CAIRO (AP) ? Egyptian security officials say 22 people have been killed in riots sparked by death sentences given to nearly two dozen soccer fans convicted of violence after a game in Port Said last year.
The security officials say most were killed in assaults on the governor's office, courthouse and prison after the sentence was handed down during a trial outside Cairo. They say two policemen also were shot to death outside the city's main prison when angry relatives tried to storm the facility.
The military has been deployed to try and restore security.
The judge sentenced 21 people to death in connection with the Feb. 1, 2012, soccer melee that killed 74 fans of the Cairo-based Al-Ahly team.
The security officials spoke on condition of anonymity in line with regulations.
'If the Royal Institution is sold, that's the end'
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Fastest-turning legged robot uses tail to take corners
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The real lesson from the bird flu storm
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Genes from nowhere: Orphans with a surprising story
Many of our genes have no obvious relatives or evolutionary history. So where did they come from?
Dwarf planet Eris may reveal quantum gravity
The Pluto-killer is at it again: studies of the small world and its moon may also knock down popular theories of dark matter and dark energy
Environmental crises may threaten pensions
Growing environmental problems, from climate change to water shortages, could wipe out many pension funds within decades
A glittering introduction to the night sky
Mark Thompson's A Down to Earth Guide to the Cosmos does what its title says - it shows how to locate stars in the night sky and explains how they work
Prophylactic progress: The story of the condom's rise
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To spot a fit partridge, check its fractal necklace
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OpenXC will set the hacker community loose on Ford's car computer systems - expect a host of apps to improve vehicles' performance and efficiency
Wallace: Wonders of nature have been solace of my life
As the letters of Alfred Russel Wallace, a co-discoverer of natural selection, are published online, he reveals what he really thought about Darwin
Snaps from space: Bleak landscapes become abstract art
New photos just tweeted from the International Space Station reveal the abstract beauty waiting in nature
Purchasing real estate can be a lucrative and enjoyable venture as you watch the growth and success of your investment over time. This can also be an incredibly time-consuming process with money to collect, tenants to find, and materials to update and maintain. If you have purchased real estate but also have other responsibilities and projects, you may not have the time to manage your investment properly. Work with a responsible property manager to help alleviate this burden. Property management companies can help in the process of locating tenants, collecting rent, and communicating with the tenants of the property. We always work hard to provide the finest property management services you will find anywhere. We understand that different forms of real estate require different approaches and we can think outside of the box. Call us today for a great solution to your property management concerns. Residential Property Management Salt Lake City
No matter how bad your morning is going, this adorable $12 Sunnyside egg mold is sure to brighten your day—unless you're some kind of monster. Its clever design traps and holds an egg's yolk so it cooks in the shape of the sun, while the egg whites are free to flow and solidify into the shape of a fluffy cloud. More »
Last time Apple bragged about the number of iOS devices it's sold, the number was 400 million. On the company earnings call today, however, Tim Cook revealed that the number of iPhones, iPads and iPods sold has surpassed the half a billion mark. To be clear, that's over 500,000,000 devices, and it means that Apple's moved a hundred million devices total since June 2012. Of those, 75 million were moved in this quarter alone. Not bad, eh?
UT Dallas researchers awarded $4.3 million to create next-generation technologiesPublic release date: 22-Jan-2013 [ | E-mail | Share ]
Contact: Lakisha Ladson LaKisha.Ladson@UTDallas.edu 972-883-4183 University of Texas at Dallas
Teams studying alternatives to silicon in integrated circuits and robust new computer networks
Two teams of researchers from The University of Texas at Dallas have been chosen to help a $194 million national network create the technologies of the next generation.
One UT Dallas team will evaluate materials to replace silicon in integrated circuits, with the goal of creating faster electronics that use dramatically less power. The other team will help design a computer architecture that allows the many types of computers used in everyday life to seamlessly communicate with one another, making it possible to build systems to avoid traffic accidents or to lock down an area in the case of an emergency.
The Semiconductor Technology Advanced Research Network, known as STARnet, is administered by the Semiconductor Research Corporation and the Defense Advanced Research Projects Agency . STARnet is made up of six centers with professors and graduate students from nearly 40 universities, including researchers in UT Dallas' Erik Jonsson School of Engineering and Computer Science.
"The top programs in the nation want to partner with us in two different areas of technology to help our country continue to lead in microelectronics," said Dr. Mark W. Spong, dean of the Jonsson School. "Our researchers are on par with top-tier research universities, and our participation shows that other academicians recognize this and seek us out."
Dr. Kyeongjae "K.J." Cho, Dr. Moon Kim, and Dr. Robert "Bob" Wallace, all professors of materials science and engineering at UT Dallas, are participating in STARnet's Center for Low Energy Systems Technology (LEAST) to solve the problem of finding a replacement for silicon in integrated circuits. Dr. Roozbeh Jafari, assistant professor of electrical engineering and Dr. Carl Sechen, professor of electrical engineering at UT Dallas, are involved in STARnet's TerraSwarm Research Center to create the architecture for seamlessly integrated computer systems.
LEAST: Reinventing Electronics
As the physical limits of integrated circuits currently made of silicon transistors are reached, LEAST researchers are looking to replace conventional 3-D silicon with nanoscale substances that increase the speed of computing done in electronics while also using less energy. Integrated circuits are used in nearly all modern electronics, such as computers, cellphones and tablets.
The UT Dallas LEAST team, which will receive about $3.4 million over five years, will explore a 2-D class of materials known as dichalcogenides, which are atomically thin but allow electrical current to be controlled as it moves through the material.
"The key for future transistor applications will be combining these 2-D materials with other types of materials such as insulators and metals used in integrated circuits to find the most powerful and efficient combination," Wallace said.
The UT Dallas team is conducting research on the interfaces of these materials.
"The ability to control the surfaces and interfaces in these types of material systems is the most important aspect of future device operations."
Besides conducting research in LEAST, Wallace, holder of the Erik Jonsson Distinguished Chair, is also a center coordinator. His previous discovery that hafnium silicates and oxides could be used in transistors to enable smaller nanoscale devices revolutionized the computer industry. Hafnium-based transistors are now used in processor chips in desktop and laptop computers, iPads and cellphones.
Cho is an expert in multiscale computer modeling related to new materials, and Kim is an expert in nanoscale electron microscopy advanced techniques that allow atom-to-atom modeling and chemical mapping of materials. The team will use this expertise in the surface and interface studies.
The world-class facilities housed in the $85 million Natural Science and Engineering Research Laboratory (NSERL) are an important factor in what enabled the UT Dallas team to be part of LEAST, Wallace said.
"UT Dallas has the state-of-the art equipment needed to contribute to LEAST and determine which materials will be used for the next generation of electronics," he said.
TerraSwarm: Linking Cyber-Worlds to the Physical World
The other UT Dallas team is developing revolutionary technology as part of STARnet's TerraSwarm Research Center.
Sensors and computers can be found in nearly all aspects of modern life, from pacemakers to air conditioners to sensors in vehicles that can tell when a driver is distracted.
TerraSwarm researchers are working toward shared data collected from the millions of individual smart sensors and other types of computers used in energy, health, environmental and personal applications.
The potential of sensor-based systems in monitoring applications goes far beyond what has been accomplished so far, Jafari said. When realized in full, these technologies can seamlessly integrate the cyber world, centered today in the cloud, with the physical/biological world, effectively blurring the gap between the two. The emerging global cyber-physical network is called the TerraSwarm, meaning that it encompasses many billions of sensors and actuators deployed across the earth.
