NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 28 March 2010
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Genetics: Hybrid vigor in tomatoes
Nanotechnology: Superconductivity in just four molecules
Medicine: Removing the guesswork from multiple sclerosis
Biotechnology: Anti-RNA therapy counters breast cancer spread
Nature: Truffle genome unearthed
Medicine: The immunology of epilepsy
Genetics: Antibody has therapeutic effect on mice with ALS
Nature: Chemoprevention cocktail for colon cancer
Immunology: Fighting cytosolic bacteria and DNA viruses
Genetics: Genetic risk variant for urinary bladder cancer
Immunology: Borrowing stress to sustain immunity
And finally…Neuroscience: Addicted to junk food
· 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] Genetics: Hybrid vigor in tomatoes
DOI: 10.1038/ng.550
A mutation in one copy of the gene SFT in tomato increases fruit yield by up to 60%, according to a report published this week in Nature Genetics. The study suggests that improved vigor in plants can result from single heterozygous mutations.
Heterosis, or hybrid vigor, is a well-known genetic phenomenon, which is characterized by increased vigor or other superior qualities in offspring from two parents that are genetically different. Heterosis has immense practical value and is widely applied in agriculture, as many crops are grown from hybrid seed. However, the genetic mechanisms underlying heterosis are not well understood.
Zachary Lippman and colleagues find that mutation of just one copy of SFT leads to increased fruit yield in tomato. Plants were tested under diverse agricultural conditions and showed consistent increases in SFT hybrid plants.
Author contact:
Zachary Lippman (Cold Spring Harbor Laboratory, New York, NY, USA)
Tel: +1 516 367 8897; E-mail: [email protected]
[2] Nanotechnology: Superconductivity in just four molecules
DOI: 10.1038/nnano.2010.41
A nanowire that contains just four molecules can be superconducting, according to research published online in Nature Nanotechnology this week. This work helps to better understand superconductivity and the materials involved.
When a superconductor is cooled below a certain temperature it is able to conduct electricity without losing any energy as heat, which is why some researchers are trying to make longer superconducting wires. However, other researchers are trying to make smaller superconducting structures, so that they can learn more about these materials.
Saw-Wai Hla and co-workers deposited molecules of an organic charge-transfer salt on a silver surface and used a technique called scanning tunnelling spectroscopy to examine the molecular islands and chains that formed on the surface. They found evidence for a superconducting gap — a classic signature of superconductivity — at temperatures within ten degrees of absolute zero. The size of this gap depended on the length of the chains, and the gap could still be seen in wires that contained just four molecules.
Author contact:
Saw-Wai Hla (Ohio University, Athens, OH, USA)
Tel: +1 740 593 1727; E-mail: [email protected]
James Brooks (Florida State University, Tallahassee, FL, USA) N&V author
Tel: +1 850 644 2836; E-mail: [email protected]
[3] Medicine: Removing the guesswork from multiple sclerosis
DOI: 10.1038/nm.2110
The therapeutic efficacy of interferon-beta – the major treatment for multiple sclerosis – depends on what immune cell type is involved in the disease, according to a report in this week’s Nature Medicine. The results suggest that MS patients who will benefit from IFN-beta treatment may be identifiable before therapy even begins.
Interferon-beta (IFN-beta) is widely used against multiple sclerosis but is not always effective, and the reasons for treatment failure are not understood. Lawrence Steinman and his colleagues studied experimental autoimmune encephalomyelitis—the mouse version of multiple sclerosis—and found that IFN-beta was successful therapeutically depending on the immune cell type that induced the disease. If symptoms were caused by so-called TH1 cells—one type of immune system helpers—IFN-beta worked, but if TH17 cells—another type of immune system helpers—were involved, IFN-beta made disease worse. Crucially, the team found that patients with multiple sclerosis who do not respond to IFN-beta had worse disease and higher levels of IL-17F, a molecule produced by TH17 cells, compared to responders.
