NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 27 December 2009
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Medicine: Making transfusion safer
Immunology: Triggering inflammation to self
Chemical Biology: Sweet digestion
Genetics: Variants associated with metabolite levels
And finally…Medicine: The neurochemistry of panic
· 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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[1] Medicine: Making transfusion safer
DOI: 10.1038/nm.2070
A molecule has been identified that can elicit a deadly immune response after blood transfusion, as reported in this week’s Nature Medicine.
Transfusion-related acute lung injury (TRALI) is a frequent cause of death after blood transfusion. TRALI is often caused by antibodies found in blood components that are directed against a protein, HNA-3a. The identity of these antibodies has so far remained unknown.
Andreas Greinacher and colleagues now show that HNA-3a is coded by the choline transporter-like protein-2 gene, and that genetic variants in this molecule change the reactivity of the protein with HNA-3a–specific antibodies.
The molecular identification of this antigen should facilitate the development of tests for blood donor screening to lower the risk of TRALI.
Author contact:
Andreas Greinacher (Ernst-Moritz-Arndt-University, Greifswald, Germany)
Tel: +49 383 486 5482; E-mail: [email protected]
[2] Immunology: Triggering inflammation to self
DOI: 10.1038/ni.1836
How proteins implicated in Alzheimer’s disease and the vascular disease atherosclerosis are recognized is revealed in a report published online this week in Nature Immunology.
Kathryn Moore and colleagues found that three cell surface proteins – TLR4, TLR6 and CD36 – previously implicated in the recognition of specific microbial patterns assemble to form a newly identified molecular complex. CD36 recognizes the atherosclerosis-associated protein oxidized LDL (oxLDL) as well as the beta-amyloid peptide linked to Alzheimer’s disease, recruiting TLR4 and TLR6 in the recognition process. Signals triggered by this tri-molecular complex in immune cells induce production of proinflammatory mediators implicated in the pathology of these diseases.
Identification of a common molecular pathway involved in triggering and maintaining inflammation in atherosclerosis and Alzheimer’s disease represents an opportunity to devise therapies that may be effective in both conditions.
Author contact:
Kathryn Moore (New York University Medical Center, NY, USA)
Tel: +1 212 263 9259; E-mail: [email protected]
[3] Chemical Biology: Sweet digestion
DOI: 10.1038/nchembio.278
New insights into how gut bacteria break down sugars is published online this week in Nature Chemical Biology. These results could have implications in the human diet.
Bacteria need sugars as food to grow. Gut bacteria, also known as ‘symbiotic’ bacteria, obtain these sugars by breaking down larger chains of sugars – or ‘complex’ sugars – found in both human diet and human cells, a process which is critical for human health and digestion. However, the specific proteins that perform these tasks along the way have been elusive. In particular, a very common complex sugar contains four different types of chemical bonds, requiring four enzymes, known as glycoside hydrolases, to cut the pieces apart.
Harry Gilbert, Gideon Davies and colleagues profile 22 of the 23 glycoside hydrolases found in one of our gut bacteria. Unexpectedly, the researchers find a wide range of enzyme functions, explaining how this species can degrade these complicated sugar structures. These findings add to our growing understanding of our bacterial symbionts and the complexities of human digestion.
Author contacts:
Gideon Davies (University of York, UK)
Tel: +44 1904 328 260; E-mail: [email protected]
Harry Gilbert (University of Georgia, Athens, GA, USA)
Tel: +1 706 583 0655; Email: [email protected]
[4] Genetics: Variants associated with metabolite levels
DOI: 10.1038/ng.507
Genetic variants associated with metabolite concentrations in human blood serum are reported in this week’s issue of Nature Genetics.
Concentrations of metabolites, such as biologically relevant amino acids, sugars, and lipids, in blood serum provide specific measurements that reflect biological activity in the body, and often provide clinically useful information. Such metabolic profiles can provide a physiological snapshot of the cells or tissues being analyzed.
