2012 (below)
2011
Several fatal brain disorders, including Parkinson's disease, are connected by the misfolding of specific proteins into disordered clumps and stable, insoluble fibrils called amyloid. Amyloid fibrils are hard to break up due to their stable, ordered structure. For example, a-synuclein forms amyloid fibrils that accumulate in Lewy Bodies in Parkinson's disease. By contrast, protein clumps that accumulate in response to environmental stress, such as heat shock, possess a less stable, disordered architecture.
Hsp104, an enzyme from yeast, breaks up both amyloid fibrils and disordered clumps. In the most recent issue of Cell, James Shorter, PhD, assistant professor of Biochemistry and Biophysics, and colleagues show that Hsp104 switches mechanism to break up amyloid versus disordered clumps. For stable amyloid-type structures, Hsp104 needs all six of its subunits, which together make a hexamer, to pull the clumps apart. By contrast, for the more amorphous, non-amyloid clumps, Hsp104 required only one of its six subunits.
Unexpectedly, the bacterial version of the Hsp104 enzyme, called ClpB, behaves differently compared to Hsp104. Bacterial ClpB uses all six subunits to break up amorphous clumps and fails to break up amyloid fibrils. Bacteria just ignore these more stable structures, whereas yeast use Hsp104 to exploit amyloid fibrils for beneficial purposes.
“One surprise is that biochemists thought that Hsp104 and ClpB hexamers worked in the same way,” says first author and graduate student in the Shorter lab Morgan DeSantis. “This is not the case.”
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Understanding
how any disease progresses is one of the first and most important steps towards
finding treatments to stop it. This has been the case for such
brain-degenerating conditions as Alzheimer's disease. Now, after several years
of incremental study, researchers at the Perelman School of Medicine, University
of Pennsylvania have been able to piece together important steps in how
Parkinson’s disease (PD) spreads from cell to cell and leads to nerve cell
death.
In short, the Penn researchers found that, in healthy mice, a single injection of synthetic, misfolded α-Syn fibrils led to a cell-to-cell transmission of pathologic α-Syn proteins and the formation of Parkinson’s α-Syn clumps known as Lewy bodies in interconnected regions of the brain. Their findings appear in this week’s issue of Science. The team was led by senior author Virginia M.-Y Lee, PhD, director of the Center for Neurodegenerative Disease Research (CNDR) and professor of Pathology and Laboratory Medicine, and first author Kelvin C. Luk, PhD, research assistant professor in the CNDR.
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James
Eberwine, PhD, Elmer Holmes Bobst Professor of Pharmacology in the
Perelman School of Medicine, and Junhyong Kim,
PhD, Edmund J. and Louise W. Kahn Professor of Biology in the School of Arts and
Sciences, will be studying the role of how messenger RNA (mRNA) molecules vary
in their function in individual cells with a five-year, $10 million grant from
the National Institutes of Health (NIH). Their award is supported by the NIH
Common Fund and is part of three initiatives of the Single Cell Analysis Program
(SCAP). Eberwine and Kim are also Co-directors of the Penn Genomic Frontiers Institute.
The goal of the Penn grant is to characterize the variability in identity and abundances of RNA molecules that are transcribed from the genome of human neurons and heart cells. These are the so-called excitable cells, those that use bioelectricity for communication and everyday functions. Many human nervous system diseases derive from changes in electrical responsiveness of neurons and heart arrhythmias account for many heart-related deaths.
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The cancer-causing form of the gene Myc alters the metabolism of mitochondria, the cell’s powerhouse, making it dependent on the amino acid glutamine for survival. In fact, 40 percent of all “hard-to-treat” cancers have a mutation in the Myc gene. Accordingly, depriving cells of glutamine selectively induces programmed cell death in cells overexpressing mutant Myc.
Using Myc-active neuroblastoma cancer cells, a team led by Howard Hughes Medical Institute (HHMI) investigator M. Celeste Simon, Ph.D., scientific director for the Abramson Family Cancer Research Institute (AFCRI), identified the proteins PUMA, NOXA, and TRB3 as executors of the glutamine-starved cells. These three proteins represent a downstream target in the Myc pathway at which to aim drugs. Roughly 25 percent of all neuroblastoma cases are associated with Myc-active cells.
The findings appear in this week’s issue of Cancer Cell. Simon is also a professor of Cell and Developmental Biology at
the Perelman School of Medicine, University of Pennsylvania. The Penn team
collaborated with colleagues from The Children’s Hospital of Philadelphia (CHOP) John
Maris and Michael
Hogarty.
