If three's a crowd, the Samsung Galaxy S III party in the US is about to get pretty stuffy. Having already reviewed AT&T and Sprint's variants -- not to mention the original I9300 before them -- we're now ready to put a third iteration through its paces, this time from the country's fourth-largest carrier, T-Mobile.
Of course, the phone itself needs no grand introduction, as it's fast become the new darling of the smartphone world. And rightfully so, in many respects: it's the first high-end device to launch on all four major mobile operators in the US (a feat in and of itself), and it's done so with minimal carrier branding, hardware changes or bloatware levies. It is, in essence, an unadulterated handset. The reason this piece of news is so wondrous is that it opens up your ability to choose your phone service based on the network, not on the actual phone each individual carrier offers.
Sadly, the big tradeoff here is the loss of an Exynos quad-core processor in exchange for a Snapdragon S4 dual-core chipset and additional RAM. Join us as we take a deeper look at the T-Mobile Galaxy S III. Is it the best phone on the network? Is it worth shelling out $280 (with a two-year contract) for the 16GB model or $330 for 32GB? How well does it perform? This and more answers await you in our full review below.
[ [ [['Connery is an experienced stuntman', 2]], 'http://yhoo.it/KeQd0p', '[Slideshow: See photos taken on the way down]', ' ', '630', ' ', ' ', ], [ [['Connery is an experienced stuntman', 7]], ' http://yhoo.it/KpUoHO', '[Slideshow: Death-defying daredevils]', ' ', '630', ' ', ' ', ], [ [['know that we have confidence in', 3]], 'http://yhoo.it/LqYjAX ', '[Related: The Secret Service guide to Cartagena]', ' ', '630', ' ', ' ', ], [ [['We picked up this other dog and', 5]], 'http://yhoo.it/JUSxvi', '[Related: 8 common dog fears, how to calm them]', ' ', '630', ' ', ' ', ], [ [['accused of running a fake hepatitis B', 5]], 'http://bit.ly/JnoJYN', '[Related: Did WH share raid details with filmmakers?]', ' ', '630', ' ', ' ', ], [ [['accused of running a fake hepatitis B', 3]], 'http://bit.ly/KoKiqJ', '[Factbox: AQAP, al-Qaeda in Yemen]', ' ', '630', ' ', ' ', ], [ [['have my contacts on or glasses', 3]], 'http://abcn.ws/KTE5AZ', '[Related: Should the murder charge be dropped?]', ' ', '630', ' ', ' ', ], [ [['have made this nation great as Sarah Palin', 5]], 'http://yhoo.it/JD7nlD', '[Related: Bristol Palin reality show debuts June 19]', ' ', '630', ' ', ' ', ], [ [['have made this nation great as Sarah Palin', 1]], 'http://bit.ly/JRPFRO', '[Related: McCain adviser who vetted Palin weighs in on VP race]', ' ', '630', ' ', ' ', ], [ [['A JetBlue flight from New York to Las Vegas', 3]], 'http://yhoo.it/GV9zpj', '[Related: View photos of the JetBlue plane in Amarillo]', ' ', '630', ' ', ' ', ], [ [['the 28-year-old neighborhood watchman who shot and killed', 15]], 'http://news.yahoo.com/photos/white-house-stays-out-of-teen-s-killing-slideshow/', 'Click image to see more photos', 'http://l.yimg.com/cv/ip/ap/default/120411/martinzimmermen.jpg', '630', ' ', 'AP', ], [ [['He was in shock and still strapped to his seat', 6]], 'http://news.yahoo.com/photos/navy-jet-crashes-in-virginia-slideshow/', 'Click image to see more photos', 'http://l.yimg.com/cv/ip/ap/default/120406/jet_ap.jpg', '630', ' ', 'AP', ], [ [['xxxxxxxxxxxx', 11]], 'http://news.yahoo.com/photos/russian-grannies-win-bid-to-sing-at-eurovision-1331223625-slideshow/', 'Click image to see more photos', 'http://l.yimg.com/a/p/us/news/editorial/1/56/156d92f2760dcd3e75bcd649a8b85fcf.jpeg', '500', ' ', 'AP', ] ]
[ [ [['did not go as far his colleague', 8]], '29438204', '0' ], [ [[' the 28-year-old neighborhood watchman who shot and killed', 4]], '28924649', '0' ], [ [['because I know God protects me', 14], ['Brian Snow was at a nearby credit union', 5]], '28811216', '0' ], [ [['The state news agency RIA-Novosti quoted Rosaviatsiya', 6]], '28805461', '0' ], [ [['measure all but certain to fail in the face of bipartisan', 4]], '28771014', '0' ], [ [['matter what you do in this case', 5]], '28759848', '0' ], [ [['presume laws are constitutional', 7]], '28747556', '0' ], [ [['has destroyed 15 to 25 houses', 7]], '28744868', '0' ], [ [['short answer is yes', 7]], '28746030', '0' ], [ [['opportunity to tell the real story', 7]], '28731764', '0' ], [ [['entirely respectable way to put off the searing constitutional controversy', 7]], '28723797', '0' ], [ [['point of my campaign is that big ideas matter', 9]], '28712293', '0' ], [ [['As the standoff dragged into a second day', 7]], '28687424', '0' ], [ [['French police stepped up the search', 17]], '28667224', '0' ], [ [['Seeking to elevate his candidacy back to a general', 8]], '28660934', '0' ], [ [['The tragic story of Trayvon Martin', 4]], '28647343', '0' ], [ [['Karzai will get a chance soon to express', 8]], '28630306', '0' ], [ [['powerful storms stretching', 8]], '28493546', '0' ], [ [['basic norm that death is private', 6]], '28413590', '0' ], [ [['songwriter also saw a surge in sales for her debut album', 6]], '28413590', '1', 'Watch music videos from Whitney Houston ', 'on Yahoo! Music', 'http://music.yahoo.com' ], [ [['keyword', 99999999999999999999999]], 'videoID', '1', 'overwrite-pre-description', 'overwrite-link-string', 'overwrite-link-url' ] ]
Scottsdale is refinancing about $88 million of bonds starting next week to save an estimated $10 million over 13 years for the McDowell Sonoran Preserve.
