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Imaging Excellence — David Gaita, a college student who participated in the 2012 Summer Undergraduate Research Program, won the “Novel Application Image of the Year” category of the Siemens Preclinical Image of the Year contest, along with his mentors. The award showcases images acquired as part of cutting-edge preclinical research using Siemens imaging systems. The award-winning images tested the feasibility of utilizing a widely used medical radioisotope, Technetium-99m (Tc-99m-MAA), to image the live goldfish brain. The winning images showed that Tc-9mm-MAA readily localizes to the gills, brain, and the suprabranchial chamber of the goldfish.  The experiment was conducted using a novel device ? specially designed and constructed by Wade Koba, operations manager of the MicroPET Core Facility ? that immobilizes aquatic animals in their natural environment. (Einstein has filed a patent application related to this research, which is available for licensing.) Results from the experiment demonstrated the ability to obtain repeated imaging without harm to the fish. This lays important groundwork for the possibility of imaging conscious zebra fish, an important vertebrate model organism used in such diverse fields as genetics, developmental biology, cancer, and immunology.  Mr. Gaita conducted his studies under the guidance of Dr. Linda Jelicks, associate professor of physiology and biophysics.

Wednesday, July 31, 2013
 

Examining Scientific Fraud — Dr. Arturo Casadevall’s research with collaborator Dr. Ferric Fang (University of Washington, Seattle), examining incidents of scientific fraud, was the “NewsFocus” feature in the January 24, 2013 issue of Science. The article chronicles how Drs. Casadevall and Ferric are taking a hard look at honesty in science and questioning the ethos of their profession. The publication, which is subscription-only, may be viewed at www.sciencemag.org. Dr. Casadevall is professor and chair of microbiology & immunology and the Leo and Julia Forchheimer Chair of Microbiology & Immunology.

Wednesday, July 31, 2013
 

Slowed Signaling Stumps Tumors  — Research by Drs. Jonathan BackerHashem Dbouk, and collaborators at the Medical Research Council Laboratory of Molecular Biology, in Cambridge, UK, may reveal a novel target for anti-cancer drugs. The scientists found a method for blocking a specific enzyme, PI3Kβ, which is known to promote tumor formation.  PI3Kβ  can be activated by receptor tyrosine kinases and by G-protein coupled receptors (GPCRs), but the mechanism of GPCR activation was unknown. The researchers identified the region of PI3Kβ required for its activation by GPCRs. Expression of a mutant PI3Kβ that cannot be activated by GPCRs, or treatment of cells with a peptide inhibitor of PI3Kβ activation, prevented control cells from becoming cancerous, and prevented the invasion of tumor cells in an in vitro metastasis assay. The data suggest that inhibition of GPCR signaling may provide a novel approach to the treatment of some cancers. Dr. Backer is a professor of molecular pharmacology. Dr. Dbouk is a recently graduated Ph.D. student in Dr. Backer’s lab. The study was featured on the cover of the December 4, 2012 issue of Science Signaling.

Wednesday, July 31, 2013
 

Insightful Research Research to Prevent Blindness (RPB) has presented Dr. Nicholas Baker with its Senior Scientific Investigator Award. This grant not only acknowledges Dr. Baker as a leader in the field of eye research, it allocates $150,000 in highly sought-after, flexible support for current research conducted by an established investigator. Dr. Baker aims to identify genes that enable some cells to prosper while neighboring cells perish. Such genes could also dictate whether a healthy eye cell will become diseased. A better understanding of the roles of these genes could reveal the causes of certain eye diseases and provide guidance for their prevention or treatment. RPB is the largest private funder of research into eye disease prevention and treatment, providing hundreds of millions of dollars in support since its inception in 1960. Dr. Baker joins a select group of 184 researchers who have been bestowed the Senior Scientific Investigator Award since its introduction in 1987. Dr. Baker is professor of ophthalmology & visual sciences, of genetics and of developmental & molecular biology.

Wednesday, July 31, 2013
 

Fate of fats and stem cells — Dr. Keisuke Ito has received $1.6 million from the National Institute of Diabetes and Digestive and Kidney Disease to study the role of lipid metabolism in the maintenance of hematopoietic stem cells (HSCs). HSCs have the potential to become all types of blood cells and are therefore important in maintaining the blood cell population throughout the lifespan of an organism. Understanding the mechanisms that determine the fate of HSCs will allow investigators to harness the potential of stem cells for clinical applications. The researchers will investigate how a key gene involved in lipid metabolism, PPARdelta, determines the fate and maintenance of this stem cell population, with a goal of identifying therapeutic approaches for manipulating the function of HSCs and clinical potential for enhancing and extending the health and well-being of patients. Dr. Ito is assistant professor of medicine and of cell biology, and director of Scientific Resources of the Stem Cell Institute.

