HUBBLE DETECTS GAS STREAMER ECLIPSES SUPERMASSIVE BLACK HOLE
From the FMS Global News Desk of Jeanne Hambleton
Embargo expired: 19-Jun-2014 2:00 PM EDT
Source Newsroom: Space Telescope Science Institute (STScI)
Citations Science Express, Jun-2014
Newswise — An international team of astronomers, using data from several NASA and European Space Agency (ESA) space observatories, has discovered unexpected behavior from the supermassive black hole at the heart of the galaxy NGC 5548, located 244.6 million light-years from Earth. This behavior may provide new insights into how supermassive black holes interact with their host galaxies.
Immediately after NASA’s Hubble Space Telescope observed NGC 5548 in June 2013, this international research team discovered unexpected features in the data. They detected a stream of gas flowing rapidly outward from the galaxy’s supermassive black hole, blocking 90 percent of its emitted X-rays.
“The data represented dramatic changes since the last observation with Hubble in 2011,” said Gerard Kriss of the Space Telescope Science Institute (STScI) in Baltimore, Maryland. “I saw signatures of much colder gas than was present before, indicating that the wind had cooled down due to a significant decrease in X-ray radiation from the galaxy’s nucleus.”
The discovery was made during an intensive observing campaign that also included data from NASA’s Swift spacecraft, Nuclear Spectroscopic Telescope Array (NuSTAR), and Chandra X-ray Observatory, as well as ESA’s X-ray Multi-Mirror Mission (XMM-Newton) and Integral gamma-ray observatory (INTEGRAL).
After combining and analyzing data from all six sources, the team was able to put together the pieces of the puzzle. Supermassive black holes in the nuclei of active galaxies, such as NGC 5548, expel large amounts of matter through powerful winds of ionized gas. For instance, the persistent wind of NGC 5548 reaches velocities exceeding 621 miles (approximately 1,000 kilometers) a second. But now a new wind has arisen, much stronger and faster than the persistent wind.
“These new winds reach speeds of up to 3,107 miles (5,000 kilometers) per second, but is much closer to the nucleus than the persistent wind,” said lead scientist Jelle Kaastra of the SRON Netherlands Institute for Space Research.
“The new gas outflow blocks 90 percent of the low-energy X-rays that come from very close to the black hole, and it obscures up to a third of the region that emits the ultraviolet radiation at a few light-days distance from the black hole.”
The newly discovered gas stream in NGC 5548 — one of the best-studied of the type of galaxy know as Type I Seyfert — provides the first direct evidence of a shielding process that accelerates the powerful gas streams, or winds, to high speeds. These winds only occur if their starting point is shielded from X-rays.
It appears the shielding in NGC 5548 has been going on for at least three years, but just recently began crossing their line of sight.
“There are other galaxies with similar streams of gas flowing outward from the direction of its central black hole, but we’ve never before found evidence that the stream of gas changed its position as dramatically as this one has,” said Kriss. “This is the first time we’ve seen a stream like this move into our line of sight. We got lucky.”
Researchers also deduced that in more luminous quasars, the winds may be strong enough to blow off gas that otherwise would have become “food” for the black hole, thereby regulating both the growth of the black hole and that of its host galaxy.
These results are being published online in the Thursday issue of Science Express.
For images and more information about Hubble, visit:
The Hubble Space Telescope is a project of international cooperation between NASA and the European Space Agency. NASA’s Goddard Space Flight Center in Greenbelt, Maryland, manages the telescope. STScI conducts Hubble science operations and is operated for NASA by the Association of Universities for Research in Astronomy, Inc., in Washington, D.C.
NEW BRAIN PATHWAYS FOR TYPE 2 DIABETES AND OBESITY
UT SOUTHWESTERN RESEARCHERS UNCOVER NEURAL PATHWAYS
From the FMS Global News Desk of Jeanne Hambleton
Released: 25-Jul-2014 2:00 PM EDT
Source Newsroom: UT Southwestern Medical Center
Citations Nature Neuroscience 17, 911–913 (2014)
Newswise — DALLAS – July 25, 2014 – Researchers at UT Southwestern Medical Center have identified neural pathways that increase understanding of how the brain regulates body weight, energy expenditure, and blood glucose levels – a discovery that can lead to new therapies for treating Type 2 diabetes and obesity.
