Nanoparticles control microfluidic applications; How a neurodegenerative disease gene kills neurons

Researchers demonstrate an easy and very flexible control over microfluidic flow by using suspended gold nanoparticles; Motor neurons secrete a mutant protein produced from a particular gene, setting off a chain of events that leads to cell death.

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

For papers that will be published online on 18 December 2005

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This press release contains:

* Nanoparticles control microfluidic applications - Nature Materials
* How a neurodegenerative disease gene kills neurons - Nature Neuroscience

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**********************NATURE MATERIALS************************
(<http://www.nature.com/naturematerials>)

[4] Nanoparticles control microfluidic applications

DOI: 10.1038/nmat1528

In the January issue of Nature Materials, Luke Lee and co-workers
demonstrate an easy and very flexible control over microfluidic flow by
using suspended gold nanoparticles. Microfluidic systems have attracted
significant interest for their applications such as biochemical analysis
systems as well as for chemistry 'labs on chips'. Traditionally, to achieve
control over the flow of liquids in microfluidic channels, complex pumps,
valves or even patterned surfaces are used.
In order to steer the direction of liquid flow, the team heated the
nanoparticles with a low-power laser causing the surrounding liquid to
evaporate. At the liquid-air interface at the front of the flow, the vapour
quickly condenses near the interface and coalesces with the original bulk
liquid, causing it to move forward. Several applications of this method are
demonstrated, including the transport of a living cell along a microfluidic
channel, and the mixing of two fluids. The simplicity of this approach could
lead to its use in large-scale integrated microfluidic circuits for
biochemical analysis, or to even to optically power nanomachines and
nanorobots in liquid environments.

Author contact:
Luke Lee (University of California-Berkeley, CA, USA)
Tel: +1 510 642 5855, E-mail: [email protected]

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

[5] Temperature rise at shear bands in metallic glasses
DOI: 10.1038/nmat1536

[6] Spatial control of the recombination zone in an ambipolar light-emitting
organic transistor
DOI: 10.1038/nmat1537

**************************NATURE NEUROSCIENCE*************************
(<http://www.nature.com/natureneuroscience>)

[16] How a neurodegenerative disease gene kills neurons

DOI: 10.1038/nn1603

Although amyotrophic lateral sclerosis (ALS) is linked to mutations in a
particular gene, how these mutations cause disease symptoms has been
unclear. Motor neurons secrete a mutant protein produced from this gene,
setting off a chain of events that leads to cell death, reports a paper in
the January issue of Nature Neuroscience.
ALS (or Lou Gehrig's disease) leads to paralysis from the death of motor
neurons in the spinal cord and brainstem. It is incurable, and patients
typically die within three to five years of disease onset. Only 5-10% of ALS
cases are inherited, but some such patients have mutations in the gene that
encodes a protein called superoxide dismutase (SOD1), an antioxidant enzyme.

Most of our current knowledge about ALS comes from analysis of mice with
mutations of the SOD1 gene. In these mice, in addition to the motor neuron
dysfunction, non-neuronal cells - such as microglia - also contribute to
disease development. Jean-Pierre Julien and colleagues now suggest how
microglia may contribute to disease development. They find that mutant SOD1
in motor neurons can bind to chromogranins, a family of proteins stored in
secretory vesicles in neurons and microglia. When these secretory vesicles
release their contents, mutant SOD1 is released into the extracellular space
and binds to microglia, causing these cells in turn to release cell
death-inducing molecules such as nitric oxide, which trigger motor neuron
death. These results therefore provide a better understanding of how ALS
symptoms develop by describing how SOD1 mutation can lead to motor neuron
death.

Author contact:
Jean-Pierre Julien (Laval University, Montreal, Canada)
Tel: +1 418 654 2296; E-mail: [email protected]

Additional contact for comment on paper:
Michael Sendtner (University of Wuerzburg, Germany)
Tel: +49 931 201 49767 or 49771 (assistant); E-mail:
[email protected]

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

[17] DWnt4 regulates the dorsoventral specificity of retinal projections in
the Drosophila melanogaster visual system
DOI: 10.1038/nn1604

[18] Molecular taxonomy of major neuronal classes in the adult mouse
forebrain
DOI: 10.1038/nn1618

[19] Calcium-dependent interaction of Lis1 with IQGAP1 and Cdc42 promotes
neuronal motility
DOI: 10.1038/nn1619

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

Nature PHYSICS (http://www.nature.com/naturephysics)

[20] Thermal equivalence of DNA duplexes without calculation of melting
temperature
DOI: 10.1038/nphys189

[21] Transition from phase slips to the Josephson effect in a superfluid 4He
weak link
DOI: 10.1038/nphys190

