GM-CSF required for the immune attack in multiple sclerosis

The neutralization of the cytokine GM-CSF could halt the development of multiple sclerosis. This was demonstrated by the research team of the immunologist Burkhard Becher at the University of Zurich in an animal model. Unlike other known cytokines, they write in the journal Nature Immunology, this messenger substance is essential for the development of the disease. By the end of this year, a clinical trial will be launched in which GM-CSF is to be neutralized in MS patients.

The immune systems main task is to protect us from pathogenic microorganisms. To do so, an armada of immune cells is diligently instructed to search for invading pathogens. The ability of immune cells to communicate with one another is vital to this protection. Mistakes in the communication can lead to 'misunderstandings' and an erroneous attack against ones own tissues. Such is the case in autoimmune diseases such as multiple sclerosis (MS), rheumatoid arthritis and juvenile diabetes, where the immune system inadvertently attacks the body. So-called helper T cells are chiefly responsible for the fatal immune response.

There are various sub-classes of helper T cells with different tasks and responsibilities. Clinicians and researchers have long been trying to ascertain which sub-class the rogue T cells that attack the body's own organs in autoimmune diseases actually belong to. T cells release certain messenger substances, known as cytokines, which in turn coordinate the appropriate immune response. Until now, the type of T-cell and, above all, the relevant cytokine that causes the inflammation in the brain and spinal cord were not known.

The research team of Professor Burkhard Becher has spent six years testing the relevant cytokines by a process of elimination in transgenic mouse models of multiple sclerosis. Over the years, they were able to cross many factors off the list before eventually hitting the jackpot with GM-CSF (granulocyte macrophage colony-stimulating factor). GM-CSF is produced by a newly discovered subclass of helper T cells. "The MS-like disease could not be induced in mice without GM-CSF," says Becher. "What's more, the disease could even be cured in MS mice if the cytokine was neutralized."

GM-CSF is not a new cytokine; we already knew that it can cause or aggravate inflammation. Apart from GM-CSF, however, all the other cytokines studied thus far only played a minor role. "GM-CSF is therefore the first T-cell cytokine that's essential for the initiation of an inflammatory reaction," says Becher. Furthermore, the researchers were able to demonstrate that the GM-CSF delivered to the brain by T cells activates the recruitment of tissue-damaging scavenger cells. "Without scavenger cells like these, the inflammation can't really get going in the first place and the neutralization of GM-CSF can even reverse the inflammatory process," says the immunologist.

Patients suffering from rheumatoid arthritis are currently being treated with neutralizing antibodies against GM-CSF in a clinical trial. A trial with MS patients is due to begin at the end of 2011. "We're extremely hopeful," says Becher enthusiastically. "But whether this form of therapy will actually help MS patients remains to be seen. Quiet optimism is the way to go," he explains.

Irrespective of the clinical trial, the team expects the study to have a significant impact on basic and clinical research. "We're really making headway; we now understand much better how an inflammatory lesion can develop in the brain."

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Contact: Burkhard Becher
becher@immunology.uzh.ch
41-446-353-701
University of Zurich

Combination therapy provides hope for cure of dangerous infections of cystic fibrosis patients

Hamilton, ON (April 24, 2011) – An over-the-counter drug used to treat diarrhea combined with minocycline, an antibiotic used to treat bacterial infections, could one day change the lives of those living with cystic fibrosis.

Researchers at McMaster University have discovered this creative approach to tackle antibiotic resistance to bacterial infections, a frequent complication of those with cystic fibrosis. Cystic fibrosis is the most common, fatal genetic disease affecting Canadian children and young adults.

"Antibiotic resistance is having a profound effect on known drugs that are used to treat illness and disease," says researcher Eric Brown, professor and chair of McMaster's Department of Biochemistry and Biomedical Sciences and member of the Michael G. DeGroote Institute for Infectious Disease Research (IIDR).

"Previous advances in treating cystic fibrosis have been in managing infection, but since infectious organisms are increasingly developing resistance to antibiotics, the importance of providing new treatments is more important than ever."

Brown, who made the discovery in collaboration with McMaster researchers Gerry Wright and Brian Coombes, found that the combination of these two drugs inhibits the growth of bacteria after screening a collection of previously approved non-antibiotic drugs within McMaster's Centre for Microbial Chemical Biology.

Their screening revealed that this particular combination using the anti-diarrhea drug loperamide increases the efficacy of the antibiotic minocycline against multidrug resistant P. aeruginosa.

