Climate change is altering North American winter bird communities in ways that models currently favored by ecologists fail to predict.
Based on patterns of animals found in different climate zones today, ecologists would expect that as habitats warm, numbers of species found there will increase, and that those species will be smaller in size and restricted to narrower geographic ranges. Ecologists at the University of California, San Diego have found that only one of those three predictions has held for North American birds over the past quarter century.
Instead, their analysis has revealed that warmer weather has favored "weedy" species, those that are adapted to a wide range of habitats and therefore easily extend their ranges. Larger birds, which are typically better disperses than smaller species, seem to have gained an advantage, they report in the early online edition of the Proceedings of the Royal Society B June 10.
"The changes, at least initially, are likely to favor generalist species, those in the best position to respond to changes," said Frank La Sorte, a post-doctoral fellow at UC San Diego and first author of the paper. "It's going to be difficult using existing spatial ecological patterns to predict the outcome of climate change."
The team based their assessment on the annual Christmas Bird Count, an event organized by the National Audubon Society in which volunteers note which birds are present within a 24 kilometer wide circle in their communities over a 24-hour period in early winter, relying on either sight or sound to identify the species.
The team found 404 sites throughout North America where birders surveyed every year between 1975 and 2001. Over that period of time, the average annual temperature of these communities increased by nearly one degree Celsius.
As spatial models predict, the numbers of species counted at each site grew as temperature climbed. But that increase could be attributed to larger and more widespread species becoming more common, a pattern not reflected by differences between ecological communities found in warmer versus cooler parts of the world.
The observation suggests that weedy species may win in a warmer world, at least initially. But it also warns ecologists that they may need to revise their models when planning conservation in the face of global climate change.
"Biodiversity is under severe threat from climate change, and the lack of long-term data makes accurate forecasting of likely impact notoriously difficult," said Walter Jetz, associate professor of biology at UC San Diego and senior author of the paper. "Our study illustrates the limitations of using spatial relationships that were established over millennia to model the ecological consequences of current climate change, which is proceeding at a very rapid rate. Rigorous assessment will require much more extensive, long-term monitoring of ecological communities."
Friday, June 19, 2009
Key Found To How Tumor Cells Invade The Brain In Childhood Cancer
Despite great strides in treating childhood leukemia, a form of the disease called T-cell acute lymphoblastic leukemia (T-ALL) poses special challenges because of the high risk of leukemic cells invading the brain and spinal cord of children who relapse.
Now, a new study in the June 18, 2009, issue of the journal Nature by scientists at NYU School of Medicine reveals the molecular agents behind this devastating infiltration of the central nervous system. The finding may lead to new drugs that block these agents and thus lower the risk of relapse.
T-ALL, a blood-borne cancer in which the bone marrow makes too many lymphocytes, or white blood cells, strikes several hundred children and adolescents in the U.S. annually. While greater than 90% percent go into remission through a combination of chemotherapy and radiation, up to one third of this group end up relapsing. These patients are at particular risk for tumor cells to invade the brain and spinal cord, and to prevent this all patients receive chemotherapy injections into the central nervous system and in some cases cranial irradiation—approaches that cause dangerous side effects, including secondary tumors and potentially permanent cognitive and developmental deficits.
“In general, T-cell acute lymphoblastic leukemia is treatable with chemotherapy and radiation,” said Ioannis Aifantis, PhD, associate professor of pathology and co-director of the Cancer Stem Cell Program at the NYU Cancer Institute, who led the new study. “But you have a very high rate of relapse. And after the relapse, it is not treatable because the cancer occurs in tricky places like the central nervous system,” said Dr. Aifantis, who is also an Early Career Scientist at the Howard Hughes Medical Institute.
“We are very proud of this research and very excited about the potential implications for new therapeutic approaches to prevent or reduce the spread of leukemic cells into the central nervous system,” said Vivian S. Lee MD, PhD, MBA, the vice dean for science, senior vice president and chief scientific officer of NYU Langone Medical Center.
In the new study, Dr. Aifantis and his colleagues found that a key protein receptor embedded on the outer surface of leukemic cells is responsible for infiltrating the brain and spinal cord. “What we have found is that leukemic cells over-express this receptor.” said Dr. Aifantis, “If you knock out this receptor, these cells will not go to the brain under any circumstances.”
Previous research had strongly implicated a famous gene regulator called Notch1 in the progression of T-ALL. The Notch1 gene (a mutated version gives fruit flies notched wings) is an oncogene, or cancer-causing gene, in humans. Certain kinds of mutations in this gene have been found in nearly half of all T-ALL patients, and current estimates suggest that the gene’s regulatory influence might be implicated in nearly 90 percent of all T-ALL cases.
