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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IN THIS ISSUE:
RESEARCH HIGHLIGHTS:
+ Stressed Mice Quicker To Get Skin Cancer
+ Preservation of Rhodospin Delays Blinding Light Damage
+ New Clue to Nerve Growth May Help Regeneration Efforts
+ Surprise! Cells Have Second Source of Phosphate
NEWS BRIEFS:
Young Investigators' Day Entries Due Jan. 11
Laboratory Animal Technician Courses
Rodent Handling and Surgery Training
Mouse Phenotyping Seminar Jan. 27
HONORS AND AWARDS:
Rose Honored for Life's Work
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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
Stressed Mice Quicker To Get Skin Cancer
Scientists at the Johns Hopkins Kimmel Cancer Center have discovered that mice exposed to stressful conditions and cancer-causing ultraviolet light develop skin cancers in less than half the time it takes for non-stressed mice. Their results are published in the December issue of the Journal of the American Academy of Dermatology.
"There's a lot of evidence pointing to the negative effects of chronic stress, which dampens our immune system and impacts various aspects of our health," says Francisco Tausk, MD, associate professor of dermatology and director of the study. "But, to help create solid treatment strategies, we need a better understanding of the mechanisms of how stressors affect skin cancer development."
Tausk exposed 40 mice to the scent of fox urine -- the mouse equivalent of big-time stress -- and large amounts of UV light. The first skin tumor in one of the mice appeared after eight weeks of testing. Mice exposed only to UV light began developing tumors 13 weeks later. By 21 weeks of testing, 14 of the 40 stressed mice had at least one tumor, and two non-stressed mice had tumors.
http://www.hopkinsmedicine.org/Press_releases/2004/12_08_04.html
J Am Acad Dermatol Dec. 2004;51(6):919-22.
http://dx.doi.org/10.1016/j.jaad.2004.08.042
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12/14/04
Preservation of Rhodopsin Delays Blinding Light Damage
In experiments with fruit flies, Johns Hopkins researchers have found that blindness induced by constant low-level light results directly from the loss of a key light-detecting protein, rather than from the overall death of cells in the retina.
Although many animals, and presumably humans, lose both their retinal cells and vision after exposure to low levels of light for long periods, the relationship between exposure and blindness had been poorly understood. Now, the Hopkins researchers report in the Dec. 14 issue of Current Biology that flies whose light-detecting protein rhodopsin was engineered to resist destruction retained their vision twice as long as normal flies.
"Everyone assumed that the blindness caused by chronic light exposure was an effect of the degeneration and loss of the retinal cells, but our experiments show these are two distinct events caused by two distinct processes," says Craig Montell, PhD, professor of biological chemistry in Hopkins' Institute for Basic Biomedical Sciences.
The light-detecting cells of fruit fly retinas share similarities with rod and cone cells of the human retina and also rely on rhodopsin to detect light and create an electrical signal that is transmitted to the brain.
In the researchers' experiments, this electrical signal was measured by an electroretinogram, which uses a contact placed on the surface of the eye. The measured signals get smaller as the flies lose their ability to see.
http://www.hopkinsmedicine.org/Press_releases/2004/12_15a_04.html
Current Biology 14 Dec. 2004;14(23):2076-2085.
http://dx.doi.org/10.1016/j.cub.2004.11.054
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12/15/04
New Clue to Nerve Growth May Help Regeneration Efforts
Johns Hopkins scientists have discovered how one family of proteins repels growing nerves and keeps them properly on track during development. The finding, described in the Dec. 15 issue of Neuron, might provide a chance to overcome the proteins' later role in preventing regrowth of injured nerves, the researchers say.
The proteins, known as chondroitin sulfate proteoglycans (CSPGs), have long been known to prevent nerve regeneration after injury by recruiting a stew of other proteins and agents, but exactly what part of the mix keeps nerves from regrowing is unknown.
In studies of nerve growth in developing rats, the Hopkins scientists have linked CSPGs' no-growth effects to a protein called semaphorin 5A. The scientists, including David Kantor, an MD/PhD candidate, found that when CSPGs bind to semaphorin 5A, growing nerves are stopped in their tracks. Blocking this particular interaction freed the nerves to continue growing.