"The possibilities of this type of shared sensing platform will revolutionize society," said Jafari, lead investigator for the UT Dallas TerraSwarm team, which will receive more than $900,000 over five years. "A fully integrated cyber-physical world presents limitless opportunities."
The key to enabling this type of technology is creating self-powered sensors and computers, and creating a networked architecture for thousands of smart sensing devices - similar to the World Wide Web - that is accessible from multiple types of electronic devices available to users.
Jafari, director of the Embedded Systems and Signal Processing Lab and a member of the Texas Analog Center of Excellence (TxACE), has experience creating wearable computers and wireless systems that monitor different aspects of human, health, behavior and thought.
"One strength we have is that we not only build the theories, but also implement them," he said.
Sechen, the other member of the UT
Dallas TerraSwarm team, is an expert in building ultra-low power digital circuits.
Jafari said TerraSwarm research includes funding to create this new architecture while also protecting individual privacy.
###
The LEAST Center is led by the University of Notre Dame, and the TerraSwarm Research Center is led by the University of California, Berkeley.
Industry partners of STARnet include Applied Materials, GLOBALFOUNDRIES Inc., IBM, Intel Corp., Micron Technology Inc., Raytheon Co., Texas Instruments Inc. and United Technologies Corp.
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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.
UT Dallas researchers awarded $4.3 million to create next-generation technologiesPublic release date: 22-Jan-2013 [ | E-mail | Share ]
Contact: Lakisha Ladson LaKisha.Ladson@UTDallas.edu 972-883-4183 University of Texas at Dallas
Teams studying alternatives to silicon in integrated circuits and robust new computer networks
Two teams of researchers from The University of Texas at Dallas have been chosen to help a $194 million national network create the technologies of the next generation.
One UT Dallas team will evaluate materials to replace silicon in integrated circuits, with the goal of creating faster electronics that use dramatically less power. The other team will help design a computer architecture that allows the many types of computers used in everyday life to seamlessly communicate with one another, making it possible to build systems to avoid traffic accidents or to lock down an area in the case of an emergency.
The Semiconductor Technology Advanced Research Network, known as STARnet, is administered by the Semiconductor Research Corporation and the Defense Advanced Research Projects Agency . STARnet is made up of six centers with professors and graduate students from nearly 40 universities, including researchers in UT Dallas' Erik Jonsson School of Engineering and Computer Science.
"The top programs in the nation want to partner with us in two different areas of technology to help our country continue to lead in microelectronics," said Dr. Mark W. Spong, dean of the Jonsson School. "Our researchers are on par with top-tier research universities, and our participation shows that other academicians recognize this and seek us out."
Dr. Kyeongjae "K.J." Cho, Dr. Moon Kim, and Dr. Robert "Bob" Wallace, all professors of materials science and engineering at UT Dallas, are participating in STARnet's Center for Low Energy Systems Technology (LEAST) to solve the problem of finding a replacement for silicon in integrated circuits. Dr. Roozbeh Jafari, assistant professor of electrical engineering and Dr. Carl Sechen, professor of electrical engineering at UT Dallas, are involved in STARnet's TerraSwarm Research Center to create the architecture for seamlessly integrated computer systems.
LEAST: Reinventing Electronics
As the physical limits of integrated circuits currently made of silicon transistors are reached, LEAST researchers are looking to replace conventional 3-D silicon with nanoscale substances that increase the speed of computing done in electronics while also using less energy. Integrated circuits are used in nearly all modern electronics, such as computers, cellphones and tablets.
The UT Dallas LEAST team, which will receive about $3.4 million over five years, will explore a 2-D class of materials known as dichalcogenides, which are atomically thin but allow electrical current to be controlled as it moves through the material.
"The key for future transistor applications will be combining these 2-D materials with other types of materials such as insulators and metals used in integrated circuits to find the most powerful and efficient combination," Wallace said.
The UT Dallas team is conducting research on the interfaces of these materials.
"The ability to control the surfaces and interfaces in these types of material systems is the most important aspect of future device operations."
Besides conducting research in LEAST, Wallace, holder of the Erik Jonsson Distinguished Chair, is also a center coordinator. His previous discovery that hafnium silicates and oxides could be used in transistors to enable smaller nanoscale devices revolutionized the computer industry. Hafnium-based transistors are now used in processor chips in desktop and laptop computers, iPads and cellphones.
Cho is an expert in multiscale computer modeling related to new materials, and Kim is an expert in nanoscale electron microscopy advanced techniques that allow atom-to-atom modeling and chemical mapping of materials. The team will use this expertise in the surface and interface studies.
The world-class facilities housed in the $85 million Natural Science and Engineering Research Laboratory (NSERL) are an important factor in what enabled the UT Dallas team to be part of LEAST, Wallace said.
"UT Dallas has the state-of-the art equipment needed to contribute to LEAST and determine which materials will be used for the next generation of electronics," he said.
TerraSwarm: Linking Cyber-Worlds to the Physical World
The other UT Dallas team is developing revolutionary technology as part of STARnet's TerraSwarm Research Center.
Sensors and computers can be found in nearly all aspects of modern life, from pacemakers to air conditioners to sensors in vehicles that can tell when a driver is distracted.
TerraSwarm researchers are working toward shared data collected from the millions of individual smart sensors and other types of computers used in energy, health, environmental and personal applications.
The potential of sensor-based systems in monitoring applications goes far beyond what has been accomplished so far, Jafari said. When realized in full, these technologies can seamlessly integrate the cyber world, centered today in the cloud, with the physical/biological world, effectively blurring the gap between the two. The emerging global cyber-physical network is called the TerraSwarm, meaning that it encompasses many billions of sensors and actuators deployed across the earth.
"The possibilities of this type of shared sensing platform will revolutionize society," said Jafari, lead investigator for the UT Dallas TerraSwarm team, which will receive more than $900,000 over five years. "A fully integrated cyber-physical world presents limitless opportunities."
The key to enabling this type of technology is creating self-powered sensors and computers, and creating a networked architecture for thousands of smart sensing devices - similar to the World Wide Web - that is accessible from multiple types of electronic devices available to users.
Jafari, director of the Embedded Systems and Signal Processing Lab and a member of the Texas Analog Center of Excellence (TxACE), has experience creating wearable computers and wireless systems that monitor different aspects of human, health, behavior and thought.
"One strength we have is that we not only build the theories, but also implement them," he said.
Sechen, the other member of the UT
Dallas TerraSwarm team, is an expert in building ultra-low power digital circuits.
Jafari said TerraSwarm research includes funding to create this new architecture while also protecting individual privacy.
###
The LEAST Center is led by the University of Notre Dame, and the TerraSwarm Research Center is led by the University of California, Berkeley.
Industry partners of STARnet include Applied Materials, GLOBALFOUNDRIES Inc., IBM, Intel Corp., Micron Technology Inc., Raytheon Co., Texas Instruments Inc. and United Technologies Corp.
[ | E-mail | Share ]
?
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.
Families of fishermen lost at sea during typhoon Pablo (Bopha) prepare to release white balloons in honor of the victims, aboard a ship in waters off General Santos City, January 19, 2013. Photo by Francis Canlas.
GENERAL SANTOS CITY, Philippines - On Saturday, January 19, General Santos City Mayor Darlene Antonino Custodio led city officials and families of fishermen in honoring those who perished and went missing during the height of super typhoon Pablo (Bopha).
