NEW YORK (AP) ? A burst of hiring in February pushed stocks higher on Wall Street.
The Dow Jones industrial average gained 67.58 points, or 0.5 percent, to 14,397.07. The index surpassed its previous record close Tuesday and logged a sixth straight increase Friday.
The Standard & Poor's 500 index rose 6.92 points, or 0.5 percent, to 1,551.18. The Nasdaq composite advanced 12.28 points, or 0.4 percent, to 3,244.37.
U.S. employers added 236,000 jobs last month and the unemployment rate fell to 7.7 percent from 7.9 percent in January, the Labor Department reported. That's far better than the 156,000 job gains and unemployment rate of 7.8 percent that economists surveyed by FactSet expected.
The strong job growth shows that employers are confident about the economy despite higher taxes and government spending cuts.
Optimism that hiring is picking up has been one of the factors bolstering the stock market this year. Stocks have also gained on evidence that the housing market is recovering and company earnings continue to growing.
Stocks have also been boosted by continuing economic stimulus from the Federal Reserve.
The U.S. central bank began buying bonds in January 2009 and is still purchasing $85 billion each month in Treasury bonds and mortgage-backed securities. That has kept interest rates near historic lows, reducing borrowing costs and encouraging investors to move money out of conservative investments like bonds and into stocks.
Investors have also been pondering what the Fed's next move will be. That question was in especially sharp focus Friday after the government reported the surge in hiring last month.
Andres Garcia-Amaya at JPMorgan Asset Management said that the strong jobs report may heighten speculation that the Fed will end its stimulus sooner than investors had anticipated, which would be a negative for the stock market.
"If the economy maintains or increases the pace of job creation....that could change the Fed's stance," said Garcia-Amaya. "That could mean that the Fed could take the 'punch bowl' away."
The Dow has gained 9.9 percent this year and is trading at record levels, having broken its previous record of 14,164 on Tuesday. The Standard & Poor's 500 index is up 8.8 percent since the start of the year, and is less than 1 percent short of its all-time high close of 1,565 set Oct. 9, 2007.
The stock market is drawing in more investors as it continues to surge.
Investors put $3.2 billion into stock mutual funds in the week ending Wednesday, data provider Lipper reported Friday. That's the ninth straight week of net inflows to stock funds, bringing this year's total to $59 billion.
Friday's jobs report strengthens the case of stock market bulls, who say the economy is gaining momentum following a long and tepid recovery after the financial crisis and Great Recession, said JJ Kinahan, chief derivatives strategist at TD Ameritrade.
"It gives hope to those that say this rally isn't just about the Fed, it's about the economy recovering," said Kinahan. "It's giving people confidence that maybe the economy is turning the corner."
The Dow is up 120 percent since reaching a 12-year low during The Great Recession. The index bottomed out almost exactly four years ago, on March 9, 2009, at 6,547. The S&P 500 has gained 129 percent since hitting its own bottom of 676 on the same date.
McDonald's contributed the most to the Dow's gains, rising $1.62, or 1.7 percent, to $98.71. The fast-food restaurant chain reported that a key sales figure fell 3.3 percent in February, but the decline wasn't as bad as analysts were expecting.
H&R Block had the biggest percentage gain on the S&P 500, advancing $2.30, or 9.2 percent, to $27.28.
The company said late Thursday that its net loss widened because of a delay to the start of this year's tax season. The stock got a boost, though, after CEO William Cobb said on a conference call that the company was winning market share, Barrington Research analyst Joe Janssen said.
The yield on the 10-year Treasury note, which moves inversely to its price, rose to 2.06 percent from 2 percent Thursday. The yield is at its highest in 11 months.
Among stocks making big moves;
? Pandora gained $2.06, or 17.6 percent, to $13.79 after the Internet radio company issued a strong profit forecast and said its mobile business was improving. Pandora also said its CEO, Joseph Kennedy, would leave.
? Skullcandy fell $1.51, or 22.5 percent, to $5.21 after the headphone maker projected a big loss and a drop in sales for the current quarter. The company said this year's results will likely be worse than in 2012.
? Foot Locker fell $2.52, or 7.1 percent, to $32.79 even after reporting that its fiscal fourth-quarter profit jumped 28 percent. An extra sales week helped boost earnings, but analysts were expecting more.
