Neuroscience: Regaining running in paralyzed rats

Summaries of newsworthy papers in Nature and Nature research journals - Genetics: Variants in prostate cancer, Medicine: Losing weight without too much energy, Geoscience: Deltas in decline, Chemical Biology: HCV lost in translation, Cell Biology: Stopping Listeria spread and Neuroscience: While you were sleeping.


For papers that will be published online on 20 September 2009
This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Neuroscience: Regaining running in paralyzed rats
Genetics: Variants in prostate cancer
Medicine: Losing weight without too much energy
Geoscience: Deltas in decline
Chemical Biology: HCV lost in translation
Cell Biology: Stopping Listeria spread
And finally... Neuroscience: While you were sleeping

· 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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HYPE: We take great care not to hype the papers mentioned on our press releases, but are sometimes accused of doing so. If you ever consider that a story has been hyped, please do not hesitate to contact us at [email protected], citing the specific example.


[1] Neuroscience: Regaining running in paralyzed rats

DOI: 10.1038/nn.2401

A complex combination of drugs, electrical stimulation and regular exercise can enable paralyzed rats to walk and even run on a treadmill. The study published online this week in Nature Neuroscience suggests that regeneration of severed nerve fibers is not required for paraplegic rats to learn to walk again. This finding may have implications for rehabilitation after spinal cord injuries

The spinal cord contains nerve circuits that can by themselves, without input from the brain, generate rhythmic activity to drive leg muscles in a way that resembles walking. Numerous studies have attempted to tap into this circuitry to help victims of spinal cord injury, but while leg motion can indeed be elicited, no weight-bearing walking has yet been achieved.

Grégoire Courtine and colleagues subjected rats to a complete spinal injury, such that they had no voluntary movement in their hind limbs. They set these paralyzed rats on a slowly moving treadmill while administering certain drugs as well as applying specific electrical currents to the spinal cord below the point of injury. This triggered the spinal rhythm-generating circuitry and elicited walking motion in the paralyzed hind limbs. Daily treadmill training over several weeks enabled full weight bearing walking, even backwards, sideways, and running.

The rats’ injury still left the connection between the brain and the spinal cord-based rhythmic walking circuitry interrupted. The rats were therefore unable to walk of their own accord. In human patients, since neuroprosthetic devices may in principle bridge spinal cord injuries to some extent, activating the spinal cord rhythmic circuitry as this study has may help in rehabilitation after spinal cord injuries.

Author contact:
Grégoire Courtine (University of Zurich, Switzerland)
Tel: +41 44634 8930; E-mail: [email protected]

[2], [3], [4] & [5] Genetics: Variants in prostate cancer

DOI: 10.1038/ng.450
DOI: 10.1038/ng.448
DOI: 10.1038/ng.452
DOI: 10.1038/ng.444

New genetic variants that are associated with increased risk of prostate cancer have been identified in four studies published online in this week’s Nature Genetics.

Two studies led by Rosalind Eeles, Julius Gudmundsson and colleagues surveyed the genomes of thousands of men with prostate cancer, which is the second most common cancer in men and affects approximately 25 per 100,000 men worldwide. Together, these studies identified eight new genetic loci that are associated with increased risk of prostate cancer. In addition, the studies report the identification of two new variants on 8q24 that confer risk of prostate cancer.

An area on 8q24 has been associated with breast, colon, and bladder cancer. Although this region contains no known protein-coding genes, the oncogene MYC is located next to this region. Douglas Easton and colleagues report a comprehensive analysis of 8q24 and identify two new regions in 8q24 that are associated with risk of prostate cancer. Meredith Yeager and colleagues also independently identified one of same new risk variants at 8q24 as Easton. Altogether, the studies emphasize the need for more research on the 8q24 locus, since future discoveries will likely be relevant to multiple types of cancer.

Author contacts:

Rosalind A Eeles (The Institute of Cancer Research, Sutton, Surrey, UK) Author paper [2]
Tel: +44 2086 613642; E-mail: [email protected]

Julius Gudmundsson (deCODE, Reykjavik, Iceland) Author paper [3]

This author can be contacted through the following media contact:

Edward Farmer (deCODE, Reykjavik, Iceland)
Tel: +44 7796 010107; E-mail: [email protected]

Douglas Easton (University of Cambridge, UK) Author paper [4]
Tel: +44 1223 740160; E-mail: [email protected]

Meredith Yeager (National Cancer Institute, Frederick, Maryland, USA) Author paper [5]
Tel: +1 301 435 7613; E-mail: [email protected]

[6] Medicine: Losing weight without too much energy

DOI: 10.1038/nm.2026

A pathway for how insulin signaling in the mouse hypothamalus - a region of the brain known to control food intake - is involved in obesity is presented in this week’s Nature Medicine. The findings could lead to a new therapeutic model for obesity intervention and weight loss treatment.

