NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 29 June 2008
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Biotechnology: Fingers point way to HIV treatment
Geoscience: Landslides drive glacial advances
Neuroscience: Cognitive therapy to control reward anticipation
Nature: Easy iPS
Medicine: A new way to treat premature ageing
Chemical Biology: A sweet route to treating Alzheimer’s disease?
Medicine: A noncoding RNA may drive Alzheimer’s disease
Geoscience: Oceanic methane production
Genetics: Thirty loci and counting for Crohn’s disease
Immunology: New anti-parasite protective mechanism
Methods: Automated imaging of worm gene expression
Immunology: Constraining neutrophil damage
Nature: Mushroom bodies feel the heat
And finally… Neuroscience: The downside of a good defence
· 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] Biotechnology: Fingers point way to HIV treatment
DOI: 10.1038/nbt1410
T cells, a type of white blood cell that is destroyed by HIV, have been made resistant to HIV infection, both in the test tube and in mice, using an enzyme designed to disrupt a specific gene. The results, published online this week in Nature Biotechnology, could lead to a clinical treatment in which the T cells of an HIV-positive individual would be isolated, genetically altered with the enzyme and then returned to the body.
HIV enters T cells by recognizing two different cell-surface receptors—a primary receptor, called CD4, and a co-receptor, such as CCR5 or CXCR4. Rare individuals who are born with mutations in the CCR5 gene lack functional CCR5 molecules on their T cells and are naturally resistant to HIV infection.
To see if this natural mechanism of viral resistance could be mimicked in normal T cells that do express functional CCR5, Carl June and colleagues deliberately disrupted the CCR5 gene using a genetic treatment. The treatment involves zinc-finger endonucleases, enzymes that cut DNA at specific sequences. By making variants of these endonucleases, researchers can control which genomic sequences are cut.
The authors designed a zinc-finger endonuclease meant to target the CCR5 gene and showed that it disrupts this gene in primary human T cells with very high specificity. When a mixture of modified and unmodified T cells was infected with HIV in a culture dish, the modified T cells survived better. Tests in a mouse model of HIV infection revealed that animals transplanted with the modified T cells had lower viral loads and higher numbers of T cells compared with animals that received unmodified T cells.
Ultimately, if clinical trials confirm the positive results in mice reported here, this treatment may be useful for restoring the immune systems of HIV-positive individuals by rendering their T cells resistant to HIV infection.
Author contact:
Carl June (University of Pennsylvania, Philadelphia, PA, USA)
Tel: +1 215 573 5745; E-mail: [email protected]
[2] Geoscience: Landslides drive glacial advances
DOI: 10.1038/ngeo249
The re-advance of the Franz Joseph Glacier that led to the formation of New Zealand’s Waiho Loop moraine during the last glacial termination was driven by a landslide from a nearby mountain, rather than climatic changes. The Waiho Loop, located in the Southern Alps of New Zealand, had been interpreted as evidence for Southern Hemisphere cooling during the Younger Dryas cold reversal.
Online this week in Nature Geoscience, James Shulmeister and colleagues study a large suite of rock samples collected from the Waiho Loop moraine – the debris material carried and deposited by the glacier. Based on an analysis of the rock types and the grain characteristics of the material, they concluded that the moraine most likely represented the products of a massive landslide, rather than typical glacier transport. They suggest that a landslide from nearby Mount Roon may have blanketed the glacier, protecting it from surface ice loss and ultimately causing the glacial advance.
The authors suggest that landslides may play a bigger role in causing isolated glacial advances than previously thought, and suggest care must be taken when interpreting similar isolated moraines elsewhere.
Author contact:
James Shulmeister (University of Canterbury, Christchurch, New Zealand)
Tel: +64 3 364 2762; E-mail: [email protected]
[3] Neuroscience: Cognitive therapy to control reward anticipation
DOI: 10.1038/nn.2141
People can dampen their anticipation of an upcoming reward by re-directing their thoughts, reports a study published online in Nature Neuroscience this week.