Wednesday, July 31, 2013
 

Fateful Regulator — Researchers led by postdoctoral fellow Dr. Britta Will and her mentor, Dr. Ulrich Steidl, have identified a new critical regulator of hematopoietic stem cell (HSC) fate called Satb1, a protein that has been linked to several types of cancer. HSCs are precursor blood cells that have the ability to mature into specialized cell types. They are guided by various factors within the cell to either commit to a particular cell lineage (differentiation commitment) or to maintain their immature form (self-renewal).  Although individual molecular mechanisms underlying each of these two opposing cell fates are understood, until recently, how they are coordinated has remained elusive. By studying stem cells lacking Satb1, the research team was able to show that the protein indeed coordinates the two processes:  Satb1 regulates self-renewal by simultaneously promoting quiescence (halting cell division) and by repressing differentiation commitment. The findings appear in the April 7 issue of Nature Immunology. Dr. Steidl is assistant professor of cell biology and of medicine (oncology).

Wednesday, July 31, 2013
 

“Leuk”ing for a Cure — Dr. Ulrich G. Steidl had received an award of $1.8 million from The National Cancer Institute to study the role of a specific gene, HLX, in causing acute myeloid leukemia (AML), a cancer of white blood cells characterized by abnormal, rapid growth that interferes with the cells’ normal functions.  The HLX gene encodes a protein that activates other genes (transcription factor); Dr. Steidl previously found that excessive amounts of HLX is associated with AML in both mouse models and in human patients.  With this funding, he will study the mechanisms by which high amounts of HLX initiate AML; the genes that HLX targets for activation, which may work in concert to cause disease; and how HLX might be manipulated to identify possible therapeutic approaches.  Dr. Steidl is assistant professor of cell biology and of medicine and is the Diane and Arthur B. Belfer Faculty Scholar in Cancer Research.

Wednesday, July 31, 2013
 

Pompe’s Circumstance  Dr. Jeffrey Pessin has been awarded $2.5 million from the National Institute of Arthritis and Musculoskeletal and Skin Diseases to study the mechanism of Pompe’s disease.  Resulting from deficiency in an enzyme that breaks down glycogen, a storage form of glucose in the liver and muscle that is the major source of energy for cells, Pompe’s disease can cause fatal heart and lung failure in infants.  The process by which cells degrade damaged or unused components and molecules is called macroautophagy and late events in this pathway are damaged in this disease.  The grant will aid Dr. Pessin’s research into the mechanism of muscle degradation in Pompe’s disease and how defects in macroautophagy contribute to this process.  Ultimately, Dr. Pessin aims to design nutritional, exercise, and drug therapies that may help restore proper function in this pathway, which also might be used to treat related diseases.  Dr. Pessin is professor of medicine and of molecular pharmacology, director of the Diabetes Research Center, and the Judy R. and Alfred A. Rosenberg Professorial Chair in Diabetes Research.

Wednesday, July 31, 2013
 

Silencing “Selfish DNA”  Transposable elements (TEs) are mobile segments of genomic DNA that are often referred to as “selfish DNA” because they insert copies of themselves into different locations within the genome where they can cause harmful mutations. For this reason, it is important that cells repress TEs. A collaborative study between the laboratories of Drs. Arthur Skoultchi and Dmitry Fyodorov, published in the April 5 issue of Science, has revealed a novel mechanism for TE silencing that appears to protect chromosomes from injury. The current model highlights small RNA interference as the major pathway for TE repression; however, the Einstein team, including first author Dr. Xingwu Lu, discovered a new pathway, which silences TEs by compacting the regions of the genome in which they are located, effectively inactivating the selfish DNA.  The researchers also show that the linker histone H1 specifically recruits a “code-writer” enzyme, Su(var)3-9, which marks the TEs for silencing. Dr. Skoultchi is professor and chair of cell biology, as well as the Judith and Burton P. Resnick Chair in Cell Biology; Dr. Fyodorov is associate professor and Dr. Lu is an associate in the same department.

Wednesday, July 31, 2013
 

Looking at Liver Functions The National Institute of Diabetes and Digestive and Kidney Disorders has awarded Drs. Allan Wolkoff and Ana Maria Cuervo $2.9 million over four years to study two processes, endocytosis and autophagy, which are fundamental to the health of liver cells. Endocytosis (how cells engulf material) and autophagy (how cells eliminate internal toxic products) are related events that involve containment of material within similar internal compartments and play critical roles in protein breakdown. Drs. Wolkoff and Cuervo will study these pathways and how they interact to contribute to the maintenance of optimal health in liver cells. Dysfunction in these two pathways is associated with a variety of human diseases and these studies will provide fundamental knowledge that may suggest therapeutic targets for restoring normal liver function or for slowing decline in related liver diseases. Dr. Wolkoff is professor of medicine and of anatomy and structural biology, director of the Marion Bessin Liver Research Center and chief of the division of gastroenterology and liver diseases in medicine. He also holds the Herman Lopata Chair in Liver Disease Research.  Dr. Cuervo is professor of developmental and molecular biology, of anatomy and structural biology and of medicine, and is co-director of the Einstein Institute for Aging Research. She also is the Robert and Renee Belfer Chair for the Study of Neurodegenerative Diseases.

Wednesday, July 31, 2013
 
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