FOR IMMEDIATE RELEASE, Tuesday, Sept. 20, 2016
CONTACT: Kristen Perfetuo, 617-638-8484, firstname.lastname@example.org
New Research Indicates Key Protein May Directly Impact Development of Colon Cancer
Discovery may lead to targeted new therapies for treatment of the disease
(Boston) – Researchers have discovered a new role of a protein that, if manipulated, may help suppress Colorectal Cancer (CRC) growth. The discovery, published online by Oncotarget journal, may lead to new therapies in managing patients with CRC.
CRC is a complex disease caused by several genetic mutations and their consequences. In more than 80-percent of CRC patients, some of these mutations can lead to an increase in b-catenin, a vital protein, leading to cancer initiation.
Researchers from Boston University School of Medicine (BUSM), led by Vipul Chitalia, MD, PhD, assistant professor of Medicine, have identified a new role of the protein, c-Cbl that it may be capable of degrading b-catenin in CRC patients.
“We believe these findings could have clinical implications in managing patients with CRC,” explains Chitalia. “For example, c-Cbl could be used as a biomarker of patient survival. The discovery may also lead to new strategies to suppress CRC growth.”
According to Chitalia, another aspect of this study is related to the method by which researchers analyze human biopsy samples. Until now, the information within biopsies, such as the amount of a specific protein, used to be determined on a semi-quantitative basis. Accurate estimation of relevant content within these images is critical for prognostic and therapeutic purposes.
BUSM researchers, led by Vijaya Kolachalama, PhD, principal investigator at the Whitaker Cardiovascular Institute at BUSM, developed a more accurate, automated and high-throughput image processing technique that was capable of uncovering hidden relationships between important proteins in cancer.
“We are excited about this discovery and the treatments that could improve the quality of life for CRC patients,” says Chitalia and his collaborators Kevan Hartshorn, MD, professor of Medicine, and Nader Rahimi, PhD, associate professor of Pathology and Laboratory Medicine “c-Cbl targeted therapy may provide a means to suppress the growth of CRC and possibly with lower side effects.”
Every year about 150,000 new cases of colorectal cancer are diagnosed in the United States. Despite surgery and new therapies, about one third of patients with the disease die from CRC annually, making it the second most common cause of cancer death.
The study was supported by the National Institutes for Health/National Cancer Institute and the Sharon Anderson American Society of Nephrology fellowship award.
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FOR IMMEDIATE RELEASE, September 20, 2016
CONTACT: Gina DiGravio, 617-638-8480, email@example.com
Researchers Investigate New Strategy to Block Growth of Colon Cancer Cells
(Boston)—Researchers from Boston University School of Medicine (BUSM) have discovered a possible strategy to treat colon cancers that are caused by the mutant KRAS gene, which is responsible for approximately half of all colon cancer cases.
The findings, which appear online in the journal Molecular Cancer Research, may lead to better therapeutic agents to treat this disease.
Colon cancer is the third leading cause of cancer-related deaths in the U.S. Routine screenings by undergoing a colonoscopy have helped reduce mortality rates, however, if the disease advances to malignancy, it can be very difficult to treat. Cancers with the KRAS gene mutation respond poorly to currently available therapeutic agents.
“Our study provides a new strategy to treat colon cancers driven by the mutant KRAS gene, which is based on targeting additional genes that cooperate with KRAS to promote tumor growth. These additional genes, notably MEK and TAK1, can be blocked by selective therapeutic agents to suppress colon cancer cellular proliferation and viability,” explained corresponding author Anurag Singh, PhD, assistant professor of pharmacology & experimental therapeutics at BUSM.
The researchers tested 40 colon cancer cell lines that were derived from human colon cancer samples for sensitivity to inhibitors of MEK and TAK1. They found that treating those cell lines with MEK and TAK1 inhibitors suppressed the growth of mutant KRAS-driven colon cancer cells significantly as compared to the control group.
