Jan. 29, 2013 ? While the wooly musk ox may like it cold, fruit flies definitely do not. They like it hot, or at least warm. In fact, their preferred optimum temperature is very similar to that of humans -- 76 degrees F.
Scientists have known that a type of brain cell circuit helps regulate a variety of innate and learned behavior in animals, including their temperature preferences. What has been a mystery is whether or not this behavior stems from a specific set of neurons (brain cells) or overlapping sets.
Now, a new study from The Scripps Research Institute (TSRI) shows that a complex set of overlapping neuronal circuits work in concert to drive temperature preferences in the fruit fly Drosophila by affecting a single target, a heavy bundle of neurons within the fly brain known as the mushroom body. These nerve bundles, which get their name from their bulbous shape, play critical roles in learning and memory.
The study, published in the January 30, 2013 edition of the Journal of Neuroscience, shows that dopaminergic circuits -- brain cells that synthesize dopamine, a common neurotransmitter -- within the mushroom body do not encode a single signal, but rather perform a more complex computation of environmental conditions.
"We found that dopamine neurons process multiple inputs to generate multiple outputs -- the same set of nerves process sensory information and reward-avoidance learning," said TSRI Assistant Professor Seth Tomchik. "This discovery helps lay the groundwork to better understand how information is processed in the brain. A similar set of neurons is involved in behavior preferences in humans -- from basic rewards to more complex learning and memory."
Using imaging techniques that allow scientists to visualize neuron activity in real time, the study illuminated the response of dopaminergic neurons to changes in temperature. The behavioral roles were then examined by silencing various subsets of these neurons. Flies were tested using a temperature gradient plate; the flies moved from one place to another to express their temperature preferences.
As it turns out, genetic silencing of dopaminergic neurons innervating the mushroom body substantially reduces cold avoidance behavior. "If you give the fly a choice, it will pick San Diego weather every time," Tomchik said, "but if you shut down those nerves, they suddenly don't mind being in Minnesota."
The study also showed dopaminergic neurons respond to cooling with sudden a burst of activity at the onset of a drop in temperature, before settling down to a lower steady-state level. This initial burst of dopamine could function to increase neuronal plasticity -- the ability to adapt -- during periods of environmental change when the organism needs to acquire new associative memories or update previous associations with temperature changes.
The study, "Dopaminergic Neurons Encode a Distributed, Asymmetric Representation of Temperature in Drosophila," was supported by the National Institute of Mental Health of the National Institutes of Health (grant number K99 MH092294).
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NEW YORK (AP) ? Chris Cuomo is leaving ABC News to host a new morning show at CNN, where new boss Jeff Zucker is moving fast to try to turn around the cable news pioneer that has fallen on hard times.
Network managing editor Mark Whitaker announced he was quitting Tuesday, officially Zucker's seventh day on the job as CNN Worldwide president. Longtime political consultants and commentators James Carville and Mary Matalin also are leaving.
Cuomo is expected to be paired with current evening anchor Erin Burnett in the mornings. CNN said Tuesday it was discussing other job options with Soledad O'Brien, who will be ending her second stint as morning show co-host.
"Chris is an accomplished anchor who is already an established name in morning television," Zucker said. "What I love about Chris is that he is passionate about every story he tells, never forgets about the viewer and represents the type of journalism that makes CNN great."
In addition to the broadcast morning shows, CNN is competing with two distinctive cable news morning programs in Fox News Channel's "Fox & Friends" and MSNBC's "Morning Joe."
Zucker was the "Today" show executive producer as the show began dominating morning television in the mid-1990s, before moving up in the NBC executive suite, and he is expected to work closely in developing the new morning show. He was largely responsible for Matt Lauer and Meredith Vieira getting their jobs at "Today."
Cuomo, the "20/20" co-anchor, is the second big defection from ABC to CNN in a little more than a month, the other being Jake Tapper.
