Nanotech energy storage breaks records

Model projections suggest ice-free Arctic Ocean by 2100, Quantum entanglement could boost communication capacity, New York sea level to rise owing to slowing ocean circulation, A brain trauma–Alzheimer’s disease connection, How nerve fibres degenerate, Many antibodies make light work and Shutting the door on obesity


For papers that will be published online on 15 March 2009

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

This press release contains:

· Summaries of newsworthy papers:

Nanotechnology: Nanotech energy storage breaks records

Chemical Biology: A pancreatic path

Geoscience: Model projections suggest ice-free Arctic Ocean by 2100

Physics: Quantum entanglement could boost communication capacity

Geoscience: New York sea level to rise owing to slowing ocean circulation

Medicine: A brain trauma–Alzheimer’s disease connection

Nature: How to make a dopamine-producing neuron

Neuroscience: How nerve fibres degenerate

Genetics: Risk factor for blood diseases

Geoscience: Temporarily oxygenated oceans 3,460 million years ago

Nature: Many antibodies make light work

Chemistry: Looking at cells in sticky situations

And finally… Medicine: Shutting the door on obesity

· 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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[1] Nanotechnology: Nanotech energy storage breaks records
DOI: 10.1038/nnano.2009.37

A new generation of energy storage is one step closer to reality, reports a paper published online this week in Nature Nanotechnology. The research improves the performance of ‘electrostatic capacitors’ — a type of device that stores energy as electric charge, rather than chemically as in batteries. Electrostatic capacitors are expected to be useful for a variety of high-power applications, including hybrid and electric cars.

To make their devices, Gary Rubloff, Sang Bok Lee and colleagues used nanosized holes at a density of 60 billion holes per square inch, and, for the first time, assembled most of their device one atomic layer at a time. As a result, their capacitors were able to provide high power levels for up to 40 times longer than existing nanoscale electrostatic capacitors.

Author contact:
Gary Rubloff (University of Maryland, College Park, MD, USA)
Tel: +1 301 405 2949; E-mail: [email protected]

[2] Chemical Biology: A pancreatic path
DOI: 10.1038/nchembio.154

Scientists have found a small compound that could direct stem cells to become insulin-secreting pancreatic beta cells. The strategy, published online this week in Nature Chemical Biology, holds great promise for transplantation therapy of metabolic diseases such as diabetes.

In the development of organs in human embryos, the pancreas progenitors develop from endoderm cells, which themselves had been derived from human embryonic stem cells (hESCs). Since it is not known what cells along the pathway will be needed for transplantation therapy, a major goal among researchers is to generate large numbers of fully mature insulin-secreting pancreatic cells, the beta cells.

The research groups of Douglas Melton and Stuart Schreiber performed a high-content screen to identify a compound, ILV, that when added to definitive endoderm derived from hESCs, generated large numbers of cells that express Pdx1 and other pancreatic markers. Implantation of the cells into mice kidney capsules further generated a population of insulin-positive cells in vivo, suggesting that they are on a key pathway towards formation of insulin-secreting beta cells.

Based on ILV’s mechanism of action, the results show that targeting the protein kinase C pathway could lead to improvements in the numbers of beta cells that can be formed.

Author contact:
Douglas Melton (Harvard University, Cambridge, MA, USA)
Tel: +1 617 495 1812; E-mail: [email protected]

[3] Geoscience: Model projections suggest ice-free Arctic Ocean by 2100
DOI: 10.1038/ngeo467

The Arctic Ocean will probably be free of sea ice during the month of September by the end of this century, suggests an analysis of climate model projections and past observations reported online in Nature Geoscience. Most current climate models underestimate the observed deterioration rate of Arctic sea-ice cover, but a robust model-based estimate for the twenty-first century is possible by combining known physical links between past and future evolutions of sea ice and the available observations.

By analysing a range of climate model simulations, Julien Boé and colleagues found a close linear relationship between the simulated summer sea-ice extent in the twentieth century and the projected rate of sea-ice decline over the twenty-first century. Calibrating these projections with satellite observations of past Arctic sea-ice cover, they estimate that full loss of sea ice in September will probably occur in the Arctic Ocean by the end of this century. Using this method, the researchers have achieved a projection of future sea-ice cover, although most models significantly underestimate the observed decline in Arctic sea-ice cover.

