2,149 research outputs found
Vortices and Superfluidity in a Strongly Interacting Fermi Gas
Quantum-degenerate Fermi gases provide a remarkable opportunity to study
strongly interacting fermions. In contrast to other Fermi systems, such as
superconductors, neutron stars or the quark-gluon plasma, these gases have low
densities and their interactions can be precisely controlled over an enormous
range. Here we report observations of vortices in such a gas that provide
definitive evidence for superfluidity. By varying the pairing strength between
two fermions near a Feshbach resonance, one can explore the crossover from a
Bose-Einstein condensate (BEC) of molecules to a Bardeen-Cooper-Schrieffer
(BCS) superfluid of loosely bound pairs whose size is comparable to, or even
larger than, the interparticle spacing. The crossover realizes a novel form of
high-T_C superfluidity and it may provide new insight for high-T_C
superconductors. Previous experiments with Fermi gases have revealed
condensation of fermion pairs. While these and other studies were consistent
with predictions assuming superfluidity, the smoking gun for superfluid
behavior has been elusive. Our observation of vortex lattices directly displays
superfluid flow in a strongly interacting, rotating Fermi gas.Comment: 14 pages, including 7 figures, submitted to Natur
Tracing Functional Antigen-Specific CCR6+ Th17 Cells after Vaccination
BACKGROUND: The function of T helper cell subsets in vivo depends on their location, and one hallmark of T cell differentiation is the sequential regulation of migration-inducing chemokine receptor expression. CC-chemokine receptor 6 (CCR6) is a trait of tissue-homing effector T cells and has recently been described as a receptor on T helper type 17 (Th17) cells. Th17 cells are associated with autoimmunity and the defence against certain infections. Although, the polarization of Th cells into Th17 cells has been studied extensively in vitro, the development of those cells during the physiological immune response is still elusive. METHODOLOGY/PRINCIPAL FINDINGS: We analysed the development and functionality of Th17 cells in immune-competent mice during an ongoing immune response. In naïve and vaccinated animals CCR6(+) Th cells produce IL-17. The robust homeostatic proliferation and the presence of activation markers on CCR6(+) Th cells indicate their activated status. Vaccination induces antigen-specific CCR6(+) Th17 cells that respond to in vitro re-stimulation with cytokine production and proliferation. Furthermore, depletion of CCR6(+) Th cells from donor leukocytes prevents recipients from severe disease in experimental autoimmune encephalomyelitis, a model for multiple sclerosis in mice. CONCLUSIONS/SIGNIFICANCE: In conclusion, we defined CCR6 as a specific marker for functional antigen-specific Th17 cells during the immune response. Since IL-17 production reaches the highest levels during the immediate early phase of the immune response and the activation of Th17 cells precedes the Th1 cell differentiation we tent to speculate that this particular Th cell subset may represent a first line effector Th cell subpopulation. Interference with the activation of this Th cell subtype provides an interesting strategy to prevent autoimmunity as well as to establish protective immunity against infections
First Observation of the Decays and B^{0}\to D^{*-}p\bar{n}$
We report the first observation of exclusive decays of the type B to D^* N
anti-N X, where N is a nucleon. Using a sample of 9.7 times 10^{6} B-Bbar pairs
collected with the CLEO detector operating at the Cornell Electron Storage
Ring, we measure the branching fractions B(B^0 \to D^{*-} proton antiproton
\pi^+) = ({6.5}^{+1.3}_{-1.2} +- 1.0) \times 10^{-4} and B(B^0 \to D^{*-}
proton antineutron) = ({14.5}^{+3.4}_{-3.0} +- 2.7) times 10^{-4}. Antineutrons
are identified by their annihilation in the CsI electromagnetic calorimeter.Comment: 9 pages postscript, also available through
http://w4.lns.cornell.edu/public/CLN
Study of the Decays B0 --> D(*)+D(*)-
The decays B0 --> D*+D*-, B0 --> D*+D- and B0 --> D+D- are studied in 9.7
million Y(4S) --> BBbar decays accumulated with the CLEO detector. We determine
Br(B0 --> D*+D*-) = (9.9+4.2-3.3+-1.2)e-4 and limit Br(B0 --> D*+D-) < 6.3e-4
and Br(B0 --> D+D-) < 9.4e-4 at 90% confidence level (CL). We also perform the
first angular analysis of the B0 --> D*+D*- decay and determine that the
CP-even fraction of the final state is greater than 0.11 at 90% CL. Future
measurements of the time dependence of these decays may be useful for the
investigation of CP violation in neutral B meson decays.Comment: 21 pages, 5 figures, submitted to Phys. Rev.
