Max Planck abrirá su primera sede del país en Medellín y Bogotá

Las universidades de Antioquia, Nacional y Colciencias firmaron acuerdo con este instituto alemán.

Foto: Archivo/EL TIEMPO

Durante el convenio entre Max Planck, Colciencias y las universidades de Antioquia y Nacional se invertirán 100.000 millones de pesos.


La Sociedad Max Planck (MP), pionera en investigación en Alemania y una de las más prestigiosas del mundo, abrió convocatoria internacional con el objetivo de encontrar un director para la sede que tendrán en Colombia a partir del próximo año.

En un hecho calificado por académicos como histórico para la ciencia nacional, las universidades de Antioquia y la Nacional, de la mano de Colciencias, firmaron un convenio con esta Sociedad, compuesta por 82 institutos ubicados en todos los continentes.

Con el apoyo de Max Planck Colombia

• la Unal, sede Bogotá, dirigirá estudios sobre la biodiversidad del país y 
• la U. de A. abordará, también con sus propios grupos de investigación, el área de la medicina y las enfermedades tropicales, campos en los que ya tiene trayectoria.

Según Alberto Uribe Correa, rector de la U. de A., este convenio es por cinco año y es la segunda sede que la Sociedad abre en Latinoamérica, después de la de Buenos Aires (Argentina).

“En marzo del próximo año directores de varios institutos Max visitarán ambas sedes universitarias con el objetivo de reconfirmar las condiciones necesarias para dar apertura a los centros que ellos administrarán en Bogotá y Medellín. Colombia entra en las grandes ligas de la investigación mundial”, dijo Uribe.

El Gobierno nacional aportará 10.000 millones de pesos por año y cada universidad 5.000 millones, para un total de 100.000 millones de pesos. Por su parte la Sociedad se encargará de las estrategias y métodos de investigación que ya han sido exitosos en otros países, de la administración del convenio, de la logística y aportará también investigadores.

“Estos cinco años serán diferentes en la manera como se investiga. Se seguirán los cánones internacionales de una entidad de primer orden mundial. En esta asociación ganan ellos y el país. Conservando la autonomía universitaria habrá libertad para que los grupos de la Universidad se asocien con MP para que desarrollen sus investigaciones”, agregó Uribe.

La mayor parte de los recursos con los que trabaja esta Sociedad provienen del gobierno alemán. En el caso local se trata de un esfuerzo grande que hacen las universidades para internacionalizar la investigación.

Este año la Universidad de Antioquia realizó otros convenios importantes de cooperación académica. El primero con la Universidad de Purdue (Indiana, Estados Unidos) y el segundo con la Universidad de Groningen (Países Bajos).

En ambas universidad reconocen que será todo un reto albergar a MP, pues implica condiciones exigentes en el campo técnico y físico. El éxito de esta organización, se lee en su página web, radica en que definen sus objetos de investigación, trabajan en las mejores condiciones y con un personal adecuado.

La Sociedad se creó en 1948, un año después de la muerte del físico alemán Max Karl Ernest Ludwig Planck, fundador de la teoría cuántica. En 1918 obtuvo el Premio Nobel de Física.

Una Sociedad con 66 años de historia
Max Planck no es un instituto sino un conjunto de organizaciones dedicadas a la investigación en Medicina, Biología, Física, Química, Tecnología, Humanidades y Ciencias Sociales. Su sede principal está ubicada en Alemania, De sus grupos científicos han salido 18 premios Nobel. Cada año publica más de 15.000 artículos en revistas científicas. Muchos de estos textos son los más citados en cada campo. Tienen 4.487 jóvenes científicos en sus grupos.



ORIGINAL: El Tiempo
OSCAR ANDRÉS SÁNCHEZ A.
MEDELLÍN

Biochip quickly tests results of cancer therapy

The inside structure of the biochip is comprised of 3 layers, each testing a key element of the therapy: drug, oxygen, and light. (Credit: Xia Lou/University of Michigan)


University of Michigan right Original Study ("A high-throughput photodynamic therapy screening platform with on-chip control of multiple microenvironmental factors")

A new type of lab-on-a-chip could make it easier to determine the effectiveness of a promising cancer treatment that combines photosensitive drugs, light, and oxygen.