According to Singh, a key goal of “precision medicine” is to identify specific vulnerabilities that can be blocked with selective and effective drugs. “With this study we have uncovered a novel pathway in a subset of colon cancers driven by mutant KRAS gene activation, representing an important axis of vulnerability with the potential to selectively treat these types of tumors in the clinic,” he added.
Funding for this study was provided by the National Institutes of Health, National Cancer Institute K99/R00 “Pathway to Independence Award” and through Boston University Institutional Start-Up Funds.
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By Ian Stevenson, Boston University Ph.D. Candidate (American & New England Studies)
One hundred years ago — August 25, 1916 — President Woodrow Wilson signed the National Park Service Organic Act, creating the National Park Service (NPS). The legislation clearly directed the NPS “to preserve the scenery and the natural and historic objects and the wild life therein and to provide for the enjoyment of the same in such manner and by such means as will leave them unimpaired for the enjoyment of future generations.”
While we take this moment to celebrate the vast national park system, the centennial also marks a hundred-year commitment by the United States government to preserve our natural and cultural heritage.
The act did not create the national park idea. Yellowstone became America’s (and the world’s) first national park 44 years earlier in 1872. Yosemitebecame a national park in 1890, but Abraham Lincoln set it aside back in 1864 as a state park, making it the first land reservation for public use by the federal government. Yet the establishment of early national parks left ambiguous how they should be used for the public good. By the turn of the twentieth century, two divergent perspectives emerged: conservation versus preservation.
The debate evolved over a half century. Frederick Law Olmsted, designer of New York City’s Central Park, in 1865 extolled Yosemite’s natural ability for moral uplift just like city parks.
President Theodore Rooseveltused his executive powers to greatly expand the number of national parks and monuments to prevent their destruction by unfettered capitalism. But he also understood the value of resource extraction and appointed Gifford Pinchot, who promoted a conservationist ethic of scientifically managed natural resources on public land, as first chief of the U.S. Forestry Service.
The battle ultimately erupted over a 1906 proposal to dam the Hetch Hetchy Valley in Yosemite to create a public water supply for San Francisco. While conservationists won when President Wilson authorized the dam in 1913, preservationists three years later convinced the U.S. Government that preservation for both aesthetic and economic reasons (tourism) necessitated the NPS.
But how has the NPS achieved preservation since?
It expanded to include properties not explicitly “natural,” such as historic battlefields from the War Department in 1933, and recreational sites like national seashores beginning in 1937. It fought against subsequent conservationist proposals, such as for a dam at Dinosaur National Monument in the 1950s.
It added to the system in novel ways by purchasing private property, starting with Cape Cod National Seashore in 1961. It partnered with local stakeholders to create shared preservation spaces, such as Boston Harbor Islands National Recreation Area in the 1990s. More recently, it has incorporated sites notable to the history of African Americans, Native Americans, the LGBT community, and others.
And how has the NPS helped define preservation? In response to increased visitation after WWII by private automobile, it instituted Mission 66 in 1956 to “modernize” the parks with new roads and invented a new building type — the visitors center. By directing visitors within the park, the NPS sacrificed some of the natural landscape for the preservation of the rest. It absorbed truly car-free “wild” preservation tracts after the environmentalist movement yielded the 1964 Wilderness Act. It expanded preservation of the built environment when the 1966 Historic Preservation Act charged the NPS with administering the National Register of Historic Places.
“I encourage you to reflect on the importance of the National Park Service as preservation organization and to get out and enjoy its legacy at sites big and small, local and away, old and new, famous and idiosyncratic, just as characterizes the American landscape and its people.”
These praiseworthy expansions of preservation through the national park system has, however, had a cost. Early national parks like Yellowstone and Yosemite only appeared “natural” after Euro-Americans forcibly evicted Native Americans. Poor, rural whites were removed from their land to create Great Smoky Mountains National Park in the 1930s. Even middle and upper class Americans on Cape Cod faced eminent domain in the 1960s as the NPS sought to preserve that coastal landscape. Today, rural Mainers protest the potential loss of traditional hunting and recreational uses in land offered by private donation to create North Woods National Park.
