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.
**This will be the last issue of the newsletter until a replacement is found for Joanna Downer in the Office of Corporate Communications.**
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IN THIS ISSUE:
+ Gene Mutation Increases Severity of But Doesn't Cause Syndrome
+ Molecule Blocks Initiation of Protein Building in Cancer Cells
+ New Neurons Take Baby Steps in the Adult Brain
+ Study Links Length of Chromosome Ends to a Rare Disease of Stem Cells
+ In Cancer, Epigenetic Changes Likely To Come Before Mutations
+ Link Discovered Between Nitric Oxide and COX-2 Inflammatory Pathways
NEWS BRIEFS:
Young Investigators' Day Deadline Jan. 10
Hiatus for the JHM Science e-Newsletter
Spring Presentation, Grant & Paper Writing Workshops
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Do you have an interesting research finding about one month from publication or presentation? Fax your manuscript or galley proofs to the Office of Corporate Communications at 410-614-8951, or identify the correct media relations person online at
http://www.hopkinsmedicine.org/mediaII/Staff/index.html
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RESEARCH HIGHLIGHTS:
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12/4/05
Gene Mutation Increases Severity of But Doesn't Cause Syndrome
Johns Hopkins scientists studying a rare inherited syndrome marked by eye and kidney problems, learning disabilities and obesity have discovered a genetic mutation that makes the syndrome more severe but that alone doesn't cause it. Their report appears in the advance online edition of Nature (Dec. 4).
The new discovery about Bardet-Beidl syndrome (BBS) came from a panoply of studies -- starting with comparative genomics and experiments with yeast, and moving to experiments with zebrafish and genetic analysis of families with the syndrome -- and mirrors what experts expect for the genetically complex common diseases that kill most Americans, like diabetes, heart disease and cancer.
"Scientists are going to have to think very hard before they discount genetic variation that appears not to directly cause a disease," says the study's leader, Nicholas Katsanis, PhD, associate professor in the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins. "The onus is on us to figure out how to dissect the effects of what appear to be silent genetic variants."
The newly identified mutation is in a gene called MGC1203.
http://www.hopkinsmedicine.org/Press_releases/2005/12_14_05.html
Nature (Published online Dec. 4, 2005)
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature04370.html
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12/9/05
Molecule Blocks Initiation of Protein Building in Cancer Cells
A natural chemical made by a New Zealand sea sponge exerts its deadly effects on cancer cells by preventing the cells' protein-building machinery from turning on, Johns Hopkins scientists report in the Dec. 9 issue of Molecular Cell.
The chemical's anti-cancer effects have been known since 1991, but this is the first comprehensive report to show how the molecule, known as pateamine A (PatA), stalls the growth of so-called eukaryotic cells.
"Agents that interfere with protein production in bacteria are already useful antibiotics, but this is the first small molecule found to interfere specifically with the earliest steps of protein production in human cells," says the study's leader, Jun Liu, PhD, a professor of pharmacology and molecular sciences in the Johns Hopkins Institute for Basic Biomedical Sciences.
Although any clinical applications of PatA or related molecules are likely many years away, Liu notes, PatA's abilities offers investigators the chance to probe the earliest steps in protein production and the biology of so-called "suicide" in human cells.
http://www.hopkinsmedicine.org/Press_releases/2005/12_28_05.html
Mol. Cell 9 Dec. 2005;20(5):709-722.
http://dx.doi.org/10.1016/j.molcel.2005.10.008
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12/11/05
New Neurons Take Baby Steps in the Adult Brain
In experiments with mice, scientists from Johns Hopkins' Institute for Cell Engineering have discovered the steps required to integrate new neurons into the brain's existing operations.
For more than a century, scientists thought the adult brain could only lose nerve cells, not gain them, but in fact, new neurons do form during adulthood in all mammals, including humans, and become a working part of the adult brain in mice at the very least.
In the first study to show how these "baby" neurons are integrated into the brain's existing networks, the Johns Hopkins researchers show that a brain chemical called GABA readies baby neurons to make connections to old ones in a part of the brain called the dentate gyrus. The discovery is described in the Dec. 11 advance online section of Nature.
"GABA is important during fetal development, but most scientists thought it would have the same role it has with adult neurons, which is to inhibit the cells' signals," says Hongjun Song, PhD, an assistant professor in the Neuroregeneration and Repair Program within ICE. "We've shown that GABA instead excites new neurons and that this is the first step toward their integration into the adult brain."
http://www.hopkinsmedicine.org/Press_releases/2005/12_22b_05.html
Nature (Published online Dec. 11, 2005)
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature04404.html
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12/16/05
Study Links Length of Chromosome Ends to a Rare Disease of Stem Cells
With seed money from Johns Hopkins' Institute of Cell Engineering, a Johns Hopkins geneticist and her team have discovered a critical link between the health of stem cells and the length of the chromosome ends within them.
Chromosome ends, or telomeres, are repetitive stretches of DNA that protect chromosomes. Each time a cell divides, its chromosome ends get a little shorter, and eventually the cell can no longer divide because its critical genetic information is exposed. In stem cells, however, a protein called telomerase normally maintains the telomeres' length, allowing the cells to divide indefinitely.
Now, the Hopkins researchers report that mice engineered to have just half the normal amount of telomerase can't maintain their stem cells' chromosome ends, bringing an early demise to stem cells that replenish the blood supply, immune system and intestine. Moreover, offspring of these mice bred to have normal levels of telomerase still exhibited early loss of stem cells, the researchers report in the Dec. 16 issue of Cell.