[22] Femtosecond laser near-field ablation from gold nanoparticles
DOI: 10.1038/nphys191

Nature MEDICINE (<http://www.nature.com/naturemedicine>)

[23] A role for the scaffolding adapter GAB2 in breast cancer
DOI: 10.1038/nm1341

[24] Fluoroquinolone-modifying enzyme: a new adaptation of a common
aminoglycoside acetyltransferase
DOI: 10.1038/nm1347

Nature IMMUNOLOGY (<http://www.nature.com/natureimmunology>)

[25] Control of human immunodeficiency virus replication by cytotoxic T
lymphocytes targeting subdominant epitopes
DOI: 10.1038/ni1281

[26] Ablation of CD22 in ligand-deficient mice restores B cell receptor
signaling
DOI: 10.1038/ni1283

[27] Intrinsic inhibition of transcription factor E2A by HLH proteins ABF-1
and Id2 mediates reprogramming of neoplastic B cells in Hodgkin lymphoma
DOI: 10.1038/ni1285

NATURE CELL BIOLOGY (<http://www.nature.com/naturecellbiology>)

[28] In situ trapping of activated initiator caspases reveals a role for
caspase-2 in heat shock-induced apoptosis
DOI: 10.1038/ncb1340

[29] Dishevelled mediates ephrinB1 signalling in the eye field through the
planar cell polarity pathway
DOI: 10.1038/ncb1344

[30] PCNA functions as a molecular platform to trigger Cdt1 destruction and
prevent re-replication
DOI: 10.1038/ncb1346

Nature STRUCTURAL & MOLECULAR BIOLOGY
(<http://www.nature.com/natstructmolbiol>)

[31] The SPRY domain of SSB-2 adopts a novel fold that presents conserved
Par-4-binding residues
DOI: 10.1038/nsmb1034

[32] Autoproteolysis coupled to protein folding in the SEA domain of the
membrane-bound MUC1 mucin
DOI: 10.1038/nsmb1035

[33] Structure of Saccaromyces cerevisiae DNA polymerase epsilon by
cryo-electron microscopy
DOI: 10.1038/nsmb1040

[34] Modulation of microRNA processing and expression through RNA editing by
ADAR deaminases
DOI: 10.1038/nsmb1041

*****************************************************************

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The following list of places refers to the whereabouts of authors on the
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AUSTRALIA
Parkville: 31
Perth: 25

BARBADOS
Bridgetown: 25

BELGIUM
Liege: 23

CANADA
Edmonton: 10
Quebec City: 16
Sainte-Foy: 16
Toronto: 28

CHINA
Beijing: 15
Hong Kong: 11

FRANCE
Angers: 13
Bois-Guillaime: 13
Bordeaux: 13
Grenoble: 22
Marseille: 12
Nantes: 13
Paris: 13
Rouen: 13

GERMANY
Berlin: 27
Dusseldorf: 1
Heidelberg: 34
Konstanz: 22
Leipzig: 1

JAPAN
Joetsu: 7
Kyoto: 14
Nagoya: 7
Tokyo: 7, 17
Tsukuba: 7
Uji: 7
Wako: 7, 16

NORWAY
Bergen: 12
Oslo: 12

RUSSIA
Moscow: 9

SOUTH AFRICA
Durban: 25

SWEDEN
Goteborg: 32
Lund: 26, 27
Umea: 33

UNITED KINGDOM
Cambridge: 1, 5, 6
London: 1
Norwich: 3
Oxford: 11, 25
Southampton: 20

UNITED STATES OF AMERICA
California
Berkeley: 1, 4, 21
La Jolla: 19, 26, 33
Moffett Field: 15
Pasadena: 21
San Diego: 28
San Francisco: 4
Sunnyvale: 15
Connecticut
New Haven: 15
District of Columbia
Washington: 29
Maryland
Bethesda: 25
Chevy Chase: 25
Frederick: 25, 29
Massachusetts
Boston: 14, 23, 24, 25, 30
Burlington: 24
North Grafton: 14
Waltham: 18
Minnesota
Minneapolis: 19
New Jersey
Raritan: 24
New Mexico
Los Alamos: 8, 25
Santa Fe: 25
New York
Cold Spring Harbor: 18
Ithaca: 8
New York: 2, 19
North Carolina
Chapel Hill: 2
Ohio
Cleveland: 5
Pennsylvania
Philadelphia: 34
Pittsburgh: 14
Tennessee
Memphis: 28
Utah
Salt Lake City: 29
Washington
Redmond: 25
Seattle: 26
Wisconsin
Madison: 19

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Published: 18 Dec 2005

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