Elizabeth Phelps and colleagues measured anticipatory physiological and neural responses to a cue which people had learned predicted monetary rewards. Each time the cue was presented, people were asked to think of either the reward predicted by the cue, or something calming that was the same colour as the cue. The calming strategy reduced activation in the striatum ¾ an area of the brain thought to be involved in expectations of reward ¾ and diminished skin conductance responses, a measure of arousal which may relate to reward anticipation.
These results suggest that emotion regulation might be useful in controlling urges elicited by reward-predicting stimuli such as drug cravings.
Author contact:
Elizabeth Phelps (New York University, NY, USA)
Tel: +1 212 998 8337; E-mail: [email protected]
[4] Nature: Easy iPS
DOI: 10.1038/nature07061
Developmental biologists have simplified the recipe for creating induced pluripotent stem cells (iPS cells), which could potentially make the technology safer for clinical treatments. The new method makes it less likely that the cells — which offer hope as tailor-made cures for people with genetic diseases — could cause complications such as cancer.
iPS cells are traditionally made by injecting adult cells with viruses carrying genes for a range of developmental factors, which ‘reprogramme’ the cells and make them revert to a more primitive developmental state. However, one of these factors, called c-Myc, can cause tumours to form.
Writing in this week’s Nature, researchers led by Hans Schöler report that a particular adult cell type in mice, called neural stem cells, can be converted to iPS cells by using just two developmental factors instead of the previous four, and without the need for c-Myc or for viral gene insertion. If the effect can be recreated in human cells it may pave the way for safer and wider application of iPS cells, for research and perhaps clinical treatments.
Author contact:
Hans Scholer (Max Planck Institute for Molecular Biomedicine, Münster, Germany)
Tel: +49 251 70365 300; E-mail: [email protected]
[5] Medicine: A new way to treat premature ageing
DOI: 10.1038/nm1786
A combination of statins and drugs for bone disorders could treat premature-ageing conditions such as Hutchinson-Gilford progeria syndrome (HGPS), reports a study published online this week in Nature Medicine.
Several forms of human premature aging, including HGPS, are caused by a mutant protein called progerin. Progerin undergoes a biochemical modification known as prenylation, which anchors it to the membrane of the cell nucleus, leading to the disease. Previous studies showed that inhibitors of the enzyme farnesyltransferase (FT), which is responsible for one form of prenylation, eliminate the nuclear abnormalities associated with progerin accumulation and lead to a small improvement of the aging-like characteristics in a mouse model of progeria.
Now, Carlos López-Otín and colleagues show that progerin is also prenylated by the enzyme geranylgeranyltransferase (GGT), which could explain the low efficiency of the FT inhibitors in previous studies. The authors also show that a combination of cholesterol-lowering drugs – statins – and drugs for certain bone disorders – aminobisphosphonates – prevents the modification of progerin, markedly improving the aging-like characteristics of progeroid mice, and increasing their life span.
These findings point to a new therapeutic approach for HGPS and other premature-aging syndromes.
Author contact:
Carlos López Otín (Universidad de Oviedo, Spain)
Tel: +34 98 510 4201; E-mail: [email protected]
[6] Chemical Biology: A sweet route to treating Alzheimer’s disease?
DOI: 10.1038/nchembio.96
Scientists have identified an enzyme inhibitor in the brain that reduces the phosphorylation of a key protein known to be associated with Alzheimer’s disease. The research, published online this week in Nature Chemical Biology, could lead to a new strategy for developing therapeutic treatments for patients with Alzheimer’s disease.
Hyperphosphorylated tau proteins tend to collect into clusters called neurofibrillary tangles. The presence of these tangles in the brain is a major hallmark of Alzheimer’s disease and associated neurodegenerative diseases called ‘tauopathies’. Scientists think that tau phosphorylation may have a reciprocal relationship with tau O-GlcNAcylation, or addition of a particular type of sugar molecule to tau. This means that increasing the levels of the sugar O-GlcNAc should decrease tau phosphorylation.
