Search

Abstract A sensitivity study for the search for the charged lepton flavor violating process $$\tau \rightarrow \gamma \mu $$ τ → γ μ at the Super $$\tau $$ τ -Charm Facility is performed with a fast simulation. With the expected performance of the current detector design and an integrated luminosity of $$1\,\textrm{ab}^{-1}$$ 1 ab - 1 corresponding to one-year of data taking, the sensitivity on the branching fraction (BF) of $$\tau \rightarrow \gamma \mu $$ τ → γ μ is estimated to be at the level of $$10^{-8}$$ 10 - 8 . The sensitivity under different detector performances are also studied. With ideal performance, the BF could be probed to be $$2.8\,\times \,10^{-8}$$ 2.8 × 10 - 8 at 90% confidence level. The sensitivity is expected to scale with the square root of the luminosity, therefore with a total luminosity of $$10\,\hbox {ab}^{-1}$$ 10 ab - 1 corresponding to ten-year of data taking, the sensitivity could reach $$8.8\,\times 10^{-9}$$ 8.8 × 10 - 9 , which is about one order of magnitude improvement upon the current best upper limit.

Abstract We report a feasibility study of pure leptonic decay $$D_s^+\rightarrow \mu ^+\nu _\mu $$ D s + → μ + ν μ by using a fast simulation software package at STCF. With an expected luminosity of $$1~\mathrm {ab}^{-1}$$ 1 ab - 1 collected at STCF at a center-of-mass energy of 4.009 GeV, the statistical sensitivity of the branching fraction is determined to be 0.3%. Combining this result with the $$c \rightarrow s$$ c → s quark mixing matrix element $$|V_{cs}|$$ | V cs | determined from the current global Standard Model fit, the statistical sensitivity of $$D_s^+$$ D s + decay constant, $$f_{D_s^+}$$ f D s + , is estimated to be 0.2%. Alternatively, combining the current results of $$f_{D_s^+}$$ f D s + calculated by lattice QCD, the statistical sensitivity of $$|V_{cs}|$$ | V cs | is determined to be 0.2%, which helps probe possible new physics beyond Standard Model. The unprecedented precision to be achieved at STCF will provide a precise calibration of QCD and rigorous test of Standard Model.

Sphingosine kinase 1 (SphK1) is an important signaling molecule for cell proliferation and survival. However, the role of SphK1 in acrylamide (ACR)-induced nerve injury remains unclear. The purpose of this study was to investigate the role and potential mechanism of SphK1 in ACR-induced nerve injury. Liquid chromatography triple quadrupole tandem mass spectrometry (LC-MS/MS) and reverse transcription-quantitative PCR (RT-qPCR) were used to detect sphingosine 1-phosphate (S1P) content in serum and SphK1 content in whole blood from an occupational work group exposed to ACR compared to a non-exposed group. For in vitro experiments, SphK1 in human SH-SY5Y neuroblastoma cells was activated using SphK1-specific activator phorbol 12-myristate 13-acetate (PMA). Our research also utilized cell viability assays, flow cytometry, western blots, RT-qPCR and related protein detection to assess activity of the mitogen activated protein kinase (MAPK) signaling pathway. The results of the population study showed that the contents of SphK1 and S1P in the ACR-exposed occupational contact group were lower than in the non-exposed group. The results of in vitro experiments showed that expression of SphK1 decreased with the increase in ACR concentration. Activating SphK1 improved the survival rate of SH-SY5Y cells and decreased the apoptosis rate. Activating SphK1 in SH-SY5Y cells also regulated MAPK signaling, including enhancing the phosphorylation of extracellular signal-regulated protein kinases (ERK) and inhibiting the phosphorylation of c-Jun N-terminal kinase (JNK) and p38. These results suggest that activating SphK1 can protect against nerve cell damage caused by ACR.