Researchers Develop Concept for New Sunscreen that Allows Body to Produce Vitamin D

February 2nd, 2016in 2016, News Releases, School of Medicine

FOR IMMEDIATE RELEASE, February 1, 2016
CONTACT: Gina DiGravio, 617-638-8480, ginad@bu.edu

Researchers Develop Concept for New Sunscreen that
Allows Body to Produce Vitamin D

(Boston)—For the first time researchers have developed a process for altering the ingredients in a sunscreen that does not impact its sun protection factor (SPF), but does allow the body to produce vitamin D.

The findings, published in the peer reviewed journal PLOS ONE, has led to the production of a new sunscreen called Solar D.

Sun exposure is the major source of vitamin D for most children and adults worldwide. It is also recognized that vitamin D deficiency and insufficiency is a major health problem that afflicts approximately 40 percent of children and 60 percent of adults. However, because of concern for increased risk for skin cancer, widespread sunscreen use has been implemented. As a result, an SPF of 30 when properly applied, reduces the capacity of the skin to produce vitamin D by almost 98 percent

According to the researchers there are several chemical compounds that are typically used in a sunscreen that efficiently absorbed varying wavelengths of UVB radiation. After removing certain ingredients the researchers compared Solar D, which has an SPF of 30, to a popular commercial sunscreen with the same SPF, and found Solar D allowed for up to 50 percent more production of vitamin D in-vitro.

“Solar D was designed with compounds with differing filter compositions to maximize vitamin D production while maintaining its sun protection for reducing erythema or burning of the skin,” explained corresponding author Michael F. Holick, PhD, MD, professor of medicine, physiology and biophysics at Boston University School of Medicine and an endocrinologist at Boston Medical Center.

Solar D is currently available in Australia and will be available in the U.S. summer 2016.

Funding for this study was provided by Exposure Scientific, LLC/Nexidus, Ltd, Pty.

 

Professor Voices — 2016 Iowa caucuses explained, analyzed

DeanSapiroThe Iowa caucuses took place yesterday, Feb. 1, and were the first major electoral event decision point in of the nominating process for the United States’ next president. Ted Cruz came in first and won the Republican caucuses and Marco Rubio made a much stronger showing than was expected, and although Hillary Clinton won in the Democratic caucuses, the result was so close that both major candidates justifiably claimed a victory.

Virginia Sapiro is a Boston University professor of political science and an expert on public opinion, political behavior and electoral politics. She is also a former director of the American National Election Studies, the major scholarly survey of American voters that has been in operation since 1948. In a blog post, Sapiro broke down how the caucuses work. Here, a brief explainer:

There were Republican caucuses and Democratic caucuses throughout the state. In both camps, advocates were allowed to speak in front of other caucus-goers about their preferred candidates to try to convince others to join them. This began at 7 p.m. CST all around Iowa (8 p.m. EST). Then what?

Republicans gathered at their locations in Iowa (there are around 700) and decided which 30 delegates will attend the Republican National Convention from Iowa this July. They did so by declaring their candidate preferences, mostly by casting secret ballots.

Democrats gathered at their locations (there are around 1,000) and completed the first process in decision which 44 delegates will attend the Democratic National Convention from Iowa in July. In addition to these 44, eight “super delegates” will attend, picked on the basis of the positions they hold in government and politics, as is the process in the Democratic party across the country, so the super delegates are not chosen through the caucus process. Democrats did this in several rounds, by standing with similar-minded voters in “preference groups,” openly displaying their candidate of choice for all to see, and then doing a head count. After the first round, any group that has less than 15 percent of the people attending is considered “not viable,” and they distribute themselves to other groups or leave for the next round. People who are undecided redistribute themselves. Any people can change which group they are standing in.

Sapiro also broke down the results of both the Republican and Democratic caucuses for us in the following Q&A:

Q: What stood out to you most from Monday’s results? Was there much that differed from expectations?

VS: The biggest piece of news was the upset of Donald Trump, and from two sides. First, Ted Cruz came in first, and comfortably. He was expected to do especially well in the Evangelical western parts of the state, but he pulled strong leads in most regions of the state. And on the other side, Marco Rubio had his “surge,” and came in a reasonably close third. On the Democratic side, Hillary Clinton was expected to win, but everyone who read the indicators knew it was going to be close. In the end it was much closer than anyone expected — virtually a tie. Bernie Sanders was expected to do very well in the college towns and generally among young and first-time voters, but he did well beyond those groups.

