Betable, a gaming platform that enables developers to use real money instead of virtual currencies, just signed one of Canada’s largest independent developers Frima Studio. Frima, which has about 350 people and is based in Quebec, is opening up a real-money gaming division called 3OAK. Instead of going their own way with acquiring gambling licenses in different countries, Frima said they chose Betable to fast-track the process. Betable is a real-money gaming platform that already has a gambling license in the U.K., so that third-party developers can incorporate real bets in their games without having to go through the legal hassle of getting their own permits. “They’ve already secured legality, which is a blessing to us,” said Mikael Lefebvre, who is a director of Frima’s 3OAK studios. “It makes our life much easier.” This is a big year for Betable as the company is trying to get ahead of a wave of developers moving into social casino style games like slots and Slingo. At the same time, a difficult economic recovery has made more domestic states at least consider loosening online gambling regulations to improve their finances. Zynga recently made its first moves toward enabling real-money gaming by applying for “preliminary finding of suitability” from the Nevada Gaming Control Board and partnering with bwin.party to offer real-money bets in the U.K. While Betable hasn’t said how many games or developers it has signed or how many players it reaches so far, the company has disclosed partnerships with developers like Big Fish Games, Digital Chocolate, SGN, Slingo and Mandala. Big Fish, in particular, is a noteworthy client because their game Big Fish Casino is consistently one of the top 20 grossing iPhone games in the U.S. Betable’s belief is that the casual gaming market is going to change over the next 18-24 months as some developers choose to pick up real-money betting and suddenly acquire a host of new “whales” or lucrative players. Those developers will suddenly be able to spend more on marketing, boosting costs for other similar game makers. At the same time, real-money gaming creates its own unique set of challenges. Managing a game economy with real money is different from one with virtual currencies, where the developer needs to tweak currency sources and sinks properly to avoid inflation or deflation. Betable also says that it legally needs to manage the direct relationship with a game’s real-money players.
Researchers discover mutations linked to relapse of childhood leukemiaPublic release date: 3-Feb-2013 [ | E-mail | Share ]
Contact: Christopher Rucas Christopher.Rucas@nyumc.org 212-404-3525 NYU Langone Medical Center / New York University School of Medicine
Finding emerged from 100 billion RNA nucleotides in 10 children with cancer
After an intensive three-year hunt through the genome, medical researchers have pinpointed mutations that leads to drug resistance and relapse in the most common type of childhood cancerthe first time anyone has linked the disease's reemergence to specific genetic anomalies.
The discovery, co-lead by William L. Carroll, MD, director of NYU Langone Medical Center's Cancer Institute, is reported in a study published online February 3, 2013, in Nature Genetics.
"There has been no progress in curing children who relapse, in spite of giving them very high doses of chemotherapy and bone marrow transplants," said Dr. Carroll.
The discovery suggests how scientists may be able to thwart a dangerous form of acute lymphoblastic leukemia, a rapidly progressing blood-borne cancer that strikes about 6,000 people in the United States every year and accounts for more than one in four pediatric cancers. Eventually, such information could help doctors detect the early emergence of chemotherapy-resistant leukemia cells in patients and switch to a different treatment strategy before the disease can fully reassert itself.
In acute lymphoblastic leukemia, abbreviated ALL, the body's bone marrow produces an abnormally large number of lymphocytes, or white blood cells. Improved treatments have increased the overall cure rate to roughly 80 percent. But Dr. Carroll says the prognosis is especially dire for some 20 percent of patients who relapse.
Medical researchers have suspected that the reemergence of disease could be due to drug resistance, but previous efforts had not uncovered any definitive pathway. For the new study, led by Dr. Carroll and graduate student Julia Meyer, researchers at five U.S. institutions spent three years analyzing multiple bone marrow samples from pediatric ALL patients for more clues to the disease's progression.