The treatment, known as photodynamic therapy (PDT), uses a unique type of drug, called a photosensitizer, that generates high-energy oxygen when activated by light, in this case an LED laser.

The oxygen reaction destroys cells locally only in the immediate surrounding area, which in this case is the tumor, without damaging other healthy cells in the rest of the body. PDT may also prompt the patient’s immune system to attack the tumor, whereas without treatment it will likely ignore it.

“PDT is a fairly complicated therapy because it requires light, oxygen, and the drug, all three of which need to be carefully controlled,” says Xia Lou, a postdoctoral fellow at the University of Michigan. “With chemotherapy, for example, you only control how much of the drug is used.”

The biochip can test the interaction of the drug, light, and oxygen simultaneously, generating results in a fraction of the time of current testing practices.

“In cancer research doctors are always looking for better drugs,” adds Lou. “But there has always been a lack in the ability to efficiently test new drugs.

“Researchers are also hoping to get more reliable test results than is the norm. We are providing more precise drug test conditions to insure that the results we are getting will more closely match the actual results from cancer treatment.”

Test all three components There are two primary challenges in PDT today:

• One is determining the best treatment plan for the patient, and 
• the other is testing the efficacy of new and existing drugs.

For example, the location of a tumor in the body will determine the amount of light needed to excite the drug, and will impact the amount of drug that is administered. Also, when testing new drugs, it is again important to know the amount of light needed to excite the oxygen reaction, and the strength of the reaction.

This adds a high level of complexity compared to conventional drug testing that only tests one component, the drug itself.

Current PDT testing methods might take more than 24 hours to acquire just 10 data points.

“With our device,” says Lou, “we can finish the testing in 1 hour and have 1,000 data points. The result is a very comprehensive understanding of how the 3 elements need to be manipulated for maximum effect in an individual patient.”

The researchers reported the details of their findings in the journal Lab on a Chip. The NSF Engineering Research Center for Wireless Integrated Microsystems, Thermo Fisher Scientific, and the National Institute of Health supported the project.

Source: University of Michigan

ORIGINAL: Futurity

by Catharine June-U. Michigan 

February 28, 2014 

Advancing brain cancer treatment through genomics

IBM and the New York Genome Center testing Watson prototype on glioblastoma

We have put Watson to work in any number of different ways and in any number of different industries. Healthcare, though, was its first real job. It’s gone to medical school, and even studied health insurance. And now Watson is working with the New York Genome Center to launch a pilot that tackles a new medical challenge – glioblastoma.

Dr. Robert Darnell, MD, PhD, President, CEO and Scientific Director of the New York Genome Center (left) and Dr. Ajay Royyuru, PhD, Director of the Computational Biology Center, IBM Research (right)

The most common kind of brain cancer, glioblastoma annually kills 13,000 people in the US alone. As a cancer of the brain, it’s difficult to take tissue samples, for one, so it can’t be examined like most other kinds of cancers. And it moves quickly. Diagnosis to death is on average only 12 months.

All cancers are a disease of the genome. It’s the genome itself that’s progressively changing from normal to abnormal when someone has cancer. When we can determine which genes start to “go bad,” we can better-determine what specific treatment would work to stop it. Therein lies the challenge: How can we better understand what is happening at a genetic level?

The key to glioblastoma’s genetic code is in the human genome. So while we know our cells’ biochemical pathways, it’s also an overwhelming amount of data – billions of DNA base sequences, plus millions of studies, medical documents and clinical records.

Different kinds of brain cancers manifest in different ways and progression rates, so finding these details about glioblastoma is a molecule-sized needle in the genome haystack.

That’s why my team – with decades of research experience in biology as a data science – and NYGC, with the expertise and resources of a dozen top hospitals and medical schools, are collaborating on a project with Watson in genomics. Our goals with this prototype and ensuing studies are to assist physicians with discovering personalized treatment for patients with glioblastoma.

Watson can read millions of pages of medical literature in seconds. By applying its natural language processing and analytics to the genome, it could find connections between what’s buried in journals about the interaction of certain genes, and where those genes are in the genome. And so, in the same way Watson evaluates and hypothesizes on other medical diagnosis based on electronic health records and a doctor’s evaluation (see a demo), it could evaluate and hypothesize about mutations in a cancer cell’s genome that caused the disease, not based on a wide demographic swath of those with similar characteristics, but for an individual based on their personal genome.