It was an emotional voyage for all who joined the ceremony.
The city mayor was so distraught she reportedly shed tears.
For the families still hoping their loved ones are still alive, it was a voyage to eventuality.
All 352 fishermen still listed as missing may have already died in the open seas that ironically sustained them in life.
They were among the 378 fishermen from this city who were caught in the middle of the perfect storm. Only 18 survivors ived to tell their harrowing ordeal.
When Pablo headed to the eastern coast of Mindanao in early December 2012, the owners of the fishing vessels hoped their fishing crews were able to find refuge and seek shelter from the destructive wrath of the typhoon.
In the end, all they could locate was their vessels? last known GPS locations based on last radio contact.
One fishing company owner recalled how their base operator had heard hoarse and fainting voices from fishermen frantically crying for help. These were followed by complete radio silence.
In the aftermath, veteran journalist and former New York Times reporter Mort Rosenblum asked why these vessels could not be tracked when they were supposed to be equipped with vessel monitoring system (VMS) as required by the convention on conservation measures (CCM) of the Western and Central Pacific Fisheries Commission (WCPFC), of which the Philippines is a member.
Rosenblum was at the 9th WCPFC meeting in Manila on December 2 to 6 when Pablo made landfall in Davao Oriental on Dec 3, 2012.
Rosenblum went straight to General Santos City after the meeting, only to learn that the vessels did not have VMS equipment.
Dino Barrientos, executive director of the Umbrella Fish Landing Association (UFLA), admitted all 51 fishing vessels that went missing were not equipped with VMS, although he said they have a complement of communications equipment such as VHF-UHF, single side band and citizen?s band radios, and GPS kits.
These communication equipment are however vulnerable to weather changes and could conk out when washed out in sea water. A break and malfunctioning of the antenna could cut them off from their home bases.
Costly lessons
VMS costs anywhere between P100,000 to P180,000 "for the two-way system." This exludes air time fee, Barrientos said.
For example, a ROM Communications ROMTraX VMS-9601 unit is priced starting at US$1,374 (approximately Php 55,811.88) excluding backup battery module.
To register, a fishing company has to pay US$50 (Php 2,031.00) per month for each unit for the base plan only. For hourly positioning, a vessel owner will have to shell out US$85 (Php 3,452.70) per month. If one wants a 15-minute reporting, the vessel owner will have to cough up US$160 (Php 6,500) per month.
The UK-based Seafish said installing a VMS could reach ?8,744 for 3-year coverage, installation and frequency rate every 5 minutes. That is roughly P550,000 for the duration or P183,000 per vessel per year.
But Dexter Teng, operations officer of TSP Marine Industries, said fees will depend on the satellite provider/server.
"Fees should not be expensive but the number of poles (where the VMS onboard sends positional and other data to server)?those are expensive. It will depend on how many poles per day," Teng said.
According to ROM Communications, "A VMS unit is about the size of a small radio with an antenna. Data is sent to a satellite orbiting the earth, relayed to a station on the ground and then sent to the designated vessel-monitoring centre in near real time or at a pre-determined time intervals.
"VMS units are available with a backup battery that allows it to continue to operate in the event of a vessel power failure."
The VMS is often referred to as the blue box of fishing vessels. However, it does not have the standard transponder of the black boxes of airplanes that will send the signal of its location in case of a plane crash.
But its back-up battery could help rescuers in the event of mishaps and distress calls in the open seas.
Resolving issues
Barrientos however said not all Philippine fishing fleet could afford to install a VMS on their vessels.
One Philippine tuna fishing fleet consists of a catcher vessel, 4 to 5 light boats and at least a fish carrier.
But Teng said the WCPFC should also address compatibility of VMS and how it works with different systems.
"These are issues that WCPFC will have to resolve," he said.
VMS was primarily designed to monitor the location of fishing vessels in relation to the origin of their catches.
Teng conceded the VMS could have helped them track, in real time, the location of their fishing vessels in relation to the path of Pablo.
"Combined with robust weather and distress monitoring system, we could have saved the lives of our fishermen," Teng said.
Dead of the night
Marfenio Tan, former president of the Soccsksargen Federation of Fishing and Allied Industries (SFFAI), said most base radio communications of fishing companies are turned off during the night, which explains why many distress calls may have gone unheard.
But it may also have not mattered at all.
Pablo was one of the strongest typhoons to hit the country in recent years.
With sustained winds of up to 260 km/h, Pablo wrought havoc unseen in Mindanao for decades.
"It was the first time our fishermen encountered a perfect storm," Tan said.
It left in its path more than 1,000 dead and over 800 missing. At least P17 billion (US$415 million) in properties, infrastructure and crops were damaged when it was all over. Some towns in Compostela Valley and Davao Oriental are yet to recover from the tragedy, with rehabilitation seen to take more than two years.
The tuna industry in General Santos City said it lost more than P640 million worth of vessels alone.
Tan said it is essential for companies to regularly monitor the weather as well as location of their fishing vessels.
Tan, a reserve commodore in the Philippine Navy, said the change of direction of Pablo may have also contributed to the unprecedented high number of fishermen casualties.
Pablo was predicted to hit landfall in Surigao del Sur but it veered several degrees southward at the very last minute, hitting with full might Baganga, Davao Oriental, on December 3.
Beyond equipment
Montgomery Montealegre said he escaped Pablo when he left their catcher vessel on November 30, a day ahead of schedule. He said the catcher boat was at coordinates 09-129, some 302 kilometers off Baganga, when he left for shore.
They were already moored in Mati, Davao Oriental on December 2 when Pablo hit landfall. His son Mark Gil was supposed to follow him on board a catcher vessel the following day. Mark Gil never made it to Mati. He is among the 109 still missing fishermen from LPS Fishing which suffered the most number of fishermen lost in thigh seas and the most number of fishing vessels (15), including 3 catcher boats.
The tuna federation here however said VMS and other communications equipment alone will not guarantee saving the lives of fishermen in distress situation.
The tuna industry and the city government do not have statistics on the number of fishermen who were lost in the seas. That could top over a thousand over the years. They now have a number to start with.
But Teng said the Pablo tragedy should also spur the government into investing in live-saving search and rescue assets. "A dedicated search and rescue (S&R) assets or two that are on call during bad weather conditions and in cases of distress calls," Teng explained. - Rappler.com
Jan. 21, 2013 ? A team of researchers based at Johns Hopkins has decoded a system that makes certain types of immune cells impervious to HIV infection. The system's two vital components are high levels of a molecule that becomes embedded in viral DNA like a code written in invisible ink, and an enzyme that, when it reads the code, switches from repairing the DNA to chopping it up into unusable pieces. The researchers, who report the find in the Jan. 21 early edition of the Proceedings of the National Academy of Sciences, say the discovery points toward a new approach to eradicating HIV from the body.
"For decades, we've seen conflicting reports on whether each of these components helped protect cells from viruses," says James Stivers, Ph.D., a professor of pharmacology and molecular sciences at the Johns Hopkins University School of Medicine's Institute for Basic Biomedical Sciences. "By plotting how much of each are found in different types of cells, as well as the cells' response to HIV, we learned that both are needed to get the protective effect."
Researchers have long known that DNA's code is made up of four building blocks called nucleotides, commonly abbreviated A, T, G, and C. Before a cell divides, DNA-copying enzymes string these nucleotides together based on existing templates, so that each of the new cells gets its own copy of the genome. But because the T nucleotide, dTTP, is very similar to dUTP, a fifth nucleotide that doesn't belong in DNA, the copying enzyme sometimes mistakenly puts in a U where there should be a T.
