Do rich people live longer?

Those looking for a magic elixir to keep them healthy and happy need look no further than their bank account. Wealth and, more broadly, socioeconomic status play powerful roles in determining how long we live.

"It's clear that those who have less wealth will have fewer years to live than those with more wealth," says James Smith, senior economist at the research group Rand. The connection is so widely accepted that researchers have given it a name: "the wealth gradient in mortality." What's far more complicated to understand is why the connection exists, and whether wealth causes better health, or vice versa.

The longest-running longitudinal study of health, run by George Vaillant, a professor of psychiatry at Harvard Medical School, found education to be one of the biggest determinants of longevity, along with behavioral factors -- excessive drinkers were more likely to die young, for example. Out of the 500-plus Harvard students and inner-city Boston men the study has followed since 1937, the Harvard students have lived an average of 10 years longer than the inner-city men, says Vaillant. In fact, three in 10 of the Harvard students reached age 90, compared with the 3% to 5% one would expect.

Among the inner-city men who attended college, health was just as good as that of Harvard students who attended college but not graduate school, says Vaillant. "(The Boston men) went to terrible colleges by Harvard standards, but they did get 16 years of education, and that absolutely evened the playing field," says Vaillant. People who go to college tend to drink less, smoke less, and are less likely to be obese, he adds, all factors that contribute to longevity. In fact, after controlling for education and other factors, Vaillant found that income alone had little effect on longevity.

People who pursue higher education, explains Vaillant, tend be more focused on the future, which probably also helps them make healthier choices. "In order to get an education, especially if you're poor, you have to think you have a future," he says.

Indeed, says Smith, one hypothesis is that "more-educated people are more forward-looking, and when they make decisions, they take into account the future more than uneducated people. A lot of things you might do don't have an immediate negative impact -- excessive drinking, smoking and doing drugs can (feel good in the short-term) -- but the fact is, it's going to kill you in the future." Another possibility is that people with higher levels of education are more likely to maintain their health, have better access to health care, and follow doctors' directions when it comes to taking pills or other instructions.

Smith's research also suggests that causality doesn't just run one way; health contributes to wealth, as well. "Because you are healthy and able to work, you are wealthier," he explains. At the same time, poor health often takes a toll on a person's wealth, either because it prevents one from working or because of expensive medical treatments. Taken together, researchers at the University of Chicago estimate that the gains in life expectancy between 1970 and 2000 resulted in an additional $3.2 trillion a year in national wealth.

Meanwhile, as income disparities continue to grow in this country, so do life expectancy disparities. According to an analysis by the Social Security Administration, life expectancy for 65-year-old men in the top half of the earnings distribution has increased by five years, to 21.5 more years. For those in the bottom half of the earnings distribution, life expectancy has increased just over one year, to 16.1 more years.

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Why some animals live longer than others

ScienceDaily (Mar. 29, 2012) Scientists at the University of Liverpool have developed a new method to detect proteins associated with longevity, which helps further our understanding into why some animals live longer than others.

The team looked at the genome of more than 30 mammalian species to identify proteins that evolve in connection with the longevity of a species. They found that a protein, important in responding to DNA damage, evolves and mutates in a non-random way in species that are longer-lived, suggesting that it is changing for a specific purpose. They found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins.

Findings show that if certain proteins are being selected by evolution to change in long-lived mammals like humans and elephants, then it is possible that these species have optimized pathways that repair molecular damage, compared to shorter-lived animals, such as mice.

The study, led by Dr Joao Pedro Magalhaes and postgraduate student, Yang Li, is the first to show evolutionary patterns in biological repair systems in long-lived animals and could, in the future, be used to help develop anti-aging interventions by identifying proteins in long-lived species that better respond to, for example, DNA damage. Proteins associated with the degradation of damaged proteins, a process that has been connected to aging, were also linked with the evolution of longevity in mammals.

Dr Magalhaes, from the University's Institute of Integrative Biology, said: "The genetic basis for longevity differences between species remains a major puzzle of biology. A mouse lives less than five years and yet humans can live to over 100 for example. If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the aging process.

"We developed a method to detect proteins whose molecular evolution correlates with longevity of a species. The proteins we detected changed in a particular pattern, suggesting that evolution of these proteins was not by accident, but rather by design to cope with the biological processes impacted by aging, such as DNA damage. The results suggest that long-lived animals were able to optimise bodily repair which will help them fend off the aging process."

The research is published in the American Aging Association's journal, Age.

