NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 06 April 2008. This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Coastal pollution could produce an unhealthy chemical cocktail - Nature Geoscience
Host-to-graft disease spread in Parkinson disease? - Nature Medicine
Common genetic variants influencing adult height - Nature Genetics
p53 hampers energy metabolism in cancer cells - 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.
PICTURES: To obtain artwork from any of the journals, you must first obtain permission from the copyright holder (if named) or author of the research paper in question (if not).
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 GEOSCIENCE ***********************************
[1] Coastal pollution could produce an unhealthy chemical cocktail
DOI: 10.1038/ngeo177
The reaction of chemical compounds in the pollution from cities and ships with sea salt aerosols from the ocean could affect air quality in coastal areas where the two meet, according to research online this week in Nature Geoscience. A team measured high levels of nitryl chloride, an active halogen implicated in ground-level ozone production, in industrially polluted air along the southeast coast of the US, implying that ozone pollution could be particularly high where industrial combustion products meet the ocean, as in many megacities around the world.
James Roberts and colleagues measured unexpectedly high levels of nitryl chloride in ship exhaust plumes along the southeast coast of the US. They show that this chemical compound is produced during the night by the reaction of the nitrogen oxides in polluted air from ships or cities with the chlorine from sea salt. With the help of the morning sunlight, nitryl oxide is rapidly split into a reactive radical that can produce ozone in combination with suitable atmospheric compounds, and nitrogen oxides.
Author contact:
James Roberts (National Oceanic and Atmospheric Administration, Boulder, CO, USA)
Tel: +1 303 497 3982, E-mail: [email protected]
Related Backstory
‘Hunting for halogen chemistry’ by James Roberts describes the field work and the background to the work
DOI: 10.1038/ngeo184
Other papers from Nature Geoscience to be published online at the same time and with the same embargo:
[2] Slow slip and frictional transition at low temperature at the Hikurangi subduction zone
DOI: 10.1038/ngeo178
*********************************** Nature MEDICINE ****************************************
(http://www.nature.com/naturemedicine)
[3], [4] & [5] Host-to-graft disease spread in Parkinson disease?
DOI: 10.1038/nm1746
DOI: 10.1038/nm1747
DOI: 10.1038/nm1752
Cell transplants have long been proposed as a possible therapy for Parkinson disease, but a series of reports in Nature Medicine suggest that the pathology may spread from the host to the transplants.
Parkinson disease results from the abnormal aggregation of a protein known as alpha-synuclein and the degeneration of the substantia nigra, a dopamine-releasing region of the midbrain. Therapies for the disease aiming at replacing the lost cells have given hope and, in the 1990s, clinical trials transplanting dopaminergic fetal brain tissue into the brains of patients with Parkinson took place.
Two independent groups led by Patrik Brundin and by Jeffrey Kordower report that the transplanted tissue in some subjects shows evidence of alpha-synuclein aggregates. This observation is striking because the grafts were too young to develop this on their own, and the fetal tissue had been placed into the striatum, a brain region that receives input from the substantia nigra but does not develop alpha-synuclein aggregates in Parkinson disease. So, in these subjects, the disease seems to have spread from the host to the graft.
But not all studies agree. A third study, led by Ole Isacson, failed to show Parkinson-like pathology in the transplants from a different set of similar subjects, finding instead a large proportion of serotonergic, and not only dopaminergic, neurons within the grafts.
As current efforts to develop cell-replacement therapies focus on the use of stem cells to generate substantia nigra-like dopaminergic neurons, the findings of these three groups on long-term transplant recipients add a level of complexity to the idea of curing Parkinson disease with grafted tissue.
Author contacts:
Patrik Brundin (Wallenberg Neuroscience Center, Lund, Sweden)
Tel: +46 46 222 05 63; E-mail: [email protected]
Jeffrey Kordower (Rush University Medical Center, Chicago, IL, USA)
Tel.: +1 312 563 3570; E-mail: [email protected]
Ole Isacson (Harvard Medical School/McLean Hospital, Belmont, MA, USA)
Tel: +1 617 855 3283; E-mail: [email protected]
********************************** NATURE GENETICS **************************************
(http://www.nature.com/naturegenetics)
[6], [7] & [8[ Common genetic variants influencing adult height
DOI: 10.1038/ng.121
DOI: 10.1038/ng.122
DOI: 10.1038/ng.125
Scientists have discovered dozens of common genetic variants influencing adult human height, according to three studies published online this week in Nature Genetics.