For their new study, Dr. Aifantis and his colleagues first introduced overactive forms of Notch1 into mice. As a result, the mice developed leukemia and the leukemic cells efficiently infiltrated the inner layers of the membrane covering the brain. “What happens is that the leukemic cells get into the cerebrospinal fluidthat protects our brain and spine, where they fill up the space and they can affect brain function, either by secreting chemicals and toxic factors or even by simple pressure,” Dr. Aifantis said.
His team then examined an array of other mouse genes to identify candidates that might fall under the regulatory spell of Notch1 to promote the brain and spinal cord infiltration. The screen revealed a promising gene for a protein named CCR7, which is embedded on the surface of lymphocytes. This chemokine receptor, as it’s known, normally senses and responds to small chemical attractants called chemokines, which act like recruitment signals for lymphocytes to converge on a specific site during the body’s response to infection or injury. In leukemia, however, these lymphocytes proliferate abnormally.
CCR7 was already known as a key player in normal lymphocyte migration and as a binding partner of two chemokines named CCL19 and CCL21. Previous studies had implicated these protein interactions in the metastasis of other tumors such as melanomas and breast cancers. Dr. Aifantis’s team also discovered that the gene for CCR7 was overactive in four of five T-ALL cell lines derived from human patients, bolstering suspicions that it played a central role in the disease. Conversely, a mutation that knocked out Notch1 also led to dramatically reduced CCR7 levels.
To characterize CCR7’s potential role in T-ALL, the researchers used two sets of mice: one in which the receptor was turned on, and a second in which it was turned off. When the team delivered an identical number of human-derived leukemic cells to both sets of mice, those with the CCR7 chemokine receptor turned off lived almost twice as long. Using bioluminescent imaging, the researchers quickly understood why: animals with the active CCR7 receptor had many more tumors. Tellingly, the T-ALL cells had infiltrated the brain and spinal cord of those mice.
Further experiments suggested that when healthy mice received leukemic cells in which the gene for CCR7 had been turned off, the cells could not migrate to the brain even though they reached other body tissues. As a result, the mice survived significantly longer than counterparts with an active copy of the gene. On the other hand, introducing a normal version of the same gene to mice otherwise lacking it was enough to recruit leukemic cells to the brain and spine.
“We wanted to determine whether CCR7 by itself was sufficient for entry into the central nervous system and that’s what this experiment shows,” Dr. Aifantis said. “By changing one specific gene, you now have your function back.”
Finally, the researchers identified the small protein that acted as the “come hither” signal for the CCR7 protein receptors. One candidate, CCL21, was undetectable in leukemic mice. But a second, CCL19, appeared in tiny veins of the brain near the infiltrating tumor cells. When the researchers introduced leukemic cells carrying a gene for CCR7 to mice that naturally lacked the CCL19 chemokine, the mice survived longer, suggesting that their increased life spans might be due to a disrupted interaction of the two proteins. The leukemic cells had no trouble infiltrating other tissue like the lymph nodes, but were completely incapable of infiltrating the brains of CCL19-deficient mice, the researchers report.
“Perhaps there are antibodies or small molecules that can block the interaction between these two proteins or reduce their interactions,” Dr. Aifantis said, “and hopefully that could be used as a type of prophylactic treatment to prevent a relapse in the central nervous system among patients who have already been treated for leukemia.” Such a treatment, he said, could prove a good alternative to the intensive and often poorly tolerated radiation and chemotherapy now used to try to block such a relapse.
The study was led by Dr. Silvia Buonamici, a post-doctoral fellow in the laboratory of Dr. Aifantis in the Department of Pathology and the NYU Cancer Institute, and in the Helen L. and Martin S. Kimmel Stem Cell Center at NYU Langone Medical Center. Other study investigators are; Thomas Trimarchi, Maria Grazia Ruocco, Linsey Reavie, Severine Cathelin, Yevgeniy Lukyanov, Jen-Chieh Tseng, Filiz Sen, Mengling Li, Elizabeth Newcomb, Jiri Zavadil, Daniel Meruelo, Sherif Ibrahim, David Zagzag, and Michael L. Dustin from NYU Langone Medical Center; Brenton G. Mar, Apostolos Klinakis, and Argiris Efstratiadis from Columbia University Medical Center; Eric Gehrie and Jonathan S. Bromberg from Mount Sinai School of Medicine; and Martin Lipp from the Max Delbrück Center for Molecular Medicine in Berlin.