"These offspring have what we have called 'occult' genetic disease -- their genetic make-up is perfectly normal, but they still have the physical problems of their parents," says Carol Greider, PhD, director and professor of molecular biology and genetics in the Johns Hopkins Institute of Basic Biomedical Sciences. "This phenomenon could complicate the hunt for disease genes." http://www.hopkinsmedicine.org/Press_releases/2005/12_23_05.html
Cell 16 Dec. 2005;123(6):1121-1131.
http://dx.doi.org/10.1016/j.cell.2005.11.020
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12/21/05
In Cancer, Epigenetic Changes Likely To Come Before Mutations
A Johns Hopkins researcher, with colleagues in Sweden and at the Fred Hutchinson Cancer Research Center, suggests that the traditional view of cancer as a group of diseases whose biological properties arise from a series of alterations within a cell's nuclear DNA may have to give way to a more complicated view. In the January issue of Nature Reviews Genetics, available online Dec. 21, he and his colleagues suggest that cancers instead begin with "epigenetic" alterations to stem cells.
"We're not contradicting the view that genetic changes occur in the development of cancers, but there also are epigenetic changes and those come first," says lead author Andrew Feinberg, MD, MPH, King Fahd Professor of Medicine and director of the Center for Epigenetics in Common Human Disease at Johns Hopkins.
Cells affected by epigenetic changes -- those that don't affect the gene's sequence of DNA but change the gene in other ways -- look normal under a microscope at low levels of resolution, Feinberg says, "but if you look carefully at the genome, you find there are subtle changes." By tracking these changes, he suggests, doctors potentially could treat people before tumors develop in much the same way as cardiologists prescribe cholesterol-lowering drugs to help prevent heart disease.
http://www.hopkinsmedicine.org/Press_releases/2005/12_21_05.html
Nature Reviews Genetics Jan. 2006;7(1):21-33.
http://www.nature.com/nrg/journal/v7/n1/full/nrg1748.html
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12/22/05
Link Discovered Between Nitric Oxide and COX-2 Inflammatory Pathways
Nitric oxide-mediated inflammation, once thought to be wholly independent of other inflammatory systems, has now been linked to another major pathway, Johns Hopkins neuroscientists report in the Dec. 23 issue of Science. The findings are likely to point scientists to novel drugs that significantly reduce the risks of taking COX-2 inhibitor pain relievers, the investigators report.
The Johns Hopkins team, led by Solomon Snyder, MD, discovered that the iNOS (inducible nitric oxide synthase)-based inflammation pathway cross-links with the more well-known COX-2 pathway that is the target of COX-2 inhibitor drugs such as Vioxx. Until now, these two major inflammatory mechanisms were assumed to be unrelated and independent of each other, the researchers say.
"The fundamental significance of this work is that it demonstrates a totally unsuspected connection between the two most important inflammatory systems in the body," says Snyder, professor and director of neuroscience in Johns Hopkins' Institute for Basic Biomedical Sciences. "The therapeutic significance is that drugs which block the binding of iNOS and COX-2 might represent novel anti-inflammatory agents or reduce the dosage needed and side effects of this family of drugs."
http://www.hopkinsmedicine.org/Press_releases/2005/12_22c_05.html
Science 23 Dec. 2005;310(5756):1966-1970.
http://www.sciencemag.org/cgi/content/full/310/5756/1966
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NEWS BRIEFS:
Young Investigators' Day Deadline Jan. 10 -- Applications for the School of Medicine's 2006 Young Investigators' Day Awards will be accepted from 9 a.m. until 3 p.m. on Tuesday, Jan. 10, 2006, in 809 PCTB. Graduate students and postdoctoral fellows in the basic science and clinical departments at the medical school are eligible, as are house staff at the Johns Hopkins Hospital. Applicants who have graduated from or left Hopkins or who have been promoted to faculty status (research associate or above) prior to Sept. 1, 2005, are not eligible. All award recipients must be present at the Young Investigators' Day celebration, which begins at 4 p.m., April 20, 2006, in Mountcastle Auditorium. Cover sheets and instructions for applicants can be found on easel posters at various locations on the East Baltimore campus. Questions can be directed to YID@jhmi.edu .
Hiatus for the JHM Science e-Newsletter -- Joanna Downer, PhD, assistant director of science communication at Johns Hopkins Medicine and the writer and editor of the JHM Science e-Newsletter, is leaving Hopkins as of Jan. 1, 2006. The JHM Science e-Newsletter will likely cease production at that point and will resume in some form when a replacement is found. Until then, find news about Johns Hopkins research at
http://www.hopkinsmedicine.org/Press_releases/index.html
Spring Presentation, Grant & Paper Writing Workshops -- The Professional Development Office is offering three workshops for faculty and postdoctoral fellows to build critical skills for presentations, grant writing and paper writing; all are held from 8:30 am until 4 pm. On Feb. 23, the PDO will hold its "Giving a Research Talk" workshop in Room 2-108 in the 1830 Building. Faculty can pay the $750 fee by tuition remission; postdocs and fellows can pay their $375 fee by M&S form or check. On March 20, the PDO will hold its grant writing workshop in Tilghman Auditorium. The fee for faculty is $1100, for postdocs and fellows the fee is $550, payable as above. On April 21, the PDO will hold its "Writing a Biomedical Research Paper" workshop in the Bodian Conference Room in the 1830 Building. The fees for this workshop are $750 for faculty and $375 for postdocs and fellows, payable as above. For more information email jhmipdo@jhmi.edu .
http://www.hopkinsmedicine.org/pdo
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--JHMI--