Arizona residents will have the first chance on Monday to buy the tax-exempt investment bonds to refinance the bonds that were issued in 2004 for the preserve, said David Smith, Scottsdale city treasurer.
"It's a refinancing that has a significant benefit for all of the citizens of Scottsdale and the preserve acquisition program going forward," Smith said.
The McDowell Sonoran Preserve includes about 21,000 acres of desert and mountainous terrain.
Scottsdale residents voted in 1994 and 2005 to support a tax hike for preserve acquisition.
The city hopes to save money with lower-interest-rate bonds that will reduce payments on that debt from Scottsdale's dedicated sales tax for the preserve.
The minimum investment in the preserve bonds is $5,000 for a period of one to 13 years.
The yield on the bonds is expected to be low, maybe 2 to 3 percent, because the city's triple-A bond rating is a low-risk investment, Smith said.
Scottsdale has a AAA bond rating from all three major rating agencies -- Moody's Investor Services, Standard & Poor's, and Fitch, he said.
Scottsdale has arranged a group of underwriters to sell the preserve bonds: J.P. Morgan, Morgan Stanley, Edward Jones, Stone & Youngberg and Wedbush Securities.
Information on the preserve bonds and underwriters is available at scottsdaleaz.gov/preservebonds.
Lee Guillory, city finance manager, said in most cases the city's bonds are purchased by large institutional investors and are available only to citizens on the secondary market.
Scottsdale residents can place orders through their brokers during Monday's exclusive retail period but the funding is not due until early July, Guillory said.
by Peter Corbett - Jun. 8, 2012 01:28 PM The Republic | azcentral.com
Scottsdale refinancing bonds to save $10M for McDowell Sonoran Preserve
Breast cancer's many driversPublic release date: 20-Jun-2012 [ | E-mail | Share ]
Contact: Nicole Davis ndavis@broadinstitute.org 617-714-7152 Broad Institute of MIT and Harvard
New genetic alterations discovered through US-Mexico sequence-analysis collaboration
Breast cancer is not a single disease, but a collection of diseases with dozens of different mutations that crop up with varying frequency across different breast cancer subtypes. Deeper exploration of the genetic changes that drive breast cancer is revealing new complexity in the leading cause of cancer death in women worldwide.
In one of the largest breast cancer sequencing efforts to date, scientists from the Broad Institute, the National Institute of Genomic Medicine in Mexico City, Beth Israel Deaconess Medical Center, and Dana-Farber Cancer Institute have discovered surprising alterations in genes that were not previously associated with breast cancer. They report their results in the June 21 issue of Nature, which is publishing a series of papers characterizing the genomic landscape of breast cancer.
One of the team's new findings, a recurrent fusion of the genes MAGI3 and AKT3 in what is known as a translocation event, was observed in tumors from a rare but aggressive form of breast cancer known as triple-negative breast cancer. This cancer does not respond to conventional hormone therapy because its tumors lack three receptors that fuel most breast cancers: estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (known as HER2). But the biological pathway that is affected by the MAGI3-AKT3 reshuffling is already the target of experimental drugs.
The other new alteration reported by the team occurred in two transcription factor genes. Recurrent mutations were detected in the gene CBFB and deletions of its partner RUNX1. Cancer-causing rearrangements of these two genes are common in blood cancers, such as acute myeloid leukemia, but their discovery in breast cancer marks the first time they have been seen in a solid cancer.
"These genes wouldn't top the list of genes you think would be mutated in breast cancer," said Alfredo Hidalgo Miranda, co-senior author of the paper and head of the cancer genomics laboratory at the National Institute of Genomic Medicine, known by its Spanish acronym INMEGEN. "That's exactly the point of doing this type of analysis. It gives you the opportunity to find those genes that you never thought would be involved in the breast cancer process."
The scientists studied two kinds of samples. They sequenced the whole exomes - the tiny fraction of the genome that encodes proteins of 103 breast cancer tumors and DNA from normal tissue from patients in Mexico and Vietnam. They also sequenced the entire genomes of 22 breast cancer tumors and matched normal tissue.
Their analysis confirmed the presence of previously known mutations, but it also turned up the unsuspected alterations.
"One of the lessons here is the real diversity of mutations in breast cancer. I think it's clear there are going to be roughly 50 or so different mutated genes in breast cancer," said Matthew Meyerson, co-senior author of the paper, Broad senior associate member, and professor of pathology at Dana-Farber Cancer Institute and Harvard Medical School. "There's a big diversity of driver genes in cancer. We don't understand what all of them are, but larger data sets will enable us to identify them."
