NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 28 August 2005
This press release is copyrighted to the Nature journals mentioned below.
* Nanoshuttles move droplets uphill - Nature Materials
* Detecting prions in blood - Nature Medicine
* Evolution discounts errors - Nature Genetics
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.
******************NATURE MATERIALS******************************
(<http://www.nature.com/naturematerials>)
[1] Nanoshuttles move droplets uphill
DOI: 10.1038/nmat1455
A paper by a group of European researchers in the September issue of Nature
Materials shows how to transform light-induced molecular motion into
macroscopic motion of liquid droplets.
Biasing the random motion of molecules is no easy task for chemists, even as
we approach the nanotechnology era. Harnessing directional molecular motion
and transforming it into measurable mechanical movement is even more of a
challenge, although it is commonplace for biological molecular motors found
in nature.
David Leigh and colleagues have now developed a surface that is covered with
wholly synthetic molecular shuttles that shift position when exposed to
light. The movement of droplets is not a direct effect of the change in
position that occurs within the individual shuttle molecules. Rather, it is
an ensemble effect that results from the change in surface wettability after
most of the shuttle molecules change position. The phenomenon is so
efficient that it generates enough energy to move a microlitre droplet up a
twelve-degree slope*. This work represents a key technological breakthrough,
and may prove useful in lab-on-a-chip environments, or for performing
chemical reactions on a tiny scale without reaction vessels.
Author contact:
David A. Leigh (University of Edinburgh, UK)
Tel: +44 131 650 4721, E-mail: [email protected]
Additional contact for comment on paper:
Donald Fitzmaurice (University College Dublin, Ireland)
Tel: + 353 1 716 2441, E-mail: [email protected]
*Please note: there are movie files available from the relevant section of
the Nature press site.
**************NATURE MEDICINE*************************
(<http://www.nature.com/naturemedicine>)
[2] Detecting prions in blood
DOI: 10.1038/nm1286
Research published in the September issue of Nature Medicine may help
minimize the spread of prion diseases in the human body.
Prion diseases, like BSE (bovine spongiform encephalopathy) and CJD
(Creutzfeldt-Jakob disease) are caused by a misfolded prion protein referred
to as PrPSc. Minimizing spread of the disease could be facilitated by the
ability to detect PrPSc in blood. Claudio Soto and colleagues have devised
an automated method, termed protein misfolding cyclic amplification, to help
do just that.
The extremely small amount of PrPSc that appears in blood makes it difficult
to detect it and diagnose the disease. But the researchers' new technique,
analogous to polymerase chain reaction for amplifying tiny samples of
genetic material, amplifies PrPSc in the test tube, which allows the
detection of PrPSc with 89% sensitivity (a measure of the probability of
correct diagnosis) and 100% specificity (i.e., the method detects no false
positives).
This is the first time PrPSc has been biochemically detected in the blood,
so the authors have raised several issues for discussion. These issues
include investigating whether all diseased animals carry PrPSc in their
blood, and how early and sensitive diagnosis will facilitate therapeutic
intervention before the appearance of clinical signs and permanent brain
damage.
Author contact:
Claudio Soto (University of Texas Medical Branch, Galveston, TX, USA)
Tel: +1 409 747 0017, E-mail: [email protected]
Other papers from Nature Medicine to be published online at the same time
and with the same embargo:
[3] Induction of interleukin-8 preserves the angiogenic response in
HIF-1alpha-deficient colon cancer cells
DOI: 10.1038/nm1294
[4] Blockade of PI3Kgamma suppresses joint inflammation and damage in mouse
models of rheumatoid arthritis
DOI: 10.1038/nm1284
[5] PI3Kgamma inhibition blocks glomerulonephritis and extends lifespan in a
mouse model of systemic lupus
DOI: 10.1038/nm1291
****************NATURE GENETICS**************************
(<http://www.nature.com/naturegenetics>)
[6] Evolution discounts errors
DOI: 10.1038/ng1621
Research in the September issue of Nature Genetics may shed new light on one
of the key hurdles associated with the development of life on Earth - how to
evolve genetic complexity.
One of the problems with the theory that living cells evolved from
replicating molecules comes from the inherent imperfection of the copying
process. Larger and more complicated molecules might be capable of
preventing or correcting their mistakes (mutations), but then the target to
be copied is larger too, increasing the chance of mutations. This dilemma,
called an "error threshold" was thought to present a lethal block to the
evolution of complex molecules.