Thus, in 2016 as in 1916, preservation issues remain constant, highlighting the continued importance of the NPS. The next century will bring new challenges as the NPS confronts maintenance demands for its current properties, struggles to attract visitors among shifting demographics, and confronts the effects of climate change, which has already reduced Glacier National Park to 25 active glaciers from 100 when founded in 1910.
As we celebrate its centennial, I encourage you to reflect on the importance of the National Park Service as a preservation organization and to get out and enjoy its legacy at sites big and small, local and away, old and new, famous and idiosyncratic, just as characterizes the American landscape and its people.
FOR IMMEDIATE RELEASE, August 10, 2016
CONTACT: Gina DiGravio, 617-638-8480, firstname.lastname@example.org
BrightFocus Foundation Awards BUSM Researchers $450K
(Boston)—Two researchers from Boston University School of Medicine (BUSM) were recently awarded grants from the BrightFocus Foundation.
Haiyan Gong, MD, PhD, professor of ophthalmology and anatomy & neurobiology whose research interests include glaucoma, received a $150,000 grant to study various cellular interactions in the eye’s drainage system using newly developed, advanced 3D electron microscopes.
Tsuneya Ikezu, MD, PhD, professor of pharmacology & experimental therapeutics and neurology, was awarded $300,000 for his work on the TREM2 molecule in the search for Alzheimer’s disease treatments.
“BrightFocus is proud to support researchers who are at the forefront of scientific discovery,” said the foundation’s President and CEO Stacy Pagos Haller. “They are pushing new frontiers of knowledge in their labs and sparking the creativity and innovation that will improve the quality of life for millions around the world.”
BrightFocus is a Maryland-based nonprofit that funds research worldwide and provides public awareness for Alzheimer’s, macular degeneration and glaucoma.
Originally established in 1848 as the New England Female Medical College, and incorporated into Boston University in 1873, Boston University School of Medicine today is a leading academic medical center with an enrollment of more than 700 medical students and 950 students pursuing degrees in graduate medical sciences. BUSM faculty contribute to more than 668 active grants and contracts, with total anticipated awards valued at more than $693 million in amyloidosis, arthritis, cardiovascular disease, cancer, infectious diseases, pulmonary disease and dermatology, among other areas. The School’s teaching affiliates include Boston Medical Center, its primary teaching hospital, the Boston VA Healthcare System, Kaiser Permanente in northern California, as well as Boston HealthNet, a network of 15 community health centers. For more information, please visit http://www.bumc.bu.edu/busm/
FOR IMMEDIATE RELEASE, August 10, 2016
CONTACT: Gina DiGravio, 617-638-8480, email@example.com
Study Reveals Association between Physical Function and Neurological Disease
(Boston)— A new study, based on data from the Framingham Heart Study (FHS) suggests a simple test of physical functioning may be able to help physicians identify individuals who are at a higher risk for developing Alzheimer’s disease and stroke.
These findings, which appear in the Journal of Alzheimer’s Disease, provide hope that there are easy-to-test clinical markers that will help physicians identify individuals who are at increased risk for common age-related neurological diseases.
It is known that as people age, there is a decline in physical capability, muscle strength and aspects of the nervous system that regulate and guide motor function and balance. Studies from recent years have shown that slow walking and weak grip strength can suggest that a person is in poor health and can even show that the individual is at high risk for poor health and disability in the future. Based on this information, researchers at Boston University School of Medicine (BUSM) were interested to learn whether the same measures of slow walking and weak grip could also predict the risk of common age-related neurological diseases.