"Typically it takes 13 to 15 years to develop a drug," says Brown. "We think that this approach could cut drug development time in half."

"These exciting research findings hold promise that a new, safer method for treating devastating lung infections in people with cystic fibrosis may be just around the corner," says Maureen Adamson, CEO, Cystic Fibrosis Canada, a charity that partnered with the Canadian Institutes of Health Research to fund the project. "These findings could impact healthcare worldwide as antibiotic resistance is a tremendous threat to many populations."

Wright, scientific director of the IIDR, adds that McMaster is one of the only universities to look at the combination of antibiotic and non-antibiotic drugs in combating bacterial resistance. But he believes this marks the beginning of using combination therapy as a more effective way to treat disease.

"This finding has opened doors to discovering the abilities of drugs when combined," he says. "Not only has antibiotic resistance become a growing threat to managing illness and disease, the use of combination therapy has added benefits. These combinations might be a way to selectively target bacteria and combat disease and leave so-called "good bacteria" intact to do other things. In effect you use fewer antibiotics to get the same effect."

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The study appears online in the journal Nature Chemical Biology on April 24.

Contact: Laura Thompson
lthomp@mcmaster.ca
905-525-9140, ext. 22196
McMaster University

RHIC Physicists Nab New Record for Heaviest Antimatter

Newly discovered antihelium-4 could be heaviest stable antinucleus detectable for decades to come

		IMAGE: This graph plots particle counts by mass, showing ordinary helium nuclei (He-3 and He-4) in orange, and their antimatter counterparts (antihelium-3 and antihelium-4) in blue. The plot illustrates that the

UPTON, NY -- Members of the international STAR collaboration at the Relativistic Heavy Ion Collider -- a particle accelerator used to recreate and study conditions of the early universe at the U.S. Department of Energy's Brookhaven National Laboratory -- have detected the antimatter partner of the helium nucleus: antihelium-4. This new particle, also known as the anti-alpha, is the heaviest antinucleus ever detected, topping a discovery announced by the same collaboration just last year*.

The new record will likely stand far longer, the scientists say, because the next weightier antimatter nucleus that does not undergo radioactive decay is predicted to be a million times more rare - and out of reach of today's technology.

"This discovery highlights the extraordinary capabilities of RHIC to investigate fundamental questions about the nature of matter, antimatter, and the early universe," said William F. Brinkman, Director of the DOE Office of Science.

Steven Vigdor, Brookhaven's Associate Lab Director for Nuclear and Particle Physics, who leads the RHIC program, said, "Barring a new breakthrough in accelerator technology, or the discovery of a completely new production mechanism, it is likely that antihelium-4 will remain the heaviest stable antimatter nucleus observed for the foreseeable future."

The STAR physicists describe the discovery in a paper in Nature, published online April 24, 2011.

The ability to create and study antimatter in conditions similar to those of the early universe is no small matter: One of the great mysteries of physics is why our universe appears to be made entirely of ordinary matter when matter and antimatter are understood to have been created in equal amounts at the time of the Big Bang.

At RHIC, head-on collisions of gold ions moving at nearly the speed of light simulate conditions just after the Big Bang. In these atomic smashups, quarks and antiquarks likewise emerge with approximately equal abundance. A major fraction of the stable antimatter produced in RHIC collisions leaves a clear signal in the STAR detector before annihilating with ordinary matter in the outer part of the experimental apparatus.

By sifting through data for half a trillion charged particles emitted from almost one billion collisions, the STAR collaboration has detected 18 examples of the unique "signature" of the antihelium-4 nucleus. Consisting of two antiprotons and two antineutrons in a stable bound state that does not undergo radioactive decay, the antihelium-4 nucleus has a negative electric charge that is twice that of an electron, while its mass is very close to four times that of a proton. Data plots show that the newly discovered anti-alphas are very cleanly separated from the lighter isotopes, and are at the expected mass.

		IMAGE: This rendering shows antihelium-4 (anti-alpha) emerging from a collision in the Relativistic Heavy Ion Collider at Brookhaven National Laboratory.

The scientists also measured the antihelium-4 production rate in nuclear interactions, and found that it is consistent with expectations based on a statistical coalescence of antiquarks from the soup of quarks and antiquarks generated in RHIC collisions. But the fact that 12 antiquarks combine to build such a complex antinucleus in a way that bears out these predictions is really quite remarkable considering it all takes place in the midst of rapidly expanding matter created at trillions of degrees and surviving for only ten trillionths of a trillionth of a second.