To prevent this, says Stivers, most human cell types have an enzyme whose job is to break down dUTP, keeping its levels very low. Another quality control measure is the enzyme hUNG2, which snips stray Us out of newly copied DNA strands, leaving the resulting holes to be filled by a different repair enzyme. Certain immune cells called resting cells lack the first quality-control mechanism because, Stivers explains, "They're not replicating their DNA and dividing, so they couldn't care less if they have a lot of dUTP."
This is a critical piece of information, Stivers says, because when a retrovirus like HIV invades a cell, its first order of business is to make a DNA copy of its own genome, then insert that copy into the host cell's genome. If there are many dUTPs floating around in the cell, they will likely make their way into the new viral DNA, and, potentially, later be snipped out by hUNG2. The question, Stivers says, left open by the conflicting results of previous studies, was what effect, if any, this process has on HIV and other viruses.
To address this question, Amy Weil, a graduate student in Stivers' laboratory, measured dUTP levels and hUNG2 activity in a variety of human cells grown in the laboratory, then exposed them to HIV. Cells with high dUTP but little hUNG2 activity succumbed easily to the virus, which appeared to function just fine with a U-ridden genome. Similarly, cells with low dUTP levels but high hUNG2 activity were susceptible to HIV. For these cells, it seemed, hUNG2 would snip out the few stray Us, but the resulting holes would be repaired, leaving the viral DNA as good as new.
But in cells with both high dUTP and vigilant hUNG2, the repair process turned into a hack job, Stivers says, leaving the viral DNA so riddled with holes that it was beyond repair. "It's like dropping a nuclear bomb on the viral genome," he says.
By showing how dUTP and hUNG2 work together to protect resting cells from infection, Stivers says, the study identifies a new pathway that could restrict HIV infection in non-dividing cells. Current anti-retroviral drugs effectively suppress the virus, but, Stivers explains, they miss copies of the virus that hide out in non-dividing cells, and "the minute you stop taking anti-retrovirals, it starts replicating again." He suggests that drug strategies could be devised to target this pathway in affected cells, possibly lessening the pool of viruses hiding out in non-dividing cells. The principle could also be applied to other retroviruses, he says, since they, like HIV, all make DNA copies of their genomes as part of the infection process.
Other authors on the paper were Devlina Ghosh, Yan Zhou, Lauren Seiple and Robert F. Siliciano of the Johns Hopkins University School of Medicine; Moira A. McMahon of the University of California, San Diego; and Adam M. Spivak of the University of Utah School of Medicine.
The study was funded by the National Institute of General Medical Sciences (grant number GM056834) and the National Institute of Allergy and Infectious Diseases Extramural Activities (grant number AI081600).
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Genetic basis of high-risk childhood cancer points to possible new drug treatment strategyPublic release date: 20-Jan-2013 [ | E-mail | Share ]
Contact: Carrie Strehlau media@stjude.org 901-595-2295 St. Jude Children's Research Hospital
St. Jude Children's Research Hospital scientists lead a study that finds new genetic defects in high-risk childhood leukemia subtypes with chromosomal loss and evidence that some patients have an inherited cancer syndrome
(MEMPHIS, Tenn. January 20, 2013) Research led by St. Jude Children's Research Hospital scientists has identified a possible lead in treatment of two childhood leukemia subtypes known for their dramatic loss of chromosomes and poor treatment outcomes.
The findings also provide the first evidence of the genetic basis for this high-risk leukemia, which is known as hypodiploid acute lymphoblastic leukemia (ALL). Normal human cells have 46 chromosomes, half from each parent, but hypodiploid ALL is characterized by fewer than 44 chromosomes. Chromosomes are highly condensed pieces of DNA, the molecule that carries the inherited instructions for assembling and sustaining a person. The research appears in the January 20 advance online edition of the scientific journal Nature Genetics.
The study, the largest ever focused on hypodiploid ALL, confirmed that this tumor has distinct subtypes distinguished by the number of chromosomes lost and the submicroscopic genetic alterations they harbor. Researchers found evidence suggesting more than one-third of patients with a subtype known as low hypodiploid ALL have Li-Fraumeni syndrome. Families with Li-Fraumeni syndrome harbor inherited mutations in the TP53 tumor suppressor gene and have a high risk of a range of cancers. Hypodiploid ALL had not previously been recognized as a common manifestation of Li-Fraumeni syndrome.
Researchers reported that the major hypodiploid subtypes are both sensitive to a family of compounds that block the proliferation of cancer cells. The compounds include drugs already used to treat other cancers. The subtypes are low hypodiploid ALL, characterized by 32 to 39 chromosomes, and near haploid ALL, which has 24 to 31 chromosomes.
"This study is a good example of the important insights that can be gained by studying the largest possible number of patients in as much detail as possible. This approach led us to key insights about these leukemia subtypes that we would otherwise have missed," said the study's senior and corresponding author, Charles Mullighan, MBBS(Hons), MSc, M.D., an associate member of the St. Jude Pathology Department. Mullighan is a Pew Scholar in Biomedical Sciences.
The near haploid and low hypodiploid ALL subtypes represent 1 to 2 percent of the estimated 3,000 pediatric ALL cases diagnosed annually in the U.S. But they account for a much larger number of ALL treatment failures. Today more than 90 percent of young ALL patients will become long-term survivors, compared to 40 percent for patients with these two high-risk subtypes. St. Jude researchers led the study in collaboration with investigators from the Children's Oncology Group, the world's largest organization devoted exclusively to childhood and adolescent cancer research.
"The cure rate for hypodiploid ALL is only about half that obtained overall for children with ALL. The findings of this study are very important and have the potential to impact how this high-risk subset of childhood ALL is treated," said Stephen Hunger, M.D., chair of the Children's Oncology Group ALL committee and one of the paper's co-authors. "This study grew out of the efforts of Hank Schueler, a teenager who died from hypodiploid ALL. He wanted to find ways to help treat other children with this type of leukemia. After he passed away, his parents established a foundation to support research in hypodiploid ALL. We thought that one way to do this was to conduct the genomic analyses reported in this paper. These findings would not have been possible without Hank's idea and without support from the Schueler family."
Researchers used a variety of laboratory techniques to look for genetic abnormalities in cancer cells from 124 pediatric patients missing at least one chromosome. The patients included 68 with near haploid ALL and 34 with low hypodiploid ALL. Investigators also checked white blood cells collected when 89 of the 124 patients were in remission. The study included whole-genome sequencing of the entire cancer and normal genomes of 20 patients with near haploid or low hypodiploid subtypes. For another 20 patients, investigators deciphered just DNA involved in protein production. Researchers also screened cancer cells from 117 adult ALL patients, including 11 with the low hypodiploid subtype.
The whole genome sequencing was done in conjunction with the St. Jude Children's Research Hospital Washington University Pediatric Cancer Genome Project. The project has sequenced the complete normal and cancer genomes of more than 600 children and adolescents with some of the most aggressive and least understood cancers.
Near haploid ALL was characterized by alterations in six genes and increased activity in key pathways that help regulate cell division and development. Disruption of these pathways, known as Ras and PI3K, has been linked to other cancers. The changes were found in 71 percent of near haploid ALL patients and included deletion of the NF1 gene. The gene had not previously been linked to high-risk leukemia. Other alterations involved the genes NRAS, KRAS, MAPK1, FLT3 and PTPN11.
