NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 08 July 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Planetary disc drive – Nature Physics
Nanocrystal shape control – Nature Materials
Common genetic risk variant for colorectal cancer – Nature Genetics
Growth factor reinforces cocaine addiction – Nature Neuroscience
Arresting autoimmunity – Nature Immunology
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
PDFs of all the papers mentioned on this release can be found in the relevant journal’s section of http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.
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NOTE: Once a paper is published, the digital object identifier (DOI) number can be used to retrieve the abstract and full text from the journal web site (abstracts are available to everyone, full text is available only to subscribers). To do this, add the DOI to the following URL: http://dx.doi.org/ (For example, http://dx.doi.org/10.1038/ng730). For more information about DOIs and Advance Online Publication, see http://www.nature.com/ng/aop/.
PLEASE CITE THE SPECIFIC NATURE JOURNAL AND WEBSITE AS THE SOURCE OF THE FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO THE APPROPRIATE JOURNAL’S WEBSITE.
***********************************************NATURE PHYSICS*****************************************
(http://www.nature.com/naturephysics)
[1] Planetary disc drive
DOI: 10.1038/nphys661
A report online this week in Nature Physics describes a physical mechanism that explains how the final stage of planet formation proceeds within an orbiting disc of dust and gas surrounding a young star.
It’s known that part of the disc spirals inwards onto the central star, dragging along planets and setting their final orbits, but it's not clear what drives this gas flow. Eugene Chiang and Ruth Murray-Clay investigate the coupling between disc magnetic fields and rotating gas. They focus on the recently discovered 'transitional' discs, whose innermost regions are swept clean of dust that might otherwise absorb charged particles and thwart the coupling. X-rays from the star are therefore able to ionize gas in the inner disc, activating a magnetic instability that drives gas towards the central star and empties the disc from the inside out. Radiation pressure from the star ensures that inflowing gas remains cleared of dust. The researchers’ calculations are consistent with observed rates of gas flow onto the star.
Author contact:
Eugene Chiang (University of California, Berkeley, CA, USA)
Tel: +1 510 642 2131; E-mail: [email protected]
Other papers from Nature Physics to be published online at the same time and with the same embargo:
[2] All-optical injection of ballistic electrical currents in unbiased silicon
DOI: 10.1038/nphys674
[3] Observation of Landau levels of Dirac fermions in graphite
DOI: 10.1038/nphys653
********************************************* NATURE MATERIALS ************************************** (http://www.nature.com/naturematerials)
[4] Nanocrystal shape control
DOI: 10.1038/nmat1957
The shape of metal nanocrystals can be accurately controlled by using a small particle of a different metal as a seed, as reported in an article online this week in Nature Materials.
Peidong Yang and co-authors reacted a platinum nanocube (~13 nanometres each side) with a palladium-based compound to produce core–shell Pt/Pd nanocrystals. By varying the reaction environment, and in particular the amount of NO2, the researchers were able to obtain three different shapes — cubes, cuboctahedra and octahedra.
Many of the physical and chemical properties of nanocrystals depend strongly on their morphology. The authors show, for example, that the catalytic activity of the cubes is quite different from that of the other two types of nanocrystals. The use of seeds represents a clear step towards the development of nanocrystals with well-defined shapes.
Author contact:
Peidong Yang (University of California, Berkley, CA, USA)
Tel: +1 510 643 1545; E-mail: [email protected]
Other papers from Nature Materials to be published online at the same time and with the same embargo:
[5] Self-assembly of metal–polymer analogues of amphiphilic triblock copolymers
DOI: 10.1038/nmat1954
[6] Protective coatings on extensible biofibres
DOI: 10.1038/nmat1956
***********************************************NATURE GENETICS **************************************
(http://www.nature.com/naturegenetics)
[7], [8] & [9] Common genetic risk variant for colorectal cancer
DOI: 10.1038/ng2085
DOI: 10.1038/ng2089
DOI: 10.1038/ng2098
A common variant on chromosome 8 that predisposes to prostate cancer also confers risk of colorectal cancer, according to three studies to be published online this week in Nature Genetics. Although a few relatively rare mutations have been identified that are associated with colorectal cancer, this is the first evidence for a common genetic risk factor. Colorectal cancer is one of the most commonly diagnosed forms of cancer.
In the first study, Richard Houlston, Ian Tomlinson and colleagues carried out a genome-wide association study for colorectal cancer and identified the most strongly associated variant on chromosome 8 as the same variant that had previously been associated with risk of prostate cancer. In the second study, Thomas Hudson, Malcolm Dunlop and colleagues screened a smaller number of variants across the genome but identified the same one on chromosome 8 as highly associated with colorectal cancer. Finally, Christopher Haiman and colleagues noted that the region on chromosome 8 that was shown to be associated with prostate cancer is also known to be amplified in individuals with colorectal cancer. Given this background they directly assessed the relevant variants in individuals with colorectal cancer and found them to be significantly more frequent than in cancer-free individuals. Haiman and colleagues also note that five other variants in this region that had been associated with prostate cancer were not associated with colorectal cancer, suggesting that the mechanism by which variants in the region contribute to cancer risk may differ depending on the type of cancer.
