News

Newswise — 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.” Ounce of prevention 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.” Stopping the flu virus 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.” Findings published The findings have been published online 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.   SEE ORIGINAL STUDY
Newswise — Research Triangle Park, NC— Pot brownies may be a thing of the past as there are new edible marijuana products, or edibles, on the market, including chocolates, candies, and cookies. These products are legally sold in Colorado and Washington, and according to a new study conducted by RTI International, changes to their labels are needed to ensure people know what they are consuming and that they are safely consuming the products. The new study published in the International Journal of Drug Policy, found that many of the adults who participated in the study are not reading labels, and if they are, information is often hard to decipher. “We discovered that people think there is too much information listed on the labels of edibles, thus potentially overlooking important information on consumption advice” said Sheryl C. Cates, corresponding author of the study and senior research policy analyst at RTI. “Our study also determined that labels often do not make it clear that the product contains marijuana, which can lead to accidental ingestion.” Researchers conducted four focus groups in Denver and Seattle with 94 adult consumers and nonconsumers. Participants revealed concerns with edible labels, and suggested that more needs to be done to inform and educate consumers and nonconsumers about the possible risks of edibles. In 2012, Colorado and Washington became the first two states in the United States to legalize marijuana for recreational use with retail sales starting in 2014. According to the Colorado Department of Revenue, edibles accounted for nearly half of total marijuana sales in the state for 2014. In Washington, edibles accounted for about 40 percent of marijuana sales according to Washington State Liquor and Cannabis Board (reported in 2016). “As the popularity of edibles grow, it is important that labels clearly and concisely provide consumers important information,” Cates said. “Web- and video-based education and using graphics on labels may be easy, cost-effective ways to inform buyers and the public.” Since conducting this research, the states of Colorado and Washington have changed some of the requirements for labeling of edibles based on increasing public concern. Lessons learned from Colorado and Washington, can help inform the labeling of edibles as additional states allow the sale of edibles for recreational use. To learn about RTI’s marijuana research, visit our Emerging Issues page. SEE ORIGINAL STUDY
Newswise — There are neurons in your skin that are wired for one purpose and one purpose only: to sense itchy things. These neurons are separate from the ones that detect pain, and yet, chemical-induced itch is often accompanied by mild pain, such as burning and stinging sensations. But when it comes to sending signals toward your brain through your spinal cord, itch and mild pain can go through the same set of spinal cord neurons, researchers report Feb. 22 in Neuron. This finding explains why pain often accompanies intense, chemical-induced itch. “To our surprise, we found the spinal cord neurons receiving the peripheral pain and itch inputs are not separate. They can receive signals from itch fibers and also pain fibers,” says Xinzhong Dong, Ph.D., professor of neuroscience at the Johns Hopkins University School of Medicine and Howard Hughes Medical Institute investigator, who led the study. These neurons, called the GRP neurons, are a way station for pain and itch signals on their way to the brain. However, GRP neurons are not passive conduits, the researchers found. “When we eliminate this population of neurons in mice, the itch response is reduced. They scratch less,” says first author Shuohao Sun, a graduate student at Johns Hopkins. “But at the same time, the pain response is actually increased.” Mice without GRP neurons spent more time rubbing and licking to alleviate their pain, induced, for example, by exposing their tails to hot water. Further experiments that tracked electrical signaling through the neurons corroborated the result. Even though the GRP neurons seemed to be forwarding mild pain signals to the next neural relay station, they also seemed to mitigate intense pain signals. “It might sound counterintuitive, but we suggest that this small group of cells actually functions like a braking system for pain,” says Sun. “This brake is not always triggered by the painful stimuli; it’s only triggered by the strong pain stimuli. When the brake is on, the signal doesn’t go through. But when you have a weak pain signal, it doesn’t trigger the brake, and the signal can go through.” The researchers have named this hypothesis “the leaky gate” model. When the mice’s GRP neurons have been destroyed, the brake lines have essentially been cut, resulting in an uncontrolled cascade of pain. The braking system may be a way for animals to detect mild pains — like the kinds associated with itchy substances — without becoming overwhelmed by the pain, the researchers say. Built-in pain management would likely be a helpful adaptation for escaping from predators while injured. At the same time, GRP neurons are not the only group of spinal cord neurons that receive and forward pain signals to the brain, and the brain itself plays a central role in translating signals from peripheral neurons into experienced sensation. Questions remain about what happens to the signals from GRP neurons after they’re transported up the spinal cord. Chronic pain and itch affect about one in 10 Americans, the authors say. A better understanding of pain and itch signals’ journey to the brain may eventually lead to new treatment options. “The next step is moving even further into the central nervous system and seeing how the signal from the secondary neuron is getting to the next relay station,” says Dong. “We go one step at a time.” Other authors on the paper are Qian Xu and Yun Guan of the Johns Hopkins University School of Medicine, and Changxiong Guo and Qin Liu of Washington University School of Medicine. This work was supported by the National Institute of Dental and Craniofacial Research (grant number R01DE022750) and the National Institute of Neurological Disorders and Stroke (grant number R01NS054791).
