Franklin, IN, United States
Franklin, IN, United States

Franklin College is a sixth form college on Chelmsford Avenue in Grimsby, North East Lincolnshire, England, serving more than 2,700 students, including adult learners. Wikipedia.


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News Article | May 17, 2017
Site: www.eurekalert.org

Athens, Ga. - University of Georgia researchers, with colleagues from the University of Tokyo, have identified a new drug target for the two most common types of myeloid leukemia, including a way to turn back the most aggressive form of the disease. They published their findings today in the journal Nature. By blocking a protein called BCAT1, the researchers were able to stop cancer cell growth in mice and human blood samples from leukemia patients. The BCAT1 protein activates the metabolism of a group of amino acids known as branched-chain amino acids, or BCAAs, that are essential building blocks of proteins in all cells and thus necessary for aggressive leukemia cells to grow. The same enzymes are also responsible for the development of brain and lung tumors. Earlier research indicated that BCAT functions to break down the BCAAs in most healthy tissues. The new paper shows for the first time that, rather than to break them down, leukemia cells use the BCAT1 pathway to produce BCAAs. By blocking the protein, researchers can reverse the disease's aggressiveness. "We wanted to understand what is driving aggressiveness in acute leukemia, and then examine whether targeting such a pathway would reverse the disease back to the treatable phase," said Takahiro Ito, senior author on the paper and assistant professor in the Franklin College of Arts and Sciences department of biochemistry and molecular biology. Chronic myeloid leukemia is a kind of blood cancer with three major clinical phases: a chronic phase, an accelerated phase and an acute or blast crisis phase. Chronic leukemia usually responds well to treatments with TKI drugs. But if the cancer is left untreated or resistance develops, mutations will eventually push the disease into the more aggressive blast crisis phase, which is often fatal. "The idea was that these indolent and aggressive leukemia cells have different ways of using nutrients such as amino acids, which regulate the balance between differentiation and cell growth," Ito said. "If we can understand what regulates that balance, we may be able to harness the pathway, to stop the disease progression or revert it back to a less aggressive disease." By analyzing blood and leukemia cells from both the indolent chronic phase and more aggressive blast crisis phase, the research team observed higher concentrations of the BCAAs in the aggressive phase. What was unclear was whether the presence of BCAAs was a consequence or a cause leading to the more aggressive phase. They identified one gene, BCAT1, encoding for an enzyme that can produce BCAAs in the leukemia cells. The team used a knock-down approach to inhibit the function of the gene, to determine BCAT's importance in the aggressive phase, testing the approach in mice and human blood samples from patients with leukemia. By blocking the BCAT1 gene, the research team was able to promote differentiation in the blast crisis cells, making the disease less aggressive and slow growing, similar to the treatable chronic phase. Importantly, although BCAT1 is high in leukemia cells, normal blood cells show low BCAT1 levels, and normal blood cells showed little impact by the BCAT1 inhibition. These findings suggest that BCAT1 may be an ideal therapeutic target that does little harm on normal blood production. Furthermore, results indicated that BCAT1 is also a key player in acute myeloid leukemia, which is more prevalent than the blast crisis chronic myeloid leukemia. Patients with AML with high BCAT1 tend to survive less than those with low BCAT1. Blocking the BCAT1 activity also proved effective on human acute myeloid leukemia cells. "The classical view is that no cells are known to produce BCAA by themselves--it is taken from the food we eat, always utilized as is or to be broken down inside the body," Ito said. "But leukemia cells actually take advantage of this enzyme, use the metabolic reaction in reverse to make BCAAs for their favor--for cell growth and progression to the more aggressive state." The researchers worked with colleagues at the Complex Carbohydrates Research Center Nuclear Magnetic Resonance facility, the UGA Cancer Center, the College of Veterinary Medicine, and the University of Tokyo in Japan. An online version of the full study is available at http://www.