One way to increase tau O-GlcNAc levels is to inhibit the enzyme that removes the sugar from tau. The O-GlcNAcase inhibitors created so far are unstable within the body, difficult to synthesize or unable to enter the brain from the bloodstream. David Vocadlo and colleagues have created an inhibitor that overcomes these problems and shown that it elevates O-GlcNAc and lowers tau phosphorylation within the body.
With this inhibitor it will now be possible to investigate O-GlcNAcase as a target for treating Alzheimer’s disease and also to explore the role of O-GlcNAc in the brain.
Author contact:
David J. Vocadlo, (Simon Fraser University, Burnaby, BC, Canada)
Tel: +1 778 782 3530; Email: [email protected]
[7] Medicine: A noncoding RNA may drive Alzheimer’s disease
DOI: 10.1038/nm1784
Scientists have found a molecular mechanism that may drive the progression of Alzheimer’s disease. The mechanism, involving the enzyme Beta secretase 1 (BACE1), is described online in Nature Medicine this week, and could become a target for future therapeutic efforts.
Many protein-coding RNAs have natural complementary partners, most of which seem to be noncoding RNAs. Claes Wahlestedt and colleagues have identified a noncoding complementary partner for the enzyme BACE1, which positively regulates the levels of BACE1 RNA and protein, and is present in people with Alzheimer’s disease and in a mouse model with similar symptoms.
Upon exposure to amyloid-beta, the molecule that results from the activity of BACE1 and that accumulates in the amyloid plaques characteristic of Alzheimer’s disease, expression of the noncoding RNA is enhanced, which increases the levels of BACE1 and generates additional amyloid-beta through a positive feedback loop.
Author contact:
Claes Wahlestedt (The Scripps Research Institute, Jupiter, FL, USA)
Tel: +1 561 799 8905; E-mail: [email protected]
[8] Geoscience: Oceanic methane production
DOI: 10.1038/ngeo234
Aerobic bacteria could produce the greenhouse gas methane in the surface waters of the world’s oceans, suggests a study published online this week in Nature Geoscience. The research indicates that marine methane production may increase in response to climate change, releasing more methane into the atmosphere in a positive feedback loop.
David Karl and colleagues measured methane production in seawater samples collected off the coast of Hawaii. They found that marine bacteria break down a phosphate-containing compound in oxygenated seawater, producing methane as a by-product. They found that methane production was greatest in phosphate-depleted waters.
The upper oceans are known to be rich in methane, relative to the atmosphere, but the precise source of this methane has perplexed researchers. Production of the gas was previously thought to be limited to oxygen-free environments unlike the sea surface.
Author contact:
David Karl (University of Hawaii, Hawaii, USA)
Tel: +1 808 956 8964; E-mail: [email protected]
[9] Genetics: Thirty loci and counting for Crohn’s disease
DOI: 10.1038/ng.175
More than 30 genetic loci have been identified that confer susceptibility to Crohn’s disease, a common inflammatory bowel disorder, according to a study published online this week in Nature Genetics. This is the most complete picture yet assembled of the genetic influences on risk of a common disease.
Three genome-wide scans for Crohn’s disease have recently been published, revealing 11 loci that lead to increased risk of the disease. Led by Mark Daly, the authors of those studies have now combined their data and conducted an overall ‘meta-analysis’, which increases the likelihood of identifying variants with modest effects on disease susceptibility. With this approach an additional 21 loci were found. Together, these 32 loci account for approximately 10% of the overall variance in disease risk, which may reflect as much as 20% of the genetic risk, given a substantial role for environmental factors. The overall picture suggests that there are a small number of loci that confer significant added risk, and a much larger number with smaller effects.
Three of the individual genes that have been implicated in Crohn’s disease have previously been shown to influence risk of type 1 diabetes and asthma, raising the possibility of common genetic mechanisms underlying these disorders.