Newswise — The implementation of state laws legalizing same-sex marriage was associated with a significant reduction in the rate of suicide attempts among high school students – and an even greater reduction among gay, lesbian and bisexual adolescents, new Johns Hopkins Bloomberg School of Public Health research suggests. The researchers, publishing Feb. 20 in JAMA Pediatrics, estimate that state-level, same-sex marriage policies were associated with more than 134,000 fewer adolescent suicide attempts per year. The study compared states that passed laws allowing same-sex marriage through Jan. 2015 to states that did not enact state-level legalization. A Supreme Court decision made same-sex marriage federal law in June of 2015. The findings show the effect that social policies can have on behavior, the researchers say. “These are high school students so they aren’t getting married any time soon, for the most part,” says study leader Julia Raifman, ScD, a post-doctoral fellow in the Department of Epidemiology at the Bloomberg School. “Still, permitting same-sex marriage reduces structural stigma associated with sexual orientation. There may be something about having equal rights – even if they have no immediate plans to take advantage of them – that makes students feel less stigmatized and more hopeful for the future.” Suicide is the second most common cause of death among people ages 15 to 24 in the United States (behind unintentional injury). Suicide rates have been rising in the U.S., and data indicate that rates of suicide attempts requiring medical attention among adolescents increased 47 percent between 2009 and 2015. Gay, lesbian and bisexual high school students are at particular risk. In the new study, 29 percent of gay, lesbian and bisexual high school students reported attempting suicide in the previous year as compared to six percent of heterosexual teens. For the study, Raifman and her colleagues analyzed data from the Youth Risk Behavior Surveillance System, a survey supported by the Centers for Disease Control and Prevention. The data included 32 of the 35 states that enacted same-sex marriage policies between Jan. 1, 2004 and Jan. 1, 2015. The researchers used data from Jan. 1, 1999 to Dec. 31, 2015 to capture trends in suicide attempts five years before the first same-sex marriage policy went into effect in Massachusetts. They were also able to compare data with states that did not enact same-sex marriage laws. They conducted state-by-state analyses, comparing, for example, suicide attempt rates in a state like Massachusetts before same-sex marriage was legalized to the period right after. State same-sex marriage legalization policies were associated with a seven percent reduction in suicide attempts among high school students generally. The association was concentrated in sexual minorities, with a 14 percent reduction in suicide attempts among gay, lesbian and bisexual adolescents. The effects persisted for at least two years. The states that did not implement same-sex marriage saw no reduction in suicide attempts among high school students. It’s unclear whether the political campaigns surrounding same-sex marriage legalization were behind the reduction in suicide attempts or the laws themselves. Still, they found that the reduction in suicide attempts wasn’t realized until after a law was enacted. In a state that would go on to pass a law two years in the future – when there was likely to be much conversation in the public about it – suicide attempts remained flat before passage. Healthy People 2020, a program run by the U.S. Department of Health and Human Services (HHS), has a goal of reducing adolescent suicide rates by 10 percent by 2020. The new research suggests that the legalization of same-sex marriage has been very effective in making progress toward that goal. Despite the large reduction in suicide attempts among gay, lesbian and bisexual high school students, this population still attempts suicide at higher rates than their straight peers. “It’s not easy to be an adolescent, and for adolescents who are just realizing they are sexual minorities, it can be even harder – that’s what the data on disparities affecting gay, lesbian, and bisexual adolescents tell us,” Raifman says. She says gay, lesbian, and bisexual adolescents are also at increased risk of substance abuse, depression and HIV. Despite evidence of disparities, she says there are no population-level programs aimed at reducing suicide attempts in gay, lesbian and bisexual students. She says schools and medical providers must understand that students who are sexual minorities are at higher risk and be on high alert. While Raifman found that legalizing same-sex marriage appears to be positively associated with reducing suicide attempts, policies that take away rights or add to stigma could have the opposite effect. “We can all agree that reducing adolescent suicide attempts is a good thing, regardless of our political views,” Raifman says. “Policymakers need to be aware that policies on sexual minority rights can have a real effect on the mental health of adolescents. The policies at the top can dictate in ways both positive and negative what happens further down.” “Difference-in-Differences Analysis of the Association Between State Same-Sex Marriage Policies and Adolescent Suicide Attempts” was written by Julia Raifman, Ellen Moscoe, Bryn Austin and Margaret McConnell. The research was supported by grants from the National Institutes of Health’s National Institute on Aging (T32AI102623) and National Institute of Mental Health (R25MH083620) as well as the Maternal and Child Health Bureau, Health Resources and Services Administration at HHS (T71-MC-00009 and T76-MC-00001).
