NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 19 October 2008
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Materials: Straight to the heart
Neuroscience: Treating Lou Gehrig’s disease with glial stem cells
Neuroscience: Excess fatty acid in Alzheimer’s disease
Chemical Biology: A sweet surprise
And finally…Carbon storage by typhoons?
· 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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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.
[1] Materials: Straight to the heart
DOI: 10.1038/nmat2299
A new kind of non-inflammatory drug-delivery vehicle for the treatment of heart disease is reported online this week in Nature Materials. Michael Davis and colleagues demonstrate that ‘polymeric microspheres’ could be a useful form of drug transportation for a range of conditions.
Many polymer-based drug-delivery materials break down in the body to form acidic by-products that cause local inflammation in the target tissue. In the treatment of inflammatory diseases, such as cardiac dysfunction following heart attacks, this inflammation is detrimental to the recovery of the tissue.
Davis and his team show that polymer microspheres loaded with a known drug can be injected directly into the heart and, because of the neutral and non-inflammatory breakdown products of the polymer, they do not worsen the already inflamed section of the heart. This improved treatment of cardiac dysfunction is a result of the controlled release of the encapsulated drug from the polymer particles, allowing the diseased area to experience a sustained amount of the drug over several days. In comparison, the direct injection of the drug without the polymer shows no such beneficial effect.
The use of a polymer delivery vehicle with non-inflammatory decomposition products could have applications in inflammatory diseases of other organs, including liver, lung and bowel.
Author contact:
Michael Davis (Emory University and Georgia Institute of Technology, Atlanta, GA, USA)
Tel: + 1 404 727 9858; E-mail: [email protected]
[2] Neuroscience: Treating Lou Gehrig’s disease with glial stem cells
DOI: 10.1038/nn.2210
Nerve cell degeneration in a mouse model of Lou Gehrig’s disease can be slowed by transplantation of healthy glial cell precursors, reports a study published online this week in Nature Neuroscience. The research could have implications for future treatment of this devastating condition.
Lou Gehrig’s disease, or amyotrophic lateral sclerosis (ALS), is caused by degeneration and death of motor neurons, the nerve cells that drive all muscles. Recent work has shown that astrocytes, a type of supporting glial cell, are also affected in ALS.
Based on these reports, Nicholas Maragakis and colleagues attempt to cure mice suffering from an ALS-like condition with a transplantation of astrocyte precursors. The transplanted cells survived in the spinal cord, and mice that received transplants survived longer, though they were not completely cured. The beneficial effect required the presence of a particular transporter protein in the astrocyte precursors. This transporter may help to remove any toxic excess of the neurotransmitter glutamate, which may be a contributing factor to ALS, from the motor neurons’ surroundings.
Author contact:
Nicholas Maragakis (Johns Hopkins University School of Medicine, Baltimore, MD, USA)
Tel: +1 410 614 9874; E-mail: [email protected]
[3] Neuroscience: Excess fatty acid in Alzheimer’s disease
DOI: 10.1038/nn.2213
Correcting altered fatty acid metabolism in the brain of mice with Alzheimer’s can reverse the cognitive deficits associated with the disease, reports a paper online this week in Nature Neuroscience. This work highlights a possible target for therapeutic intervention in patients with the disease.
Using a mouse model of Alzheimer’s disease, Lennart Mucke and colleagues observed a specific increase in an omega-6 fatty acid, known as arachidonic acid, and also an increase in the product of its metabolism. Because Amyloid-beta peptide – whose abnormal deposits are seen in Alzheimer’s patients’ brains – affects the activation of an arachidonic acid-metabolizing enzyme, the researchers blocked the action of this enzyme. The mice then showed significant improvement in some learning and memory tasks.
Author contact:
Lennart Mucke (Gladstone Institute of Neurological Disease, San Francisco, CA, USA)
Tel: +1 415 734 2504; E-mail: [email protected]
[4] Chemical Biology: A sweet surprise
DOI: 10.1038/nchembio.116
Scientists have discovered a new cellular pathway that controls synthesis of a well-known sugar. The research, published online this week in Nature Chemical Biology, has global implications for cell biology due to the large number of roles for the sugar.
The sugar, CD15 antigen, or Lewis x (Le), is typically found on the cell surface and is important in both the immune system and in cell differentiation. Until now, it was believed that, when needed on the cell surface, it was synthesized from scratch by machinery inside the cell and then sent to the surface.
Robert Sackstein and Samah Zeineb Gadhoum show that a related sugar structure, sialyl-CD15, which carries an extra molecule called sialic acid and is also present on the cell surface, is directly changed to CD15. This shows that sialyl-CD15 serves partly as a storehouse for CD15. This surprising new route means that scientists will need to rethink how CD15 and sialic acid control cell function.