Q: How can we explain what happened in the Iowa caucuses?

VS: In one sense, you have to have been there to know. In a primary, people go to the polls and individually case their ballots. But at a caucus, there’s a lot of discussion and argument, especially on the Democratic side, where they stand out in the open to be counted, continuing to argue all the way, while the Republicans cast secret ballots. Bernie Sanders’ appeal is a very emotional one, well represented by the “They’ve all come to look for America” ad. Sanders’ ability to draw people into engagement, and to support his candidacy with enthusiasm and small donations has been very impressive. He promises big things, and he touches those who are angry and frustrated with the state of the economy and politics today. Hillary Clinton’s appeal — a progressive who can get things done — has not grabbed a lot of people with the same resonance, certainly not the young, especially.  Sanders was enormously strong among the very young and the economically least well off, and according to polls he still does much better among men than women. Clinton did much better among older voters and among women. Of course we can’t tell much about race because Iowa is a very homogeneously white state.

On the Republican side, Ted Cruz’s organization and the support of talk radio and religious groups were crucial. Cruz walked away with the very conservative vote. For Marco Rubio, he has been labeled the “mainstream Republican” alternative, and that appeal has worked.

On both sides, attacks on “the media” and “the establishment” also were very appealing. That seems to be a winner with much of the public. 

Q: New Hampshire is up next. What impact will the Iowa results have on the N.H. primary next week and the others beyond that? 

VS: Donald Trump and Bernie Sanders have been predicted for some time to be the winners in New Hampshire. Trump is perhaps more vulnerable than he was, and Ted Cruz and Marco Rubio will have a strong running start to close that gap in the next week. But it is only a week — and there are still many candidates vying for a good show in N.H. On the Democratic side, Bernie Sanders is likely to “break the internet” — as one CNN commentator said — collecting contributions over the next few days. He will have a large infusion of donations, and his strong lead in N.H. is likely to be reinforced by the strength he showed in Iowa. Above all, we know, both races will continue for some time, certainly through Super Tuesday, on March 1. The results in Iowa have assured that. After New Hampshire, Sanders will encounter states that will be a much steeper climb for him, though, so we’ll all keep watching.

Q: Will we see the candidate roster slim down soon?

VS: Last night, we saw Democratic candidate Martin O’Malley and Republican contender Mike Huckabee withdraw from the race, and we are likely to see some more Republicans withdraw soon. But even for those further down the ticket, we are unlikely to see the race limited to the top three before Super Tuesday.

For additional commentary by Boston University experts, follow us on Twitter at @BUexperts and on Instagram at @buexperts.

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Opioid Prescribing for Chronic Pain — Achieving the Right Balance through Education

January 27th, 2016in 2016, News Releases, School of Medicine

EMBARGOED by the NEJM until Wednesday, January 27, 2016, 5 p.m. ET
CONTACT: Gina DiGravio, 617-638-8480, ginad@bu.edu

Opioid Prescribing for Chronic Pain — Achieving the Right Balance through Education

(Boston)–In recent decades, the United States has seen a dramatic increase in opioid prescribing for chronic pain. That growth has been associated with increasing misuse of these medications, leading to alarming increases in unintentional opioid overdose deaths.

In a perspective in this week’s New England Journal of Medicine, Daniel Alford, MD, MPH, associate professor of medicine and assistant dean of Continuing Medical Education and director of the Safe and Competent Opioid Prescribing Education (SCOPE of Pain) program at Boston University School of Medicine (BUSM), recommends that prescriber education is the best approach to addressing the prescription opioid-misuse epidemic, allowing for individualized care on the basis of a patient’s needs after a careful benefit–risk assessment.

According to Alford, a key problem is that clinician education around pain management and safe opioid prescribing has been lacking. As opposed to blunt regulatory solutions that decrease access to opioids in an indiscriminant way, education is a more finely tuned approach that can empower clinicians to make appropriate, well-informed treatment decisions for every patient at each clinical encounter. “Education has the potential to both reduce overprescribing and ensure that patients in need retain access to opioids,” explained Alford, who is also medical director of Boston Medical Center’s Office-based Opioid Treatment (OBOT) program.