The mutations in CBFB and RUNX1 point to the importance of understanding cell differentiation - how cells become specialized and transcription factors that regulate that process of cell differentiation in epithelial tissue, which lines the inner and outer surfaces of the body. Further studies are needed to unravel that relationship, the authors concluded.
For the current study, inspecting the novel fusion gene MAGI1-AKT3 more closely showed not only that the translocation can transform normal cells into cancer cells, but also that the protein produced by the gene is insensitive to certain drugs now in clinical trials, yet sensitive to others.
In general, fusion genes are created within the same chromosome or across different chromosomes when parts of one gene join parts of another to become a novel gene that wouldn't normally exist. Like the CBFB and RUNX1 mutations, translocations are also more common in blood cancers but until now have rarely been detected in solid tumors, especially breast cancer.
This particular MAGI1-AKT3 fusion gene produces a fusion protein that acts in the PI 3-kinase pathway as an oncogene, or a gene that drives cancer, revealing a new target for potential therapy. The kinase pathway controls a multitude of cellular functions. When a gene is mutated in this pathway, the result is uncontrolled cell growth, a hallmark of cancer.
Other gene mutations in this pathway are well-known, but MAGI1-AKT3 is a first.
"This is the first translocation event resulting in an oncogenic fusion protein that has been identified in this pathway," said Alex Toker, a professor in the department of pathology at Beth Israel Deaconess and Harvard Medical School. "That's important because this is one of the most frequently mutated pathways in human cancer, especially in women's cancers such as breast, ovarian, and endometrial cancer."
The most frequently mutated pathway is also the most studied and, from a pharmaceutical perspective, among the most "druggable."
In laboratory dishes, tests confirmed that the novel structure of proteins encoded by the fusion gene provided no place for some drugs to bind but offered targets for other drugs.
"There are many additional studies that need to be performed using mouse models of disease that would recapitulate the expression of this protein in the mammary gland, in addition to the mechanism by which this protein promotes the effects associated with malignancy," Toker said. "These are all experiments that are under way."
Once the mechanism at work in triple-negative breast cancer is understood through animal models, the next step would be to test chemical compounds to see how effective they might be at targeting cells that harbor this fusion gene's protein.
Beyond these scientific findings, the study also represents a closer look at the Latino population, thanks to the collaboration between the Broad and INMEGEN forged through the Slim Initiative in Genomic Medicine.
"The Slim Initiative in Genomic Medicine aims to support the discovery of the genetic basis of diseases such as type 2 diabetes mellitus and several types of cancer which have a profound public health impact in Mexico and Latin America," said Roberto Tapia-Conyer, director general of the Carlos Slim Health Institute. "This novel bi-national scientific collaboration is contributing to put the Latin American genome on the map of the second generation worldwide genome studies."
INMEGEN scientists had previously built a large breast cancer study and then scientists at both the Broad and INMEGEN exchanged clinical, biological, and computational information.
"From the Mexican point of view, you can say the Latino population has not been extensively characterized using genomic methods," Hidalgo Miranda said. "This is a significant contribution to the knowledge of the architecture of breast tumors in this particular population."
The study represented a first opportunity to study the genetic basis of breast cancer in Mexico. Larger studies will be required to determine whether differences in the spectrum of mutations exist between different populations, but this was an important first step toward that goal.
###
Contributors to the work also include, from the Broad and its Harvard-affiliated hospitals: Shantanu Banerji (co-first author), Kristian Cibulskis (co-first author), Kristin K. Brown (co-first author), Scott L. Carter, Abbie M. Frederick, Michael S. Lawrence, Andrey Y. Sivachenko, Carrie Sougnez, Lihua Zou, Maria L. Cortes, Shouyong Peng, Kristin G. Ardlie, Daniel Auclair, Fujiko Duke, Joshua Francis, Joonil Jung, Robert C. Onofrio, Melissa Parkin, Nam H. Pho, Alex. H. Ramos, Steven E. Schumacher, Nicolas Stransky, Kristin M. Thompson, Jose Baselga, Rameen Beroukhim, Kornelia Polyak, Dennis C. Sgroi, Andrea L. Richardson, Eric S. Lander, Stacey B. Gabriel, Levi A. Garraway, Todd R. Golub, and Gad Getz (co-senior author). From Mexico: Claudia Rangel-Escareno (co-first author), Juan C. Fernandez-Lopez, Veronica Bautista-Pina, Antonio Maffuz-Aziz, Valeria Quintanar-Jurado, Rosa Rebollar-Vega, Sergio Rodriguez-Cuevas, Sandra L. Romero-Cordoba, Laura Uribe-Figueroa, Gerardo Jimenez-Sanchez, and Jorge Melendez-Zajgla.
The research was conducted as part of the Slim Initiative in Genomic Medicine, a project funded by the Carlos Slim Health Institute in Mexico. The work was also supported by grants from the National Institutes of Health and the National Cancer Institute.