Karsten Suhre and colleagues determined the serum concentrations of 163 metabolites in over 2000 individuals. They then scanned the genomes of these individuals and identified nine genetic locations that are each associated with different metabolic measurements. For eight out of the nine regions, the genetic variant is located within or close to genes whose functions are correlated with the production of the associated metabolite.
These results provide insights into the common genetic variants that regulate human metabolism.
Author contact:
Karsten Suhre (German Research Center for Environmental Health, Neuherberg, Germany)
Tel: +49 31872627; E-mail: [email protected]
[5] And finally…Medicine: The neurochemistry of panic
DOI: 10.1038/nm.2075
Orexin, a brain peptide best known for its link to the sleep disorder narcolepsy, participates in the pathophysiology of panic disorder, according to a report in this week’s Nature Medicine.
In people with panic disorder – characterized by recurrent panic attacks – there is evidence of decreased brain inhibition and marked increases in autonomic and respiratory responses after intravenous infusions of sodium lactate—a common test for panic disorder. In rats, a brain region known as the DPH participates in anxiety-like states and is similarly vulnerable to sodium lactate.
The DPH has a large number of neurons that contain orexin—a peptide involved in arousal and vigilance states. Philip Johnson and his colleagues therefore investigated the role of orexin in panic anxiety and found that activation of orexin neurons leads to a panic-prone state in rats. Silencing the hypothalamic orexin gene with RNA interference or with orexin-receptor blockers prevented the panic responses.
The team also found that humans with panic anxiety have elevated levels of orexin in the cerebrospinal fluid compared to subjects without panic anxiety. These results indicate that the orexin system may constitute a potential new target to treat panic disorder.
Author contact:
Philip Johnson (Indiana University School of Medicine, Indianapolis, IN, USA)
Tel: +1 317 278 9047; 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 BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[6] Transcriptional profiling of growth perturbations of the human malaria parasite Plasmodium falciparum
DOI: 10.1038/nbt.1597
[7] Design of phosphodiesterase 4D (PDE4D) allosteric modulators for enhancing cognition with improved safety
DOI: 10.1038/nbt.1598
[8] Reengineering a receptor footprint of adeno-associated virus enables selective and systemic gene transfer to muscle
DOI: 10.1038/nbt.1599
[9] Nucleotide-resolution analysis of structural variants using BreakSeg and a breakpoint library
DOI: 10.1038/nbt.1600
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[10] An in vitro translation, selection and amplification system for peptide nucleic acids
DOI: 10.1038/nchembio.280
[11] Substrate-dependent proton antiport in neurotransmitter:sodium symporters
DOI: 10.1038/nchembio.284
NATURE GENETICS (http://www.nature.com/naturegenetics)
[12] Alterations in the ankyrin domain of TRPV4 cause congenital distal SMA, scapuloperoneal SMA and HMSN2C
DOI: 10.1038/ng.508
[13] Scapuloperoneal spinal muscular atrophy and CMT2C are allelic disorders caused by alterations in TRPV4
DOI: 10.1038/ng.509
[14] Mutations in TRPV4 cause Charcot-Marie-Tooth disease type 2C
DOI: 10.1038/ng.512
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[15] CTLA-4 suppresses the pathogenicity of self antigen–specific T cells by cell-intrinsic and cell-extrinsic mechanisms
DOI:10.1038/ni.1835
Nature MEDICINE (http://www.nature.com/naturemedicine)
