Energy Deposition in Adjacent LHC Superconducting Magnets from Beam Loss at LHC Transfer Line Collimators

Injection intensities for the LHC are over an order of magnitude above the damage threshold. The collimation system in the two transfer lines is designed to dilute the beam sufficiently to avoid damage in case of accidental beam loss or mis-steered beam. To maximise the protection for the LHC most of the collimators are located in the last 300 m upstream of the injection point where the transfer lines approach the LHC machine. To study the issue of possible quenches following beam loss at the collimators part of the collimation section in one of the lines, TI 8, together with the adjacent part of the LHC has been modeled in FLUKA. The simulated energy deposition in the LHC for worst-case accidental losses and as well as for losses expected during a normal filling is presented

Photon echo quantum memories in inhomogeneously broadened two level atoms

Here we propose a solid-state quantum memory that does not require spectral holeburning, instead using strong rephasing pulses like traditional photon echo techniques. The memory uses external broadening fields to reduce the optical depth and so switch off the collective atom-light interaction when desired. The proposed memory should allow operation with reasonable efficiency in a much broader range of material systems, for instance Er3+ doped crystals which have a transition at 1.5 um. We present analytic theory supported by numerical calculations and initial experiments.Comment: 7 pages, 8 figure

Experimental realization of light with time separated correlations by rephasing amplified spontaneous emission

Amplified spontaneous emission is a common noise source in active optical systems, it is generally seen as being an incoherent process. Here we excite an ensemble of rare earth ion dopants in a solid with a {\pi}-pulse, resulting in amplified spontaneous emission. The application of a second {\pi}-pulse leads to a coherent echo of the amplified spontaneous emission that is correlated in both amplitude and phase. For small optical thicknesses, we see evidence that the amplified spontaneous emission and its echo are entangled.Comment: 6 pages, 5 figures, the supplementary information pdf was uploaded with latex source files. This version accepted for publication in PR

Age-Related Differences in Executive Functions Within High-Level Youth Soccer Players

Background: When measuring executive functions (EF), it is common for athletes to be assessed on their ability to detect and process explicit sources of information. Yet not all of the information is perceived explicitly in an environment. Aim: This study aimed to include a new assessment that measures the impact of implicitly perceived congruent and incongruent visual precues on response times. Method: Seventy-four male soccer players: U12 (n=15), U13 (n=17), U17 (n=21) and U19 (n=21) representing a German 1st league club were assessed on four cognitive tasks. Results: The MANOVAs revealed a multivariate effect of age group on a reactive stress tolerance task (F(6,140)=11.670, p&lt;0.001, ES=0.38) and a Stop Signal Reaction Time task (F(6,144)=6.142, p&lt;0.001, ES=0.20). A one-way ANOVA revealed an age group effect for response accuracy in a multiple-object-tracking task (F(3,74)=4.05, p=0.01, ES=0.14). Lastly, a within-subjects effect of congruency on the implicit precued task (F(1,74)=51.32, p&lt;0.001, ES=0.41) and a between-subjects effect of age group (F(3,74)=4.30, p=0.008, ES=0.15) was observed. Interpretation: The results provided support for including an implicit precueing task, while the overall testing demonstrated that the magnitude of the increase in EF performance between ages was greater across the younger age groups compared to the older age groups.&#x0D;  </jats:p

Endoplasmic reticulum and lysosomal Ca2+ stores are remodelled in GBA1-linked Parkinson disease patient fibroblasts.

Mutations in β-glucocerebrosidase (encoded by GBA1) cause Gaucher disease (GD), a lysosomal storage disorder, and increase the risk of developing Parkinson disease (PD). The pathogenetic relationship between the two disorders is unclear. Here, we characterised Ca2+ release in fibroblasts from type I GD and PD patients together with age-matched, asymptomatic carriers, all with the common N370S mutation in β-glucocerebrosidase. We show that endoplasmic reticulum (ER) Ca2+ release was potentiated in GD and PD patient fibroblasts but not in cells from asymptomatic carriers. ER Ca2+ signalling was also potentiated in fibroblasts from aged healthy subjects relative to younger individuals but not further increased in aged PD patient cells. Chemical or molecular inhibition of β-glucocerebrosidase in fibroblasts and a neuronal cell line did not affect ER Ca2+ signalling suggesting defects are independent of enzymatic activity loss. Conversely, lysosomal Ca2+ store content was reduced in PD fibroblasts and associated with age-dependent alterations in lysosomal morphology. Accelerated remodelling of Ca2+ stores by pathogenic GBA1 mutations may therefore feature in PD