FHS participants between the ages of 35 and 84 years were asked to walk a certain distance as fast as they could without running, and the time taken to complete the walk was recorded. Researchers also recorded the participant’s maximum force on an object to estimate their handgrip strength. These participants were followed for up to 11 years.
After analyzing the results, the researchers found that individuals who had slow walking speeds and weak grip strength had a significant increase in risk of Alzheimer’s disease. Additionally, participants older than 65 years had a higher risk of stroke if their hand grip strength was weak. “These findings suggest that measuring walking speed and handgrip strength can help predict who is at a higher risk of Alzheimer’s disease and stroke. If these findings are confirmed, these measures can serve as additional tools to screen people for stroke or dementia,” explained corresponding author Galit Weinstein, PhD, adjunct assistant professor of neurology at BUSM.
The FHS consistently has been shown to be a reliable source of data. The authors admit, however, that the sample population is overwhelmingly of European ancestry and that further studies are needed to extend the findings to other populations. Regardless, there was still a strong association and these measures are simple, cheap and easy to perform and therefore could one day be used in any clinical setting,” added Weinstein.
Funding for this study was provided by a contract from the NHLBI to the Framingham Heart Study (HHSN268201500001L) and by grants from the NIA (AG008122) and NINDS (NS019750) to Dr. Sudha Seshadri.
FOR IMMEDIATE RELEASE, August 5, 2016
CONTACT: Gina DiGravio, 617-638-8480, firstname.lastname@example.org
New Director of the Boston University Master’s Program in Genetic Counseling Named
(Boston)–Kathleen Berentsen Swenson, MS, CGC, MPH, has been named the new director of the Boston University Master’s Program in Genetic Counseling. Berentsen has been with the program since 2010 as a course instructor and capstone mentor.
Berentsen brings 16 years of experience in genetic counseling in various clinical settings across many specialties including prenatal, pediatrics, neurology and cancer. She has been an advocate at the national level with the Children’s Tumor Foundation and at the community level with the Dominican Women’s Development Center for the WH/I GENE coalition project. In addition, she possesses experience in public health having worked with the New York State Department of Health.
Berentsen is an experienced educator and clinician across a broad spectrum of genetic counseling domains, ranging from prenatal genetic counseling to the development of a telephone-based counseling platform. Most recently, she worked at Counsyl, Inc. as a clinical product specialist where she oversaw education for hereditary cancer genetics and mentorship of graduate students and internal employees. Prior to that, she served as a genetic counselor at Beth Israel Deaconess Medical Center in their Cancer Genetics and Prevention Program.
Berentsen earned her undergraduate degree in natural sciences and psychology from Muhlenberg College in 1997, her master’s degree in human genetics from Sarah Lawrence College in 2000 and a master’s degree in public health from Columbia University in 2008.
FOR IMMEDIATE RELEASE, August 4, 2016
CONTACT: Gina DiGravio, 617-638-8480, email@example.com
Study Analyses How Epigenetics Regulate Vital Functions from Bacteria to Humans
(Boston)–After the emergence of single-celled organisms some billions of years ago, nature started experimenting with how to diversify gene function without changing the sequence of the DNA, such that the blue print remains conserved, but allows gene products to have different functions. As multicellular organisms evolved, this process of maintenance and function were provided by mechanisms which are called “epigenetics”. Epigenetics allow genes to function differently by adding chemical ‘tags’ to DNA or to proteins that surround the DNA. Recent studies suggest that in more developed eukaryotes the changes in the protein that help DNA fold regulate how much chemical ‘tag’ will be attached to DNA and vice versa.