Author contacts:
Robert Sackstein (Brigham and Women's Hospital, Boston, MA, USA)
Tel: +1 617 525 5604; Email: [email protected]
Samah Zeineb Gadhoum (Brigham and Women's Hospital, Boston, MA, USA)
Tel: +1 617 525 5550, Email: [email protected]
[5] And finally… Carbon storage by typhoons?
DOI: 10.1038/ngeo333
Tropical cyclones could have a significant role in the transfer of atmospheric carbon dioxide to long-term deposits in the deep ocean, suggests research online this week in Nature Geoscience. The global importance of this carbon sequestration remains to be assessed, but this link in the carbon cycle will be highly sensitive to any future changes in the frequency or intensity of tropical cyclones.
Robert Hilton and colleagues analysed the sediment composition of Taiwan’s LiWu river during periods of flooding induced by tropical cyclones, seeking to quantify the proportion of young organic carbon in the river – that is, carbon recently taken up from the atmosphere. By looking at decades of river erosion, they estimate that 80–90% of this carbon is transported during cyclone-induced floods.
The findings suggest that both the frequency and intensity of typhoons can strongly affect the seaward transport of terrestrial young organic carbon. Such dense, sediment-laden floods are often injected directly into the deep ocean, potentially providing a mechanism for long-term carbon burial.
Author contact:
Robert Hilton (University of Cambridge, UK)
Tel: +44 1223 333 455; E-mail: [email protected]
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Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[6] 53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility
DOI: 10.1038/nature07433
[7] Strong effect of dispersal network structure on ecological dynamics
DOI: 10.1038/nature07395
[8] Sox18 induces development of the lymphatic vasculature in mice
DOI: 10.1038/nature07391
[9] 53BP1 facilitates long-range DNA end-joining during V(D)J recombination
DOI: 10.1038/nature07476
[10] The zinc-finger protein Zelda is a key activator of the early zygotic genome in Drosophila
DOI: 10.1038/nature07388
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[11] A model for transmission of the H3K27me3 epigenetic mark
DOI: 10.1038/ncb1787
[12] IAPs contain an evolutionarily conserved ubiquitin-binding domain that regulates NF-kB as well as cell survival and oncogenesis
DOI: 10.1038/ncb1789
[13] The TBP–PP2A mitotic complex bookmarks genes by preventing condensin action
DOI: 10.1038/ncb1790
[14] Scaffolding function of PAK in the PDK1–Akt pathway
DOI: 10.1038/ncb1795
NATURE GENETICS (http://www.nature.com/naturegenetics)
[15] Structure and function of a transcriptional network activated by the MAPK Hog1
DOI: 10.1038/ng.235
[16] Tbc1d1 mutation in lean mouse strain confers leanness and protects from diet-induced obesity
DOI: 10.1038/ng.244
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[17] Putative greigite magnetofossils from the Pliocene epoch
DOI: 10.1038/ngeo335
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[18] Transforming growth factor-beta ‘reprograms’ the differentiation of T helper 2 cells and promotes an interleukin 9–producing subset
DOI: 10.1038/ni.1659
[19] Proteolytic cleavage in an endolysosomal compartment is required for Toll-like receptor 9 activation
DOI: 10.1038/ni.1669
[20] Nedd4 augments the adaptive immune response by promoting ubiquitin-mediated degradation of Cbl-b in activated T cells
DOI: 10.1038/ni.1670
NATURE MATERIALS (http://www.nature.com/naturematerials)
[21] Printable ion-gel gate dielectrics for low-voltage polymer thin-film transistors on plastic
DOI: 10.1038/nmat2291
[22] Tunnelling spectra of individual magnetic endofullerene molecules
DOI: 10.1038/nmat2300
[23] Ultrahigh stress and strain in hierarchically structured hollow nanoparticles
DOI: 10.1038/nmat2295
[24] Electron and phonon renormalization near charged defects in carbon nanotubes
DOI: 10.1038/nmat2296
Nature MEDICINE (http://www.nature.com/naturemedicine)
[25] Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma
DOI: 10.1038/nm.1877
