Longevity drugs get attention

Interest in longevity drugs continues to grow as new research points to the tonic effects of resveratrol. The implications could be huge for any developer like Sirtris, a startup founded in 2004 to develop drugs with the same effects as resveratrol. On Monday, the company completed its sale to GlaxoSmithKline for $720 million.

The cited research suggested red wine may be much more potent than was thought in extending human lifespan. The study is based on dosing mice with resveratrol, an ingredient of some red wines. Serious scientists have long derided the idea of life-extending elixirs, but the door has now been opened to drugs that exploit an ancient biological survival mechanism, that of switching the body's resources from fertility to tissue maintenance. The improved tissue maintenance seems to extend life by cutting down on the degenerative diseases of aging.

The reflex can be prompted by a famine like diet, known as caloric restriction, which extends the life of laboratory rodents by up to 30 percent but is far too hard for most people to keep to and in any case has not been proven to work in humans.

Research started nearly 20 years ago by Leonard Guarente of the Massachusetts Institute of Technology showed recently that the famin-induced switch to tissue preservation might be triggered by activating the body's sirtuins. Sinclair, a former student of Guarente, then found in 2003 that sirtuins could be activated by some natural compounds, including resveratrol, previously known as just an ingredient of certain red wines.

EXCERPTED FROM: Fierce Biotech; The New York Times

Google opens shop at NASA

Google Inc. has signed a 40-year lease to secure space for a huge office complex that will be built on a federal government research center near the Internet search leader's Silicon Valley headquarters.

Google anticipates needing the additional space (1.2 million-ft) for the thousands of workers it expects to hire as tries to mine more profits from the Internet's advertising market and expand into other areas of technology and media. The NASA deal sets Google's initial rent for 42.2 acres of land at $3.66 million per year. Google didn't estimate how much it would cost to build the new campus, which will begin construction in 2013 and will include some housing for employees. Google expects to start the final phase of the campus in 2022.

Excerpted from: Associated Press

GE : $20M for medical imaging

Hartford, Conn. (AP) - General Electric Co., the international conglomerate with a stake in everything from GE Healthcare and the Univ. of Pittsburgh Medical Center are each putting up $20 million to establish Omnyx LLC, a business to develop and commercialize technology allowing doctors to store and display on computers, digital images of human tissue from microscope slides, allowing colleagues anywhere to participate in consultations. GE Healthcare, a division of Fairfield-based GE, already manufactures imaging for radiology and cardiology.

Other companies, such as Aperio Technologies Inc. in Vista, Calif., already are in the business of scanning biopsies and transforming computers into virtual microscopes. The advantage for doctors, researchers and medical teachers is that biopsy images can be shared electronically and vast amounts of information can be stored in databases.

Transforming biopsies and human tissues into digital images also helps improve the study and diagnosis of diseases such as cancer and micro-organisms that can lead to lung ailments such as tuberculosis.

Omnyx promises to come up with a product in about two years that will speed up scanning materials from a slide into a digital file from between two and five minutes now to about half a minute, he said. GE and the University of Pittsburgh Medical Center believe Omnyx could reap revenue of $500 million - 25% of the worldwide market - in three or four years.

Excerpted: Associated Press

Related links:  General Electric,  Univ. of Pittsburgh Medical Center,  Aperio Technologies

Artifical neuron membrane could open doors in Alzheimer's R & D

Researchers at the National Institute of Standards and Technology (NIST) and three collaborating institutions are using a new laboratory model of the membrane surrounding neurons in the brain to study how a protein long suspected of a role in early-stage Alzheimer's disease actually impairs a neuron's structure and function. The team's findings are reported in a new paper in the Biophysical Journal.

The brain's neurons transmit nerve impulses down a long stem that is surrounded by a two-layer membrane. In the neuron's normal, "rest" state, this membrane actively sorts sodium ions to the outside of the cell and potassium ions to the inside. To transmit a nerve impulse, an electrochemical change ripples down the membrane in advance of the impulse, making it temporarily more permeable and allowing the ions to swap places. That in turn changes the electrical potential across the membrane, allowing the impulse to pass. Afterwards, the membrane returns to rest and begins sorting the ions again.

Medical experts have hypothesized for years that small polypeptides called amyloid beta peptides somehow create a "leaky" membrane that disrupts this balanced back-and-forth switching of the electrical potential and, in turn, normal impulse transmission. Alzheimer's disease-the progressive brain disorder that is the nation's sixth leading cause of death-is believed to start with such breakdowns. As the disease progresses, amyloid beta peptides clump together to form plaques that further destroy nerve function.

