For Immediate Release: April 25, 2013
Contact: Jenny Eriksen Leary, 617-638-6841, email@example.com
(Boston) – A study conducted by researchers at Boston University School of Medicine (BUSM) provides new evidence that longwave ultraviolet light (UVA) induces a protein that could result in premature skin aging. The findings demonstrate that aspects of photoaging, the process of skin aging by chronic exposure to ultraviolet radiation, could be linked to genetic factors that accelerate the aging process when induced by the environment.
The study, published in the Journal of Investigative Dermatology, was led by BUSM co-authors Thomas M. Ruenger MD, PhD, professor and vice chair of the department of dermatology, and Hirotaka Takeuchi, MS.
Photoaging is attributed to continuous exposure to UVA and shortwave ultraviolet light (UVB) rays over a long period of time and affects skin surfaces most often exposed to sunlight, including the face, ears, hands and neck. The UVA or UVB rays can be from the sun or from synthetic sources, such as tanning beds. Progerin is a protein that has been associated with both normal and abnormal aging. In Hutchinson Gilford Progeria syndrome, a genetic disorder characterized by a vast acceleration of aging of most organs, expression and accumulation of progerin is caused by a mutation in the Lamin A gene.
In this study, skin cells were cultured and exposed to UVB or UVA rays and then examined for expression and accumulation of progerin. The results showed that progerin is induced by ultraviolet light, specifically UVA rays, and that this induction is mediated by reactive oxygen species causing alternative splicing of the LaminA gene pre-mRNA.
“This, to our knowledge, is the first time that induction of progerin is described in response to an external agent,” said Ruenger, who also is professor of pathology and laboratory medicine at BUSM and a dermatologist at Boston Medical Center. “Our results reveal a novel mechanism by which UVA rays, which are often emitted from tanning beds, may play a role in the acceleration of photoaging of the skin.”
The researchers also note that some aspects of photoaging should be regarded as a process of damage-accelerated intrinsic aging and that intrinsic and extrinsic aging are interdependent.
For Immediate Release: April 11, 2013
Contact: Jenny Eriksen Leary, 617-638-6841, firstname.lastname@example.org
(Boston) – Researchers from Boston University School of Medicine (BUSM) have pinpointed a genetic signature for chronic obstructive pulmonary disease (COPD) from airway cells harvested utilizing a minimally invasive procedure. The findings provide a novel way to study COPD and could lead to new treatments and ways to monitor patient’s response to those treatments. The study is published online in the American Journal of Respiratory and Critical Care Medicine.
Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that leads to the loss of lung function primarily caused by cigarette smoking. It causes coughing, wheezing, shortness of breath, chest tightness and other symptoms that make it difficult to breathe. While there are treatments and lifestyle changes that can help people cope with COPD, there currently is no cure and there are no effective therapies to reduce the rate of lung function decline. According to the National Institutes of Health’s National Heart, Lung, and Blood Institute (NHLBI), which partially funded the study, COPD is the third leading cause of death in the United States, resulting in approximately 135,000 deaths each year.
“There have been limited molecular studies of COPD given the inaccessibility and invasiveness of obtaining lung tissue,” said Katrina Steiling, MD, MSc, assistant professor of medicine at BUSM who served as the study’s first author. The researchers hypothesized that while COPD primarily affects the tissue deep within the lung, the effects of COPD might be detectable in relatively accessible tissue throughout the respiratory tract. This echoes previous work they had done that found that cancer found deep in the lung could be detected by cancer-specific patterns of gene expression in the largest airways connected to the windpipe, far from the tumor.
To examine their hypothesis, the research team used airway cells obtained during a bronchoscopy, a procedure that involves putting a small camera into the airway through the nose or mouth. During the procedure, which can be done while a patient is awake under local anesthesia or moderate sedation, a cytology brush is used to gently scrape the sides of airways to collect cells.
They examined 238 samples from current and former smokers that had been collected by Stephen Lam, MD, a collaborator from the University of British Columbia. Eighty seven of the samples were from patients who had been diagnosed with mild to moderate COPD based on their lung function. The other 151 samples represented patients who did not have COPD based on these criteria.
When the researchers compared the airway samples from both groups, they found that 98 genes were expressed at different levels in those diagnosed with COPD compared to those without COPD. In order to determine how similar the airway cell changes were to lung tissue cells, the researchers compared their results with previously published findings on the gene expression changes associated with COPD in lung tissue. The results of the comparison demonstrate that the changes that occur in the airway cell samples in those diagnosed with COPD were similar to the changes in lung tissue cells of individuals with the disease despite the airway cells coming from regions of the lung not thought to be altered by disease.
“Our data shows that there are consistent gene-expression changes that occur in both airway and lung tissue cells in individuals with COPD,” said Avrum Spira, MD, MSc, Alexander Graham Bell professor of medicine and chief of the division of computational biomedicine at BUSM who served as one of the senior co-authors of the study. Spira also is a physician in the pulmonary, critical care and allergy department at Boston Medical Center.
