375 research outputs found
Measurement of the \u3csup\u3e32\u3c/sup\u3eS(p,d)\u3csup\u3e31\u3c/sup\u3eS Reaction and Its Astrophysical Implications
The 30P(p,γ)31S reaction plays a crucial role in the synthesis of heavier nuclear species, from Si to Ca, in nova outbursts on ONe White Dwarfs [26, 28, 35]. However, its rate is very uncertain as a result of the lack of spectroscopic information on the levels above proton threshold in 31S. The currently adopted rate of this reaction, based on statistical Hauser-Feshbach calculations [36], could have an uncertainty as much as a factor of 100 higher or lower under nova conditions [26].
To reduce these uncertainties, we have measured differential cross sections for the 32S(p,d)31S reaction and determined excitation energies for states in 31S. A total of 26 states in 31S were observed, including 17 above the proton threshold. Five new states were observed. Uncertainties in the excitation energies of states in the high energy region were significantly reduced. Spin and parity values were determined or constrained for 15 of the strongly populated levels through a distorted wave Born approximation (DWBA) analysis of the angular distributions, of which 6 were made for the first time.
A new 30P(p,γ)31S reaction rate was calculated utilizing the present experimental spectroscopic information. We confirmed the spin-parity assignment of 1/2+ for the state at 6263 keV which dominates the 30P(p,γ)31S reaction rate at lower tempera- tures in nova, while the state at 6544 keV dominates at temperatures above 0.2 GK (1 GK=1.0×109 Kelvin). Our results indicate that the 30P(p,γ)31S rate based on our resonance calculations is reduced by up to a factor of 10 at nova temperatures compared to the previous rate.
Nova element synthesis calculations using the new 30P(p,γ)31S reaction rate were performed, and predictions of isotopic abundance patterns were obtained. Production of elements in the Si-Ca mass region are found to be altered by as much as 40% using the new rate. Important isotopic ratios are found to agree well with observations on presolar grains thought to have a nova origin [34]. Of special interest are the close- to-solar 29Si/28Si ratio and large excess in 30Si/28Si found in our simulations, which are the most important features pointing to a nova origin of such grains
A super-Eddington wind scenario for the progenitors of type Ia supernovae: binary population synthesis calculations
The super-Eddington wind scenario has been proposed as an alternative way for
producing type Ia supernovae (SNe Ia). The super-Eddington wind can naturally
prevent the carbon--oxygen white dwarfs (CO WDs) with high mass-accretion rates
from becoming red-giant-like stars. Furthermore, it works in low-metallicity
environments, which may explain SNe Ia observed at high redshifts. In this
article, we systematically investigated the most prominent single-degenerate
WD+MS channel based on the super-Eddington wind scenario. We combined the
Eggleton stellar evolution code with a rapid binary population synthesis (BPS)
approach to predict SN Ia birthrates for the WD+MS channel by adopting the
super-Eddington wind scenario and detailed mass-accumulation efficiencies of
H-shell flashes on the WDs. Our BPS calculations found that the estimated SN Ia
birthrates for the WD+MS channel are ~0.009-0.315*10^{-3}{yr}^{-1} if we adopt
the Eddington accretion rate as the critical accretion rate, which are much
lower than that of the observations (<10% of the observed SN Ia birthrates).
This indicates that the WD+MS channel only contributes a small proportion of
all SNe Ia. The birthrates in this simulation are lower than previous studies,
the main reason of which is that new mass-accumulation efficiencies of H-shell
flashes are adopted. We also found that the critical mass-accretion rate has a
significant influence on the birthrates of SNe Ia. Meanwhile, the results of
our BPS calculations are sensitive to the values of the common-envelope
ejection efficiency.Comment: 14 pages, 9 figures, 1 table, accepted for publication in Astronomy
and Astrophysic
Targeting Radioresistant Breast Cancer Cells by Single Agent CHK1 Inhibitor via Enhancing Replication Stress
Radiotherapy (RT) remains a standard therapeutic modality for breast cancer patients. However, intrinsic or acquired resistance limits the efficacy of RT. Here, we demonstrate that CHK1 inhibitor AZD7762 alone significantly inhibited the growth of radioresistant breast cancer cells (RBCC). Given the critical role of ATR/CHK1 signaling in suppressing oncogene-induced replication stress (RS), we hypothesize that CHK1 inhibition leads to the specific killing for RBCC due to its abrogation in the suppression of RS induced by oncogenes. In agreement, the expression of oncogenes c-Myc/CDC25A/c-Src/H-ras/E2F1 and DNA damage response (DDR) proteins ATR/CHK1/BRCA1/CtIP were elevated in RBCC. AZD7762 exposure led to significantly higher levels of RS in RBCC, compared to the parental cells. The mechanisms by which CHK1 inhibition led to specific increase of RS in RBCC were related to the interruptions in the replication fork dynamics and the homologous recombination (HR). In summary, RBCC activate oncogenic pathways and thus depend upon mechanisms controlled by CHK1 signaling to maintain RS under control for survival. Our study provided the first example where upregulating RS by CHK1 inhibitor contributes to the specific killing of RBCC, and highlight the importance of the CHK1 as a potential target for treatment of radioresistant cancer cells
Targeting Radioresistant Breast Cancer Cells by Single Agent CHK1 Inhibitor via Enhancing Replication Stress