-Elizabeth Cooney, Broad Institute
Paper(s) cited:
Banerji S et al. Sequence analysis of mutations and translocations across breast cancer subtypes. Nature June 21, 2012. DOI: 10.1038/nature11154
About the Broad Institute of Harvard and MIT
The Eli and Edythe L. Broad Institute of Harvard and MIT was launched in 2004 to empower this generation of creative scientists to transform medicine. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.
Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to http://www.broadinstitute.org.
About the Carlos Slim Health Institute
The Carlos Slim Health Institute is a non-profit organization created in 2007 by the initiative of Mr. Carlos Slim-Hel with the purpose of generating solutions in order to help solving Mexico's and Latin America's main public health problems focusing on the most deprived populations.
The institute seeks to achieve its objectives by fostering alliances with Mexican and foreign public, private and social institutions in order to support the adoption of innovative, sustainable and replicable solutions aimed at improving the health of the population, such as the use of mobile technologies in health care, on-line based distance learning, translating scientific research into applicable tools, etc. http://www.salud.carlosslim.org
About the National Institute of Genomic Medicine
The National Institute of Genomic Medicine (INMEGEN) is the eleventh National Institute of Health in Mexico, founded in 2004. INMEGEN's mission is to contribute to the health care of the Mexican population by developing cutting-edge scientific research and well-trained human resources in order to apply the knowledge of genomic medicine through innovation, state-of-the-art technology, and strategic partnerships, all the while complying with universal ethical principles.
INMEGEN's main research areas focus on principal complex diseases in Mexico, including population genomics of the Mexican population, genomics of metabolic diseases (diabetes mellitus and obesity), cancer, infectious diseases, cardiovascular diseases, nutrigenomics, and pharmacogenomics.
One of the features of INMEGEN's innovative culture is scientific research and development of technology, which leads to goods and services that can then be used to contribute to better health care for the Mexican people in the knowledge-based economy.
www.inmegen.gob.mx
About Beth Israel Deaconess Medical Center
Beth Israel Deaconess Medical Center is a patient care, research and teaching affiliate of Harvard Medical School and ranks third in National Institutes of Health funding among independent hospitals nationwide. BIDMC is clinically affiliated with the Joslin Diabetes Center and is a research partner of the Dana-Farber/Harvard Cancer Center. BIDMC is the official hospital of the Boston Red Sox. For more information, visit http://www.bidmc.harvard.edu.
About Dana-Farber Cancer Institute
Dana-Farber Cancer Institute (http://www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Boston Children's Hospital as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber or Facebook: http://www.facebook.com/danafarbercancerinstitute.
[ | 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.
Breast cancer's many driversPublic release date: 20-Jun-2012 [ | E-mail | Share ]
Contact: Nicole Davis ndavis@broadinstitute.org 617-714-7152 Broad Institute of MIT and Harvard
New genetic alterations discovered through US-Mexico sequence-analysis collaboration
Breast cancer is not a single disease, but a collection of diseases with dozens of different mutations that crop up with varying frequency across different breast cancer subtypes. Deeper exploration of the genetic changes that drive breast cancer is revealing new complexity in the leading cause of cancer death in women worldwide.
In one of the largest breast cancer sequencing efforts to date, scientists from the Broad Institute, the National Institute of Genomic Medicine in Mexico City, Beth Israel Deaconess Medical Center, and Dana-Farber Cancer Institute have discovered surprising alterations in genes that were not previously associated with breast cancer. They report their results in the June 21 issue of Nature, which is publishing a series of papers characterizing the genomic landscape of breast cancer.
One of the team's new findings, a recurrent fusion of the genes MAGI3 and AKT3 in what is known as a translocation event, was observed in tumors from a rare but aggressive form of breast cancer known as triple-negative breast cancer. This cancer does not respond to conventional hormone therapy because its tumors lack three receptors that fuel most breast cancers: estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (known as HER2). But the biological pathway that is affected by the MAGI3-AKT3 reshuffling is already the target of experimental drugs.
The other new alteration reported by the team occurred in two transcription factor genes. Recurrent mutations were detected in the gene CBFB and deletions of its partner RUNX1. Cancer-causing rearrangements of these two genes are common in blood cancers, such as acute myeloid leukemia, but their discovery in breast cancer marks the first time they have been seen in a solid cancer.
"These genes wouldn't top the list of genes you think would be mutated in breast cancer," said Alfredo Hidalgo Miranda, co-senior author of the paper and head of the cancer genomics laboratory at the National Institute of Genomic Medicine, known by its Spanish acronym INMEGEN. "That's exactly the point of doing this type of analysis. It gives you the opportunity to find those genes that you never thought would be involved in the breast cancer process."
The scientists studied two kinds of samples. They sequenced the whole exomes - the tiny fraction of the genome that encodes proteins of 103 breast cancer tumors and DNA from normal tissue from patients in Mexico and Vietnam. They also sequenced the entire genomes of 22 breast cancer tumors and matched normal tissue.
Their analysis confirmed the presence of previously known mutations, but it also turned up the unsuspected alterations.
"One of the lessons here is the real diversity of mutations in breast cancer. I think it's clear there are going to be roughly 50 or so different mutated genes in breast cancer," said Matthew Meyerson, co-senior author of the paper, Broad senior associate member, and professor of pathology at Dana-Farber Cancer Institute and Harvard Medical School. "There's a big diversity of driver genes in cancer. We don't understand what all of them are, but larger data sets will enable us to identify them."