Author contact:
Julien Boé (University of California, Los Angeles, CA, USA)
Tel: +1 310 206 5257; E-mail: [email protected]

[4] Physics: Quantum entanglement could boost communication capacity
DOI: 10.1038/nphys1224

The laws of quantum mechanics could help to transmit classical – or binary – information more efficiently, suggests a paper online this week in Nature Physics. This finding solves a problem considered to be one of the most important open questions in the field of quantum information theory – can the effects of quantum mechanics be harnessed for sending classical ‘bits of information?’

In recent years, there has been intense research activities aimed at using quantum-mechanical effects — which govern the behaviour of particles at the smallest length scales — for the purposes of communication and computation. A key property that has been harnessed is known as quantum entanglement, but it has been unclear whether this can help transmit classical information efficiently through quantum communication channels. Several conjectures say that quantum entanglement is of no help in such situations.

Matthew Hastings now shows, on a fundamental level, that these conjectures are false. The practical significance of these findings remains to be shown, however they will be of immediate relevance to how the capacity of quantum communication channels can be calculated, and therefore for predicting in which communication tasks quantum effects can be of potential use.

Author contact:
Matthew Hastings (Los Alamos National Laboratory, NM, USA)
Tel: +1 505 665 9730; E-mail: [email protected]

[5] Geoscience: New York sea level to rise owing to slowing ocean circulation
DOI: 10.1038/ngeo462

Regional sea level along the northeastern coast of the United States, particularly near New York, is expected to rise almost twice as fast as global sea levels during the twenty-first century, according to a study online in Nature Geoscience. The rising waters in this particular region are attributed to a slowing of the North Atlantic Ocean circulation, as estimated by a range of state-of-the-art climate models.

Jianjun Yin and colleagues analysed climate projections from a set of global climate models under a variety of greenhouse-gas emission scenarios. They find that sea levels in the North Atlantic Ocean adjust to the projected slowing of the meridional overturning circulation. Their model projection attributes 15–23 cm of the rise in New York sea level by the year 2100 to changes in the North Atlantic Ocean circulation, compared with 36–51 cm of total sea-level rise in this location.

This work suggests that the northeast coast of the US is among the regions most vulnerable to future changes in sea level through variations in ocean circulation.

Author contact:
Jianjun Yin (Florida State University, Tallahassee, FL, USA)
Tel: +1 850 644 4841; E-mail: [email protected]

[6] Medicine: A brain trauma–Alzheimer’s disease connection
DOI: 10.1038/nm.1940

Two enzymes implicated in Alzheimer’s disease may also have a role in traumatic brain injury, according to research online this week in Nature Medicine.

Amyloid-beta peptides, pathological hallmarks of Alzheimer’s disease, accumulate rapidly after traumatic brain injury in humans. Mark Burns and his colleagues now show that blocking either beta- or gamma-secretase, enzymes required for production of Amyloid-beta, can reduce deficits in movement and behavior and reduce neuronal loss after experimentally inflicted brain injury in mice.

The authors propose that these two secretases, which are being actively pursued in the fight against Alzheimer’s disease, could also be promising targets to treat traumatic brain injury.

Author contact:
Mark Burns (Georgetown University, Washington, DC, USA)
Tel: +1 202 687 4735; E-mail: [email protected]

[7] Nature: How to make a dopamine-producing neuron
DOI: 10.1038/nature07929

A ‘control switch’ that instructs immature cells to become dopamine-expressing neurons is revealed in this week's Nature. The findings could help stem-cell researchers wishing to make replacement dopaminergic neurons for people with Parkinson’s disease.

Nuria Flames and Oliver Hobert show that the protein AST-1 is needed to drive and maintain the differentiation of dopaminergic nerves cells in the nematode worm Caenorhabditis elegans. If the protein is absent, dopaminergic differentiation is impaired; adding the protein activates the dopamine production pathway.

Dopamine-producing neurons have been implicated in many activities including motor control cognition, motivation and pleasure. Many different genes have been implicated in their production, but AST-1 seems to be at the top of the pathway. Given that the protein and its functions are conserved in vertebrates, it is now a therapeutically relevant target for influencing dopaminergic cell production and maintenance.