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Duality of Longevity Drug Explained

Rapamycin-induced longevity in mice can be uncoupled from diabetes-inducing side effects

Newswise PHILADELPHIA A Penn- and MIT-led team explained how rapamycin, a drug that extends mouse lifespan, also causes insulin resistance. The researchers showed in an animal model that they could, in principle, separate the effects, which depend on inhibiting two protein complexes, mTORC1 and mTORC2, respectively.

The study suggests that molecules that specifically inhibit mTORC1 may combat age-related diseases without the insulin-resistance side effect, which can predispose people to diabetes.

Senior author Joseph A. Baur, PhD, assistant professor of Physiology, Perelman School of Medicine, University of Pennsylvania, and colleagues at the Whitehead Institute for Biomedical Research and Broad Institute, Massachusetts Institute of Technology, in Cambridge, MA, describe their work in this weeks issue of Science. Baur is also a member of Penns Institute for Diabetes, Obesity, and Metabolism.

The hope is that in the future, we will be able to develop molecules that target mTORC1 specifically, separating out the beneficial effects of rapamycin on aging and disease, and leaving behind the insulin-resistance side effect, says Baur.

Our results demonstrate that reduced mTORC1 signaling is sufficient to extend lifespan and mTORC2 signaling has profound effects on metabolism, says co-first author Lan Ye, PhD, postdoctoral fellow in the Baur lab. Our findings indicate that mTORC2 may be an important player in the pathogenesis of type 2 diabetes and metabolic syndrome."

One Compound, Many Effects Rapamycin extends the lifespan of yeast, flies, and mice and is also an immunosuppressant drug for organ transplants and an anti-cancer drug. It was first discovered as a byproduct of Streptomycin hygroscopicus, a bacterium found in a soil sample from Easter Island, an island also known as Rapa Nui, hence the name. Rapamycin was originally developed as an antifungal agent, but that use was abandoned when it was discovered to have immunosuppressive properties.

The mTOR complexes, for mammalian (or mechanistic) target of rapamycin, are proteins that regulate cell growth, movement, and survival, as well as protein synthesis and transcription. Specifically, there are two mTOR complexes and one mTOR protein. The mTOR protein is the core of both complexes (mTORC1 and mTORC2), which behave differently based on their associated proteins. One or both of the mTOR complexes can be inappropriately activated in certain cancers, and dual-specific inhibitors are being developed as chemotherapeutic agents.

Several theories have been put forward by researchers to explain the observations that patients receiving rapamycin are more prone to developing glucose intolerance, which can lead to diabetes. Chronic treatment with rapamycin impairs glucose metabolism and the correct functioning of insulin in mice, despite extending lifespan. The research team demonstrated that rapamycin disrupts mTORC2 in the mice, and that mTORC2 is required for the insulin-mediated suppression of glucose metabolism in the liver.

On the other hand, they also demonstrated that decreasing mTORC1 signaling was sufficient to extend lifespan independently from changes in glucose metabolism. They used a mouse strain in which mTORC1 activity was decreased and saw that lifespan was extended by 14 percent, yet the animals had normal glucose metabolism and insulin sensitivity.

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Duality of Longevity Drug Explained

Genetic study yields longevity clue

Published: March. 29, 2012 at 7:36 PM

LIVERPOOL, England, March 29 (UPI) -- British scientists say their genetic studies have helped detect proteins associated with longevity, helping explain why some animals live longer than others.

The researchers examined the genome of more than 30 mammalian species to identify proteins that evolve in connection with the longevity of a species, the University of Liverpool reported Thursday.

A particular protein -- involved in responding to DNA damage -- evolves and mutates in a non-random way in species that are longer-lived, the researchers found, suggesting it is changing for a specific purpose.

The study is the first to show evolutionary patterns in biological repair systems in long-lived animals, they said.

The findings may help develop anti-aging interventions by identifying proteins in long-lived species that better respond to DNA damage, they said.

"The genetic basis for longevity differences between species remains a major puzzle of biology," researcher Joao Pedro Magalhaes said. "A mouse lives less than five years and yet humans can live to over 100, for example.

"If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the aging process."

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Genetic study yields longevity clue

Plan to merge labs for biofuel research criticized

A plan by Lawrence Berkeley Laboratory to merge its energy labs into a major new research facility in Richmond where scientists would work to develop biofuels through genetic engineering came under fire Wednesday by activists who fear that dangerous new microbes would be created there.

And even if the venture succeeds in transforming plants into biofuels by altering the genes of microbes, the activists argued, the Richmond lab could become an unregulated front for corporate interests and turn millions of acres of croplands used to grow food in underdeveloped countries into huge plantations for energy production.