With the help of the Children's Oncology Group, a multi-institutional clinical trials consortium supported by the National Cancer Institute, the researchers analyzed the entire transcriptomeor the full sequence of RNA from 10 children with pediatric B lymphoblastic leukemia, the most common subtype of ALL. RNA is an essential intermediary in the cellular process that uses DNA blueprints to assemble specific proteins, thus a leukemia transcriptome gives researchers a view of all active genes within the cancerous cells.
For each patient, the team pieced together a complete sequence of RNA extracted from the bone marrow at three time points: at diagnosis, during remission, and upon relapse some months or years later. All told, the project required the researchers to sequence, or spell out, 100 billion letters of RNA. By comparing the before and after sequences, the team found that each patient had acquired between one and six mutations that changed the genetic code over the course of the disease. In some cases researchers were able to detect these mutations in a very small subset (0.01 percent) of the tissue samples at diagnosis so that these cells likely expanded because their drug resistant properties provided the leukemia cells with a survival advantage.
In all, the team documented 20 relapse-specific mutationsnone of which had previously been implicated in ALL recurrences. Intriguingly, two patients harbored a mutation in the same gene, NT5C2, which encodes a protein that normally regulates some building blocks used to construct DNA but also can degrade an important class of drugs called purine analogues used in ALL therapy.
When the researchers fully sequenced the NT5C2 gene in 61 other cases in which pediatric ALL patients had relapsed, they found five more mutations that altered the gene's coding region. Further experiments suggested that these NT5C2 mutations all increased the protein's enzymatic activity, making the cancer cells more resistant to a chemotherapy treatment designed to force the cells to kill themselves. All seven patients with NT5C2 mutations relapsed within three years of the initial diagnosisan early, particularly hard-to-treat re-emergence likely mediated by the drug resistance.
Armed with the new knowledge, Dr. Carroll says doctors may be better equipped to identify patients likely to relapse. "We plan to test the feasibility of screening patients during therapy using sophisticated sequencing technology to pick up low-level mutations in NT5C2 and other genes indicating that a mutant clone is growing," he says. His team is researching whether that advance warning could allow doctors to administer separate drugs to beat back the cancer cells, and is also working on a strategy to directly inhibit the mutant enzyme.
###
The study co-authors include Julia A. Meyer, Jinhua Wang, Laura A. Hogan, Smita Dandekar, Zuojian Tang, Jiri Zavadil, Timothy Cardozo, Elizabeth Raetz, and Debra J. Morrison at NYU Langone Medical Center; Jun J. Yang and William E. Evans at St. Jude Children's Research Hospital; Jay P. Patel and Ross L. Levine at Memorial Sloan-Kettering Cancer Center; Paul Zumbo, Sheng Li, and Christopher E. Mason at Weill Cornell Medical College of Cornell University; and Stephen. P. Hunger at the University of Colorado School of Medicine and Children's Hospital Colorado.
The research was supported by the National Institutes of Health and National Cancer Institute, with additional support from the American Society of Hematology and St. Baldrick's Foundation.
About the NYU Cancer Institute:
The research mission of the NYU Cancer Institute is to discover the origins of cancer and use that knowledge to eradicate the personal and societal burden of cancer in our community and around the world. Fifteen research programs are organized as scientific research programs, focused on the fundamental biology of cancer in general, and as disease-specific research programs centered on individual types of cancer, such as breast or lung cancer. Translational research, a hallmark of the institute, is finding new ways to integrate the extraordinary growth and understanding made in basic research with the ever-growing need for the development of new therapies and approaches in the clinic to a variety of cancers that have remained difficult to treat. To help translate discovery into clinical practice, the NYU Cancer Institute has embarked on five programs that integrate efforts in laboratory investigation and clinical care: cancer targets and novel therapeutics, community and environment, integrative health, molecular oncology/cancer genomics, and immune- and stem-cell-based therapies.