Author contact:
Mark Daly (Harvard Medical School, Boston, MA, USA)
Tel: +1 617 643 3290; E-mail: [email protected]
[10] Immunology: New anti-parasite protective mechanism
DOI: 10.1038/ni.1629
Scientists have discovered how the immune system fights Toxoplasma gondii, a parasite that causes the disease toxoplasmosis in humans, according to a paper online this week in Nature Immunology.
Immune cells called CD8+ T lymphocytes are required to fight T. gondii, which can cause severe disease in humans with weak immune systems. These cells recognize parasite-derived protein fragments displayed on the surface of infected cells. Nilabh Shastri and colleagues show that a fragment of the T. gondii protein called GRA6 is a target of CD8+ T lymphocytes and induces a protective immune response in mice.
They also showed that the host cell protein ERAAP, which acts as a scissor to ‘clip’ proteins into fragments, is required for the production of this protective GRA6 fragment. This is the first time ERAAP has been shown to have a specific and protective role in the immune response to pathogens.
Author contact:
Nilabh Shastri (University of California, Berkeley, CA, USA)
Tel: +1 510 643 9197; E-mail: [email protected]
[11] Methods: Automated imaging of worm gene expression
DOI: 10.1038/nmeth.1228
A system to monitor gene expression during embryonic development of the worm C. elegans is published online this week in Nature Methods.
Understanding the process of development, where a fertilized egg gives rise to a multicellular organism, is a major goal in biological research. This would be helped greatly by defining which genes are expressed in every cell during development. C. elegans is ideal for such studies because it is transparent and relatively simple, and because its lineage — that is, the pattern of cell divisions over the course of its development — has been previously defined.
Bob Waterston and colleagues apply automated imaging to monitor the timing and relative expression levels of fluorescent indicators for four individual genes, each encoding an important transcription factor, in the C. elegans embryo. They could identify precisely which cells expressed the gene of interest up until the 350-cell stage of development, which includes all but the last round of cell division in the worm embryo.
This sets the stage for a systematic analysis of reporters for many more genes, which will help reveal the entire range of expressed genes for every cell during development in this organism.
Author contact:
Robert Waterston (University of Washington School of Medicine, Seattle, WA, USA)
Tel: +1 206 685 7347; E-Mail: [email protected]
[12] Immunology: Constraining neutrophil damage
DOI: 10.1038/ni.1628
The way in which neutrophils – the immune system’s ‘first responders’ – migrate into target tissues is reported online this week in Nature Immunology.
Neutrophils are the ‘look-out’ white blood cells that can exit the bloodstream at the first sign of infection and travel to its source. Here they can release their payload of noxious chemicals in an attempt to stave off the invaders.
Jingsong Xu and colleagues identify an intracellular signaling molecule, called MYLK, that is required for neutrophil movement. MYLK links the ‘danger’ signals sensed outside cells to their intracellular structure, allowing them to change shape and direction, as well as increasing their ‘adhesive’ properties needed to crawl through blood vessels.
Xu’s group shows MYLK-deficient neutrophils are less able to enter lung tissues in response to septic infections. However, this defect is not a bad thing as neutrophil-mediated collateral damage is the leading cause of acute respiratory distress syndrome (ARDS), a potential lethal complication of sepsis-induced lung injury. By identifying the signaling pathway between MYLK and the cell structure, scientists can start to develop potential new targets for treating ARDS.
Author contact:
Jingsong Xu (University of Illinois College of Medicine, Chicago, IL, USA)
Tel: +1 312 996 6919; E-mail: [email protected]
[13] Nature: Mushroom bodies feel the heat
DOI: 10.1038/nature07090
The part of the brain centre that determines the desired temperature in Drosophila has been identified in a paper in this week’s Nature. Mushroom bodies (already known to control learning and sleep in flies), and the activity of certain signalling proteins within them, are essential for controlling temperature-favouring behaviour.
Various thermoresponsive ion channels have been previously identified as temperature sensors, but how and where temperature information is interpreted and processed in the brain remains unknown.