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When a virus such as influenza invades our bodies, interferon proteins are among the first immune molecules produced to fight off the attack. A study by scientists from the University of Pennsylvania School of Veterinary Medicine offers a new strategy for enhancing the effects of interferon in fighting off infection. The research suggests that, by targeting a particular molecule in the interferon signaling pathway, specially designed drugs may be able to boost the activity of a person’s own interferon, augmenting the immune system’s fight against viruses. It’s possible that the same drugs might also be effective against some types of cancer and certain autoimmune conditions.
Serge Fuchs, a professor of cell biology in Penn Vet’sDepartment of Animal Biology and director of the School’s Mari Lowe Comparative Oncology Center, was the senior author on the paper published in theProceedings of the National Academy of Sciences.
“The practical significance of our study is a demonstration of the ability to use emerging pharmaceuticals to reactivate an individual’s own interferon or to use a reduced dose to get the same effect,” Fuchs said.
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An international effort led by researchers at the Perelman School of Medicine at Penn has resulted in positive phase 3 clinical trial results for a new medicine to treat patients suffering from a rare and deadly cholesterol disorder. Penn researchers report in The Lancet that lomitapide, a first-in-class microsomal triglyceride transfer protein (MTP) inhibitor, substantially and stably reduced LDL cholesterol (the “bad” cholesterol) in patients with the orphan disease homozygous familial hypercholesterolemia (HoFH). Lomitapide works by inhibiting MTP, which is required for the production of VLDL — the precursor to LDL.
Senior study author Daniel J. Rader, MD, chief, Division of Translational Medicine and Human Genetics, has treated HoFH patients for more than two decades. In the early 1990s, Rader worked with colleagues to determine that mutations in MTP were the cause of a rare condition characterized by absent LDL in the blood, establishing MTP as a therapeutic target to reduce LDL. His colleagues then went on to discover the MTP inhibitor lomitapide at Bristol-Myers Squibb (BMS). Rader led a study at Penn in the late 1990s showing that lomitapide substantially reduced LDL in patients with moderately elevated LDL. However, because the agent caused some gastrointestinal side effects and increased liver fat, BMS decided to abandon further development of lomitapide for a much larger population of patients with elevated levels of cholesterol. Rader convinced BMS to donate the drug to Penn so that he could continue to develop it in patients with HoFH. Based on its mechanism and on a study in a rabbit model of the disease, Rader felt it would be effective against HoFH.
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A new study by researchers at the Perelman School of Medicine at the University of Pennsylvania demonstrates in an animal model that a commonly used inhaled anesthetic drug, isoflurane, works by directly causing sleep-promoting neurons in the brain to activate, thereby hijacking our natural sleep circuitry. The findings are the latest work by investigators in the Center for Anesthesia Research at Penn who are exploring how anesthetics interact within the central nervous system to cause a state of unconsciousness. Thenew research is published the latest edition of the journal Current Biology.
"Despite more than 160 years of continuous use in humans, we still do not understand how anesthetic drugs work to produce the state of general anesthesia," said study author Max B. Kelz, MD, PhD, assistant professor of Anesthesiology and Critical Care. "We show in this new work that a commonly used inhaled anesthetic drug directly causes sleep-promoting neurons to fire. We believe that this result is not simply a coincidence. Rather, our view is that many general anesthetics work to cause unconsciousness in part by commandeering the brain’s natural sleep circuitry, which initiates our nightly journey into unconsciousness."
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Scott Halpern of Medicine discusses a new end-of-life studies center that researches one of “health care's most contentious and painful areas.”
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Medicine's Virginia Lee and John Trojanowski discuss the need for drug discovery to combat the “natural disaster of our millennium,” neurodegenerative disease.
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Nearly 100 years after a British neurologist first mapped the blind spots caused by missile wounds to the brains of soldiers, Perelman School of Medicine researchers at the University of Pennsylvania have perfected his map using modern-day technology. Their results create a map of vision in the brain based upon an individual's brain structure, even for people who cannot see. Their result can, among other things, guide efforts to restore vision using a neural prosthesis that stimulates the surface of the brain. The study appears in the latest issue of Current Biology, a Cell Press journal.
"By measuring brain anatomy and applying an algorithm, we can now accurately predict how the visual world for an individual should be arranged on the surface of the brain," said senior author Geoffrey Aguirre, MD, PhD, assistant professor of Neurology. "We are already using this advance to study how vision loss changes the organization of the brain."