The study was supported by grants from the National Institutes of Health, the American Cancer Society, the Dana Foundation, The Chemotherapy Foundation, the Alex’s Lemonade Stand Foundation, the Lauri Strauss Leukemia foundation, the G&P Foundation, an NYU School of Medicine Molecular Oncology and Immunology training grant, the American Society of Hematology, the Juvenile Diabetes Research Foundation, the National Cancer Institute, a gift from the Berrie Foundation, and a fellowship from the Jane Coffin Childs Memorial Fund for Medical Research.
Now, a new study in the June 18, 2009, issue of the journal Nature by scientists at NYU School of Medicine reveals the molecular agents behind this devastating infiltration of the central nervous system. The finding may lead to new drugs that block these agents and thus lower the risk of relapse.
T-ALL, a blood-borne cancer in which the bone marrow makes too many lymphocytes, or white blood cells, strikes several hundred children and adolescents in the U.S. annually. While greater than 90% percent go into remission through a combination of chemotherapy and radiation, up to one third of this group end up relapsing. These patients are at particular risk for tumor cells to invade the brain and spinal cord, and to prevent this all patients receive chemotherapy injections into the central nervous system and in some cases cranial irradiation—approaches that cause dangerous side effects, including secondary tumors and potentially permanent cognitive and developmental deficits.
“In general, T-cell acute lymphoblastic leukemia is treatable with chemotherapy and radiation,” said Ioannis Aifantis, PhD, associate professor of pathology and co-director of the Cancer Stem Cell Program at the NYU Cancer Institute, who led the new study. “But you have a very high rate of relapse. And after the relapse, it is not treatable because the cancer occurs in tricky places like the central nervous system,” said Dr. Aifantis, who is also an Early Career Scientist at the Howard Hughes Medical Institute.
“We are very proud of this research and very excited about the potential implications for new therapeutic approaches to prevent or reduce the spread of leukemic cells into the central nervous system,” said Vivian S. Lee MD, PhD, MBA, the vice dean for science, senior vice president and chief scientific officer of NYU Langone Medical Center.
In the new study, Dr. Aifantis and his colleagues found that a key protein receptor embedded on the outer surface of leukemic cells is responsible for infiltrating the brain and spinal cord. “What we have found is that leukemic cells over-express this receptor.” said Dr. Aifantis, “If you knock out this receptor, these cells will not go to the brain under any circumstances.”
Previous research had strongly implicated a famous gene regulator called Notch1 in the progression of T-ALL. The Notch1 gene (a mutated version gives fruit flies notched wings) is an oncogene, or cancer-causing gene, in humans. Certain kinds of mutations in this gene have been found in nearly half of all T-ALL patients, and current estimates suggest that the gene’s regulatory influence might be implicated in nearly 90 percent of all T-ALL cases.
For their new study, Dr. Aifantis and his colleagues first introduced overactive forms of Notch1 into mice. As a result, the mice developed leukemia and the leukemic cells efficiently infiltrated the inner layers of the membrane covering the brain. “What happens is that the leukemic cells get into the cerebrospinal fluidthat protects our brain and spine, where they fill up the space and they can affect brain function, either by secreting chemicals and toxic factors or even by simple pressure,” Dr. Aifantis said.
His team then examined an array of other mouse genes to identify candidates that might fall under the regulatory spell of Notch1 to promote the brain and spinal cord infiltration. The screen revealed a promising gene for a protein named CCR7, which is embedded on the surface of lymphocytes. This chemokine receptor, as it’s known, normally senses and responds to small chemical attractants called chemokines, which act like recruitment signals for lymphocytes to converge on a specific site during the body’s response to infection or injury. In leukemia, however, these lymphocytes proliferate abnormally.
CCR7 was already known as a key player in normal lymphocyte migration and as a binding partner of two chemokines named CCL19 and CCL21. Previous studies had implicated these protein interactions in the metastasis of other tumors such as melanomas and breast cancers. Dr. Aifantis’s team also discovered that the gene for CCR7 was overactive in four of five T-ALL cell lines derived from human patients, bolstering suspicions that it played a central role in the disease. Conversely, a mutation that knocked out Notch1 also led to dramatically reduced CCR7 levels.
To characterize CCR7’s potential role in T-ALL, the researchers used two sets of mice: one in which the receptor was turned on, and a second in which it was turned off. When the team delivered an identical number of human-derived leukemic cells to both sets of mice, those with the CCR7 chemokine receptor turned off lived almost twice as long. Using bioluminescent imaging, the researchers quickly understood why: animals with the active CCR7 receptor had many more tumors. Tellingly, the T-ALL cells had infiltrated the brain and spinal cord of those mice.