The study, published in Nature Neuroscience, found that melanocortin 4 receptors (MC4Rs) expressed by neurons that control the autonomic nervous system are key in regulating glucose metabolism and energy expenditure, said senior author Dr. Joel Elmquist, Director of the Division of Hypothalamic Research, and Professor of Internal Medicine, Pharmacology, and Psychiatry.
“A number of previous studies have demonstrated that MC4Rs are key regulators of energy expenditure and glucose homeostasis, but the key neurons required to regulate these responses were unclear,” said Dr. Elmquist, who holds the Carl H. Westcott Distinguished Chair in Medical Research, and the Maclin Family Distinguished Professorship in Medical Science, in Honor of Dr. Roy A. Brinkley.
“In the current study, we found that expression of these receptors by neurons that control the sympathetic nervous system, seem to be key regulators of metabolism. In particular, these cells regulate blood glucose levels and the ability of white fat to become ‘brown or beige’ fat.”
Using mouse models, the team of researchers, including co-first authors Dr. Eric Berglund, Assistant Professor in the Advanced Imaging Research Center and Pharmacology, and Dr. Tiemin Liu, a postdoctoral research fellow in Internal Medicine, deleted MC4Rs in neurons controlling the sympathetic nervous system.
This manipulation lowered energy expenditure and subsequently caused obesity and diabetes in the mice. The finding demonstrates that MC4Rs are required to regulate glucose metabolism, energy expenditure, and body weight, including thermogenic responses to diet and exposure to cold. Understanding this pathway in greater detail may be a key to identifying the exact processes in which type 2 diabetes and obesity are developed independently of each other.
In 2006, Dr. Elmquist collaborated with Dr. Brad Lowell and his team at Harvard Medical School to discover that MC4Rs in other brain regions control food intake but not energy expenditure.
The American Diabetes Association lists Type 2 diabetes as the most common form of diabetes. The disease is characterized by high blood glucose levels caused by the body’s lack of insulin or inability to use insulin efficiently, and obesity is one of the most common causes.
Future studies by Dr. Elmquist’s team will examine how melanocortin receptors may lead to the “beiging” of white adipose tissue, a process that converts white adipose to energy-burning brown adipose tissue.
Other UT Southwestern researchers involved in the study include Dr. Philipp Scherer, Director of the Touchstone Center for Diabetes Research, Professor of Internal Medicine and Cell Biology, and holder of the Gifford O. Touchstone, Jr. and Randolph G. Touchstone Distinguished Chair in Diabetes Research; Dr. Kevin Williams, Assistant Professor of Internal Medicine; Dr. Syann Lee, Instructor of Internal Medicine; Dr. Jong-Woo Sohn, postdoctoral research fellow; and Charlotte Lee, senior research scientist.
The study was supported by the National Institutes of Health, the American Diabetes Association, and the American Heart Association.
About UT Southwestern Medical Center
UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty includes many distinguished members, including six who have been awarded Nobel Prizes since 1985. Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 91,000 hospitalized patients and oversee more than 2 million outpatient visits a year.
NEW CLUE HELPS EXPLAIN HOW BROWN FAT BURNS ENERGY
Investigators identify a major transciption fact that drives brown fat’s thermogenic process
From the FMS Global News Desk of Jeanne Hambleton
Embargo expired: 3-Jul-2014 12:00 PM EDT
Source Newsroom: Beth Israel Deaconess Medical Center
Newswise — BOSTON – The body contains two types of fat cells, easily distinguished by color: White and brown. While white fat serves to store excess calories until they are needed by the body, brown adipocytes actually burn fat by turning it into heat.
Ever since it was discovered that adult humans harbor appreciable amounts of brown fat, investigators have been working to better understand its thermogenic fat-burning properties with the ultimate goal of developing novel therapies to combat obesity and diabetes.
Now, research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) adds another piece to the puzzle, demonstrating that the transcription factor IRF4 (interferon regulatory factor 4) plays a key role in brown fat’s thermogenic process, regulating energy expenditure and cold tolerance. The findings appear in the July 3 issue of the journal Cell.
“The discovery several years ago that brown fat plays an active role in metabolism suggested that if we could manipulate the number or activity of these fat cells, we could force our bodies to burn extra calories,” explains the study’s senior author Evan Rosen, MD, PhD, an investigator in the Division of Endocrinology, Diabetes and Metabolism at BIDMC and Associate Professor of Medicine at Harvard Medical School.
