UVA

Brazil
Brazil

Time filter

Source Type

News Article | March 1, 2017
Site: www.eurekalert.org

The University of Virginia Health System is teaming up with the Virginia Tech Transportation Institute to study novice drivers with autism to determine if they would benefit from specialized training to help them become better, safer drivers and feel more comfortable behind the wheel. Researchers will use a high-tech driving simulator and on-road driving to compare the driving performance of novice drivers with autism with those of novice drivers without autism. The researchers also will look at a group of much more experienced drivers without autism. "With this, we will be able to determine if there is a specific need to give these folks [with autism] further attention and support even after they have a driver's license," said UVA School of Medicine researcher Dan Cox, PhD. "Possibly just to become safer drivers, but also possibly to reduce collisions and driving mishaps." Cox, of UVA's Department of Psychiatry and Neurobehavioral Sciences, noted that the driving abilities of novice drivers with autism -- including reaction time, vision and cognitive abilities -- tend to be similar to those of any individual. Novice drivers with autism, however, may feel additional anxiety about driving in some cases. "Where things become challenging," Cox said, "is in the flexibility and the integration and the multitasking involved in on-road driving." Cox and his colleagues at the Virginia Tech Transportation Institute (VTTI) want to determine if specialized training can help them with those challenges. During the study, Cox will place participants in UVA's high-tech driving simulator, which offers a controlled environment for testing and assessment. "The neat thing about virtual reality is that you can just focus on one task at a time, which you can't in the real world," Cox said. "You can just focus on maintaining speed control, then you can focus on lane position, then once they master that, you can worry about ability to brake. In the real world, you're just thrust out there and you have to deal with it all at the same time." After completing the simulation, study participants will drive on real roads using a research vehicle car VTTI has outfitted with advanced data collection instrumentation. VTTI researchers will then will analyze key safety-related driver behavior. Cox and his colleagues will ultimately compare the simulation with the in-car driving to determine if additional interventions or countermeasures could benefit teen drivers, especially those with autism, and, if so, what form they should take. "These are novice drivers who have been approved. They've satisfied all the DMV requirements for independent drivers. Our goal is to determine if they differ from those without autism, and we then want to determine how these novice drivers in the virtual world and on road differ from experienced drivers," Cox said. "Once you know the differences, you can really drill down in terms of how to do interventions to neutralize those differences." To participate Cox is seeking to recruit 10 novice drivers with autism and 10 without. The novice drivers must have had their licenses for less than 12 months. He also plans to evaluate 10 experienced drivers with more than 10 years behind the wheel, a group Cox expects to draw from the parents of the novice drivers. Trial participants will receive $30 in compensation and an individualized report of their strengths and weaknesses in terms of driving abilities and skills. A single visit to UVA will be required. For more information, contact UVA at (434) 924-8021 or (434) 924-5913. The study is IRB-HSR #19577. The work is being supported by a $60,000 grant from 4-VA, a collaborative partnership of UVA, Tech, George Mason University, James Madison University and Old Dominion University.


