NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 16 December 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Fast-rising sea levels - Nature Geoscience
Meteoritic boost to biodiversity? - Nature Geoscience
In the right direction - Nature Photonics
Silicon nanowires stay current - Nature Nanotechnology
Genetic risk factor for ALS - Nature Genetics
Genetic susceptibility to Kawasaki disease - Nature Genetics
A pathway controlling body temperature - Nature Neuroscience
Control of EGFR in breast cancer cell invasion - Nature Cell Biology
· 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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****************************** NATURE GEOSCIENCE **********************************
[1] Fast-rising sea levels
DOI: 10.1038/ngeo.2007.28
Sea levels rose by between 0.6 and 2.6 metres per century during the last interglacial period 120,000 years ago, suggests a paper published online in Nature Geoscience this week. These figures are well above the IPCC’s estimated rise of 0.18 to 0.58 metres for the coming century and indicate that sea levels can quickly adjust to climatic changes.
Eelco Rohling and colleagues studied changes in the salinity of Red Sea water and reconstructed the sea-level-dependent water exchange between the basin and the open ocean across the straits. Their high-resolution records point to at least one period of rapid sea-level rise during the last interglacial period. At that time, global mean temperatures were about 2 degrees Celsius warmer than today, but with a different regional temperature distribution.
Author contact:
Eelco Rohling (National Oceanography Centre, Southampton, UK)
Tel: +44 23 8059 3042; E-mail: [email protected]
[2] Meteoritic boost to biodiversity?
DOI: 10.1038/ngeo.2007.37
The breakup of an asteroid and the resultant meteoritic bombardment of Earth probably led to more varied environmental conditions and a marked spurt in the number of new species around 470 million years ago, suggests a study online this week in Nature Geoscience. These results are surprising as meteorite impacts are often more commonly associated with mass extinctions.
Birger Schmitz and colleagues studied rocks of Middle Ordovician age from the Baltic and Scandinavian region as well as from China, and documented the diversity of ancient clam-like organisms and the abundance of material of meteoritic origin. They found that the marked increase in biodiversity - as inferred from the number of fossils of various species - occurred at precisely the same time as an increase in meteoritic bombardment in those regions.
Meteoritic impacts on Earth have often been linked to major extinction events - for example, the end-Cretaceous impact 65 million years ago is implicated in the demise of the dinosaurs. This study suggests, however, that depending on their size, frequency and timing in Earth’s evolution, impacts could have also created conditions that were conducive to an increase in the diversity of plant and animal life.
Author contact:
Birger Schmitz (University of Lund, Sweden)
Tel: +46 46 222 8265; E-mail: [email protected]
********************************** NATURE PHOTONICS **********************************
(http://www.nature.com/nphoton)
[3] In the right direction
DOI: 10.1038/nphoton.2007.252
An artificial material capable of guiding light in three dimensions on a tiny scale could be used to form compact optical circuits. The technique, reported online in Nature Photonics this week, has the potential to be as important to photonics as the miniaturization of transistors was to electronics.
Paul Braun and his colleagues start with a structure similar to naturally found opals, and use it as a frame to create a silicon-based photonic crystal. They can then controllably introduce crystal imperfections that trap the infrared light and direct its flow, guiding it around sharp 90° bends or splitting it into two paths. All this is done on a length scale of just a few millionths of a metre.
Author contact:
Paul Braun (University of Illinois at Urbana-Champaign, Urbana, IL, USA)
Tel: +1 217 244 7293; E-mail: [email protected]
****************************** NATURE NANOTECHNOLOGY **************************
[4] Silicon nanowires stay current
DOI: 10.1038/nnano.2007.411
Lithium-ion batteries that have a nanowire component could last much longer and store up to ten times more charge than conventional batteries. A paper online this week in Nature Nanotechnology reports that these batteries, with anodes made from silicon nanowires.
Rechargeable lithium-ion batteries are found in numerous portable electronics - from iPods to laptops. Typically, carbon is used as the anode electrode in these batteries, but silicon anodes should be able to store up to ten times more charge. The problem with silicon is that the repeated insertion and extraction of lithium ions causes it to degrade and fall apart, leading to poor battery performance over time.
The anodes designed by Yi Cui and co-workers are made from silicon nanowires that are grown directly on a stainless steel substrate, which serves as the current collector. These anodes reach the maximum theoretical charge capacity for silicon on the first charge cycle and stay close to 75% of this maximum over many charge and discharge cycles. The study attributes the success of the silicon nanowire anodes to a combination of excellent electrical contact with the substrate, improved strain relief and the one-dimensional electrical properties of silicon nanowires.