Alford points out clinicians have limited tools at their disposal to help patients with severe chronic pain and the reimbursement system favors the use of medications alone, despite evidence supporting multimodal pain management. Moreover, whereas clinicians can use objective measures to guide their management of other chronic diseases, here they must rely solely on the patient’s (or family’s) reports of benefits (such as improved function) and harms (such as loss of control).

Alford believes voluntary prescriber education may be insufficient to address this problem and that mandatory education may be required. “If so, it will be important to link mandated education to medical licensure to avoid having clinicians opt out — since that could lead to reduced treatment access, as well as burnout among the clinicians who opt in,” he added.

Alford believes that the medical profession is compassionate enough and bright enough to learn how to prescribe opioids, when they are indicated, in ways that maximize benefit and minimize harm. “Though managing chronic pain is complicated and time consuming and carries risk, we owe it to our patients to ensure access to comprehensive pain management, including the medically appropriate use of opioids.”

Professor Voices — Internet levels playing field for “long shot” candidates

dino_christenson (1)Defying expectations, Bernie Sanders is ahead in New Hampshire, and tied with Hillary Clinton in Iowa as the race to be the Democratic nominee continues. Nationally, Sanders’ numbers are also on the rise.

What has contributed to Sanders’ success? A lot of it may have to do with the web. The 74-year-old candidate has raised millions of dollars online and recently launched a volunteer app for smartphones.

We asked Dino Christenson, a Boston University College of Arts & Sciences political science professor, about the link between Sanders’s success and Internet savvy in a Q&A:

Q: How is Bernie Sanders’ campaign using the web to their advantage?

DC: Sanders has been quite successful at using the web for fundraising—especially from small donors—as well as for campaign organizing, voter outreach, and advertising. He has taken a comprehensive approach, which is becoming the norm in campaigns.

Q: How is Sanders’ online strategy different than other candidates?

DC: Actually, I don’t think it is very different. From a historical perspective, Sanders looks like many long shot candidates of the past, like Howard Dean in 2003, Ron Paul and Barack Obama in 2007. Like Sanders, these candidates were less tapped into elite party networks and received a smaller share of media coverage and traditional funding at the onset of their campaigns, and thus they relied heavily on the Internet.

Q: Do his tactics seem more effective than Barack Obama’s were during his campaign?

DC: Not yet, they don’t. Sanders is doing a good job fundraising and communicating with voters. However, I think Sanders’ chances of overcoming the front-runner, Hillary Clinton, and taking the nomination are considerably lower than Obama’s at this stage in 2008.

Of course, winning may be only one of a campaign’s objectives. Sanders’ online appeals have helped him to reach larger audiences, and his success in online fundraising has allowed him to stay in the race and affect important policy discussions.

Q: Why is the Internet important to today’s political landscape?

DC: Because the Internet is a new and unique feature of campaigns. That is, a candidate’s presence on the Internet is not the same as nor is it a mere result of media coverage and polls. Moreover, its effects on campaigns are different. A strong online presence is a uniquely powerful tool for generating small donor contributions, quickly raising contributions after victories, and maximizing support in early state contests.

Q: What kind of candidates does the Internet typically help?

DC: This is a great question. All candidates are not the same, and the potential for the Internet to help them varies. Our research suggests that the Internet is particularly helpful to long shot candidates, providing them the traditionally lacking exposure to voters and access to fundraising necessary for them to compete with the front-runners in a long nomination campaign.

Q: Given the benefits of the Internet, can candidates do anything to increase their presence on the web?

DC: Again it depends on the candidate. Long shots are better able to boost their web presence than front-runners, who start at relatively higher levels. By focusing their campaign spending on marketing and travel, long shot candidates can drive up their web presence, and capitalize on it in the aforementioned ways.

Q: So then, is the Internet a good thing for nomination campaigns?

DC: It is most certainly a notable change, since many see recent trends in the primary calendar, like frontloading and compaction, as benefiting front-runners. Frontloading means that candidates must compete earlier to gather funds and organize campaigns, which benefits those with insider support and donor networks, or front-runners. A compacted calendar means that long shots without nationally organized campaigns in place have less time to convert strong early performances into fundraising and organization before the next contest. But our work, and perhaps the present success of Sanders, suggests that the Internet is bucking both of these trends and leveling the playing field.