These results raise the tantalizing possibility of identifying what patients will derive benefit from IFN-beta even before the treatment begins — a prospect with important clinical and financial implications.
Author contact:
Lawrence Steinman (Stanford University School of Medicine, Stanford, CA, USA)
Tel: +1 650 725 6401; E-mail: [email protected]
[4] Biotechnology: Anti-RNA therapy counters breast cancer spread
DOI: 10.1038/nbt.1618
A new type of therapy that prevents the metastatic spread of breast cancer in a mouse model of breast cancer is presented online this week in Nature Biotechnology. Although the safety and efficacy of this therapy needs to be researched before testing in humans, the study provides a proof of principle that could one day prove beneficial for treating breast cancer.
Metastasis is responsible for the vast majority of cancer related deaths, but several factors have hampered the development of therapeutics for patients with these secondary tumors. One problem has been insufficient understanding of the molecular mechanisms involved in cancer invasion and progression, as well as a resulting lack of targets for therapeutic intervention. Recently, there has been a focus on a class of nucleic acid molecules—called microRNAs—that are important in controlling the expression of genes in normal cells, but are also implicate in the development and progression of disease. Some microRNAs are key regulators of metastasis formation. In addition, a new type of drug termed antagomirs—which are nucleic acid molecules capable of binding to complementary microRNA sequence—have recently been described that can target specific cellular microRNAs for destruction.
Robert Weinberg and colleagues now show the feasibility of using antagomirs in cancer metastasis treatment. By inhibiting a pro-metastatic microRNA with intravenously injected antagomir, they prevent the establishment of new metastases from aggressive breast tumors in mice. Their antagomir therapy has no effect on the growth of the primary tumor or on established metastases, but reduces the number of newly formed metastases by about 80%.
Author contact:
Robert Weinberg (Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA)
Tel: +1 617 258 5159; E-mail: [email protected]
[5] Nature: Truffle genome unearthed
DOI: 10.1038/nature08867
The newly sequenced black truffle genome provides important insights into fungal sex and fruiting, and the evolution of symbiotic relationships between fungi and plant roots. The sequence is revealed in this week’s Nature.
The Périgord black truffle (Tuber melanosporum Vittad.) lives in symbiotic harmony with the roots of European oak trees, where its fruiting bodies are highly sought as a gastronomic delight. Comparison of its DNA with that of the symbiotic fungus Laccaria bicolor reveals the truffle genome to be unusually poor in genes but rich in mobile genetic elements called transposons. And the two fungi appear to have evolved two very different ‘molecular toolkits’ for their symbiotic lifestyles, Francis Martin and colleagues show.
Worldwide demand for the black truffle has fuelled intense efforts at cultivation. So analysing the genetic traits related to fruiting and symbiosis should ultimately help boost crop production.
Author contact:
Francis Martin (Institut National de la Recherche Agronomique, Champenoux, France)
Tel: +33 383 39 40 80; E-mail: [email protected]
[6] Medicine: The immunology of epilepsy
DOI: 10.1038/nm.2127
A signaling pathway known for its role in immune defense responses is also involved in epilepsy, according to a report in this week’s Nature Medicine. The discovery could potentially be useful in the development of new anti-convulsant agents.
Brain inflammation is a major factor in epilepsy, but the impact of specific inflammatory molecules on the disease is not fully understood. Using several models of epilepsy in mice, Annamaria Vezzani and her colleagues discovered that release of a molecule called HMGB1 from neurons and glia and its interaction with a receptor key for the immune response against pathogens—TLR4—promoted seizures.
The researchers also found that blocking the action of HMGB1 and TLR4 decreased seizure frequency. Mice lacking TLR4 were also resistant to manipulations known to induce seizures. Last, increased levels of HMGB1 and TLR4 in epileptogenic tissue from patients pointed to the potential human relevance of this mechanism, which could be targeted to develop new anticonvulsant agents.