In struggling with weight gain, one approach is to eat less food. However, reducing food intake leads to a natural decrease in the amount of energy used, and this consequently contributes to a relapse of obesity. Various hormones, such as insulin, play a key regulatory role in the process of food intake and energy expenditure.

Insulin is known to inhibit food intake through FoxO1, a transcription factor, in hypothalamic neurons. Domenico Accili and colleagues observed that by significantly reducing the amount of FoxO1 in the hypothalamus, mice would reduce their food intake without also decreasing their energy use. They also show that FoxO1 in the hypothalamus inversely impacts the local concentration of Cpe, an enzyme that is required for the proper maturation of key hormones that also regulate food intake. An independent experiment where Cpe was over-expressed showed that this enzyme protected mice from weight gain without changing energy use, confirming the relationship between FoxO1 and Cpe.

The separation of food intake from energy spending allows for new therapeutic possibilities in obesity.

Author contact:
Domenico Accili (Columbia University, New York, NY, USA)
Tel: +1 212 851 5332; E-mail: [email protected]

[7] Geoscience: Deltas in decline

DOI: 10.1038/ngeo629

Eighty-five percent of the world’s largest deltas have experienced severe flooding over the past decade, according to the authors of an overview article published online in Nature Geoscience. The authors predict that the amount of deltaic land vulnerable to flooding could rise by 50% if sea-level rise occurs as projected for the twenty-first century.

James Syvitski and colleagues assessed the overall state of 33 major delta systems across the globe from satellite measurements and historical maps. They found that only nine of these deltas were keeping up with sea-level rise, and, of those, four were barely breaking even. They attribute the relative sinking of delta surfaces primarily to human interference - the sinking deltas were affected by upstream damming and river diversions, which limited the amount of new sediments carried to the delta. At some sites the recovery of oil and gas also led to sediment compaction.

Increasing rates of sea-level rise in response to greenhouse gas emissions will only increase the likelihood that swollen rivers and storm surges will flood these vulnerable areas.

Author contact:
James Syvitski (INSTAAR, University of Colorado, Boulder, CO, USA)
Tel: +1 303 735 5482; E-mail: [email protected]

[8] Chemical Biology: HCV lost in translation

DOI: 10.1038/nchembio.217

A method for inhibiting the ability of Hepatitis C virus to hijack cellular machinery and therefore spread is reported online this week in Nature Chemical Biology. The work could prove a promising strategy for treating viral infections.

The RNA genome of Hepatitis C virus (HCV) harbors a site called the IRES that is recognized by host ribosomes and is needed for translation of the RNA into viral proteins. A subdomain of the IRES is the target for a class of compounds that blocks replication of the virus. By using fluorescent labeling, guided by the three-dimensional structure of the viral RNA, Thomas Hermann and colleagues found that these inhibitors work by changing the conformation of the IRES such that the RNA is removed from the ribosome.

Inhibiting the ability of HCV and other viruses to hijack the cellular machinery is a promising strategy for treating viral infections.

Author contact:
Thomas Hermann, (University of California, San Diego, La Jolla, CA, USA)
Tel: +1 858 534 4467 ; E-mail: [email protected]

[9] Cell Biology: Stopping Listeria spread

DOI: 10.1038/ncb1964

A common mechanism by which Listeria, a type of bacteria, spreads from cell to cell during infection is reported online this week in Nature Cell Biology. The finding could prove useful in looking at ways to halt the development of diseases linked to Listeria, such as gastroenteritis.

Listeria monocytogenes is a highly virulent foodborne bacteria. It is responsible for listeriosis, which is linked to gastroenteritis in healthy individuals and more serious types of infections in pregnant women and those with weak immune systems.

During Listeria infection, bacteria replicate inside host cells, but it was unclear how the bacteria could then spread to infect other cells. Keith Ireton and colleagues show that certain molecules expressed by Listeria loosen the 'tension' of the membrane in infected host cells, allowing the bacteria to protrude and spread between cells more easily. This may be a common mechanism by which infectious agents promote cell-to-cell spreading during infection.

