mice. Once we have better inhibitors, they can be clinically tested.

**More information: http://www.nature. … o/index.html

Japanese researchers find compound responsible for halitosis may help in development of valuable treatments

The compound responsible for bad breath may help speed the development of stem cells from dental pulp into valuable treatments for patients, according to Japanese researchers.
Hydrogen sulphide (H2S), the noxious mix that smells of rotten eggs and is a major cause of halitosis, appears to help transform the cells into liver cells, said a team from Nippon Dental University, Tokyo. It collected stem cells from the pulp – the central part of the tooth made up of connective tissue and cells – from patients undergoing routine extractions before separating them into a group incubated in an H2S chamber and a control group.
They were analysed after three, six and nine days, to see whether they changed into liver cells and tested for their effectiveness, including the ability to store glycogen, which is converted to glucose when the body needs energy, and collect urea, the by-product of protein metabolism, which is transferred by the kidneys from blood to urine.
The researchers, whose findings are published in the Journal of Breath Research, published by the Institute of Physics, said their work suggested liver cells could be produced in high numbers to a high quality. Lead author Ken Yaegaki said: "High purity means there are less 'wrong cells' that are being differentiated to other tissues, or remaining as stem cells … These facts suggest that patients undergoing transplantation with the hepatic cells may have almost no possibility of developing teratomas (malignant tumours) or cancers.
"Until now, nobody has produced the protocol to regenerate such a huge number of hepatic cells for human transplantation. Compared to the traditional method or suing fetal bovine serum to produce the cells, our method is productive and, most importantly, safe."
Anthony Hollander, head of cellular and molecular medicine at Bristol University, said: "This is interesting work in a new direction but there's a long way to go to see if it is usable therapeutically."
The real test of a liver cell was whether it could metabolise specific toxins and that would require experiments on enzyme function, he said.

**Published in "THE GUARDIAN"