Next-to-leading-order QCD corrections to e+e−→H+γe^+e^-\to H+\gamma

The associated production of Higgs boson with a hard photon at lepton collider, i.e., $e^+e^-\to H\gamma$, 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 $H\to \gamma\gamma, Z\gamma$, the $e^+e^-\to H\gamma$ 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 $H+\gamma$ 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 ($\sqrt{s}<300$ GeV), thus of negligible impact on Higgs factory such as CEPC. Nevertheless, when the energy is boosted to the ILC energy range ($\sqrt{s}\approx 400$ GeV), QCD corrections may enhance the leading-order cross section by $20\%$. In any event, the $e^+e^-\to H\gamma$ process has a maximal production rate $\sigma_{\rm max}\approx 0.08$ fb around $\sqrt{s}= 250$ 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 $\propto 1/s$ , but the latter undergoes a much faster decrease $\propto 1/s^2$.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