This is the twice-per-month electronic newsletter for basic, preclinical and translational research news related to the Johns Hopkins School of Medicine. Please forward freely. Direct comments or questions to Joanna Downer, PhD, in the Office of Corporate Communications (4-5105, jdowner1@jhmi.edu).
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*** Top Scientists at Hopkins for Jan. 28 Symposium ***
IN THIS ISSUE:
RESEARCH HIGHLIGHTS:
+ Hearing's "Off-Switch" Borrowed from Muscles
+ Antibiotics Protect Nerves in Mice by Turning on Genes
+ First Step in Protein Building Revealed
NEWS BRIEFS:
***Top Scientists at Hopkins for Jan. 28 Symposium***
Mouse Phenotyping Seminar Jan. 27
New Animal Research Protocol Forms
Laboratory Animal Technician Courses
AWARDS AND HONORS:
Freischlag Named Editor of Archives of Surgery
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Do you have an interesting research finding about one month from publication or presentation? Send manuscripts to Joanna Downer at jdowner1@jhmi.edu or fax to 410-614-8951. Information about awards and honors received by laboratory personnel and others is welcomed also.
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RESEARCH HIGHLIGHTS:
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12/8/04
Hearing's "Off-Switch" Borrowed from Muscles
In experiments with rats, Johns Hopkins researchers have discovered that the shut-off switch for the auditory system is quite similar to an "on" switch previously known principally in muscle. The findings appear in the Dec. 8 issue of the Journal of Neuroscience.
Calcium was already known to be a key factor in both systems. It helps trigger contraction of muscles, and it helps the brain rapidly shut off the ear's sound-detecting "hair cells," named for the spiky projections that help translate sound waves into electricity. However, the amount of calcium coming into hair cells in response to the brain's signals has always seemed too small to do the trick.
Now the Hopkins researchers report that the small influx of calcium triggered by the "shut-off" nerve causes a flood of calcium to be released from a reservoir sitting just inside the hair cell. That flood, in turn, quiets the hair cell by stimulating its release of potassium.
"We've known the response to the nerve is practically immediate, and people had suggested that perhaps the cells had a reservoir of calcium that made it possible," says Paul Fuchs, Ph.D., professor of otolaryngology--head and neck surgery, of neuroscience and of biomedical engineering and director of the Cochlear Neurotransmission Laboratory at the Center for Hearing and Balance at Johns Hopkins. "Our evidence strongly supports this idea and shows how it happens. The similarities to the situation in muscle is striking."
In both systems, the reservoir of calcium is just inside the cell and extends along the cell's connection with the nerve, maximizing the impact of the incoming calcium. Moreover, the researchers discovered that the flood gates are so-called ryanodine receptors and are triggered to open by nicotinic receptors in hair cells, as in muscle.
http://www.hopkinsmedicine.org/Press_releases/2004/12_08a_04.html
J Neurosci. 8 Dec. 2004;24(49):11160-11164.
http://www.jneurosci.org/cgi/content/full/24/49/11160
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1/5/05
Antibiotics Protect Nerves in Mice by Turning on Genes
A family of antibiotics that includes penicillin may help prevent nerve damage and death in a wide variety of neurological diseases, including Lou Gehrig's disease, dementia, stroke, and epilepsy, Johns Hopkins researchers have found.
The antibiotics' beneficial effects, discovered in experiments in the lab and with mice, are unrelated to their ability to kill bacteria, the researchers report in the Jan. 6 issue of Nature. Instead, the drugs squelch the dangerous side of a brain chemical called glutamate by turning on at least one gene, thereby increasing the number of transporters that remove glutamate from nerves.
In mice engineered to develop the equivalent of Lou Gehrig's disease, daily injections of an antibiotic called ceftriaxone, started just as symptoms tend to surface, delayed both nerve damage and symptoms and extended survival by 10 days compared to untreated animals. Lou Gehrig's disease, or amyotrophic lateral sclerosis (ALS), in people causes progressive weakness and paralysis and ends in death, usually within three to five years of diagnosis.
"We're very excited by these drugs' abilities," says Jeffrey Rothstein, MD, PhD, director of the Robert Packard Center for ALS Research at Johns Hopkins and a professor of neurology and of neuroscience. "They show for the first time that drugs, not just genetic engineering, can increase numbers of specific transporters in brain cells. This approach has potential applications in numerous neurologic and psychiatric conditions that arise from abnormal control of glutamate."
http://www.hopkinsmedicine.org/Press_releases/2005/01_05_05.html
[See full release for Conflict of Interest statement.]