About NYU Langone Medical Center:
NYU Langone Medical Center, a world-class, patient-centered, integrated, academic medical center, is one of the nation's premier centers for excellence in clinical care, biomedical research and medical education. Located in the heart of Manhattan, NYU Langone is composed of four hospitals Tisch Hospital, its flagship acute care facility; the Hospital for Joint Diseases, one of only five hospitals in the nation dedicated to orthopaedics and rheumatology; Hassenfeld Pediatric Center, a comprehensive pediatric hospital supporting a full array of children's health services; and the Rusk Institute of Rehabilitation Medicine, the world's first university-affiliated facility devoted entirely to rehabilitation medicine plus NYU School of Medicine, which since 1841 has trained thousands of physicians and scientists who have helped to shape the course of medical history. The medical center's tri-fold mission to serve, teach and discover is achieved 365 days a year through the seamless integration of a culture devoted to excellence in patient care, education and research. For more information, go to www.NYULMC.org.
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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.
Researchers discover mutations linked to relapse of childhood leukemiaPublic release date: 3-Feb-2013 [ | E-mail | Share ]
Contact: Christopher Rucas Christopher.Rucas@nyumc.org 212-404-3525 NYU Langone Medical Center / New York University School of Medicine
Finding emerged from 100 billion RNA nucleotides in 10 children with cancer
After an intensive three-year hunt through the genome, medical researchers have pinpointed mutations that leads to drug resistance and relapse in the most common type of childhood cancerthe first time anyone has linked the disease's reemergence to specific genetic anomalies.
The discovery, co-lead by William L. Carroll, MD, director of NYU Langone Medical Center's Cancer Institute, is reported in a study published online February 3, 2013, in Nature Genetics.
"There has been no progress in curing children who relapse, in spite of giving them very high doses of chemotherapy and bone marrow transplants," said Dr. Carroll.
The discovery suggests how scientists may be able to thwart a dangerous form of acute lymphoblastic leukemia, a rapidly progressing blood-borne cancer that strikes about 6,000 people in the United States every year and accounts for more than one in four pediatric cancers. Eventually, such information could help doctors detect the early emergence of chemotherapy-resistant leukemia cells in patients and switch to a different treatment strategy before the disease can fully reassert itself.
In acute lymphoblastic leukemia, abbreviated ALL, the body's bone marrow produces an abnormally large number of lymphocytes, or white blood cells. Improved treatments have increased the overall cure rate to roughly 80 percent. But Dr. Carroll says the prognosis is especially dire for some 20 percent of patients who relapse.
Medical researchers have suspected that the reemergence of disease could be due to drug resistance, but previous efforts had not uncovered any definitive pathway. For the new study, led by Dr. Carroll and graduate student Julia Meyer, researchers at five U.S. institutions spent three years analyzing multiple bone marrow samples from pediatric ALL patients for more clues to the disease's progression.
With the help of the Children's Oncology Group, a multi-institutional clinical trials consortium supported by the National Cancer Institute, the researchers analyzed the entire transcriptomeor the full sequence of RNA from 10 children with pediatric B lymphoblastic leukemia, the most common subtype of ALL. RNA is an essential intermediary in the cellular process that uses DNA blueprints to assemble specific proteins, thus a leukemia transcriptome gives researchers a view of all active genes within the cancerous cells.
For each patient, the team pieced together a complete sequence of RNA extracted from the bone marrow at three time points: at diagnosis, during remission, and upon relapse some months or years later. All told, the project required the researchers to sequence, or spell out, 100 billion letters of RNA. By comparing the before and after sequences, the team found that each patient had acquired between one and six mutations that changed the genetic code over the course of the disease. In some cases researchers were able to detect these mutations in a very small subset (0.01 percent) of the tissue samples at diagnosis so that these cells likely expanded because their drug resistant properties provided the leukemia cells with a survival advantage.
In all, the team documented 20 relapse-specific mutationsnone of which had previously been implicated in ALL recurrences. Intriguingly, two patients harbored a mutation in the same gene, NT5C2, which encodes a protein that normally regulates some building blocks used to construct DNA but also can degrade an important class of drugs called purine analogues used in ALL therapy.
