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Article Released Sun-6th-January-2008 18:00 GMT
Contact: Ruth Institution: Nature Publishing Group
 Anatomy of a pandemic flu threat

Summaries of other newsworthy papers include Walking after spinal rewiring in Nature Medicine and First sign of trouble in Nature Immunology


For papers that will be published online on 06 January 2008

This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Walking after spinal rewiring – Nature Medicine

Anatomy of a pandemic flu threat – Nature Biotechnology

First sign of trouble – Nature Immunology

· 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 Press contacts for the Nature journals are listed at the end of this release.

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*******************************************Nature MEDICINE********************************************

[1] Walking after spinal rewiring
DOI: 10.1038/nm1682

Rewiring of nerve fibres in the spinal cord helps rats to regain the ability to walk after injury, reports a paper online this week in Nature Medicine.

People with spinal cord injury lose the ability to walk, partly because nerve fibres from motor neurons in the brain are severed or crushed. Efforts to induce functional recovery have largely concentrated on finding ways to regrow these damaged fibres through the lesion. However, regeneration has proven very difficult to achieve.

Michael Sofroniew and colleagues report that there may be an easier way to restore walking after spinal cord injury. They find that neurons within intact portions of the spinal cord near the lesion rewire after injury. These spinal neurons can then relay signals from the brain to neurons below the lesion and restore walking in injured animals. These findings suggest that harnessing spinal neuron rewiring may be a simpler way to induce functional recovery after spinal cord injury.

Author contact:
Michael Sofroniew (University of California, Los Angeles, CA, USA)
Tel: +1 310 794 4944; E-mail:

Other papers from Nature Medicine to be published online at the same time and with the same embargo:

[2] Endothelin B receptor mediates the endothelial barrier to T cell homing to tumors and disables immune therapy
DOI: 10.1038/nm1699

*******************************************NATURE BIOTECHNOLOGY*********************************

[3] Anatomy of a pandemic flu threat
DOI: 10.1038/nbt1375

Widespread transmission of bird flu between humans would require the virus to develop the ability to recognize umbrella-shaped structures in the human respiratory tract. This finding, reported online this week in Nature Biotechnology, promises to change how scientists monitor human adaptation of flu viruses and how doctors diagnose and treat both seasonal influenza and a potential H5N1 pandemic.

Most human flu pandemics are thought to have arisen from mutant viruses that combine features of both animal and human influenzas, but knowing exactly what to look for when analyzing new variants is key to anticipating an outbreak. Flu viruses attack by binding sugar chains that line the airways and lungs. The chemical linkages between the sugar molecules in these chains differ between humans and birds, and until now it has been assumed that bird flu viruses adapt to humans simply by acquiring mutations that enable them to attach to human sugar linkages.

Ram Sasisekharan and colleagues show that human adaptation depends on the shape assumed by the flexible sugar chains rather than the type of linkage. Bird flu viruses currently require cone-shaped sugar chains to infect birds, so the umbrella shape found in humans has protected most of us from avian flu. One implication of this finding is that bird flu strains that might have triggered alarm may not be a cause for undue concern provided that they cannot bind umbrella-shaped sugar chains.

Author contact:
Ram Sasisekharan (Massachusetts Institute of Technology, Cambridge, MA, USA)
Tel: +1 617 258 9494; E-mail:

Additional contact for comment on paper:
Carole Bewley (National Institutes of Health, Bethesda MD, USA)
Tel: +1 301 594 5187; E-mail:

Other papers from Nature Biotechnology to be published online at the same time and with the same embargo:

[4] Peptide-conjugated antisense oligonucleotides for targeted inhibition of a transcriptional regulator in vivo
DOI: 10.1038/nbt1366

*******************************************NATURE IMMUNOLOGY ************************************

[5] First sign of trouble
DOI: 10.1038/ni1556

Expression of a single stress response protein, even in the absence of ‘danger’ signals displayed by invading microbes or dying cells, triggers massive reorganization and activation of immune cells, according to a paper published online this week in Nature Immunology.

Previous studies questioned whether stress response proteins, which are often found on the surfaces of tumours, are sufficient to activate immune defences. Adrian Hayday and co-workers designed a mouse in which expression of the stress response protein Rae1 could be turned on and off in the skin, on demand. Rae1 induction provoked reorganization of skin-resident immune cells and infiltration of activated immune cells from the blood. Surprisingly, some affected skin-resident immune cell populations promoted, whereas others suppressed, tumour rejection.