The mutations in CBFB and RUNX1 point to the importance of understanding cell differentiation - how cells become specialized and transcription factors that regulate that process of cell differentiation in epithelial tissue, which lines the inner and outer surfaces of the body. Further studies are needed to unravel that relationship, the authors concluded.
For the current study, inspecting the novel fusion gene MAGI1-AKT3 more closely showed not only that the translocation can transform normal cells into cancer cells, but also that the protein produced by the gene is insensitive to certain drugs now in clinical trials, yet sensitive to others.
In general, fusion genes are created within the same chromosome or across different chromosomes when parts of one gene join parts of another to become a novel gene that wouldn't normally exist. Like the CBFB and RUNX1 mutations, translocations are also more common in blood cancers but until now have rarely been detected in solid tumors, especially breast cancer.
This particular MAGI1-AKT3 fusion gene produces a fusion protein that acts in the PI 3-kinase pathway as an oncogene, or a gene that drives cancer, revealing a new target for potential therapy. The kinase pathway controls a multitude of cellular functions. When a gene is mutated in this pathway, the result is uncontrolled cell growth, a hallmark of cancer.
Other gene mutations in this pathway are well-known, but MAGI1-AKT3 is a first.
"This is the first translocation event resulting in an oncogenic fusion protein that has been identified in this pathway," said Alex Toker, a professor in the department of pathology at Beth Israel Deaconess and Harvard Medical School. "That's important because this is one of the most frequently mutated pathways in human cancer, especially in women's cancers such as breast, ovarian, and endometrial cancer."
The most frequently mutated pathway is also the most studied and, from a pharmaceutical perspective, among the most "druggable."
In laboratory dishes, tests confirmed that the novel structure of proteins encoded by the fusion gene provided no place for some drugs to bind but offered targets for other drugs.
"There are many additional studies that need to be performed using mouse models of disease that would recapitulate the expression of this protein in the mammary gland, in addition to the mechanism by which this protein promotes the effects associated with malignancy," Toker said. "These are all experiments that are under way."
Once the mechanism at work in triple-negative breast cancer is understood through animal models, the next step would be to test chemical compounds to see how effective they might be at targeting cells that harbor this fusion gene's protein.
Beyond these scientific findings, the study also represents a closer look at the Latino population, thanks to the collaboration between the Broad and INMEGEN forged through the Slim Initiative in Genomic Medicine.
"The Slim Initiative in Genomic Medicine aims to support the discovery of the genetic basis of diseases such as type 2 diabetes mellitus and several types of cancer which have a profound public health impact in Mexico and Latin America," said Roberto Tapia-Conyer, director general of the Carlos Slim Health Institute. "This novel bi-national scientific collaboration is contributing to put the Latin American genome on the map of the second generation worldwide genome studies."
INMEGEN scientists had previously built a large breast cancer study and then scientists at both the Broad and INMEGEN exchanged clinical, biological, and computational information.
"From the Mexican point of view, you can say the Latino population has not been extensively characterized using genomic methods," Hidalgo Miranda said. "This is a significant contribution to the knowledge of the architecture of breast tumors in this particular population."
The study represented a first opportunity to study the genetic basis of breast cancer in Mexico. Larger studies will be required to determine whether differences in the spectrum of mutations exist between different populations, but this was an important first step toward that goal.
###
Contributors to the work also include, from the Broad and its Harvard-affiliated hospitals: Shantanu Banerji (co-first author), Kristian Cibulskis (co-first author), Kristin K. Brown (co-first author), Scott L. Carter, Abbie M. Frederick, Michael S. Lawrence, Andrey Y. Sivachenko, Carrie Sougnez, Lihua Zou, Maria L. Cortes, Shouyong Peng, Kristin G. Ardlie, Daniel Auclair, Fujiko Duke, Joshua Francis, Joonil Jung, Robert C. Onofrio, Melissa Parkin, Nam H. Pho, Alex. H. Ramos, Steven E. Schumacher, Nicolas Stransky, Kristin M. Thompson, Jose Baselga, Rameen Beroukhim, Kornelia Polyak, Dennis C. Sgroi, Andrea L. Richardson, Eric S. Lander, Stacey B. Gabriel, Levi A. Garraway, Todd R. Golub, and Gad Getz (co-senior author). From Mexico: Claudia Rangel-Escareno (co-first author), Juan C. Fernandez-Lopez, Veronica Bautista-Pina, Antonio Maffuz-Aziz, Valeria Quintanar-Jurado, Rosa Rebollar-Vega, Sergio Rodriguez-Cuevas, Sandra L. Romero-Cordoba, Laura Uribe-Figueroa, Gerardo Jimenez-Sanchez, and Jorge Melendez-Zajgla.
The research was conducted as part of the Slim Initiative in Genomic Medicine, a project funded by the Carlos Slim Health Institute in Mexico. The work was also supported by grants from the National Institutes of Health and the National Cancer Institute.
-Elizabeth Cooney, Broad Institute
Paper(s) cited:
Banerji S et al. Sequence analysis of mutations and translocations across breast cancer subtypes. Nature June 21, 2012. DOI: 10.1038/nature11154
About the Broad Institute of Harvard and MIT
The Eli and Edythe L. Broad Institute of Harvard and MIT was launched in 2004 to empower this generation of creative scientists to transform medicine. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.
Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to http://www.broadinstitute.org.
About the Carlos Slim Health Institute
The Carlos Slim Health Institute is a non-profit organization created in 2007 by the initiative of Mr. Carlos Slim-Hel with the purpose of generating solutions in order to help solving Mexico's and Latin America's main public health problems focusing on the most deprived populations.
The institute seeks to achieve its objectives by fostering alliances with Mexican and foreign public, private and social institutions in order to support the adoption of innovative, sustainable and replicable solutions aimed at improving the health of the population, such as the use of mobile technologies in health care, on-line based distance learning, translating scientific research into applicable tools, etc. http://www.salud.carlosslim.org
About the National Institute of Genomic Medicine
The National Institute of Genomic Medicine (INMEGEN) is the eleventh National Institute of Health in Mexico, founded in 2004. INMEGEN's mission is to contribute to the health care of the Mexican population by developing cutting-edge scientific research and well-trained human resources in order to apply the knowledge of genomic medicine through innovation, state-of-the-art technology, and strategic partnerships, all the while complying with universal ethical principles.
INMEGEN's main research areas focus on principal complex diseases in Mexico, including population genomics of the Mexican population, genomics of metabolic diseases (diabetes mellitus and obesity), cancer, infectious diseases, cardiovascular diseases, nutrigenomics, and pharmacogenomics.
One of the features of INMEGEN's innovative culture is scientific research and development of technology, which leads to goods and services that can then be used to contribute to better health care for the Mexican people in the knowledge-based economy.
www.inmegen.gob.mx
About Beth Israel Deaconess Medical Center
Beth Israel Deaconess Medical Center is a patient care, research and teaching affiliate of Harvard Medical School and ranks third in National Institutes of Health funding among independent hospitals nationwide. BIDMC is clinically affiliated with the Joslin Diabetes Center and is a research partner of the Dana-Farber/Harvard Cancer Center. BIDMC is the official hospital of the Boston Red Sox. For more information, visit http://www.bidmc.harvard.edu.
About Dana-Farber Cancer Institute
Dana-Farber Cancer Institute (http://www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Boston Children's Hospital as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber or Facebook: http://www.facebook.com/danafarbercancerinstitute.
[ | 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.
WTNH) -- A national advocacy group has filed a complaint against Hartford Hospital for using live animals for surgical training.
The nonprofit group says state-of-the-art simulators are used at most health facilities.
The Physicians Committee for Responsible Medicine says it really comes down to the use of live animals, in the case of Hartford Hospital, a pig under anesthesia, to train doctors on emergency medical procedures to be performed on humans, instead of using the latest technology available.
Dr. Marjorie Cramer said, "I have a lot of trouble with the concept of using an animal, which doesn't really resemble a human very much, has different thickness of skin, has different tissues underneath the skin."
The alternative is using a simulator, which closely resembles human tissue. A training tool approved by the American College of Surgeons.
Dr. Cramer is a retired plastic surgeon and is one of a handful of doctors who signed what they say is a criminal complaint against Hartford Hospital, that still uses live animals to train doctors in emergency medical procedures.
"If I were in a huge car accident and came into an emergency room and had someone try to save my life, I would feel a lot better had they practiced on a human based simulator," Dr. Cramer said.
A statement issued by Hartford Hospital says its' treatment of animals strictly adheres to the guidelines of the National Association of Biomedical Research stating "...scientific and medical knowledge developed through biomedical research and training has saved countless lives, has alleviated great pain and suffering, and has improved both animal and human health."
The nonprofit advocacy organization filed the complaint, alleging the hospital is in violation of animal cruelty.
"It is animal cruelty because it is gratuitous," said Dr. John Pippin. "It is unnecessary."
Dr. John Pippin is the PCRM Director of Academic Affairs.
"We've met resistance at every level," Dr. Pippin said. "We can't establish a dialogue about this so we feel compelled to take this to the next level."
He added Hartford Hospital is among five programs out of 278 in the U.S. and Canada still using live animals for trauma training.
The group has filed the complaint with the state's attorney for the Hartford Judicial District and is seeking for action to be taken.
To assist you in losing weight, drink ice water. When really cold water gets into your system, you begin a cool down mode. The process of warming the water causes your body to work a little harder. Drink ice cold water rather than other unhealthy options, such as soft drinks.
Eat more low-calorie foods that are also filling. If you eat a salad, or even just a few veggies prior to a meal, they will somewhat fill you up before you get stuck in to that calorie-laden main course. Drinking a glass of water, tea, coffee or another sugar-free beverage can also achieve the same result.
Put some extra protein in your breakfast in place of that high carbohydrate bagel or toast and avoid the hungry feeling that often before lunch. Protein makes you feel fuller for an extended period, so you will be less likely to reach for snacks between meals.
The portions you eat are an important part of any weight loss goals. Generally, the meat you eat should be about 3 ounces, or the size of your hand?s palm. It?s been proven that people who pay attention to what they?re eating tend to weight less.
Once you have had breakfast, only drink water. Water does have sugar, calories, or fat and provides you with the hydration your body needs. Consuming water post will help you knock off the pounds with less difficulty.
You should always make sure you get a lot of sleep. Try to get at least eight hours each night. Staying awake can just hurt your chances to lose weight. Having enough sleep can help your metabolism get corrected so that you can burn your food.
