42 research outputs found
Genetic risk scores associated with baseline lipoprotein subfraction concentrations do not associate with their responses to fenofibrate
Lipoprotein subclass concentrations are modifiable markers of cardiovascular disease risk. Fenofibrate is known to show beneficial effects on lipoprotein subclasses, but little is known about the role of genetics in mediating the responses of lipoprotein subclasses to fenofibrate. A recent genomewide association study (GWAS) associated several single nucleotide polymorphisms (SNPs) with lipoprotein measures, and validated these associations in two independent populations. We used this information to construct genetic risk scores (GRSs) for fasting lipoprotein measures at baseline (pre-fenofibrate), and aimed to examine whether these GRSs also associated with the responses of lipoproteins to fenofibrate. Fourteen lipoprotein subclass measures were assayed in 817 men and women before and after a three week fenofibrate trial. We set significance at a Bonferroni corrected alpha <0.05 (p < 0.004). Twelve subclass measures changed with fenofibrate administration (each p = 0.003 to <0.0001). Mixed linear models which controlled for age, sex, body mass index (BMI), smoking status, pedigree and study-center, revealed that GRSs were associated with eight baseline lipoprotein measures (p < 0.004), however no GRS was associated with fenofibrate response. These results suggest that the mechanisms for changes in lipoprotein subclass concentrations with fenofibrate treatment are not mediated by the genetic risk for fasting levels
Pion, kaon, proton and anti-proton transverse momentum distributions from p+p and d+Au collisions at GeV
Identified mid-rapidity particle spectra of , , and
from 200 GeV p+p and d+Au collisions are reported. A
time-of-flight detector based on multi-gap resistive plate chamber technology
is used for particle identification. The particle-species dependence of the
Cronin effect is observed to be significantly smaller than that at lower
energies. The ratio of the nuclear modification factor () between
protons and charged hadrons () in the transverse momentum
range GeV/c is measured to be
(stat)(syst) in minimum-bias collisions and shows little
centrality dependence. The yield ratio of in minimum-bias d+Au
collisions is found to be a factor of 2 lower than that in Au+Au collisions,
indicating that the Cronin effect alone is not enough to account for the
relative baryon enhancement observed in heavy ion collisions at RHIC.Comment: 6 pages, 4 figures, 1 table. We extended the pion spectra from
transverse momentum 1.8 GeV/c to 3. GeV/
Demonstration of the temporal matter-wave Talbot effect for trapped matter waves
We demonstrate the temporal Talbot effect for trapped matter waves using
ultracold atoms in an optical lattice. We investigate the phase evolution of an
array of essentially non-interacting matter waves and observe matter-wave
collapse and revival in the form of a Talbot interference pattern. By using
long expansion times, we image momentum space with sub-recoil resolution,
allowing us to observe fractional Talbot fringes up to 10th order.Comment: 17 pages, 7 figure
Azimuthal anisotropy at RHIC: the first and fourth harmonics
We report the first observations of the first harmonic (directed flow, v_1),
and the fourth harmonic (v_4), in the azimuthal distribution of particles with
respect to the reaction plane in Au+Au collisions at the Relativistic Heavy Ion
Collider (RHIC). Both measurements were done taking advantage of the large
elliptic flow (v_2) generated at RHIC. From the correlation of v_2 with v_1 it
is determined that v_2 is positive, or {\it in-plane}. The integrated v_4 is
about a factor of 10 smaller than v_2. For the sixth (v_6) and eighth (v_8)
harmonics upper limits on the magnitudes are reported.Comment: 6 pages with 3 figures, as accepted for Phys. Rev. Letters The data
tables are at
http://www.star.bnl.gov/central/publications/pubDetail.php?id=3
Transverse-momentum correlations on from mean- fluctuations in Au-Au collisions at 200 GeV
We present first measurements of the pseudorapidity and azimuth
bin-size dependence of event-wise mean transverse momentum
fluctuations for Au-Au collisions at GeV. We invert that
dependence to obtain autocorrelations on differences
interpreted to represent velocity/temperature
distributions on (). The general form of the autocorrelations
suggests that the basic correlation mechanism is parton fragmentation. The
autocorrelations vary strongly with collision centrality, which suggests that
fragmentation is strongly modified by a dissipative medium in the more central
Au-Au collisions relative to peripheral or p-p collisions. \\Comment: 7 pages, 3 figure
Mid-rapidity anti-proton to proton ratio from Au+Au collisions at GeV
We report results on the ratio of mid-rapidity anti-proton to proton yields
in Au+Au collisions at \rts = 130 GeV per nucleon pair as measured by the
STAR experiment at RHIC. Within the rapidity and transverse momentum range of
and 0.4 1.0 GeV/, the ratio is essentially independent of
either transverse momentum or rapidity, with an average of for minimum bias collisions. Within errors, no
strong centrality dependence is observed. The results indicate that at this
RHIC energy, although the -\pb pair production becomes important at
mid-rapidity, a significant excess of baryons over anti-baryons is still
present.Comment: 5 pages, 3 figures, accepted by Phys. Rev. Let
A molecular portrait of epithelial–mesenchymal plasticity in prostate cancer associated with clinical outcome
The propensity of cancer cells to transition between epithelial and mesenchymal phenotypic states via the epithelial–mesenchymal transition (EMT) program can regulate metastatic processes, cancer progression, and treatment resistance. Transcriptional investigations using reversible models of EMT, revealed the mesenchymal-to-epithelial reverting transition (MErT) to be enriched in clinical samples of metastatic castrate resistant prostate cancer (mCRPC). From this enrichment, a metastasis-derived gene signature was identified that predicted more rapid cancer relapse and reduced survival across multiple human carcinoma types. Additionally, the transcriptional profile of MErT is not a simple mirror image of EMT as tumour cells retain a transcriptional “memory” following a reversible EMT. This memory was also enriched in mCRPC samples. Cumulatively, our studies reveal the transcriptional profile of epithelial–mesenchymal plasticity and highlight the unique transcriptional properties of MErT. Furthermore, our findings provide evidence to support the association of epithelial plasticity with poor clinical outcomes in multiple human carcinoma types