Nature 6 Jan. 2005;433(7021):73-77.
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v433/n7021/full/nature03180_fs.html
(This is a long URL. If the hyperlink fails, copy and paste entire URL into browser.)
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1/20/05
First Step in Protein Building Revealed
A team led by Johns Hopkins scientists has unraveled the first step in translating genetic information in order to build a protein, only to find that it's not one step but two. The findings are published in the Jan. 21 issue of Molecular Cell.
In a series of experiments, the scientists discovered that when yeast's protein-building machinery recognizes the starting line for a gene's instructions, it first alters its structure and then releases a factor known as eIF1, a step necessary to let it continue reading the assembly instructions. Even though yeast are the most primitive relatives of humans, the protein-building machinery, or ribosomes, of each are quite similar.
"It's impossible to know for sure whether eIF1 is released completely in living creatures, but in our laboratory experiments that is clearly the case," says Jon Lorsch, PhD, professor of biophysics and biophysical chemistry, one of the departments in Johns Hopkins' Institute for Basic Biomedical Sciences. "Even if it isn't released completely in intact cells, our results would indicate that it must be very loosely associated for translation to begin."
Scientists already knew that without eIF1, the ribosome can start reading the gene's RNA instructions at places other than a particular three-block piece of RNA known as the start codon. And excessive amounts of eIF1 are associated with cardiac hypertrophy, or an enlarged heart.
While eIF1's role in cardiac hypertrophy remains a mystery, the new discovery reveals exactly how eIF1 regulates the ribosome's activity. By using fluorescence resonance energy transfer, or FRET, the research team was able to demonstrate that eIF1's mere presence on the yeast ribosome prevents the machinery from getting started. Only after its release from the complex -- triggered by recognition of the start codon -- can the ribosome start making proteins, says graduate student David Maag, first author of the paper.
http://www.hopkinsmedicine.org/Press_releases/2005/01_21a_05.html
Molecular Cell 21 Jan 2005;17(2):265-275.
http://www.molecule.org/content/article/abstract?uid=PIIS1097276504007737
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NEWS BRIEFS:
Top Scientists at Hopkins for Jan. 28 Symposium -- Scientific luminaries David Baltimore, Stuart Schreiber, John Kuriyan, Cori Bargmann, Mary-Claire King and Sydney Brenner are the featured speakers for a Jan. 28 symposium "Toward the Third New Biology," which will start at 10:30 a.m. in the Wood Basic Science Auditorium, 725 N. Wolfe St. Overflow seating will be available in West Lecture Hall. The speakers will discuss their work and the growing role of chemistry and mathematics in biology research in this celebration of the role of interdisciplinary research in the post-genomic era. The symposium was organized by the McKusick-Nathans Institute of Genetic Medicine and the Institute for Basic Biomedical Sciences.
http://www.insidehopkinsmedicine.org/news/news_detail.cfm?id=2780
http://www.hopkinsmedicine.org/Press_releases/2005/01_21_05.html
Mouse Phenotyping Seminar Jan. 27 -- Cory Brayton, DVM, a visiting associate professor of comparative medicine and head of the new rodent phenotyping center, will present "Phenotyping: Nature vs. Nurture; Background Genetics and Environmental Factors," Jan. 27 from noon until 1 p.m. in Ross 403.
New Animal Research Protocol Forms -- The Animal Care and Use Committee revised the animal use protocol forms in October 2004. Beginning February 2005, protocols submitted using the old forms will not be accepted. To obtain a current form visit:
http://www.jhu.edu/animalcare/forms1.html
Laboratory Animal Technician Courses -- On alternating Fridays, 8 a.m. to 9 a.m., the Animal Care and Use Committee presents Assistant Laboratory Animal Technician classes in Phipps Room 340, and Laboratory Animal Technician classes in the Traylor Room 707. The classes constitute a course which continuously cycles, so participants may begin at any point or pick up a schedule and attend those lectures of particular interest. For more information on this series, contact Kinta Diven at 443-287-3743 or kdiven1@jhmi.edu; to register send email to acuc@jhmi.edu.
AWARDS AND HONORS:
Freischlag Named Editor of Archives of Surgery -- Julie Freischlag, MD, the William Stewart Halsted Professor and Director of the Department of Surgery at the Johns Hopkins School of Medicine and surgeon in chief of The Johns Hopkins Hospital, has been appointed editor of the Archives of Surgery, one of the JAMA/Archives journals published by the American Medical Association.
http://www.hopkinsmedicine.org/Press_releases/2005/01_17_05.html
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--JHMI--