A new study published by Boston University School of Medicine researchers in the journal of Genetics and Epigenetics, provides a comparative analysis of the evolution of epigenetic mechanisms from prokaryotes (bacteria) to simple eukaryotes (multi-cellular) to more complex eukaryotes (humans). Bacteria evolved billions of years ago, and even at that early stage, nature started the process of allowing bacterial DNA to perform different functions without changing the order by which DNA is organized. This was achieved by adding a chemical ‘tag’ to one of the subunits of DNA. The group of atoms that gets attached can vary based on the organism. This simple modification is important for bacterial survival, and allows bacteria to fight infections. It is striking though that the attachment site of the ‘tag’ shifted to a different subunit on DNA as eukaryotes developed. Viruses also learned how to use this “tagging” process to their advantage. The virus HIV, which causes AIDs, hides from an individual’s immune system by removing a particular ‘tag’ from the proteins that fold DNA.
According to corresponding author Sibaji Sarkar, PhD, instructor of medicine at BUSM, it is intriguing to observe how nature shifted the site of ‘tag’ addition from bacteria to mammals. “The addition of ‘tagging’ proteins that are involved in folding DNA in eukaryotes provided another dimension,” he explains.
He adds, “If we closely observe the process of regeneration in some eukaryotes including zebra fish, when a portion is cut out, it is clear that the present gene pool in the DNA provides the necessary healing process to regenerate the section of the organism. We may gain tremendous knowledge to understand how stem cells can become so many types of organs by studying this process.” It appears that epigenetic mechanisms regulate this process. The most striking event which describes this type of multifaceted formation of organs and tissues from one cell (fertilized egg) is embryogenesis.
When mammals reproduce, the DNA sequences that are inherited cannot be altered, but from the time that the sperm fertilizes the egg, every step proceeds according to a set of rules until the tissues and organs are differentiated. Different sets of genes are used for each step of development. For example, the ‘tags’ in the egg are erased after fertilization and then rewritten. The proteins that rewrite this process are governed by the same proteins that fold the DNA in the mother’s egg. It is reasonable, therefore, to believe that the characteristics of mom’s folding proteins may dictate which type of ‘tag’ will take place in her offspring DNA. It is known that the epigenetic alterations of ‘tagging’ are regulated by environmental effects. The authors suggest that environmental factors and the mother’s lifestyle will thus affect ‘tagging’ of the offspring DNA, which will dictate how the offspring genes will be utilized. Interestingly, epigenetic changes also take place throughout life depending on the life style of the person.
This article includes the description of altered epigenetic changes which may lead to many types of diseases including metabolic syndrome, cardiovascular disease, autoimmune diseases, neurological disorders, aging and cancer.
The authors proposed another hypothesis which could explain how cancer cells increase copy numbers of tumor promoting genes and decrease or delete tumor inhibiting genes. Sarkar added, “Cancer cells possibly hijack a mechanism operative in normal cells which provides way how the methyl tagged DNA will be untagged by cutting the DNA at the site of tag and repairing it. It is an interesting idea which needs to be tested.”
The epigenetic process of ‘tagging’ that is utilized by living organisms from bacteria to humans is a gold mine for understanding the normal functions of cells and determining where, when, and how these steps deviate from normal behavior to cause disease conditions, a process which is still not well understood.
BUSM co-authors on the study include: Amber Willbanks, Meghan Leary, Molly Greenshields, Camila Tyminski, Karolina Lapinska, and Kathryn Haskins. Sarah Heerboth is from Vanderbilt School of Medicine.
FOR IMMEDIATE RELEASE, August 3, 2016
Contact: Gina DiGravio, 617-638-8480, firstname.lastname@example.org
Squash and Science: A New Pathway to STEM Success
(Boston)–Boston University School of Medicine’s (BUSM) CityLab program has received a Science Education Partnership Award (SEPA) from the National Institutes of Health (NIH). The $1.3 million grant will support a new partnership that combines afterschool squash training and academic STEM (Science, Technology, Engineering and Math) enrichment programs. This collaboration will build upon CityLab’s success in providing rich laboratory-based STEM experiences that inspire and prepare young people to develop an awareness of scientific research and critical thinking skills that inspire careers in STEM fields. City Lab has been funded by NIH for 25 consecutive years. Institutions of higher education around the country as well as internationally have adopted CityLab’s model of outreach in STEM education.