Author contact:
Oliver Hobert (Columbia University, New York, NY, USA)
Tel: +1 212 305 0063; E-mail: [email protected]

[8] Neuroscience: How nerve fibres degenerate
DOI: 10.1038/nn.2290

An enzyme inside nerve cells that is crucial for nerve fibre degeneration in fruit flies and mice is identified in a paper online in Nature Neuroscience this week.

Degeneration of the axon fibres that connect nerve cells in the brain is common after brain injury and in many neurological diseases. This research may therefore prove important for treatment of hereditary neuropathy, glaucoma, and neurodegenerative diseases such as Alzheimer’s disease or Parkinson’s disease.

Aaron DiAntonio and colleagues removed the antennae of fruit flies, thereby severing the axons of smell neurons in flies. In normal flies, the remaining axon fragments rapidly deteriorated, but in flies lacking the enzyme known as DLK, the axons were preserved. Similarly, the cutting of sensory nerve cell axons in mice usually leads to rapid degeneration, but if the nerve cells lacked DLK, their axons did not decompose after being cut.

Author contact:
Aaron DiAntonio (Washington University School of Medicine, St. Louis, MO, USA)
Tel: + 1 314 362 9925; Email: [email protected]

[9], [10], & [11] Genetics: Risk factor for blood diseases
DOI: 10.1038/ng.334
DOI: 10.1038/ng.341
DOI: 10.1038/ng.342

A common genetic sequence abnormality that enhances the likelihood of acquiring a mutation in a gene linked to blood diseases has been identified, according to three studies published online this week in Nature Genetics.
Nicholas Cross, Robert Kralovics, and Ross Levine carried out independent case-control studies to identify a collection of mutations that occur in the JAK2 gene, that do not arise from random mutagenesis but rather are specifically determined by the DNA sequence. JAK2 is a protein with enzymatic activity that is linked to the abnormal production of several types of blood cells, called myeloproliferative neoplasms, found in patients with who suffer from this disorder.

Myeloproliferative neoplasms arise from the bone marrow and over 50% of patients afflicted with this blood disorder carry the JAK2 mutation and suffer from the overproduction of red blood cells, platelets, or fibrous connective tissue. Understanding the underlying inherited sequence partly explains the predisposition for acquiring mutations in certain disease-specific genes and may help explain why some individuals are at higher risk in developing a disease.

Author contacts:
Nicholas Cross (University of Southampton, UK) Author paper [9]
Tel: + 44 1722 429080; Email: [email protected]

Robert Kralovics (Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria) Author paper [10]
Tel: + 43 14 0400 5464; Email: [email protected]

Ross Levine (Memorial Sloan-Kettering Cancer Center, New York, NY, USA) Author paper [11]
Tel: +1 646 888 2767; Email: [email protected]

[12] Geoscience: Temporarily oxygenated oceans 3,460 million years ago
DOI: 10.1038/ngeo465

Tiny crystals of the iron mineral haematite provide evidence for an oxygenated water body 3,460 million years ago, reports a paper online this week in Nature Geoscience. This evidence indicates that microorganisms capable of producing oxygen through photosynthesis were present at this time, predating the oldest unambiguous fossils of photosynthetic microbes by about 800 million years.

Hiroshi Ohmoto and colleagues analysed the chemical characteristics of grains of haematite found in a jasper formation of Western Australia. They found that the grains, which developed in an early sea that existed over what is now Pilbara, Australia, probably formed as the result of an interaction between hydrothermal fluids and oxygen-rich sea water. The group suggests that organisms capable of photosynthesis must therefore have been present in sufficient numbers to at least occasionally oxygenate this body of water.

Author contact:
Hiroshi Ohmoto (Pennsylvania State University, University Park, PA, USA)
Tel: +1 814 865 4074; E-mail: [email protected]

[13] Nature: Many antibodies make light work
DOI: 10.1038/nature07930

Scientists have characterized antibodies from ‘slow progressing’ HIV patients. They find that rather than having one antibody that recognizes the virus really well, they have a diverse range of antibodies that each recognizes the virus in a different way. The study, published online this week in Nature, has important implications for vaccine development.