Their protests reflect deep concerns about the dramatic new science called "synthetic biology," an unfamiliar term that in part involves engineering the genes of microbes to transform worthless plants like switchgrass into potentially unlimited sources of energy. The controversy also recalls an epic time in science nearly 40 years ago when manipulating genes was in its infancy and the public was deeply fearful that some genetically altered "Andromeda Strain" microbe might escape and imperil the world with unknown diseases.

That fear was largely ended when, after a 1975 conference at Asilomar near Monterey, biologists, lawyers and physicians agreed on enforceable guidelines for proceeding with genetic engineering projects.

It marked the first time that scientists agreed to be regulated and led to the public start of recombinant DNA research and what would become the huge international biotech industry.

Concerns about engineering "synthetic biology" are arising anew among activists.

On Wednesday, they gathered at the Center for Genetics and Society in Berkeley to express their concerns that the new research lab would be a poorly regulated entity with ties to unknown energy companies, that the work there would expose employees to dangerous microbes and, if successful, ultimately rob undeveloped nations of their croplands.

"This is a wild, wild, dangerous world," said Becky McClain, a onetime molecular biologist at a Pfizer lab in Connecticut who claimed that she had been sickened by a genetically engineered virus and was fired for speaking out about it.

"We can't afford to leave it to the corporations to self-regulate," said McClain, who won a $1.37 million lawsuit against Pfizer as a whistle-blower.

Gopal Dayaneni, an Oakland organizer, argued that the entire project - with so many engineered microbes - should never be built where earthquake hazards are high.

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Plan to merge labs for biofuel research criticized

New insights into how cells duplicate their DNA

ScienceDaily (Mar. 29, 2012) In the beginning ... but how do you begin? That question has long perplexed scientists in fields from cosmology to anthropology. Fortunately, researchers at the Office of Science's Brookhaven National Lab (Brookhaven Lab) are beginning to get at the answer on a small but important scale -- in biology.

Specifically, the researchers looked at how cells begin to duplicate their DNA, so they can then begin to replicate themselves. DNA is the essential stuff of beginnings. Its double strands -- which consist of chemical 'letters' or base pairs -- tell cells how to remake themselves; how to build the protein machines that keep them alive and make them distinct. So before they divide, cells have to duplicate their DNA.

This is a relatively straightforward affair for bacteria (and other simple cells, also called prokaryotes) since they typically only have a single loop of DNA, even though it can be millions of base pairs long. As a consequence, they have just a single point along the strand where the copying starts, called an origin of replication.

However, most of biology that can be seen with the naked eye -- animals and plants and even humble yeast -- is composed of more complicated cells called eukaryotes. Eukaryotes have much more DNA, which is tightly wound into distinct pieces, or spindles, called chromosomes, each of which may have many origins of replication. 'Top gun' cells, say those in humans, have a need for speed, since they have some 3.4 billion DNA base pairs, all of which have to be pulled apart and copied. So in order to finish in a reasonable amount of time, those cells have to begin copying their DNA simultaneously at tens of thousands of different points.

But how do they begin? Namely, how do protein machines find and bind to the right spots along the DNA strands, and then set them up for copying? That's what the team at Brookhaven Lab studied. They used an imaging method known as cryo-electron microscopy to take extremely high resolution images of how the right proteins come together at the right point on the DNA strands, forming a structure called an "origin recognition complex" (ORC). The lab's first-of-a-kind images (taken using yeast cells, which are also eukaryotes), showed how the shape of the complex changes as it sets the DNA up for duplication.

Scientists then gathered additional details about individual parts of the structure from previously made X-ray crystallography images, which showed the positions of many individual portions of the complex. Then they took all of their information and ran a detailed computer simulation, which gave scientists a good idea of how the whole process works.

That's important since beginnings can go bad, and uncontrolled cell division is the hallmark of many cancers. The new insights from Brookhaven Lab might lead to new ways to attack cancers at a basic level, one reason that the research was also supported by the National Institutes of Health.

But there's also a deeper reason to do basic research. Beginnings are one of the most precious opportunities of all, the chance to create, to discover. That's what happens with each new experiment run at National Laboratories supported by the Office of Science: Each day it's a new chance to begin againin the beginning.

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Posted in DNA

DNA evidence contaminated in case of MI6 spy found in bag

A second area of the investigation has also proved futile, the pre-inquest review heard. While police released sketches of a Mediterranean couple who allegedly let themselves into Mr Williams' flat, the coroner referred to the couple as a "red herring".

Gareth Williams' family believe an unknown third party, a "member of some agency specialising in the dark arts of the secret service," was either present when he died or entered the flat afterward to destroy or remove evidence, Anthony O'Toole, the family's lawyer, said.

