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Archive - Oct 29, 2015

Electric Eels Use Sophisticated Electrical System As Both Weapon and Sensory Tool

The electric eel may be one of the most remarkable predators in the entire animal kingdom. That is the conclusion of Kenneth Catania, Ph.D., Stevenson Professor of Biological Sciences at Vanderbilt University, who has spent the last three years studying the way this reclusive South American fish uses electric fields to navigate through the muddy waters of the Amazon and Orinoco basins where it lives, to locate hidden prey, and to stun them into submission. Electric eels can grow to lengths exceeding eight feet and weights of more than 44 pounds. Over two thirds of the eel's body is filled with specialized cells called electrocytes that store electricity like small biological batteries. When the eel is threatened or attacking prey, these cells discharge simultaneously, emitting electrical discharges of at least 600 volts, five times the voltage of a standard U.S. wall socket. "Historically, electric eels have been viewed as unsophisticated, primitive creatures that have a single play in their playbook: shocking their prey to death," said Dr. Catania. "But it turns out that they can manipulate their electric fields in an intricate fashion that gives them a number of remarkable abilities." One of the biologist's latest discoveries, reported online on October 28, 2015 in the journal Current Biology, is that the eels have a special maneuver that allows them to double the electrical shock that they can deliver to particularly large or difficult prey. This article is titled “Electric Eels Concentrate Their Electric Field to Induce Involuntary Fatigue in Struggling Prey.” The eel's electrical system essentially provides it with a wireless Taser that it uses to stun its prey. In a study published last year, Dr.

HHMI Develops First Light Microscope (IsoView) Capable of Imaging Large, Non-Transparent Specimens at Sub-Second Temporal Resolution and Sub-Cellular Spatial Resolution in All Dimensions

A new microscope developed at the Howard Hughes Medical Institute's (HHMI’s) Janelia Research Campus in Virginia is giving scientists a clearer, more comprehensive view of biological processes as they unfold in living animals. The microscope produces images of entire organisms, such as a zebrafish or fruit fly embryo, with enough resolution in all three dimensions so that each cell appears as a distinct structure. What's more, the new microscope does so at speeds fast enough to watch cells move as a developing embryo takes shape and to monitor brain activity as it flashes through neuronal circuits. Nearly two years in development, Janelia group leader Dr. Philipp Keller says his team has built the first light microscope capable of imaging large, non-transparent specimens at sub-second temporal resolution and sub-cellular spatial resolution in all dimensions. Dr. Keller and his team at Janelia aim to understand how a functioning nervous system emerges in an embryo. Over the last five years, they have devised several imaging technologies that make it possible to image large biological samples at high speed. His lab's newest microscope, called the IsoView light sheet microscope, overcomes a final challenge--improving spatial resolution--without sacrificing the performance features of his team's previous microscopes. The IsoView microscope is described in an article published online on October 26, 2015, in the journal Nature Methods. The article is titled “Whole-Animal Functional and Developmental Imaging with Isotropic Spatial Resolution.” The publication includes complete building plans for the microscope and the associated image processing software developed by Dr. Keller's team. In 2012, Dr. Keller's team developed the SiMView microscope, which provides fast three-dimensional imaging of large specimens.