When the researchers fully sequenced the NT5C2 gene in 61 other cases in which pediatric ALL patients had relapsed, they found five more mutations that altered the gene's coding region. Further experiments suggested that these NT5C2 mutations all increased the protein's enzymatic activity, making the cancer cells more resistant to a chemotherapy treatment designed to force the cells to kill themselves. All seven patients with NT5C2 mutations relapsed within three years of the initial diagnosisan early, particularly hard-to-treat re-emergence likely mediated by the drug resistance.
Armed with the new knowledge, Dr. Carroll says doctors may be better equipped to identify patients likely to relapse. "We plan to test the feasibility of screening patients during therapy using sophisticated sequencing technology to pick up low-level mutations in NT5C2 and other genes indicating that a mutant clone is growing," he says. His team is researching whether that advance warning could allow doctors to administer separate drugs to beat back the cancer cells, and is also working on a strategy to directly inhibit the mutant enzyme.
###
The study co-authors include Julia A. Meyer, Jinhua Wang, Laura A. Hogan, Smita Dandekar, Zuojian Tang, Jiri Zavadil, Timothy Cardozo, Elizabeth Raetz, and Debra J. Morrison at NYU Langone Medical Center; Jun J. Yang and William E. Evans at St. Jude Children's Research Hospital; Jay P. Patel and Ross L. Levine at Memorial Sloan-Kettering Cancer Center; Paul Zumbo, Sheng Li, and Christopher E. Mason at Weill Cornell Medical College of Cornell University; and Stephen. P. Hunger at the University of Colorado School of Medicine and Children's Hospital Colorado.
The research was supported by the National Institutes of Health and National Cancer Institute, with additional support from the American Society of Hematology and St. Baldrick's Foundation.
About the NYU Cancer Institute:
The research mission of the NYU Cancer Institute is to discover the origins of cancer and use that knowledge to eradicate the personal and societal burden of cancer in our community and around the world. Fifteen research programs are organized as scientific research programs, focused on the fundamental biology of cancer in general, and as disease-specific research programs centered on individual types of cancer, such as breast or lung cancer. Translational research, a hallmark of the institute, is finding new ways to integrate the extraordinary growth and understanding made in basic research with the ever-growing need for the development of new therapies and approaches in the clinic to a variety of cancers that have remained difficult to treat. To help translate discovery into clinical practice, the NYU Cancer Institute has embarked on five programs that integrate efforts in laboratory investigation and clinical care: cancer targets and novel therapeutics, community and environment, integrative health, molecular oncology/cancer genomics, and immune- and stem-cell-based therapies.
About NYU Langone Medical Center:
NYU Langone Medical Center, a world-class, patient-centered, integrated, academic medical center, is one of the nation's premier centers for excellence in clinical care, biomedical research and medical education. Located in the heart of Manhattan, NYU Langone is composed of four hospitals Tisch Hospital, its flagship acute care facility; the Hospital for Joint Diseases, one of only five hospitals in the nation dedicated to orthopaedics and rheumatology; Hassenfeld Pediatric Center, a comprehensive pediatric hospital supporting a full array of children's health services; and the Rusk Institute of Rehabilitation Medicine, the world's first university-affiliated facility devoted entirely to rehabilitation medicine plus NYU School of Medicine, which since 1841 has trained thousands of physicians and scientists who have helped to shape the course of medical history. The medical center's tri-fold mission to serve, teach and discover is achieved 365 days a year through the seamless integration of a culture devoted to excellence in patient care, education and research. For more information, go to www.NYULMC.org.
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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.