News Article | February 15, 2017
Site: www.eurekalert.org

BOSTON - (February 14, 2017) - Joslin Diabetes Center will take part in two clinical trials this year to test artificial pancreas systems designed to automatically monitor and regulate blood glucose levels in people with type 1 diabetes, which would replace traditional methods of managing the disease such as testing blood glucose levels by finger stick or using continuous glucose monitoring systems with separate, non-integrated delivery of insulin by either injections or a pump. Lori Laffel, MD, MPH, Chief of the Pediatric, Adolescent, and Young Adult Section at Joslin Diabetes Center, is Principal Investigator at the Joslin site for the trials, which are among four major research efforts being funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH) to test and refine artificial pancreas systems. If successful, the trials could lead to applications for regulatory approval for use of the devices by people with type 1 diabetes, helping to improve glucose control and reduce the burden of diabetes self-management. Joslin is a site for the International Diabetes Closed-Loop Trial being led by the University of Virginia in Charlottesville (UVA). The trial will provide clinical results of an automated insulin delivery system that features a reconfigured smartphone running advanced algorithms that link wirelessly to a continuous glucose monitor and an insulin pump that the patient wears, as well as a remote-monitoring site, aimed at keeping blood glucose levels in range. In addition, Joslin will be a site for a trial later this year that will compare a hybrid model of an artificial pancreas approved in September 2016 by the U.S. Food and Drug Administration to a next-generation system. One hundred adolescents and young adults (ages 14-30) will test each system for three months during the trial, which will be led by the International Diabetes Center in Minneapolis and the Schneider Medical Center in Israel. "We are entering an era of exceptional opportunity for patients living with type 1 diabetes, with regard to improving glycemic control and enhancing the quality of life for our patients," said Dr. Laffel. "We are very pleased at Joslin to contribute to advancing this initiative through our participation in this important research." The trials are funded under NIH grant numbers DK108483 and DK108611. Joslin Diabetes Center is world-renowned for its deep expertise in diabetes treatment and research. Joslin is dedicated to finding a cure for diabetes and ensuring that people with diabetes live long, healthy lives. We develop and disseminate innovative patient therapies and scientific discoveries throughout the world. Joslin is an independent, non-profit institution affiliated with Harvard Medical School, and one of only 11 NIH-designated Diabetes Research Centers in the U.S. For more information, please visit http://www. .


News Article | February 15, 2017
Site: www.prweb.com

Our culture cherishes youth. Youth is associated with innovation, passion, and well-being. People are searching for ways to maintain their energy and beauty as the years pile on. “Aging is a natural part of life that holds many benefits. On average, people become happier and more content with maturity. But aging has some cons, such as bodily pain and undesired looks. Nowadays, medicine can help people maintain the beauty of their youth as they get older,” says Dr. Suzanne Friedler with Advanced Dermatology PC. One skin issue of particular concern for men and women alike are age spots. “Age spots, or Lentigines, are small patches of light brown or black skin. They are harmless blemishes that appear with age, usually after the 40-year mark. They appear on areas that are consistently exposed to ultra violet light from the sun, such as the face, back of the hands, shoulders, forearms and upper back,” says Dr. Frielder. What causes age spots and who gets them? According to Dr. Friedler, “When an area of the skin is exposed to excessive UV light, those skin cells will produce more melanin, the pigment that gives skin the dark look. In young peoples’ skin, new cells regenerate rapidly to replace the damaged cells. However, this process slows down in older people and these damaged cells clump together and form these brown or black patches.” Dr. Friedler also notes that people with fair skin develop age spots more often since their skin is more susceptible to damage from UV light. Are age spots cancerous? “Before engaging in any treatment, the patient should consult a physician. It’s possible that these dark patches are cancerous cells rather than benign spots of excess melanin. A trained physician will provide the proper diagnosis.” Treatment options for Age spots Creams: Creams can be prescribed or bought over-the-counter. They work by bleaching the damaged area and slowly removing the color. The creams use hydroquinone with or without retinoids, such as tretinoin. This bleaching process takes months to complete. “It’s crucial that people apply sunscreen to the treatment area during this period, since these bleaching creams can make the skin cells more sensitive to damage from UV light,” adds Dr. Friedler. Lasers: Lasers can target specific pigment cells (melanocytes) in the skin and leave the surrounding tissue unharmed. This process is quick and the effects are immediate. Other laser treatments resurface the skin by removing the damaged cells and reveal the healthy cells beneath. Both laser treatments are highly effective. Microneedling: This treatment involves causing micro-injuries to the damaged cells with tiny needles. The body responds by producing new cells to heal over the damaged area, thus blocking the brown skin cells. Several treatments may be required to get the best results. Chemical Peel: This process involves applying a patch of chemicals to the damaged cells. These chemicals burn off the top layer of cells and reveal the healthy cells beneath. Dr. Friedler stresses not to worry about any ill effects, “chemical peels not only remove the damaged cells, but also promote healthy collagen production.” Cryosurgery: This treatment is prescribed if the physician suspects that the spots could be cancerous. It involves applying liquid nitrogen to the damaged cells, which freezes and kills them. Dermabrasion: This treatment involves sanding off the outer layers of damaged skin to reveal the healthy cells beneath. Despite the slew of treatment options, Dr. Friedler stresses the importance of prevention as the best treatment. Wearing sunscreen throughout the year, even in the winter, will reduce the likelihood of developing age spots. Always make sure you buy a broad-spectrum sunscreen that protects against both UVA and UVB rays with an SPF of at least 15.” Suzanne J. Friedler, M.D. F.A.A.D., is a board certified fellow of the American Academy of Dermatology, with expertise in many areas of medical and cosmetic dermatology. She has been with Advanced Dermatology PC since 2002. Advanced Dermatology P.C. and the Center for Laser and Cosmetic Surgery (New York & New Jersey) is one of the leading dermatology centers in the nation with 18 locations in New York and New Jersey, offering highly experienced physicians in the fields of cosmetic and laser dermatology as well as plastic surgery and state-of-the-art medical technologies. http://www.advanceddermatologypc.com.