It is a good idea to eat meals around the same hour each day. This allows you to stay on schedule and refrain from having snacks at random times during the day. Stick to a consistent eating schedule.
You should visit and bookmark blogs dedicated to weight loss or bodybuilding. If you aren?t feeling up to the task of losing weight, head over to a site you bookmarked to get motivated again. Once you begin to read the positive and uplifting stories online, you will start to get inspired and continue on your weight loss journey.
Are you hoping to lose weight this year? Then you have been reading the right article. You are now armed with information regarding tips, techniques and strategies, all that could lead to effective loss of weight. May you experience a great success!
The Galaxy S III is the official phone of the London Olympics, and Samsung's teamed up with Eurosport to give S III owners a way of watching the summer's games on-the-go. Download the Eurosport Player app for Android on your S III, and you'll qualify for a free month-long subscription that can be activated between July 14 and August 12, letting you watch Eurosport's Olympic coverage live.
European Galaxy S III owners (excluding Italy, for some reason) can download the Eurosport Player app from Google Play or Samsung Apps in preparation, though it won't become active until July 14. Unfortunately it looks like this promotion won't be available on the North American S III when it launches later this month.
Most people understand that relocating can be a discomfort, but moving companies can certainly lessen the burden so long as one selects the right one. Relocation companies are professional packers, transporters, and can even unpack possessions. Most are effective, cautious, and dependable simply because their reputations are at risk. Nevertheless, some are better than others so looking around, comparing companies, their prices, services, and so on is a wise ?move.? Here are some simple steps:
Gather multiple relocating quotes from many different companies. There are trusted web sites out there that offer estimating services for this particular purpose. One of the best of these web sites is movingquotes.net.
Speak to a number of companies over the phone. Ask what services they do and do not offer. Request they send these things in writing. They ought to be able to produce a detailed description of the duties, a warranty, and common costs.(The final price ought to be able to be obtained once assessed personally by a business representative.) Communication is key. Establish clearly and early on what each of your responsibilities will and can not be. After interviewing a number of companies, this ought to help choose the most beneficial one for your needs and goals.
After deciding upon a business, request one contact person who can respond to all of your concerns and one you might contact whenever you want, should a crisis arise. If a business cannot or will not provide such a person, you might want to reexamine your option.
Generally a business will send a representative to the house to assess the job and can also offer the opportunity to voice issues over any special breakable, precious items. They ought to also be able to advise about disconnecting and reconnecting the appliances you plan to take to your new house. They may offer lists or spreadsheets of particular services. The representatives ought to also note any unique issues their movers may encounter, such as stairs, elevators, steep grades, and heavy furniture. He ought to be able to tell you what items they will pack and how and what your duties will be. That is a great time to make unique mention of any and all delicate items you might own and how you wish them handled.
If you plan to put some belongings into storage, the moving business can offer guidance to you concerning this.
While they will likely consist of relocation insurance against any lost or damaged items done in transit, it may be a good idea to purchase some additional personal insurance for added protection. While following these steps may appear a little overwhelming, in the long run it is well worth the efforts and can save time, energy and money. The right business can help ease the stresses that come along with moving and get the ?load? off your mind!
ScienceDaily (June 5, 2012) ? U.S. researchers are perfecting simulations that show a nuclear weapon's performance in precise molecular detail, tools that are becoming critical for national defense because international treaties forbid the detonation of nuclear test weapons.
The simulations must be operated on supercomputers containing thousands of processors, but doing so has posed reliability and accuracy problems, said Saurabh Bagchi, an associate professor in Purdue University's School of Electrical and Computer Engineering.
Now researchers at Purdue and high-performance computing experts at the National Nuclear Security Administration's (NNSA) Lawrence Livermore National Laboratory have solved several problems hindering the use of the ultra-precise simulations. NNSA is the quasi-independent agency within the U.S. Department of Energy that oversees the nation's nuclear security activities.
The simulations, which are needed to more efficiently certify nuclear weapons, may require 100,000 machines, a level of complexity that is essential to accurately show molecular-scale reactions taking place over milliseconds, or thousandths of a second. The same types of simulations also could be used in areas such as climate modeling and studying the dynamic changes in a protein's shape.
Such highly complex jobs must be split into many processes that execute in parallel on separate machines in large computer clusters, Bagchi said.
"Due to natural faults in the execution environment there is a high likelihood that some processing element will have an error during the application's execution, resulting in corrupted memory or failed communication between machines," Bagchi said. "There are bottlenecks in terms of communication and computation."
These errors are compounded as long as the simulation continues to run before the glitch is detected and may cause simulations to stall or crash altogether.
"We are particularly concerned with errors that corrupt data silently, possibly generating incorrect results with no indication that the error has occurred," said Bronis R. de Supinski, co-leader of the ASC Application Development Environment Performance Team at Lawrence Livermore. "Errors that significantly reduce system performance are also a major concern since the systems on which the simulations run are very expensive."
Advanced Simulation and Computing is the computational arm of NNSA's Stockpile Stewardship Program, which ensures the safety, security and reliability of the nation's nuclear deterrent without underground testing.
New findings will be detailed in a paper to be presented during the Annual IEEE/IFIP International Conference on Dependable Systems and Networks from June 25-28 in Boston. Recent research findings were detailed in two papers last year, one presented during the IEEE Supercomputing Conference and the other during the International Symposium on High-Performance Parallel and Distributed Computing.