Recently, two independent studies reported that common variants near two genes, HMGA2 and GDF5, are associated with variation in human height in the general population. Using substantially larger sample sizes, three groups now report the discovery of dozens of additional variants influencing adult height.
The newly discovered variants explain up to 4% of normal height variation in populations of European ancestry. Individuals carrying predominantly ‘tall’ versions of these variants are, on average, 5 cm taller than individuals carrying only a few of the ‘tall’ variants.
Many of the height-associated variants reside near genes known or suspected to have a role in skeletal development. Others reside near genes that control how cells grow and divide.
Height is considered a classic complex trait with a strong heritable component. Therefore, understanding the genetic basis of this model trait may shed light on the genetic architecture of other traits, including those influencing risk of common diseases.
Author contacts:
Timothy Frayling (Peninsula Medical School, Exeter, UK)
Tel: +44 1392 262935; E-mail: [email protected]
Kari Stefansson (deCODE Genetics, Reykjavik, Iceland)
Tel: +354 570 1900; E-mail: [email protected]
Joel Hirschhorn (Broad Institute of Harvard and MIT, Cambridge, MA, USA)
Tel: +1 617 919 2129; E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[9] Rare independent mutations in renal salt handling genes contribute to blood pressure variation
DOI: 10.1038/ng.118
***************************** NATURE CELL BIOLOGY ************************************
(http://www.nature.com/naturecellbiology)
[10] p53 hampers energy metabolism in cancer cells
DOI: 10.1038/ncb1724
The tumour suppressor p53 can limit tumour development by inhibiting aerobic glycolysis reports a paper published online this week in Nature Cell Biology.
Cancer cells normally shift their metabolism to aerobic glycolysis - the conversion of glucose to lactic acid in the presence of oxygen - which confers an advantage in sustaining tumour growth.
p53 activity is lost in over half of human tumours; its primary role is to eliminate cells that have undergone oncogenic transformation by inducing cell growth arrest or programmed cell death. Nobuyuki Tanaka and colleagues found, by looking at p53-deficient primary fibroblasts, that loss of p53 leads to higher glucose metabolism, and demonstrated that this requires de-repression of the transcription factor NF-kB and one of its target genes called GLUT3.
This work reveals an additional function of p53 in restricting cell proliferation through suppression of NF-kB, which is important for maintaining normal levels of glucose metabolism and cell growth.
Author contact:
Nobuyuki Tanaka (Nippon Medical School, Kawasaki-shi, Japan)
Tel: +81 44 733 1860; E-mail: [email protected]
Other papers from Nature Cell Biology to be published online at the same time and with the same embargo:
[11] Mature ribosomes are selectively degraded upon starvation by an autophagy pathway requiring the Ubp3p/Bre5p ubiquitin protease
DOI: 10.1038/ncb1723
*****************************************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[12] Single-molecule analysis of human telomerase monomer
DOI: 10.1038/nchembio.82
Nature PHYSICS (http://www.nature.com/naturephysics)
[13] A thermodynamic unification of jamming
DOI: 10.1038/nphys934
[14] Single-atom gating of quantum-state superpositions
DOI: 10.1038/nphys930
NATURE MATERIALS (http://www.nature.com/naturematerials)
[15] Epitaxial graphene on ruthenium
DOI: 10.1038/nmat2166
[16] A chemically driven insulator-metal transition in non-stoichiometric and amorphous gallium oxide