Author contacts:
Richard Houlston (Institute of Cancer Research, Sutton, UK)
Tel: +44 208 722 4175; E-mail: [email protected]
Ian Tomlinson (London Research Institute, Cancer Research UK)
Tel: +44 207 269 2884; E-mail: [email protected] Authors paper [7]
Thomas Hudson (The Ontario Institute for Cancer Research, Toronto, Ontario, Canada)
Tel: +1 416 673 6650; E-mail: [email protected]
Malcolm Dunlop (University of Edinburgh, UK)
Tel: +44 131 467 8439; E-mail: [email protected] Authors paper [8]
Christopher Haiman (University of Southern California, Los Angeles, CA, USA)
Tel: +1 323 865 0429; E-mail: [email protected] Author paper [9]
Additional media contact:
Emma Gilgunn-Jones (Press Officer, Cancer Research UK, London, UK)
Tel: +44 207 061 8311 or +44 7050 264 059; E-mail: [email protected]
Cancer Research UK press office is able to arrange interviews with the UK based authors
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[10] Loss of GLIS2 causes nephronophthisis in humans and mice by increased apoptosis and fibrosis
DOI: 10.1038/ng2072
[11] Bi-orientation of achiasmatic chromosomes in meiosis I oocytes contributes to aneuploidy in mice
DOI: 10.1038/ng2065
*******************************************NATURE NEUROSCIENCE ***********************************
(http://www.nature.com/natureneuroscience)
[12] Growth factor reinforces cocaine addiction
DOI: 10.1038/nn1929
Release of a growth factor in the nucleus accumbens – a brain area mediating reward – is necessary for the development and relapse of cocaine addiction, reports a paper in the August issue of Nature Neuroscience.
Addictive drugs are thought to ‘hijack’ reward systems in the brain, causing neurons to be persistently more responsive to drug-associated cues and stressors. David Self and colleagues report that four hours after cocaine self-administration, rats show an increase in brain-derived neurotrophic factor (BDNF) in the nucleus accumbens. Preventing this increase in BDNF reduced cocaine self-administration and the propensity to relapse, whereas giving the rats daily BDNF injections after cocaine self-administration increased cocaine-seeking behaviour and relapse.
Moreover, using mice that were genetically engineered to lack BDNF only in the nucleus accumbens in adulthood, they showed that BDNF release in the nucleus accumbens did not affect the initial rewarding effects of cocaine, but did dramatically alter the development of addiction. If similar mechanisms mediate addiction in humans, these results could suggest possible approaches to addiction treatment.
Author contact:
David Self (University of Texas Southwestern Medical Center, Dallas, TX, USA)
Tel: +1 214 648 1237; E-mail: [email protected]
Additional contact for comment on paper:
Geoffrey Schoenbaum (University of Maryland School of Medicine, Baltimore, MD, USA)
Tel: +1 410 706 3814; E-mail: [email protected]
Other papers from Nature Neuroscience to be published online at the same time and with the same embargo:
[13] Opposing roles in neurite growth control by two seven-pass transmembrane cadherins
DOI: 10.1038/nn1933
[14] Dual subcellular roles for LIS1 and dynein in radial neuronal migration in live brain tissue
DOI: 10.1038/nn1934
[15] A functional link between area MSTd and heading perception based on vestibular signals
DOI: 10.1038/nn1935
[16] Molecular genetic visualization of a rare subset of unmyelinated sensory neurons that may detect gentle touch
DOI: 10.1038/nn1937
[17] A functional role for EGFR signaling in myelination and remyelination
DOI: 10.1038/nn1938
*******************************************NATURE IMMUNOLOGY ************************************
(http://www.nature.com/natureimmunology)
[18] Arresting autoimmunity
DOI: 10.1038/ni1489
A study to be published online this week in Nature Immunology reveals how T lymphocytes survive to induce several types of autoimmune disease, including multiple sclerosis.
Working with a mouse version of multiple sclerosis, Gang Pei and colleagues study a protein called beta-arrestin 1, a factor known to regulate gene expression in all cells. Pei’s team reports that beta-arrestin 1 helps promote survival of T lymphocytes, which increases the duration of inflammation. In the absence of beta-arrestin 1 a critical factor required for T lymphocyte survival is not produced. Consistently, T lymphocytes lacking beta-arrestin 1 survive less well and cause much less brain inflammation in a mouse model of multiple sclerosis.