Author contact:
Annamaria Vezzani (Mario Negri Institute for Pharmacological Research, Milan, Italy)
Tel: +39 02 39 014 410; E-mail: [email protected]
[7] Genetics: Antibody has therapeutic effect on mice with ALS
DOI: 10.1038/ng.557
A biological treatment targeting the protein CD40L has a therapeutic effect on mice with amyotrophic lateral sclerosis (ALS), reports a new study published in Nature Genetics. The study suggests that ALS progression may be amenable to treatments that target the immune response.
ALS is a progressive neurodegenerative disease that leads to neuron loss in the brain and spinal cord and eventual paralysis. ALS affects approximately 2 per 100,000 individuals worldwide and is typically fatal within 5 years of diagnosis.
Steven Perrin and colleagues administered a monoclonal antibody to CD40L to mice with a mutation in SOD1 – a commonly used mouse model for ALS. They found that the anti-CD40L antibody delayed onset of paralysis and on average, led to a 40% extension of life duration after the first signs of paralysis.
Author contact:
Steven Perrin (ALS Therapy Development Institute, Cambridge, MA, USA)
Tel: +1 617 441 7236; E-mail: [email protected]
[8] Nature: Chemoprevention cocktail for colon cancer
DOI: 10.1038/nature08871
Treating premalignant colorectal cells with a protein cocktail that ‘persuades’ them to commit cell suicide may prove a useful method of cancer chemoprevention, a Nature paper suggests.
The treatment, devised by Xiangwei Wu and colleagues, targets a molecular pathway altered early in tumorigenesis. Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) and all-trans-retinyl acetate (RAc) treatment caused premalignant intestinal polyp cells to commit suicide in a mouse model and a human biopsy study.
Critically, normal cells appear unaffected by the treatment, suggesting that the therapy could be beneficial in preventing human colon cancer. Also, this type of cell death is triggered by short-term, intermittent treatment cycles, so the authors hope that the potential side effects and costs associated with long-term treatment could be minimized and controlled.
Author contact:
Xiangwei Wu (MD Anderson Cancer Center, Houston, TX, USA)
Tel: +1 713 745 2867; E-mail: [email protected]
[9] & [10] Immunology: Fighting cytosolic bacteria and DNA viruses
DOI: 10.1038/ni.1859
DOI: 10.1038/ni.1864
The first biochemical and genetic evidence that the DNA sensor, AIM2, is critical for immunity against certain bacterial infections and DNA viruses is reported in two papers online this week in Nature Immunology.
The AIM2 inflammasome is a multi-protein complex that induces the release of certain substances which are known to be critical for host defense against microbial invasion. Two groups – one led by Kate Fitzgerald and the other by Emad Alnemri – generated mice lacking AIM2 in order to test the effects of its loss on immune responses. They found that AIM2 is critical for immunity against Francisella tularensis, the causative agent of the infectious disease, tularemia. In addition, Fitzgerald’s group found AIM2 inflammasome activation is critical for a type of poxvirus and mouse cytomegalovirus infection. It is also partially involved in Listeria monocytogenes infection which gives rise to the bacterial infection listeriosis.
Future studies may go on to clarify what other intracellular microbial bacteria and viruses depend on AIM2.
Author contacts:
Emad Alnemri (Thomas Jefferson University, Philadelphia, PA, USA) Author paper [9]
Tel: +1 215 503 4632; E-mail: [email protected]
Kate Fitzgerald (University of Massachusetts, Worcester, MA, USA) Author paper [10]
Tel: +1 508 856 6518; E-mail: [email protected]
[11] Genetics: Genetic risk variant for urinary bladder cancer
DOI: 10.1038/ng.558
Another genetic variant associated with risk of urinary bladder cancer is reported in a study published in Nature Genetics.
Urinary bladder cancer (UBC) is the ninth most common cancer and affects approximately 350,000 people worldwide. Cigarette smoking and occupationally-related exposure to specific carcinogens are known risk factors for UBC, although genetic risk factors are also thought to be involved in UBC susceptibility.