Dr Fiona Wilcox, the London coroner investigating the bizarre death of the 31-year-old code breaker and maths genius, told the hearing at Westminster coroner's court that whether Mr Williams was alive inside the bag and locked it himself "was at the very heart of this inquiry". Experts say it is very unlikely he could have locked himseld inside the bag.

Speculation

Speculation and theories about the death have ranged from a solo sex game gone wrong to murder by foreign agents.

Police found Mr Williams' body in his Pimlico flat on 23 August 2010. The keys to the padlock were inside the bag and he is believed to have died a week before the discovery of his body.

The coroner also revealed a long witness list of about 30 people who will be called when the five-day hearing begins in April.

Among those testifying will be experts from Counter Terrorism Command, known as SO15, vetted to examine Mr Williams' computers and phones found at the scene.

A number of agents, listed only by an initial, will testify from MI6 and GCHQ, the government communications headquarters, where Mr Williams worked before his secondment to MI6.

Police have also revealed Mr Williams visited bondage websites months before his death and accessed sites were people were tied up. Tickets to a drag show and women's clothing valued at 15,000 were also found in the central London flat.

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DNA evidence contaminated in case of MI6 spy found in bag

Posted in DNA

Wetherby to Waco – DNA lab's demise

30 March 2012 Last updated at 01:05 ET By John Henry BBC News, Wetherby

Scientists working at the Forensic Science Service laboratories in West Yorkshire led the world in DNA profiling, the senior scientist at the site said.

The 150-strong team of experts at the lab off Audby Lane handled crucial evidence from a number of high-profile cases for police forces across the globe.

But 35 years after it opened and began using the cutting-edge forensic techniques that were the stuff of television dramas, its doors have shut for the last time.

Principal Forensic Scientist Tim Clayton said the closure would "lead to the loss of 1,000 years' experience".

Forensic work has been distributed to police forces and private sector providers because the Home Office said the service was economically unviable and incurred "huge losses".

The union Prospect said it was "deeply disappointed" by the closure.

Mr Clayton said that during a "purple patch" of a decade from the early 1990s most of the major DNA investigations across the world went through the laboratory.

He said: "This lab had, by historical accident, developed DNA technology that developed into the [DNA] database.

"From 1993 this lab had a world-leading role despite its minor geographical significance, leading the whole of the UK and international excellence in the field of DNA.

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Wetherby to Waco - DNA lab's demise

Posted in DNA

Biology professor wins national award for contributions to citizen science

MEDIA CONTACT: Hilary Dickinson at dickinsonh@beloit.edu or 608-363-2849

Marion Field Fass named 2012 winner by the National Center for Science and Civic Engagement

Marion Field Fass, biology professor and co-chair of Beloits health and society interdisciplinary program, has won the 2012 William E. Bennett Award for Extraordinary Contributions to Citizen Science. The announcement was made on Wednesday by the Science Education for New Civic Engagements and Responsibilities.

Dr. Fass has been a distinguished, long-time, unflagging, unfailing, and imaginative contributor to the precursor health and higher education and HIV/AIDS education work that led to the creation of Science Education for New Civic Engagements and Responsibilities (SENCER), wrote David Burns, the executive director of the National Center for Science and Civic Engagement, in a letter to Beloit College President Scott Bierman.

First presented in 2009, the William E. Bennett Award for Extraordinary Contributions to Citizen Science was established by NCSCE and named in honor of its first recipient for his lifetime contributions to citizen science. The award is given annually to an individual and/or a team whose SENCER and other related activities have made exemplary and extraordinary contributions to citizen science.

I'm really honored to be receiving the Bennett Award for Contributions to Citizen Science, Fass said. It is really an honor for the institution that has nurtured and supported SENCER approaches across the curriculum. Science at Beloit College is exceptional in that we encourage students to focus on real world problems as they learn the basic concepts and methods of these disciplines. The SENCER approach complements the work of the BioQUEST Curriculum Consortium and the CHEMLinks project, which both originated at Beloit College, that have really pushed the boundaries of science pedagogy.

Fass will be honored at the annual SENCER Summer Institute in San Jose, Calif., in August when she will share her thoughts on her work and this award. She was nominated for the award by her colleagues in the department of biology and the health and society program.

Marion has demonstrated unwavering dedication to the creation and communication of interdisciplinary opportunities that guide students and faculty to a better understanding of the intersection and overlap between science and civic issues, wrote Fasss colleagues in their nomination letter.