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We couldn’t live without our immune systems, always tuned to detect and eradicate invading pathogens and particles. But sometimes the immune response goes overboard, triggering autoimmune diseases like lupus, asthma or inflammatory bowel disease.
A
new study led by Christopher
Hunter, professor and chair in the Department of Pathobiology in
Penn’s School of Veterinary Medicine and Aisling O’Hara Hall, a
doctoral candidate in the Immunology
Graduate Group, has now identified a crucial signaling molecule involved in
counterbalancing the immune system attack.
“The immune response is like driving a car,” said Hunter. “You hit the accelerator and develop this response that’s required to protect you from a pathogen, but, unless you have a brake to guide the response, then you’ll just careen off the road and die because you can’t control the speed of the response.”
The study is published in the September issue of the journal Immunity.
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Researchers from the Perelman School of Medicine at Penn have been awarded a $3.7 million grant from the National Institutes of Health (NIH) to establish a new translational interdisciplinary research center to explore the role of sex and gender in behavioral health.
The new Center for the Study of Sex and Gender in Behavioral Health will be led by C. Neill Epperson, MD, associate professor of Psychiatry and founder and director of the Penn Center for Women's Behavioral Wellness, as principal investigator, along with Tracy L. Bale, PhD, Center co-director and associate professor of Psychiatry at the Perelman School of Medicine and director, Neuroscience Center at Penn's School Of Veterinary Medicine.
“It is well established that sex and gender are critical determinants of mental health and mental illness. But what isn’t clear is how hormonal developmental milestones such as puberty and early life traumatic events interact to impact neuropsychiatric health in women across the lifespan,” said Dr. Epperson. “Using behavioral and molecular models of stress and reproductive neuroendocrinology, psychophysiology, and neuroimaging, the new Center for the Study of Sex and Gender in Behavioral Health will investigate the unique mechanisms at play in women’s behavioral health.”
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How does one’s experience of an event get translated into a memory that can be accessed months, even years later? A team led by University of Pennsylvania scientists has come closer to answering that question, identifying key molecules that help convert short-term memories into long-term ones. Joshua Hawk (right), now a postdoctoral research fellow at Yale University, led the study, which was conducted as part of his Ph.D. work in the Neuroscience Graduate Group at Penn. He worked with Ted Abel (left), PhD, Penn’s Brush Family Professor of Biology.
“There are many drugs
available to treat some of the symptoms of diseases like schizophrenia,” Abel
said, “but they don’t treat the cognitive deficits that patients have, which can
include difficulties with memory. This study looks for more specific targets to
treat deficits in cognition.”
Published in the Journal of Clinical Investigation, the study focused on a group of proteins called nuclear receptors, which have been implicated in the regulation of a variety of biological functions, including memory formation.
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Researchers at the Perelman School of Medicine at the University of Pennsylvania report in a new study that thickening of the heart’s right ventricle is associated with an increased risk of heart failure and cardiovascular death in patients without clinical cardiovascular disease at baseline. The study is published online ahead of print in the journal Circulation.
“In most studies of the heart, researchers have focused on the more-easily-imaged left ventricle, the region of the heart affected by systemic high blood pressure and other common conditions,” said study author Steven Kawut, M.D., M.S., associate professor of Medicine and Epidemiology and director of the Pulmonary Vascular Disease Program at Penn. “But we know from the results of this study and previous work that focusing attention on the right ventricle (RV) is critical in our understanding of many conditions of the heart and lungs. This research revealed that approximately one in 10 heart failure events and cardiovascular deaths may be attributed to thickening of the RV in adults without clinical cardiovascular disease at baseline.”
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Yvonne
Paterson, PhD, professor of Microbiology (Cell & Molecular Biology and Immunology Graduate Groups), at the
Perelman School of Medicine, and professor and associate dean, at the School of
Nursing, has been awarded an almost $5 million renewal by the National Institute
for General Medical Sciences for the University of Pennsylvania Postdoctoral
Opportunities in Research and Training, or PENN-PORT, the postdoctoral-training
program she leads.
This program funds 15 postdoctoral fellows who teach in local colleges and universities that have a significant minority enrollment. The PENN-PORT program combines a traditional, three-year postdoctoral research training with a two-year mentored teaching experience at one of three partner minority-serving institutions: Lincoln University, Rutgers University-Camden, and Delaware County Community College.
The goals of the postdoctoral program are to enhance research-oriented teaching at the partner institutions; to promote research collaborations between faculty members at the three partner institutions and Penn; and to encourage minority students to enter graduate school and increase minority participation in biomedical research.