To investigate the effects of treatment on the COPD-associated gene expression changes, the researchers collaborated with a team led by Maarten van den Berge, MD, PhD, from the University of Groningen Medical Center in the Netherlands that had collected airway cells from COPD patients before and after they started steroid therapy. They found that the expression of some genes that changed due to COPD reversed their expression after treatment and started to look more like the levels seen in current or former smokers without COPD.
“Part of the COPD ‘signature’ reverses with therapy, suggesting that examining airway cells might be a minimally invasive tool for monitoring the disease and evaluating the response to therapy more quickly in order to determine the best course of treatment for each individual patient,” said Marc Lenburg, PhD, associate professor in computational biomedicine and bioinformatics at BUSM and the study’s other senior co-author.
“Studying COPD using the large airway opens up some really exciting new avenues of research that could also improve care for patients with COPD,” said Spira. “While we are still at an early stage, I envision being able to examine airway cells from my patients with COPD to determine what is causing the disease and, from that information, recommend a more specific and effective treatment.”
Funding for this research was provided in part by the National Institutes of Health’s (NIH) NHLBI under grant award number 1R01 HL095388 (PI: Spira/Lenburg) and the NIH’s National Center for Advancing Translational Science through the Boston University Clinical and Translational Science Institute under award number KL2RR025770.
Boston University Henry M. Goldman School of Dental Medicine Expands Elective Externship Program to Two University Sites in China
FOR IMMEDIATE RELEASE: April 8, 2013
Contact: Mary Becotte: 617-638-5147, email@example.com
Boston—Boston University Henry M. Goldman School of Dental Medicine (GSDM) will expand its Global Elective Externship program during the 2013–14 academic year to include an exchange program with two institutions in China: Shanghai Jiaotong University School of Stomatology (SJUSS), located in Shanghai, and the Fourth Military Medical University School of Stomatology (FMMUSS), located in Xi’an. GSDM students and residents will have the opportunity to do one- or two-week rotations in Oral and Maxillofacial Surgery under supervision by SJUSS and FMMUSS faculty. In return, GSDM will accept students and scholars from SJUSS and FMMUSS for clinical observation and/or research experience in various specialties at GSDM.
In his Strategy for a Global University, Boston University President Robert A. Brown states, “I believe that the future success and impact of Boston University as a great private research university will be interwoven with our presence as a truly global university in the 21st century.” Through these new exchange programs with FMMUSS and SJUSS, GSDM plans to extend its international dental externship program initiatives and to help fulfill the mission President Brown writes about. GSDM Dean Jeffrey W. Hutter said, “It is an honor and privilege to contribute to the global profile of this great University.”
The two-week externship training program at GSDM has already provided fourth-year DMD students at GSDM the chance to travel to Guatemala, Mexico, Haiti, Honduras, Nicaragua, Ukraine, and Jamaica for rotations. These rotations allow opportunities for the continued growth of the students’ clinical and critical thinking skills in treating diverse patient populations, along with the development of their cultural competencies. The externship locations in China will provide the added opportunity of observing and assisting in clinical practice in a hospital setting.
GSDM provides exemplary Advanced Specialty Education Programs in the recognized specialty areas of Dental Public Health, Endodontics, Oral & Maxillofacial Surgery, Orthodontics & Dentofacial Orthopedics, Pediatric Dentistry, Periodontics, and Prosthodontics. Students and residents from SJUSS and FMMUSS will benefit from observing world renowned leaders in dental specialties and patient treatment in technologically advanced settings, along with research being conducted in Biomaterials & Restorative Sciences, Health Policies & Health Services, Molecular & Cell Biology, and Oral Biology.
BUSM Study Reveals B cells as Therapeutic Targets to Alter Obesity-Associated Inflammation and Type 2 Diabetes
FOR IMMEDIATE RELEASE, March 12, 2013,
Jenny Eriksen Leary, 617-638-6841, firstname.lastname@example.org
(Boston) – New research from Boston University School of Medicine (BUSM) reveals that B cells regulate obesity-associated inflammation and type 2 diabetes through two specific mechanisms. The study, published in the Proceedings of the National Academy of Sciences, indicates the importance of continuing to explore B cells as a therapeutic target to treat these diseases. Barbara Nikolajczyk, PhD, associate professor of microbiology at BUSM, is the study’s senior author.
The incidence of diabetes continues to rise at alarming rates. According to the National Institute of Diabetes and Digestive and Kidney Diseases, the disease now affects approximately 25.8 million Americans. In 2007, the National Institutes of Health estimated that the direct and indirect costs of diabetes were a staggering $174 billion.