Newswise — LOS ANGELES – Cedars-Sinai neuroscientists have uncovered processes involved in how the human brain creates and maintains short-term memories. “This study is the first clear demonstration of precisely how human brain cells work to create and recall short-term memories,” said Ueli Rutishauser, PhD, associate professor of Neurosurgery in the Cedars-Sinai Department of Neurosurgery and the study’s senior author. “Confirmation of this process and the specific brain regions involved is a critical step in developing meaningful treatments for memory disorders that affect millions of Americans.” The study’s findings, published online Feb. 20 and in the April print edition of Nature Neuroscience, involve a type of brain cell, called a persistently active neuron, that is vital for supporting short-term memory. Results indicate that this specific type of neurons remain active for several seconds when a person is required to memorize an object or image and recall it at a later time. The findings reveal critical new information on how the human brain stores and maintains short-term memories – the ability to remember ideas, thoughts, images and objects during a time frame of seconds to minutes. Short-term memory is essential for making decisions and mental calculations. “Because impaired short-term memory severely weakens someone’s ability to complete everyday tasks, it is essential to develop a better understanding of this process so new treatments for memory disorders can be developed,” said Jan Kamiński, PhD, a neuroscientist at Cedars-Sinai and lead author of the study. Researchers found persistently active neurons in the medial frontal lobe as well as the medial temporal lobe. The neurons remained active even after the patient stopped looking at an image or object. Until now, the medial temporal lobe was thought to be involved only in the formation of new long-term memories. Now, however, the new findings show that both areas of the brain are critical for maintaining short-term memory and rely upon the ongoing activity of the neurons for memorization. During the study, a team of Cedars-Sinai neurosurgeons implanted electrodes to precisely locate the source of seizures in 13 epilepsy patients. Investigators then studied the electrical activity of individual neurons while patients performed a memory test. During the test, patients viewed a sequence of three images, followed by a two-to-three-second delay. Then patients were shown another image and were asked to decide whether they had previously seen the image. “A surprising finding of this new study is that some of the persistently active neurons were only active if the patient memorized a specific image,” Kamiński said. “For example, the researchers discovered a neuron that reacted every time the patient memorized an image of Han Solo, a character in the movie Star Wars, but not any other memory.” Another key finding of the study was a correlation between the strength of the neurons’ activity and the ability to later make use of the memory. “We noticed that the larger the increase in activity, the more likely the patient was to remember the image. In contrast, if the neuron’s activity was weak, the patient forgot the image and thus lost the memory,” said Adam N. Mamelak, MD, professor of Neurosurgery, director of Functional Neurosurgery at Cedars-Sinai and a co-author of the study. Keith L. Black, MD, chair of the Department of Neurosurgery at Cedars-Sinai, said the breakthrough can be credited to the partnership between neurosurgery and neurology clinicians working with neuroscientists. “This unique collaboration allows us to discover the mechanisms of memory in the human brain,” Black said. “This is key for moving closer to finding treatments for memory disorders, epilepsy and other diseases.” Rutishauser said a next step is understanding how multiple areas of the brain work together to support short-term memory. “Now that specific neurons that support short-term memory have been discovered, we have a way to study their interaction systematically,” he said. Other Cedars-Sinai study contributors included Jeffrey Chung, MD, director of the Epilepsy Program and the Neurophysiology Laboratory; and Shannon Sullivan, research associate. Ian Ross, MD, a neurosurgeon at Huntington Memorial Hospital also contributed. This work was supported by National Science Foundation grant 1554105, National Institute of Mental Health grant R01MH110831, the McKnight Endowment Fund for Neuroscience, a NARSAD Young Investigator grant from the Brain & Behavior Research Foundation (23502), and the Pfeiffer Foundation. # # #
