597 research outputs found
Excited Heavy Quarkonium Production at the LHC through -Boson Decays
Sizable amount of heavy-quarkonium events can be produced through -boson
decays at the LHC. Such channels will provide a suitable platform to study the
heavy-quarkonium properties. The "improved trace technology", which disposes
the amplitude at the amplitude-level, is helpful for deriving
compact analytical results for complex processes. As an important new
application, in addition to the production of the lower-level Fock states
and , we make a further study on the
production of higher-excited -quarkonium Fock states
, and . Here
stands for the -charmonium,
-quarkonium and -bottomonium respectively. We show
that sizable amount of events for those higher-excited states can also be
produced at the LHC. Therefore, we need to take them into consideration for a
sound estimation.Comment: 7 pages, 9 figures and 6 tables. Typo errors are corrected, more
discussions and two new figures have been adde
Heavy Quarkonium Production at LHC through Boson Decays
The production of the heavy -quarkonium, -quarkonium
and -quarkonium states (-quarkonium for short), via
the semi-inclusive decays, has been systematically studied within the
framework of the non-relativistic QCD. In addition to the two color-singlet
-wave states, we also discuss the production of the four color-singlet
-wave states and (with ) together with the two color-octet components
and . Improved
trace technology is adopted to derive the simplified analytic expressions at
the amplitude level, which shall be useful for dealing with the following
cascade decay channels. At the LHC with the luminosity and the center-of-mass energy TeV, sizable
heavy-quarkonium events can be produced through the boson decays, i.e.
, and
-wave charmonium events per year can be obtained; and
, and -wave
-quarkonium events per year can be obtained. Main theoretical
uncertainties have also been discussed. By adding the uncertainties caused by
the quark masses in quadrature, we obtain KeV, KeV, KeV and eV.Comment: 24 pages, 12 figures. References updated. To be published in
Phys.Rev. D. To match the published versio
Microarray-based analysis of microRNA expression in breast cancer stem cells
<p>Abstract</p> <p>Background</p> <p>This study aimed to determine the miRNA profile in breast cancer stem cells (BCSCs) and to explore the functions of characteristic BCSC miRNAs.</p> <p>Methods</p> <p>We isolated ESA<sup>+</sup>CD44<sup>+</sup>CD24<sup>-/low </sup>BCSCs from MCF-7 cells using fluorescence-activated cell sorting (FACS). A human breast cancer xenograft assay was performed to validate the stem cell properties of the isolated cells, and microarray analysis was performed to screen for BCSC-related miRNAs. These BCSC-related miRNAs were selected for bioinformatic analysis and target prediction using online software programs.</p> <p>Results</p> <p>The ESA<sup>+</sup>CD44<sup>+</sup>CD24<sup>-/low </sup>cells had up to 100- to 1000-fold greater tumor-initiating capability than the MCF-7 cells. Tumors initiated from the ESA<sup>+</sup>CD44<sup>+</sup>CD24<sup>-/low </sup>cells were included of luminal epithelial and myoepithelial cells, indicating stem cell properties. We also obtained miRNA profiles of ESA<sup>+</sup>CD44<sup>+</sup>CD24<sup>-/low </sup>BCSCs. Most of the possible targets of potential tumorigenesis-related miRNAs were oncogenes, anti-oncogenes or regulatory genes.</p> <p>Conclusions</p> <p>We identified a subset of miRNAs that were differentially expressed in BCSCs, providing a starting point to explore the functions of these miRNAs. Evaluating characteristic BCSC miRNAs represents a new method for studying breast cancer-initiating cells and developing therapeutic strategies aimed at eradicating the tumorigenic subpopulation of cells in breast cancer.</p
Boson Decays to Meson and Its Uncertainties
The programming new collider with high luminosity shall provide
another useful platform to study the properties of the doubly heavy meson
in addition to the hadronic colliders as LHC and TEVATRON. Under the `New Trace
Amplitude Approach', we calculate the production of the spin-singlet and
the spin-triplet mesons through the boson decays, where
uncertainties for the production are also discussed. Our results show
KeV and
KeV, where the errors are caused by
varying and within their reasonable regions.Comment: 11 pages, 5 figures, 2 tables. To be published in Eur.Phys.J.