News Article | May 17, 2017
Site: www.sciencedaily.com

University of Georgia researchers, with colleagues from the University of Tokyo, have identified a new drug target for the two most common types of myeloid leukemia, including a way to turn back the most aggressive form of the disease. They published their findings today in the journal Nature. By blocking a protein called BCAT1, the researchers were able to stop cancer cell growth in mice and human blood samples from leukemia patients. The BCAT1 protein activates the metabolism of a group of amino acids known as branched-chain amino acids, or BCAAs, that are essential building blocks of proteins in all cells and thus necessary for aggressive leukemia cells to grow. The same enzymes are also responsible for the development of brain and lung tumors. Earlier research indicated that BCAT functions to break down the BCAAs in most healthy tissues. The new paper shows for the first time that, rather than to break them down, leukemia cells use the BCAT1 pathway to produce BCAAs. By blocking the protein, researchers can reverse the disease's aggressiveness. "We wanted to understand what is driving aggressiveness in acute leukemia, and then examine whether targeting such a pathway would reverse the disease back to the treatable phase," said Takahiro Ito, senior author on the paper and assistant professor in the Franklin College of Arts and Sciences department of biochemistry and molecular biology. Chronic myeloid leukemia is a kind of blood cancer with three major clinical phases: a chronic phase, an accelerated phase and an acute or blast crisis phase. Chronic leukemia usually responds well to treatments with TKI drugs. But if the cancer is left untreated or resistance develops, mutations will eventually push the disease into the more aggressive blast crisis phase, which is often fatal. "The idea was that these indolent and aggressive leukemia cells have different ways of using nutrients such as amino acids, which regulate the balance between differentiation and cell growth," Ito said. "If we can understand what regulates that balance, we may be able to harness the pathway, to stop the disease progression or revert it back to a less aggressive disease." By analyzing blood and leukemia cells from both the indolent chronic phase and more aggressive blast crisis phase, the research team observed higher concentrations of the BCAAs in the aggressive phase. What was unclear was whether the presence of BCAAs was a consequence or a cause leading to the more aggressive phase. They identified one gene, BCAT1, encoding for an enzyme that can produce BCAAs in the leukemia cells. The team used a knock-down approach to inhibit the function of the gene, to determine BCAT's importance in the aggressive phase, testing the approach in mice and human blood samples from patients with leukemia. By blocking the BCAT1 gene, the research team was able to promote differentiation in the blast crisis cells, making the disease less aggressive and slow growing, similar to the treatable chronic phase. Importantly, although BCAT1 is high in leukemia cells, normal blood cells show low BCAT1 levels, and normal blood cells showed little impact by the BCAT1 inhibition. These findings suggest that BCAT1 may be an ideal therapeutic target that does little harm on normal blood production. Furthermore, results indicated that BCAT1 is also a key player in acute myeloid leukemia, which is more prevalent than the blast crisis chronic myeloid leukemia. Patients with AML with high BCAT1 tend to survive less than those with low BCAT1. Blocking the BCAT1 activity also proved effective on human acute myeloid leukemia cells. "The classical view is that no cells are known to produce BCAA by themselves -- it is taken from the food we eat, always utilized as is or to be broken down inside the body," Ito said. "But leukemia cells actually take advantage of this enzyme, use the metabolic reaction in reverse to make BCAAs for their favor -- for cell growth and progression to the more aggressive state."