Author contact:
Keith Ireton (University of Central Florida, Orlando, FL, USA)
Tel: +1 407 882 2278; E-mail: [email protected]

[10] Neuroscience: While you were sleeping

DOI: 10.1038/nn.2391

Patients in vegetative and minimally conscious states still appear capable of acquiring certain forms of learning, reports a study published this week in Nature Neuroscience. This suggests that some of these patients could have partially preserved conscious processing that may not be apparent in behavior.

Tristan Bekinschtein and his colleagues used a conditioning technique, where subjects learnt to associate a tone with a subsequent puff of air to the eye. The association led to anticipatory muscle activity around the eye as soon as the tone was presented.

It was previously thought that learning this sort of association between a tone and an air puff requires explicit awareness of the relationship between the two stimuli. However, the vegetative patients also showed these anticipatory changes in muscle activity in response to the tone. This activity increased closer to the time that the air puff was expected, and the team found that patients who showed this type of conditioning were more likely to later show increased behavioral responsiveness.

The anticipatory learning did not happen in normal subjects who were given general anesthesia. This suggests that such learning cannot happen in unconscious states. Instead, patients in vegetative and minimally conscious states may have some preserved consciousness which is not visible via intentional movements or verbal responses, but which is still enough to support some types of learning.

Author contact:
Tristan Bekinschtein (MRC Cognition and Brain Sciences Unit, Cambridge, UK)
Tel: +44 1223 355294; E-mail: [email protected]


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

Nature (

[11] Role of the polycomb protein EED in the propagation of repressive histone marks
DOI: 10.1038/nature08398


[12] A proteomics approach to discovering natural products and their biosynthetic pathways
DOI: 10.1038/nbt.1565


[13] MyosinV controls PTEN function and neuronal cell size
DOI: 10.1038/ncb1961

[14] Regulation of endoplasmic reticulum stress response by a BBF2H7-mediated Sec23a pathway is essential for chondrogenesis
DOI: 10.1038/ncb1962

[15] Signalling mediated by the endoplasmic reticulum stress transducer OASIS is involved in bone formation
DOI: 10.1038/ncb1963

[16] Intracellular fluid flow in rapidly moving cells
DOI: 10.1038/ncb1965

[17] The planar cell polarity effector Fuz is essential for targeted membrane trafficking, ciliogenesis and mouse embryonic development
DOI: 10.1038/ncb1966


[18] The yeast Wsc1 cell surface sensor behaves like a nanospring in vivo
DOI: 10.1038/nchembio.220


[19] A microbial source of phosphonates in oligotrophic marine systems
DOI: 10.1038/ngeo639

[20] Frictional resistance of faults during accelerating and decelerating earthquake slip
DOI: 10.1038/ngeo637


[21] CARD9 facilitates microbe-elicited production of reactive oxygen species by regulating the LyGDI-Rac1 complex
DOI: 10.1038/ni.1788

[22] Runx-CBFbeta complexes control expression of the transcription factor Foxp3 in regulatory T cells
DOI: 10.1038/ni.1795


[23] Linking catalyst composition to chirality distributions of as-grown single-walled carbon nanotubes by tuning NixFe1_x nanoparticles
DOI: 10.1038/nmat2531

[24] Morphology-dependent zeolite intergrowth structures leading to distinct internal and outer-surface molecular diffusion barriers
DOI: 10.1038/nmat2530

[25] Imaging single atoms using secondary electrons with an aberration-corrected electron microscope
DOI: 10.1038/nmat2532


[26] Activation of the NLRP3 inflammasome in dendritic cells induces IL-1b-dependent adaptive immunity against tumors
DOI: 10.1038/nm.2028

[27] Kcne2 deletion uncovers its crucial role in thyroid hormone biosynthesis
DOI: 10.1038/nm.2029


[28] Tn-seq: high-throughput parallel sequencing for fitness and genetic interaction studies in microorganisms
DOI: 10.1038/nmeth.1377

[29] An approach for extensibly profiling the molecular states of cellular subpopulations
DOI: 10.1038/nmeth.1375


[30] Anticipating the perceived risk of nanotechnologies
DOI: 10.1038/nnano.2009.265

[31] Performance of monolayer graphene nanomechanical resonators with electrical readout
DOI: 10.1038/nnano.2009.267


[32] Far-ultraviolet plane-emission handheld device based on hexagonal boron nitride
DOI: 10.1038/nphoton.2009.167