Knowing the production rate of these antinuclei is important to a wide range of scientific disciplines, including searches for new phenomena in the cosmos. For example, it ties in with the scientific goals of an experiment known as the Alpha Magnetic Spectrometer (AMS), which will be delivered to the International Space Station via one of the last space shuttle missions, currently scheduled for launch in late April 2011. This experiment will search for antimatter in space.

"If AMS were to find evidence for the existence of bulk antimatter elsewhere in the cosmos, the new measurement from the STAR experiment would provide the quantitative background rate for comparison," said Hank Crawford, a STAR collaborator from the University of California, Berkeley, Space Sciences Laboratory. "An observation of antihelium-4 by the AMS experiment could indicate the existence of large quantities of antimatter somehow segregated from the matter in our universe," he said.

In 2010, the Large Hadron Collider at CERN, the European laboratory for nuclear and particle physics research, began its own collisions of heavy nuclei at energies more than an order of magnitude higher than at RHIC. Experiments there also have the capability to study production of antinuclei, and it will be interesting to see what those experiments find at higher energies.

"The discovery of the antihelium-4 nucleus also has special synergy with a major scientific anniversary: the 100th anniversary of Ernest Rutherford's seminal gold foil experiments, in which he used ordinary-matter helium-4 (alpha) particles to probe the structure of matter," said Brookhaven physicist Aihong Tang, a member of the STAR collaboration and a lead author on the Nature paper. "These experiments, conducted in 1911, established the very existence of atomic nuclei for the first time, and marked the dawn of our modern understanding of atoms."

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The STAR collaboration is composed of 54 institutions from 12 countries. Research at RHIC is funded primarily by the U.S. Department of Energy's Office of Science and by various national and international collaborating institutions, with support from many funding agencies (see: http://www.bnl.gov/rhic/funding.asp) Measurement capabilities vital to antihelium-4 identification were added to the STAR experiment in 2009 with the installation of a large time-of-flight detector. This device was constructed jointly by U.S. and Chinese institutions and was funded jointly by DOE's Office of Science and the National Natural Science Foundation of China, China's Ministry of Science and Technology, and the Chinese Academy of Sciences. The antihelium-4 discovery is being announced simultaneously in the U.S. and in China.

Related Links

* 2010 Antimatter discovery at RHIC: http://www.bnl.gov/bnlweb/pubaf/pr/PR_display.asp?prID=1075

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Contact: Kendra Snyder
ksnyder@bnl.gov
631-344-8191
DOE/Brookhaven National Laboratory

RNA dynamics deconstructed

Technique offers detailed view of how RNA levels change

RNA plays a critical role in directing the creation of proteins, but there is more to the life of an RNA molecule than simply carrying DNA's message. One can imagine that an RNA molecule is born, matures, and eventually, meets its demise. Researchers at the Broad have developed an approach that offers many windows into the lifecycle of these essential molecules and will enable other scientists to investigate what happens when something in a cell goes wrong. They describe their approach, which offers high resolution and a comprehensive scope, in a Nature Biotechnology article published online on April 24.

"People are discovering more and more how the RNA lifecycle is at the heart of problems we see in disease, but we actually understand a lot less about it than we understand about many other cellular processes," said Aviv Regev, a core faculty member of the Broad Institute and a co-senior author on the paper.

Regev and her colleagues have developed a method that allows them to tease apart the different stages of this lifecycle by measuring how much messenger RNA is produced and how much is degraded. The balance of these two processes contributes to the changes seen in RNA levels in a cell over time, much the way that birth and death rates contribute to a country's total population.

RNA levels are dynamic – they change in response to certain stimuli. For this study, the researchers examined dendritic cells, which are involved in the body's immune response, as a model. They exposed these cells to a stimulus that resembled a pathogen and then looked at RNA changes before and after exposure.

"We wanted to understand how cells regulate RNA levels, and if regulation happens at the step of producing the molecule, degrading the molecule, or processing it," said Michal Rabani, first author of the paper and an MIT graduate student at the Broad. "Each of these steps can affect the level of active RNA molecules in cells. If you want to understand what happens when things go wrong, you have to understand how things work when they work as they should."

The researchers' approach allows them to look at a specific cell type and see changes in the expression of all genes. This combination of breadth and specificity offers a systematic view of how RNA changes over time. "If we want to look at specific neurons in the brain or a specific cell that's lying between other kinds of cells in the lung, this technique allows us to zoom in on one process in one cell among a billion other cells. This is the case in many diseases, a short circuit in one specific cell type, and now we have a great tool to find it," said Ido Amit, a co-senior author of the paper and a scientist at the Broad.