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Researchers Discover Key Pathway Involved in Blood Vessel Occlusion

January 14th, 2016in 2016, News Releases, School of Medicine

FOR IMMEDIATE RELEASE, January 14, 2016
CONTACT: Gina DiGravio, 617-638-8480, ginad@bu.edu

Researchers Discover Key Pathway Involved in Blood Vessel Occlusion

(Boston)–Researchers have made a breakthrough in understanding blood vessel occlusion by discovering a novel pathway involved in this process.

The findings, which appear in the journal Blood, may lead to new treatments for clotting associated with atherosclerosis, cancer, heart attacks and strokes.

Clotting (thrombosis) is an important function of blood to prevent excessive bleeding, but it can become inappropriately activated during a stroke or heart attack. Earlier studies led by these same researchers identified that a protein called lysyl oxidase (LOX) is increased in certain blood cancers that have a high risk of clotting. However, the mechanism through which increased LOX leads to clotting was unknown until now.

In an experimental model that increased LOX activity in platelets (blood cells involved in clotting), researchers found that the time needed to form a blood clot after injury to the blood vessels was reduced. These platelets were more likely to form a clot and researchers pinpointed the specific receptor on the platelets affected by the oxidation activity of LOX. This receptor is responsible for platelet adhesion to proteins (collagen) in blood vessels.

“By using interdisciplinary approaches, we were able to extend discovery of basic mechanisms to in vivo studies” explains corresponding author Katya Ravid, DSc, PhD, professor of medicine and biochemistry at Boston University School of Medicine. Post-doctoral fellow, Dr. Shinobu Matsuuras is the study’s first author.

This study has implications for various other diseases, such as vascular restenosis (blood vessel narrowing) and chronic kidney disease, in which there are high levels of LOX and increased blood clotting related complications.

Researchers Discover Novel Factor in Parkinson’s Disease

January 12th, 2016in 2016, News Releases, School of Medicine

FOR IMMEDIATE RELEASE, January 12, 2016
CONTACT: Gina DiGravio, 617-638-8480, ginad@bu.edu

 Researchers Discover Novel Factor in Parkinson’s Disease

Discovery May Lead to Better Understanding of Disease, Early Diagnosis and Therapeutic Development

Boston–A team of local researchers have discovered a previously unknown cellular defect in patients with idiopathic Parkinson’s disease, and identified a sequence of pathological events that can trigger or accelerate premature death of certain neurons in the brain seen in this disease.

The findings, published in the journal Nature Communications, will provide a better understanding and further research towards a possible cure of Parkinson’s disease, which is a neurodegenerative disorder that affects movement and other vital functions in nearly one million people in the United States. Despite advances in understanding the causes of familial forms of this disease, the most prevalent idiopathic form of Parkinson’s disease remains a mystery.

Boston University School of Medicine (BUSM) researchers discovered that the cells of people with idiopathic Parkinson’s disease have a previously unknown defect in the function of a specific PLA2g6 protein, causing dysfunction of calcium homeostasis that can determine whether some cells will live or die.

“Idiopathic or genetic dysfunction of calcium signaling triggers a sequence of pathological events leading to autophagic dysfunction, progressive loss of dopaminergic neurons and age-dependent impairment of vital motor functions typical for Parkinson’s disease,“ explained corresponding author Victoria Bolotina, PhD, professor of medicine at BUSM.

“Discovery of this new mechanism associated with human Parkinson’s disease and our ability to mimic this pathology in a novel genetic model opens new opportunities for finding a cure for this devastating neurodegenerative disease,” she added.

This work was partially supported by research grant awards from The Michael J. Fox Foundation for Parkinson’s Research, the US National Institutes of Health, SERVIER Research Institute and the Department of Medicine at Boston University School of Medicine.

Researchers Find Shared Molecular Response to Tobacco Smoke and Indoor Air Pollution

January 11th, 2016in 2016, News Releases, School of Medicine

FOR IMMEDIATE RELEASE, January 11, 2016
CONTACT: Gina DiGravio, 617-638-8480, ginad@bu.edu

Researchers Find Shared Molecular Response to Tobacco Smoke and Indoor Air Pollution

(Boston)—Exposure to certain household air pollutants may cause some of the same molecular changes as smoking cigarettes.