While CityLab has been available to all students, the current grant will focus on outreach to underrepresented groups in STEM. According to the experts, many urban minority middle and high school students lack exposure to authentic laboratory science experiences that can have a profound influence on their academic performance in school and ultimately their career trajectories. “We now have a unique opportunity to build a new program that will reach many underrepresented minorities students and position them for undergraduate STEM success,” explained Carl Franzblau, PhD, founder of CityLab and professor of biochemistry at BUSM.
The squash education movement for urban youth has been highly successful in preparing young students for success in college. However the current academic offerings of these programs focus on English Language Arts and mathematics with less preparation in STEM, therefore missing tremendous opportunities to develop interest in tSTEM fields. CityLab is partnering with Fordham University and squash organizations in Boston and New York to enrich and enhance STEM education for students from communities underrepresented in STEM. Most of the students will be among the first generation in their families to attend college.
“We will build upon the laboratory investigations developed by CityLab to create engaging STEM experiences in the context of athletics and exercise physiology,” said Don DeRosa, director of CityLab and MobileLab and clinical associate professor at BU’s School of Education. “Our premise is to leverage student interest in exercise and athletics to engage students in learning STEM concepts and skills.”
“Our vision is to develop a national model for informal precollege biomedical science education that can be infused into a myriad of similar athletic/academic enrichment programs,” added Franzblau.
In 1991, BUSM pioneered CityLab, an innovative, biotechnology learning laboratory serving students and teachers in grades 7–12 to provide access to state-of-the-art biotechnology laboratory facilities and curriculum, unavailable to most school systems. Teachers from Massachusetts and neighboring states bring their students to CityLab where they solve problems by applying the same techniques and concepts of genetics and molecular biology used in research laboratories today. Since it began, more than 100,000 students have participated in hands-on, discovery-oriented investigations and thousands of teachers have attended workshops at CityLab or aboard the MobileLab that brings the laboratory directly to schools. Both CityLab and MobileLab have been successfully replicated both nationally and internationally.
About NIH SEPA Program
NIH’s SEPA program is designed to improve life science literacy throughout the nation through innovative educational programs. SEPA-supported projects create partnerships among biomedical and clinical researchers and K-12 teachers and schools, museums and science centers, media experts, and other educational organizations.
Jupiter’s great red spot heats planet’s upper atmosphere
BU scientists answer elusive question in new study
(BOSTON) – Researchers from Boston University’s (BU) Center for Space Physics report today in Nature that Jupiter’s Great Red Spot may provide the mysterious source of energy required to heat the planet’s upper atmosphere to the unusually high values observed.
Sunlight reaching Earth efficiently heats the terrestrial atmosphere at altitudes well above the surface–even at 250 miles high, for example, where the International Space Station orbits. Jupiter is over five times more distant from the Sun, and yet its upper atmosphere has temperatures, on average, comparable to those found at Earth. The sources of the non-solar energy responsible for this extra heating have remained elusive to scientists studying processes in the outer solar system.
“With solar heating from above ruled out, we designed observations to map the heat distribution over the entire planet in search for any temperature anomalies that might yield clues as to where the energy is coming from,” explained Dr. James O’Donoghue, research scientist at BU, and lead author of the study.
Astronomers measure the temperature of a planet by observing the non-visible, infrared (IR) light it emits. The visible cloud tops we see at Jupiter are about 30 miles above its rim; the IR emissions used by the BU team came from heights about 500 miles higher. When the BU observers looked at their results, they found high altitude temperatures much larger than anticipated whenever their telescope looked at certain latitudes and longitudes in the planet’s southern hemi-sphere.
“We could see almost immediately that our maximum temperatures at high altitudes were above the Great Red Spot far below–a weird coincidence or a major clue?” O’Donoghue added.