Type 2 diabetes, which is a common result of obesity, occurs when the body produces insulin but cannot use it properly (insulin resistance) or the body does not produce enough insulin. The body needs insulin to absorb glucose and generate energy. If the body does not produce and respond to insulin appropriately, it can, over time, lead to various complications such as cardiovascular disease, nerve damage, kidney disease and blindness.
Previous research has shown that B cells, which are white blood cells of the immune system, promote inflammation and can lead to the development of type 2 diabetes, but the mechanisms underlying B cell function were unclear.
The results of this study shed light on that question and indicate that B cells secrete a pro-inflammatory ratio of proteins called cytokines, which directly promote the insulin resistance that characterizes type 2 diabetes. The researchers also demonstrated that B cells directly regulate inflammatory T cells, an immune cell type known to cause insulin resistance in animal models of disease.
“Now that we have identified the specific mechanisms by which B cells promote inflammation, we can help develop novel, targeted approaches to treat type 2 diabetes,” said Nikolajczyk. “Our study supports the continued exploration of FDA-approved B cell depletion drugs, which are known to be generally safe and effective, as novel agents to prevent obesity-associated inflammation and type 2 diabetes.”
Research included in this study was supported in part by the National Institutes of Health’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) under grant award numbers R21DK089270 and R56DK096525 (PI: Nikolajczyk) and R56DK090455 (PI: Gerald Denis); the NIDDK’s Boston Area Diabetes Endocrinology Research Center Pilot Program and the Boston Nutrition Obesity Research Center under grant award number DK046200; the NIH’s National Institute of Dental and Craniofacial Research under grant award number 5R21DE021154 (PI: Nikolajczyk); the NIH’s National Institute of Allergy and Infectious Diseases (NIAID) Immunology Training Program under grant award number AI007309; the NIH’s National Heart, Lung, and Blood Institute’s Hematology Training Program under grant award number HL007501; and the Evans Center for Interdisciplinary Biomedical Research at BUSM (PI: Nikolajczyk and Denis).
FOR IMMEDIATE RELEASE: November 19, 2012
WASHINGTON, D.C. – Three organizations representing America’s research universities today launched a website that aims to inform policymakers and the public of the impact that the upcoming budget sequester would have on federal funding for university research. The organizations – the Association of American Universities (AAU), the Association of Public and Land-grant Universities (APLU) and The Science Coalition (TSC) – urge Congressional leaders and the President to act quickly to develop a comprehensive, balanced solution to America’s fiscal crisis that avoids steep cuts to scientific research, which pays a substantial return on investment in the form of job creation, workforce development and economic growth.
Collectively, the three sponsoring organizations represent more than 200 of the country’s leading academic research institutions. Their website, www.ScienceWorksForUS.org, provides data on the impact that sequestration – the across-the-board spending cut scheduled to take effect on Jan. 2, 2013 – is likely to have next year on academic research in all 50 states and the District of Columbia. While the estimated reduction in research funding ranges from the hundreds of millions of dollars for large, research-intensive states to less than $10 million for smaller states, every state will experience a significant impact given the catalytic effect research universities have on local and state economies. The website also provides numerous examples of the essential role that federally funded university research plays in today’s economy and the impact it has on society at large.
“Federal funding for research represents only 2 percent of the total federal budget, but it pays enormous dividends,” said Philip DiStefano, Chancellor of the University of Colorado Boulder, which is a member of AAU, APLU and TSC. “The numbers might not look huge, but the potential negative impact of reduced research on the economy would have long-lasting effects. That is because basic scientific research produces the discoveries that lead to countless treatments and cures that improve health, provide for our energy needs, fuel the new technologies that spark businesses and economic growth, improve our security, and help us better understand the world around us. ”
Federal funding for research is currently at the lowest level in the past decade in real dollars. The caps on discretionary spending mandated by the Budget Control Act (BCA) of 2011 will likely further depress research funding over the next decade. And sequestration requires additional cuts in federal spending on research and development – beyond those that will result from the BCA spending caps – of more than $12 billion in 2013 and nearly $95 billion over the life of the sequester.
“It is essential that America get itself on a sustainable financial path that reduces deficits and makes room for needed investments in the country’s future,” said Sally Mason, president of the University of Iowa and another AAU, APLU, TSC member. “We urge Congress and the President to work together now to enact a long-term plan to reduce budget deficits, prevent the arbitrary and harmful cuts of sequestration, and provide for continued investments in scientific research that will help build a better America.”
ScienceWorksForUS is a project of the Association of American Universities (AAU), the Association of Public and Land-grant Universities (A۰P۰L۰U) and the Science Coalition (TSC) to demonstrate the tremendous impact that federally funded university based research has on the nation and on the lives of all Americans, particularly the role it plays in improving health and spurring economic growth.
AAU: Barry Toiv: email@example.com
or Ann Speicher firstname.lastname@example.org, 202-408-7500
APLU: Paul Hassen email@example.com, 202-478-6073
TSC: Lauren Pulte firstname.lastname@example.org, 202-429-6875