Eors Szathmáry and colleagues have calculated that many mutations may not
after all be lethal to real replicators. They examined the effects of real
mutations (copying mistakes) on the predicted structure of real RNA enzymes,
called ribozymes, and found that many mutations are likely to have no
effect, or even to cancel out the damage caused by other mutations. This
reprieve from "mutational meltdown" is enough to allow a genome size of
seven thousand bases or RNA "letters", which is big enough to allow the
survival of a minimal genome in the RNA world. The idea of an error
threshold is still of great interest as a way to battle viruses today by
using drugs to drive the virus's copying process beyond the level of
mistakes it can tolerate.
Author contact:
Eors Szathmary (Collegium Budapest, Institute for Advanced Study, Hungary)
Tel: +36 1 224 8300, E-mail: [email protected]
Additional contact for comment on paper:
Edward C. Holmes (Penn State University, University Park, PA, USA)
Tel: +1 814 863 4689, E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time
and with the same embargo:
[7] Genome-wide analysis of mouse transcripts using exon microarrays and
factor graphs
DOI: 10.1038/ng1630
******************************************************************
Items from other Nature journals to be published online at the same time and
with the same embargo:
Nature (<http://www.nature.com/nature>)
[10] A SUMOylation-dependent pathway mediates transrepression of
inflammatory response
genes by PPAR-gamma
DOI: 10.1038/nature03988
[11] Calcium triggers exit from meiosis II by targeting the APC/C inhibitor
XErp1 for degradation
DOI: 10.1038/nature04093
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnolgy)
[12] Production of human monoclonal antibody in eggs of chimeric chickens
DOI: 10.1038/nbt1132
Nature NEUROSCIENCE (<http://www.nature.com/natureneuroscience>)
[13] Targeting BACE1 with siRNAs ameliorates Alzheimer disease
neuropathology in a transgenic model
DOI: 10.1038/nn1531
[14] Spatial navigation impairment in mice lacking cerebellar LTD: a motor
adaptation deficit?
DOI: 10.1038/nn1532
[15] Acoustic environment determines phosphorylation state of the Kv3.1
potassium channel in auditory neurons
DOI: 10.1038/nn1533
[16] Inferring another's expectation from action: the role of peripheral
sensation
DOI: 10.1038/nn1535
NATURE CELL BIOLOGY (<http://www.nature.com/naturecellbiology>)
[17] Neddylation and deneddylation regulate Cul1 and Cul3 protein
accumulation
DOI: 10.1038/ncb1301
[18] Ubiquitin ligase component Cul4 associates with Clr4 histone
methyltransferase to assemble heterochromatin
DOI: 10.1038/ncb1300
*************************************************************
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.
CANADA
Montreal: 9
Toronto: 7
FRANCE
Lyon: 9
Paris: 9, 14
GERMANY
Martinsried near Munich: 11
Munich: 16
HUNGARY
Budapest: 6
IRAN
Shahrekoed: 14
ITALY
Bologna: 1
Collerato Giacosa: 4
Turin: 4
JAPAN
Asahikawa: 3
Kyoto: 8
Osaka: 8
THE NETHERLANDS
Groningen: 1
Rotterdam: 14
SPAIN
Barcelona: 6
Madrid: 2, 5
SWITZERLAND
Basel: 4
Geneva: 4, 5
TAIWAN
Taipei: 17
UNITED KINGDOM
Edinburgh: 1
Leicester: 15
Poole: 16
UNITED STATES OF AMERICA
California
Burlingame: 12
La Jolla: 10, 13
Los Angeles: 12
Milpitas: 12
Connecticut
Farmington: 15
New Haven: 15
Maryland
Bethesda: 18
Massachusetts
Boston: 3
New Jersey
Newark: 16
New York
Buffalo: 15
North Carolina
Research Triangle Park: 10
Texas
College Station: 12
Houston: 18
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]
For media inquiries relating to editorial content/policy for the Nature
Research Journals, please contact the journals individually:
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Kathy Aschheim
Tel: +1 212 726 9346; E-mail: [email protected]
Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]
Nature Chemical Biology (Boston)
Beatrice Chrystall
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 Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Maria Bellantone
Tel: +44 20 7843 4556; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
Ed Feng
Tel: +1 212 726 9351; E-mail: [email protected]
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