Low hypodiploid ALL in both adults and children was linked to mutations in the TP53 tumor suppressor gene. The gene was altered in 91 percent of pediatric patients with the ALL subtype and in 10 of the 11 adults with low hypodiploid ALL included in the study. Other common alterations involved RB1, another tumor suppressor gene.
About 38 percent of children with low hypodiploid ALL also carried TP53 abnormalities in non-cancerous blood cells. The mutations included many previously linked to Li-Fraumeni syndrome, which is characterized by changes in TP53.
Further evidence linking low hypodiploid ALL to Li-Fraumeni syndrome came when researchers found the same TP53 mutation in two generations of the same family. The father was 31 years old when he was found to have a brain tumor associated with Li-Fraumeni syndrome. His son later developed low hypodiploid ALL.
"Identification of children with low-hypodiploid ALL and inherited TP53 mutations could help expand the use of life-saving cancer screening," said Linda Holmfeldt, Ph.D., a St. Jude postdoctoral fellow. She and Lei Wei, Ph.D., of the St. Jude Department of Computational Biology and formerly of Pathology, are the study's co-first authors. "Screening helps save lives by finding cancers much earlier when the odds of a cure are greatest," Holmfeldt said.
Investigators also reported deletions involving Ikaros gene family members that are rare in other ALL patients. The genes play a role in normal immune system development. The IKZF3 gene, also known as AIOLOS, was deleted in 13 percent of near haploid ALL patients. IKZF3 was deleted in nearly 53 percent of patients with low hypodiploid ALL.
Despite such differences, when researchers tested a variety of compounds against cells from both subtypes growing in the laboratory, they found compounds that targeted the PI3K pathway inhibited proliferation. Researchers are testing the effectiveness of these drugs in mouse models.
###
The authors are Ernesto Diaz-Flores and Mignon Loh, both of University of California School of Medicine, San Francisco; Michael Walsh, Jinghui Zhang, Debbie Payne-Turner, Michelle Churchman, Shann-Ching Chen, Kelly McCastlain, Jared Becksfort, Jing Ma, Gang Wu, Letha Phillips, Guangchun Song, John Easton, Matthew Parker, Xiang Chen, Michael Rusch, Kristy Boggs, Bhavin Vadodaria, Erin Hedlund, Christina Drenberg, Sharyn Baker, Deqing Pei, Cheng Cheng, Geoffrey Neale, David Ellison, Sheila Shurtleff, Ching-Hon Pui, Raul Ribeiro, Susana Raimondi and James Downing, all of St. Jude; Anna Andersson of St. Jude and Lund University Hospital, Sweden; Samir Patel and Susan Heatley, both formerly of St. Jude; Li Ding, Charles Lu, Robert Fulton, Lucinda Fulton, Yashodhan Tabib, David Dooling, Kerri Ochoa, Elaine Mardis and Richard Wilson, all of Washington University; Mark Minden, Princess Margaret Hospital/University Health Network, Toronto; Ian Lewis and L. Bik To, both of the Institute of Medical and Veterinary Science, Adelaide, Australia; Paula Marlton, Princess Alexandra Hospital, Queensland, Australia; Andrew Roberts, Royal Melbourne Hospital, Australia; Gordana Raca and Wendy Stock, both of University of Chicago School of Medicine; Hans Drexler, German Collection of Microorganisms and Cell Cultures, Braunschweig, Germany; Ross Dickins, Walter & Eliza Hall Institute of Medical Research, Parkville, Australia; Meenakshi Devidas, University of Florida, Gainesville; Andrew Carroll, University of Alabama at Birmingham; Nyla Heerema and Julie Gastier-Foster, the Ohio State University; Brent Wood, Seattle Children's Hospital; and Michael Borowitz, Johns Hopkins Hospital, Baltimore.
The research was funded in part by the Pediatric Cancer Genome Project, including Kay Jewelers, a lead partner; The Henry Schueler 41&9 Foundation in conjunction with Partnership4Cures; the St. Baldrick's Foundation, grants (CA156329, CA21765, GM92666, CA98543, CA98413, CA114766 and CA023944) from the National Cancer Institute and National Institutes of Health; the AACR Gertrude B. Elion Cancer Research Award, Swedish Research Council and ALSAC.
St. Jude Children's Research Hospital
St. Jude Children's Research Hospital is internationally recognized for its pioneering research and treatment of children with cancer and other life-threatening diseases. The hospital's research has helped push overall survival rates for childhood cancer from less than 20 percent when the institution opened to almost 80 percent today. It is the first and only National Cancer Institute-designated Comprehensive Cancer Center devoted solely to children, and no family ever pays St. Jude for anything. For more information, visit www.stjude.org. Follow us on Twitter @StJudeResearch.
The Children's Oncology Group
The Children's Oncology Group is the world's largest organization devoted exclusively to childhood and adolescent cancer research. The Children's Oncology Group (COG) unites more than 8,000 experts in childhood cancer at more than 200 leading children's hospitals, universities, and cancer centers across North America, Australia, New Zealand, and parts of Europe in the fight against childhood cancer. Today, more than 90 percent of the 13,500 children and adolescents diagnosed with cancer each year in the United States are cared for at COG member institutions. Research performed by the Children's Oncology Group institutions over the past fifty years has transformed childhood cancer from a virtually incurable disease to one with a combined 5-year survival rate of 80 percent. COG's mission is to improve the cure rate and outcome for all children with cancer.
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.
Genetic basis of high-risk childhood cancer points to possible new drug treatment strategyPublic release date: 20-Jan-2013 [ | E-mail | Share ]
Contact: Carrie Strehlau media@stjude.org 901-595-2295 St. Jude Children's Research Hospital
St. Jude Children's Research Hospital scientists lead a study that finds new genetic defects in high-risk childhood leukemia subtypes with chromosomal loss and evidence that some patients have an inherited cancer syndrome
(MEMPHIS, Tenn. January 20, 2013) Research led by St. Jude Children's Research Hospital scientists has identified a possible lead in treatment of two childhood leukemia subtypes known for their dramatic loss of chromosomes and poor treatment outcomes.
The findings also provide the first evidence of the genetic basis for this high-risk leukemia, which is known as hypodiploid acute lymphoblastic leukemia (ALL). Normal human cells have 46 chromosomes, half from each parent, but hypodiploid ALL is characterized by fewer than 44 chromosomes. Chromosomes are highly condensed pieces of DNA, the molecule that carries the inherited instructions for assembling and sustaining a person. The research appears in the January 20 advance online edition of the scientific journal Nature Genetics.
The study, the largest ever focused on hypodiploid ALL, confirmed that this tumor has distinct subtypes distinguished by the number of chromosomes lost and the submicroscopic genetic alterations they harbor. Researchers found evidence suggesting more than one-third of patients with a subtype known as low hypodiploid ALL have Li-Fraumeni syndrome. Families with Li-Fraumeni syndrome harbor inherited mutations in the TP53 tumor suppressor gene and have a high risk of a range of cancers. Hypodiploid ALL had not previously been recognized as a common manifestation of Li-Fraumeni syndrome.
Researchers reported that the major hypodiploid subtypes are both sensitive to a family of compounds that block the proliferation of cancer cells. The compounds include drugs already used to treat other cancers. The subtypes are low hypodiploid ALL, characterized by 32 to 39 chromosomes, and near haploid ALL, which has 24 to 31 chromosomes.