A study in the journal Carcinogenesis reports non-smoking women living in rural China who burn smoky (bituminous) coal for heating and cooking had gene expression patterns in buccal (cheek) epithelial cells similar to those present in the cheek cells of active cigarette smokers. The study, conducted by investigators at Boston University School of Medicine (BUSM), the U.S. National Cancer Institute (NCI), and others, is the first to identify genomic alterations that result from exposure to smoky coal.

Approximately three billion people in the world use coal and biomass (charcoal, wood, animal dung and crop waste) for cooking and heating. “Lung cancer rates among non-smoking women in China’s rural counties, where smoky coal is used extensively, are among the highest in the world,” noted Qing Lan, MD, PhD, MPH, senior investigator at the NCI, and co-senior author of the study.

Avrum Spira, MD, MS, professor of medicine, pathology and laboratory medicine at BUSM and co-senior and co-corresponding author of the study, has previously shown that tobacco smoke induces gene expression changes throughout the epithelium of the respiratory tract. Since smoky coal is also an established risk factor for lung cancer and other non-malignant respiratory diseases, the researchers were interested to examine whether smoky coal had a similar effect on the respiratory tract.

“While lung cancer in this population has been linked to the usage of smoky coal, as compared to smokeless (anthracite) coal, the molecular changes experienced by those exposed to these indoor air pollutants remained unclear,” said Nathaniel Rothman, MD, MPH, MHS, senior investigator at the NCI, and a co-author of the study.

To understand the physiologic effects of this exposure Spira and his collaborators at NCI analyzed buccal epithelial cells collected from healthy, non-smoking female residents of Xuanwei and Fuyuan county who burned smoky and smokeless coal. Genome-wide gene-expression profiles were examined and changes associated with coal type were compared. The researchers identified 282 genes as differentially expressed in the buccal epithelium of women exposed to smoky versus smokeless coal.

“We then compared our smoky coal gene-expression signature to gene-expression changes observed in tobacco users and found that smoky coal emissions elicited similar physiologic effects. These results shed new light on the molecular mechanisms associated with smoky coal exposure and may provide a biological basis for the increased risk of lung cancer,” explained Spira, who is also director of the Boston University Cancer Center and a pulmonologist at Boston Medical Center. “We hope genomic profiling of the biologic response to solid fuel emissions will ultimately lead to the development of clinically relevant biomarkers,” he added.

“Ultimately, this and other studies of the health effects from indoor air pollution due to smoky combustion highlight the importance of switching to cleaner fuels,” concluded Lan.

Funding for this study was provided by National Institutes of Health/National Institute of Environmental Health Sciences (3U01ES16035-03S1) and the Intramural Research Program of the US National Cancer Institute.

Epigenetic Regulation of Metastatic Breast Cancer Progression Could Guide Prognosis and Future Therapies

January 11th, 2016in 2015, News Releases, School of Medicine

FOR IMMEDIATE RELEASE: January 7, 2016
CONTACT:
Gina DiGravio, 617-638-8480, ginad@bu.edu

Epigenetic Regulation of Metastatic Breast Cancer Progression
Could Guide Prognosis and Future Therapies

(Boston)–A gene that plays a role in the development of breast cancer to metastatic disease has been identified which may help to predict disease progression and serve as a target for the development of future breast cancer therapies.

These findings by Boston University School of Medicine (BUSM) researchers currently appear in the journal Proceedings of the National Academy of Sciences.

Researchers have identified a gene called serum deprivation response (SDPR) and the mechanisms by which this gene is down-regulated, or silenced, in breast cancer cells promoting tumor spread. Using a breast cancer progression model, the team identified that aggressive, metastatic breast cancer cells had little or no genetic expression of SDPR and furthermore that when it is over-expressed (or turned on) this gene in models of breast cancer cells with propensity for metastasis, there was a significant reduction in the incidence of metastatic disease.

Despite the advent of advanced technologies, the discovery of new metastasis suppressor genes such as SDPR that prevent the spread of breast cancer to distal sites using genomic efforts has been slow potentially due to their primary mode of regulation by epigenetic mechanisms as shown in this case by the researchers at BUSM. The current study reveals the importance of gene regulation by epigenetic rather than genetic mechanisms enabling the cancer cells to readily adapt to new microenvironments of the various organs of the human body at sites away from the initial sites at which the cancer cells formed.