Circuitry of cells involved in immunity, autoimmune diseases exposedPublic release date: 6-Mar-2013 [ | E-mail | Share ]
Contact: Marjorie Montemayor-Quellenberg mmontemayor-quellenberg@partners.org 617-534-2208 Brigham and Women's Hospital
Autoimmune disease connections point to interplay between salt and genetic factors
Boston, MA New work from the Broad Institute's Klarman Cell Observatory, Brigham and Women's Hospital, Harvard University, MIT, and Yale University expands the understanding of how one type of immune cell known as a T helper 17 or Th17 cell develops, and how its growth influences the development of immune responses. By figuring out how these cells are "wired," the researchers make a surprising connection between autoimmunity and salt consumption, highlighting the interplay of genetics and environmental factors in disease susceptibility. The results of their work appear in three companion papers in Nature this week.
The researchers concentrated on T cells because of their important roles in clearing foreign pathogens and in various autoimmune diseases. "The question we wanted to pursue was: how does the highly pathogenic, pro-inflammatory T cell develop?" said Vijay Kuchroo, co-director of the Center for Infection and Immunity at Brigham and Women's Hospital's Biomedical Research Institute and a Broad associate member. Kuchroo is also a professor of neurology at Harvard Medical School. "Once we have a more nuanced understanding of the development of the pathogenic Th17 cells, we may be able to pursue ways to regulate them or their function."
The human immune system is in a state of delicate balance: too little activity leaves a person vulnerable to foreign invaders, but too much activity threatens to harm the body it ought to protect. When this delicate balance is broken, it can lead to autoimmune diseases. But little is known about the molecular circuitry that maintains or upsets such a fine equilibrium.
"We wanted to understand how the body gets the right kinds of immune cells in the right amount, and how it keeps those cells at the right activity level so that they are not too active but also not underactive," said Aviv Regev, a Broad Institute core member and an associate professor of biology at MIT. Regev is also an Early Career Scientist at Howard Hughes Medical Institute and the director of the Klarman Cell Observatory at the Broad. "The value in doing an unbiased analysis is that we're able to understand a lot more about the molecular biology at play and identify novel players in this process."
Th17 cells can promote inflammation that is important for protection against pathogens, but they have also been implicated in diseases like multiple sclerosis, psoriasis, rheumatoid arthritis, and ankylosing spondylitis. Treatment options for some of these diseases, such as psoriasis, include manipulating T cell function.
David Hafler's group at Yale University studies human autoimmune diseases in general and the role of Th17 cells in particular, and has collaborated with Kuchroo's group for many years. "These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment," said Hafler, Gilbert H. Glaser Professor of Neurology, professor of immunobiology, chair of Department of Neurology, and senior author of one of this week's Nature papers.
Some genes have been previously tied to Th17 development, but the research team wanted a more comprehensive view. One of the challenges of studying cell development, however, is that cells, particularly immune cells, change and evolve over time. The researchers chose to take frequent snapshots 18 over the course of three days to see what was happening within the T cells as they grew from nave cells into more specialized Th17 cells. From these snapshots, they used computational algorithms to begin to stitch together a network of molecular changes happening as the cells matured.
With this initial information in hand, the researchers systematically tested their model by silencing genes one-by-one, which could help reveal the most important points in the network and untangle their biological meaning.
To do so, they needed a technology that would allow them to silence genes without perturbing the cells in the process. Although RNA interference (RNAi) is a powerful way to turn off individual genes, most RNAi techniques rely on viruses as delivery vehicles. When scientists tried to perturb the T cells using these traditional techniques, cells either changed or died, limiting the effectiveness of these strategies.
"This was a real challenge," said Kuchroo. "Every time we tried to downregulate a gene with existing technologies, the cell would change. We didn't know if we were looking at the right thing. We needed a new technology something that could have a dramatic but precise effect."
A solution came from an unlikely source. Harvard professor and Broad associate member Hongkun Park and his lab in the departments of chemistry and chemical biology and of physics had been working on a computer-chip-like structure to interact with brain cells. Co-first authors Alex Shalek and Jellert Gaublomme along with other lab members had developed a bed of silicon nanowires miniscule needles designed to pierce cells.
"We learned that we could use these needles to deliver molecules into cells in a minimally invasive fashion," said Park. "And as Vijay and Aviv taught me, there are lots of things that this allows you to do that you could not do before. It's been an eye-opening experience."