News Article | April 17, 2017
Site: www.eurekalert.org

Athens, Ga. - When Hurricane Katrina struck Louisiana in 2005, cities inland saw an influx of evacuees escaping the storm and its aftermath. Now, a new University of Georgia study predicts that this could happen again as a result of sea-level rise. In a paper published today in Nature Climate Change, researchers estimate that approximately 13.1 million people could be displaced by rising ocean waters, with Atlanta, Houston and Phoenix as top destinations for those forced to relocate. The study is the first attempt to model the destination of millions of potentially displaced migrants from heavily populated coastal communities. "We typically think about sea level rise as a coastal issue, but if people are forced to move because their houses become inundated, the migration could affect many landlocked communities as well," said the study's lead author, Mathew Hauer, who completed his doctoral degree in the Franklin College of Arts and Sciences department of geography. While sea-level rise assessments are numerous and may help plan for the development of critical infrastructure, few research studies have grappled with where displaced people and families will go. No previous studies model how migration caused by sea-level rise will affect population other than in the directly affected coastal areas. Relationships between environmental stressors and migration are highly complex, as responses range from short-term, temporary migration to permanent, long-distance migration. Sea-level rise is a unique environmental stressor because it permanently converts habitable land to uninhabitable water. The new study combines estimates of populations at risk from sea-level rise within a migrations systems simulation to estimate both the number and destinations of potential sea-level rise migrations in the U.S. over the coming century. "Some of the anticipated landlocked destinations, such as Las Vegas, Atlanta and Riverside, California, already struggle with water management or growth management challenges," Hauer said. "Incorporating accommodation strategies in strategic long-range planning could help alleviate the potential future intensification of these challenges." A full version of the study is available at https:/


News Article | April 17, 2017
Site: www.prweb.com

LearnHowToBecome.org, a leading resource provider for higher education and career information, has released its list of Indiana’s best colleges for 2017. Of the 46 schools honored, 44 four-year schools made the list with University of Notre Dame, Purdue University, DePauw University, Valparaiso University and Butler University taking the top five spots. Ivy Tech Community College and Ancilla College were also included as the best two-year schools in the state. A list of all schools is included below. “Education can make a huge difference when it comes to the job market,” said Wes Ricketts, senior vice president of LearnHowToBecome.Org. “These schools in Indiana have not only shown a commitment to providing quality degree programs, but also the employment services that contribute to student success as they pursue careers.” To be included on the “Best Colleges in Indiana” list, schools must be regionally accredited, not-for-profit institutions. Each college is also scored on additional data that includes annual alumni earnings 10 years after entering college, employment and academic services offered, student/teacher ratio, graduation rate and the availability of financial aid. Complete details on each college, their individual scores and the data and methodology used to determine the LearnHowToBecome.org “Best Colleges in Indiana” list, visit: Indiana’s Best Colleges for 2017 include: Ancilla College Anderson University Ball State University Bethel College-Indiana Butler University Calumet College of Saint Joseph DePauw University Earlham College Franklin College Goshen College Grace College and Theological Seminary Hanover College Huntington University Indiana Institute of Technology Indiana State University Indiana University-Bloomington Indiana University-East Indiana University-Kokomo Indiana University-Northwest Indiana University-Purdue University-Fort Wayne Indiana University-Purdue University-Indianapolis Indiana University-South Bend Indiana University-Southeast Indiana Wesleyan University Ivy Tech Community College Manchester University Marian University Martin University Oakland City University Purdue University-Calumet Campus Purdue University-Main Campus Purdue University-North Central Campus Rose-Hulman Institute of Technology Saint Joseph’s College Saint Mary-of-the-Woods College Saint Mary's College Taylor University Trine University Trine University-Regional/Non-Traditional Campuses University of Evansville University of Indianapolis University of Notre Dame University of Saint Francis-Fort Wayne University of Southern Indiana Valparaiso University Wabash College About Us: LearnHowtoBecome.org was founded in 2013 to provide data and expert driven information about employment opportunities and the education needed to land the perfect career. Our materials cover a wide range of professions, industries and degree programs, and are designed for people who want to choose, change or advance their careers. We also provide helpful resources and guides that address social issues, financial aid and other special interest in higher education. Information from LearnHowtoBecome.org has proudly been featured by more than 700 educational institutions.