Jupiter’s Great Red Spot (GRS) is one of the marvels of our solar system. Discovered within years of Galileo’s introduction of telescopic astronomy in the 17th Century, its swirling pattern of colorful gases is often called a “perpetual hurricane.” The GRS has varied is size and color over the centuries, spans a distance equal to three earth-diameters, and has winds that take six days to complete one spin. Jupiter itself spins very quickly, completing one revolution in only ten hours.
“The Great Red Spot is a terrific source of energy to heat the upper atmosphere at Jupiter, but we had no prior evidence of its actual effects upon observed temperatures at high altitudes,” ex-plained Dr. Luke Moore, a study co-author and research scientist in the Center for Space Physics at BU.
Solving an “energy crisis” on a distant planet has implications within our solar system, as well as for planets orbiting other stars. As the BU scientists point out, the unusually high temperatures far above Jupiter’s visible disk is not a unique aspect of our solar system. The dilemma also occurs at Saturn, Uranus and Neptune, and probably for all giant exoplanets outside our solar system.
“Energy transfer to the upper atmosphere from below has been simulated for planetary atmospheres, but not yet backed up by observations,” O’Donoghue said. “The extremely high temperatures observed above the storm appear to be the ‘smoking gun’ of this energy transfer, indicating that planet-wide heating is a plausible explanation for the ‘energy crisis.'”
The observations reported today and funded by NASA, were analyzed by O’Donoghue and Moore in collaboration with colleagues Thomas Stallard and Henrik Melin from the University of Leicester in the UK. Data taken spanned nine hours on the night of December 4, 2012, at the In-frared Telescope Facility (IRTF) on Mauna Kea, Hawaii, which is operated by the University of Hawaii under contract NNH14CK55B.
Founded in 1839, Boston University is an internationally recognized institution of higher educa-tion and research. With more than 33,000 students, it is the fourth-largest independent university in the United States. BU consists of 16 schools and colleges, along with a number of multi-disciplinary centers and institutes integral to the University’s research and teaching mission. In 2012, BU joined the Association of American Universities (AAU), a consortium of 62 leading research universities in the United States and Canada.
After nearly 5 years of space travel, NASA’s spacecraft Juno will finally enter Jupiter’s orbit on Monday, July 4. Several Boston University faculty and research scientists are available to comment, one of whom was directly involved with a joint project with the Hubble Space Telescope and Juno.
John Clarke is a professor of astronomy and the director of BU’s Center for Space Physics and an expert in planetary atmospheres. He has had some involvement with the Juno spacecraft. He is a co-investigator on a program with the Hubble Space Telescope focused on images of Jupiter’s aurora that has worked with Juno measurements of solar wind approaching Jupiter over the past month. Contact Clarke at 617–353–0247 or email@example.com.
Michael Mendillo is a professor of astronomy and part of the faculty roster at BU’s Center for Space Physics. He is an expert on space physics, planetary atmospheres, and observations and models. Previously, Mendillo initiated a planetary astronomy research effort at BU that led to discoveries of extraordinary large, tenuous atmospheres of sodium gas on Jupiter. Contact Mendillo at 617–353–2629 or firstname.lastname@example.org.
Luke Moore is a research scientist at BU’s Center for Space Physics, and earned his Ph.D. at BU. He studies study planetary atmospheres, focusing mostly on the ionospheres of Jupiter and Saturn. He has studied the heating of Jupiter’s upper atmosphere via the Great Red Spot, and could comment on any Juno results that link the lower and upper regions of Jupiter’s atmosphere. Contact Moore at 617–358–3906 or email@example.com.
Marissa Vogt is a research scientist at BU’s Center for Space Physics. Her research includes planetary magnetic fields, and has studied Jupiter’s magnetosphere and aurora. One of Juno’s other prime mission goals is to study the magnetic field of Jupiter. Contact Vogt at 617–686–1782 or firstname.lastname@example.org.