Both men found their paths to higher-profile jobs at ABC blocked. Cuomo, who was news anchor at "Good Morning America" from 2006 to 2009, was passed over for George Stephanopoulos as co-host of that show while Tapper twice didn't get a shot at the anchor job on "This Week," first when Stephanopoulos left and then when he returned to the Sunday show.
Both Cuomo and Tapper will have their own daily programs on CNN, which generally runs third in the ratings behind Fox and MSNBC but improves during big news events.
Cuomo wasn't made available for comment. He said in a statement that "this is a fantastic opportunity to do what I value the most and hopefully to do the work that I do best."
CNN was scooped on the announcement of Cuomo's hiring by the newsman's older brother, New York Gov. Andrew Cuomo, who mentioned it during a radio interview Tuesday morning.
ABC News moved quickly to replace Cuomo, appointing correspondent David Muir as Elizabeth Vargas' new co-host on the prime-time newsmagazine.
Whitaker came to CNN in 2011 as senior vice president and managing editor and tried to expand CNN's programming, opening a film division and hiring Morgan Spurlock and Anthony Bourdain for weekend shows that haven't started yet.
With Zucker and "his own forceful ideas" about CNN's direction and programming options, Whitaker said the new chief deserved a chance to build his own management team.
The Cajun commentator Carville, a former Bill Clinton political aide, has delivered opinions on CNN since 2002. His wife, Mary Matalin, came on at the end of the Bush administration in 2009.
___
Associated Press writer Michael Gormley in Albany, N.Y. contributed to this report.
Caddo Holdings bought Lakewood Towers in 2010. (HFF LP)
A Dallas commercial real estate investor has put its five local office properties up for sale.
But officials with Caddo Holdings say they plan to buy other buildings in the state.
Caddo Holdings has hired HFF LP to sell the buildings in Dallas? Uptown and Lakewood districts.
The three Uptown buildings were purchased in late 2011 and are the 7-story Crosstex Energy building at 2501 Cedar Springs, the five-story 3400 Carlisle building on Lemmon Avenue and the three-story 2811 McKinney building near the Quadrangle.
Caddo is also trying to sell its 2-building Lakewood Towers office complex on Gaston Avenue in East Dallas. It acquired the Lakewood property in 2010.
Lakewood Towers is 85.5 percent leased and the Uptown buildings are between 83 and 100 percent rented.
Caddo Holdings bought the Crosstex building in 2011. (HFF LP)
?We executed on our plans on those assets ahead of schedule so decided to have HFF take them to market,? Caddo Holdings Dustin Schilling said. ?We have aggressive acquisition plans for Texas and are acquiring additional buildings.?
Caddo Holdings is a private investor formed in 2009 by Schilling and partners Justin Engler, Tim Slaughter.
MOSCOW (AP) ? Russia stepped up efforts Friday to resolve a dispute with neighbor Kazakhstan over its demand to reduce the number of commercial satellite launches from the Russian-leased Baikonur cosmodrome.
Kazakhstan, which in the past suspended Russian rocket launches after previous failures spilled toxic rocket fuel, has demanded that Russia cuts the number of Proton rockets lifting off from Baikonur from 17 to 12 this year.
Russian Foreign Minister Sergey Lavrov downplayed the dispute after talks in Moscow with his Kazakh counterpart Friday.
"The issue regarding the number of launches is linked to Kazakhstan's concerns about their impact on environment," Lavrov said. "Russia is taking all the necessary steps to address environmental aspects by using improved Proton-M booster rockets. There is no sensation about it, just working issues."
The dispute has threatened to cloud relations between the two ex-Soviet neighbors. Moscow would lose half a billion dollars if Kazakhstan succeeds in cutting the number of launches, according to Russia's pro-government daily Izvestia, which reported the Kazakh demand. The paper also said Moscow was threatening Kazakhstan with countermeasures.
Izvestia on Thursday quoted a note from Russia's Roscosmos space agency warning that the country would opt out of joint projects with Kazakhstan if it doesn't withdraw its demand for Russia to scale down its scheduled rocket launches from Baikonur.