[26] The miR-15a–miR-16-1 cluster controls prostate cancer progression by targeting multiple oncogenic activities
DOI: 10.1038/nm.1880
NATURE METHODS (http://www.nature.com/nmeth)
[27] Decision tree-driven tandem mass spectrometry for shotgun proteomics
DOI: 10.1038/nmeth.1260
[28] Linking SNPs to CAG repeat length in Huntington’s disease patients
DOI: 10.1038/nmeth.1261
[29] Directed enzyme evolution via small and effective neutral drift libraries
DOI: 10.1038/nmeth.1262
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[30] Upscaling, integration and electrical characterization of molecular junctions
DOI: 10.1038/nnano.2008.305
[31] Giant negative thermal expansion in magnetic nanocrystals
DOI: 10.1038/nnano.2008.309
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[32] Fractional differentiation by neocortical pyramidal neurons
DOI: 10.1038/nn.2212
NATURE PHOTONICS (http://www.nature.com/nphoton)
[33] Bifacial dye-sensitized solar cells
DOI: 10.1038/nphoton.2008.224
Nature PHYSICS (http://www.nature.com/naturephysics)
[34] High-resolution scanning electron microscopy of an ultracold quantum gas
DOI: 10.1038/nphys1102
[35] Localization of ultrasound in a three-dimensional elastic network
DOI: 10.1038/nphys1101
[36] Probing warm dense lithium by inelastic X-ray scattering
DOI: 10.1038/nphys1103
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[37] Pore loops of the AAA+ ClpX machine grip substrates to drive translocation and unfolding
DOI: 10.1038/nsmb.1503
[38] FANCI phosphorylation functions as a molecular switch to turn on the Fanconi anemia pathway
DOI: 10.1038/nsmb.1504
[39] Activation of Slo1 BK chanells by Mg2+ coordinated between the voltage sensor and RCK1 domains
DOI: 10.1038/nsmb.1507
[40] PDGFRA/NG2 glia generate myelinating oligodendrocytes and piriform projection neurons in adult mice
DOI: 10.1038/nn.2220
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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: 8
Melbourne: 8, 12
Parkville: 8
BELGIUM
Brussels: 18, 25
Mons: 30
BRAZIL
Belo Horizonte: 24
Duque de Caxias: 24
CANADA:
Manitoba: 35
CHINA
Hong Kong: 8
DENMARK
Copenhagen: 11, 12
FRANCE
Gif-sur-Yvette: 17, 40
Grenoble: 35
Palaiseau: 36
GERMANY
Berlin: 16, 22
Darmstadt: 36
Essen: 18
Hannover: 12
Mainz: 34
Munich: 24
Nuthetal: 16
IRAN
Ahwaz: 38
IRELAND
Dublin: 11
ISRAEL
Jerusalem: 15
Rehovot: 29
ITALY
Alessandria: 12
Catania: 26
Milan: 8, 26, 30
Rome: 26
Turin: 12, 26
JAPAN
Fukuoka: 38
Hiroshima: 38
Hyogo: 31, 33
Kyoto: 38
Saga: 31
Tokyo: 14
MEXICO
San Luis Potosi: 24
NETHERLANDS
Eindhoven: 30
Groningen: 30
Leiden: 16
Utrecht: 17
PAKISTAN
Kohat: 36
POLAND
Warsaw: 12
Poznan: 12
SOUTH KOREA
Seoul: 21
SWEDEN
Stockholm: 16
SWITZERLAND
Lausanne: 33
TAIWAN
Hualien: 5
Taipei: 5
UNITED KINGDOM
Belfast: 36
Cambridge: 5
Coventry: 36
Didcot: 36
Edinburgh: 11
London: 18, 40
Oxford: 36
UNITED STATES OF AMERICA
California
Berkeley: 23
Carlsbad: 2
Davis: 3, 7
Livermore: 36
San Francisco: 3
Colorado
Denver: 20
Georgia
Atlanta: 1
Illinois
Urbana: 35
Iowa
Iowa City: 20
Kansas
Lawrence: 22
Kentucky
Lexington: 13
Maryland
Baltimore: 2, 9
Bethesda: 9
Massachusetts
Boston: 3, 4, 25, 38
Cambridge: 15, 19, 37
Charlestown: 28
Worcester: 28
Minnesota
Minneapolis: 21, 23
St Paul: 21
Missouri
Kansas City:
St Louis: 9, 39
New York
Cold Spring Harbor: 6, 12
Ithaca: 22
New York: 6, 9, 10
Rochester: 24
Ohio
Columbus: 36
Pennsylvania
Philadelphia: 20
South Carolina
Clemson: 24
Utah
Salt Lake City: 10
Washington
Seattle: 32
Wisconsin
Madison: 27
PRESS CONTACTS…
For media inquiries relating to embargo policy for all the Nature Research Journals:
Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]
Katherine Anderson (Nature New York)
Tel: +1 212 726 9231; E-mail: [email protected]
Ruth Francis (Head of Press, 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 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)
Alison Stoddart
Tel: +44 20 7843 4593; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: [email protected]
Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]
Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; 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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