346 research outputs found
Biola Hour Highlights, 1976 - 10
Interview with Dr.Samuel H. Sutherland Special Youth Panel with Ron Hafer, Jerry Root, and Frank Mercer Panel Discussions with Richard Chase, Charles Feinberg, and Samuel Sutherland This We Believe Introduction by Richard Chase Satan by Robert Moroscohttps://digitalcommons.biola.edu/bhhs/1032/thumbnail.jp
Biola Hour Highlights, 1976 - 10
Interview with Dr.Samuel H. Sutherland Special Youth Panel with Ron Hafer, Jerry Root, and Frank Mercer Panel Discussions with Richard Chase, Charles Feinberg, and Samuel Sutherland This We Believe Introduction by Richard Chase Satan by Robert Moroscohttps://digitalcommons.biola.edu/bhhs/1032/thumbnail.jp
Biola Hour Highlights, 1976 - 11
A Police Officer\u27s View of Life: A Personal Testimony by Robert Vernon Panel Discussions with Richard Chase, Charles Feinberg, and Samuel Sutherland Psalm 63: How Strong is Your Desire for God by Al Sanders Titus for Today\u27s Christian by Curtis Mitchellhttps://digitalcommons.biola.edu/bhhs/1033/thumbnail.jp
Bostonia: The Boston University Alumni Magazine. Volume 11
Founded in 1900, Bostonia magazine is Boston University's main alumni publication, which covers alumni and student life, as well as university activities, events, and programs
Steep Faint-end Slopes of Galaxy Mass and Luminosity Functions at z>=6 and the Implications for Reionisation
We present the results of a numerical study comparing photometric and
physical properties of simulated z=6-9 galaxies to the observations taken by
the WFC3 instrument aboard the Hubble Space Telescope. Using cosmological
hydrodynamical simulations we find good agreement with observations in
color-color space at all studied redshifts. We also find good agreement between
observations and our Schechter luminosity function fit in the observable range,
Muv<= -18, provided that a moderate dust extinction effect exists for massive
galaxies. However beyond what currently can be observed, simulations predict a
very large number of low-mass galaxies and evolving steep faint-end slopes from
alpha_L = -2.15 at z=6 to alpha_L = -2.64 at z=9, with a dependence of
|alpha_L| \propto (1+z)^0.59. During the same epoch, the normalization phi*
increases and the characteristic magnitude Muv* becomes moderately brighter
with decreasing redshift. We find similar trends for galaxy stellar mass
function with evolving low-mass end slope from alpha_M = - 2.26 at z=6 to
alpha_M = -2.87 at z=9, with a dependence of |alpha_M| \propto (1+z)^0.65.
Together with our recent result on the high escape fraction of ionizing photons
for low-mass galaxies, our results suggest that the low-mass galaxies are
important contributor of ionizing photons for the reionisation of the Universe
at z>=6.Comment: Revised metadata, 16 pages, 5 tables, 17 figures. MNRAS, in pres
Thermal Conductivity across the Phase Diagram of Cuprates: Low-Energy Quasiparticles and Doping Dependence of the Superconducting Gap
Heat transport in the cuprate superconductors YBaCuO and
LaSrCuO was measured at low temperatures as a function of
doping. A residual linear term kappa_{0}/T is observed throughout the
superconducting region and it decreases steadily as the Mott insulator is
approached from the overdoped regime. The low-energy quasiparticle gap
extracted from kappa_{0}/T is seen to scale closely with the pseudogap. The
ubiquitous presence of nodes and the tracking of the pseudogap shows that the
overall gap remains of the pure d-wave form throughout the phase diagram, which
excludes the possibility of a complex component (ix) appearing at a putative
quantum phase transition and argues against a non-superconducting origin to the
pseudogap. A comparison with superfluid density measurements reveals that the
quasiparticle effective charge is weakly dependent on doping and close to
unity.Comment: 12 pages, 9 figure
Recommended from our members
ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer.
ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer.
We have previously shown that during pregnancy the E-twenty-six (ETS) transcription factor ELF5 directs the differentiation of mammary progenitor cells toward the estrogen receptor (ER)-negative and milk producing cell lineage, raising the possibility that ELF5 may suppress the estrogen sensitivity of breast cancers. To test this we constructed inducible models of ELF5 expression in ER positive luminal breast cancer cells and interrogated them using transcript profiling and chromatin immunoprecipitation of DNA followed by DNA sequencing (ChIP-Seq). ELF5 suppressed ER and FOXA1 expression and broadly suppressed ER-driven patterns of gene expression including sets of genes distinguishing the luminal molecular subtype. Direct transcriptional targets of ELF5, which included FOXA1, EGFR, and MYC, accurately classified a large cohort of breast cancers into their intrinsic molecular subtypes, predicted ER status with high precision, and defined groups with differential prognosis. Knockdown of ELF5 in basal breast cancer cell lines suppressed basal patterns of gene expression and produced a shift in molecular subtype toward the claudin-low and normal-like groups. Luminal breast cancer cells that acquired resistance to the antiestrogen Tamoxifen showed greatly elevated levels of ELF5 and its transcriptional signature, and became dependent on ELF5 for proliferation, compared to the parental cells. Thus ELF5 provides a key transcriptional determinant of breast cancer molecular subtype by suppression of estrogen sensitivity in luminal breast cancer cells and promotion of basal characteristics in basal breast cancer cells, an action that may be utilised to acquire antiestrogen resistance
Gemcitabine Plus Bevacizumab Compared With Gemcitabine Plus Placebo in Patients With Advanced Pancreatic Cancer: Phase III Trial of the Cancer and Leukemia Group B (CALGB 80303)
The combination of gemcitabine plus bevacizumab produced a 21% response rate and a median survival of 8.8 months in a multicenter phase II trial in patients with metastatic pancreatic cancer. These encouraging data led Cancer and Leukemia Group B (CALGB) to conduct a double-blind, placebo-controlled, randomized phase III trial of gemcitabine/bevacizumab versus gemcitabine/placebo in advanced pancreatic cancer patients
Application of a stochastic modeling to evaluate tuberculosis onset in patients treated with tumor necrosis factor inhibitors
In this manuscript we apply stochastic modeling to investigate the risk of
reactivation of latent mycobacterial infections in patients undergoing
treatment with tumor necrosis factor inhibitors. First, we review the
perspective proposed by one of the authors in a previous work and which
consists in predicting the occurrence of reactivation of latent tuberculosis
infection or newly acquired tuberculosis during treatment; this is based on
variational procedures on a simple set of parameters (e.g. rate of reactivation
of a latent infection). Then, we develop a full analytical study of this
approach through a Markov chain analysis and we find an exact solution for the
temporal evolution of the number of cases of tuberculosis infection
(re)activation. The analytical solution is compared with Monte Carlo
simulations and with experimental data, showing overall excellent agreement.
The generality of this theoretical framework allows to investigate also the
case of non-tuberculous mycobacteria infections; in particular, we show that
reactivation in that context plays a minor role. This may suggest that, while
the screening for tuberculous is necessary prior to initiating biologics, when
considering non-tuberculous mycobacteria only a watchful monitoring during the
treatment is recommended. The framework outlined in this paper is quite general
and could be extremely promising in further researches on drug-related adverse
events.Comment: 26 pages, 7 figure
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