Russia has a lease to use Kazakhstan's Soviet-built launch pad until 2050 and pays an annual fee of $115 million. It has continued to rely on Baikonur for all its manned missions and most of its commercial satellite launches.
This isn't the first time Kazakh authorities have voiced worries over the environmental impact of Russia's space program. Previously, they have briefly suspended Russian launches from Baikonur following the spill of highly toxic rocket fuel after failed launches of the heavylift Proton booster rocket, the main cash cow of Russia's space program.
Moscow also has the Plesetsk launch pad in the north of Russia but that is used mostly for launches of military satellites. It has moved to reduce its dependence on Kazakhstan by building a new cosmodrome in the far east.
The Vostochny cosmodrome, where construction started in 2011, is located 5,500 kilometers (3,400 miles) east of Moscow, and just about 100 kilometers (60 miles) away from the border with China.
The first rocket launch from the Vostochny cosmodrome is set to be conducted by 2015. An unmanned mission to the moon is also planned for the same year. In 2018 it is slated to launch a first manned mission.
Personal injury law is a broad term used in cases involving any number of unrelated actions such as car accidents, dog bites, wrongful death, or slip and fall (premises liability), which result in physical and/or psychological harm to an individual. When such incidents occur, the victim seeking justice and compensation should seek out the representation of a personal injury attorney.
Personal injury law is principally based upon tort law. A basic definition of a tort is a ?civil wrong?. The law of torts is very basic and predicated upon the idea that an injured party should be compensated in some way for the harm that was caused to them by the ?tortfeasor? (the person responsible for the act) or the ?tort? act. Ideally, the injured party should be compensated for any losses they have suffered whether they are physical, emotional or economic in nature.
The word tort comes from the Latin ?tortus?, meaning ?twisted? or ?crooked?. As the word was adopted into the English language, it was used to describe an act that was twisted, or not straight and became synonymous with the word ?wrong?. As the word fell out of use by the general public, it was retained in the legal arena to describe the types of cases taken up by personal injury attorneys.
All personal injury matters boil down to the concept of negligence. The elements of proving negligence are (1) duty ? each of us, no matter our role in society, owe a duty to one another, whether we are operating a motor vehicle, walking a dog or managing a property. If that duty is not upheld or is (2) breached, and that breach (3) causes (4) damages to another person, the person who committed the wrongful act (the tortfeasor) is negligent.
R. Klettke is a freelance writer. He writes about personal injury and medical malpractice law and other matters of jurisprudence.
Important Advisory: This article is not intended to provide legal advice upon which you or anyone else should rely in making any decisions regarding the instituting or prosecuting of a legal claim. Laws and rules relating to the bringing of a claim vary widely from state to state. You should always contact a personal injury attorney to obtain information as to the rules and the laws pertaining to any claim you might have.
HealthyUNCG, the university employee health promotion program, would like to invite you to participate in a research study designed to examine the effectiveness of health and wellness coaching on weight loss. All UNCG employees are eligible to participate.
HealthyUNCG is offering the Taking Pounds OFF Sensibly (TOPS) program. This research study will combine weight management strategies from the nationally recognized TOPS program with individual or small group health and wellness coaching sessions. Each week all participants will attend a 1 hour session.
Registration in the national TOPS program is required, $29.50/year.
Participants will not receive compensation or reimbursement for joining TOPS or for participating in the study. Participants will receive TOPS program materials as part of their registration fee and health & wellness coaching services for free.
All information is confidential and only group data will be used for the study. You may participate in the TOPS program even if you do not participate in the research study.
Attend the information and sign-up session on Thursday, Jan. 24, noon in the Dogwood Room of EUC
For further information about the study, TOPS ? and to register for an information session ? visit http://healthy.uncg.edu
You may contact Michelle Cathorall, the director of HealthyUNCG and PI of the study,with any questions. She can be reached at healthy_uncg@uncg.edu or by phone at 334-9743.