"This study is a good example of the important insights that can be gained by studying the largest possible number of patients in as much detail as possible. This approach led us to key insights about these leukemia subtypes that we would otherwise have missed," said the study's senior and corresponding author, Charles Mullighan, MBBS(Hons), MSc, M.D., an associate member of the St. Jude Pathology Department. Mullighan is a Pew Scholar in Biomedical Sciences.
The near haploid and low hypodiploid ALL subtypes represent 1 to 2 percent of the estimated 3,000 pediatric ALL cases diagnosed annually in the U.S. But they account for a much larger number of ALL treatment failures. Today more than 90 percent of young ALL patients will become long-term survivors, compared to 40 percent for patients with these two high-risk subtypes. St. Jude researchers led the study in collaboration with investigators from the Children's Oncology Group, the world's largest organization devoted exclusively to childhood and adolescent cancer research.
"The cure rate for hypodiploid ALL is only about half that obtained overall for children with ALL. The findings of this study are very important and have the potential to impact how this high-risk subset of childhood ALL is treated," said Stephen Hunger, M.D., chair of the Children's Oncology Group ALL committee and one of the paper's co-authors. "This study grew out of the efforts of Hank Schueler, a teenager who died from hypodiploid ALL. He wanted to find ways to help treat other children with this type of leukemia. After he passed away, his parents established a foundation to support research in hypodiploid ALL. We thought that one way to do this was to conduct the genomic analyses reported in this paper. These findings would not have been possible without Hank's idea and without support from the Schueler family."
Researchers used a variety of laboratory techniques to look for genetic abnormalities in cancer cells from 124 pediatric patients missing at least one chromosome. The patients included 68 with near haploid ALL and 34 with low hypodiploid ALL. Investigators also checked white blood cells collected when 89 of the 124 patients were in remission. The study included whole-genome sequencing of the entire cancer and normal genomes of 20 patients with near haploid or low hypodiploid subtypes. For another 20 patients, investigators deciphered just DNA involved in protein production. Researchers also screened cancer cells from 117 adult ALL patients, including 11 with the low hypodiploid subtype.
The whole genome sequencing was done in conjunction with the St. Jude Children's Research Hospital Washington University Pediatric Cancer Genome Project. The project has sequenced the complete normal and cancer genomes of more than 600 children and adolescents with some of the most aggressive and least understood cancers.
Near haploid ALL was characterized by alterations in six genes and increased activity in key pathways that help regulate cell division and development. Disruption of these pathways, known as Ras and PI3K, has been linked to other cancers. The changes were found in 71 percent of near haploid ALL patients and included deletion of the NF1 gene. The gene had not previously been linked to high-risk leukemia. Other alterations involved the genes NRAS, KRAS, MAPK1, FLT3 and PTPN11.
Low hypodiploid ALL in both adults and children was linked to mutations in the TP53 tumor suppressor gene. The gene was altered in 91 percent of pediatric patients with the ALL subtype and in 10 of the 11 adults with low hypodiploid ALL included in the study. Other common alterations involved RB1, another tumor suppressor gene.
About 38 percent of children with low hypodiploid ALL also carried TP53 abnormalities in non-cancerous blood cells. The mutations included many previously linked to Li-Fraumeni syndrome, which is characterized by changes in TP53.
Further evidence linking low hypodiploid ALL to Li-Fraumeni syndrome came when researchers found the same TP53 mutation in two generations of the same family. The father was 31 years old when he was found to have a brain tumor associated with Li-Fraumeni syndrome. His son later developed low hypodiploid ALL.
"Identification of children with low-hypodiploid ALL and inherited TP53 mutations could help expand the use of life-saving cancer screening," said Linda Holmfeldt, Ph.D., a St. Jude postdoctoral fellow. She and Lei Wei, Ph.D., of the St. Jude Department of Computational Biology and formerly of Pathology, are the study's co-first authors. "Screening helps save lives by finding cancers much earlier when the odds of a cure are greatest," Holmfeldt said.
Investigators also reported deletions involving Ikaros gene family members that are rare in other ALL patients. The genes play a role in normal immune system development. The IKZF3 gene, also known as AIOLOS, was deleted in 13 percent of near haploid ALL patients. IKZF3 was deleted in nearly 53 percent of patients with low hypodiploid ALL.
Despite such differences, when researchers tested a variety of compounds against cells from both subtypes growing in the laboratory, they found compounds that targeted the PI3K pathway inhibited proliferation. Researchers are testing the effectiveness of these drugs in mouse models.
###
The authors are Ernesto Diaz-Flores and Mignon Loh, both of University of California School of Medicine, San Francisco; Michael Walsh, Jinghui Zhang, Debbie Payne-Turner, Michelle Churchman, Shann-Ching Chen, Kelly McCastlain, Jared Becksfort, Jing Ma, Gang Wu, Letha Phillips, Guangchun Song, John Easton, Matthew Parker, Xiang Chen, Michael Rusch, Kristy Boggs, Bhavin Vadodaria, Erin Hedlund, Christina Drenberg, Sharyn Baker, Deqing Pei, Cheng Cheng, Geoffrey Neale, David Ellison, Sheila Shurtleff, Ching-Hon Pui, Raul Ribeiro, Susana Raimondi and James Downing, all of St. Jude; Anna Andersson of St. Jude and Lund University Hospital, Sweden; Samir Patel and Susan Heatley, both formerly of St. Jude; Li Ding, Charles Lu, Robert Fulton, Lucinda Fulton, Yashodhan Tabib, David Dooling, Kerri Ochoa, Elaine Mardis and Richard Wilson, all of Washington University; Mark Minden, Princess Margaret Hospital/University Health Network, Toronto; Ian Lewis and L. Bik To, both of the Institute of Medical and Veterinary Science, Adelaide, Australia; Paula Marlton, Princess Alexandra Hospital, Queensland, Australia; Andrew Roberts, Royal Melbourne Hospital, Australia; Gordana Raca and Wendy Stock, both of University of Chicago School of Medicine; Hans Drexler, German Collection of Microorganisms and Cell Cultures, Braunschweig, Germany; Ross Dickins, Walter & Eliza Hall Institute of Medical Research, Parkville, Australia; Meenakshi Devidas, University of Florida, Gainesville; Andrew Carroll, University of Alabama at Birmingham; Nyla Heerema and Julie Gastier-Foster, the Ohio State University; Brent Wood, Seattle Children's Hospital; and Michael Borowitz, Johns Hopkins Hospital, Baltimore.
The research was funded in part by the Pediatric Cancer Genome Project, including Kay Jewelers, a lead partner; The Henry Schueler 41&9 Foundation in conjunction with Partnership4Cures; the St. Baldrick's Foundation, grants (CA156329, CA21765, GM92666, CA98543, CA98413, CA114766 and CA023944) from the National Cancer Institute and National Institutes of Health; the AACR Gertrude B. Elion Cancer Research Award, Swedish Research Council and ALSAC.
St. Jude Children's Research Hospital
St. Jude Children's Research Hospital is internationally recognized for its pioneering research and treatment of children with cancer and other life-threatening diseases. The hospital's research has helped push overall survival rates for childhood cancer from less than 20 percent when the institution opened to almost 80 percent today. It is the first and only National Cancer Institute-designated Comprehensive Cancer Center devoted solely to children, and no family ever pays St. Jude for anything. For more information, visit www.stjude.org. Follow us on Twitter @StJudeResearch.