The scientists harnessed an existing technique to trace the fate of newly produced RNA and paired it with a new sequencing-based technology that counts molecules of mRNA. The results also gave the researchers a view of some of the in-between steps, during which mRNA is edited or processed – an unexpected but serendipitous finding. "That's the beauty of sequencing: it has a very extensive view so it shows you things you didn't expect to see," said Regev.

A key aspect of the approach is that the researchers were able to take "snapshots" of RNA levels over very short time intervals. Strung together, these snapshots reveal not only how the amount of RNA changes, but also the short-lived, intermediate phases of the RNA lifecycle that are otherwise impossible to detect. "This allows us many windows into the world of RNA," said Amit.

One critical application of the new method is in following up on leads from disease studies, such as mutated genes in cancer or other diseases that impact the RNA lifecycle. "In the past, you would know that there's a mutation and there's even a suspicion of what the gene does, but it would have been extraordinarily hard to see the effect of the mutation on these types of processes in the cell," said Regev, who is also an assistant professor at MIT and an early career scientist at the Howard Hughes Medical Institute. The researchers hope that their newly developed technique will enable others to gain deep insights into how gene mutations disrupt RNA levels, and in turn, what proteins are made.

"We're decomposing these RNA levels, breaking them down into each separate step, so that we can understand what happens at each of these steps and how they interact with each other to produce the final read out," said Rabani. "It's a very complex system, but understanding it could eventually help us understand what goes wrong when things don't work."

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This work was supported by the Richard Merkin Foundation for Stem Cell Research at the Broad Institute through a gift that Regev describes as essential for the project's success.

Paper cited:

Rabani M et al. Metabolic labeling of RNA uncovers principles of RNA production and degradation dynamics in mammalian cells. Nature Biotechnology. April 24, 2011. DOI: 10.1038/nbt.1861

About the Broad Institute of Harvard and MIT

The Eli and Edythe L. Broad Institute of Harvard and MIT was launched in 2004 to empower this generation of creative scientists to transform medicine. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.

Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to http://www.broadinstitute.org.

About the Richard Merkin Foundation for Stem Cell Research at the Broad Institute

The Richard Merkin Foundation for Stem Cell Research at the Broad Institute seeks to fund Broad Institute-affiliated scientists to develop a novel and comprehensive "toolbox" of experimental methods and computational algorithms and to apply those tools to understand cellular circuitry in stem cells, with the goal of being able to manipulate those circuits for both biological knowledge and medical applications.

Contact: Nicole Davis
ndavis@broadinstitute.org
617-714-7152
Broad Institute of MIT and Harvard

Brain cell migration during normal development may offer insight on how cancer cells spread

SEATTLE – By shedding new light on how cells migrate in the developing brain, researchers at Fred Hutchinson Cancer Research Center also may have found a new mechanism by which other types of cells, including cancer cells, travel within the body. The findings by Jonathan Cooper, Ph.D., member and director of the Hutchinson Center's Basic Sciences Division, and Yves Jossin, Ph.D., a research fellow in Cooper's laboratory, published online April 24 in Nature Neuroscience, could lead to a better understanding of neurological development and, possibly, cancer metastasis.

During normal development cells divide, arrange themselves in appropriate patterns, and specialize to form discrete tissues and organs. For the body to develop properly, cells must coordinate their migratory patterns and the process by which they differentiate, or evolve from less-specialized cells into more-specialized cell types. A lack of such coordination leads to disordered development and, in some cases, cancer.

Jossin and Cooper set out to analyze how cells migrate in the cerebral cortex of the developing brain. The cerebral cortex, gray matter of the cerebrum, is the brain's command and control center where cognition and planning occur, and it is particularly well developed in humans.

The cerebral cortex is composed of horizontal layers of nerve cells, or neurons, which are specialized for different functions and connected vertically into circuits. If some neurons are in the wrong layers, the wiring can be defective and neurological disorders including epilepsy, autism and schizophrenia may result.

In the fetus, the cortex grows "from the inside out" via the sequential addition of new neurons, which move from the inside, pass between neurons in previously established intermediate layers, and form new layers on the outside. How the migrations are regulated remains unclear despite years of study.