Immune cells engineered in lab to resist HIV infection, Stanford study showsPublic release date: 22-Jan-2013 [ | E-mail | Share ]
Contact: Ruthann Richter richter1@stanford.edu 650-725-8047 Stanford University Medical Center
STANFORD, Calif. Researchers at the Stanford University School of Medicine have found a novel way to engineer key cells of the immune system so they remain resistant to infection with HIV, the virus that causes AIDS.
A new study describes the use of a kind of molecular scissors to cut and paste a series of HIV-resistant genes into T cells, specialized immune cells targeted by the AIDS virus. The genome editing was made in a gene that the virus uses to gain entry into the cell. By inactivating a receptor gene and inserting additional anti-HIV genes, the virus was blocked from entering the cells, thus preventing it from destroying the immune system, said Matthew Porteus, MD, an associate professor of pediatrics at Stanford and a pediatric hematologist/oncologist at Lucile Packard Children's Hospital.
"We inactivated one of the receptors that HIV uses to gain entry and added new genes to protect against HIV, so we have multiple layers of protection what we call stacking," said Porteus, the study's principal investigator. "We can use this strategy to make cells that are resistant to both major types of HIV."
He said the new approach, a form of tailored gene therapy, could ultimately replace drug treatment, in which patients have to take multiple medications daily to keep the virus in check and prevent the potentially fatal infections wrought by AIDS. The work was done in the laboratory, and clinical trials would still be needed to determine whether the approach would work as a therapy.
"Providing an infected person with resistant T cells would not cure their viral infection," said Sara Sawyer, PhD, assistant professor of molecular genetics and microbiology at the University of Texas-Austin and a co-author of the study. "However, it would provide them with a protected set of T cells that would ward off the immune collapse that typically gives rise to AIDS."
The study will be published in the Jan. 22 issue of Molecular Therapy.
One of the big challenges in treating AIDS is that the virus is notorious for mutating, so patients must be treated with a cocktail of drugs known as highly active antiretroviral therapy or HAART which hit it at various stages of the replication process. The researchers were able to get around that problem with a new, multi-pronged genetic attack that blocks HIV on several fronts. Essentially, they hope to mimic HAART through genetic manipulation.
The technique hinges on the fact that the virus typically enters T cells by latching onto one of two surface proteins known as CCR5 and CXCR4. Some of the latest drugs now used in treatment work by interfering with these receptors' activity. A small number of people carry a mutation in CCR5 that makes them naturally resistant to HIV. One AIDS patient with leukemia, now famously known as the Berlin patient, was cured of HIV when he received a bone marrow transplant from a donor who had the resistant CCR5 gene.
Scientists at Sangamo BioSciences in Richmond, Calif., have developed a technique using a protein that recognizes and binds to the CCR5 receptor gene, genetically modifying it to mimic the naturally resistant version. The technique uses a zinc finger nuclease, a protein that can break up pieces of DNA, to effectively inactivate the receptor gene. The company is now testing its CCR5-resistant genes in phase-1 and -2 trials with AIDS patients at the University of Pennsylvania.
The Stanford scientists used a similar approach but with an added twist. They used the same nuclease to zero in on an undamaged section of the CCR5 receptor's DNA. They created a break in the sequence and, in a feat of genetic editing, pasted in three genes known to confer resistance to HIV, Porteus said. This technique of placing several useful genes at a particular site is known as "stacking."
Incorporating the three resistant genes helped shield the cells from HIV entry via both the CCR5 and CXCR4 receptors. The disabling of the CCR5 gene by the nuclease, as well as the addition of the anti-HIV genes, created multiple layers of protection.
Blocking HIV infection through both the CCR5 and CXCR4 receptors is important, Porteus said, as it hasn't been achieved before by genome editing. To test the T cells' protective abilities, the scientists created versions in which they inserted one, two and all three of the genes and then exposed the T cells to HIV.