Further experiments suggested that when healthy mice received leukemic cells in which the gene for CCR7 had been turned off, the cells could not migrate to the brain even though they reached other body tissues. As a result, the mice survived significantly longer than counterparts with an active copy of the gene. On the other hand, introducing a normal version of the same gene to mice otherwise lacking it was enough to recruit leukemic cells to the brain and spine.
“We wanted to determine whether CCR7 by itself was sufficient for entry into the central nervous system and that’s what this experiment shows,” Dr. Aifantis said. “By changing one specific gene, you now have your function back.”
Finally, the researchers identified the small protein that acted as the “come hither” signal for the CCR7 protein receptors. One candidate, CCL21, was undetectable in leukemic mice. But a second, CCL19, appeared in tiny veins of the brain near the infiltrating tumor cells. When the researchers introduced leukemic cells carrying a gene for CCR7 to mice that naturally lacked the CCL19 chemokine, the mice survived longer, suggesting that their increased life spans might be due to a disrupted interaction of the two proteins. The leukemic cells had no trouble infiltrating other tissue like the lymph nodes, but were completely incapable of infiltrating the brains of CCL19-deficient mice, the researchers report.
“Perhaps there are antibodies or small molecules that can block the interaction between these two proteins or reduce their interactions,” Dr. Aifantis said, “and hopefully that could be used as a type of prophylactic treatment to prevent a relapse in the central nervous system among patients who have already been treated for leukemia.” Such a treatment, he said, could prove a good alternative to the intensive and often poorly tolerated radiation and chemotherapy now used to try to block such a relapse.
The study was led by Dr. Silvia Buonamici, a post-doctoral fellow in the laboratory of Dr. Aifantis in the Department of Pathology and the NYU Cancer Institute, and in the Helen L. and Martin S. Kimmel Stem Cell Center at NYU Langone Medical Center. Other study investigators are; Thomas Trimarchi, Maria Grazia Ruocco, Linsey Reavie, Severine Cathelin, Yevgeniy Lukyanov, Jen-Chieh Tseng, Filiz Sen, Mengling Li, Elizabeth Newcomb, Jiri Zavadil, Daniel Meruelo, Sherif Ibrahim, David Zagzag, and Michael L. Dustin from NYU Langone Medical Center; Brenton G. Mar, Apostolos Klinakis, and Argiris Efstratiadis from Columbia University Medical Center; Eric Gehrie and Jonathan S. Bromberg from Mount Sinai School of Medicine; and Martin Lipp from the Max Delbrück Center for Molecular Medicine in Berlin.
The study was supported by grants from the National Institutes of Health, the American Cancer Society, the Dana Foundation, The Chemotherapy Foundation, the Alex’s Lemonade Stand Foundation, the Lauri Strauss Leukemia foundation, the G&P Foundation, an NYU School of Medicine Molecular Oncology and Immunology training grant, the American Society of Hematology, the Juvenile Diabetes Research Foundation, the National Cancer Institute, a gift from the Berrie Foundation, and a fellowship from the Jane Coffin Childs Memorial Fund for Medical Research.
Diesel engines clean up their act
Some good news for a change.
A new study shows that 2007 diesel engines are belching out 90% less pollution than 2004 models when it comes to many toxic emissions. Some say the improvements will save lives.
The report by the Coordinating Research Council, a nonprofit research group, found that emissions of fine particulate matter, a dangerous pollutant that can get into people's lungs, has decreased by 99%. That's 89% lower than 2007 EPA standards.
Smog-producing hydrocarbons and carbon monoxide emissions also passed EPA standards with flying colors, dropping more than 90%, according to the study. Nitrogen oxides, another culprit in smog production, went down 70%, or 10% below required levels.
The improvements will save lives.
EPA's standards apply only to new diesel engines. California remains the only state to force truckers to clean up existing diesel engines, through controversial rules adopted in December 2009.
A new study shows that 2007 diesel engines are belching out 90% less pollution than 2004 models when it comes to many toxic emissions. Some say the improvements will save lives.
The report by the Coordinating Research Council, a nonprofit research group, found that emissions of fine particulate matter, a dangerous pollutant that can get into people's lungs, has decreased by 99%. That's 89% lower than 2007 EPA standards.
Smog-producing hydrocarbons and carbon monoxide emissions also passed EPA standards with flying colors, dropping more than 90%, according to the study. Nitrogen oxides, another culprit in smog production, went down 70%, or 10% below required levels.