News Article | March 2, 2017
Site: www.medicalnewstoday.com

Of the more than 3 million people with breast cancer in the United Stated, about 10 percent carry an inherited mutation in their BRCA1 gene. In health, the gene is responsible for suppressing tumors. In disease, the gene goes terribly awry. Scientists at the Virginia Tech Carilion Research Institute found that breast cancer cells can trigger the self-destruction of the tumor-suppressing BRCA1 proteins. They published their results in Scientific Reports, a Nature journal. "There are different ways in which DNA damage can be repaired. The breast cancer susceptibility protein, BRCA1, has an interesting mechanism as a tumor suppressor," said Deborah Kelly, an assistant professor at the Virginia Tech Carilion Research Institute and senior author on the paper. "Unfortunately, where there are mutations in BRCA1, there's a significant decrease in its ability to repair DNA and cells are more likely to become cancerous." Scientists knew the mutations promoted cancer, but they didn't know exactly how BRCA1 physically changed, or how those changes prevented the protein from participating in DNA repair. Kelly and her team focused on a highly prevalent BRCA1 mutation to begin to understand not only the structural changes, but also the functional fallout. Using molecular imaging and biochemical tools, the researchers examined human cancer cells and found that mutated BRCA1 proteins were destroyed under stressful, oxidative cellular conditions. The proteins were unable to properly repair damaged DNA. "The system we use mimics the chain of events resulting from the inappropriate breakdown of estrogen, which produces molecules known as reactive oxygen species that can modify DNA and proteins, contributing to cancer," Kelly said. Healthy cells can manage the damage caused by reactive oxygen species, also called free radicals, with repair proteins. Kelly and her team saw that typical BRCA1 proteins remained relatively stable, but mutated BRCA1 proteins significantly reduced in number. Cells tag the mutated BRCA1 protein for destruction with a molecule called ubiquitin, according to Kelly. The cells then destroy the ubiquitin-tagged BRCA1 proteins, leading to a decrease in their ability to repair DNA lesions. Kelly and her team are not the first to identify ubiquitination, but they are the first to recognize that the process increases in response to the BRCA1 mutation. They suspect that the BRCA1 mutation causes a small misfolding that allows even more ubiquitin to attach to the protein. "Some ubiquitin modifications actually enhance the function of proteins, but, in this case, it acts as a target for degradation," said Kelly, who is also an assistant professor of biological sciences at Virginia Tech's College of Science. "Compared with non-mutated BRCA1 proteins, the ubiquitination process heightens the destruction of mutated BRCA1 proteins. The levels are lowered to a point where its power to assist in genomic maintenance is compromised." The process of ubiquitation is already a target for a potential therapeutic treatment, according to Kelly. It's theoretically possible for enzymes to block or remove the ubiquitin, allowing cells to potentially enhance or restore BRCA1's function as a tumor suppressor. "We demonstrated that protein levels, genetic mutations, and the chemical changes in proteins after they are made, known as post-translational modifications - particularly ubiquitination - can affect BRCA1's functional state in breast cancer cells," Kelly said. "Based on the results of this work, the next logical step is to test mechanistic-based therapies, such as enzymes that remove ubiquitin to restore the physical properties of the mutated BRCA1." Current experiments in the Kelly Lab involve determining the 3D structures of healthy and mutated BRCA1 using high resolution cryo-electron microscopy. This information may help scientists more fully understand the extent to which some individuals with BRCA1 mutations are more disposed to cancer than others, based on physical changes to the BRCA1 protein structure. The research was supported by the Virginia Tech Carilion Research Institute, the Commonwealth Health Research Board, the Concern Foundation, the National Cancer Institute of the National Institutes of Health, and the UVA-VTC Neuroscience Seed Fund Award.