[16] Tumor-mediated liver X receptor-alpha activation inhibits CC chemokine receptor-7 expression on dendritic cells and dampens antitumor responses
DOI: 10.1038/nm.2074
NATURE METHODS (http://www.nature.com/nmeth)
[17] Adaptive optics via pupil segmentation for high resolution imaging in biological tissues
DOI: 10.1038/nmeth.1411
[18] Chronic microsensors for longitudinal, subsecond dopamine detection in behaving animals
DOI: 10.1038/nmeth.1412
[19] Two-color, two-photon uncaging of glutamate and GABA
DOI: 10.1038/nmeth.1413
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[20] Representing information in cell assemblies: Persistent activity in the dentate gyrus mediated by semilunar granule cells
DOI: 10.1038/nn.2458
[21] The descending corticocollicular pathway mediates learning-induced auditory plasticity
DOI: 10.1038/nn.2466
[22] HDAC1 nuclear export induced by pathological conditions is essential for the onset of axonal damage
DOI: 10.1038/nn.2471
[23] Ischemia-induced neurogenesis of neocortical layer 1 progenitor cells
DOI: 10.1038/nn.2473
[24] A single fear-inducing stimulus induces a transcription-dependent switch in synaptic AMPAR phenotype
DOI: 10.1038/nn.2474
[25] Amyloid-beta from axons and dendrites reduces local spine number and plasticity
DOI: 10.1038/nn.2476
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[26] STIM1 gates the store-operated calcium channel ORAI1 in vitro
DOI: 10.1038/nsmb.1724
[27] Loqs and R2D2 act sequentially in the siRNA pathway in Drosophila
DOI: 10.1038/nsmb.1735
*****************************************************
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
Parkville: 3
AUSTRIA
Graz: 12
Innsbruck: 4
Vienna: 9
CANADA:
Toronto: 9
FRANCE
Ameins : 3
Strasbourg: 23
Toulouse: 3
GERMANY
Berlin: 2
Bochum: 1
Greifswald: 1
Hamburg: 6
Heidelberg: 9
Munich: 4, 12
Neuherberg: 4
Planegg-Martinsried: 4
Weihenstephan: 4
HUNGARY
Budapest: 24
ICELAND
Reykjavik: 7
ITALY
Milan: 16
Segrate : 16
JAPAN
Aichi: 23
Gunma: 24
Kyoto: 23
Saitama: 23
Tokyo: 19, 23
MALI
Bamako: 14
NETHERLANDS
Groningen: 12
Nijmegen: 12
NEW ZEALAND
Auckland: 12
SINGAPORE
Singapore: 6
SWEDEN
Huddinge: 16
Lund: 5
UNITED KINGDOM
Cambridge: 4, 9
Glasgow: 12
London: 4, 12, 22
Newcastle: 3, 12
Nottingham: 21
Oxford: 21
York: 3
UNITED STATES OF AMERICA
California
Berkeley: 25
La Jolla: 25
Stanford: 9
Connecticut
New Haven: 9
Florida
Gainesville: 8
Georgia
Athens: 3
Illinois
Chicago: 13, 25, 27
Evanston: 27
Woodridge: 7
Indiana
Indianapolis: 5
Louisiana
New Orleans: 24
Maryland
Baltimore: 14
Bethesda: 14
Massachusetts
Boston: 2, 13, 26
Cambridge: 10, 14
Charlestown: 2
Worcester: 2
Minnesota
Rochester: 13
Missouri
St Louis: 2, 15
New Jersey
Piscataway: 22
New York
Bronx: 24
Cold Spring Harbor: 25
New York: 2, 11, 22
North Carolina
Chapel Hill: 8
Durham: 13
Ohio
Cleveland: 20
Pennsylvania
Chadds Ford: 17
Philadelphia: 19
University Park: 24
Texas
Houston: 16
Virginia
Ashburn: 17
Harrisonburg: 14
Washington
Seattle: 18
Wisconsin
Madison: 8
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]
Neda Afsarmanesh (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 Biotechnology (New York)
Michael Francisco
Tel: +1 212 726 9288; E-mail: [email protected]
Nature Cell Biology (London)
Sowmya Swaminathan
Tel: +44 20 7843 4656; E-mail: [email protected]
Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail: [email protected]
Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail: [email protected]
Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; 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)
Vincent Dusastre
Tel: +44 20 7843 4531; 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)
Sabbi Lall
Tel: +1 212 726 9326; E-mail: [email protected]
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