Antibody responses to an inactivated SARS-CoV-2 vaccine in individuals aged from 50 to 102 years
ObjectivesTo assess antibody responses to an inactivated SARS-CoV-2 vaccine in individuals aged 50 and older.MethodsWe conducted a post-market cross-sectional seroepidemiology study. We recruited 4,632 vaccinated individuals aged 50 and older, measured their total serum SARS-CoV-2-specific antibody (TA), and collected correlates. The primary outcome was the geometric mean titer (GMT) of TA, and the secondary outcome was the decline of TA with age. Univariate, bivariate, and multivariate analyses were used to examine the associations of the TA GMT with age, and trend analyses were used to test whether their associations were significant.ResultsAll participants had a detectable TA, which was generally at a low level across all age groups. The TA GMT (95% CI) in AU/mL was 3.05 (2.93, 3.18); the corresponding arithmetic mean (95% CI) was 17.77 (16.13, 19.42) in all participants and 4.33 (3.88, 4.84), 3.86 (3.49, 4.28), 3.24 (2.92, 3.59), 2.77 (2.60, 2.96), and 2.65 (2.48, 2.83) in the age groups of 50-54, 55-59, 60-64, 65-74, and 75 years or older, respectively. The TA GMT decreased with age with a Ptrend < 0.001. The TA GMT was significantly lower in those with hypertension or diabetes compared to those with neither.ConclusionThe inactivated SARS-CoV-2 vaccine is effective in individuals aged 50 and older. This is the first study that has found an inverse dose-response relationship between ages and the low-level TAs. Older people, especially those with chronic diseases, should get the SARS-CoV-2 vaccine, and their vaccination frequency, dose, and method may need to be different from those of younger people
Clinical characteristics and genetic analysis of pediatric patients with sodium channel gene mutation-related childhood epilepsy: a review of 94 patients
ObjectiveThis study aimed to examine the clinical and gene-mutation characteristics of pediatric patients with sodium channel gene mutation-related childhood epilepsy and to provide a basis for precision treatment and genetic counseling.MethodsThe clinical data from 94 patients with sodium channel gene mutation-related childhood epilepsy who were treated at Hunan Children's Hospital from August 2012 to December 2022 were retrospectively evaluated, and the clinical characteristics, gene variants, treatment, and follow-up status were analyzed and summarized.ResultsOur 94 pediatric patients with sodium channel gene variant-related childhood epilepsy comprised 37 girls and 57 boys. The age of disease onset ranged from 1 day to 3 years. We observed seven different sodium channel gene variants, and 55, 14, 9, 6, 6, 2, and 2 patients had SCNlA, SCN2A, SCN8A, SCN9A, SCN1B, SCN11A, and SCN3A variants, respectively. We noted that 52 were reported variants and 42 were novel variants. Among all gene types, SCN1A, SCN2A, and SCN8A variants were associated with an earlier disease onset age. With the exception of the SCN1B, the other six genes were associated with clustering seizures. Except for variants SCN3A and SCN11A, some patients with other variants had status epilepticus (SE). The main diagnosis of children with SCN1A variants was Dravet syndrome (DS) (72.7%), whereas patients with SCN2A and SCN8A variants were mainly diagnosed with various types of epileptic encephalopathy, accounting for 85.7% (12 of 14) and 88.9% (8 of 9) respectively. A total of five cases of sudden unexpected death in epilepsy (SUDEP) occurred in patients with SCN1A, SCN2A, and SCN8A variants. The proportion of benign epilepsy in patients with SCN9A, SCN11A, and SCN1B variants was relatively high, and the epilepsy control rate was higher than the rate of other variant types.ConclusionSodium channel gene variants involve different epileptic syndromes, and the treatment responses also vary. We herein reported 42 novel variants, and we are also the first ever to report two patients with SCN11A variants, thereby increasing the gene spectrum and phenotypic profile of sodium channel dysfunction. We provide a basis for precision treatment and prognostic assessment
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