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Penn Medicine research presented on July 19th at the 2012 Alzheimer's Association International Conference (AAIC) shows that an anti-tau treatment called epithilone D (EpoD) was effective in preventing and intervening the progress of Alzheimer's disease in animal models, improving neuron function and cognition, as well as decreasing tau pathology.
"This drug effectively hits a tau target by correcting tau loss of function, thereby stabilizing microtubules and offsetting the loss of tau due to its formation into neurofibrillary tangles in animal models, which suggests that this could be an important option to mediate tau function in Alzheimer's and other tau-based neurodegenerative diseases," said John Trojanowski, MD, PhD, (Neuroscience Graduate Group). "In addition to drugs targeting amyloid, which may not work in advanced Alzheimer's disease, our hope is that this and other anti-tau drugs can be tested in people with Alzheimer's disease to determine whether stabilizing microtubules damaged by malfunctioning tau protein may improve clinical and pathological outcomes."
Bristol-Myers Squibb, who developed and owns the rights to the drug, has started enrolling patients into a phase I clinical trial in people with mild Alzheimer's disease.
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Researchers are hopeful that new advances in tissue engineering and regenerative medicine could one day make a replacement liver from a patient’s own cells, or animal muscle tissue that could be cut into steaks without ever being inside a cow. Bioengineers can already make 2D structures out of many kinds of tissue, but one of the major roadblocks to making the jump to 3D is keeping the cells within large structures from suffocating; organs have complicated 3D blood vessel networks that are still impossible to recreate in the laboratory.
Now, University of Pennsylvania researchers have developed an innovative solution to this perfusion problem: they’ve shown that 3D printed templates of filament networks can be used to rapidly create vasculature and improve the function of engineered living tissues.
The research was conducted by a team led by postdoctoral fellow Jordan S. Miller and Christopher S. Chen, the Skirkanich Professor of Innovation in the Department of Bioengineering at Penn (CAMB), along with Sangeeta N. Bhatia, Wilson Professor at MIT, and postdoctoral fellow Kelly R. Stevens in Bhatia’s laboratory.
Their work was published in the journal Nature Materials.
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Researchers have long been interested in discovering the ways that human brains represent thoughts through a complex interplay of electrical signals. Recent improvements in brain recording and statistical methods have given researchers unprecedented insight into the physical processes underlying thoughts.
A new study by University of Pennsylvania and Thomas Jefferson University scientists brings this work one step closer to actual mind reading by using brain recordings to infer the way people organize associations between words in their memories.
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The research was conducted by professor Michael J. Kahana, PhD (Neuroscience, left) and former graduate student Jeremy R. Manning, PhD (right), a 2011 graduate of the Neuroscience Graduate Group. They collaborated with other members of Kahana’s laboratory, as well as with research faculty at Thomas Jefferson University Hospital. |
Their study was published in The Journal of Neuroscience.
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Psoriasis is an independent risk for Type 2 Diabetes, according to a new study by researchers with the Perelman School of Medicine at the University of Pennsylvania, with the greatest risk seen in patients with severe psoriasis. Researchers estimate that an additional 115,500 people will develop diabetes each year due to the risk posed by psoriasis above and beyond conventional risk factors. The research is published in the latest issue of the Archives of Dermatology, a JAMA Network publication.
"These data suggest that patients with psoriasis are at increased risk for developing diabetes even if they don't have common risk factors such as obesity," said senior author Joel M. Gelfand, MD, MSCE (Epidemiology and Biostatistics group). "Patients with psoriasis should eat a healthy diet, get regular exercise, and see their physician for routine preventative health screenings such as checks of blood pressure, cholesterol, and blood sugar."
Psoriasis is a common inflammatory skin disease affecting over 7.5 million Americans and causes thick, inflamed, scaly patches of skin. The disease has previously been associated with increased risk of myocardial infarction, stroke, metabolic syndrome and cardiovascular mortality.
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The healthy human intestine is colonized with over 100 trillion
beneficial, or commensal, bacteria of many different species. In healthy people,
these bacteria are limited to the intestinal tissues and have a number of
helpful properties, including aiding in the digestion of food and promoting a
healthy immune system. However, several chronic human diseases, including
HIV/AIDS, inflammatory bowel disease, viral hepatitis, and obesity are
associated with the spread of these intestinal commensal bacteria to the blood
stream and other peripheral tissues, which can cause chronic inflammation.