Connecting medical literature to the genome 

Today, we know and have detailed medical literature on the biochemical pathways our genes take. But we don’t know where in the genome these cancerous perturbations happen in that molecular network of interactions. So, we’re loading Watson with genome data from NYGC, along with medical literature to map out where these deviations happen. Watson will be able to see that, in the context of given cancer mutations in the genome, which pathways matter. And in the context of those interactions, suggest evidence of potential treatments.

IBM Watson and New York Genome Center. Video: IBM SocialMedia

This journey takes clinicians from trials, to validating what genomic knowledge improves treatment, to routine analysis that helps patients. Ultimately, we want to see our partners at NYGC and physicians upload genomic data into the Watson Genome on the cloud, where the system could quickly synthesize a personalized report of available evidence of treatment options.

ORIGINAL: IBM Research

By Dr. Ajay Royyuru, Director of IBM Research’s Computational Biology Center

Researchers Cure Diabetes in Mice

Researchers in California have turned skin cells in mice into insulin producing beta cells, effectively curing the animals of diabetes. They hope to achieve similar results in human cells, paving the way to an eventual cure for a disease that affects millions of people around the world.

Original story by Ben Gruber for Reuters:

ORIGINAL: Singularity Web

by Socrates

Nikola Danaylov

Can Gene Therapy Cure HIV?

Why It Matters

There is no cure for HIV, which can cause AIDS. In 2012, 1.6 million people died of AIDS-related illnesses.

The immune cells of HIV patients can be genetically engineered to resist infection, say researchers. In a small study in humans, scientists report that by creating a beneficial mutation in T cells, they may be able to nearly cure patients of HIV.

In a study published in the New England Journal of Medicine on Wednesday, researchers report that they can use genome editing to re-create the rare mutations responsible for protecting about 1 percent of the population from the virus in infected patients. They report that some of the patients receiving the genome-modifying treatment showed decreased viral loads during a temporary halt of their antiretroviral drugs. In one patient, the virus could no longer be detected in his blood.


Zinc-finger nucleases are one of a few genome-editing tools that researchers use to create specific changes to the genomes of living organisms and cells (see “Genome Surgery”). Scientists have previously used genome-editing techniques to modify DNA in human cells and nonhuman animals, including monkeys (see “Monkeys Modified with Genome Editing”). Now, the NEJM study suggests the method can also be safely used in humans.

From each participating patient, the team harvested bone marrow stem cells, which give rise to T cells in the body. They then used a zinc finger nuclease to “break” copies of the CCR5 gene that encodes for proteins on the surface of immune cells that are a critical entry point of HIV. The stem cells were then infused back into each patient’s bloodstream. The modification process isn’t perfect, so only some of the cells end up carrying the modification. “About 25 percent of the cells have at least one of the CCR5 genes interrupted,” says Edward Lanphier, CEO of Sangamo Biosciences, the Richmond, California, biotech company that manufactures zinc finger nucleases.

Because the cells are a patient’s own, there is no risk of tissue rejection. The modified stem cells then give rise to modified T cells that are more resistant to infection by HIV, say the researchers.

One week after the infusion, researchers were able to find modified T cells in the patients’ blood. Four weeks after the infusion, six of the 12 patients in the study temporarily stopped taking their antiretroviral drugs so the researchers could assess the effect of the genome-editing treatment on the amount of the virus in the patients’ bodies. In four of these patients, the amount of HIV in the blood dropped. In one patient, the virus could no longer be detected at all. The team later discovered that this best responder had naturally already had one mutated copy of the CCR5 gene.

Patients who carry one broken copy of the CCR5 progress to AIDS more slowly than those who don’t, says Bruce Levine, a cell and gene therapy researcher at the University of Pennsylvania School of Medicine and coauthor on the study. Because all of the cells in that best-responder patient already carried one disrupted copy of CCR5, the modification by the zinc finger nuclease led to T cells with no functional copies of the gene. That means the cells are fully resistant to HIV infection. The team is now working to increase the number of immune cells that end up carrying two broken copies of CCR5.

ORIGINAL: Technology Review