Though the T cells with the single- and double-gene modifications were somewhat protected against an onslaught of HIV, the triplets were by far the most resistant to infection. These triplet cells had more than 1,200-fold protection against HIV carrying the CCR5 receptor and more than 1,700-fold protection against those with the CXCR4 receptor, the researchers reported. The T cells that hadn't been altered succumbed to infection with 25 days.
Porteus said he views the work as an important step forward in developing a gene therapy for HIV.
"I'm very excited about what's happened already," he said. "This is a significant improvement in that first-generation application."
He said a potential drawback of the strategy is that while the nuclease is designed to create a break in one spot, it could possibly cause a break elsewhere, leading to cancer or other cell aberration. He said it's also possible the cells may not tolerate the genetic change.
"It's possible the cells won't like the proteins they're asked to express, so they won't grow," he said.
But he said he believes both problems are technically surmountable. He said the researchers' next step is to test the strategy in T cells taken from AIDS patients, and then move on to animal testing. He said he hopes to begin clinical trials within three to five years.
Though the method is labor-intensive, requiring a tailored approach for each patient, it would save patients from a lifelong dependence on antiretroviral drugs, which have adverse side effects, Porteus noted.
He said he also hopes to adapt these techniques for use against other diseases, such as sickle cell anemia, one of his areas of interest. Porteus works with patients in the Pediatric Bone Marrow Transplant service at Packard Children's.
In addition to Sawyer, he collaborated with Richard Voit, a former Stanford graduate student who is now an MD/PhD candidate at the University of Texas Southwestern Medical Center, and Moira McMahon, PhD, a former postdoctoral scholar at Stanford who is now at the University of California-San Diego.
###
The study was supported by a grant from the American Foundation for AIDS Research and by a Laurie Krauss Lacob Faculty Scholar Award from the Lucile Packard Foundation for Children's Health.
Information about Stanford's Department of Pediatrics, which also supported the work, is available at http://pediatrics.stanford.edu.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
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Immune cells engineered in lab to resist HIV infection, Stanford study showsPublic release date: 22-Jan-2013 [ | E-mail | Share ]
Contact: Ruthann Richter richter1@stanford.edu 650-725-8047 Stanford University Medical Center
STANFORD, Calif. Researchers at the Stanford University School of Medicine have found a novel way to engineer key cells of the immune system so they remain resistant to infection with HIV, the virus that causes AIDS.
A new study describes the use of a kind of molecular scissors to cut and paste a series of HIV-resistant genes into T cells, specialized immune cells targeted by the AIDS virus. The genome editing was made in a gene that the virus uses to gain entry into the cell. By inactivating a receptor gene and inserting additional anti-HIV genes, the virus was blocked from entering the cells, thus preventing it from destroying the immune system, said Matthew Porteus, MD, an associate professor of pediatrics at Stanford and a pediatric hematologist/oncologist at Lucile Packard Children's Hospital.
"We inactivated one of the receptors that HIV uses to gain entry and added new genes to protect against HIV, so we have multiple layers of protection what we call stacking," said Porteus, the study's principal investigator. "We can use this strategy to make cells that are resistant to both major types of HIV."
He said the new approach, a form of tailored gene therapy, could ultimately replace drug treatment, in which patients have to take multiple medications daily to keep the virus in check and prevent the potentially fatal infections wrought by AIDS. The work was done in the laboratory, and clinical trials would still be needed to determine whether the approach would work as a therapy.
"Providing an infected person with resistant T cells would not cure their viral infection," said Sara Sawyer, PhD, assistant professor of molecular genetics and microbiology at the University of Texas-Austin and a co-author of the study. "However, it would provide them with a protected set of T cells that would ward off the immune collapse that typically gives rise to AIDS."
The study will be published in the Jan. 22 issue of Molecular Therapy.