David Artis, PhD, (Immunology, Cell & Molecular Biology), and Gregory F. Sonnenberg, PhD, a postdoctoral researcher in the Artis lab, have identified that immune cells, called innate lymphoid cells, are resident in the intestinal tissues of healthy humans, mice, and non-human primates, and are critical in limiting the location of commensal bacteria. If the innate lymphoid cells are depleted in mice, commensal bacteria move to peripheral tissues and promote inflammation.
"A fundamental question that has puzzled researchers for many years is how did the human body evolve to accommodate all these commensal bacteria and keep them in their correct locations?," asks Artis. "The indication from these studies is that the body may have many different pathways to limit the spread of commensal bacteria and these pathways may be tailored to specific types of bacteria."
The research was published in the current edition of Science.
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The Perelman School of Medicine at the University of Pennsylvania, in
collaboration with the University of Pennsylvania School of Nursing and School
of Dental Medicine, has been designated a national Center of Excellence in Pain
Education (CoEPEs) by the National Institutes of Health (NIH).
"Pain is one of the primary reasons that patients seek medical care," said John T. Farrar, MD, PhD (Epidemiology & Biostatistics group), co-principal investigator of the new center. "Learning how to properly diagnose the underlying cause and how to effectively treat both acute and chronic pain needs to be an important focus of medical education. The interprofessional collaboration between three Penn schools in this endeavor is pivotal to our mission to help redefine pain education in the U.S. health care system and improve the lives of all of our patients."
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By pairing an intimate knowledge of immune-system function with a deep understanding of statistical physics, a cross-disciplinary team at the University of Pennsylvania, led by senior authors Christopher Hunter, professor and chair of the Pathobiology Department in Penn’s School of Veterinary Medicine (Cell & Molecular Biology and Immunology Graduate Groups), and Andrea Liu, the Hepburn Professor of Physics in the Department of Physics and Astronomy, has arrived at a surprising finding: T cells use a movement strategy to track down parasites that is similar to strategies that predators such as monkeys, sharks and blue-fin tuna use to hunt their prey.
With this new insight into immune-cell movement patterns, scientists will be able to create more accurate models of immune-system function, which may, in turn, inform novel approaches to combat diseases from cancer to HIV/AIDS to arthritis.
The study, published in the journal Nature, was conducted in mice infected with the parasite Toxoplasma gondii.
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A new study published by researchers at the Perelman School of Medicine at the University of Pennsylvania, the Broad Institute, and Massachusetts General Hospital, challenges the conventional concept that raising a person's HDL levels (good cholesterol) will always help lower their risk of a heart attack. In the study, published in May 17 edition of The Lancet, the research team analyzed previously identified DNA sequence variations directly associated with elevated HDL levels in humans. After analyzing the genes of roughly 170,000 individuals, the team discovered that none of these established genetic variations actually reduced the risk of heart attack.
"The concept that genetic data can directly test the relationship between a biomarker like HDL to heart attack is an extremely potent one. Through our research, we have found that all roads that raise HDL do not always lead to the promise land of reduced risk of heart attack," said Benjamin F. Voight, PhD (PHRM), lead author of the new study. "These data have important implications for future development of therapies based on raising HDL levels."
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A team of University of Pennsylvania researchers has
recently been recognized by the National Science Foundation for the development
of computer models that will be instrumental in improving the design of
pharmaceuticals on an atomic scale.
Led by Ravi Radhakrishnan, PhD (BMB, GCB), the team also included Portonovo Ayyaswamy, PhD (Engineering) as well as David Eckmann, PhD, MD, and Vladimir Muzykantov, PhD (PHRM).
The team received a “Research Highlight” from the NSF’s Division of Chemical, Bioengineering, Environmental & Transport Systems, and the work for which they were honored was published in the Biophysical Journal.
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Nancy Bonini, PhD (NGG), Gideon Dreyfuss, PhD (CAMB, BMB), and Beatrice H. Hahn, MD (CAMB), of the University of Pennsylvania have been elected members of the National Academy of Sciences, considered one of the highest honors that can be accorded a U.S. scientist or engineer.
Cited for “their distinguished and continuing achievements in original
research,” the three scientists are part of the 2012 Academy class of 84 members
and 21 foreign associates.
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Garret FitzGerald, MD
(GCB), is among the 44 newly elected Fellows and eight newly elected Foreign
Members to the Royal Society.