News Article | April 19, 2017
Site: www.eurekalert.org

Athens, Ga. - As allergy sufferers can attest, thunderstorm activity can exacerbate asthma and respiratory ailments. In fall 2016, when strong storms moved across southeastern Australia, a major thunderstorm asthma epidemic struck Melbourne and the surrounding area. High grass pollen concentrations dispersed by strong, gusty winds led to multiple deaths and a flood of residents seeking medical attention for respiratory problems. Now, University of Georgia researchers are exploring new ways of predicting thunderstorm asthma outbreaks that may one day provide early warnings for health professionals, emergency management officials and residents in affected areas. The study, published by researchers from UGA and Emory University in the Journal of Applied Meteorology and Climatology, is one of the first to specifically include well-known aspects of thunderstorm diagnostics often used by meteorologists to assess storm severity. According to the study, the combination of rainfall, winds and lightning from thunderstorms in conjunction with pollen or mold spores can worsen asthma symptoms. Rainfall and high humidity rupture bioaerosols, particularly rye grass pollen grains. Thunderstorm electrical activity contributes further pollen fragmentation, and gusty winds can spread pollen granules ahead of the storm. Several of the factors in combination may result in these events reaching epidemic proportions. "Thunderstorm asthma is a very complex phenomenon and involves interactions of allergens like grass pollens, thunderstorms and susceptible groups of people," said lead author Andrew J. Grundstein, professor of geography in UGA's Franklin College of Arts and Sciences. "Our study may help anticipate significant thunderstorms by employing a technique that helps identify wind magnitudes commonly associated with thunderstorm asthma outbreaks." By cross-referencing several forecast modeling tools, and especially as the modeling accuracy and resolution of the tools improve, the public and emergency service providers can be better prepared for the incidence of thunderstorm asthma events. "While this study does not yet provide the capability of predicting thunderstorm asthma outbreaks, our methodology may provide a key piece to the puzzle for alerting public health officials about what storms may trigger an episode and which ones may not," said co-author Marshall Shepherd, Georgia Athletic Association Distinguished Professor of Geography and Atmospheric Sciences. Other authors on the study include Paul Miller, graduate research assistant in the department of geography at UGA, and Stefanie Sarnat, associate professor of environmental health in the Rollins School of Public Health at Emory University. An online version of the full study is available at http://journals.


News Article | April 20, 2017
Site: www.eurekalert.org

Athens, Ga. - Increasing water temperatures are responsible for the accumulation of a chemical called nitrite in marine environments throughout the world, a symptom of broader changes in normal ocean biochemical pathways that could ultimately disrupt ocean food webs, according to new research from the University of Georgia. Nitrite is produced when microorganisms consume ammonium in waste products from fertilizers, treated sewage and animal waste. Too much nitrite can alter the kinds and amounts of single-celled plants living in marine environments, potentially affecting the animals that feed on them, said James Hollibaugh, co-author of the study published recently in Environmental Science and Technology. It also could lead to toxic algal blooms and create dead zones where no fish or animals can live. "Rising ocean temperatures are changing the way coastal ecosystems--and probably terrestrial ecosystems, too--process nitrogen," said Hollibaugh, Distinguished Research Professor of Marine Sciences in UGA's Franklin College of Arts and Sciences. "Much of the global nitrogen cycle takes place in the coastal zone." Hollibaugh and researcher Sylvia Schaefer found midsummer peaks in concentrations of nitrite alongside massive increases in numbers of the microorganisms that produce it in the coastal waters off Sapelo Island, Georgia, in data collected over the course of eight years. Although most researchers believe nitrite accumulation is a consequence of oxygen deficiency in a marine environment, Hollibaugh and Schaefer thought something else had to be driving the accumulation. "The paradigm taught when I was in school was that hypoxia, or lack of oxygen, results in nitrite accumulation," Hollibaugh said. "But the Georgia coast does not go hypoxic. It just didn't fit." After performing lab experiments that exposed the single-celled organisms known as Thaumarchaea to varying water temperatures, the researchers discovered that higher temperatures prompted the microorganisms to produce more nitrite. "The microorganisms involved in this process are very tolerant to low oxygen levels," Schaefer said. "Typically, two groups of microorganisms work in really close concert with one another to convert ammonium to nitrate so that you don't see nitrite really accumulate at all, but we found that the activity of those two groups was decoupled as a result of the increased water temperatures." To see if the pattern held beyond the island, Schaefer and Hollibaugh analyzed environmental monitoring data from 270 locations across the U.S., France and Bermuda, ultimately affirming the relationship between higher temperatures and nitrite accumulation. This dependence on temperature wasn't appreciated by the research community until now, and it can have widespread consequences even beyond coastal water quality management, Hollibaugh said. "The same process, though we didn't look at it specifically, takes place in regards to fertilizing soil for agricultural purposes," he said. "It affects farmers and their efficient use of fertilizer--when they should apply it and what form it should be in--and ultimately much of that fertilizer will end up in the waterways, which can lead to algal blooms that choke out other species." Nitrite accumulation can also result in more production of nitrous oxide, a powerful greenhouse gas that has more of an effect on climate change per molecule than carbon dioxide, Hollibaugh said. That nitrous oxide production then increases global temperatures more, causing more nitrite accumulation and creating a positive feedback loop. "If you live on a marsh and look out over the water, you're probably not going to notice it, but if you like shellfish, like to fish, like recreational water sports, then these findings do matter," Hollibaugh said. "The information gained from monitoring programs, like the ones we used to analyze temperature and nitrite data across the country and in other countries, can be used not only to forecast what is going to happen down the road and the longer-term consequences of management decisions, but also to come up with potential solutions for the problem. The data collected by these programs are important for wise management of our resources." The study was published in Environmental Science and Technology and is available at http://pubs. . The research was supported the National Science Foundation's Division of Ocean Sciences grants 13-35838 and 12-37130.