Jo Appleby, a lecturer in Human Bioarchaeology, at University of Leicester, School of Archaeology and Ancient History, who led the exhumation of the remains found during a dig at a Leicester car park, speaks at the university Monday Feb. 4, 2013. Tests have established that a skeleton found , including this skull, are "beyond reasonable doubt" the long lost remains of England's King Richard III, missing for 500 years.(AP Photo/Rui Vieira, PA) UNITED KINGDOM OUT - NO SALES - NO ARCHIVES
Jo Appleby, a lecturer in Human Bioarchaeology, at University of Leicester, School of Archaeology and Ancient History, who led the exhumation of the remains found during a dig at a Leicester car park, speaks at the university Monday Feb. 4, 2013. Tests have established that a skeleton found , including this skull, are "beyond reasonable doubt" the long lost remains of England's King Richard III, missing for 500 years.(AP Photo/Rui Vieira, PA) UNITED KINGDOM OUT - NO SALES - NO ARCHIVES
Jo Appleby, a lecturer in Human Bioarchaeology, at University of Leicester, School of Archaeology and Ancient History, who led the exhumation of the remains found during a dig at a Leicester car park, speaks at the university Monday Feb. 4, 2013. Tests have established that a skeleton found , including this skull, are "beyond reasonable doubt" the long lost remains of England's King Richard III, missing for 500 years.(AP Photo/Rui Vieira, PA) UNITED KINGDOM OUT - NO SALES - NO ARCHIVES
Undated photo made available by the University of Leicester, England, Monday Feb. 4, 2013 of the earliest surviving portrait of Richard III in Leicester Cathedral, ahead of an announcement about the identity of the skeleton found underneath a car park last September. Richard was immortalized in a play by Shakespeare as a hunchbacked usurper who left a trail of bodies ? including those of his two young nephews, murdered in the Tower of London ? on his way to the throne. (AP Photo/ University of Leicester)
Undated photo made available by the University of Leicester, England, Monday Feb. 4 2013 of the skull found at the Grey Friars excavation in Leicester, potentially the long lost remains of England's King Richard III, ahead of an announcement about the identity of the skeleton found underneath a car park last September. Richard was immortalized in a play by Shakespeare as a hunchbacked usurper who left a trail of bodies ? including those of his two young nephews, murdered in the Tower of London ? on his way to the throne. (AP Photo/ University of Leicester)
Michael Ibsen, a descendant of England's King Richard III, from whom DNA samples were taken, listens during a press conference Monday Feb. 4, 2013 at the University of Leicester Council Chamber building, regarding the exhumation of the remains found during a dig at a Leicester car park. Tests have established that a skeleton found are "beyond reasonable doubt" the long lost remains of King Richard III, missing for 500 years.(AP Photo/Rui Vieira, PA) UNITED KINGDOM OUT - NO SALES - NO ARCHIVES
LEICESTER, England (AP) ? He wore the English crown, but he ended up defeated, humiliated and reviled.
Now things are looking up for King Richard III. Scientists announced Monday that they had found the monarch's 500-year-old remains under a parking lot in the city of Leicester ? a discovery Richard's fans say will rewrite the history books.
University of Leicester researchers say tests on a battle-scarred skeleton unearthed last year prove "beyond reasonable doubt" that it is the king, who died at the Battle of Bosworth Field in 1485, and whose remains have been missing for centuries.
"Richard III, the last Plantaganet King of England, has been found," said the university's deputy registrar, Richard Taylor.
Bone specialist Jo Appleby said study of the bones provided "a highly convincing case for identification of Richard III."
And DNA from the skeleton matched a sample taken from a distant living relative of Richard's sister. Geneticist Turi King said Michael Ibsen, a Canadian carpenter living in London, share with the skeleton a rare strain of mitochondrial DNA. She said combined with the archaeological evidence, that left little doubt the skeleton belonged to Richard.
Ibsen said he was "stunned" to discover he was related to the king ? he is a 17th great-grand-nephew of Richard's older sister.
"It's difficult to digest" he said.
Richard III ruled England between 1483 and 1485, during the decades-long tussle over the throne known as the Wars of the Roses. His brief reign saw liberal reforms, including introduction of the right to bail and the lifting of restrictions on books and printing presses.
His rule was challenged, and he was defeated and killed by the army of Henry Tudor, who took the throne as King Henry VII.
The last English monarch to die in battle, Richard was depicted in a play by William Shakespeare as a hunchbacked usurper who left a trail of bodies ? including those of his two princely nephews, murdered in the Tower of London ? on his way to the throne.
Many historians say that image is unfair, and argue Richard's reputation was smeared by his Tudor successors. That's an argument taken up by the Richard III Society, set up to re-evaluate the reputation of a reviled monarch.