Just as the thin needle of a syringe can be inserted into the skin and cause no more than a small pinching sensation, nanowires can be inserted into cells, causing minimal disruption. Using this new technology, the team teased apart the network, piece by piece, by deleting each of the key genes required in the development of Th17 cells.
With the help of co-first author Nir Yosef, a postdoc at the Broad and Brigham and Women's Hospital, the team found that Th17 cells are governed by two networks, seemingly at odds with each other: one network positively regulates the cells, coaxing them to increase in number while suppressing the development of other cells. The other negatively regulates them, having the opposite effect.
"It's a system in perfect tension," said Regev. "It both suppresses and promotes Th17 cell creation, keeping the cells at equilibrium."
Through this analysis, one particular gene stood out to the researchers: SGK1. The gene plays an important role in the cells' development, and when turned off in mice, Th17 cells are not produced.
SGK1 had not been described in T cells before, but it has been found in cells in the gut and in kidneys, where it plays a role in absorbing salt.
Based on this, two teams of researchers set out to test the connection between salt and autoimmunity Kuchroo, Regev, and their colleagues working with mouse cells and mouse models, and Hafler's team working with human cells.
Through efforts led by co-first author and Brigham and Women's Hospital postdoc Chuan Wu, the team found that they could induce more severe forms of autoimmune diseases, and at higher rates, in mice fed a high-salt diet than in those that were fed a normal mouse diet. Kuchroo notes though that the high-salt diet alone did not cause autoimmune diseases the researchers had to induce disease, in this case by injecting a self-antigen to prompt the mouse immune system to respond.
"It's not just salt, of course," Kuchroo said. "We have this genetic architecture genes that have been linked to various forms of autoimmune diseases, and predispose a person to developing autoimmune diseases. But we also suspect that environmental factors infection, smoking, and lack of sunlight and Vitamin D may play a role. Salt could be one more thing on the list of predisposing environmental factors that may promote the development of autoimmunity."
"One important question is: how can one think of these results in the context of human health?" said Regev. "It's premature to say, 'You shouldn't eat salt because you'll get an autoimmune disease.' We're putting forth an interesting hypothesis a connection between salt and autoimmunity that now must be tested through careful epidemiological studies in humans."
The researchers plan to harness the cell circuitry data to identify and follow up on potential drug targets. Kuchroo notes that the published work and future studies are only possible because of the interdisciplinary team brought together by shared questions about cell circuitry.
"We often work in isolation in our areas of expertise, but this is the kind of work I could not have done in my own lab, and that Hongkun and Aviv could not have done in their respective labs," said Kuchroo. "We needed this unique combination of tools and technologies to come together around this problem. Looking forward, we'll need the tools and intellect of different disciplines in order to solve big problems in biology and medicine."
###
Support for this work was provided by the National Human Genome Research Institute, the National Institutes of Health, National Multiple Sclerosis Society, the Klarman Cell Observatory, Guthy Jackson Foundation, and the Austrian Science Fund.
This press release was provided by the Broad Institute.
Brigham and Women's Hospital (BWH) is a 793-bed nonprofit teaching affiliate of Harvard Medical School and a founding member of Partners HealthCare. BWH has more than 3.5 million annual patient visits, is the largest birthing center in New England and employs more than 15,000 people. The Brigham's medical preeminence dates back to 1832, and today that rich history in clinical care is coupled with its national leadership in patient care, quality improvement and patient safety initiatives, and its dedication to research, innovation, community engagement and educating and training the next generation of health care professionals. Through investigation and discovery conducted at its Biomedical Research Institute (BRI), BWH is an international leader in basic, clinical and translational research on human diseases, involving nearly 1,000 physician-investigators and renowned biomedical scientists and faculty supported by nearly $625 million in funding. BWH continually pushes the boundaries of medicine, including building on its legacy in organ transplantation by performing the first face transplants in the U.S. in 2011. BWH is also home to major landmark epidemiologic population studies, including the Nurses' and Physicians' Health Studies, OurGenes and the Women's Health Initiative. For more information and resources, please visit BWH's online newsroom.
The Eli and Edythe L. Broad Institute of MIT and Harvard was founded in 2003 to empower this generation of creative scientists to transform medicine with new genome-based knowledge. 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 www.broadinstitute.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.
