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SHANGHAI (AP) ? Angry Birds is migrating to China.
Rovio, the Finnish gaming company behind Angry Birds has opened its Shanghai office and outlined plans for activity parks and stores across China, one of its biggest markets.
Angry Birds, currently the second most popular paid iPhone app, has a huge fan base in China, with much merchandise available in stores and online but most of it pirated.
The makers of the game, which features bubbly headed peevish birds attacking their enemies, the pigs, hopes it will be able to convert that popularity into legitimate sales.
"We expect to be more Chinese than the Chinese people, and we will add more and Chinese cultural elements to our products," Peter Vesterbacka, founder of "Angry Birds," said Thursday.
Rovio's initiatives so far in China have included moon cakes for the mid-Autumn Festival. It is opening stores in Shanghai and Beijing next month and is building an activity park in Shanghai's Tongji University.
It also plans a theme park in the nearby city of Haining, similar to its Angry Birds Land at Finland's Sarkanniemi Amusement Park.
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Contact: Daphne Watrin
d.watrin@iospress.nl
31-206-883-355
IOS Press
Amsterdam, NL, June 14, 2012 No effective treatments are currently available for the prevention or cure of Alzheimer's disease (AD), the most frequent form of dementia in the elderly. The most recognized risk factors, advancing age and having the apolipoprotein E ?4 gene, cannot be modified or treated. Increasingly, scientists are looking toward other risk factors to identify preventive and therapeutic strategies. Much attention recently has focused on the metabolic syndrome (MetS), with a strong and growing body of research suggesting that metabolic disorders and obesity may play a role in the development of dementia.
A new supplement to the Journal of Alzheimer's Disease provides a state-of-the-art assessment of research into the link between metabolic syndrome and cognitive disorders. The supplement is guest edited by Vincenza Frisardi, of the Department of Neurological and Psychiatric Sciences, University of Bari, and the Geriatric Unit and Gerontology-Geriatrics Research Laboratory, IRCCS, Foggia, Italy, and Bruno P. Imbimbo, Research and Development Department, Chiesi Farmaceutici, Parma, Italy.
The prevalence of MetS and obesity has increased over the past several decades. MetS is a cluster of vascular and metabolic risk factors including obesity, hypertension, an abnormal cholesterol profile, and impaired blood glucose regulation. "Although molecular mechanisms underlying the relationship between MetS and neurological disorders are not fully understood, it is becoming increasingly clear that cellular and biochemical alterations observed in MetS may represent a pathological bridge between MetS and various neurological disorders," explains Dr. Frisardi.
Type 2 diabetes (T2D) has been linked with cognitive impairment in a number of studies. The risk for developing both T2D and AD increases proportionately with age, and evidence shows that individuals with T2D have a nearly twofold higher risk of AD than nondiabetic individuals.
Paula I. Moreira, Faculty of Medicine and Center for Neuroscience and Cell Biology, University of Coimbra, Portugal, outlines some of the likely mechanisms. Both AD and T2D present similar abnormalities in the mitochondria, which play a pivotal role in cellular processes that impair their ability to regulate oxidation in the cell. Human amylin, a peptide that forms deposits in the pancreatic cells of T2D patients, shares several properties with amyloid- plaques in the Alzheimer's brain. Insulin resistance is another feature shared by both disorders. Impairment of insulin signalling is directly involved in the development of tau tangles and amyloid (A) plaques. "Understanding the key mechanisms underlying this deleterious interaction may provide opportunities for the design of effective therapeutic strategies," Dr. Moreira notes.
In another article, author, Jos A. Luchsinger of the Division of General Medicine, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, notes that while there seems to be little dispute that T2D can cause cerebrovascular disease and vascular cognitive impairment, whether T2D can cause late onset AD remains to be determined. "Although the idea is highly speculative, the association between T2D and cognitive impairment may not be causal. Several lines of evidence provide some support to the idea that late onset Alzheimer's disease could cause T2D, or that both could share causal pathways," he notes. He reviews epidemiological, imaging, and pathological studies and clinical trials to provide insight. "Given the epidemic of T2D in the world, it's important to determine whether the association between T2D and cognitive impairment, particularly late onset AD, is causal and if so, what are the mechanisms underlying it."
Dr. Frisardi notes that most efforts by the pharmaceutical industry have been directed against the production and accumulation of amyloid-. "Unfortunately, these efforts have not produced effective therapies yet, since the exact mechanisms of AD are largely unknown. Given that the onset of AD most likely results from the interaction of genetic and environmental factors, the research agenda should consider new platforms of study, going beyond the monolithic outlook of AD, by synthesizing epidemiological, experimental, and biological data under a unique pathophysiological model as a point of reference for further advances in the field."
###
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Contact: Daphne Watrin
d.watrin@iospress.nl
31-206-883-355
IOS Press
Amsterdam, NL, June 14, 2012 No effective treatments are currently available for the prevention or cure of Alzheimer's disease (AD), the most frequent form of dementia in the elderly. The most recognized risk factors, advancing age and having the apolipoprotein E ?4 gene, cannot be modified or treated. Increasingly, scientists are looking toward other risk factors to identify preventive and therapeutic strategies. Much attention recently has focused on the metabolic syndrome (MetS), with a strong and growing body of research suggesting that metabolic disorders and obesity may play a role in the development of dementia.