Jossin and Cooper now report the discovery of signals that control a particular stage in a cortical neuron's journey. New neurons initially move in a straight line, from the inside to the outside, until they reach a layer called the intermediate zone. This zone contains relatively few neurons but many connecting fibers, or axons. When new neurons reach this layer, they lose their way and start wandering – up, down, left and right, frequently changing direction. When, seemingly by chance, they emerge from the intermediate zone, they realign with their original direction of movement and speed ahead through layers of differentiated neurons towards the outer surface of the cortex.

The researchers aimed to determine how neurons get back on track after they emerge from the chaos of the intermediate zone. They identified a signaling protein, called Reelin, which is made by cells in the outermost layer of the cortex. It has been known for years that mutations in the Reelin gene cause profound cortical layering abnormalities in rodents and people, but it has been unclear which stage of neuron migration goes awry when Reelin is absent.

The new study shows that new neurons respond to Reelin as they emerge from the intermediate zone. "This is remarkable because the top layer of the cortex, where Reelin is made, is widely separated from the top of the intermediate zone, where it acts, so the Reelin protein must be diffuse," Cooper said. "It is also remarkable that Reelin seems not to be a direction signal itself. Rather, Reelin triggers changes in the membranes of the migrating neurons that allow the cells to respond to direction signals."

The researchers show that a membrane protein called N-cadherin increases on the surface of neurons when the neurons encounter Reelin. The surface increase in N-cadherin allows the cell to choose the appropriate direction for its next stage of migration. "This represents a new and surprising function for N-cadherin," Jossin said, "because normally this protein acts as a cellular stabilizer and not as an orchestrator of migration."

For example, elsewhere in the cortex, N-cadherin forms tight adhesions between adjacent cells and prevents them from moving. Indeed, the general role for cadherins in the body is to stabilize sheets of cells and organize tissues by holding cells together.

"The new role for N-cadherin in orienting migrating cells is quite unexpected and suggests that cadherins on the surface of other types of normal or cancer cells may also be involved in helping them move rather than stay in place," Jossin said. "This finding could provide new clues to how normal and cancerous cells migrate within the body," he said.

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This research was funded in part by the National Institutes of Health and a Marie Curie Fellowship from the European Union.

At Fred Hutchinson Cancer Research Center, our interdisciplinary teams of world-renowned scientists and humanitarians work together to prevent, diagnose and treat cancer, HIV/AIDS and other diseases. Our researchers, including three Nobel laureates, bring a relentless pursuit and passion for health, knowledge and hope to their work and to the world.www.fhcrc.org

Contact: Kristen Woodward
kwoodwar@fhcrc.org
206-667-5095
Fred Hutchinson Cancer Research Center

Tecnalia develops a system for heat collection from asphalt pavements

Tecnalia, through its Construction Unit, is participating in the Pavener project, aimed at developing a system for collecting the solar energy absorbed by asphalt paved surfaces. The two-year project is being led by the Campezo Group. The Group is focusing on quality control and research project development through its Research and Quality Control Laboratory, and presently this is one of its key projects.

The system involves collecting solar energy accumulated in pavements by circulating a fluid through pipes installed below the surface. This method works similarly to a solar collector incorporated into the pavement. The system can be implemented below any paved surface exposed to solar radiation, such as roads, pavements, car parks, airport landing runways and aprons, etc. Asphalted paved surfaces can heat up 70 degrees in days of strong sunlight, and given the large paved surface area available, there is a great potential for the recovery of this energy.

Multiple applications

The system can be designed for multiple applications, the most novel of these being its use as a solar collector, with great potential in the building sector. Incorporating concepts such as heat storage and heat pumps into the developed system, the accumulated solar energy may be used in low-temperature applications such as the air-conditioning of buildings, sports and leisure centres, swimming pools, and hot water supply. Another potential application of the system is its use for maintaining the temperature of the asphalt above freezing levels in winter, thus preventing the formation of ice on the roads. Apart from the benefits to road safety, this would reduce the amount of salt needed to be used to prevent frost.

The system would reduce consumption of fossil fuels, as well as greenhouse gas emissions to the atmosphere, as a renewable source of energy is exploited. Moreover, the maintenance required for roads is reduced, as road surface temperature can be maintained stable both in winter and in summer, thus reducing the appearance of cracks and grooves in the paved surfaces. An additional advantage of the system is the reduction of the urban heat island effect, as excess heat is extracted from the paved surfaces.

Simulation tasks

The Construction Unit at Tecnalia is researching into the thermal and mechanical properties of the system through experimental simulations and measurements, with the goal of optimising the system configuration depending on the application. Structural stability and thermal behaviour are the key aspects to consider in the development of the system.