News Article | February 28, 2017
Site: www.eurekalert.org

Of the more than 3 million people with breast cancer in the United Stated, about 10 percent carry an inherited mutation in their BRCA1 gene. In health, the gene is responsible for suppressing tumors. In disease, the gene goes terribly awry. Scientists at the Virginia Tech Carilion Research Institute found that breast cancer cells can trigger the self-destruction of the tumor-suppressing BRCA1 proteins. They published their results today (5 a.m. Eastern Time, Tuesday, Feb. 28) in Scientific Reports, a Nature journal. "There are different ways in which DNA damage can be repaired. The breast cancer susceptibility protein, BRCA1, has an interesting mechanism as a tumor suppressor," said Deborah Kelly, an assistant professor at the Virginia Tech Carilion Research Institute and senior author on the paper. "Unfortunately, where there are mutations in BRCA1, there's a significant decrease in its ability to repair DNA and cells are more likely to become cancerous." Scientists knew the mutations promoted cancer, but they didn't know exactly how BRCA1 physically changed, or how those changes prevented the protein from participating in DNA repair. Kelly and her team focused on a highly prevalent BRCA1 mutation to begin to understand not only the structural changes, but also the functional fallout. Using molecular imaging and biochemical tools, the researchers examined human cancer cells and found that mutated BRCA1 proteins were destroyed under stressful, oxidative cellular conditions. The proteins were unable to properly repair damaged DNA. "The system we use mimics the chain of events resulting from the inappropriate breakdown of estrogen, which produces molecules known as reactive oxygen species that can modify DNA and proteins, contributing to cancer," Kelly said. Healthy cells can manage the damage caused by reactive oxygen species, also called free radicals, with repair proteins. Kelly and her team saw that typical BRCA1 proteins remained relatively stable, but mutated BRCA1 proteins significantly reduced in number. Cells tag the mutated BRCA1 protein for destruction with a molecule called ubiquitin, according to Kelly. The cells then destroy the ubiquitin-tagged BRCA1 proteins, leading to a decrease in their ability to repair DNA lesions. Kelly and her team are not the first to identify ubiquitination, but they are the first to recognize that the process increases in response to the BRCA1 mutation. They suspect that the BRCA1 mutation causes a small misfolding that allows even more ubiquitin to attach to the protein. "Some ubiquitin modifications actually enhance the function of proteins, but, in this case, it acts as a target for degradation," said Kelly, who is also an assistant professor of biological sciences at Virginia Tech's College of Science. "Compared with non-mutated BRCA1 proteins, the ubiquitination process heightens the destruction of mutated BRCA1 proteins. The levels are lowered to a point where its power to assist in genomic maintenance is compromised." The process of ubiquitation is already a target for a potential therapeutic treatment, according to Kelly. It's theoretically possible for enzymes to block or remove the ubiquitin, allowing cells to potentially enhance or restore BRCA1's function as a tumor suppressor. "We demonstrated that protein levels, genetic mutations, and the chemical changes in proteins after they are made, known as post-translational modifications - particularly ubiquitination - can affect BRCA1's functional state in breast cancer cells," Kelly said. "Based on the results of this work, the next logical step is to test mechanistic-based therapies, such as enzymes that remove ubiquitin to restore the physical properties of the mutated BRCA1." Current experiments in the Kelly Lab involve determining the 3D structures of healthy and mutated BRCA1 using high resolution cryo-electron microscopy. This information may help scientists more fully understand the extent to which some individuals with BRCA1 mutations are more disposed to cancer than others, based on physical changes to the BRCA1 protein structure. Brian Gilmore and Yanping Liang, both research associates in Kelly's laboratory, are co-first authors on this paper. Carly Winton, a graduate research assistant who has since graduated with a master's degree from Virginia Tech's Department of Biomedical Engineering and Mechanics; Vasiliea Karageorge, an undergraduate research assistant at Roanoke College; Kaya Patel, a research associate who now attends Tulane University School of Medicine; Cameron Varano, a third-year doctoral student in Virginia Tech's Translational Biology, Medicine, and Health graduate program; and William Dearnaley, a postdoctoral associate in Kelly's laboratory, contributed to the study. Zhi Sheng, an assistant professor at the Virginia Tech Carilion Research Institute, advised on the cancer biology work and aided with the microscopy imaging. The research was supported by the Virginia Tech Carilion Research Institute, the Commonwealth Health Research Board, the Concern Foundation, the National Cancer Institute of the National Institutes of Health, and the UVA-VTC Neuroscience Seed Fund Award.