Jaeseob Kim and colleagues have carried out a large behavioural genetic screen of Drosophila mutants. They discovered that the temperature preferred by Drosophila is mainly determined by the levels of an intracellular messenger, cAMP, and a signalling protein, PKA, and by their activity in the mushroom body.
The discovery of the involvement of these proteins in the mushroom bodies provides new insight into how the set point temperature might be established in mammals for the purpose of body temperature regulation.
Author contact:
Jaeseob Kim (Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea)
Tel: +82 11 438 2632; E-mail: [email protected]
[14] And finally… Neuroscience: The downside of a good defence
DOI: 10.1038/nn.2152
Many babies experience a temporary lack of oxygen during birth, and some children suffer long-lasting brain damage as a consequence. A study published online in Nature Neuroscience this week provides a potential explanation for this effect, by identifying a specific pathway by which low oxygen can disturb the development of an immature nervous system.
Although complete loss of oxygen rapidly kills nerve cells, which may explain some of the lasting damage, low oxygen levels are also known to switch on an evolutionarily ancient defensive mechanism in all cells. This mechanism is dependent on the transcription factor HIF-1. HIF-1 enhances anaerobic metabolism and blood vessel growth. But it is not known whether HIF-1 exerts any specific effects on nerve cells.
Roger Pocock and Oliver Hobert exposed pregnant roundworms to very low levels of oxygen, and then studied the nervous system in the offspring. They found very specific defects in the embryonic migration and axon growth of particular – but not all – nerve cells. Low oxygen increased expression of a receptor that is known to function in axon growth and migration, Vab-1. The specific nerve cell defects did not occur in mutant worms lacking either HIF-1 or Vab-1.
Author contacts:
Oliver Hobert (Columbia University, New York, NY, USA)
Tel: +1 212 305 0063; E-mail: [email protected]
Roger Pocock (Columbia University, New York, NY, USA)
Tel: +1 212 305 0065; 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)
[15] Treatment of arthritis with a selective inhibitor of c-Fos/activator protein-1
DOI: 10.1038/nbt1412
[16] An orally delivered small-molecule formulation with antiangiogenic and anticancer activity
DOI: 10.1038/nbt1415
[17] Electrostatic readout of DNA microarrays with charged microspheres
DOI: 10.1038/nbt1416
NATURE GENETICS (http://www.nature.com/naturegenetics)
[18] Conservation of the H19 noncoding RNA and H19-IGF2 imprinting mechanism in therians
DOI: 10.1038/ng.168
[19] Identification of renal Cd36 as a determinant of blood pressure and risk for hypertension
DOI: 10.1038/ng.164
[20] Gain-of-function mutations in TRPV4 cause autosomal dominant brachyolmia
DOI: 10.1038/ng.166
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[21] Two-stage subduction history under North America inferred from multiple-frequency tomography
DOI: 10.1038/ngeo231
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[22] Differently phosphorylated forms of the cortactin homolog HS1 mediate distinct functions in natural killer cells
DOI: 10.1038/ni.1630
NATURE MATERIALS (http://www.nature.com/naturematerials)
[23] The true toughness of human cortical bone measured with realistically short cracks
DOI: 10.1038/nmat2221
[24] High-performance dye-sensitized solar cells based on solvent-free electrolytes produced from eutectic melts