The researchers have developed automated methods to detect a glitch soon after it occurs.
"You want the system to automatically pinpoint when and in what machine the error took place and also the part of the code that was involved," Bagchi said. "Then, a developer can come in, look at it and fix the problem."
One bottleneck arises from the fact that data are streaming to a central server.
"Streaming data to a central server works fine for a hundred machines, but it can't keep up when you are streaming data from a thousand machines," said Purdue doctoral student Ignacio Laguna, who worked with Lawrence Livermore computer scientists. "We've eliminated this central brain, so we no longer have that bottleneck."
Each machine in the supercomputer cluster contains several cores, or processors, and each core might run one "process" during simulations. The researchers created an automated method for "clustering," or grouping the large number of processes into a smaller number of "equivalence classes" with similar traits. Grouping the processes into equivalence classes makes it possible to quickly detect and pinpoint problems.
"The recent breakthrough was to be able to scale up the clustering so that it works with a large supercomputer," Bagchi said.
Lawrence Livermore computer scientist Todd Gamblin came up with the scalable clustering approach.
A lingering bottleneck in using the simulations is related to a procedure called checkpointing, or periodically storing data to prevent its loss in case a machine or application crashes. The information is saved in a file called a checkpoint and stored in a parallel system distant from the machines on which the application runs.
"The problem is that when you scale up to 10,000 machines, this parallel file system bogs down," Bagchi said. "It's about 10 times too much activity for the system to handle, and this mismatch will just become worse because we are continuing to create faster and faster computers."
Doctoral student Tanzima Zerin and Rudolf Eigenmann, a professor of electrical and computer engineering, along with Bagchi, led work to develop a method for compressing the checkpoints, similar to the compression of data for images.
"We're beginning to solve the checkpointing problem," Bagchi said. "It's not completely solved, but we are getting there."
The checkpointing bottleneck must be solved in order for researchers to create supercomputers capable of "exascale computing," or 1,000 quadrillion operations per second.
"It's the Holy Grail of supercomputing," Bagchi said.
The research has been funded by Lawrence Livermore and the National Science Foundation. The work also involves Lawrence Livermore scientists Greg Bronevetsky, Dong H. Ahn, Martin Schulz and IBM Austin researcher Mootaz Elnozahy.
Share this story on Facebook, Twitter, and Google:
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by Purdue University. The original article was written by Emil Venere.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Note: If no author is given, the source is cited instead.
Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
Buckingham Palace says Prince Philip, 90-year-old husband of Queen Elizabeth II, has been hospitalized with a bladder infection.
Monday's announcement comes as the U.K. is celebrating the queen's Diamond Jubilee.
The palace said he had been taken to hospital as "a precautionary measure" and would remain under observation for a few days, meaning that he will miss the latter part of the queen's Diamond Jubilee celebrations.
Queen off to the races as jubilee events begin
The palace said the prince, who will turn 91 on Saturday, was taken to the King Edward VII Hospital in London from Windsor Castle. It said he would remain in hospital under observation for a few days.
British music royalty was set to celebrate Queen Elizabeth II on Monday with a Buckingham Palace concert featuring acts from throughout her 60-year-reign. Philip will miss the concert.
On Sunday, Prince Philip joined the queen and senior royals on the River Thames in cold and blustery weather for a pageant in honor of Elizabeth's 60 years on the throne.
Stars to rock palace, but will queen enjoy it?
The prince, who married then then-Princess Elizabeth in 1947, has cut back on official engagements in recent years, but still maintains a busy schedule. He spent four nights in the hospital at Christmas after suffering chest pains, and underwent a successful coronary stent procedure to clear a blocked artery.
He has been at the queen's side during engagements across Britain to mark the jubilee, and appeared in good spirits as he traveled down the river on a barge Sunday, despite the harsh weather.
Video: Historic St. Paul?s Cathedral prepares for Jubilee
The palace said Philip was "understandably, disappointed about missing this evening's Diamond Jubilee Concert," as well as a St. Paul's Cathedral service and other jubilee events planned for Tuesday.
The Associated Press contributed reporting to this story.
Extent: 0.1 Linear feet, in one oversize manuscript box
The Coney Island Jockey Club was founded during the late 19th century by Leonard Jerome and William Kissam Vanderbilt. During its early existence the club held horse races at the Propect Park fairgrounds, and in 1880 the club built the Sheepshead Bay Race Track, where its races were held thereafter. The collection spans the period 1889 to 1899 and contains the club?s founding resolution; programs broadsides; and ephemera, such as passes, badges, and tickets from races organized by the club.
Names:
Places:
Coney Island (New York, N.Y.)
Sheepshead Bay (New York, N.Y.)
Subjects:
Clubs ? New York (State) ? Kings County
Horse racing ? New York (State) ? Kings County
Sports ? New York (State) ? Kings County
Types of material:
Articles of incorporation.
Programs (documents)
Tickets
View Finding Aid
If you'd like to make an appointment to use this collection, or have a question, please fill out our online form.
![[ Back to EurekAlert! ]](http://www.eurekalert.org/images/back2e.gif){kind=small}
Public release date: 20-Jun-2012
Share ] 
