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Energy Department Ups Investment In Advanced Biofuels, Funds Four Projects Developing Cost-Effective Enzymes In another sign of the promise that biofuels hold for the future, the U.S. Department of Energy (DOE) announced four projects that will significantly move forward research and development of advanced enzymes necessary for producing cost-effective cellulosic biofuels. Four projects by members of the Biotechnology Industry Organization (BIO) received DOE matching grants totaling $33.8 million to develop cost-efficient enzymes for cellulosic biofuel production by 2012. These enzymes will be instrumental in fulfilling the renewable fuel standard put forward in the Energy Independence and Security Act of 2007. "The biofuels industry has taken off," said Brent Erickson, executive vice president at BIO. "There are already 21 cellulosic biorefineries planned or under construction throughout the United States. Ongoing research and development in enzymes and other biorefinery processes is critical to rapidly building advanced biofuel production capacity. This production will not only provide long-term environmental benefits by lowering greenhouse gas emissions and encouraging sustainable agricultural practices, but also help liberate the U.S. from its dependence on petroleum." The four announced projects include: - DSM Innovation Center, Inc., (Parsippany, N.J.) with Abengoa Bioenergy New Technologies (York, Neb.) - Development of a Commercial Enzymes System fro Lignocellulosic Biomass Saccharification. - Genencor - A Division of Danisco (Palo Alto, Calif.) - Enhancing Cellulase Commercial Performance for the Lignocellulosic Biomass Industry. - Novozymes, Inc. (Davis, Calif.) - Project Decrease - Development of a Commercial-Ready Enzyme Application System for Ethanol. - Verenium Corporation (San Diego) - Commercialization of Customized Cellulase Solutions for Biomass Saccharification. For more information on sustainable production of advanced biofuel, visit http://biofuelsandclimate.wordpress.com/. Upcoming BIO Events - Partnering for Global Health March 10-12, 2008 Washington, DC - BIO-Europe Spring April 7-9, 2008 Madrid, Spain - BIO National Venture Conference April 22-23, 2008 Boston, Mass. - World Congress on Industrial Biotechnology & Bioprocessing April 27-30, 2008 Chicago, Ill. - 2008 BIO International Convention June 17-20, 2008 San Diego, Calif. About BIO BIO represents more than 1,150 biotechnology companies, academic institutions, state biotechnology centers and related organizations across the United States and in more than 30 other nations. BIO members are involved in the research and development of innovative healthcare, agricultural, industrial and environmental biotechnology technologies. BIO also produces the annual BIO International Convention, the world's largest gathering of the biotechnology industry, along with industry-leading investor and partnering meetings held around the world. http://www.bio.org
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The results raise the possibility that treatments to reduce uric acid might slow the decline of renal function in patients with diabetes. "Thus we have the hope of having a means to thwart the loss of kidney function while function is still in a relatively preserved stage," comments Dr. Elizabeth T. Rosolowsky of Joslin Diabetes Center, Boston. The researchers measured serum uric acid concentration in 675 patients with type 1 diabetes. On screening tests, 311 patients had small amounts of the protein albumin in the urine. This result--called microalbuminuria--is generally regarded as a harbinger of kidney function loss in diabetic kidney disease (nephropathy). The other 364 patients had normal urine albumin levels. None of the patients had higher levels of albumin (albuminuria) representing more advanced diabetic nephropathy. Nevertheless, one in five had some impairment of kidney function on a standard test, the glomerular filtration rate. "Our research showed that loss of kidney function takes place even in the absence of albuminuria in patients with type 1 diabetes," says Dr. Rosolowsky. In contrast, the serum uric acid level was consistently related to kidney function--the higher the uric acid, the lower the kidney function. "The serum concentration of uric acid in these patients varied in a manner consistent with its having played a role in this early loss of kidney function," according to Dr. Rosolowsky. Urine albumin is commonly measured to identify patients with type 1 diabetes at risk of developing nephropathy. "Historically, it was believed that the start of kidney function loss happened only when the amount of leakage of albumin into the urine had reached a certain level," Dr. Rosolowsky explains. "However, recent studies by our group have suggested that kidney function loss may start much earlier in some patients with type 1 diabetes." Other studies have suggested that increased serum uric acid levels are associated with loss of kidney function, and may even be a causative factor. If higher uric acid levels do contribute to loss of kidney function, then the findings may offer a new approach to treating diabetic kidney disease. "The serum uric acid concentration is modifiable by drugs or by decreasing the intake of dietary protein, the main source of uric acid," says Dr. Rosolowsky. "If follow-up studies, already underway, demonstrate that serum uric acid concentration predicts the course of early decline in kidney function, then clinical trials would be justified to test whether modifying serum uric acid concentration also modifies the course of renal function decline in type 1 diabetic patients with high normoalbuminuria or microalbuminuria." Adapted from materials provided by American Society of Nephrology, via EurekAlert!, a service of AAAS.