"Science impacts on most aspects of modern life, improving our understanding of the world and playing an increasing role as we grapple with problems such as feeding a growing global population and keeping an aging population healthy. These scientists who have been elected to the Fellowship of the Royal Society are among the world's finest. They follow in the footsteps of luminaries such as Newton, Darwin and Einstein and I am delighted to welcome them into our ranks," noted Sir Paul Nurse, President of the Royal Society.
"I am deeply honored by this recognition of the efforts and accomplishments of those with whom I have been privileged to work," said FitzGerald.
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The 24-hour internal clock controls many aspects of human behavior and physiology, including sleep, blood pressure, and metabolism. Disruption in circadian rhythms leads to increased incidence of many diseases, including metabolic disease and cancer. Each cell of the body has its own internal timing mechanism, which is controlled by proteins that keep one another in check.
One of these proteins, called Rev-erb alpha, was thought to have a subordinate role because the clock runs fairly normally in its absence. New work, published in Genes and Development this month, from the lab of Mitchell Lazar, MD, PhD (CAMB, GCB, PRHM), found that a closely related protein called Rev-erb beta serves as a back-up for Rev-erb alpha. When both are not functioning, the cellular clock loses its time-keeping function.
The two Rev-erbs work together to control fat metabolism, and in their absence, the liver fills with fat. These findings establish the Rev-erbs as major regulators of both clock function and metabolism.
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When poet Walt Whitman wrote that we "contain multitudes," he was speaking metaphorically, but he was correct in the literal sense. Every human being carries over 100 trillion individual bacterial cells within the intestine -- ten times more cells than comprise the body itself.
Now, David Artis, PhD (IMUN, CAMB), along with postdoctoral fellow David Hill, PhD, and collaborators from The Children's Hospital of Philadelphia and institutions in Japan and Germany, have found that these commensal bacteria might play an important role in influencing and controlling allergic inflammation. The commensal relationship that develops between humans and internal bacteria is one in which both humans and bacteria derive benefits.
The study -- appearing this week in Nature Medicine -- suggests that therapeutic targeting of immune cell responses to resident gut bacteria may be beneficial in treating allergic diseases.
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Insulin resistance in the
brain precedes and contributes to cognitive decline above and beyond other known
causes of Alzheimer's disease, according to a new study by researchers from
Penn's Perelman School of Medicine. This is the first study to directly
demonstrate that insulin resistance occurs in the brains of people with
Alzheimer's disease. The study is now online in the Journal of Clinical
Investigation.
"Our research clearly shows that the brain's ability to respond to insulin, which is important for normal brain function, is going offline at some point...We believe that brain insulin resistance may be an important contributor to the cognitive decline associated with Alzheimer's disease," said senior author, Steven E. Arnold, MD (NGG).
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A growing body of evidence
underscores the importance of human gut bacteria in modulating human health,
metabolism, and disease. Yet bacteria are only part of the story. Viruses that
infect those bacteria also shape who we are. Frederic D.
Bushman, PhD (CAMB, GCB), led a study published this month in the
Proceedings of the National Academy of Sciences that sequenced the DNA of
viruses -- the virome -- present in the gut of healthy people.
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Dennis E. Discher,
PhD (CAMB, PHRM), has been elected to the National Academy of Engineering for
his accomplishments in "elucidation of the effects of mechanical forces on cell
physiology and stem cell development."
Election to the National Academy of Engineering is among the highest professional distinctions accorded to an engineer. Academy membership honors those who have made outstanding contributions to "engineering research, practice, or education, including, where appropriate, significant contributions to the engineering literature," and to the "pioneering of new and developing fields of technology, making major advancements in traditional fields of engineering, or developing/implementing innovative approaches to engineering education."
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The molecular pathway that carries time-of-day signals from the body's
internal clock to ultimately guide daily behavior is like a black box,
says Amita Sehgal, PhD (CAMB, NGG) the John Herr Musser
Professor of Neuroscience and Co-Director, Comprehensive Neuroscience Center, at
the Perelman School of Medicine, University of Pennsylvania.
Now, new research from the Sehgal lab is taking a peek inside, describing a molecular pathway and its inner parts that connect the well-known clock neurons to cells governing rhythms of rest and activity in fruit flies. Sehgal is also an investigator with the Howard Hughes Medical Institute.
The other co-author on the study is Wenyu Luo, PhD, a CAMB doctoral student who recently defended her dissertation. The findings, which will be featured on the cover of the February 17th issue of Cell, are published online this week.
"Most colleagues would say that we have some understanding of how the clock works and how it is synchronized with light,” says Sehgal. “But we are just beginning to get a glimpse of how the clock drives behavior in the rest of an organism's systems."
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