Author contact:
Yi Cui (Stanford University, CA, USA)
Tel: +1 650 723 4613; E-mail [email protected]
Other papers from Nature Nanotechnology to be published online at the same time and with the same embargo:
[5] Carrier-mediated magnetoelectricity in complex oxide heterostructures
DOI: 10.1038/nnano.2007.412
************************************** NATURE GENETICS **************************
(http://www.nature.com/naturegenetics)
[6] Genetic risk factor for ALS
DOI: 10.1038/ng.2007.52
Scientists have identified a variant in the gene DPP6 that increases susceptibility to amyotrophic lateral sclerosis, reports a paper to be published online this week in Nature Genetics. Amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease) is an untreatable and fatal disorder caused by degeneration of motor neurons in the brain and spinal cord.
While mutations in genes have been found that cause rare cases of familial ALS, there has been much more limited success in identifying genetic influences on non-familial (sporadic) ALS, which accounts for more than 90% of cases.
Leonard van den Berg and colleagues carried out a genome-wide association study of more than 1,700 individuals with the disease and more than 1,900 healthy controls, sampled from three European populations, and including recently reported data from affected individuals in the United States. A single variant in DPP6 was associated with ALS in each population, increasing risk by approximately 30%. This is the first genetic risk factor identified for sporadic ALS in the context of a genome-wide study, and is the first to be found consistently in multiple populations. DPP6 encodes a dipeptidyl-peptidase-like protein, an enzyme found predominantly in the brain whose expression has been shown to be increased in rats in response to spinal cord injury.
Author contact:
Leonard van den Berg (University Medical Center, Utrecht, The Netherlands)
Tel: +31 302 506 506; E-mail: [email protected]
[7] Genetic susceptibility to Kawasaki disease
DOI: 10.1038/ng.2007.59
A variant in a gene called ITPKC is associated with increased susceptibility to Kawasaki disease, reports a paper to be published online this week in Nature Genetics. Kawasaki disease is characterized by acute inflammation of the vascular system in infants and children, and if left untreated can lead to lethal coronary artery aneurysms.
Kawasaki disease tends to run in families, suggesting that there are genetic components to disease risk. It is also 10-20 times more common in Japan than in Western countries. Yoshihiro Onouchi and colleagues identified a region on chromosome 19 that was linked with the disease, and in particular a series of variants across four genes in the region were found more frequently in individuals with the disease than in healthy controls. The authors focused on one of these genes, ITPKC, which they regarded as the best candidate. ITPKC encodes an enzyme that is part of a signaling pathway with a critical role in certain cells of the immune system (T-cells). The authors went on to show that one of the risk variants reduces the expression of ITPKC, and that lower levels of ITPKC promote activation of T-cells. This is consistent with the marked activation of the immune system seen in Kawasaki disease.
Finally, the authors suggest that the association of ITPKC with Kawasaki disease may have immediate clinical implications. Approximately 10-20% of affected individuals are resistant to the standard treatment of intravenous immunoglobulins, but individuals with the ITPKC risk variant are 4-5 times more likely to fail to improve on the standard therapy. If these individuals could be identified with a genetic test, they could be offered alternative and more intensive therapies.
Author contact:
Yoshihiro Onouchi (SNP Research Center, RIKEN, Yokohama, Japan)
Tel: +81 45 503 9347; E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[8] Common genetic variants at the CRAC1 (HMPS) locus on chromosome 15q13.3 influence colorectal cancer risk in the UK population
DOI: 10.1038/ng.2007.41
[9] RNA toxicity in myotonic muscular dystrophy induces NKX2-5 expression
DOI: 10.1038/ng.2007.28
********************************* NATURE NEUROSCIENCE **************************
(http://www.nature.com/natureneuroscience)
[10] A pathway controlling body temperature
DOI: 10.1038/nn2027
Scientists have identified neurons that relay temperature information from sensory fibres in the spinal cord to the thermoregulatory control centre in the brain, reports a study in the January issue of Nature Neuroscience. This neural pathway transmits temperature information to the brain regions that produce physiological changes to defend the body against the effects of low temperatures.
Kazuhiro Nakamura and Shaun Morrison used two types of tracers in rats to identify an area in the brainstem containing neurons that receive information from temperature sensory fibres and then send this information to the central thermoregulatory control area. These neurons, in a part of the brain called the lateral parabrachial nucleus, increased their activity in response to skin cooling. Blocking the activity of the neurons abolished shivering, metabolic and cardiac responses to cooling, while stimulating the neurons produced these protective responses. Physiological responses to cooling persisted when the pathway mediating temperature perception was disrupted, suggesting that the two pathways are distinct.