Newswise — PHILADELPHIA— Cervical cancer is the leading cause of cancer deaths for women low- and middle-income countries, including Botswana, where 75 percent of cervical cancer patients suffer from advanced forms of the disease. These patients can face wait times as long as five months after diagnosis before receiving lifesaving treatment. A new, multidisciplinary model of cervical cancer care developed by a University of Pennsylvania team based in Botswana cut the delay between diagnosis and treatment by more than 50 percent, according to research published this month in the Journal of Global Oncology. Limited access to preventive screenings combined with the HIV epidemic are driving the high rate of cervical cancer in Botswana, which has the second highest HIV prevalence in the world. The risk of developing cervical cancer in women infected with HIV is three- to six–fold higher than those who are HIV-negative. In Botswana, more than two-thirds of all cervical cancer cases occur among women who are also living with HIV. However, radiation therapy is not available at in public clinics in Botswana, requiring patients to seek care at private hospitals, which can be a cumbersome process with wait times as long as five months. “With so many women suffering from advanced cervical cancer in Botswana, long delays between treatment and diagnosis can mean the difference between life and death,” said Surbhi Grover, MD, MPH, director of Global Radiation Oncology in the Perelman School of Medicine at the University of Pennsylvania and head of Oncology at Princess Marina Hospital in Botswana. “We saw an urgent need to develop a care program that gives cervical cancer patients the treatment they need as quickly as possible.” Grover and her fellow researchers at Princess Marina Hospital developed a multidisciplinary team (MDT) approach to streamline care and communication between providers and get patients to treatment facilities faster. Weekly care team meetings were established across providers, including radiation oncologists, clinical oncologists, gynecologists, nurse coordinators, and palliative care specialists to discuss patient cases and develop treatment plans. The teams also worked to together to submit paperwork and other documentation, further reducing delays in treatment and simplifying the overall process. “While this type of model might seem common in the United States or other developed countries, it’s actually a quite complicated process that lacks a global standard of guidelines,” Grover said. “We saw many different models across the world, but no published outcomes on how to successfully implement an MDT approach for cervical cancer care.” Over a six-month period, the team saw 135 patients, 60 percent of whom were diagnosed with cervical cancer and 42 percent had locally advanced cancer the required chemo-radiation. However, thanks to the MDT model, 62 percent of those patients required only one clinic visit to coordinate care, reducing the time between diagnosis and treatment initiation by more than 50 percent, with the median delay from biopsy to treatment initiation cut to 39 days from an average of 108 days before the new care model. “With this model, we’ve shown that the MDT approach works in a resource-limited setting and actually helps address several challenges providers face,” Grover said. “Many of our patients must travel long distances or face other barriers that prevent them from returning to the clinic for multiple visits. Offering patients a comprehensive treatment plan during one clinic visit is a game-changer.” Similar MDT models are being developed for head and neck cancer, breast cancer, and palliative care in Botswana. A follow-up clinic is also being piloted where patients with gynecological cancer receive continued follow-up care after chemotherapy and radiation are complete. All patients seen in the Penn MDT clinic will be linked to this new clinic and will receive regular communication about follow-up care. “What this approach really shows is the importance of integrated care and treatment models,” Grover said. “We hope our MDT model will be applied on a broad scale across many different illnesses and clinics in resource-limited settings worldwide.” ###
Newswise — Australia could save AUD $3.4 billion (USD $2.3 billion) in healthcare costs over the remaining lifetimes of all Australians alive in 2010 by instituting a combination of taxes on unhealthy foods and subsidies on fruits and vegetables, according to a new study published in PLOS Medicine by Linda Cobiac, from the University of Melbourne, Australia and colleagues. An increasing number of Western countries have implemented or proposed taxes on unhealthy foods and drinks in an attempt to curb rates of dietary-related diseases, however the cost-effectiveness of combining various taxes and subsidies is not well-understood. In the new study, researchers modeled the effect of taxes on saturated fat, salt, sugar, and sugar-sweetened beverages and a subsidy on fruits and vegetables on the Australian population of 22 million alive in 2010. They simulated how different combinations of these taxes and subsidies—designed so there would be less than a one percent change in total food expenditure for the average household—impacted the death and