Fass has taught biology at Beloit College since 1991 and served as chair of the department from 2009-2011. Among her many affiliations, she is currently a faculty member at the SENCER Summer Institute, a SENCER leadership fellow, a member of the American Public Health Association, and an executive board member of the Wisconsin Health Education Network. Fass earned a B.A. from the University of Pennsylvania and a doctorate from Johns Hopkins University. For more information on Fass, see her biography here.

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Pine Manor College Awarded $600,000 National Science Foundation Grant to Support Women Studying Biology

BOSTON, MA--(Marketwire -03/29/12)- Pine Manor College announced today it is the recipient of a $600,000 grant from the National Science Foundation. The grant will provide 20 Pine Manor biology students with targeted educational support, research opportunities and financial aid, enabling them to continue their studies and enter the workforce or pursue graduate degrees.

"We're proud of this partnership with the National Science Foundation and its decision to invest in Pine Manor's students," said Dr. Alane Shanks, president of Pine Manor College. "This grant is really a tribute to the outstanding work of our students and faculty."

In 2008, the National Science Foundation awarded Pine Manor a grant of more than $570,000 to help educate the first 20 BioScholars. Building on this success, with the 2012 grant, Pine Manor will select 20 new students during the next two years.

"We believe this program makes a real difference in the lives of these students and allows women to pursue careers in science after receiving the excellent education Pine Manor offers," President Shanks said. "Each year, a number of promising biology students lack the resources to stay in school and graduate. Our experience with this program has taught us that access plays a crucial role in helping students continue to graduation and beyond."

Each participant will receive a scholarship up to a maximum of $10,000 annually. This scholarship support will continue for the BioScholars through to graduation.

The students will also be enrolled in an Honors Colloquium in Biology, a senior research internship, and workshops to help them obtain graduate school admission and/or life sciences employment. Biology and math tutors will also work with the BioScholars.

Pine Manor College, one of the most diverse liberal arts colleges in the nation, is celebrating its centennial this year.

About Pine Manor CollegePine Manor College is a private, affordable four-year liberal arts college dedicated to preparing women for roles of inclusive leadership and social responsibility in their workplaces, families and communities. The College consistently ranks among the most diverse B.A. liberal arts colleges in the nation, according to US News & World Report's America's Best Colleges. Pine Manor College is located in Chestnut Hill, Mass., five miles from Boston. http://www.pmc.edu.

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Pine Manor College Awarded $600,000 National Science Foundation Grant to Support Women Studying Biology

The Readers’ Writers: Author and biochemist Robert L. Switzer, PhD

Retired professor emeritus of biochemistry Robert Switzers book A Family Farm: Life on an Illinois Dairy Farm is his own familys rich history and loving devotion to the life they chose. Within the pages live four generations, from the start of the farm in 1916 to its heart-wrenching dismantlement under an auctioneers gavel in 1991. A Family Farm isnt just the journey of the Switzer farm, it is our own odyssey as a civilization, and a warning that if we do not tend to the strengths, labors and devotion that provided our foundations, we, too, could become an interesting exhibit in a quaint museum.

Readers wont just learn about the rigors of farm life, but about the people themselves as we follow the authors mother filled with dreams of a scholarly future, only to see the Great Depression snuff those dreams, and her return to the farm with her husband who performed his chores and taught in a rural schoolhouse as well. The story is an emotional rollercoaster, because thats what small farm life is.

Q. You and your brother Steve left farm life to pursue other careers, thereby unknowingly dooming your familys farm. Is this book a strand of conscience cleansing as well as the documenting of a rich history?

A. Near the end of his life, Dad coaxed Steve and me to keep the farm in the family, even though he knew that neither of us were free to operate it. It was a painful moment, but we wouldnt lie to himwe intended to sell the farm after he was gone. Economic and practical factors overrule sentiment in the passing of small family farms.

On a more personal level, I think the decision hurt Steve more than it did me. I confess that I was happy to leave the farm, and I was fortunate to be able to pursue a career in scientific research and education that I loved. Brashly, I never looked back until I was much older.

Q. What do you believe first inspired your grandparents to choose farming in northwest Illinois, especially considering they primarily utilized outdated methodology for their time?

A. They were like many rural people of the time: they stayed where they grew up and they did what they knew. Neither Grandpa nor Grandma had an education beyond the eighth grade, and they had grown up on farms. They were slow to adopt new methods and equipment because they were always cash-poor. Grandpa had an additional handicap: he suffered from narcolepsy, so he was afraid of falling asleep while operating motorized machinery.

Q. As your parents early dreams had involved scholarly pursuits, how instrumental were they to your decision to bring your academic dreams to fruition?