The researchers found increased cation movement across the normally strong barrier at the higher concentrations of the peptides. The data support the hypothesis that membrane "leakiness" is not due to a permanent hole being formed but rather to an aggregation of amyloid beta peptides in the membrane that allows cations to be passed from peptide to peptide across the bilayer, like a baton handed off by relay runners.

The researchers are continuing to use their model system to better understand the role amyloid beta peptides play in early-stage Alzheimer's disease. Future plans include investigating how amyloid beta peptide aggregates arrange themselves in the membrane, how the peptide aggregates affect or influence calcium channels (portals for calcium ion movement) in the membrane, and how the peptides interact with membranes constructed with other types of lipids.

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Human cells QC manager

Researchers in Japan and Canada have discovered a key component of the quality control mechanism that operates inside human cells-sometimes too well. The breakthrough has significant implications for the development of new treatments for cystic fibrosis (CF) and some other hereditary diseases, the researchers say.

Researchers have discovered the important role played by an enzyme called ERdj5 inside the cell's endoplasmic reticulum (ER). The ER acts as a sort of packaging plant that folds and prepares proteins for distribution inside or outside the cell. But when proteins are misfolded in the ER, they must be destroyed in a degradation process-and that is where ERdj5 comes into play.

"ERdj5 is like a quality control inspector," explains Thomas. "If you ever owned an AMC Pacer and you now drive a BMW, you know the difference quality control can make. That's what ERdj5 does, it recognizes when a protein has 'manufacturing defects' and degrades it before it can be distributed."

The ERdj5 enzyme is the first protein found to be capable of breaking the disulfide bonds that hold the misfolded proteins together in the ER. Once those bonds are broken, the researchers say ERdj5 also helps other enzymes and molecules break down the misfolded proteins completely so that the constituent amino acids can be recycled for further protein synthesis.

SOURCE: McGill Univ.
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Van Gogh's hidden works are brought to life

European researchers are reporting the first use of a powerful new imaging technique to reveal with unprecedented detail a Van Gogh under a Van Gogh-the portrait of a woman hidden underneath one of the fabled Dutch Master's landscapes.

Joris Dik and colleagues note that Vincent van Gogh, one of the founding fathers of modern painting, saved canvas by painting-over as many as one-third of his early period works with new or modified pictures. However, current imaging tools used by museums are unable to clearly visualize many of these hidden images, which offer unique and intimate insights into the artist's works, the researchers say.

In the new study, the researchers used their new non-destructive technique, called Synchrotron Radiation-based X-Ray Fluorescence (XRF) Elemental Mapping, to analyze Van Gogh's Patch of Grass painting. Although conventional imaging techniques previously showed that the painting contained the hidden image of a woman's head, the details were blurred. The new technique reveals more detailed information about the chemical composition of the hidden paint layers. As a result, the scientists could construct a clearer and more colorful image of the hidden head. The image even includes brush strokes and facial features such as eyes, nose, mouth, and chin. The reconstructed image shows the dark, somber-head of a Dutch peasant woman, similar to a series of head portraits from Van Gogh's early career, the researchers say.

SOURCE: American Chemical Society
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Ancient Frog - Killing Fungus Returns

Batrachochytrium dendrobatidis (Bd) is a chytrid fungus that lives on keratin, a type of protein found in the skin of amphibians, and is particularly deadly for certain species of frogs. Studies have shown that, once Bd is introduced to a habitat, up to 50 percent of amphibian species and 80 percent of individuals may die within one year. The fungus has been studied for the past decade, yet scientists still do not know much about how Bd kills its host. Because it is so ancient, it differs wildly from most known species, and many of its genes have unknown functions.

Key findings from the 2004 Global Amphibian Assessment state that 43 percent of all frog species are declining in population, with less than one percent showing increases. Although there are many reasons for frog decline, including climate change and habitat loss, Bd is seriously affecting a growing number of species.

"This fungus is really bizarre," said Erica Bree Rosenblum, assistant professor of biological sciences at the University of Idaho and lead author of a recent study published in the Proceedings of the National Academy of Sciences. "It's a member of a group of ancient fungi that are at least a half billion years old. But it only recently began killing amphibians and unequivocally is responsible for a lot of the catastrophic frog die-offs during the past decade."