The society's Philippa Langley, who helped launch the search for the king, said she could scarcely believe her quest had paid off.
"Everyone thought that I was mad," she said. "It's not the easiest pitch in the world, to look for a king under a council car park."
Now, she said, "a wind of change is blowing, one that will seek out the truth about the real Richard III."
For centuries, the location of Richard's body has been unknown. Records say he was buried by the Franciscan monks of Grey Friars at their church in Leicester, 100 miles (160 kilometers) north of London. The church was closed and dismantled after King Henry VIII dissolved the monasteries in 1538, and its location eventually was forgotten.
Then, last September, archaeologists searching for Richard dug up the skeleton of an adult male who appeared to have died in battle.
Appleby said the 10 injuries to the body were inflicted by weapons like swords, daggers and halberds and were consistent with accounts of Richard being struck down in battle ? his helmet knocked from his head ? before his body was stripped naked and flung over the back of a horse in disgrace.
She said some scars, including a knife wound to the buttock, bore the hallmarks of "humiliation injuries" inflicted after death.
The remains also displayed signs of scoliosis, which is a form of spinal curvature, consistent with contemporary accounts of Richard's appearance, though not with Shakespeare's description of him as "deform'd, unfinished," hunchback.
Researchers conducted a battery of scientific tests, including radiocarbon dating to determine the skeleton's age. They found the skeleton belonged to a man aged between his late 20s and late 30s who died between 1455 and 1540. Richard was 32 when he died in 1485.
The discovery is a boon for the city of Leicester, which has bought a building next to the parking lot to serve as a visitor center and museum.
The mayor, Peter Soulsby, said the monarch would be interred in the city's cathedral and a memorial service would be held.
Asked if the late king would get a state funeral, Prime Minister David Cameron's spokesman Jean-Christophe Gray said it was a matter for the university.
People react as the coffin with the remains of Cambodia's late former King Norodom Sihanouk is taken on chariots through Phnom Penh, as his funeral procession begins, February 1, 2013. Sihanouk died at age 89 of heart failure on October 15, 2012 and his body will be cremated on February 4, 2013. REUTERS/Samrang Pring
People react as the coffin with the remains of Cambodia's late former King Norodom Sihanouk is taken on chariots through Phnom Penh, as his funeral procession begins, February 1, 2013. Sihanouk died at age 89 of heart failure on October 15, 2012 and his body will be cremated on February 4, 2013. REUTERS/Samrang Pring
Being the caregiver for an aging loved one can be exceptionally stressful. Not only are you handling physical responsibilities of addressing your loved one?s daily needs such as helping him move around, taking care of housekeeping and cooking responsibilities, and keeping his finances and medical needs organized, but you are also coping with the emotional challenges of watching a loved one age. Though many seniors are capable of maintaining active and vital lifestyles throughout the entirety of their lives; other seniors cope with debilitating physical and cognitive challenges that can be extremely difficult for loved ones to accept. You remember this senior when he was young, and it can be difficult for you to deal with the changes that he is undergoing a regular basis.
Experiencing caregiver stress and fatigue is not about you not being a good enough caregiver. It is not an indication that you don?t care enough about your aging loved one, or that you are not capable of fulfilling his needs. It is perfectly normal for anyone who is taken on the responsibilities of being an in home care provider for an aging adult to cope with emotional challenges and physical exhaustion. This is especially true of the senior who you are caring for is a beloved family member. You may push yourself excessively hard to be available and do more than you should. This is why it is extremely common for caregivers to report poor health, emotional stress and difficulty in other relationships after becoming an in home care provider.
By acknowledging caregiver stress and fatigue, you are able to address these challenges and overcome them effectively so you are able to be the best caregiver possible.