Circuitry of cells involved in immunity, autoimmune diseases exposedPublic release date: 6-Mar-2013 [ | E-mail | Share ]
Contact: Marjorie Montemayor-Quellenberg mmontemayor-quellenberg@partners.org 617-534-2208 Brigham and Women's Hospital
Autoimmune disease connections point to interplay between salt and genetic factors
Boston, MA New work from the Broad Institute's Klarman Cell Observatory, Brigham and Women's Hospital, Harvard University, MIT, and Yale University expands the understanding of how one type of immune cell known as a T helper 17 or Th17 cell develops, and how its growth influences the development of immune responses. By figuring out how these cells are "wired," the researchers make a surprising connection between autoimmunity and salt consumption, highlighting the interplay of genetics and environmental factors in disease susceptibility. The results of their work appear in three companion papers in Nature this week.
The researchers concentrated on T cells because of their important roles in clearing foreign pathogens and in various autoimmune diseases. "The question we wanted to pursue was: how does the highly pathogenic, pro-inflammatory T cell develop?" said Vijay Kuchroo, co-director of the Center for Infection and Immunity at Brigham and Women's Hospital's Biomedical Research Institute and a Broad associate member. Kuchroo is also a professor of neurology at Harvard Medical School. "Once we have a more nuanced understanding of the development of the pathogenic Th17 cells, we may be able to pursue ways to regulate them or their function."
The human immune system is in a state of delicate balance: too little activity leaves a person vulnerable to foreign invaders, but too much activity threatens to harm the body it ought to protect. When this delicate balance is broken, it can lead to autoimmune diseases. But little is known about the molecular circuitry that maintains or upsets such a fine equilibrium.
"We wanted to understand how the body gets the right kinds of immune cells in the right amount, and how it keeps those cells at the right activity level so that they are not too active but also not underactive," said Aviv Regev, a Broad Institute core member and an associate professor of biology at MIT. Regev is also an Early Career Scientist at Howard Hughes Medical Institute and the director of the Klarman Cell Observatory at the Broad. "The value in doing an unbiased analysis is that we're able to understand a lot more about the molecular biology at play and identify novel players in this process."
Th17 cells can promote inflammation that is important for protection against pathogens, but they have also been implicated in diseases like multiple sclerosis, psoriasis, rheumatoid arthritis, and ankylosing spondylitis. Treatment options for some of these diseases, such as psoriasis, include manipulating T cell function.
David Hafler's group at Yale University studies human autoimmune diseases in general and the role of Th17 cells in particular, and has collaborated with Kuchroo's group for many years. "These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment," said Hafler, Gilbert H. Glaser Professor of Neurology, professor of immunobiology, chair of Department of Neurology, and senior author of one of this week's Nature papers.
Some genes have been previously tied to Th17 development, but the research team wanted a more comprehensive view. One of the challenges of studying cell development, however, is that cells, particularly immune cells, change and evolve over time. The researchers chose to take frequent snapshots 18 over the course of three days to see what was happening within the T cells as they grew from nave cells into more specialized Th17 cells. From these snapshots, they used computational algorithms to begin to stitch together a network of molecular changes happening as the cells matured.
With this initial information in hand, the researchers systematically tested their model by silencing genes one-by-one, which could help reveal the most important points in the network and untangle their biological meaning.
To do so, they needed a technology that would allow them to silence genes without perturbing the cells in the process. Although RNA interference (RNAi) is a powerful way to turn off individual genes, most RNAi techniques rely on viruses as delivery vehicles. When scientists tried to perturb the T cells using these traditional techniques, cells either changed or died, limiting the effectiveness of these strategies.
"This was a real challenge," said Kuchroo. "Every time we tried to downregulate a gene with existing technologies, the cell would change. We didn't know if we were looking at the right thing. We needed a new technology something that could have a dramatic but precise effect."
A solution came from an unlikely source. Harvard professor and Broad associate member Hongkun Park and his lab in the departments of chemistry and chemical biology and of physics had been working on a computer-chip-like structure to interact with brain cells. Co-first authors Alex Shalek and Jellert Gaublomme along with other lab members had developed a bed of silicon nanowires miniscule needles designed to pierce cells.
"We learned that we could use these needles to deliver molecules into cells in a minimally invasive fashion," said Park. "And as Vijay and Aviv taught me, there are lots of things that this allows you to do that you could not do before. It's been an eye-opening experience."