News Article | December 1, 2016
Site: www.eurekalert.org

Researchers at the University of Georgia have received a $2.78 million grant from the National Institutes of Health to study CRISPR-Cas, a powerful gene editing tool derived from a defense mechanism evolved in bacteria and other single-celled organisms. Like a pair of molecular scissors, CRISPR-Cas allows scientists to precisely edit sequences of DNA in everything from plants to humans, and it could one day be used to silence the genes that predispose humans to myriad diseases, including cancer, diabetes, cardiovascular disorders and mental illnesses. "This is a technology that has taken the scientific world by storm," said Michael Terns, Distinguished Research Professor of Biochemistry and Molecular Biology in UGA's Franklin College of Arts and Sciences and principal investigator for the project. "But there are still a lot of things that we don't know, and this project will help us expand and refine our ability to exploit CRISPR for research and biomedicine." CRISPR is often discussed as a single entity, but there are actually many different CRISPR-Cas systems, Terns said, and researchers are only beginning to understand the complex molecular processes that make these systems work. Fundamentally, CRISPR-Cas is a defense mechanism that single-celled organisms use to ward off attacks from viruses and other invaders. For example, when a bacterium is attacked by a virus, it captures some of the virus's DNA, chops it up into pieces and incorporates a segment of the viral DNA into its own genome. It then uses this DNA to make RNAs that bind with a protein, and this complex seeks out and destroys the viral DNA. As the bacterium experiences more threats, it accumulates a bank of past infections in a special part of its genetic code called CRISPRs--short for clustered regularly interspaced short palindromic repeats. "This ability to cleave DNA is what makes CRISPR-Cas such a powerful research tool, but we don't yet fully understand how many CRISPR-Cas systems capture foreign DNA sequences or how they selectively recognize and destroy foreign nucleic acids," Terns said. "This grant will give us the freedom to explore these processes, which will ultimately speed the development of new methods to fight human disease." In particular, Terns hopes that their discoveries will lead to new methods of combating pathogenic bacteria, especially those that have become resistant to antibiotics. However, Terns is quick to point out that this project is focused primarily on basic science and the examination of fundamental biological processes. "Basic science is what gave us CRISPR in the first place; nobody knew that the most powerful gene editing tool in the world would come from single-celled organisms until scientists did the basic research to discover it," he said. "I don't think CRISPR has revealed all its secrets yet, and there may be even more powerful genetic tools waiting to be found." Terns' research is funded by a grant from NIH's Maximizing Investigators' Research Award, or MIRA. The goal of MIRA is to increase the efficiency and efficacy of National Institute of General Medical Sciences funding by providing investigators with greater stability and flexibility, thereby enhancing scientific productivity and the chances for important breakthroughs.