Here are some tips for overcoming caregiver stress and fatigue:
Take time every day for yourself. Even if this is just a bubble bath or half an hour spend reading a book, carve out some time that will be about focusing only on use of you can decompress and relax
Participate in a senior care support group where you can find others who are dealing with the same challenges in gain emotional support
Hire a home care provider to be in the home one or two days per week so that you have time off
Start writing in a journal daily so you have place to express your emotions
Forgive yourself for feeling these things, and allow yourself to take the time off that you desire.
When researching options for caregivers in Duxbury, MA call us at (339) 707-0012. Home care counselors at Hahn Home Health Care are available to talk with you about your in-home care needs including how to reduce caregiver stress while providing better, affordable care. We are an elder care agency providing Home Health Care in Duxbury, MA.
MANILA, Philippines ? Ateneo and Far Eastern University battled to a 1-1 draw on Thursday but the Blue Eagles kept the top spot in the UAAP season 75 men?s football tournament.
Midfielder Carlo Liay scored on a header to equalize in the 89th minute, which kept the Blue Eagles undefeated in the tournament with seven wins and three draws for 24 points.
Eric Giganto put FEU in the scoreboard early with a goal in the 12th minute, but yielded a last minute goal and failed to pounce on the chance to wrest the number one seeding.
The Tamaraw booters, though, kept their hold of the second spot with 22 points on seven wins, two setbacks and a draw.
Meanwhile, La Salle defeated National University, 2-0, to secure third place in the other game at the football fields inside the Ateneo campus.
Don Rabaya scored both goals for the Green Archers, who improved to 21 points on seven wins and three losses.
The Bulldogs, on their first shot at men?s football, absorbed their eight setback with two losses and a draw for seven points.
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Jan. 30, 2013 ? Searching for common elements in seemingly incompatible scientific theories may lead to the discovery of new ones that revolutionize our understanding of the world.
Such is the idea behind a mathematical framework Princeton University researchers developed that strips away the differences between scientific laws and theories to reveal how the ideas are compatible. In a recent report in the journal Physical Review Letters, the authors explain how the mathematical model finds common ground between the famously at-odds physics equations that govern classical and quantum mechanics.
In their paper, the researchers attempt to reconcile classical and quantum mechanics. Simply put, classical mechanics -- based on the ideas of English scientist Isaac Newton -- describes the ordered laws of motion for large objects and systems. Quantum mechanics relates more to the chaotic motion and activity of microscopic particles.
Lead author Denys Bondar, a postdoctoral research associate in Princeton's Department of Chemistry, explained that the Princeton framework -- called operational dynamic modeling -- is intended to streamline the development of novel theories, a typically painstaking process that can be for naught if the end result does not agree with experimental data. The framework unpacks and mathematically tests the basic algebra of a theory against that of observed data. If they reconcile, the newborn theory might be valid, Bondar said.
"We have a new theoretical tool that we can use to look at old problems and try to solve new problems," Bondar said. He worked with second author Renan Cabrera, a Princeton postdoctoral research associate in chemistry; senior researcher Herschel Rabitz, Princeton's Charles Phelps Smyth '16 *17 Professor of Chemistry; Robert Lompay, a physics graduate student at Uzhgorod National University in Ukraine; and Misha Ivanov, a physics professor at Imperial College London.
The Princeton model builds on theorems that Austrian physicist Paul Ehrenfest developed in the 20th century to illustrate the similarities between classical and quantum mechanics. Putting these theorems into action, Bondar and his colleagues pared the differences between these branches of physics down to a single mathematical consideration: to commute or not to commute. This Shakespearean-sounding crossroads relates to whether the result relies on the order of the experimental measurements.
If the same conclusion can be drawn regardless of how the measurements are arranged, the theory is commutative. If the result depends on a specific sequence, it is non-commutative. At this point, any novel theory can be characterized as classical or quantum, Bondar said. If the theory is commutative it is classical; if not, it has quantum elements.
"Scientists are taught from the time they are students that classical and quantum mechanics can never be reconciled," Bondar said. "But now we have one equation for classical and quantum mechanics. We can make the transition from classical to quantum mechanics in a smooth and straightforward way."