morbidity rates of Australians as well as healthcare spending over the remainder of their lives. The greatest impact, the researchers concluded, came from a sugar tax, which could avert 270,000 disability-adjusted life years (DALYs, or years of healthy lifespan across the population lost due to disease). “That is a gain of 1.2 years of healthy life for every 100 Australians alive in 2010,” the authors say. “Few other public health interventions could deliver such health gains on average across the whole population.” A salt tax was estimated to save 130,000 DALYS over the remainder of the lives of Australians alive in 2010, a saturated fat tax 97,000 DALYs, and a sugar-sweetened beverage tax 12,000 DALYs. Combined with taxes, the fruit and vegetable subsidies made for additional averted DALYs and reduced health sector spending, but on their own were not estimated to lead to a clear health benefit. Overall, when combined to maximize benefits, the taxes and subsidies could save an estimated 470,000 DALYs and reduce spending by AUD $3.4 billion (USD $2.3 billion). “Simulation studies, such as ours, have uncertainty. For example, we are reliant on other research estimating the responsiveness of the public to changes in food prices. There are also implementation issues for the food industry.” “Nevertheless, this study adds to the growing evidence of large health benefits and cost-effectiveness of using taxes and regulatory measures to influence the consumption of healthy foods,” the authors say. “We believe that with such large potential health benefits for the Australian population and large benefits in reducing health sector spending…the formulation of a tax and subsidy package should be given more prominent and serious consideration in public health nutrition strategy.” “Several countries have imposed taxes on sugary drinks, with the UK the latest to consider such a policy. Our research suggests that even bigger health gains and cost savings may be possible with food taxes and subsidies on a wider range of foods.” Research Article Funding: LJC was supported by a National Health and Medical Research Council Fellowship (Grant number 1036771; www.nhmrc.gov.au). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.   Competing Interests:LJC is a member of the Editorial Board of PLOS Medicine. Citation:Cobiac LJ, Tam K, Veerman L, Blakely T (2017) Taxes and Subsidies for Improving Diet and Population Health in Australia: A Cost-Effectiveness Modelling Study. PLoS Med 14(2): e1002232. doi:10.1371/journal.pmed.1002232   Author Affiliations:Centre for Health Policy, School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia School of Public Health, The University of Queensland, Herston, Queensland, Australia, Burden of Disease Epidemiology, Equity and Cost-Effectiveness Programme, Department of Public Health, University of Otago, Wellington, Wellington, New Zealand     SEE ORIGINAL STUDY
Newswise — WINSTON-SALEM, N.C. – In medieval Europe, when astrology and blood-letting were frequently employed in the diagnosis and treatment of disease, one therapy for rabies was to place some pieces of hair from the rabid dog onto the victim’s bite wound. It didn’t work. But it did give rise to the notion that “the hair of the dog that bit you” – a drink – can cure a hangover. This concept is rather ancient, too, having first appeared in print in 1546. It doesn’t work, either. “There’s no scientific evidence that having an alcoholic drink will cure a hangover,” said Laura Veach, Ph.D., director of screening and counseling intervention services and training in the Department of Surgery at Wake Forest Baptist Medical Center. “It will, at best, postpone one.” A hangover develops when an elevated concentration of alcohol in the blood caused by drinking falls sharply after drinking stops. The symptoms – usually some combination of headache, thirst, fatigue, dizziness, nausea and general grumpiness – reach their peak when the blood-alcohol level hits zero. “Taking a drink the morning after may temporarily make you feel better because you’re putting alcohol back into the system,” said Veach, who holds a doctoral degree in counseling. “But it doesn’t cure the hangover; it just sort of tricks you by masking the symptoms. They’re going to show up eventually.” So is there no cure? “Rest, hydration and aspirin can help some, but they won’t make the hangover go away,” Veach said. “The only real cure is time.” What if you want to help somebody who’s tipsy, buzzed, smashed or otherwise inebriated get sobered up? You give them black coffee, right? “No, all that does is give you a wide-awake drunk,” Veach said. The liver, she explained, detoxifies alcohol in the system and does so at only one rate, which is about one drink per hour. “There’s nothing we know of that can speed up that process,” Veach said. “Not drinking coffee, taking a shower, standing on your head, getting slapped, walking around outside in the cold. Nothing.”