Nature PHYSICS (

[33] Superfluidity of polaritons in semiconductor microcavities
DOI: 10.1038/nphys1364

[34] Vacuum ultraviolet frequency combs from below-threshold harmonics
DOI: 10.1038/nphys1398

[35] Topology-driven quantum phase transitions in time-reversal-invariant anyonic quantum liquids
DOI: 10.1038/nphys1396

[36] Non-local observables and lightcone-averaging in relativistic thermodynamics
DOI: 10.1038/nphys1395


[37] Phosphoproteomics reveals new ERK MAP kinase targets and links ERK to nucleoporin-mediated nuclear transport
DOI: 10.1038/nsmb.1656

[38] Active site remodelling switches HIV specificity of antiretroviral TRIMCyp
DOI: 10.1038/nsmb.1667

[39] Structural and kinetic determinants of protease substrates
DOI: 10.1038/nsmb.1668

[40] Distinct promoter dynamics of the basal transcription factor TBP across the yeast genome
DOI: 10.1038/nsmb.1674

[41] Neural activity predicts attitude change in cognitive dissonance
DOI: 10.1038/nn.2413



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.

Buenos Aires: 10

Brisbane: 2
Parkville: 4
Victoria: 2, 4, 26

Ghent: 26
Louvain-la-Neuve: 18
Machelen: 24

Sofia: 2

Montreal: 2, 16
Toronto: 9
Vancouver: 30

Santiago: 26

Shanghai: 2

Helsinki: 5
Tampere: 2, 3

Dijon: 26
Orleans: 26
Orsay: 26
Paris: 26, 33
St Cloud: 26
Villejuif: 26

Augsburg: 36
Berlin: 27
Bonn: 35
Hannover: 2
Karlsruhe: 6
Meulheim an der Ruhr: 24
Osnabruck: 18
Wurzburg: 9

Reykjavik: 3

Dublin: 39

Haifa: 16

Candiolo: 3
Milan: 38
Povo: 33

Chiba: 32
Higashi-Hiroshima: 20
Ibaraki: 25, 32
Kumamoto: 15
Kyoto: 20, 37
Miyazaki: 14, 15
Nara: 15
Osaka: 14, 15
Saitama: 37
Tokushima: 37
Tokyo: 6, 14, 15, 37
Tsukuba: 7

Seoul: 17

Nijmegen: 3
Utrecht: 24, 40

Tromso: 5
Trondheim: 5

Torun: 24

St. Petersburg: 1

Calayayud: 3
Tudela: 3
Zaragoza: 3

Stockholm: 5
Umea: 5

Epalinges: 26
Geneva: 2
Lausanne: 33
Zurich: 1, 35

Bangkok: 2

Bristol: 2, 4
Cambridge: 2, 4, 10, 38
Dundee: 13
London: 2, 5, 11, 13, 17, 38
Manchester: 24
Nottingham: 2, 4
Oxford: 2, 4, 5, 36
Southampton: 7
Surrey: 2, 4

Berkeley: 41
Davis: 16, 41
La Jolla: 8, 39
Los Angeles: 1, 2, 5
Pasadena: 35
San Francisco: 27
Santa Barbara: 30, 35, 41
Stanford: 2, 16, 20
Boulder: 7, 34
Denver: 5
Orlando: 9
Atlanta: 5
Tampa: 2
Honolulu: 2, 5
Chicago: 3
Des Plaines: 24
Urbana: 12
Baton Rouge: 7, 34
Bethesda: 2, 5, 6
Frederick: 5
Gaithersburg: 5
Bedford: 8
Boston: 5, 6, 26, 28
Cambridge: 40
Woods Hold: 7, 19
Ann Arbor: 2
Rochester: 2
St Louis: 3, 5
New Hampshire
Hanover: 7
New Jersey
Murray Hill: 31
Piscataway: 11
New York
Bronx: 27
New York: 6, 7, 11, 22, 25, 27, 31, 38
North Carolina
Winston-Salem: 5
Cleveland: 23
Philadelphia: 2
South Carolina
Columbia: 19
Nashville: 3
Austin: 17
Dallas: 29
Houston: 17, 21
Salt Lake City: 2
Seattle: 2, 22


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)
Craig Mak
Tel: +1 212 726 9284; E-mail: [email protected]

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 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: ma[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)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]

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Published: 20 Sep 2009

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Cancer Research