News Article | February 22, 2017
Site: www.eurekalert.org

Two drugs used to treat asthma and allergies may offer a way to prevent a form of pneumonia that can kill up to 40 percent of people who contract it, researchers at the University of Virginia School of Medicine have found. Influenza pneumonia results when a flu infection spreads to alveolar air sacs deep within the lungs. Normally, a flu infection does not progress that far into the lower respiratory tract, but when it does, the results can be deadly. "If infection is severe enough, and the immune response is potent enough, you get injury to these cells and are no longer able to get sufficient oxygen exchange," explained UVA researcher Thomas J. Braciale, MD, PhD. "As a result of the infection of the cells, you can develop lethal pneumonia and die." But early administration of the two asthma drugs, Accolate and Singulair, could prevent the infection of the alveolar cells deep in the lower respiratory tract, Braciale's research suggests. "The excitement of this is the possibility of someone coming to see the physician with influenza that looks a little more severe than usual and treating them with the drugs Singulair or Accolate and preventing them from getting severe pneumonia," he said. "The fatality rate from influenza pneumonia can be pretty high, even with all modern techniques to support these patients. Up to 40 percent. So it's a very serious problem when it occurs." Unlike bacterial pneumonia, influenza pneumonia is caused by a virus. That makes it very difficult to treat - and makes the possibility of prevention all the more tantalizing. "When we look at pandemic strains of influenza that have high mortality rates, one of the best adaptations of those pandemic viruses is their ability to infect these alveolar epithelial cells," explained researcher Amber Cardani, PhD. "It's one of the hallmarks for certain strains that cause the lethality in these pandemics." Once influenza spreads deep into the lungs, the body's own immune response can prove harmful, resulting in severe damage to the alveolar air sacs. "It's an important observation the field is coming to," Cardani said. "We really need to limit the infection of these lower respiratory airways." The researchers determined that the alveolar epithelial cells are typically protected from influenza infection by immune cells called alveolar macrophages. In some instances, however, the flu virus can prevent the macrophages from carrying out their protective function, allowing the epithelial cells to become vulnerable to infection. "It's not as though they lack alveolar macrophages, it's just that their alveolar macrophages don't work right when they get exposed to the flu," Braciale said. "And those are the types of patients, who potentially would eventually go to the intensive care unit, that we think could be treated early in infection with Accolate or Singulair to prevent infection of these epithelial cells and prevent lethal infection." For their next steps, the researchers are consulting with colleagues to determine if patients being treated with Accolate and Singulair are less likely to develop influenza pneumonia during flu outbreaks. "This was a totally unexpected observation," Braciale said. "When I told multiple colleagues who are infectious disease or pulmonary physicians, they were absolutely flabbergasted." The findings have been published by the scientific journal PLOS Pathogens. It was written by Cardani, Adam Boulton, Taeg S. Kim and Braciale. Braciale and Cardani are both part of UVA's Department of Microbiology, Immunology and Cancer Biology and UVA's Beirne B. Carter Center for Immunology Research. Braciale's primary appointment is with the Department of Pathology. The work was supported by the National Institutes of Health, grant R01AI015608-35, and the NIH's National Institute of General Medical Sciences, grants T32 GM007055 and T32 GM007055.