Gladstone iPSC Nobel Laureate Elected to National Academy of Medicine

Nobel Laureate (2012) Shinya Yamanaka (photo), M.D., Ph.D., a Senior Investigator at the Gladstone Institutes in San Francisco and inventor of induced pluripotent stem cells (iPSCs), has been elected to the National Academy of Medicine. “This latest accomplishment further acknowledges Shinya’s tremendous contributions to the fields of science and medicine. His discovery of induced pluripotent stem cells has revolutionized biomedical research and has the potential to improve the lives of millions. This distinction is well deserved,” says Gladstone President R. Sanders “Sandy” Williams, M.D. “It is a great honor to be named to this distinguished institution and join such an esteemed group of scientists. It is especially meaningful that the decision is made by a panel of my peers,” says Dr. Yamanaka, who is also the L.K. Whittier Foundation Investigator in Stem Cell Biology at Gladstone, a Professor of Anatomy at the University of California, San Francisco (UCSF), and Director and Professor at the Center for iPS Cell Research and Application (CiRA), Kyoto University in Japan. Election to the National Academy of Medicine, formerly the Institute of Medicine, is considered one of the highest accomplishments in the fields of health and medicine and recognizes individuals around the world who have demonstrated outstanding professional achievement and commitment to service. “Our newly elected members represent the brightest, most influential, and passionate people in health, science, and medicine in our nation and internationally,” said Academy President Victor J. Dzau in a press release (http://nam.edu/nam-elects-80-new-members/) announcing this year’s election of new members. “They are at the top of their fields and are committed to service.

CTL-Associated Antigen-4 Immunoglobulin (CTLA4Ig) Suppresses Liver Damage in New Mouse Model of Acute Hepatitis B Infection

A promising new avenue for treating hepatitis B has been reported by researchers at Hiroshima University in Japan who have developed a new animal model of the disease. Approximately two million people worldwide have been exposed to hepatitis B virus. Liver transplantation is often necessary to save the lives of patients who have severe liver damage that results from acute overreaction of the immune system. To develop therapies against acute hepatitis, an appropriate animal model is necessary. “The number of patients who can receive liver transplantation is limited, so there is an urgent need to develop new treatment options,” said Professor Kazuaki Chayama of Hirioshima University. Professor Chayama and his research group used mice with so-called “humanized” livers, and injected them with human blood. They found that hepatitis in these “human hepatocyte chimeric mice” was caused by white blood cells known as cytotoxic T lymphocytes (CTLs) that were specifically targeted to hepatitis B virus. This was very similar to human acute hepatitis B. The researchers also found that treating the mice with a molecule called CTL-associated antigen-4 immunoglobulin (CTLA4Ig) suppressed damage to liver cells infected with hepatitis B virus, suggesting that this might be a potential approach to treatment in humans. The mouse model should also be useful for studying the immunological reactions and viral clearance in hepatitis B virus infection, the authors note in their article posted online on August 5, 2015 in the Journal of Virology.

Rockefeller-Led Research Reveals Key Cancer-Promoting Activity of Histone Demethylase Enzyme (JMJD1C) in Acute Myeloid Leukemia (AML), and Perhaps Other Myeloid Leukemias; Possible New Drug Target

New treatment options are badly needed for acute myeloid leukemia (AML), a relatively rare form of cancer. The malignancy begins in the bone marrow, and from there, can spread rapidly to the bloodstream, depriving the body of the essential blood cells that carry oxygen and fight infections. Now, new work from a team led by Rockefeller University researchers in New York City has revealed a potential genetic weakness of this leukemia, offering insights into the molecular mechanisms behind AML, and suggesting a new target for drug development. Previously, researchers had identified a variety of mutations associated with this disease, including a DNA rearrangement found in approximately 15 percent of patients. The abnormal DNA-binding protein produced as a result of this rearrangement takes on entirely new functions, dramatically altering a set of genes that are turned on in a cell to promote the cancer. But how this mutation effects these changes has remained a mystery. In their new work published in the October 15, 2015 issue of Genes and Development, the researchers describe how they identified the molecular mechanism responsible for this gene activation. Their article is titled “JMJD1C Is Required for the Survival of Acute Myeloid Leukemia by Functioning As a Coactivator for Key Transcription Factors.” The research team, led by Dr. Robert G. Roeder, Arnold and Mabel Beckman Professor and Head of Rockefeller's Laboratory of Biochemistry and Molecular Biology, began by searching for proteins that interact with the mutant protein, known as AE (AML/ETO) fusion protein, which is produced by the DNA rearrangement. Their screen identified JMJD1C, an enzyme that removes chemical tags, known as methyl groups, from histones, which are proteins contained in chromosomes.