DOI: 10.1038/nmat2224
[25] Mapping the spatial distribution of charge carriers in LaAlO3/SrTiO3 heterostructures
DOI: 10.1038/nmat2223
Nature MEDICINE (http://www.nature.com/naturemedicine)
[26] Hepatic insulin resistance directly promotes formation of cholesterol gallstones
DOI: 10.1038/nm1785
NATURE METHODS (http://www.nature.com/nmeth)
[27] Detection of heteromerization of more than two proteins by sequential BRET-FRET
DOI:10.1038/nmeth.1229
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[28] Engineered elastomeric proteins with dual elasticity can be controlled by a molecular regulator
DOI: 10.1038/nnano.2008.168
[29] Contact and edge effects in graphene devices
DOI: 10.1038/nnano.2008.172
[30] Carbon nanotube coating improves neuronal recordings
DOI: 10.1038/nnano.2008.174
[31] Formation of chiral branched nanowires by the Eshelby Twist
DOI: 10.1038/nnano.2008.179
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[32] Action potentials contribute to neuronal signaling in C. elegans
DOI: 10.1038/nn.2131
[33] Directed differentiation of hippocampal stem/progenitor cells in the adult brain
DOI: 10.1038/nn.2148
[34] Gating the pore of P2X receptor channels
DOI: 10.1038/nn.2151
Nature PHYSICS (http://www.nature.com/naturephysics)
[35] Superconductivity and quantum criticality in the heavy-fermion system beta-YbAlB4
DOI: 10.1038/nphys1002
[36] Two-photon probe of the Jaynes–Cummings model and controlled symmetry breaking in circuit QED
DOI: 10.1038/nphys1016
[37] Pairing fluctuations in the pseudogap state of copper-oxide superconductors probed by the Josephson effect
DOI: 10.1038/nphys1017
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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
Melbourne: 18
BELGIUM
Brussels: 9
Ghent: 9
Leuven: 9, 20
Liege: 9
CANADA:
Burnaby: 6
Montreal: 9
Toronto: 9
Vancouver: 28
CHINA
Changchun: 24
COLOMBIA
Medellin: 7
CROATIA
Zagreb: 25
CZECH REPUBLIC
Prague: 19
FRANCE
Grenoble: 5
Marcoussis: 37
Marseille: 5
Orsay: 37
Palaiseau: 25, 37
Paris: 9, 37
Sophia Antipolis: 21
GERMANY
Aachen: 4
Berlin: 19
Garching: 36
Munich: 21, 36
Munster: 4
Stuttgart: 29
ITALY
Modena: 27
JAPAN
Kanagawa: 36
Kashiwa: 35
Kobe: 15
Kyoto: 35
Saitama: 20
Tokyo: 15, 20, 36
Toyama: 15
Tsukuba: 36
NEW ZEALAND
Christchurch: 2
SOUTH KOREA
Daejeon: 13
SPAIN
Barcelona: 25, 27
Bilbao: 36
Oviedo: 5
Pamplona: 27
SWEDEN
Stockholm: 7, 27
SWITZERLAND
Lausanne: 24, 29
Zurich: 33
UNITED KINGDOM
Cambridge: 9, 18, 35
Edinburgh: 9
Exeter: 9
London: 9, 19
Newcastle: 9
Oxford: 9
York: 6
UNITED STATES OF AMERICA
California
Berkeley: 1, 10, 17, 23
Irvine: 35
La Jolla: 33
Los Angeles: 7, 9, 20
Richmond: 1
San Francisco: 19
Stanford: 31
Connecticut
Groton: 7
New Haven: 9
District of Columbia
Washington: 7
Florida
Jupiter: 7
Tallahassee: 35
Hawaii
Honolulu: 8
Illinois
Chicago: 9, 12, 26
Maywood: 19
Maryland
Baltimore: 9, 27
Bethesda: 34
Massachusetts
Boston: 9, 16, 26
Cambridge: 8, 9
Michigan
Ann Arbor: 19
Detroit: 19
Missouri
St Louis: 22
New Jersey
Newark: 3
Princeton: 21
New Mexico
Los Alamos: 35
New York
New York: 3, 11, 14
Pennsylvania
Philadelphia: 1
Pittsburgh: 9
Tennessee
Nashville: 30
Texas
Dallas: 30
Denton: 30
San Antonio: 18
Utah
Salt Lake City: 32
Washington
Seattle: 11
URUGUAY
Montevideo: 20
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 Biotechnology (New York)
Peter Hare
Tel: +1 212 726 9284; 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 Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]
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