Lambertus Kiemeney, Kari Stefansson, and colleagues analyzed 4,739 European individuals with UBC and found that a variant near the gene FGFR3 is associated with risk of UBC. Somatic, or acquired, mutations in FGFR3 are commonly found in low-grade bladder tumours.
Author contacts:
Lambertus Kiemeney (Radboud University, Nijmegen, Netherlands)
Tel: +31 24 3613745; E-mail: [email protected]
Kari Stefansson (deCODE Genetics, Reykjavik, Iceland)
Tel: +354 570 1900; Email: [email protected]
Edward Farmer (deCODE Genetics) Media contact
Tel: +44 7796 010107; E-mail: [email protected]
[12] Immunology: Borrowing stress to sustain immunity
DOI: 10.1038/ni.1857
Signaling molecules involved in the body’s stress responses also take part in the immune system’s anti-microbial responses, according to a study published online this week in Nature Immunology.
Many bacteria share distinct molecular components that are rapidly recognized by ‘pattern recognition receptors’ on immune cells, which once alerted, activate an immune response. Laurie Glimcher and colleagues found a subset of these receptors also activates XBP1 — a protein previously shown to control cellular stress responses. The scientists show major bacterial pathogens, including those causing tuberculosis, tularemia and listeriosis, activate this XBP1 pathway.
Unlike classical stress responses, which can lead to cell death, XBP1 activation by microbial components enhances the host’s inflammatory responses. This response reduces bacterial numbers and contributes to the control of infection.
Author contact:
Laurie Glimcher (Harvard School of Public Health, Boston, MA, USA)
Tel: +1 617 432 0622; E-mail: [email protected]
[13] And finally…Neuroscience: Addicted to junk food
DOI: 10.1038/nn.2519
High-calorie food can be just as addictive as smoking or the abuse of drugs suggests work published online this week in Nature Neuroscience. Although the findings cannot be directly transferred to human obesity, the study shows that overconsumption of high-calorie food can trigger addiction-like responses in the brain, and that junk food can turn rats into compulsive eaters in a laboratory setting.
Addicts are known to show blunted activation of brain circuits responsible for reward in response to normally positive experiences. Paul Kenny and colleagues measured rats’ sensitivity to rewarding experiences. When the researchers regularly offered rats a choice of high-calorie foods such as bacon, sausage, cake, and chocolate, in addition to their regular, healthier but less appetizing chow, the animals over-consumed calories and gained weight rapidly. Their reward sensitivity also plummeted, as has been shown before for addictive drugs. This blunting of reward response persisted for at least two weeks after the high-calorie food was no longer available.
A true addict, whether rat or human, will also compulsively consume their drug even when it is clearly detrimental to their own health. To test this, the team trained their rats to expect painful foot shocks when seeing a light signal. Although normal rats stop eating even the most delicious junk food when the light comes on, the obese rats used to a high-calorie diet just kept feeding.
The scientists also found decreased levels of a specific dopamine receptor in the overweight rats, as has been reported in humans addicted to drugs. Artificially decreasing levels of this dopamine receptor in another group of rats accelerated their loss of reward sensitivity when given access to the high-calorie food diet.