News Article | November 22, 2016
Site: www.eurekalert.org

A team of scientists led by researchers at the University of Georgia has developed a new mouse model that closely mimics fetal brain abnormalities caused by the Zika virus in humans. This model, described in a paper published recently in the journal Development, may help scientists better understand how the Zika virus affects different cell types in the developing brain, which could hasten the creation of new treatments and diagnostics. Spread mostly by the bite of an infected mosquito, the Zika virus can pass from a pregnant woman to her fetus. This can result in microcephaly, a birth defect in which the brain does not develop properly, resulting in a smaller than normal head. "A lot of the discussion about Zika has focused on microcephaly, and while that is certainly important, we found that the virus causes additional devastating damages to the developing brain as well," said Jianfu "Jeff" Chen, an assistant professor of genetics in UGA's Franklin College of Arts and Sciences. Most notably, Chen and his colleagues, including postdoctoral fellow Qiang Shao and graduate student Stephanie Herrlinger, found that Zika infection leads to abnormal blood vessel formation in the brain and a leaky blood-brain barrier, which normally protects the brain from potentially harmful pathogens. "In addition to neural progenitor cell disruption, which is a classical cause of human microcephaly, we also observed massive death of neuronal cells in our mouse model," Chen said. "This combined with the disruption of the vascular system and the blood-brain barrier results in microcephaly and extensive brain damage." Therefore, he added, "It's not just that the brain is smaller than normal; it is severely injured as a result of the infection, and we need to understand all these effects if we are going to develop successful therapies." The researchers created their model by injecting Zika virus that was isolated in Mexico from an infected mosquito into the brain of mouse embryos. They were then able to observe the neurological effects after the mice were born. "A lot of scientists are looking for postnatal mouse models to study the effects of Zika virus infection, but the virus often causes premature birth in mice," Chen said. "The virus-infected pups in our model were carried to term, and they were born alive. This is important, because some infected babies were also born alive in humans, and establishing a postnatal mouse model will be a good start to understand potential neurological complications after virus infection." Ultimately, the researchers hope that this model will prove useful as researchers around the world work to understand the unique disease mechanisms of the Zika virus and test new therapeutics. For a full version of the study, see http://dev. This research was supported by grants from the National Institutes of Health under grant numbers R00HD073269, R01NS096176, and R01NS097231.


News Article | December 1, 2016
Site: www.eurekalert.org

A new statistical review of 62 studies with over 13,000 individuals found that narcissism has a modest but reliable positive relationship with a range of social media behaviors. The largest effects were with the number of friends/followers narcissists had and frequency of status updates, followed by selfie postings, according to University of Georgia psychology researchers. The two strains of narcissistic behavior--grandiose narcissism and vulnerable narcissism--showed different relationships to social media use. Grandiose narcissism, the more extroverted, callous form, positively related to time spent on social media, the frequency of updates, number of friends/followers, and the frequency of posting selfies. Vulnerable narcissism, the more insecure form, did not show any relationship to social media, but there was relatively little research on this form of narcissism. "The stories you have heard about grandiose narcissism on social media are probably true," said the study's senior author, Keith Campbell, a professor of psychology in the UGA Franklin College of Arts and Sciences. Campbell, co-author of the best-selling "The Narcissism Epidemic," notes that "when you engage with social media, you will be engaging with more narcissism than might really exist in the world. This might distort your view of the world as being more narcissistic than it is." "It is important to remember that these are only correlations, however," said the study's lead author, Jessica McCain, a graduate student in the Behavioral and Brain Sciences Program in the UGA Franklin College of Arts and Sciences department of psychology. "This is not evidence that social media causes narcissism or vice versa. Theoretically, we suspect that individuals with pre-existing narcissism are drawn to social media, but the present evidence only establishes that the two are related." "Networks on social media aren't designed by people in Silicon Valley," Campbell said. "They are built one link at a time by users. And narcissists seem to be central to this build-out." The study, "Narcissism and Social Media Use: A Meta-Analytic Review," was published in the early online edition of Psychology of Popular Media Culture and is available at http://psycnet. .