Future work is needed to understand the mechanism through which Rae1 expression induces such large-scale changes in the skin immune system, and to determine whether manipulation of Rae1 expression might hold therapeutic utility in the treatment of tumours.

Author contact:
Adrian Hayday (King’s College London, UK)
Tel: +44 207 188 3078; E-mail:

Other papers from Nature Immunology to be published online at the same time and with the same embargo:

[6] Transcription factor EBF restricts alternative lineage options and promotes B cell fate commitment independently of Pax5
DOI: 10.1038/ni1555

Items from other Nature journals to be published online at the same time and with the same embargo:


[7] Glyoxylate carboligase lacks the canonical active site glutamate of thiamine-dependent enzymes
DOI: 10.1038/nchembio.62

[8] A forward chemical genetic screen reveals an inhibitor of the Mre11–Rad50–Nbs1 complex
DOI: 10.1038/nchembio.63


[9] The same sequence variant on 9p21 associates with myocardial infarction, abdominal aortic aneurysm and intracranial aneurysm
DOI: 10.1038/ng.72

[10] Deletions and epimutations affecting the human 14q32.2 imprinted region in individuals with paternal and maternal upd(14)-like phenotypes
DOI: 10.1038/ng.2007.56

[11] Role of retrotransposon-derived imprinted gene, Rtl1, in the feto-maternal interface of mouse placenta
DOI: 10.1038/ng.2007.51

[12] Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism
DOI: 10.1038/ng.62

[13] Ultraconservation identifies a small subset of extremely constrained developmental enhancers
DOI: 10.1038/ng.2007.55


[14] CNS-derived glia ensheath peripheral nerves and mediate motor root development
DOI: 10.1038/nn2025

[15] NGF-promoted axon growth and target innervation requires GITRL-GITR signaling
DOI: 10.1038/nn2034


[16] Epitope tagging of endogenous proteins in somatic cells for genome-wide ChIP-chip studies
DOI: 10.1038/nmeth1170

[17] Highly inclined thin illumination enables clear single-molecule imaging in cells
DOI: 10.1038/nmeth1171


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.

Innsbruck: 12

Aartselaar: 12
Brussels: 12
Leuven: 12
Liege: 9, 12

Aarhus: 9
Copenhagen: 9
Glostrup: 9

Helsinki: 9
Kupoio: 9

Paris: 8

Erlangen: 12
Freiberg: 6
Halle: 7
Heidelberg: 12

Alexandroupolis: 2

Kopavogur: 9
Reykjavik: 9

Beer-Sheva: 7

Rome: 9
Perugia: 15
Torino: 2

Akita: 10
Chiba: 10
Fukuoka: 10
Ibaraki: 11
Ichikawa: 10
Kagoshima: 10
Kanagawa: 11, 17
Niigata: 11
Numazu: 10
Osaka: 10
Saitama: 10, 17
Shizuoka: 18
Takamatsu: 10
Tokyo: 10, 11
Yokohama: 10, 11

Groningen: 9
Heerlen: 9
Nijmegen: 9
Utrecht: 9

Dunedin: 9

Ansan: 14

Huddinge: 9
Malmo: 9

Cambridge: 10
Cardiff: 15
London: 5, 9, 12
Oxford: 12

Berkeley: 13
Los Angeles: 1
Walnut Creek: 13
New Haven: 5
Atlanta: 3, 9
Chicago: 6
Indianapolis: 12
Bethesda: 8
Boston: 15, 16
Cambridge: 3
Ann Arbor: 2
Detroit: 9
Minneapolis: 5
Rochester: 6
New York
New York: 4, 8
North Carolina
Durham: 9
Cleveland: 16
Oklahoma City: 12
Philadelphia: 2, 6, 9
Pittsburgh: 9
Nashville: 14
Austin: 8


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Tel: +44 20 7843 4502; E-mail:

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Tel: +44 20 7843 4562; E-mail:

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Nature Biotechnology (New York)
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Tel: +1 212 726 9284; E-mail:

Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail:

Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail:

Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail:

Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail:

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail:

Nature Materials (London)
Fabio Pulizzi
Tel: +44 207 014 4024; E-mail:

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail:

Nature Methods (New York)
Allison Doerr
Tel: +1 212 726 9393; E-mail:

Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email:

Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail:

Nature Photonics (Tokyo))
Oliver Graydon
Tel: +81 3 3267 8776; E-mail:

Nature Physics (London)
Alison Wright
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Nature Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail:

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Keywords associated to this article: nerve fibres, spinal cord, flu pandemics, stress response protein, immunology
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