Demonstrating a role for beta-arrestin 1 in prolonging survival of aggressive T lymphocytes associated with autoimmune disease provides a possible target for reducing such diseases. Whether blocking the function of beta-arrestin 1 will help multiple sclerosis patients, however, remains a question for future investigation.
Author contact:
Gang Pei (Shanghai Institutes for Biological Sciences, China)
Tel: +86 21 5492 1371; E-mail: [email protected]
Other papers from Nature Immunology to be published online at the same time and with the same embargo:
[19] Interleukin 15–mediated survival of natural killer cells is determined by interactions among Bim, Noxa and Mcl-1
DOI: 10.1038/ni1487
***************************************************************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE (http://www.nature.com/nature)
[20] DAI (DLM-1/ZBP1) is a cytosolic DNA sensor and an activator of innate immune response DOI: DOI: 10.1038/nature06013
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[21] A new thiamin salvage pathway
DOI: 10.1038/nchembio.2007.13
Nature MEDICINE (http://www.nature.com/naturemedicine)
[22] E3 ubiquitin ligase Cblb regulates the acute inflammatory response underlying lung injury
DOI: 10.1038/nm1607
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[23] Cables links Robo-bound Abl kinase to N-cadherinbound beta-catenin to mediate Slit-induced modulation of adhesion and transcription
DOI: 10.1038/ncb1614
[24] Plasma membrane nanoswitches generate high-fidelity Ras signal transduction
DOI: 10.1038/ncb1615
[25] Multi-step pericellular proteolysis controls the transition from individual to collective cancer cell invasion
DOI: 10.1038/ncb1616
[26] Regulated ATP release from astrocytes through lysosome exocytosis
DOI: 10.1038/ncb1620
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[27] Crystal structure of the thioesterase domain of human fatty acid synthase inhibited by Orlistat
DOI: 10.1038/nsmb1265
[28] Structural basis for nick recognition by a minimal pluripotent DNA ligase
DOI: 10.1038/nsmb1266
NATURE METHODS (http://www.nature.com/nmeth)
[29] Red-shifted Renilla reniformis luciferase variants for imaging in living subjects
DOI: 10.1038/nmeth1070
[30] Luciferase-YFP fusion tag with enhanced emission for single-cell luminescence imaging
DOI: 10.1038/nmeth1069
***************************************************************************************************************
GEOGRAPHICAL LISTING OF AUTHORS
The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.
AUSTRALIA
Brisbane: 24
Melbourne: 19
Nedlands: 19
Parkville: 19
CANADA:
Montreal: 8
Ottawa: 8
Toronto: 2, 5, 8
Vancouver: 25
Winnipeg: 10
CHINA
Beijing: 26
Jiangsu: 26
Shanghai: 18, 26
Wuhan: 26
FRANCE
Marseille: 8
Paris: 8, 19
Villejuif: 8
GERMANY
Berlin: 10
Cologne: 10
Heidelberg: 10
Wurzburg: 25
JAPAN
Aichi: 19
Chiba: 13
Kyoto: 13
Osaka: 30
Sapporo: 20, 30
Tokyo: 20
SWEDEN
Solna: 11
Stockholm: 11
SWITZERLAND
Basel: 21
UNITED KINGDOM
Birmingham: 7
Edinburgh: 8
Harrow: 7
London: 7, 8
Newcastle: 11
Nottingham: 7
Oxford: 7
Surrey: 7
Sutton: 7
UNITED STATES OF AMERICA
California
Berkeley: 1, 4
Los Angeles: 9, 29
Pasadena: 16
San Francisco: 23, 25
Santa Barbara: 6
Stanford: 29
Connecticut
New Haven: 12
District of Columbia
Washington: 17
Hawaii
Honolulu: 9
Illinois
Chicago: 22, 25
Iowa
Iowa City: 23
Maryland
Baltimore: 16
Bethesda: 8
Gaithersburg: 8
Massachusetts
Boston: 9, 12
Cambridge: 9
Waltham: 13
Michigan
Ann Arbor: 10
Missouri
St Louis: 15, 24
New Jersey
Piscataway: 3
New York
Albany: 16
Ithaca: 21
New York: 10, 14, 28
North Carolina
Chapel Hill: 5, 16, 25
Winston-Salem: 27
Texas
Dallas: 12
Virginia
Richmond: 17
Washington
Seattle: 8
PRESS CONTACTS…
For media inquiries relating to embargo policy for all the Nature Research Journals:
Katherine Anderson (Nature London)
Tel: +44 20 7843 4502; E-mail: [email protected]
Ruth Francis (Senior Press Officer, Nature, London)
Tel: +44 20 7843 4562; E-mail: [email protected]
For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:
Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]
Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail: [email protected]
Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]
Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Maria Bellantone
Tel: +44 20 7843 4556; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Methods (New York)
Allison Doerr
Tel: +1 212 726 9393; E-mail: [email protected]
Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]
Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail: [email protected]
Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]
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