News Article | November 10, 2016
Site: www.eurekalert.org

Increased enrollment in the Supplemental Nutrition Assistance Program in Georgia contributed to the growth of grocery retailers at all levels from 2007 to 2014. A new paper from University of Georgia researchers used U. S. Department of Agriculture and Georgia Division of Family and Children Services data sets to track the increase in retailers accepting SNAP benefits during what is known as the Great Recession. The publicly available data suggest that increased enrollment in the program improves access to food for SNAP beneficiaries by acting as an indirect subsidy to retailers. The study, "Growth in SNAP Retailers Was Associated With Increased Client Enrollment in Georgia During the Great Recession," was published in the November issue of Health Affairs. The paper connects enrollment increases with the growth in the number of food retailers. The researchers divided food stores into four categories: large, midsize, small and specialty retailers. Between 2008 and 2011, the number of SNAP enrollees increased by 87 percent; between 2007 and 2014, the number of SNAP retailers in Georgia increased by 82 percent, primarily due to growth in the number of small retailers. "In one of the roughest economic patches of the last 100 years, we see this huge boom in stores, which seems counterintuitive. During the recession, rather than closing their doors, we saw the number of SNAP retailers double," said Jerry Shannon assistant professor in the UGA Franklin College of Arts and Sciences department of geography and lead author on the study. "I think that points to the fact that SNAP is very much an economic stimulus and that during times of economic hardship, stores rely on SNAP as much as consumers might. Especially for small stores, it can be a vital source of financial support." The study differentiates how much of the growth was represented by the opening of new stores versus existing stores becoming authorized SNAP retailers. For small stores like the Dollar General chains, gas stations, convenience stores and pharmacies, the breakdown was split roughly 50-50. "SNAP is framed often, and rightly so, as an important support for people who have low incomes. It defrays food insecurity, provides counter-cyclical support for folks when the economy is tough and then tails off when things get better," Shannon said. "That's important, but from practically the genesis of the program, it was designed to support retailers during those rough times as well." The foundation for SNAP was the 1933 Agricultural Adjustment Act. The program, referred to as the Federal Surplus Relief Corporation, was established during the Great Depression, when prices for crops fell and farms across America were struggling to deal with the excess supply. To support farmers, the federal government purchased basic farm commodities at discount prices and distributed them among hunger relief agencies in states and local communities. To formalize food distribution and to avoid duplicating efforts by local relief agencies, the Food Stamp Program was first implemented in 1939 under the administration of President Franklin D. Roosevelt. Over time, the program changed and evolved, maintaining its goal to achieve a more effective use of agricultural overproduction, improve levels of nutrition among individuals with low incomes and provide an economic stimulus to farmers, distributors and retailers. In 2015, the program served over 45 million individuals, and over 250,000 retailers were authorized to accept SNAP benefits nationwide. "When we think about food deserts, or food accessibility, SNAP can help support stores, as it already does in low-income neighborhoods," Shannon said. "But it also highlights the dependence of those stores on SNAP. During the recent economic downturn, convenience stores were most sensitive to the increased enrollment, though they are not generally places where we think of buying healthy foods." Shannon says the research supports new rule changes proposed by the USDA that would require SNAP retailers to provide healthy food as an effective way of improving access to healthy foods more generally. "The data support interventions that would try to help improve nutritional quality of foods available to consumers. It also suggests how SNAP might be useful for other alternative food sites like farmers markets or other local food efforts--programs that help consumers link up with nearby producers," he said. Co-authors on the study are Sarah Shannon, assistant professor in the department of sociology in UGA's Franklin College; Grace Bagwell Adams, assistant professor in the department of health policy and management in the UGA College of Public Health; and Jung Sun Lee, associate professor in the department of foods and nutrition in the UGA College of Family and Consumer Sciences.

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