According to the researchers this work is crucial as metastatic dissemination of breast cancer cells represents a significant clinical obstacle to curative therapy and spreading of the cancer is the major cause of death of patients affected by breast and other cancers. “It is of utmost importance to understand the underlying molecular mechanisms that facilitate/prevent cancer metastasis,” explains corresponding author Sam Thiagalingam, BUSM associate professor of medicine, genetics and genomics, pathology and laboratory medicine.

The researchers also found that SDPR loss was not limited to breast cancer, as tumor samples from bladder, colorectal, lung, pancreatic and ovarian cancers as well as sarcomas also exhibited loss of SDPR expression based on in silico meta-analysis of publicly available data, suggesting its functional role as a metastasis suppressor is likely to impact multiple cancers.

“While this is a significant advance in deciphering the molecular basis of the metastatic disease and may help to predict progression to metastatic cancer, its potential importance in the development of future precision cancer therapies have yet to be worked out from the identification of druggable targets regulated by SDPR,“ added Thiagalingam.

Sait Ozturk, PhD, the lead author of the paper was a graduate student at BUSM in Molecular and Translational Medicine Program. This work was supported by grants from Susan G. Komen for the Cure (KG081435) and the NIH (CA165707). Additional support for this work was provided by a Seed grant from the BU Genome Science Institute and the Research Promotion Foundation of Cyprus (DIDATOR 0609/24).

Experts media alert – State of the Union 2016

presidential-sealPresident Obama is set to deliver his final State of the Union Address. Boston University presidential historian Tom Whalen shares his thoughts on the president’s last address:

“Like all second termers delivering their final State of the Union address, President Obama will try mightily to show he is still politically relevant. He will remind the Republican controlled chamber that he will brandish the veto pen just as fast as they can pass bills overturning the Affordable Care Act.

“In terms of specific domestic issues, he will no doubt make one last stab at greater gun control and comprehensive immigration reform, which will give the likely Democratic presidential nominee, Hillary Clinton, some pretty good talking points on the campaign trail.

“At this point, that’s about all that can be expected. Like it or not, Obama is a lame duck.”

Contact Whalen at 617-353-4785 or tjw64@bu.edu.

For additional commentary by Boston University experts, follow us on Twitter at @BUexperts

Chronic Traumatic Encephalopathy in 25-year-old Former Football Player

January 5th, 2016in 2016, News Releases

FOR IMMEDIATE RELEASE: January 4, 2016
CONTACT: Gina DiGravio-Wilczewski at 617-638-8480 or ginad@bu.edu

JAMA Neurology

Chronic Traumatic Encephalopathy in 25-year-old Former Football Player

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder associated with repetitive head impacts and can be diagnosed only by autopsy after death. In an article published online by JAMA Neurology, Ann C. McKee, M.D., of the Boston University School of Medicine, and coauthors write an observation letter about CTE pathology in a 25-year-old former college football player who experienced more than 10 concussions while playing football, the first occurring when he was 8 years old. The authors note that, to their knowledge, this is the first autopsy-confirmed case to include neuropsychological testing to document the type of cognitive issues that present with CTE. The young man played football for 16 years, beginning when he was 6 and including three years of Division I college football. During his freshman year of college, he experienced a concussion with momentary loss of consciousness followed by headaches, neck pain and other symptoms that included difficulty with memory and concentration. He stopped playing football in his junior year because of ongoing symptoms, began failing his classes and eventually left school before earning a degree. The player, who had a family history of addiction and depression, later had difficulty maintaining a job and began using marijuana to help headaches and anxiety and to help him sleep. He died of cardiac arrest that was secondary to Staphylococus aureus endocarditis.

To read the full article, please visit the For The Media website.

(JAMA Neurol. Published online January 4, 2015. doi:10.1001/jamaneurol.2015.3998. Available pre-embargo to the media at http://media.jamanetwork.com.)

Editor’s Note: The study includes funding/support disclosures. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

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For more information, contact JAMA Network Media Relations at 312-464-JAMA (5262) or email mediarelations@jamanetwork.org.