A new supplement to the Journal of Alzheimer's Disease provides a state-of-the-art assessment of research into the link between metabolic syndrome and cognitive disorders. The supplement is guest edited by Vincenza Frisardi, of the Department of Neurological and Psychiatric Sciences, University of Bari, and the Geriatric Unit and Gerontology-Geriatrics Research Laboratory, IRCCS, Foggia, Italy, and Bruno P. Imbimbo, Research and Development Department, Chiesi Farmaceutici, Parma, Italy.
The prevalence of MetS and obesity has increased over the past several decades. MetS is a cluster of vascular and metabolic risk factors including obesity, hypertension, an abnormal cholesterol profile, and impaired blood glucose regulation. "Although molecular mechanisms underlying the relationship between MetS and neurological disorders are not fully understood, it is becoming increasingly clear that cellular and biochemical alterations observed in MetS may represent a pathological bridge between MetS and various neurological disorders," explains Dr. Frisardi.
Type 2 diabetes (T2D) has been linked with cognitive impairment in a number of studies. The risk for developing both T2D and AD increases proportionately with age, and evidence shows that individuals with T2D have a nearly twofold higher risk of AD than nondiabetic individuals.
Paula I. Moreira, Faculty of Medicine and Center for Neuroscience and Cell Biology, University of Coimbra, Portugal, outlines some of the likely mechanisms. Both AD and T2D present similar abnormalities in the mitochondria, which play a pivotal role in cellular processes that impair their ability to regulate oxidation in the cell. Human amylin, a peptide that forms deposits in the pancreatic cells of T2D patients, shares several properties with amyloid- plaques in the Alzheimer's brain. Insulin resistance is another feature shared by both disorders. Impairment of insulin signalling is directly involved in the development of tau tangles and amyloid (A) plaques. "Understanding the key mechanisms underlying this deleterious interaction may provide opportunities for the design of effective therapeutic strategies," Dr. Moreira notes.
In another article, author, Jos A. Luchsinger of the Division of General Medicine, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, notes that while there seems to be little dispute that T2D can cause cerebrovascular disease and vascular cognitive impairment, whether T2D can cause late onset AD remains to be determined. "Although the idea is highly speculative, the association between T2D and cognitive impairment may not be causal. Several lines of evidence provide some support to the idea that late onset Alzheimer's disease could cause T2D, or that both could share causal pathways," he notes. He reviews epidemiological, imaging, and pathological studies and clinical trials to provide insight. "Given the epidemic of T2D in the world, it's important to determine whether the association between T2D and cognitive impairment, particularly late onset AD, is causal and if so, what are the mechanisms underlying it."
Dr. Frisardi notes that most efforts by the pharmaceutical industry have been directed against the production and accumulation of amyloid-. "Unfortunately, these efforts have not produced effective therapies yet, since the exact mechanisms of AD are largely unknown. Given that the onset of AD most likely results from the interaction of genetic and environmental factors, the research agenda should consider new platforms of study, going beyond the monolithic outlook of AD, by synthesizing epidemiological, experimental, and biological data under a unique pathophysiological model as a point of reference for further advances in the field."
###
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
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IRON MOUNTAIN -- Many pet owners feel attached to their furry friends, taking them along for car rides and errands.? But as the summer heat moves in, leaving pets in the car can be dangerous.
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What should you do if you see a distressed pet left in a vehicle?? Diane Luczak, Manager of the Almost Home Animal Shelter, says pets should never be left in the vehicle with temperatures over 60 degrees.? The situation can cause heat stroke, severe dehydration, seizures and even death.? She says if you find pets left in a hot vehicle, call animal control
"Call am animal control officer; also go into the store and report it at the service desk and describe the make of the car, and, you know, the dog, so they could page the owner," said Luczak.????
Stacy Christiansen Smith says if you would not be comfortable sitting in the car with the windows only down a couple inches, don't do it to your dog.
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There's no more stopping Japan from restarting and blasting again online its suspended nuclear reactors.
This weekend, Japan, a year after being struck by a debilitating earthquake and tsunami that destroyed one of its nuclear reactors, is ready to bring back to life two of its suspended nuclear power plants.
The two reactors are in the western town of Ohi. Town Mayor Shinobu Tokioka on Thursday said he allowed the restarting of the idle nuclear reactor amid concerns on possible power shortages.
Japan has a total of 54 nuclear reactors, but all have been shutdown amid public clamor of safety concerns. The people likewise pressured federal government that all reactors undergo maintenance and rigid stress tests owing to the Fukushima meltdown crisis.
Although public perception to reopening the nuclear power plants still remain negative, the federal government have been saying the use of nuclear energy is important to Japan's economy.
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Moreover, according to financial site Penny Stock Detectives, all energy sources, when studied side by side, nuclear energy does far exceed the capacities of other energy sources by at least over 90 per cent capacity utilisation.
With the reopening of Japan's nuclear reactors, uranium demand is expected to regain strength.
"Nuclear power will remain a large source of energy production over the next decade to support the increase in energy usage, driving up demand for uranium," financial newsletter Profit Confidential said.
The world's consumption of uranium in 2011 reached 69,000 tonnes, The Australian reported, citing data from the World Nuclear Association. Majority or 80 per cent came directly from mines, while the rest from secondary sources such as commercial stockpiles and decommissioned nuclear weapons.
A possible supply shortage of uranium is seen two years from now, what with several new nuclear power plants expected to go online in?China, India and Russia between now and 2014.
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