The improvements will save lives.
EPA's standards apply only to new diesel engines. California remains the only state to force truckers to clean up existing diesel engines, through controversial rules adopted in December 2009.
EPA targets cement industry emissions
Environmentalists and industry representatives pleaded their case with federal regulators Tuesday over rules that would slash toxic emissions from cement kilns, the top source of mercury emissions in California.The Environmental Protection Agency issued proposed regulations for Portland cement kilns earlier this year, after more than a decade of pressure from environmental groups. The rules aim to reduce the industry's mercury emissions by an estimated 81% to 93% annually, as well as cut emissions of hydrocarbons, particulate matter and hydrochloric acid.The EPA projects that the changes could save billions of dollars and hundreds of lives a year, but cement industry officials say they will drive up the price of cement, and possibly drive the industry to countries that have lower pollution standards. The rules would "undermine the stability of the domestic cement industry, endangering thousands of jobs and the supply of a basic construction material for uncertain environmental benefits," Andy O'Hare, a spokesman for the Portland Cement Assn., told EPA officials at the hearing in downtown Los Angeles."This regulation will help all Californians breathe easier, particularly the dozens of California communities neighboring cement kilns," Otana Jakpor, a Riverside high school student speaking for the American Lung Assn., told the EPA panel. "It will reduce hundreds of thousands of tons of toxic chemicals that harm young people. And it will do so with technology that already exists. . . . As a young person who lives in an area with some of the worst air pollution in the country, I feel especially passionate about this."
Portland cement kilns, which produce the key ingredient in concrete, account for 90% of the state's airborne mercury, which can affect the nervous system, cognitive function and kidneys, and can cause respiratory failure and death at high exposures, according to the EPA. Cement kilns emit hazardous chemicals as they burn coal, petroleum coke or industrial waste to heat raw materials including limestone ore, which also can contain mercury and other elements. The process produces "clinker," which is cooled, ground and mixed with gypsum. In 2008, high levels of the toxic carcinogen hexavalent chromium were traced to piles of clinker outside the TXI Riverside cement plant, which has since shut down. "We think of California as not having coal-fired power plants, but we really do," said Miriam Rotkin-Ellman, a scientist with the Natural Resources Defense Council. "We have these cement kilns that basically operate as small coal-fired power plants, and some of them aren't so small."California is the nation's largest producer of cement, and houses 11 of the nation's 163 Portland cement plants, including the Lehigh Southwest plant in Tehachapi, which has historically been one of the industry's worst mercury polluters.The EPA is accepting public comments on the proposed rules through Sept. 4. A second hearing will take place in Dallas today and a third in Washington on Thursday
Portland cement kilns, which produce the key ingredient in concrete, account for 90% of the state's airborne mercury, which can affect the nervous system, cognitive function and kidneys, and can cause respiratory failure and death at high exposures, according to the EPA. Cement kilns emit hazardous chemicals as they burn coal, petroleum coke or industrial waste to heat raw materials including limestone ore, which also can contain mercury and other elements. The process produces "clinker," which is cooled, ground and mixed with gypsum. In 2008, high levels of the toxic carcinogen hexavalent chromium were traced to piles of clinker outside the TXI Riverside cement plant, which has since shut down. "We think of California as not having coal-fired power plants, but we really do," said Miriam Rotkin-Ellman, a scientist with the Natural Resources Defense Council. "We have these cement kilns that basically operate as small coal-fired power plants, and some of them aren't so small."California is the nation's largest producer of cement, and houses 11 of the nation's 163 Portland cement plants, including the Lehigh Southwest plant in Tehachapi, which has historically been one of the industry's worst mercury polluters.The EPA is accepting public comments on the proposed rules through Sept. 4. A second hearing will take place in Dallas today and a third in Washington on Thursday
New York 'carbon counter' sign shows greenhouse gases in real time
New Yorkers leaving Penn station and the tenor Andrea Bocelli's concert at Madison Square Garden stadium were confronted with an unusual advert yesterday – a huge sign showing greenhouse gas levels in the atmosphere.
Updated in real time, using projections from monthly measurements of CO2 and other greenhouse gases by Massachusetts Institute of Technology, the Carbon Counter is designed to get everyone to reduce their emissions.
Kevin Parker, the global head of Deutsche Bank's asset management division, which put up the 21-metre sign, said: "Carbon in the atmosphere has reached an 800,000-year high. We can't see greenhouse gases, so it is easy to forget that they are accumulating rapidly."
Yesterday the counter, which uses 40,960 low-energy LEDs and carbon-offsets its electricity usage, gave a figure of 3.64tn tonnes.