The performance of the system will be further studied after the construction of a prototype installation.

Bing Energy relocates to partner with FSU on high-tech fuel cells

		IMAGE: This is Professor Jim P. Zheng of Florida State University. Click here for more information.

Florida Gov. Rick Scott today announced that Bing Energy Inc. of Chino, Calif., has selected Tallahassee as the new site of the company's world headquarters. The company, in collaboration with Professor Jim P. Zheng of The Florida State University, is planning to turn revolutionary nanotechnology pioneered at FSU into a better, faster, more economical and commercially viable fuel cell. The move is expected to create at least 244 jobs paying an average wage of $41,655 in Florida.
"I am proud to welcome Bing Energy and thank them for recognizing that Florida is the best state in the nation," Scott said. "As governor, I am continuing to make it the best place to do business. This is only the beginning. Just as Bing Energy was convinced to bring jobs here, I am talking to companies across the nation. I am letting them know that our reduction in the business tax burden, commitment to job creation, and Florida's world-class work force mean we are open for business."
Bing Energy, a manufacturer of state-of-the-art components for polymer electrolyte membrane fuel cells, will begin production in March 2011 and serve the domestic and international energy markets.
"We know that, with the continuing support of Gov. Scott, the Legislature and the people of Florida, our institutions of higher learning will continue to foster innovation, and jobs will continue to cluster around those innovations," said Florida State University President Eric J. Barron. "The breakthrough research by Drs. Wang and Zheng and the company's decision to come to Florida confirm that the investment made in their work by our state and the federal government has realized its commercial potential. Bing Energy represents the future, and Florida State is proud to be a part of it."

		IMAGE: This is President Barron (foreground) and Florida Governor Rick Scott (background).

Bing is moving its global headquarters to Tallahassee to work in partnership with Zheng, who has pioneered a fuel cell that incorporates a thin membrane composed of carbon nanotubes, reducing the need for expensive platinum components that, until now, have made fuel cells too expensive to be widely marketed. Zheng's technology is based on pioneering research and development of buckypaper conducted at Florida State's High-Performance Materials Institute. The institute's director, Professor Ben Wang, is the assistant vice president for research at Florida State.
Bing Energy's innovation promises to produce a fuel cell that is more efficient, more durable and significantly less expensive – benefits that could transform the transportation and power generation sectors.
Joining Scott and Barron in celebrating Bing Energy's move to Tallahassee were Bing Energy CFO Dean Minardi, Tallahassee Mayor John Marks, and representatives from the Economic Development Council of Tallahassee/Leon County Inc.
"We all know the world's existing energy-use pattern is unsustainable," Minardi said. "A commercially viable fuel cell will transform the way we drive, reducing our dependence on fossil fuels. It will transform the way we deliver energy to neighborhoods, ensuring reliability and eliminating the risk of brownouts."
Bing Energy's move to Florida is tied to a $1.9 million award the company recently received from the Governor's Office of Tourism, Trade and Economic Development. The award is a Qualified Target Industry (QTI) Tax Refund in support of job creation. The local Tallahassee and Leon County governments are also supporting Bing Energy by each providing a 10 percent match on the QTI Award.
Gov. Scott has stated that creating jobs is his top priority. As governor, he has announced plans to create 700,000 jobs over the next seven years by implementing accountability budgeting, reducing government spending, enacting regulatory reform, focusing on job growth and retention, investing in world class state universities, reducing property taxes and phasing out the business income tax.
Local officials expressed delight that Tallahassee was chosen by Bing Energy as its relocation site.
"Our organization identified tax incentives and work-force training programs that gave Tallahassee the edge over other communities under consideration," said Kim Williams, chairman of the Economic Development Council of Tallahassee/ Leon County Inc. "This is a perfect example of why connecting industry, education and government is so important. In this case, these connections helped us to retain our talent, as well as our university technologies and commercialization within our community."
Tallahassee Mayor John Marks spoke of the importance of creating jobs in his community and "retaining one of our greatest assets, our work-force talent. The city of Tallahassee is committed to doing our part to help this promising company establish its roots in our community."
Marks' comments were echoed by John Dailey, chairman of the Leon County Commission.
"The county is committed to working with our public and private sectors, especially our universities, to help businesses locate in our community," Dailey said.

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Additional information on the Bing Energy-FSU licensing agreement is available at http://www.fsu.com/News/FSU-signs-licensing-agreement-with-technology-company-Bing-Energy.