Author contact:
Paul Kenny (The Scripps Research Institute, Jupiter, FL, USA)
Tel: +1 561 228 2231; E-mail: [email protected]
**********************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[14] Double Holliday junctions are intermediates of DNA break repair
DOI: 10.1038/nature08868
[15] Fructose 1,6-bisphosphate aldolase/phosphatase may be an ancestral gluconeogenic enzyme
DOI: 10.1038/nature08884
NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[16] High-resolution DNA analysis of human embryonic stem cell lines reveals culture-induced copy number changes and loss of heterozygosity
DOI: 10.1038/nbt.1615
[17] Derivation, propagation and controlled differentiation of human embryonic stem cells in suspension
DOI: 10.1038/nbt.1616
[18] Self-sufficient control of urate homeostasis in mice by a synthetic circuit
DOI: 10.1038/nbt.1617
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[19] Atomic mutagenesis reveals A2660 of 23S ribosomal RNA as key to EF-G GTPase activation
DOI: 10.130/nchembio.341
NATURE CHEMISTRY (http://www.nature.com/nchem)
[20] Charge-transfer-induced structural rearrangements at both sides of organic/metal interfaces
DOI: 10.1038/nchem.591
[21] The rational design of helium bonds
DOI: 10.1038/nchem.596
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[22] Tropical dehydration processes constrained by the seasonality of stratospheric deuterated water
DOI: 10.1038/ngeo822
[23] Young off-axis volcanism along the ultraslow-spreading Southwest Indian ridge
DOI: 10.1038/ngeo824
[24] The role of oceanic plateau subduction in the Laramide orogeny
DOI: 10.1038/ngeo829
NATURE MATERIALS (http://www.nature.com/naturematerials)
[25] Uni-directional liquid spreading on asymmetric nanostructured surfaces
DOI: 10.1038/nmat2726
Nature MEDICINE (http://www.nature.com/naturemedicine)
[26] The regulatory subunits of PI3K, p85a and p85b, interact with XBP-1 and increase its nuclear translocation
DOI: 10.1038/nm.2099
[27] A regulatory subunit of phosphoinositide 3-kinase increases the nuclear accumulation of X-box–binding protein-1 to modulate the unfolded protein response
DOI: 10.1038/nm.2121
[28] Pomc-expressing progenitors give rise to antagonistic neuronal populations in hypothalamic feeding circuits
DOI: 10.1038/nm.2126
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[29] Self-powered nanowire devices
DOI: 10.1038/nnano.2010.46
[30] An extended defect in graphene as a metallic wire
DOI: 10.1038/nnano.2010.53
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[31] Asymmetric rostro-caudal inhibition in the primary olfactory cortex
DOI: 10.1038/nn.2524
[32] The amygdala encodes specific sensory features of an aversive reinforcer
DOI: 10.1038/nn.2520
[33] Reduction in endocannabinoid tone is a homeostatic mechanism for specific inhibitory synapses
DOI: 10.1038/nn.2517
[34] Lateral prefrontal cortex and self-control in intertemporal choice
DOI: 10.1038/nn.2516
[35] p75NTR-dependent, myelin-mediated axon degeneration maintains the specificity of axonal connectivity in the intact nervous system
DOI: 10.1038/nn.2513
NATURE PHOTONICS (http://www.nature.com/nphoton)
[36] Graphene photodetectors for high-speed optical communications
DOI: 10.1038/nphoton.2010.40
[37] Amplification of long-range surface plasmons by a dipolar gain medium
DOI: 10.1038/nphoton.2010.37
[38] Heralded noiseless linear amplification and distillation of entanglement
DOI: 10.1038/nphoton.2010.35
Nature PHYSICS (http://www.nature.com/naturephysics)
[39] Quantum to classical transition in a single-ion laser
DOI: 10.1038/nphys1627
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[40] Crystal structure of the carnitine transporter and insights into the antiport mechanism
DOI: 10.1038/nsmb.1788
[41] Structural basis for telomerase catalytic subunit TERT binding to RNA template and telomeric DNA
DOI: 10.1038/nsmb.1777
