10,563 research outputs found
The imbalanced antiferromagnet in an optical lattice
We study the rich properties of the imbalanced antiferromagnet in an optical
lattice. We present its phase diagram, discuss spin waves and explore the
emergence of topological excitations in two dimensions, known as merons, which
are responsible for a Kosterlitz-Thouless transition that has never
unambiguously been observed.Comment: 4 pages, 5 figures, RevTe
About the detection of gravitational wave bursts
Several filtering methods for the detection of gravitational wave bursts in
interferometric detectors are presented. These are simple and fast methods
which can act as online triggers. All methods are compared to matched filtering
with the help of a figure of merit based on the detection of supernovae signals
simulated by Zwerger and Muller.Comment: 5 pages, proceedings of GWDAW99 (Roma, Dec. 1999), to appear in Int.
J. Mod. Phys.
Detection of a branched alkyl molecule in the interstellar medium: iso-propyl cyanide
The largest non-cyclic molecules detected in the interstellar medium (ISM)
are organic with a straight-chain carbon backbone. We report an interstellar
detection of a branched alkyl molecule, iso-propyl cyanide (i-C3H7CN), with an
abundance 0.4 times that of its straight-chain structural isomer. This
detection suggests that branched carbon-chain molecules may be generally
abundant in the ISM. Our astrochemical model indicates that both isomers are
produced within or upon dust grain ice mantles through the addition of
molecular radicals, albeit via differing reaction pathways. The production of
iso-propyl cyanide appears to require the addition of a functional group to a
non-terminal carbon in the chain. Its detection therefore bodes well for the
presence in the ISM of amino acids, for which such side-chain structure is a
key characteristic.Comment: This is the author's version of the work. It is posted here by
permission of the AAAS for non-commercial use. The definitive version was
published in Science 345, 1584 (2014), doi:10.1126/science.125667
Involvement of Inflammation in Tau Pathology and Mechanisms That Drive Neurodegeneration in Alzheimer\u27s Disease
Two of the hallmarks of neurodegenerative disorders, such as Alzheimer\u27s disease (AD), are (1) the appearance of proteinaceous deposits in inclusion bodies containing aggregates of ubiquitinated proteins and (2) activated microglia and astrocytes surrounding the diseased neurons. In Alzheimer\u27s disease, the intracellular inclusion bodies are known as neurofibrilary tangles (NFT). The mechanisms leading to inclusion body formation and their role in the progression of neurodegeneration are still largely unknown.
Many of the proteins that accumulate in inclusion bodies depend on the ubiquitin/proteasome pathway (UPP) for their degradation. This pathway is responsible for the bulk (∼80%) of intracellular protein degradation. Because of its central role in the removal of mutated and misfolded proteins by degradation, disruption of the UPP is particularly relevant to the accumulation of aberrant proteins observed in aging-related neurodegenerative disorders, such as AD. Besides containing ubiquitinated proteins, one of the major components of NFTs is the microtubule associated protein tau . Tau protein is abundant in neurons and is a highly soluble protein. Tau must be cleaved first to function as a seed for its self aggregation.
Our main hypothesis is that toxic inflammation factors released by microglia and astrocytes will damage proteins in neurons causing protein misfolding. An abrupt or chronic increase in damaged proteins will overwhelm the proteasome, particularly in old age when proteasome activity is clearly impaired. If not resolved, the ensuing accumulation of ubiquitinated proteins is potently toxic and drives the cell to activate a death pathway, therefore launching apoptosis. Caspase activation associated with apoptosis leads to caspase-mediated proteolysis of a variety of proteins including tau, which is a microtubule stabilizing protein. Tau cleavage will destabilize microtubules and cause the collapse of the cell structure. In addition, tau cleavage will promote protein aggregation. All of these events culminate in neurodegeneration.
We tested our hypothesis by incubating neuronal cells with the cytotoxic product of inflammation prostaglandin J2 (PGJ2). As we proposed, the initial event observed upon PGJ2 treatment was the accumulation of ubiquitinated proteins. This was followed by apoptosis coinciding with caspase activation and tau cleavage, culminating in protein aggregation and cell death. In other studies, we established a direct correlation between proteasome impairment (accomplished by a genetic manipulation of its chymotrypsin-like activity) with an increased vulnerability to stress conditions induced by the heavy metal cadmium. Finally, we identified a unique aging-dependent mechanism that contributes to proteasome dysfunction in Drosophila melanogaster. Our studies were the first to show that the major proteasome form in old flies is the weakly active 20S core particle, while in younger flies the fully assembled 26S holoenzyme is the preponderant proteasome form.
In conclusion, these studies support the view that maintaining proteasome activity is critical to cell survival. If proteasome activity is disrupted by inflammation or oxidative stress or even by the build-up of mutant proteins, this will have a catastrophic effect on cell survival resulting in the induction of apoptosis. The ensuing activation of caspase-mediated proteolysis will lead to partial cleavage of a variety of proteins including tau that will in turn promote protein aggregation culminating in neurodegeneration. This neurodegenerative process is exacerbated at later stages in life, because proteasome function seems to decline abruptly at an old age. A better understanding of the mechanisms leading to the build-up of protein aggregates will open up new targets for treatment of neurodegenerative disorders, such as AD, that are associated with chronic inflammation and protein aggregation
BEC-BCS crossover in an optical lattice
We present the microscopic theory for the BEC-BCS crossover of an atomic
Fermi gas in an optical lattice, showing that the Feshbach resonance underlying
the crossover in principle induces strong multiband effects. Nevertheless, the
BEC-BCS crossover itself can be described by a single-band model since it
occurs at magnetic fields that are relatively far away from the Feshbach
resonance. A criterion is proposed for the latter, which is obeyed by most
known Feshbach resonances in ultracold atomic gases.Comment: 4 pages, 3 figure
A strongly interacting Bose gas: Nozi\`eres and Schmitt-Rink theory and beyond
We calculate the critical temperature for Bose-Einstein condensation in a gas
of bosonic atoms across a Feshbach resonance, and show how medium effects at
negative scattering lengths give rise to pairs reminiscent of the ones
responsible for fermionic superfluidity. We find that the formation of pairs
leads to a large suppression of the critical temperature. Within the formalism
developed by Nozieres and Schmitt-Rink the gas appears mechanically stable
throughout the entire crossover region, but when interactions between pairs are
taken into account we show that the gas becomes unstable close to the critical
temperature. We discuss prospects of observing these effects in a gas of
ultracold Cs133 atoms where recent measurements indicate that the gas may be
sufficiently long-lived to explore the many-body physics around a Feshbach
resonance.Comment: 8 pages, 8 figures, RevTeX. Significantly expanded to include effects
beyond NS
Scanning and data extraction from crop collecting mission documents
Poster presented at TDWG 2009, Montpellier (France). 9 - 13 Nov 2009
- …