The Children's Oncology Group
The Children's Oncology Group is the world's largest organization devoted exclusively to childhood and adolescent cancer research. The Children's Oncology Group (COG) unites more than 8,000 experts in childhood cancer at more than 200 leading children's hospitals, universities, and cancer centers across North America, Australia, New Zealand, and parts of Europe in the fight against childhood cancer. Today, more than 90 percent of the 13,500 children and adolescents diagnosed with cancer each year in the United States are cared for at COG member institutions. Research performed by the Children's Oncology Group institutions over the past fifty years has transformed childhood cancer from a virtually incurable disease to one with a combined 5-year survival rate of 80 percent. COG's mission is to improve the cure rate and outcome for all children with cancer.
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.
Jan. 20, 2013 ? Marked for death with molecular tags that act like a homing signal for a cell's protein-destroying machinery, a pivotal enzyme is rescued by another molecule that sweeps the telltale targets off in the nick of time.
The enzyme, called TRAF3, lives on to control a molecular network that's implicated in a variety of immune system-related diseases if left to its own devices.
The University of Texas MD Anderson scientists identified TRAF3's savior and demonstrated how it works in a paper published online January 20 in Nature.
By discovering the role of OTUD7B as TRAF3's protector, Shao-Cong Sun, Ph.D., professor in MD Anderson's Department of Immunology, and colleagues filled an important gap in their understanding of a molecular pathway discovered in Sun's lab.
"Genetic defects or constant degradation of TRAF3 lead to the uncontrolled activity of what we call the non-canonical NF-kB pathway. This in turn, is associated with autoimmune diseases and lymphoid malignancies such as multiple myeloma and B cell lymphomas," Sun said. "Understanding how the degradation of TRAF3 is regulated is extremely important."
Dodging annihilation, turning the tables
Sun earlier found an alternative, or non-canonical, pathway that activates the protein complex known as NF-kB, a family of proteins that turns on genes that are important in immune response, inflammation, cell growth and survival, and development.
They found that NF-kB activity increases when TRAF3 has the homing targets, called ubiquitins, attached to it and is destroyed by the proteasome, a complex of proteins that hunts down ubiquitin-decorated proteins.
When TRAF3 evades attack, it turns that same destructive mechanism against NIK, a protein that's central to NF-kB activity, by tagging it with ubiquitins.
The key question was: What regulates TRAF3's destruction and, in the process, controls NF-kB?
OTUD7B emerges
Sun and colleagues had a candidate, the enzyme OTUD7B, also known by its more lyrical name, Cezanne. It was genetically quite similar to another enzyme active in the canonical pathway for NF-kB called A20. Both were known deubiquitinases, enzymes that cleave ubiquitin polymers. A20 is not active in the non-canonical NFkB pathway.
By applying inducers of the non-canonical NK-kB pathway to cells derived from OTUD7B-deficient mice, the researchers found:
? Degradation of TRAF3 and accumulation of its target, NIK
? Ubiquitination of TRAF3
Cells with OTUD7B intact suppressed non-canonical NF-kB signaling.
Varied immune effects in mice
Knocking out the OTUD7B gene caused biological changes in mice, but it did not kill them, as occurs when A20 is knocked out.
Mice with OTUD7B suppressed had greatly increased lymphoid cell growth in the lining of the intestine and hyper-responsiveness to antigens by B cells. "If these two symptoms occur persistently, as they did in the knockout mice, they may contribute to autoimmunity or inflammation," Sun said.
However, knockout mice also had an improved immune response to the lethal intestinal bacterial pathogen C. rodentium. All of the mice with normal OTUD7B died of the bacterial infection, while 75 percent of the knockout mice survived.
Teasing out the reasons for these effects and developing OTUD7B as a target for inhibitors to boost immunity in the lining of the intestine will take more research, Sun said.
"It's important to know that TRAF3 has opposing roles in regulating activation of T cells and B cells, indicating that OTUD7B has a cell-type specific function. So, as with many other research findings, it might take considerably more effort to assess the therapeutic potential of OTUD7B," Sun said.
Co-authors with Sun are first author Hongbo Hu, George Brittain, Jae-Hoon Chang, Nahum Puebla-Osorio, Jin Jin, Anna Zal, Yichuan Xiao, Xuhong Cheng, Mikyoung Chang, Tomasz Zal, and Chengming Zhu; and Yang-Xin Fu, of the University of Chicago. Zal, Zhu and Sun also are affiliated with The University of Texas Graduate School of Biomedical Sciences at Houston.
This study was supported by grants from the National Institutes of Health (numbers AI057555, AI064639, GM84459, CA137059, and T32CA009598), including MD Anderson's NCI Cancer Center Support Grant and the Sister Institution Network Fund of MD Anderson Cancer Center.
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The above story is reprinted from materials provided by University of Texas M. D. Anderson Cancer Center, via Newswise.
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Journal Reference:
Hongbo Hu, George C. Brittain, Jae-Hoon Chang, Nahum Puebla-Osorio, Jin Jin, Anna Zal, Yichuan Xiao, Xuhong Cheng, Mikyoung Chang, Yang-Xin Fu, Tomasz Zal, Chengming Zhu, Shao-Cong Sun. OTUD7B controls non-canonical NF-?B activation through deubiquitination of TRAF3. Nature, 2013; DOI: 10.1038/nature11831
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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Rhythmic gymnasts train at the Caledonian Gymnasium on Andersons Bay Rd last week. Photo by Craig Baxter.
The future of Dunedin's Caledonian Gymnasium and Bowling Club and the city council's support for gymnastics in the city is to be considered by councillors.
Any decisions, however, are unlikely to take effect in the next financial year.
The issue of the Andersons Bay Rd gymnasium's future was raised by the Dunedin Gymnastic Academy (DGA) during last year's annual planning round.
The DGA says the ageing facility does not meet modern recreation expectations and limits growth in their sport.
It also questions whether the location of the gymnasium in an area of significant commercial growth is any longer appropriate.
A report to councillors considering the 2013-14 budget recommends councillors approve further staff investigations into several options.
They are: retaining the status quo, which requires about $80,000 investment over the 30 years of the building's remaining useful life and $250,000-$300,000 in the next two to three years to keep the facility going at its current level of service; sell the land of the gymnasium and/or the next door bowling club and realise about $2.5 to $3 million; redevelop, in two stages, the current gymnasium for about $4.3 million; or sell the land and build a new purpose-built facility in the Ice Stadium car park in Victoria Rd, also for about $4.3 million.
In the scenarios that require sale of the bowling club land, valued at about $1.5 million, the 32 members would have to find new clubs to play for.
The redevelopment option would involve initially improving the standard of the building at a cost of about $1.8 million.
A second stage in five to 10 years' time would double the floor space and include an underground car park.
The total cost could also be increased, as it is listed as an earthquake-prone building and requires a structural assessment before July next year.
The report informed councillors that before DGA could begin to fundraise for new facilities, a decision needed to be made about the future of the Caledonian sports hub and what support, if any, could be expected from the council.
DGA could raise $1.8 million over two to three years, but if it needed to raise the full cost of an upgrade or new facility, that would take up to 10 years.
Staff advised council support could be in principle, by supporting the development and renewal of existing building, through the provision of a green field space for a new facility, and/or making a capital contribution from the sale of the gymnasium or bowling club.
There is no funding in the draft annual plan for gymnastics facility improvement.
A commitment from council around the preferred direction was sought, the report said.