At current rates, the counter's figures are expected to rise by 2bn tonnes a month. The concentration of carbon dioxide in the atmosphere stands at about 387 parts per million (ppm), up by more than a third on pre-industrial revolution levels of about 280ppm.
Ronald Prinn, professor of atmospheric science at MIT, explained the data behind the sign: "The number on the counter is based on global measurements. It shows the total estimated tonnage of greenhouse gases expressed as their equivalent amounts of carbon dioxide, with seasonal and other natural cyclical variations removed to more clearly reveal the underlying long-term trends driven by human and other activity."
Updated in real time, using projections from monthly measurements of CO2 and other greenhouse gases by Massachusetts Institute of Technology, the Carbon Counter is designed to get everyone to reduce their emissions.
Kevin Parker, the global head of Deutsche Bank's asset management division, which put up the 21-metre sign, said: "Carbon in the atmosphere has reached an 800,000-year high. We can't see greenhouse gases, so it is easy to forget that they are accumulating rapidly."
Yesterday the counter, which uses 40,960 low-energy LEDs and carbon-offsets its electricity usage, gave a figure of 3.64tn tonnes.
At current rates, the counter's figures are expected to rise by 2bn tonnes a month. The concentration of carbon dioxide in the atmosphere stands at about 387 parts per million (ppm), up by more than a third on pre-industrial revolution levels of about 280ppm.
Ronald Prinn, professor of atmospheric science at MIT, explained the data behind the sign: "The number on the counter is based on global measurements. It shows the total estimated tonnage of greenhouse gases expressed as their equivalent amounts of carbon dioxide, with seasonal and other natural cyclical variations removed to more clearly reveal the underlying long-term trends driven by human and other activity."
Denmark to power electric cars by wind in vehicle-to-grid experiment
Cars could be the solution to the intermittent nature of wind power if a multimillion European project beginning on a Danish island proves successful.
The project on the holiday island of Bornholm will use the batteries of parked electric cars to store excess energy when the wind blows hard, and then feed electricity back into the grid when the weather is calm.
The concept, known as vehicle-to-grid (V2G) is widely cited among greens as a key step towards a low-carbon future, but has never been demonstrated. Now, the 40,000 inhabitants of Bornholm are being recruited into the experiment. Denmark is already a world leader in wind energy and has schemes to replace 10% of all its vehicles with electric cars, but the goal on the island is to replace all petrol cars.
Currently 20% of the island's electricity comes from wind, even though it has enough turbines installed to meet 40% of its needs. The reason it cannot use the entire capacity is the intermittency of the wind: many turbines are needed to harness sufficient power in breezes, but when gales blow the grid would overload, so some turbines are disconnected.
So the aim of the awkwardly named Electric Vehicles in a Distributed and Integrated Market using Sustainable Energy and Open Networks Project – Edison for short – is to use V2G to allow more turbines to be built and provide up to 50% of the island's supply without making the grid crash.
Each electric vehicle will have battery capacity reserved to store wind power for the island rather than for travelling. This means it acts like a buffer, says Dieter Gantenbein, a researcher at IBM's Zurich Research Laboratory. IBM is developing the software needed for the island's smart grid, and will showcase its work next week. When the cars are plugged in and charging their batteries, they will absorb any additional load the grid cannot cope with and then feed it back to power homes when needed, he says.
"It's never been tried at this scale," says Hermione Crease of Cambridge-based Sentec, which develops smart grid software. There are plenty of smart grid trials already under way, usually involving the use of software to monitor and manage supply and demand, for example, by temporarily switching off industrial cooling units during periods of peak load, she says. But unlike these so-called "negawatt" approaches, proving that cars can be used as part of the grid has yet to attempted.
Andrew Howe of RLTec in London, another smart grid technology firm, says many important questions need answers. It is not clear, for example, how the cost and lifetime of batteries will influence the economics of such a system.
These are the kinds of issue the project seeks to shed light on, says the project manager Jørgen Christensen of the Danish Energy Association, which with technology companies Siemens and Dong and the government are running the scheme.
The project on the holiday island of Bornholm will use the batteries of parked electric cars to store excess energy when the wind blows hard, and then feed electricity back into the grid when the weather is calm.
The concept, known as vehicle-to-grid (V2G) is widely cited among greens as a key step towards a low-carbon future, but has never been demonstrated. Now, the 40,000 inhabitants of Bornholm are being recruited into the experiment. Denmark is already a world leader in wind energy and has schemes to replace 10% of all its vehicles with electric cars, but the goal on the island is to replace all petrol cars.