One of the big challenges in treating AIDS is that the virus is notorious for mutating, so patients must be treated with a cocktail of drugs known as highly active antiretroviral therapy or HAART which hit it at various stages of the replication process. The researchers were able to get around that problem with a new, multi-pronged genetic attack that blocks HIV on several fronts. Essentially, they hope to mimic HAART through genetic manipulation.
The technique hinges on the fact that the virus typically enters T cells by latching onto one of two surface proteins known as CCR5 and CXCR4. Some of the latest drugs now used in treatment work by interfering with these receptors' activity. A small number of people carry a mutation in CCR5 that makes them naturally resistant to HIV. One AIDS patient with leukemia, now famously known as the Berlin patient, was cured of HIV when he received a bone marrow transplant from a donor who had the resistant CCR5 gene.
Scientists at Sangamo BioSciences in Richmond, Calif., have developed a technique using a protein that recognizes and binds to the CCR5 receptor gene, genetically modifying it to mimic the naturally resistant version. The technique uses a zinc finger nuclease, a protein that can break up pieces of DNA, to effectively inactivate the receptor gene. The company is now testing its CCR5-resistant genes in phase-1 and -2 trials with AIDS patients at the University of Pennsylvania.
The Stanford scientists used a similar approach but with an added twist. They used the same nuclease to zero in on an undamaged section of the CCR5 receptor's DNA. They created a break in the sequence and, in a feat of genetic editing, pasted in three genes known to confer resistance to HIV, Porteus said. This technique of placing several useful genes at a particular site is known as "stacking."
Incorporating the three resistant genes helped shield the cells from HIV entry via both the CCR5 and CXCR4 receptors. The disabling of the CCR5 gene by the nuclease, as well as the addition of the anti-HIV genes, created multiple layers of protection.
Blocking HIV infection through both the CCR5 and CXCR4 receptors is important, Porteus said, as it hasn't been achieved before by genome editing. To test the T cells' protective abilities, the scientists created versions in which they inserted one, two and all three of the genes and then exposed the T cells to HIV.
Though the T cells with the single- and double-gene modifications were somewhat protected against an onslaught of HIV, the triplets were by far the most resistant to infection. These triplet cells had more than 1,200-fold protection against HIV carrying the CCR5 receptor and more than 1,700-fold protection against those with the CXCR4 receptor, the researchers reported. The T cells that hadn't been altered succumbed to infection with 25 days.
Porteus said he views the work as an important step forward in developing a gene therapy for HIV.
"I'm very excited about what's happened already," he said. "This is a significant improvement in that first-generation application."
He said a potential drawback of the strategy is that while the nuclease is designed to create a break in one spot, it could possibly cause a break elsewhere, leading to cancer or other cell aberration. He said it's also possible the cells may not tolerate the genetic change.
"It's possible the cells won't like the proteins they're asked to express, so they won't grow," he said.
But he said he believes both problems are technically surmountable. He said the researchers' next step is to test the strategy in T cells taken from AIDS patients, and then move on to animal testing. He said he hopes to begin clinical trials within three to five years.
Though the method is labor-intensive, requiring a tailored approach for each patient, it would save patients from a lifelong dependence on antiretroviral drugs, which have adverse side effects, Porteus noted.
He said he also hopes to adapt these techniques for use against other diseases, such as sickle cell anemia, one of his areas of interest. Porteus works with patients in the Pediatric Bone Marrow Transplant service at Packard Children's.
In addition to Sawyer, he collaborated with Richard Voit, a former Stanford graduate student who is now an MD/PhD candidate at the University of Texas Southwestern Medical Center, and Moira McMahon, PhD, a former postdoctoral scholar at Stanford who is now at the University of California-San Diego.
###
The study was supported by a grant from the American Foundation for AIDS Research and by a Laurie Krauss Lacob Faculty Scholar Award from the Lucile Packard Foundation for Children's Health.
Information about Stanford's Department of Pediatrics, which also supported the work, is available at http://pediatrics.stanford.edu.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
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Public release date: 22-Jan-2013
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