Author contact:
Kazuhiro Nakamura (Oregon Health & Science University, Beaverton, OR, USA)
Tel: +1 503 418 2671; E-mail: [email protected]
Other papers from Nature Neuroscience to be published online at the same time and with the same embargo:
[11] MuSK controls where motor axons grow and form synapses
DOI: 10.1038/nn2026
[12] On and off domains of geniculate afferents in cat primary visual cortex
DOI: 10.1038/nn2029
[13] Activity-dependent gating of lateral inhibition in the mouse olfactory bulb
DOI: 10.1038/nn2030
********************************** NATURE CELL BIOLOGY ****************************
(http://www.nature.com/naturecellbiology)
[14] Control of EGFR in breast cancer cell invasion
DOI: 10.1038/ncb1672
A mechanism explaining how epidermal growth factor (EGF) regulates breast cancer cell invasion is published online this week in Nature Cell Biology. The findings could contribute to the development of more specific anti-cancer drugs.
Highly proliferating, invasive breast cancer cells often express abnormally high levels of the EGF receptor (EGFR), and this is known to control both cell division and migration. In an effort to clarify the molecular pathways that are activated by EGFR specifically during cancer cell invasion ? as opposed to normal cell migration ? Hisataka Sabe and colleagues identify the protein GEP100 as a factor that directly links activated EGFR to Arf6, a protein that is often over expressed in breast cancer cells and promotes cancer cell invasion.
At high levels of GEP100, (as found in cancer cells), Arf6 was activated, allowing non-invasive cells to become invasive with stimulation of EGFR; conversely, when GEP100 was inhibited, metastasis was prevented in mice that had been injected with highly invasive breast cancer cells. Levels of GEP100 were enriched in clinical samples taken from invasive breast carcinomas, and the presence of GEP100 and EGFR correlated with tumour malignancy.
Inhibition of EGFR is an important anti-cancer treatment, although EGF also controls the growth of many normal cells. Thus, these findings could contribute to the development of more specific anti-cancer drugs that, by targeting GEP100, could efficiently block the pro-invasive activity of EGFR and inhibit the metastatic process.
Author contact:
Hisataka Sabe (Osaka Bioscience Institute, Japan)
Tel: +81 6 6872 4814; E-mail: [email protected]
Other papers from Nature Cell Biology to be published online at the same time and with the same embargo:
[15] ARF1 is directly involved in dynamin-independent endocytosis
DOI: 10.1038/ncb1666
[16] Unified mode of centromeric protection by shugoshin in mammalian oocytes and somatic cells
DOI: 10.1038/ncb1667
[17] Eithelial coating controls mesenchymal shape change through tissue-positioning effects and reduction of surface-minimizing tension
DOI: 10.1038/ncb1669
[18] Kif3a constrains beta-catenin-dependent Wnt signalling through dual ciliary and non-ciliary mechanisms
DOI: 10.1038/ncb1670
[19] Nuroepithelial progenitors undergo LGN-dependent planar divisions to maintain self-renewability during mammalian neurogenesis
DOI: 10.1038/ncb1673
***************************************************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
Nature PHYSICS (http://www.nature.com/naturephysics)
[20] Magnetic flux periodicity of h/e in superconducting loops
DOI: 10.1038/nphys813
[21] Charge fractionalization in quantum wires
DOI: 10.1038/nphys810
[22] Efficient coupling of photons to a single molecule and the observation of its resonance fluorescence
DOI: 10.1038/nphys812
NATURE MATERIALS (http://www.nature.com/naturematerials)
[23] Effects of elastic anisotropy on strain distributions in decahedral gold nanoparticles
DOI: 10.1038/nmat2083
[24] Electrically driven phase transition in magnetite nanostructures
DOI: 10.1038/nmat2084
Nature MEDICINE (http://www.nature.com/naturemedicine)
[25] G12-G13-LARG-mediated signaling in vascular smooth muscle is required for salt-induced hypertension
