592 research outputs found
Next-to-leading-order QCD corrections to
The associated production of Higgs boson with a hard photon at lepton
collider, i.e., , is known to bear a rather small cross
section in Standard Model, and can serve as a sensitive probe for the potential
new physics signals. Similar to the loop-induced Higgs decay channels , the process also starts at one-loop
order provided that the tiny electron mass is neglected. In this work, we
calculate the next-to-leading-order (NLO) QCD corrections to this associated
production process, which mainly stem from the gluonic dressing to
the top quark loop. The QCD corrections are found to be rather modest at lower
center-of-mass energy range ( GeV), thus of negligible impact on
Higgs factory such as CEPC. Nevertheless, when the energy is boosted to the ILC
energy range ( GeV), QCD corrections may enhance the
leading-order cross section by . In any event, the
process has a maximal production rate fb around
GeV, thus CEPC turns out to be the best place to look for this
rare Higgs production process. In the high energy limit, the effect of NLO QCD
corrections become completely negligible, which can be simply attributed to the
different asymptotic scaling behaviors of the LO and NLO cross sections, where
the former exhibits a milder decrement , but the latter undergoes
a much faster decrease .Comment: v4, 11 pages, 6 figures, 2 tables; errors in Appendix are fixed;
version accepted for publication at PL
Calcium-Dependent and Synapsin-Dependent Pathways for the Presynaptic Actions of BDNF
We used cultured hippocampal neurons to determine the signaling pathways mediating brain-derived neurotrophic factor (BDNF) regulation of spontaneous glutamate and GABA release. BDNF treatment elevated calcium concentration in presynaptic terminals; this calcium signal reached a peak within 1 min and declined in the sustained presence of BDNF. This BDNF-induced transient rise in presynaptic calcium was reduced by SKF96365, indicating that BDNF causes presynaptic calcium influx via TRPC channels. BDNF treatment increased the frequency of miniature excitatory postsynaptic currents (mEPSCs). This response consisted of two components: a transient component that peaked within 1 min of initiating BDNF application and a second component that was sustained, at a lower mEPSC frequency, for the duration of BDNF application. The initial transient component was greatly reduced by removing external calcium or by treatment with SKF96365, as well as by Pyr3, a selective blocker of TRPC3 channels. In contrast, the sustained component was unaffected in these conditions but was eliminated by U0126, an inhibitor of the MAP kinase (MAPK) pathway, as well as by genetic deletion of synapsins in neurons from a synapsin triple knock-out (TKO) mouse. Thus, two pathways mediate the ability of BDNF to enhance spontaneous glutamate release: the transient component arises from calcium influx through TRPC3 channels, while the sustained component is mediated by MAPK phosphorylation of synapsins. We also examined the ability of these two BDNF-dependent pathways to regulate spontaneous release of the inhibitory neurotransmitter, GABA. BDNF had no effect on the frequency of spontaneous miniature inhibitory postsynaptic currents (mIPSCs) in neurons from wild-type (WT) mice, but surprisingly did increase mIPSC frequency in synapsin TKO mice. This covert BDNF response was blocked by removal of external calcium or by treatment with SKF96365 or Pyr3, indicating that it results from calcium influx mediated by TRPC3 channels. Thus, the BDNF-activated calcium signaling pathway can also enhance spontaneous GABA release, though this effect is suppressed by synapsins under normal physiological conditions.MOE (Min. of Education, S’pore)Published versio
Ultrafast fluorescent decay induced by metal-mediated dipole-dipole interaction in two-dimensional molecular aggregates
Two-dimensional molecular aggregate (2DMA), a thin sheet of strongly
interacting dipole molecules self-assembled at close distance on an ordered
lattice, is a fascinating fluorescent material. It is distinctively different
from the single or colloidal dye molecules or quantum dots in most previous
research. In this paper, we verify for the first time that when a 2DMA is
placed at a nanometric distance from a metallic substrate, the strong and
coherent interaction between the dipoles inside the 2DMA dominates its
fluorescent decay at picosecond timescale. Our streak-camera lifetime
measurement and interacting lattice-dipole calculation reveal that the
metal-mediated dipole-dipole interaction shortens the fluorescent lifetime to
about one half and increases the energy dissipation rate by ten times than
expected from the noninteracting single-dipole picture. Our finding can enrich
our understanding of nanoscale energy transfer in molecular excitonic systems
and may designate a new direction for developing fast and efficient
optoelectronic devices.Comment: 9 pages, 6 figure
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