Currently 20% of the island's electricity comes from wind, even though it has enough turbines installed to meet 40% of its needs. The reason it cannot use the entire capacity is the intermittency of the wind: many turbines are needed to harness sufficient power in breezes, but when gales blow the grid would overload, so some turbines are disconnected.
So the aim of the awkwardly named Electric Vehicles in a Distributed and Integrated Market using Sustainable Energy and Open Networks Project – Edison for short – is to use V2G to allow more turbines to be built and provide up to 50% of the island's supply without making the grid crash.
Each electric vehicle will have battery capacity reserved to store wind power for the island rather than for travelling. This means it acts like a buffer, says Dieter Gantenbein, a researcher at IBM's Zurich Research Laboratory. IBM is developing the software needed for the island's smart grid, and will showcase its work next week. When the cars are plugged in and charging their batteries, they will absorb any additional load the grid cannot cope with and then feed it back to power homes when needed, he says.
"It's never been tried at this scale," says Hermione Crease of Cambridge-based Sentec, which develops smart grid software. There are plenty of smart grid trials already under way, usually involving the use of software to monitor and manage supply and demand, for example, by temporarily switching off industrial cooling units during periods of peak load, she says. But unlike these so-called "negawatt" approaches, proving that cars can be used as part of the grid has yet to attempted.
Andrew Howe of RLTec in London, another smart grid technology firm, says many important questions need answers. It is not clear, for example, how the cost and lifetime of batteries will influence the economics of such a system.
These are the kinds of issue the project seeks to shed light on, says the project manager Jørgen Christensen of the Danish Energy Association, which with technology companies Siemens and Dong and the government are running the scheme.
Consumers could get up to $4,500 for new car
Car shoppers could take advantage of government incentives worth up to $4,500 this summer to send their old gas guzzler to the scrap heap in favor of a more fuel-efficient new vehicle.
President Barack Obama is expected to sign into law the “cash for clunkers” program, which was approved by the Senate on Thursday. For owners of low-mileage models such as the 1994 Ford Bronco, 1998 Nissan Pathfinder or the 1995 Chevrolet Blazer, the plan could give them a reason to visit their local car dealer during an economic downturn.
“I’ve been sitting on the fence for about a year,” said Jim Seegraves, 44, of East Lansing, Mich., who has been looking to replace his 2000 GMC Sierra pickup truck. “This legislation will help me get over the hump and get the car that I want.”
The bill provides $1 billion for the auto sales program from July through November and the Congressional Budget Office expects that with a total of $4 billion, about 1 million new vehicles could be purchased. The government is expected to implement the program by early August.
Automakers and their unions have lobbied heavily for the incentives to help the auto industry boost sales and stabilize General Motors Corp. and Chrysler Group LLC, which have received billions of dollars for government-led bankruptcies. In May, U.S. auto sales were 34 percent lower than a year ago and the industry expects to sell less than 10 million vehicles in the U.S. in 2009, compared to more than 16 million in 2007.
Here’s how the plan works: Car owners could get a voucher worth $3,500 if they traded in a vehicle getting 18 miles per gallon or less for one getting at least 22 mpg. The voucher would grow to $4,500 if the new car’s mileage was 10 mpg higher than the old vehicle. The mpg figures are listed on the car’s window sticker.
Owners of sport utility vehicles, pickup trucks or minivans getting 18 mpg or less could receive a voucher for $3,500 if their new truck or SUV got at least 2 mpg higher than their old vehicle. The voucher would increase to $4,500 if the mileage of the new truck or SUV was at least 5 mpg higher than the older vehicle.
The program was aimed at replacing older vehicles — built in model year 1984 or later — and would not make financial sense for someone owning a vehicle with a trade-in value greater than $3,500 or $4,500.
A 1998 Jeep Cherokee 4-wheel-drive with about 150,000 miles, for example, might only get $1,000 to $1,500 as a trade-in vehicle, according to estimates by Kelley Blue Book. Since the 1998 Cherokee gets about 17 mpg, an owner could parlay it into a new Ford Escape Hybrid — 2009 versions get 28-to-32 mpg — and maximize their trade-in to $4,500.
Dealers would apply the vouchers to the purchase or lease of a qualifying vehicle and ensure that the older vehicles are crushed or shredded. The new vehicle must have a manufacturer’s suggested retail price of less than $45,000.
The program is not without critics.
Jeremy Anwyl, chief executive of Edmunds.com, a Web site for car shoppers, said it would struggle to provide 250,000 new vehicle sales. Most of the qualifying vehicles would be at least 10 years old and many owners would be less inclined to take on a new car payment or unable to afford a new vehicle.