A. Their influence, especially the influence of my mother, can hardly be overstated. She had been an excellent student, completed a college degree with honors in 1931, and had an opportunity to pursue graduate studies in biology at Cornell, but was frustrated by the Great Depression. In some sense, I was acting out her dream in becoming a university professor. I think Dads feelings were more ambivalent; he was proud of what I accomplished, but hurt a bit by my rejection of the farm life he had chosen. In his own way Dad was something of an intellectual, though. He enjoyed discussing history, politics and literature. I recall him reciting fragments of French poetry while we were milking cows.

Q. You wisely elected to include photographs and artwork in your book. How supportive has your and your brothers families been to this project?

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The Readers’ Writers: Author and biochemist Robert L. Switzer, PhD

Honors Students Lead Effort to Plant Campus Garden

(KATV, Source: UofA) Fayetteville - University of Arkansas Honors College students have led a campus-wide effort to plant a community garden that will provide fresh produce and flowers to the Full Circle Campus Food Pantry, a student-run emergency food assistance program recently honored at the White House. Two years of research and planning, along with countless hours of hands-on work with soil, compost and seedlings will culminate in the dedication of the new campus community garden at 3:30 p.m. on Monday, April 2.

Emily Crossfield, an honors biochemistry major in the J. William Fulbright College of Arts and Sciences has led the effort to get the garden in the ground. More than 50 students from multiple disciplines have worked together to design and plant the garden, fostering connections across campus. Crossfield said for her the project is as much about the people as the plants.

"I'm meeting people I never would have met otherwise," said Crossfield, who also serves as director of sustainability for the Associated Student Government. She sees the garden as an important tool for promoting community as the campus grows.

"As a freshman in a big class you can feel lost, but if you're working with 10 other students in the garden, you're going to get to know each other pretty well," she said.

Inspired by community gardens that she saw while studying in Berlin, Crossfield decided to plant a campus community garden as the capstone project required for her minor in sustainability. Her efforts have revolved around finding a good site and building partnerships across campus. The Associated Student Government and Residents' Interhall Congress have provided substantial funding for the garden, with additional support from the department of facilities management and two registered student organizations, GroGreen and the Horticulture Club.

"Emmy has worked hard to bring a lot of people together on this, and there have been lots of ups and downs," said Curt Rom, a professor of horticulture and honors program director for the Bumpers College. "She has provided the leadership to get this garden going."

The new garden builds on research by Samantha Jones, a recent honors graduate of Bumpers College who surveyed 86 universities with community gardens and visited six of them to document best practices in her honors thesis. Her feasibility study, directed by Rom, was undertaken after an earlier garden located at the university's Agricultural Research and Extension Center proved not to be sustainable.

The location of the new garden, close to two residence halls should help ensure ongoing support.

"You need the garden to be visible, where people pass by it, notice it and can easily take care of it," Crossfield said.

The site is not without challenges. Sandwiched between two four-story wings of Maple Hill, the garden is short on sunlight in certain areas and hampered by poor soil. The students have divided the small plot into three zones based on the amount of sunlight received, planting shade-loving perennials and herbs such as basil, rosemary and sage in the back of the garden. Two truckloads of topsoil and one truckload of compost, some of it recycled from residence hall food waste, have created a rich bed for growing broccoli, peppers, squash and tomatoes. One-half of the fresh produce will go to the student volunteers, while one-half will be donated to the Full Circle Campus Food Pantry. The students will also plant day lilies, cannas, irises and hostas to donate to the food pantry and to the chancellor's office for use at university events.

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Westhampton junior receives national research scholarship

Emily McFadden, a Westhampton College junior and biochemistry major, recently received the national Beckman Scholarship for outstanding undergraduate research in the chemistry and biological sciences.

The Beckman Scholars Program , established in 1997, was designed to provide scholarships that contribute significantly in advancing the education, research training and personal development of select students in biochemistry and its relative fields, according to the programs website. The nationwide scholarship is awarded to six undergraduate students each year.

McFadden, one of the six students selected to receive the scholarship in 2012 , said the $19,200 grant would cover her research costs for the next two summers and her senior year.

The grant funds travel to symposiums and conferences across the country where I can present my research, McFadden said. It also plays for supplies in my lab.

McFaddens research, which she has been conducting for the past year and a half, takes place in a Gottwald biochemistry lab with the help of a faculty mentor.

Ive been researching a specific enzyme involved in DNA repair, McFadden said. My upcoming project is looking at an alternative enzyme, and comparing the two to see how their efficiency in DNA repair is different.

McFadden said the final culmination of her research would take place next summer, when she would present her project results at the Beckman Scholars Conference in California.