Rosenblum's study uses some of the most advanced genetic technology available in an attempt to understand how the fungus works at the most basic level. Rosenblum and her colleagues sequenced Bd's entire genome and compared the expression of genes in two phases of the fungus's life - the zoospore and sporangia stages. They have identified several gene families for future study, including one strong candidate that may be a key element in the killing process.

The zoospore stage is the earliest form of the fungus when it is just a single cell swimming around looking for a host on which to grow. Once it embeds itself into an amphibian's skin, it grows into a more complex form called the sporangia stage. In this stage, Bd grows on the keratin in the frog's skin, creating more zoospores to spread the disease and, often, killing the host.

By looking at which genes are turned on when the fungus actively is destroying the skin but turned off when the fungus is doing little more than swimming around, scientists hope to find candidates for genes responsible for both spreading the fungus and killing the frogs.

The study flags many genes as potentially important, but Rosenblum identifies one family as particularly interesting. Known as fungalysin metallopeptidase, it has only one or few representatives in similar fungi that do not kill frogs. But in this deadly fungus, genes in the family appear 29 times. Additionally, the genes generally are turned on when the fungus is infecting frogs, but turned off in the zoospore stage.

Although this gene family is an excellent candidate for the pathogen's killing ability, it is not yet certain. Discovering with certainty which genes raise or lower the fungi's killing ability is a long process, partly because the fungus is so far removed from other organisms in the evolutionary tree.

"This fungus is strange and different, partly because it is so ancient," said Rosenblum. "One of the really amazing and wonderful things about this genetic technology is that we can take something we don't know anything about, sequence its whole genome, look at what each gene is doing in different life stages, and learn a tremendous amount about the organism."

Rosenblum's research is featured in the October 13-17 edition of Proceedings of the National Academy of Sciences Online Early Edition, article #08-04173, and is posted at www.pnas.org.
Copyright 2008 Scientific Computing, Advantage Business Media
Excerpted from: http://www.scientificcomputing.com/Ancient-Frog-Killing-Fungus-Returns.aspx

Secret of speedy, strong dolphins solved

There was something peculiar about dolphins that stumped prolific British zoologist Sir James Gray in 1936. He had observed the sea mammals swimming at a swift rate of more than 20 miles per hour, but his studies had concluded that the muscles of dolphins simply weren't strong enough to support those kinds of speeds. The conundrum came to be known as "Gray's Paradox."

For decades the puzzle prompted much attention, speculation, and conjecture in the scientific community. But now, armed with cutting-edge flow measurement technology, researchers at Rensselaer Polytechnic Institute have tackled the problem and conclusively solved Gray's Paradox.

After studying dolphins, Gray said in 1936 that they are not capable of producing enough thrust, or power-induced acceleration, to overcome the drag created as the mammal sped forward through the water. This drag should prevent dolphins from attaining significant speed, but simple observation proved otherwise-a paradox. In the absence of a sound explanation, Gray theorized that dolphin skin must have special drag-reducing properties.

More than 70 years later, Timothy Wei, professor and acting dean of Rensselaer's School of Engineering, has developed a tool that conclusively measures the force a dolphin generates with its tail.

Wei created this new state-of-the-art water flow diagnostic technology by modifying and combining force measurement tools developed for aerospace research with a video-based flow measurement technique known as Digital Particle Image Velocimetry, which can capture up to 1,000 video frames per second.

Wei videotaped two bottlenose dolphins, Primo and Puka, as they swam through a section of water populated with hundreds of thousands of tiny air bubbles. He then used sophisticated computer software to track the movement of the bubbles. The color-coded results show the speed and in what direction the water is flowing around and behind the dolphin, which allowed researchers to calculate precisely how mush force the dolphin was producing.

Wei also used this technique to film dolphins as they were doing tail-stands, a trick where the dolphins "walk" on water by holding most of their bodies vertical above the water while supporting themselves with short, powerful thrusts of their tails.

The results show that dolphins produce on average about 200 pounds of force when flapping their tail-about 10 times more force than Gray originally hypothesized.

"It turns out that the answer to Gray's Paradox had nothing to do with the dolphins' skin," Wei said. "Dolphins can certainly produce enough force to overcome drag. The scientific community has known this for a while, but this is the first time anyone has been able to actually quantitatively measure the force and say, for certain, the paradox is solved."

SOURCE: Rensselaer Polytechnic Institute

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