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In the journal Optics Letters, the team describes how they used optical technology to examine tissue samples taken from different autopsies and correctly identified which samples came from people who had Alzheimer's disease. Alzheimer's currently afflicts some 4.5 million Americans and is the most common cause of dementia among older people in the United States. "We're primarily interested in finding a way of diagnosing and monitoring Alzheimer's disease during life," says U.S. Department of Veterans Affairs Research Scientist Eugene Hanlon. "We think this technique has a lot of potential for detecting the disease early on." The new technique developed by Hanlon and his collaborators at Harvard Medical School/Beth Israel Deaconess Medical Center and Boston University can detect alterations to the optical properties of the brain that occur as the tissue undergoes microscopic changes due to Alzheimer's--sometimes far in advance of clinical symptoms. The technique is now being tested for its effectiveness at diagnosing Alzheimer's disease in living people. For several years, Hanlon and his colleagues have looked at the possibility of analyzing the brain with near-infrared light, which has the advantage of being able to safely penetrate the skull and pass harmlessly through the brain. Inside the head, some of the infrared light scatters, however, and how the light scatters can tell researchers about the condition of the brain. In their paper, the team reports observing an optical effect due to the presence of microscopic features of Alzheimer's. Amyloid plaques, one of the telltale signs of Alzheimer's disease, scatter light differently from normal brain tissue. What Hanlon and his colleagues showed was that as the microscopic plaques accumulate, the optical properties of the brain change. The team found that this change is detectable and that their technique could quantify differences between in-vitro samples and correctly identify signs of Alzheimer's. This technique will be a boon to medicine if it is able to detect microscopic changes that can be related to disease progression. While techniques like MRI are good at identifying the gross anatomical features associated with Alzheimer's, they cannot detect more microscopic changes. Although Alzheimer's disease is one of the leading causes of death in the United States, claiming tens of thousands of American lives a year, there is no definitive way to diagnose it--at least not while someone is alive. After someone with Alzheimer's dies, pathologists can perform an autopsy and examine slices of the brain under the microscope, looking for the same signs that Alois Alzheimer first recognized when he identified the disease more than a century ago. Finding accumulations of amyloid plaques in the brain substance and tangle-like proteins in nerve cells is the only way to confirm with certainty that someone had Alzheimer's while they were alive. Since there is no way to safely examine the brains of living people this way, doctors currently diagnose Alzheimer's disease using other methods. They rely on reviewing medical histories, administering physical exams, and taking into account the results of a battery of neuropsychological assessments that measure cognitive performance. A positive diagnosis is made when all other possible causes have been eliminated, but even under the best of circumstances, these diagnoses can be incorrect 10 percent of the time or more. Accurate, early detection of Alzheimer's could save many lives. While there is no cure for the disease, clinically proven treatments can slow its progress--especially if they are administered early on. Moreover, being able to follow the disease progression over time would greatly enhance the ability of researchers and pharmaceutical companies to find new and improved drugs and treatment strategies for people at all stages of the disease. A current rich area of research seeks to get information about what is going on in the brain without actually looking at the tissue. Some scientists, for instance, look at whether proteins and other biomarkers in the blood or spinal fluid indicate disease progression. Others try to image the brain with established techniques like MRI or PET scans. Optical methods, like the one used by the Bedford researchers, are an emerging approach to imaging. The research was funded by the U.S. Department of Veterans Affairs, the National Science Foundation, and a New Concept Award from the Center for Integration of Medicine & Innovative Technology. Journal reference: "Scattering Differentiates Alzheimer Disease In Vitro," by Eugene B. Hanlon et al., Optics Letters, Vol. 33, No. 6, March 15, pp. 624-26, abstract at http://www.opticsinfobase.org/abstract.cfm?URI=ol-33-6-624. Adapted from materials provided by Optical Society of America.
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