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

Physicians and patients like to believe that early detection of cancer extends life, and quality of life. If a cancer is present, you want to know early, right? An analysis of cancer screenings by a University of Virginia statistician and a researcher at the National Cancer Institute indicates that early diagnosis of a cancer does not necessarily result in a longer life than without an early diagnosis. And screenings - such as mammograms for breast cancer and prostate-specific antigen tests for prostate cancer - come with built-in risks, such as results mistakenly indicating the presence of cancer (false positives), as well as missed diagnoses (false negatives). Patients may undergo harsh treatments that diminish quality of life while not necessarily extending it. Yet the benefits of early diagnosis through screening often are touted over the risks. "It is difficult to estimate the effect of over-diagnosis, but the risk of over-diagnosis is a factor that should be considered," said Karen Kafadar, a UVA statistics professor and co-author of a study being presented Sunday at a session of the 2017 meeting of the American Association for the Advancement of Science. "How many diagnosed cases would never have materialized in a person's lifetime, and gone successfully untreated? Treatments sometimes can cause harm, and can shorten life or reduce quality of life." Kafadar is not advocating against screening, but her findings show that frequent screening comes with its own risks. As a metric for evaluation, reduction in mortality is considered the standard. So if a disease results in 10 deaths per 100,000 people in a year, and screening reduces the deaths to six per 100,000 people, then there seems to be an impressive 40 percent reduction in mortality. However, a more meaningful metric, Kafadar said, may be: "How much longer can a person whose case was screen-detected be expected to live, versus a case that was diagnosed only after clinical symptoms appeared?" This issue becomes harder to discern - how long a patient survives after a diagnosis versus how long the patient might have lived anyway. Some cancer cases might never become apparent during a person's lifetime without screening, but with screening might be treated unnecessarily, such as for a possibly non-aggressive cancer. And some aggressive forms of disease may shorten life even when caught early through screening. Kafadar and her collaborator, National Cancer Institute statistician Philip Prorok, gathered long-term data from several study sources, including health insurance plans and the National Cancer Institute's recently completed long-term randomized control trial on prostate, lung, colorectal and ovarian cancer, to consider several factors affecting the value of screening - over-diagnosis, lead time on a diagnosis and other statistical distortions - to look at not just how many people die, but also life extension. "People die anyway of various causes," Kafadar said, "but most individuals likely are more interested in, 'How much longer will I live?' Unfortunately, screening tests are not always accurate, but we like to believe they are." Because the paper considers together the factors that affect statistical understanding of the effectiveness of screening, rather than looking at each of these factors in isolation as previous studies have done, it offers a new statistical methodology for teasing out the relative effects of cancer screening's benefits and risks.


News Article | March 1, 2017
Site: www.marketwired.com

MCLEAN, VA--(Marketwired - March 01, 2017) - The MITRE Corporation and the University of Virginia School of Engineering and Applied Science are launching a Systems Engineering Fellowship for Federal Employees intended to help train the next generation of government technology leaders. MITRE is accepting applications through May 26. The program offers military and civilian government employees hands-on project and research experience at MITRE with an accelerated master's degree in systems engineering from UVA. The 12-month program and coursework with UVA faculty take place at MITRE's McLean, Va., campus. An applicant's government employer pays all costs, including salary, UVA tuition, and materials.The sponsoring employer also supports the temporary assignment of its employee to MITRE and relocation to the Washington, D.C., Metro area for one year. Participants will work on projects on behalf of MITRE's federal government sponsors in areas including aviation, civil systems, cybersecurity, defense and intelligence, healthcare, homeland security, and the judiciary. "We are pleased to team with the University of Virginia School of Engineering to help federal employees tackle the systems engineering challenges of today and tomorrow through a unique combination of academic training and work experience," said Alfred Grasso, MITRE president and CEO. "The program will combine six decades of system engineering experience with a contemporary and internationally recognized engineering curriculum to provide a disciplined, hands-on approach to dealing with the increasingly complex challenges facing our nation today." "UVA Engineering is committed to preparing engineering leaders who will help create a better, more advanced society," said UVA Engineering Dean Craig Benson. "We are honored to partner with MITRE to make this excellent opportunity available to federal employees, who play such important roles. Our Accelerated Master's Program is renowned for providing a rigorous, real-world, project-based experience, while allowing working professionals to earn their degrees within a timeframe that is realistic for them." The program's inaugural cohort will begin on August 23. Visit mitre.org for more information about the fellowship experience, eligibility, and Frequently Asked Questions. The MITRE Corporation is a not-for-profit organization that operates research and development centers sponsored by the federal government. Learn more about MITRE at www.mitre.org. The University of Virginia School of Engineering and Applied Science is dedicated to creating knowledge, technologies, and leaders for an advanced society. UVA Engineering's popular Accelerated Master's Program in Systems Engineering started in 1999 to help working professionals earn their degree in a year. Read more about the program here.