Some individuals infected with HIV are able to control the virus and therefore progress very slowly to disease. It is known that they have high levels of anti-virus antibodies but until now little was known about how effective these antibodies are.

Michel Nussenzweig and colleagues used cloning techniques to characterize the antibodies from six ‘slow progressing’ patients infected with HIV. The group find that these patients have a wide range of antibodies that bind to different parts of the virus. The antibodies seem to act as a team to broadly neutralize the virus in cell culture, but none of them was able to do this by itself.

The antibodies were also able to recognize a range of HIV strains, suggesting that having many different types of antibody might be better than having one ‘super’ antibody that focuses on one part of the virus, which can easily mutate.

A vaccine that mimics this naturally occurring antibody response in non-immune patients could be a useful tool to help fight the virus.

Author contact:
Michel Nussenzweig (The Rockefeller University, New York, NY, USA)
Tel: +1 212 327 8067; E-mail: [email protected]

[14] Chemistry: Looking at cells in sticky situations
DOI: 10.1038/nchem.120

A molecular rotor that can measure changes in the viscosity of the fluid inside a single cell as it dies is reported online in Nature Chemistry this week. Measurements from this rotor show that there is a significant viscosity increase on cell death and this may lead to new opportunities in drug-delivery research and cancer therapy.

Photodynamic therapy involves a chemical sensitizer being introduced into cells that produces a toxic substance on exposure to light. This is a promising cancer treatment because the light can be accurately targeted and only cells in a specific area are killed whereas others are left untouched.

Marina Kuimova, Peter Ogilby and co-workers designed and made a sensitizer molecule that not only promotes the formation of an important cytotoxic agent — so-called singlet oxygen — but simultaneously allows the viscosity of the cell contents to be measured by monitoring how much they fluoresce. They found that the increase in viscosity affects both how quickly the toxic agent is formed, and how quickly it can react with other molecules in the cell — both important factors in the efficiency of photodynamic therapy. This research offers a general strategy for monitoring diffusion dynamics inside cells, which could also lead to a better understanding of other cellular processes such as signalling and mass transport.

Author contact:
Marina Kuimova (Imperial College London, UK)
Tel: +44 20 7589 5111; E-mail: [email protected]

Peter Ogilby (University of Aarhus, Denmark)
Tel: +45 8942 3863; E-mail: [email protected]

[15] And finally… Medicine: Shutting the door on obesity
DOI: 10.1038/nm.1937

Knocking out an enzyme responsible for the metabolism of fat in the intestine protects mice from obesity, reports research published online in Nature Medicine this week. The findings suggest a possible new target for reducing obesity.

Humans are efficient in absorbing fat within their diet and assimilating it into adipose tissue for the storage of energy. Although this ability suggests an advantage in times of calorie deprivation, it contributes to obesity when dietary fat is abundant. Robert Farese, Jr., and his colleagues show that the intestinal enzyme MGAT2 is crucial for the buildup of fat in mice.

They find that the absence of MGAT2 protects mice on a high-fat diet against developing obesity, high cholesterol and fatty liver. Although food intake and fat absorption are normal in MGAT2-deficient mice, entry of dietary fat into the circulation is reduced, favoring the partitioning of fat toward energy dissipation instead of towards storage in the adipose tissue.

As MGAT2 is an intestinal enzyme that can, in principle, be readily accessible to pharmacological inhibition, these results point to a new target in the fight against obesity that may have medical potential before long.

Author Contact:
Robert Farese, Jr. (University of California, San Francisco, CA, USA)
Tel: +1 415 734 2000; E-mail: [email protected]

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


[16] Protein kinase DYRK2 is a scaffold that facilitates assembly of an E3 ligase
DOI: 10.1038/ncb1848

[17] Store-operated cyclic AMP signalling mediated by STIM1
DOI: 10.1038/ncb1850

[18] Myosin IIIa boosts elongation of stereocilia by transporting espin 1 to the plus ends of actin filaments
DOI: 10.1038/ncb1851

[19] p53-cofactor JMY is a multifunctional actin nucleation factor
DOI: 10.1038/ncb1852

[20] Characterization of the interface between normal and transformed epithelial cells
DOI: 10.1038/ncb1853

[21] Absence of nucleolar disruption after impairment of 40S ribosome biogenesis reveals an rpL11-translation-dependent mechanism of p53 induction
DOI: 10.1038/ncb1858