Newswise — WASHINGTON — In the first successful randomized trial of its kind, researchers have provided preliminary evidence that telephone-based smoking cessation counseling given to smokers shortly after undergoing lung cancer screening can be effective at helping people stop smoking. “We found that at this teachable moment — a time when smokers are thinking about their health and may be ready to make a change — offering help makes a difference, and may help save lives,” says the study’s lead researcher, Kathryn L. Taylor, PhD, a behavioral scientist and a professor of oncology at Georgetown Lombardi Comprehensive Cancer Center. The study published February 14 in the journal Lung Cancer, was led by researchers at Georgetown Lombardi and conducted with 92 participants at three centers — MedStar Georgetown University Hospital in Washington, DC, Hackensack University Medical Center in New Jersey, and Lahey Hospital and Medical Center in Massachusetts. “Millions of current smokers are now eligible for lung cancer screening, so this setting represents an important opportunity to exert a large public health impact on cessation among smokers who are at very high risk for multiple tobacco-related disorders,” she says. “This is a great way to engage smokers who have not sought out cessation help.” These study findings were so promising that investigators have been funded through NIH to conduct a much larger study of telephone-based cessation counseling. It will enroll 1,300 patients at five medical centers nationwide. Lung cancer screening recommendations issued in 2013 by the U.S. Preventive Services Task Force suggest that people who have smoked long enough to have accumulated a minimum of 30 pack-years (i.e., one pack per day for 30 years, or two packs per day for 15 years, etc.) should have an annual low-dose CT lung cancer screening test. The idea is to intervene early enough that disease spotted on the screening can be effectively treated. In the U.S., lung cancer is the leading cancer killer in both men and women — almost 160,000 Americans were expected to die from lung cancer in 2016, according to the American Lung Association. Taylor points out that the NIH has said that effective smoking cessation programs should be a part of screening programs, and has funded several groups of researchers to develop effective strategies. In this preliminary study, 92 people about to undergo lung cancer screening agreed to receive either telephone counseling or standard of care (a list of free and low-cost cessation resources). Once participants received their screening results, they were randomized to one of the two groups, each with 46 participants. Each group had an equal number of participants with abnormal screening findings, indicating possible precancerous lesions or chronic obstructive pulmonary disease (COPD). Each group also contained an equal number of participants with minor abnormalities on their screen, as well as those with normal results. None of the participants were diagnosed with lung cancer. Participants in the telephone-counseling group were given their first session after finding out their screening results. Over the next three months, six 10-15 minute sessions were conducted. At the end of the study, a nicotine saliva test was given to participants who said they had quit in order to confirm their abstinence. Researchers found that eight (17 percent) people in the telephone counseling group had verifiably quit, compared to two (4 percent) in the other group. “If this preliminary study is replicated, telephone counseling has the potential to improve cessation in a setting that reaches a large number of hard-to-reach, long-term smokers who are at very high risk for multiple tobacco-related diseases,” Taylor says. Charlotte Hagerman, who along with Taylor, offered the telephone counseling to participants, describes the counseling as “a motivational intervention. Everyone acknowledged that smoking is very harmful to their health, but some people thought it was too late to change their fate. Counseling helped them understand that it is not too late.” Population-based studies have shown that older smokers who quit can have an increased life expectancy, Taylor says. Hagerman says there were also a number of participants who “were ready to quit, and were very excited to receive the help we were offering. I found this very gratifying, and felt that what we were doing was important and mattered to people,” says Hagerman, who was trained as a tobacco treatment specialist for the study. “More than 50 percent of participants said in their first interview that they were not ready to quit, yet some of these people did quit. This finding indicates that it is important to offer the cessation intervention to everyone who undergoes lung cancer screening, and not only those who are already considering quitting. This is exactly what we hope for – to be able to reach the people who are not already planning to quit on their own,” says Taylor. In addition to Taylor and Hagerman, co-authors from Georgetown University Medical Center include George Luta, PhD; Paula G. Bellini, MA; and Cassandra Stanton, PhD. David B. Abrams, PhD, and Ray Niaura, PhD, are Georgetown faculty and also affiliated with the Schroeder Institute for Tobacco Research