Ill have the opportunity to show my work to the members of the Beckman Foundation, as well as any other scientists who may be interested in my findings, McFadden said.

Michelle Hamm , associate professor of chemistry at the University of Richmond , serves as McFaddens mentor and nominated McFadden to receive the scholarship.

Emily is a bright and talented student with a passion for science, Hamm said. The Beckman award is for future scientific leaders, and I thought that description fit Emily well.

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Westhampton junior receives national research scholarship

Winners named in Marin elementary school science fair

Students in the fourth through sixth grades throughout Marin entered 115 projects in the annual Marin County Elementary Science Fair sponsored by the Marin County Office of Education.

The projects were on display Tuesday at Vallecito Elementary School in San Rafael. Students developed a hypothesis, tested that hypothesis through data collection and analysis and then developed conclusions based on their investigations.

Grand Prize winners are:

Behavioral science: Lizzie Ferguson, sixth grade, Saint Mark's School, "The Eyes and Ears of Learning."

Engineering science: Jack Eisele and Quinn Woodhead, sixth grade, Saint Mark's School, "Insulating Fun."

Environmental science: Blake Benson, Nick Cauz and Jack De Graves, fifth grade, Dixie Elementary School, "Lead Is In What?"

Life science: Sasa Plichta, fourth grade, Brookside School Upper Campus, "How Does Light Affect Egg Laying In Chickens?"

Physical science: Daniel Ongaro, sixth grade, St. Anselm School, "Which Pipe Can Retain The Most Heat?"

Also, the Marin County Dental Society Award was presented to Payton Alonzo and Cassidy Bruner, fifth grade, Brookside School Upper Campus, "Which Toothpaste Works Best to Remove Stains From An Eggshell?"

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Winners named in Marin elementary school science fair

Syneron to Highlight New Opportunities & Trends in the Dynamic Body Shaping Market at the 2012 Anti-Aging Medicine …

YOKNEAM, ISRAEL--(Marketwire -03/29/12)- Syneron Medical Ltd. (NASDAQ: ELOS - News), the leading global aesthetic device company, announced today that it will host a joint symposium on Body Shaping featuring its VelaShape body contouring system and the recently acquired UltraShape focused ultrasound fat lipolysis system at the 2012 Anti-Aging Medicine World Congress & Medispa Conference in Monte Carlo. The symposium will feature an overview of Syneron's complementary product offerings for body shaping and a review of the pre-clinical and clinical experience with the UltraShape system. It will also feature two thought-leading physician speakers that will discuss their experience with the VelaShape and UltraShape systems.

Event: Brunch Symposium - "NEW Opportunities & Trends in the Dynamic Body Shaping Arena"

Speakers: Shimon Eckhouse, Ph.D., Co-founder and Chairman of the Board of Directors of Syneron Medical

Lior Greenbaum, Ph.D., Clinical Director of UltraShape

Chris Inglefield, M.D., Plastic Surgery Clinic at the London Bridge Hospital

Dean Adel, M.D., Head of Plastic Surgery Division at Rabin - Schneider Medical Center, Petah Tikva

Click here for speaker biographies and event agenda.

Time: 11:00 am

Location: Le Meridien Beach Plaza Hotel 22 Avenue Princesse Grace Monte Carlo 98000 Monaco

Louis P. Scafuri, Chief Executive Officer of Syneron Medical, said, "The symposium provides the first opportunity following the acquisition of UltraShape for Syneron to highlight the synergies associated with our proprietary technologies and the UltraShape focused ultrasound technology to deliver comprehensive body shaping treatments. More than 7,000 VelaShape systems have been sold worldwide since its launch, demonstrating the strong patient demand for body contouring treatments with our safe and efficacious els technology. We believe there is a tremendous opportunity to offer our VelaShape customers the UltraShape system to further enhance their patients' body shaping results. Syneron remains committed to be the global market leader in non-invasive body contouring."

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Syneron to Highlight New Opportunities & Trends in the Dynamic Body Shaping Market at the 2012 Anti-Aging Medicine ...

On the path to age-defying therapies

Public release date: 29-Mar-2012 [ | E-mail | Share ]

Contact: Nicole Giese Rura rura@wi.mit.edu 617-258-6851 Whitehead Institute for Biomedical Research

FINDINGS: The drug rapamycin has been shown to extend lifespan in lab animals, yet rapamycin has also been linked to impaired glucose tolerance and insulin sensitivity, two hallmarks of diabetes. By teasing apart rapamycin's activity at the cellular level, researchers at Whitehead Institute and the University of Pennsylvania have determined that inhibiting only the protein cluster known as the mechanistic target of rapamycin complex 1 (mTORC1) prolongs life in mice without adversely affecting glucose tolerance or insulin sensitivity.