[22] ccbe1 is required for embryonic lymphangiogenesis and venous sprouting
DOI: 10.1038/ng.321

[23] Human mutation rate associated with DNA replication timing
DOI: 10.1038/ng.363


[24] Cyclicity in Cordilleran orogenic systems
DOI: 10.1038/ngeo469


[25] Cloning polymer single crystals through self-seeding
DOI: 10.1038/nmat2405


[26] Amplification-free Illumina sequencing-library preparation facilitates improved mapping and assembly of (G+C)-biased genomes
DOI: 10.1038/nmeth.1311


[27] Dopant profiling and surface analysis of silicon nanowires using capacitance–voltage measurements


[28] Endoplasmic reticulum stress in disorders of myelinating cells
DOI: 10.1038/nn.2273

[29] Traveling waves in developing cerebellar cortex mediated by asymmetrical Purkinje cell connectivity
DOI: 10.1038/nn.2285

[30] Proteoglycan interactions with Sonic Hedgehog specify mitogenic responses
DOI: 10.1038/nn.2287

[31] miR-124 regulates adult neurogenesis in the subventricular zone stem cell niche
DOI: 10.1038/nn.2294


[32] All-optical high-speed signal processing with silicon–organic hybrid slot waveguides

Nature PHYSICS (

[33] Measuring photon bunching at ultrashort timescale by two-photon absorption in semiconductors
DOI: 10.1038/nphys1218

[34] Observation of terahertz radiation coherently generated by acoustic waves
DOI: 10.1038/nphys1219

[35] Effects of macromolecular crowding and DNA looping on gene regulation kinetics
DOI: 10.1038/nphys1222

[36] Signature of magnetic monopole and Dirac string dynamics in spin ice
DOI: 10.1038/nphys1227


[37] The pathway of hepatitis C virus mRNA recruitment to the human ribosome
DOI: 10.1038/nsmb.1572

[38] Precursor-product discrimination by La protein during tRNA metabolism
DOI: 10.1038/nsmb.1573

[39] TRF2 functions as a protein hub and regulates telomere maintenance by recognizing specific peptide motifs
DOI: 10.1038/nsmb.1575


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.

Perth: 12

Vienna: 10

Ghent: 32

Calgary: 30
Toronto: 38

Nanjing: 25

Aarhus: 14

Lyon: 36
Mulhouse: 25
Orsay: 20
Palaiseau: 33
Paris: 33

Berlin: 13
Darmstadt: 25
Freiburg: 9, 25
Heidelberg: 9
Karlsruhe: 32
Oberkochen: 32
Ulm: 9

Athens: 9

Budapest: 29

Bari: 17
Chieti: 18
Milan: 21

Fukuoka: 12
Hiroshima: 20
Kagoshima: 12
Tochigi: 29

Rotterdam: 22
Utrecht: 22

Daejeon: 1

Uppsala: 35

Basel: 21
Zurich: 32

Bournemouth: 9
Cambridge: 26
Didcot: 14
London: 14, 20, 29
Oxford: 14, 19
Southampton: 9


Mobile: 28

Tucson: 24

Berkeley: 18, 27, 37
Davis: 37
La Jolla: 22
Livermore: 34
Los Angeles: 3, 19
San Francisco: 15, 19, 22

New Haven: 16

District of Columbia
Washington: 6

Tallahassee: 5

Chicago: 28
Urbana: 5

Bethesda: 13, 18, 38
College Park: 1, 18

Boston: 11, 13, 21, 23, 30
Cambridge: 2, 11, 15, 35
Charlestown: 13
Medford: 23
West Roxbury: 17

St Louis: 8

New Hampshire
Exeter: 30

New Jersey
Princeton: 5

New Mexico
Los Alamos: 4, 34

New York
New York: 7, 9, 11, 13, 31

North Carolina
Charlotte: 18
Durham: 34

Cincinnati: 21

Portland: 30

Bethlehem: 32
University Park: 12

Houston: 11, 39
San Antonio: 17

Seattle: 23

Madison: 15


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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 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)
Lily Khidr
Tel: +1 212 726 9324; E-mail: [email protected]

Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; 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 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: 15 Mar 2009

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