"CSPGs are a critical obstacle to nerve regeneration after injury, and without details about what's really happening, it's impossible to rationally intervene," says study leader Alex Kolodkin, PhD, professor of neuroscience in Johns Hopkins' Institute for Basic Biomedical Sciences. "We studied nerve growth, rather than re-growth, but our work provides a starting point for identifying more partners of CSPGs and for finding targets to try to counter these proteins' effects in nerve regeneration."
http://www.hopkinsmedicine.org/Press_releases/2004/12_15_04.html
Neuron 15 Dec. 2004;44(6):961-975.
http://dx.doi.org/10.1016/j.neuron.2004.12.002
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12/15/04
Surprise! Cells Have Second Source of Phosphate
For 50 years, thousands of labs around the world have studied cells' critical internal communications, and scientists had assumed the speakers were known. But now, in the Dec. 17 issue of Science, Johns Hopkins researchers report finding not just a new participant, but a brand new conversation that has implications for treating disease and understanding biology.
Much of cells' internal communication revolves around two very important words -- "stop" and "go" -- elicited when a small bit, called phosphate, is added onto proteins. This addition turns protein activities up or down and fine tunes cells' responses to what's happening outside their borders.
The source of these phosphate bits has been known -- a molecule called adenosine triphosphate, or ATP. But in their new report, the Johns Hopkins scientists describe a brand new source of phosphate that seems to work with as many proteins as targeted by ATP, but in a completely different way.
"Nobody in a million years would have thought there was another way for cells to add phosphate groups to proteins other than using ATP," says Solomon Snyder, MD, professor and director of neuroscience, one of the departments in the Institute for Basic Biomedical Sciences. "Addition of phosphates to proteins -- phosphorylation -- is the most fundamental signaling mechanism in all life, and the new source of phosphate represents a very different kind of process than the one we've known about."
Unlike ATP, the new phosphate source, known as inositol pyrophosphate (IP7), modifies proteins without the help of an enzyme, the researchers report. Their early evidence also suggests IP7 might be most important in regulating the release of chemicals in the brain and in controlling the cellular machinery that builds proteins.
http://www.hopkinsmedicine.org/Press_releases/2004/12_16_04.html
Science 17 Dec 2004;306(5704):2101-2105.
http://www.sciencemag.org/cgi/content/full/306/5704/2101
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NEWS BRIEFS:
Young Investigators' Day Entries Due Jan. 11 -- Applications for awards of the 28th annual School of Medicine Young Investigators' Day are due by 3 p.m. Tuesday, Jan. 11, 2005, in Room 501A, Pre-Clinical Teaching Building. The awards recognize basic and clinical research undertaken by applicants while registered as students or postdoctoral fellows. Student applicants who graduated or left Hopkins prior to Sept. 1, 2004, are not eligible. Postdoctoral applications who were promoted to faculty or left Hopkins before Sept. 1 also are not eligible. Detailed instructions are available on the Call for Abstracts boards located throughout the East Baltimore campus. All winners must be present at Young Investigators' Day, April 14, 2005. Download the coversheet at: http://www.mbg.jhmi.edu/cv/YID.pdf
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.
Rodent Handling and Surgery Training -- The next monthly Rodent Handling Seminar and Lab will be held Jan. 13 starting at 9 a.m. in Ross 403. The next all-day Rodent Surgery Seminar and Lab will be held Feb. 10 starting at 9 a.m. in Ross 403. Subsequent surgery sessions for 2005 are scheduled for April 14, June 9, Aug. 11, Oct. 13, and Dec. 8. For more information on these seminars or to register, email acuc@jhmi.edu or call Trish Matos at 443-287-3744.
Mouse Phenotyping Seminar Jan. 27 -- Cory Brayton, DVM, a visiting associate professor of comparative medicine and head of the new phenotyping core, will present "Phenotyping: Nature vs. Nurture; Background Genetics and Environmental Factors," Jan. 27 from noon until 1 p.m. in Ross 403.
HONORS AND AWARDS:
Rose Honored for Life's Work -- Noel R. Rose, MD, PhD, professor of pathology and of microbiology and immunology and director of the Center for Autoimmune Disease Research, has received two honors for his contributions to autoimmune disease research and microbiology. At the 4th International Congress on Autoimmunity held in Budapest, Hungary, in Nov. 2004, Rose received the AESKU Award for Lifetime Contribution to Autoimmunity. In addition, the American Society for Microbiology has informed him that, at its general meeting in Atlanta in June 2005, he will receive the 2005 ASM Founders Distinguished Service Award.
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