The benefit of the model, Cabrera said, is that experimental systems can be constructed more in accordance with particular mechanics as they are being developed. In addition, it can reveal if and how a novel theory relates to classical or quantum mechanics in a way that might not have been considered initially, he said.
"This model allows us to experience mathematically classical or quantum theories in a more similar way than before and find common ground only differentiated by the ability to commute or not commute," Cabrera said.
Robert Gilmore, a physics professor at Drexel University, said that the Princeton framework is a unique and well-designed initial step toward bringing classical and quantum mechanics under the same theoretical roof. Gilmore is familiar with the work, but had no role in it.
The researchers "provide the smoothest possible transition from quantum mechanics to classical mechanics," Gilmore said. "Their vision is that it is possible to formulate physical theory in such a way that both classical mechanics and quantum mechanics play by the same rules. In order to do this, they upend one of the classical early results of quantum mechanics: the Ehrenfest theorems."
Though the model is simple -- its experimental basis is the position and velocity of a single electron -- it could be matured to describe more complicated physical phenomena, Gilmore said.
"In order to deepen our understanding of quantum mechanics, this theory must be extended in several directions," he said. "This paper seems to provide one footing for a larger foundation that will be needed to build a more comprehensive theory including both classical and quantum mechanics."
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Journal Reference:
Denys Bondar, Renan Cabrera, Robert Lompay, Misha Ivanov, Herschel Rabitz. Operational Dynamic Modeling Transcending Quantum and Classical Mechanics. Physical Review Letters, 2012; 109 (19) DOI: 10.1103/PhysRevLett.109.190403
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Betable, a gaming platform that enables developers to use real money instead of virtual currencies, just signed one of Canada’s largest independent developers Frima Studio. Frima, which has about 350 people and is based in Quebec, is opening up a real-money gaming division called 3OAK. Instead of going their own way with acquiring gambling licenses in different countries, Frima said they chose Betable to fast-track the process. Betable is a real-money gaming platform that already has a gambling license in the U.K., so that third-party developers can incorporate real bets in their games without having to go through the legal hassle of getting their own permits. “They’ve already secured legality, which is a blessing to us,” said Mikael Lefebvre, who is a director of Frima’s 3OAK studios. “It makes our life much easier.” This is a big year for Betable as the company is trying to get ahead of a wave of developers moving into social casino style games like slots and Slingo. At the same time, a difficult economic recovery has made more domestic states at least consider loosening online gambling regulations to improve their finances. Zynga recently made its first moves toward enabling real-money gaming by applying for “preliminary finding of suitability” from the Nevada Gaming Control Board and partnering with bwin.party to offer real-money bets in the U.K. While Betable hasn’t said how many games or developers it has signed or how many players it reaches so far, the company has disclosed partnerships with developers like Big Fish Games, Digital Chocolate, SGN, Slingo and Mandala. Big Fish, in particular, is a noteworthy client because their game Big Fish Casino is consistently one of the top 20 grossing iPhone games in the U.S. Betable’s belief is that the casual gaming market is going to change over the next 18-24 months as some developers choose to pick up real-money betting and suddenly acquire a host of new “whales” or lucrative players. Those developers will suddenly be able to spend more on marketing, boosting costs for other similar game makers. At the same time, real-money gaming creates its own unique set of challenges. Managing a game economy with real money is different from one with virtual currencies, where the developer needs to tweak currency sources and sinks properly to avoid inflation or deflation. Betable also says that it legally needs to manage the direct relationship with a game’s real-money players.
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Public release date: 3-Feb-2013
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Experiencing caregiver stress and fatigue is not about you not being a good enough caregiver. It is not an indication that you don?t care enough about your aging loved one, or that you are not capable of fulfilling his needs. It is perfectly normal for anyone who is taken on the responsibilities of being an in home care provider for an aging adult to cope with emotional challenges and physical exhaustion. This is especially true of the senior who you are caring for is a beloved family member. You may push yourself excessively hard to be available and do more than you should. This is why it is extremely common for caregivers to report poor health, emotional stress and difficulty in other relationships after becoming an in home care provider.