[42] Coilin-dependent snRNP assembly is essential for zebrafish embryogenesis
DOI: 10.1038/nsmb.1783
[43] Structural characterization of a capping protein interaction motif defines a family of actin filament regulators
DOI: 10.1038/nsmb.1792
[44] A potent and highly specific FN3 monobody inhibitor of the Abl SH2 domain
DOI: 10.1038/nsmb.1793
**********************************************************
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: 38
Sydney: 24
AUSTRIA
Innsbruck: 19, 39
Vienna: 36, 44
BELGIUM
Leuven: 11
CANADA:
Ottawa: 37
Toronto: 35
CHINA
Beijing: 40
Hong Kong: 20
CZECH REPUBLIC
Brno: 16
FINLAND
Helsinki: 16
Tampere: 16
Turku: 16
FRANCE
Champenoux: 5
Evry: 5
Marseille: 5
Orsay: 32
Saint-Genes-Champanelle: 5
Thiverval Grignon: 5
Versailles: 5
Villeurbanne: 18
GERMANY
Bochum: 20
Bonn: 10, 16
Braunschweig: 2, 39
Dortmund: 11
Dresden: 42
Freiburg: 15
Goettingen: 5, 42
Heidelberg: 11
Karlsruhe: 20, 22
Lutherstadt Wittenberg: 11
Saarbrucken: 39
Stuttgart: 20
HUNGARY
Budapest: 11
ISRAEL
Haifa: 16
Jerusalem: 16, 17
Rehovot: 1
ITALY
Bologna: 5
Brescia: 11
L’Aquila: 5
Milan: 6
Parma: 5
Perugia: 5
Rome: 5
Turin: 5, 11
Urbino: 5
Varese: 6
JAPAN
Ibaraki: 2
Kashiwa: 41
Kawaguchi: 2
Tokyo: 26, 27
NETHERLANDS
Amsterdam: 3, 6
Heemstede: 6
Maastricht: 11
Nijmegen: 3, 11
Utrecht: 11, 22
POLAND
Krakow: 32
PORTUGAL
Lisbon: 39
ROMANIA
Cluj-Napoca: 11
SINGAPORE
Proteos: 43
SLOVAKIA
Banska Bystrica: 11
SOUTH KOREA
Yongin: 9
SPAIN
Castelldefels: 39
Huesca: 11
Madrid: 20
Zaragoza: 11
SWEDEN
Gothenburg: 11
Stockholm: 11, 16
SWITZERLAND
Basel: 18, 34
Fribourg: 18
Lausanne: 20
Zurich: 18, 34
TURKEY
Zonguldak: 11
UNITED KINGDOM
Birmingham: 11
Cambridge: 22
Leeds: 11
London: 11, 16, 21
Manchester: 11
Oxford: 11
Sheffield: 16
UNITED STATES OF AMERICA
Alabama
Birmingham: 3
California
Carlsbad: 3
Davis: 14
Los Angeles: 11
Palo Alto: 3
Pasadena: 24
San Francisco: 14
Stanford: 3
Florida
Jupiter: 13
Tampa: 30
Georgia
Atlanta: 29
Illinois
Chicago: 44
Indiana
Bloomington: 20
Maryland
Baltimore: 10, 33
Massachusetts
Boston: 12, 26, 27
Cambridge: 4, 7, 14, 23, 25
Woods Hole: 23
Worcester: 10
Missouri
St Louis: 43
New Jersey
Princeton: 22
New York
Cold Spring Harbor: 1
New York: 4, 28, 31, 32, 34
Orangeburg: 32
Yorktown Heights: 36
Ohio
Athens: 2
Pennsylvania
Philadelphia: 9, 41
Texas
Houston: 8
San Antonio: 8
Washington
Seattle: 14, 16
Wyoming
Laramie: 23
VENEZUELA
Caracas: 35
PRESS CONTACTS…
For media inquiries relating to embargo policy for all the Nature Research Journals:
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Tel: +44 20 7843 4658; E-mail: [email protected]
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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:
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Nature Cell Biology (London)
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Nature Chemical Biology (Boston)
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Tel: +1 617 475 9241, E-mail: [email protected]
Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail: [email protected]
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Myles Axton
Tel: +1 212 726 9324; E-mail: [email protected]
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Nature Materials (London)
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Tel: +44 20 7843 4531; E-mail: [email protected]
Nature Medicine (New York)
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Nature Nanotechnology (London)
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Tel: +44 20 7014 4019; Email: [email protected]
Nature Neuroscience (New York)
Kalyani Narasimhan
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Tel: +44 20 7843 4555; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
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Tel: +1 212 726 9326; E-mail: [email protected]
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