Radiotherapy (RT) remains a standard therapeutic modality for breast cancer patients. However, intrinsic or acquired resistance limits the efficacy of RT. Here, we demonstrate that CHK1 inhibitor AZD7762 alone significantly inhibited the growth of radioresistant breast cancer cells (RBCC). Given the critical role of ATR/CHK1 signaling in suppressing oncogene-induced replication stress (RS), we hypothesize that CHK1 inhibition leads to the specific killing for RBCC due to its abrogation in the suppression of RS induced by oncogenes. In agreement, the expression of oncogenes c-Myc/CDC25A/c-Src/H-ras/E2F1 and DNA damage response (DDR) proteins ATR/CHK1/BRCA1/CtIP were elevated in RBCC. AZD7762 exposure led to significantly higher levels of RS in RBCC, compared to the parental cells. The mechanisms by which CHK1 inhibition led to specific increase of RS in RBCC were related to the interruptions in the replication fork dynamics and the homologous recombination (HR). In summary, RBCC activate oncogenic pathways and thus depend upon mechanisms controlled by CHK1 signaling to maintain RS under control for survival. Our study provided the first example where upregulating RS by CHK1 inhibitor contributes to the specific killing of RBCC, and highlight the importance of the CHK1 as a potential target for treatment of radioresistant cancer cells
RNA-Seq Analyses of the Role of miR-21 in Acute Pancreatitis
Background/Aims: Our previous study demonstrated that a deficiency of microRNA 21 (miR-21) protects mice from acute pancreatitis, yet the underlying molecular networks associated with miR-21 in pancreatitis and pancreatitis-associated lung injury remain unexplored. Methods: We used next generation sequencing to analyze gene expression profiles of pancreatic tissues from wild-type (WT) and miR-21 knockout (KO) mice treated with caerulein by using a 1-day treatment protocol. The Database for Annotation, Visualization, and Integrated Discovery gene annotation tool and Ingenuity Pathway Analysis were used to analyze the molecular pathways, while quantitative real-time PCR, western blotting, and immunohistochemistry were used to explore the molecular mechanisms. Results: We identified 152 differentially expressed genes (DEGs) in pancreata between WT and KO mice treated with caerulein. Cellular biogenesis and metabolism were the major pathways affected between WT and KO mice, whereas cell death and inflammatory response discriminated between WT and KO mice under acute pancreatitis. We validated 16 DEGs, consisting of 6 upregulated genes and 10 downregulated genes, involved in pancreatic injury. In particular, the upregulation of Pias3 and downregulation of Hmgb1 in KO pancreata coincided with a reduced severity of pancreatitis. In addition, we found Hmgb1 stimulation resulted in the overexpression of miR-21 in peripheral blood mononuclear cells, and deletion of miR-21 led to a reduction of caerulein-induced acute pancreatitis-associated lung injury by repressing Hmgb1 expression. Conclusion: Our data support the hypothesis that miR-21 modulates the inflammatory response during acute pancreatitis through the upregulation of Pias3 and downregulation of Hmgb1. Our findings further underscore a role for miR-21 in the promotion of acute pancreatitis
Multidifferential study of identified charged hadron distributions in -tagged jets in proton-proton collisions at 13 TeV
Jet fragmentation functions are measured for the first time in proton-proton
collisions for charged pions, kaons, and protons within jets recoiling against
a boson. The charged-hadron distributions are studied longitudinally and
transversely to the jet direction for jets with transverse momentum 20 GeV and in the pseudorapidity range . The
data sample was collected with the LHCb experiment at a center-of-mass energy
of 13 TeV, corresponding to an integrated luminosity of 1.64 fb. Triple
differential distributions as a function of the hadron longitudinal momentum
fraction, hadron transverse momentum, and jet transverse momentum are also
measured for the first time. This helps constrain transverse-momentum-dependent
fragmentation functions. Differences in the shapes and magnitudes of the
measured distributions for the different hadron species provide insights into
the hadronization process for jets predominantly initiated by light quarks.Comment: All figures and tables, along with machine-readable versions and any
supplementary material and additional information, are available at
https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-013.html (LHCb
public pages
Study of the decay
The decay is studied
in proton-proton collisions at a center-of-mass energy of TeV
using data corresponding to an integrated luminosity of 5
collected by the LHCb experiment. In the system, the
state observed at the BaBar and Belle experiments is
resolved into two narrower states, and ,
whose masses and widths are measured to be where the first uncertainties are statistical and the second
systematic. The results are consistent with a previous LHCb measurement using a
prompt sample. Evidence of a new
state is found with a local significance of , whose mass and width
are measured to be and , respectively. In addition, evidence of a new decay mode
is found with a significance of
. The relative branching fraction of with respect to the
decay is measured to be , where the first
uncertainty is statistical, the second systematic and the third originates from
the branching fractions of charm hadron decays.Comment: All figures and tables, along with any supplementary material and
additional information, are available at
https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-028.html (LHCb
public pages
Measurement of the ratios of branching fractions and
The ratios of branching fractions
and are measured, assuming isospin symmetry, using a
sample of proton-proton collision data corresponding to 3.0 fb of
integrated luminosity recorded by the LHCb experiment during 2011 and 2012. The
tau lepton is identified in the decay mode
. The measured values are
and
, where the first uncertainty is
statistical and the second is systematic. The correlation between these
measurements is . Results are consistent with the current average
of these quantities and are at a combined 1.9 standard deviations from the
predictions based on lepton flavor universality in the Standard Model.Comment: All figures and tables, along with any supplementary material and
additional information, are available at
https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-039.html (LHCb
public pages
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