DOI: 10.1038/nm1666
[26] Modification of kidney barrier function by the urokinase receptor
DOI: 10.1038/nm1696
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[27] Modifying murine von Willebrand factor A1 domain for in vivo assessment of human platelet therapies
DOI: 10.1038/nbt1373
Nature IMMUNOLOGY (http://www.nature.com/natureimmunology)
[28] ‘Tuning’ of type I interferon-induced Jak-STAT1 signaling by calcium-dependent kinases in macrophages
DOI: 10.1038/ni1548
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[29] Subunit organization and functional transitions in Ci-VSP
DOI: 10.1038/nsmb1320
[30] Distinct binding modes specify the recognition of methylated histones H3K4 and H4K20 by JMJD2A-tudor
DOI: 10.1038/nsmb1326
[31] Structural basis for the catalytic mechanism of phosphothreonine lyase
DOI: 10.1038/nsmb1329
[32] Structural basis for activation of the autoinhibitory C-terminal kinase domain of p90 RSK2
DOI: 10.1038/nsmb1347
[33] Structural basis for synaptic adhesion mediated by neuroligin-neurexin interactions
DOI: 10.1038/nsmb1350
NATURE METHODS (http://www.nature.com/nmeth)
[34] Vector and parameters for targeted transgenic RNAi in Drosophila melanogaster
DOI: 10.1038/nmeth1146
[35] Integrating spatially resolved three-dimensional MALDI IMS with in vivo magnetic resonance imaging
DOI: 10.1038/nmeth1147
[36] Tracking transmitter-gated P2X cation channel activation in vitro and in vivo
DOI: 10.1038/nmeth1144
[37] A proteome chip approach reveals new DNA base damage recognition activities in Escherichia coli
DOI: 10.1038/nmeth1148
***************************************************************************************************************
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
Darlinghurst: 9
Melbourne: 26
BELGUIM
Antwerp: 6
Leuven: 6, 26
CANADA:
Montreal: 12
Quebec: 9, 26
Toronto: 17
Vancouver:
CHINA
Beijing: 31
Hubei: 2
Jinan: 31
DENMARK
Copenhagen: 2
FRANCE
Evry: 26
Toulouse: 23
GERMANY
Augsburg: 20
Hamburg: 25
Hannover: 25
Heidelberg: 25
Homburg: 26
Manheim: 25
Munich: 26
Tubingen: 1
GREECE
Crete: 28
HUNGARY
Budapest: 25
INDIA:
Bangalore: 15
IRELAND
Dublin: 24
ISRAEL
Rehovot: 21
ITALY
Milan: 26
JAPAN
Aichi: 7, 19
Chiba: 7
Fukuoka: 7
Gunma: 7
Kangawa: 7
Kobe: 16, 19
Kyoto: 14
Oita: 14
Okayama: 7
Osaka: 14, 16
Matsumoto: 7
Saitama: 7
Tochigi: 7
Tokyo: 7, 16
NETHERLANDS
Amsterdam: 6
Groningen: 6
Nigmegen: 6
Utrecht: 6
RUSSIA
Moscow: 20
SINGAPORE
Singapore: 22
SPAIN
Madrid: 26
Vigo: 23
SWEDEN
Lund: 2
Umea: 6
SWITZERLAND
Basel: 8
Zurich: 22
TAIWAN
Keelung: 37
UNITED KINGDOM
Birmingham: 8
Cambridge: 1
Edinburgh: 8
Harrow: 8
London: 8
Manchester: 8
Oxford: 8
Southampton: 1
Sutton: 8
UNITED STATES OF AMERICA
California
Berkeley: 4, 29
La Jolla: 7, 26
Los Angeles: 6, 36
Pleasanton: 4
San Diego: 7
San Francisco: 12, 18, 31
Santa Barbara: 5
Stanford: 4
Connecticut
New Haven: 21, 28
Storrs: 12
Illinois
Chicago: 32, 33, 37
Urbana: 3
Maryland
Baltimore: 37
Bethesda: 6, 25
Massachusetts
Boston: 7, 26, 34
Cambridge: 21
Woods Hole: 2
Michigan
Ann Arbor: 26
Minnesota
Austin: 32
Rochester: 30
New Jersey
Murray Hill: 21
New York
New York: 11, 12, 26, 27, 28
Rochester: 9
Ohio
Columbus: 2
Oregon
Beaverton: 10
Pennsylvania
Pittsburgh: 13
Tennessee
Nashville: 35
Texas
Houston: 24
Virginia
Ashburn: 34
Charlottesville: 9
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 journalsindividually:
Nature Biotechnology (New York)
Peter Hare
Tel: +1 212 726 9284; E-mail: [email protected]
Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]
Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]
Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: [email protected]
Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Fabio Pulizzi
Tel: +44 207 014 4024; 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 Photonics (Tokyo))
Oliver Graydon
Tel: +81 3 3267 8776; 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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