“Now that we have identified a major factor driving this process, we can look for new approaches to exploit this for therapeutic benefit.”
Turned on by cold temperatures and by certain hormones and drugs, including epinephrine, brown fat generates heat through the actions of a group of genes collectively termed the thermogenic gene expression program, the best known of which encodes uncoupling protein 1 (UCP1). UCP1 dissipates, or wastes, energy in the mitochondria of brown fat cells, causing heat generation as a byproduct.
“There has been intense interest in how the UCP1 gene is regulated, with most attention focused on a molecule called PGC1-alpha,” explains Rosen.”PGC1-alpha was discovered 15 years ago in the lab of coauthor Bruce Spiegelman, and is a transcriptional co-factor, which means that it indirectly drives the transcription of genes like UCP1 because it lacks the ability to bind to DNA itself. This suggested that there must be a bona fide transcription factor, or DNA binding protein, that was mediating the effects of PGC-1alpha, but despite years of work and several promising candidates, no clear partner for PGC-1alpha had been discovered to increase thermogenesis. It turns out that IRF4 is that partner.”
Interferon regulatory factors (IRFs) play important roles in the regulation of the immune system. Rosen’s group had previously identified IRF4 as a key element in adipocyte development and lipid handling, having discovered that IRF4 expression is induced by fasting in fat and that animals that lack IRF4 in adipose tissue are obese, insulin resistant and cold intolerant.
In this new work, led by first author Xingxing Kong, PhD, a postdoctoral fellow in the Rosen lab, the scientists hypothesized that in addition to serving as a key regulator of lipolysis, IRF4 might also play a direct thermogenic role in brown fat.
Experiments in mouse models confirmed their hypothesis, demonstrating that IRF4 is induced by cold and cAMP in adipocytes and is sufficient to promote increased thermogenic gene expression, energy expenditure and cold tolerance. Conversely, loss of IRF4 in brown fat resulted in reduced thermogenic gene expression and energy expenditure, obesity and cold intolerance. Finally, the researchers showed that IRF4 physically interacts with PGC-1 alpha to promote UCP1 expression and thermogenesis.
“We’ve known a lot about how these genes are turned on by cold or when stimulated by catelcholamine drugs such as epinephrine,” explains Rosen.
“But we did not know what was turning on this gene program at the molecular level. With this new discovery of IRF4’s key transcriptional role, perhaps we can identify new drug targets that directly affect this pathway, which might be more specific than simply giving epinephrine-like drugs, which drive up heart rate and blood pressure.”
In addition to Rosen and Kong, coauthors include BIDMC investigators Tiemin Liu (now at the University of Texas Southwestern Medical Center), Songtao Yu (now at Northwestern University Feinberg School of Medicine), Xun Wang and Sona Kang; Alexander Banks, Lawrence Kazak, Rajesh R. Rao, Paul Cohen, James C. Lo, Sandra Kleiner and Bruce M. Spiegelman of Dana-Farber Cancer Institute; and Yu-Hua Tseng, Aaron M. Cypess and Ruidan Xue of Joslin Diabetes Center.
This study was funded, in part by National Institutes of Health grants R01 DK31405 and R01 DK085171 and an American Heart Association postdoctoral fellowship to Xingxing Kong.
Beth Israel Deaconess Medical Center is a patient care, teaching and research affiliate of Harvard Medical School, and currently ranks third in National Institutes of Health funding among independent hospitals nationwide.
The BIDMC health care team includes Beth Israel Deaconess Hospital-Milton, Beth Israel Deaconess Hospital-Needham, Beth Israel Deaconess Hospital-Plymouth, Anna Jaques Hospital, Cambridge Health Alliance, Lawrence General Hospital, Signature Health Care, Commonwealth Hematology-Oncology, Beth Israel Deaconess HealthCare, Community Care Alliance, and Atrius Health. BIDMC is also clinically affiliated with the Joslin Diabetes Center and Hebrew Senior Life and is a research partner of Dana-Farber/Harvard Cancer Center. BIDMC is the official hospital of the Boston Red Sox. For more information, visit http://www.bidmc.org.
Back tomorrow with more news. Jeanne