RELEVANCE: With this novel understanding of how rapamycin produces its anti-aging effects, researchers may be able to develop a drug that specifically targets mTORC1, thereby promoting longevity while preventing the adverse effects associated with rapamycin.

CAMBRIDGE, Mass. (March 29, 2012) One of the secrets to a longer, healthier life is simply to eat less. When subjected to calorie restriction (CR), typically defined as a 20-40% reduction in caloric intake with corresponding maintenance of proper nutrition, animals in labs not only live longer, but also have improved insulin sensitivity and glucose tolerance, both of which decline during aging.

Yet, for all of its benefits, CR's restricted diet is a stumbling block for most Americans. If only we had a drug that could do the same thing.

Well, we do, sort of. The drug rapamycin, which is used for immunosuppression in organ transplantations, mimics the longevity effects of CR and may tap into the same cellular pathway as CR. Unlike CR, however, rapamycin actually impairs glucose tolerance and insulin sensitivity, two hallmarks of diabetes. Clearly, rapamycin is doing something CR is not.

To understand better rapamycin's benefits and risks, researchers from the lab of Whitehead Institute Member David Sabatini and Joseph Baur, assistant professor of Physiology, at the University of Pennsylvania's Perelman School of Medicine, have discovered precisely how rapamycin is behaving at the cellular level. Their intriguing results are published this week in the journal Science.

"We know that despite its adverse effects, rapamycin still prolongs lifespan, so there's a potential that we could make it better by just having lifespan affected and not induce the adverse effects," says Sabatini, who is a professor of biology at MIT and a Howard Hughes Medical Institute (HHMI) investigator. "The data in this paper suggest that it's possible."

Rapamycin, which is also called sirolimus and marketed in the United States as Rapamune, is a known inhibitor of the mechanistic target of rapamycin complex 1 (mTORC1), a protein complex that regulates many cellular processes linked to growth and differentiation. mTORC1 is part of a cellular signaling pathway, called mTOR, which responds to nutrients and growth factors. Mechanistic target of rapamycin complex 2 (mTORC2) is also part of the mTOR pathway and regulates insulin signaling.

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On the path to age-defying therapies

Anatomy of a Smokies search

Things werent looking good. After five days of searching and zero clues, a massive search for a missing man in the Great Smoky Mountain National Park was at a critical juncture.

Lets try to make another hard push for this guy today, Joe Ponds, a supervisory park ranger, told a group of about 60 search-and-rescuers gathered near a makeshift command center last Thursday morning, March 22.

Searchers were upbeat that today would be the day the day they would get a break in the search, that they would find their guy or at the very least, a sign that he was still out there.

Marching orders were clear. Check all natural or manmade shelters. Talk to anyone and everyone they saw. Keep their eyes peeled for any leads such as a reported sighting or a Camel Crush cigarette butt, the brand Derek Lueking smoked.

Following the daily pep talk, nearly three dozen searchers split into 14 teams to begin the sixth day of combing through the densely forested national park where Lueking, 24, of Louisville, Tenn., disappeared that previous Saturday morning.

Hope was still alive that Lueking would be found. The unseasonably warm weather has given him a better chance at survival than typically afforded lost hikers this time of year.

SEE ALSO: Motives of missing man remains a mystery

But, one cannot ignore the fact that by day six, most lost hikers would have already been found. Searchers believed Lueking was ill prepared for an extended trip into the woods, taking nothing more than a daypack with him.

At this point, about 90 percent of missing hiker cases have resolved themselves either the search team finds the person or they emerge from the woods on their own, said Bob Miller, a spokesman for the Great Smoky Mountain National Park.

There is no set number of days, however, when search crews decide its time to pull the plug. As long as there are leads, the park rangers would keep at it.

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Anatomy of a Smokies search

Client Build 5 UPDATE: Personal Super Computer 2011 (SR-2 X5690 OCZ Vertex 3 GTX590 Nvidia Tesla) – Video

06-06-2011 12:48 Ok everyone, here is the much anticipated update and progress report on my Client Build 5: PSC 2011. We've had somewhat of a rough going on things, fitment issues on the mobo tray, defective motherboard and some paint issues. Allow these setbacks have been unfortunate, we've made a lot of progress as well. This build is going to be epic! 🙂 Enjoy, Trubyd44 T

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Client Build 5 UPDATE: Personal Super Computer 2011 (SR-2 X5690 OCZ Vertex 3 GTX590 Nvidia Tesla) - Video