Further investigations would then take place and staff would report back to the Community Development Committee in September, with any implications to be considered as part of the 2014-15 annual plan process if appropriate.debbie.porteous@odt.co.nz
The Xerox DocuMate 3125 is a duplexing desktop scanner with a 50-sheet automatic document feeder (ADF). It provides one-touch scanning from 9 preset and customizable scan profiles, either from your computer or the scanner itself. Though its OCR performance was reasonably good, particularly in grayscale mode, its scanning speeds were somewhat slow, especially for searchable PDF.
With an 11.2 by 6.5 inch footprint (WD), the 3125 is reasonably compact and should easily fit on a desk; it weighs 5.1 pounds. It has a straight-through paper path, and can scan documents up to 8.5 inches wide and 38 inches long, and business cards as well as plastic cards up to 0.8 mm thick. It has an ultrasonic double-feed detection sensor to catch paper misfeeds.
To the right of the ADF is the single-character LCD that's used to display the number of the current Visioneer OneTouch scan profile (as well as error messages)?you can choose between preset and customizable, numbered scan profiles, that you can switch between with up and down arrows.
Scanning You can initiate scans directly from the scanner, by choosing a profile and hitting either the Simplex or Duplex button below the LED, or the OneTouch interface on your computer or. You can also scan from the bundled programs (PaperPort and OmniPage); the 3125 includes Twain, WIA, and ISIS drivers, so you can also scan from nearly any program that has a scan command.
Like most document scanners, the 3125 can scan at up to 600 dpi; it can scan in black and white, grayscale, or color. The default OneTouch scanning profiles and destinations include Scan (image PDF); PDF (searchable PDF); Print (BMP); E-mail (PDF); Fax (BMP); OCR (RTF); Archive (searchable PDF, 300 dpi); Business Card (BMP); and Paint (BMP). It can scan to PDF, searchable PDF, JPEG, TIFF, and BMP formats; it can also scan to RTF and other document formats if you install either the included PaperPort or OmniPage Pro.
Software Software includes Visioneer OneTouch, Nuance PaperPort for document management, Nuance OmniPage Pro 17 for OCR. ?Although it can scan business cards, it doesn't have a business card management program, so if you want to use the 3125 for business card scanning and management, you'll have to supply your own software.
Speed The DocuMate 3125 has a rated speed of 25 pages per minute (ppm) for simplex scanning and 44 images per minute (ipm) where each side of a page counts as one image. In speed testing using the OneTouch default settings (image PDF, black and white, 200 dpi), the 3125 was a bit short of that, tallying 21.4 ppm simplex and 30 ipm for duplex. The Editors' Choice Canon imageFormula DR-C125, rated at 25 ppm and 50 ipm for simplex and duplex scanning, matched its rated speeds: We clocked it at 25.4 ppm simplex and 50 ipm duplex. The Kodak i2400, rated at 30 ppm simplex and 60 ipm duplex, tested at 28.3 ppm in simplex and 53 ipm in duplex.
The 3125 has two default searchable PDF scan destinations in OneTouch: PDF (200 ppi black and white) and Archive (300 dpi black and white). (The Image PDF setting is simply called Scan.) Its speed for scanning in simplex at 300 ppi (3:28) was actually somewhat faster than at 200 ppi (3:52), though that was reversed in duplex scanning, with it averaging 8:08 in simplex and 8:22 in duplex. When I switched to grayscale mode for 200 ppi simplex scanning, it was a bit faster, taking 3:15. But regardless of the resolution and mode, it is sluggish for a scanner at its price and speed rating in scanning to searchable PDF.
When we tested it last year, the Editors' Choice Canon imageFormula DR-C125 was particularly impressive as it didn't slow down at all when scanning to sPDF (searchable PDF) format, which is generally the preferred format for document management applications. We clocked the Canon at a minute flat in scanning our 25-page test document in both simplex and duplex modes. The Kodak i2400 took 1:34 to scan our test document in simplex to searchable PDF.
OCR In scanning to OCR using the default OneTouch OCR setting (black and white, 300 ppi RTF format), quality was somewhat inconsistent. With our Arial test font, it was perfect at reading 5-point type, but had at least one error in several larger sizes up to 12 point. With Times New Roman it was perfect at 8 point, with 1 error in both 10 and 12 points.
I also tried scanning to OCR in grayscale mode (at 300 ppi), and there it did reasonably well. In Times New Roman, it was perfect down to 8 points, with a single mistake at 6 points. With the Arial font, although it read 8-point type perfectly, it had one mistake at 12 points, one at 10 points, and one at 6 points. It did a relatively good job with most of our nonstandard text fonts.
The Xerox DocuMate 3125 is a reasonable choice for a desktop business scanner at its price, if you don't need to scan to searchable PDF format. It offers duplex scanning and a 50-sheet ADF. You can choose any of 9 programmable scan profiles using arrow buttons for one-touch scanning. Its OCR performance is reasonably good, particularly in grayscale mode. The 3125 lacks a business card management program, so if you want to scan business cards with it, you should either already have such a program or be ready to buy one (and factor that into your cost). ?
Its scan speed at default settings was a bit below its rated speed, in both simplex and?especially?duplex. It slowed down greatly at scanning to searchable PDF, taking more than 4 times as long as the Editors' Choice Canon DR-C125 for simplex scanning, and more than 8 times as long for duplex. If you scan to searchable PDF, there are much faster choices than the Xerox DocuMate 3125, but otherwise it's a pretty typical scanner for its price, though it doesn't offer anything to make it stand out from the pack.
More Scanner Reviews: ??? Xerox DocuMate 3125 ??? Epson WorkForce WF-3540 ??? Brother ImageCenter ADS-2500W ??? VuPoint Solutions Magic Wand with AutoFeed Dock PDS-ST450-VP ??? VuPoint Solutions Digital Film and Slide Converter FC-C520-VPD ?? more
What if you were trapped in the story of Romeo and Juliet? Who would you be, and how far will you go to change your character's fate and escape the story before its to late.
Owner:
Game Masters:
This topic is an Out Of Character part of the roleplay, ?Written In The Stars?. Anything posted here will also show up there.
Topic Tags:
Forum for completely Out of Character (OOC) discussion, based around whatever is happening In Character (IC). Discuss plans, storylines, and events; Recruit for your roleplaying game, or find a GM for your playergroup.
This definitely looks interesting.
"She offered herself to the big, bad wolf and didn't scream when he took the first bite."
bandgeek
Member for 1 years
This looks interesting, I may not be able to participate though since I have never read the real story. A suggestion to get people involved easier and so people don't get confused, maybe use face claims. Just a suggestion, not trying to steal your roleplay :)
BraceBlaze
Member for 1 years
You Don't Have to Know the Story to roleplay, it would be good if you did, but your don't need to :)
That is a really good suggestion actual :)
Sapphire Tears
Member for 0 years
May I reserve Juliet?
Oh, and if you do put up FC's, you should also allow people to choose their own, just in case someone already has an idea in mind. :D (unlike me, who has no idea. XD)
bandgeek
Member for 1 years
Yes you can :)
Okay, I'll probably keep the descriptions put put up they can make it anyway they want the description is just there for an idea of who they are. Thank you for the idea ^^
Sapphire Tears
Member for 0 years
@bandgeek: Someone has requested to compete with you for the role of Juliet, so I agreed to it, and said if she has a better character then you she would be able to take the character.
Sapphire Tears
Member for 0 years
Post a reply
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