Just as the thin needle of a syringe can be inserted into the skin and cause no more than a small pinching sensation, nanowires can be inserted into cells, causing minimal disruption. Using this new technology, the team teased apart the network, piece by piece, by deleting each of the key genes required in the development of Th17 cells.
With the help of co-first author Nir Yosef, a postdoc at the Broad and Brigham and Women's Hospital, the team found that Th17 cells are governed by two networks, seemingly at odds with each other: one network positively regulates the cells, coaxing them to increase in number while suppressing the development of other cells. The other negatively regulates them, having the opposite effect.
"It's a system in perfect tension," said Regev. "It both suppresses and promotes Th17 cell creation, keeping the cells at equilibrium."
Through this analysis, one particular gene stood out to the researchers: SGK1. The gene plays an important role in the cells' development, and when turned off in mice, Th17 cells are not produced.
SGK1 had not been described in T cells before, but it has been found in cells in the gut and in kidneys, where it plays a role in absorbing salt.
Based on this, two teams of researchers set out to test the connection between salt and autoimmunity Kuchroo, Regev, and their colleagues working with mouse cells and mouse models, and Hafler's team working with human cells.
Through efforts led by co-first author and Brigham and Women's Hospital postdoc Chuan Wu, the team found that they could induce more severe forms of autoimmune diseases, and at higher rates, in mice fed a high-salt diet than in those that were fed a normal mouse diet. Kuchroo notes though that the high-salt diet alone did not cause autoimmune diseases the researchers had to induce disease, in this case by injecting a self-antigen to prompt the mouse immune system to respond.
"It's not just salt, of course," Kuchroo said. "We have this genetic architecture genes that have been linked to various forms of autoimmune diseases, and predispose a person to developing autoimmune diseases. But we also suspect that environmental factors infection, smoking, and lack of sunlight and Vitamin D may play a role. Salt could be one more thing on the list of predisposing environmental factors that may promote the development of autoimmunity."
"One important question is: how can one think of these results in the context of human health?" said Regev. "It's premature to say, 'You shouldn't eat salt because you'll get an autoimmune disease.' We're putting forth an interesting hypothesis a connection between salt and autoimmunity that now must be tested through careful epidemiological studies in humans."
The researchers plan to harness the cell circuitry data to identify and follow up on potential drug targets. Kuchroo notes that the published work and future studies are only possible because of the interdisciplinary team brought together by shared questions about cell circuitry.
"We often work in isolation in our areas of expertise, but this is the kind of work I could not have done in my own lab, and that Hongkun and Aviv could not have done in their respective labs," said Kuchroo. "We needed this unique combination of tools and technologies to come together around this problem. Looking forward, we'll need the tools and intellect of different disciplines in order to solve big problems in biology and medicine."
###
Support for this work was provided by the National Human Genome Research Institute, the National Institutes of Health, National Multiple Sclerosis Society, the Klarman Cell Observatory, Guthy Jackson Foundation, and the Austrian Science Fund.
This press release was provided by the Broad Institute.
Brigham and Women's Hospital (BWH) is a 793-bed nonprofit teaching affiliate of Harvard Medical School and a founding member of Partners HealthCare. BWH has more than 3.5 million annual patient visits, is the largest birthing center in New England and employs more than 15,000 people. The Brigham's medical preeminence dates back to 1832, and today that rich history in clinical care is coupled with its national leadership in patient care, quality improvement and patient safety initiatives, and its dedication to research, innovation, community engagement and educating and training the next generation of health care professionals. Through investigation and discovery conducted at its Biomedical Research Institute (BRI), BWH is an international leader in basic, clinical and translational research on human diseases, involving nearly 1,000 physician-investigators and renowned biomedical scientists and faculty supported by nearly $625 million in funding. BWH continually pushes the boundaries of medicine, including building on its legacy in organ transplantation by performing the first face transplants in the U.S. in 2011. BWH is also home to major landmark epidemiologic population studies, including the Nurses' and Physicians' Health Studies, OurGenes and the Women's Health Initiative. For more information and resources, please visit BWH's online newsroom.
The Eli and Edythe L. Broad Institute of MIT and Harvard was founded in 2003 to empower this generation of creative scientists to transform medicine with new genome-based knowledge. 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 www.broadinstitute.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.
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