“You’ve got to consider the profile of consumers who drive these vehicles,” Anwyl said.
Budget-conscious Republicans in the Senate opposed it, along with environmental-leaning lawmakers who said it failed to encourage the purchase of high-mileage cars and didn’t apply to used vehicles. Someone could receive a voucher for buying a new Hummer, they noted, pointing to analysts who said it would primarily benefit owners of older-model pickup trucks, SUVs and minivans.
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Vote and discuss: Will you be trading in a clunker?
Dealers say it will be a valuable tool to lure more shoppers to their showrooms. Many intend to advertise heavily and combine the government plan with other incentives, providing some help at a time when the industry is struggling to sell cars.
“Anything to jump-start the economy,” said Jason Robinson, a car salesman with AutoServ of Tilton, N.H. “There’s not much sense of urgency out in the market right now.”
President Barack Obama is expected to sign into law the “cash for clunkers” program, which was approved by the Senate on Thursday. For owners of low-mileage models such as the 1994 Ford Bronco, 1998 Nissan Pathfinder or the 1995 Chevrolet Blazer, the plan could give them a reason to visit their local car dealer during an economic downturn.
“I’ve been sitting on the fence for about a year,” said Jim Seegraves, 44, of East Lansing, Mich., who has been looking to replace his 2000 GMC Sierra pickup truck. “This legislation will help me get over the hump and get the car that I want.”
The bill provides $1 billion for the auto sales program from July through November and the Congressional Budget Office expects that with a total of $4 billion, about 1 million new vehicles could be purchased. The government is expected to implement the program by early August.
Automakers and their unions have lobbied heavily for the incentives to help the auto industry boost sales and stabilize General Motors Corp. and Chrysler Group LLC, which have received billions of dollars for government-led bankruptcies. In May, U.S. auto sales were 34 percent lower than a year ago and the industry expects to sell less than 10 million vehicles in the U.S. in 2009, compared to more than 16 million in 2007.
Here’s how the plan works: Car owners could get a voucher worth $3,500 if they traded in a vehicle getting 18 miles per gallon or less for one getting at least 22 mpg. The voucher would grow to $4,500 if the new car’s mileage was 10 mpg higher than the old vehicle. The mpg figures are listed on the car’s window sticker.
Owners of sport utility vehicles, pickup trucks or minivans getting 18 mpg or less could receive a voucher for $3,500 if their new truck or SUV got at least 2 mpg higher than their old vehicle. The voucher would increase to $4,500 if the mileage of the new truck or SUV was at least 5 mpg higher than the older vehicle.
The program was aimed at replacing older vehicles — built in model year 1984 or later — and would not make financial sense for someone owning a vehicle with a trade-in value greater than $3,500 or $4,500.
A 1998 Jeep Cherokee 4-wheel-drive with about 150,000 miles, for example, might only get $1,000 to $1,500 as a trade-in vehicle, according to estimates by Kelley Blue Book. Since the 1998 Cherokee gets about 17 mpg, an owner could parlay it into a new Ford Escape Hybrid — 2009 versions get 28-to-32 mpg — and maximize their trade-in to $4,500.
Dealers would apply the vouchers to the purchase or lease of a qualifying vehicle and ensure that the older vehicles are crushed or shredded. The new vehicle must have a manufacturer’s suggested retail price of less than $45,000.
The program is not without critics.
Jeremy Anwyl, chief executive of Edmunds.com, a Web site for car shoppers, said it would struggle to provide 250,000 new vehicle sales. Most of the qualifying vehicles would be at least 10 years old and many owners would be less inclined to take on a new car payment or unable to afford a new vehicle.
“You’ve got to consider the profile of consumers who drive these vehicles,” Anwyl said.
Budget-conscious Republicans in the Senate opposed it, along with environmental-leaning lawmakers who said it failed to encourage the purchase of high-mileage cars and didn’t apply to used vehicles. Someone could receive a voucher for buying a new Hummer, they noted, pointing to analysts who said it would primarily benefit owners of older-model pickup trucks, SUVs and minivans.
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Vote and discuss: Will you be trading in a clunker?
Dealers say it will be a valuable tool to lure more shoppers to their showrooms. Many intend to advertise heavily and combine the government plan with other incentives, providing some help at a time when the industry is struggling to sell cars.
“Anything to jump-start the economy,” said Jason Robinson, a car salesman with AutoServ of Tilton, N.H. “There’s not much sense of urgency out in the market right now.”
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