A Search for
We report results of a search for in a sample of 9.7 million
charged meson decays. The search uses both and
decay modes of the , and demands exclusive reconstruction of the
companion decay to suppress background. We set an upper limit on the
branching fraction at 90%
confidence level. With slight modification to the analysis we also establish
at 90% confidence
level.Comment: 10 ages postscript, also available through
http://w4.lns.cornell.edu/public/CLN
Measurements of B --> D_s^{(*)+} D^{*(*)} Branching Fractions
This article describes improved measurements by CLEO of the and branching fractions, and first evidence
for the decay , where
represents the sum of the , , and
L=1 charm meson states. Also reported is the first
measurement of the polarization in the decay . A partial reconstruction technique, employing only the fully
reconstructed and slow pion from the decay, enhances sensitivity. The observed branching fractions are
, , and , where the first error is statistical,
the second systematic, and the third is due to the uncertainty in the branching fraction. The measured longitudinal
polarization, , is consistent with
the factorization prediction of 54%.Comment: 26 pages (LaTeX), 15 figures. To be submitted to PR
Improved Measurement of the Pseudoscalar Decay Constant
We present a new determination of the Ds decay constant, f_{Ds} using 5
million continuum charm events obtained with the CLEO II detector. Our value is
derived from our new measured ratio of widths for Ds -> mu nu/Ds -> phi pi of
0.173+/- 0.021 +/- 0.031. Taking the branching ratio for Ds -> phi pi as (3.6
+/- 0.9)% from the PDG, we extract f_{Ds} = (280 +/- 17 +/- 25 +/- 34){MeV}. We
compare this result with various model calculations.Comment: 23 page postscript file, postscript file also available through
http://w4.lns.cornell.edu/public/CLN
Genetic profiling of chromosome 1 in breast cancer: mapping of regions of gains and losses and identification of candidate genes on 1q
Chromosome 1 is involved in quantitative anomalies in 50–60% of breast tumours. However, the structure of these anomalies and the identity of the affected genes remain to be determined. To characterise these anomalies and define their consequences on gene expression, we undertook a study combining array-CGH analysis and expression profiling using specialised arrays. Array-CGH data showed that 1p was predominantly involved in losses and 1q almost exclusively in gains. Noticeably, high magnitude amplification was infrequent. In an attempt to fine map regions of copy number changes, we defined 19 shortest regions of overlap (SROs) for gains (one at 1p and 18 at 1q) and of 20 SROs for losses (all at 1p). These SROs, whose sizes ranged from 170 kb to 3.2 Mb, represented the smallest genomic intervals possible based on the resolution of our array. The elevated incidence of gains at 1q, added to the well-established concordance between DNA copy increase and augmented RNA expression, made us focus on gene expression changes at this chromosomal arm. To identify candidate oncogenes, we studied the RNA expression profiles of 307 genes located at 1q using a home-made built cDNA array. We identified 30 candidate genes showing significant overexpression correlated to copy number increase. In order to substantiate their involvement, RNA expression levels of these candidate genes were measured by quantitative (Q)-RT–PCR in a panel of 25 breast cancer cell lines previously typed by array-CGH. Q–PCR showed that 11 genes were significantly overexpressed in the presence of a genomic gain in these cell lines, and 20 overexpressed when compared to normal breast
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