DOI: 10.1038/nmat2164
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[17] Large-area ultrathin films of reduced graphene oxide as a transparent and flexible electronic material
DOI:10.1038/nnano.2008.83
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[18] Oligomeric amyloid-beta peptide disrupts phosphatidylinositol-4,5-bisphosphate metabolism
DOI: 10.1038/nn.2100
[19] TRPV1 exhibits dynamic ionic selectivity during agonist stimulation
DOI: 10.1038/nn.2102
[20] Functional identification of sensory mechanisms required for developmental song learning
DOI: 10.1038/nn.2103
[21] Rapid silencing of preBötzinger Complex somatostatin-expressing neurons induces persistent apnea in adult awake rats
DOI: 10.1038/nn.2104
[22] Corollary discharge circuits for saccadic modulation of the pigeon visual system
DOI: 10.1038/nn.2107
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[23] Phosphatidylinositol-3-OH kinase and nutrient-sensing mTOR pathways control T lymphocyte trafficking
DOI: 10.1038/ni.1603
[24] Phosphatase SHP-1 promotes TLR- and RIG-I-activated production of type I interferon by inhibiting the kinase IRAK1
DOI: 10.1038/ni.1604
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[25] Signal sequence-independent membrane targeting of ribosomes containing short nascent peptides within the exit tunnel
DOI: 10.1038/nsmb.1402
[26] A conserved rRNA methyltransferase regulates ribosome biogenesis
DOI: 10.1038/nsmb.1408
[27] Sequence-directed DNA export guides chromosome translocation during sporulation in Bacillus subtilis
DOI: 10.1038/nsmb.1412
NATURE METHODS (http://www.nature.com/nmeth)
[28] BAC TransgeneOmics: A high throughput method for exploration of protein function in mammals
DOI: 10.1038/nmeth.1199
[29] Spheroid-based engineering of a human vasculature in mice
DOI: 10.1038/nmeth.1198
[30] Improved genetic manipulation of human embryonic stem cells
DOI: 10.1038/nmeth.1200
************************************************************************************
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.
AUSTRIA
Vienna: 28
CANADA:
Calgary: 1
Halifax: 5
Montreal: 5
Toronto: 28
CHINA
Beijing: 22
Shanghai: 24
DENMARK
Aarhus: 7
Copenhagen: 7
Glostrup: 7
FINLAND
Helsinki: 8
Jakobstad: 8
GERMANY
Aachen: 16
Braunschweig: 16
Darmstadt : 16
Dresden : 28
Freiburg: 29
Giessen: 16
Heidelberg: 29
Mannheim: 29
Munich: 8, 28
Neuherberg: 8
Witten: 25
ICELAND
Reykjavik: 7
ITALY
Cagliari: 8
JAPAN
Kanagawa: 10
NETHERLANDS
Amsterdam: 23
Leiden: 30
Nijmegen: 7
Utrecht: 30
NEW ZEALAND
Lower Hutt: 2
SWEDEN
Lund: 3
Malmo: 8
SWITZERLAND
Basel: 29
Lausanne: 6
Zurich: 11
UNITED KINGDOM
Bristol: 6
Cambridge: 6, 8, 12, 23, 28
Cardiff: 23
Dundee: 6, 23
Exeter: 6
Glasgow: 6
Leeds: 6
Leicester: 6
London: 3, 6, 23
Nottingham: 30
Oxford: 6, 28
UNITED STATES OF AMERICA
California
Berkeley: 27
La Jolla: 21
Los Angeles: 13, 21
San Diego: 27
Dan Jose: 14
San Francisco: 23
Santa Cruz: 13
Stanford: 14
Colorado
Boulder: 1
Connecticut
New Haven: 9
Florida
Tampa: 4
Illinois
Chicago: 4, 28
Urbana: 20
Maryland
Baltimore: 7, 8, 19
Bethesda: 8, 9
Gaithersburg: 8
Massachusetts
Belmont: 5
Boston: 8, 9
Cambridge: 8
Framingham: 9
Michigan
Ann Arbor: 8
New Hampshire
Durham: 1
New Jersey
Piscataway: 17
New York
New York: 4, 18
Rochester: 26
Upton: 15
North Carolina
Chapel Hill: 8
Pennsylvania
King of Prussia: 6
Philadelphia: 5
Virginia
Richmond: 26
Washington
Seattle: 1
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]
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 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)
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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