News Article | December 29, 2016
Site: www.techtimes.com

Researchers have developed a new warning system that can effectively foresee a toxic algal bloom in a body of water and in turn help resource managers to avert its development well in advance. Toxic algae are the tiny poisonous plants blooming in reservoirs and lakes that pose a severe threat to the ecosystem. The natural toxins produced by the algae are not only poisonous to the aquatic life but also have a huge and adverse impact on the ecosystems. The harmful effects of Harmful Algal Blooms (HABs) include: According to NOAA, HABs are a cause of concern as they not only harmfully affect the marine ecosystems and human health, but are also a threat to the local and regional economies. A study related to the process of reversing algae bloom was carried out by researchers at UVA, the University of Wisconsin-Madison, the Cary Institute of Ecosystem Studies, and Rutgers University. It was found in the research that automated monitoring systems that spot the phenomenon of "regime shift" — such as speedy development of algae leading to exhaustion of oxygen levels in water— can effectively forecast full-sized blooming of algae beforehand and, in turn, can help resource managers in preventing their development. The researchers performed related experiments in a secluded lake in Michigan. The process included initiating a full-scale algae blossoming in the lake by slowly supplementing it with nutrients, and then closely monitoring it. Once the bloom in the lake reached certain predecided limits, the researchers stopped the flow of events. It was found that the growth of algae rapidly declined. Environmental scientist Michael Pace, who led the study, revealed that their automated system perceived early warnings about two weeks before the bloom. "In the experiment where nutrient inputs were cut off when early warnings occurred, the algae bloom was reversed. These whole-lake experiments show that early warning systems can be used to manage algae blooms in lakes, if rapid reductions of nutrient inputs or treatments for algae are possible," said Pace. Pace also noted that instead of depending on early forewarnings it would be a better option to monitor and keep the nutrient inputs in check from the beginning in such a way that algal blooms don't occur at all. The study is published in the journal Proceedings of the National Academy of Sciences. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


News Article | March 3, 2017
Site: www.prweb.com

Beauty Routines, outfits of the day, and latest looks, should all start with the same step – Sun Protection. The stunning differences of our skin should be celebrated, but always protected against the damaging effects of UVA/UVB radiation. Sun Therapè Pro Sport is launching an online campaign to encourage the use of sunscreen in any activity. The need to protect and preserve our skin unites every color and condition. Using the hash tag #theskinyourein, Sun Therapè Pro Sport is asking influencers to tell a ‘skin story’ – Your skin is yours, just yours; you know what it needs, what it likes, and how if feels. A unifying social campaign, the brand hopes Bloggers across the nation will post about their skin in regards to how it performs. Original and compelling stories, since the sun is always with us as we run, walk, jump, bike, climb, hike, stretch, dance, golf, play tennis, chase after kids, kick a ball, swing a bat, and go over the rim. Originally formulated for athletes, Sun Therapè Pro Sport is a dual sunscreen/moisturizer that is non-oily, absorbs quickly, and dries to a silky finish. “Active people don’t want to feel there is a greasy residue on their bodies while they perform,” said Victoria Elizabeth, Professional Golfer, LPGA. “Sun Therapè Pro Sport keeps my grip intact while preserving my skin’s integrity. The Skin You’re In should be protected by a full spectrum SPF with the beauty bonus of age-defying antioxidants.” While those regularly outside think more about environmental damage, Sun Therapè Pro Sport is using this influencer campaign as an authentic reminder to preserve skin through social storytelling. With over 5200 hours of sun exposure a decade, and skin cancer statistics climbing daily, there in no better time to remind everyone to PROTECT The Skin You’re In with Sun Therapè Pro Sport broad spectrum SPF 35. See you in the sunshine.

Loading UVA collaborators
Loading UVA collaborators