and Policy Studies. Jenna A. Kramer, NP and Eric D. Anderson, MD are from MedStar Georgetown University Hospital in Washington, DC; Shawn Regis, PhD, Andrea McKee, MD, and Brady McKee, MD, are from Lahey Hospital and Medical Center, Burlington, MA; and Harry Harper, MD and Michael Ramsaier, BS are from Hackensack University Medical Center, Hackensack, NJ. The authors report having no personal financial interests related to the study. The study was supported by the Prevent Cancer Foundation and Georgetown Lombardi’s NCI Cancer Center Support Grant P30 CA051008. About Georgetown Lombardi Comprehensive Cancer CenterGeorgetown Lombardi Comprehensive Cancer Center is designated by the National Cancer Institute as a comprehensive cancer center — the only cancer center of its kind in the Washington, DC area. A part of Georgetown University Medical Center and MedStar Georgetown University Hospital, Georgetown Lombardi seeks to improve the diagnosis, treatment, and prevention of cancer through innovative basic and clinical research, patient care, community education and outreach, and the training of cancer specialists of the future. Connect with Georgetown Lombardi on Facebook (Facebook.com/GeorgetownLombardi) and Twitter (@LombardiCancer). About Georgetown University Medical CenterGeorgetown University Medical Center (GUMC) is an internationally recognized academic medical center with a three-part mission of research, teaching and patient care (through MedStar Health). GUMC’s mission is carried out with a strong emphasis on public service and a dedication to the Catholic, Jesuit principle of cura personalis -- or "care of the whole person." The Medical Center includes the School of Medicine and the School of Nursing & Health Studies, both nationally ranked; Georgetown Lombardi Comprehensive Cancer Center, designated as a comprehensive cancer center by the National Cancer Institute; and the Biomedical Graduate Research Organization, which accounts for the majority of externally funded research at GUMC including a Clinical and Translational Science Award from the National Institutes of Health. Connect with GUMC on Facebook (Facebook.com/GUMCUpdate), Twitter (@gumedcenter) and Instagram (@gumedcenter).
Newswise — Only one new drug has become available over the past 50 years for the estimated 1.5 million Americans and five million-plus people worldwide suffering from lupus, but new research has identified a previously unknown mechanism involved in the immune response that could provide an alternative therapy target. Lupus (also known as systemic lupus erythematosus) is a chronic autoimmune disease in which the immune system is unable to distinguish the difference between foreign invaders, such as viruses and bacteria, from its own healthy body tissue, so it attacks itself, damaging skin, joints, and kidneys – among other organs – in the process. The disease is also marked by elevated levels of type I interferon, a substance normally secreted by immune cells in response to viral infections. The origin of the interferon signature in lupus has remained a mystery for years. While working to solve this enigma, researchers, including Iwona Buskiewicz, Ph.D., and Andreas Koenig, Ph.D., assistant professors of pathology and laboratory medicine at the University of Vermont’s Larner College of Medicine, uncovered an unexpected finding: a protein that normally signals an immune system pathway during viral infections was spontaneously activated in lupus patients, even in the absence of viral infection. Their results were published recently in the journal Science Signaling. “Typically, this protein – mitochondrial antiviral signaling or MAVS – is responsible for recognizing viral infections,” explains Buskewicz, who adds that her team’s publication is “the first paper showing that the interferon pathway can be activated by something other than viral infection or nucleic acids.” The culprit of this phenomenon? Oxidative stress in cells, which is sufficient to induce the clustering of MAVS at the mitochondria – the energy-producing organelles within each cell – and drive interferon production in the absence of viruses. Why it is located at the mitochondria is still a missing piece of the puzzle, Buskewicz admits. She and her colleagues’ findings suggest that in lupus patients, environmental stress may contribute to their production of type I interferon, which normally helps regulate immune system activity. In their study, introduction of an anti-oxidant reversed the clustering of MAVS and prevented the subsequent production of interferon. Buskiewicz and her colleagues believe that MAVS could be targeted therapeutically with antioxidants directed to the mitochondria.The next step for the research team members, who in addition to the Larner College of Medicine at the University of Vermont, hail from the Wellcome Trust, University of Glasgow, SUNY Upstate Medical Center, and Weill Cornell Medical College, is to collaborate with rheumatologists to further explore a potential therapy, by examining the degree of MAVS clustering and interferon levels before and after antioxidant therapy.“We need to develop a drug that can revive the mitochondria,” she says. “A more focused antioxidant therapy targeting the particular organelle may have more efficacy.”