Experimental Measurement of the Berry Curvature from Anomalous Transport

Geometrical properties of energy bands underlie fascinating phenomena in a wide-range of systems, including solid-state materials, ultracold gases and photonics. Most famously, local geometrical characteristics like the Berry curvature can be related to global topological invariants such as those classifying quantum Hall states or topological insulators. Regardless of the band topology, however, any non-zero Berry curvature can have important consequences, such as in the semi-classical evolution of a wave packet. Here, we experimentally demonstrate for the first time that wave packet dynamics can be used to directly map out the Berry curvature. To this end, we use optical pulses in two coupled fibre loops to study the discrete time-evolution of a wave packet in a 1D geometrical "charge" pump, where the Berry curvature leads to an anomalous displacement of the wave packet under pumping. This is both the first direct observation of Berry curvature effects in an optical system, and, more generally, the proof-of-principle demonstration that semi-classical dynamics can serve as a high-resolution tool for mapping out geometrical properties

Tideglusib Rescues Neurite Pathology of SPG11 iPSC Derived Cortical Neurons

Mutations in SPG11 cause a complicated autosomal recessive form of hereditary spastic paraplegia (HSP). Mechanistically, there are indications for the dysregulation of the GSK3β/βCat signaling pathway in SPG11. In this study, we tested the therapeutic potential of the GSK3β inhibitor, tideglusib, to rescue neurodegeneration associated characteristics in an induced pluripotent stem cells (iPSCs) derived neuronal model from SPG11 patients and matched healthy controls as well as a CRISPR-Cas9 mediated SPG11 knock-out line and respective control. SPG11-iPSC derived cortical neurons, as well as the genome edited neurons exhibited shorter and less complex neurites than controls. Administration of tideglusib to these lines led to the rescue of neuritic impairments. Moreover, the treatment restored increased cell death and ameliorated the membranous inclusions in iPSC derived SPG11 neurons. Our results provide a first evidence for the rescue of neurite pathology in SPG11-HSP by tideglusib. The current lack of disease-modifying treatments for SPG11 and related types of complicated HSP renders tideglusib a candidate compound for future clinical application

Evidence for the η_b(1S) Meson in Radiative Υ(2S) Decay

We have performed a search for the η_b(1S) meson in the radiative decay of the Υ(2S) resonance using a sample of 91.6 × 10^6 Υ(2S) events recorded with the BABAR detector at the PEP-II B factory at the SLAC National Accelerator Laboratory. We observe a peak in the photon energy spectrum at E_γ = 609.3^(+4.6)_(-4.5)(stat)±1.9(syst) MeV, corresponding to an η_b(1S) mass of 9394.2^(+4.8)_(-4.9)(stat) ± 2.0(syst) MeV/c^2. The branching fraction for the decay Υ(2S) → γη_b(1S) is determined to be [3.9 ± 1.1(stat)^(+1.1)_(-0.9)(syst)] × 10^(-4). We find the ratio of branching fractions B[Υ(2S) → γη_b(1S)]/B[Υ(3S) → γη_b(1S)]= 0.82 ± 0.24(stat)^(+0.20)_(-0.19)(syst)

New Perspectives for Spinal Cord Stimulation in Parkinson’s Disease-Associated Gait Impairment: A Systematic Review

Parkinson’s Disease is a neurodegenerative disorder manifesting itself as a hypokinetic movement impairment with postural instability and gait disturbance. In case of failure and/or limited response, deep brain stimulation has been established as an alternative and effective treatment modality. However, a subset of PD patients with gait impairment represents a therapeutic challenge. A systematic review (2000–2023) was performed using PubMed, Embase, Web of Science, Scopus, and Cochrane Library databases to determine the efficacy, stimulation waveform/parameters, spine level, and outcome measures of spinal cord stimulation using different waveforms in PD patients with and without chronic pain. Spinal cord stimulation responsiveness was assessed within the pre-defined follow-up period in three groups (short-term follow-up = 0–3 months; intermediate follow-up = 3–12 months; and long-term follow-up = more than 12 months). In addition, we briefly outline alternative neurostimulation therapies and the most recent developments in closed-loop spinal cord stimulation relevant to PD. In summary, 18 publications and 70 patients from uncontrolled observational trials were included, with low-quality evidence and conflicting findings. First and foremost, the currently available data do not support the use of spinal cord stimulation to treat PD-related gait disorders but have confirmed its usefulness for PD-associated chronic pain.This research received no external funding

Measurement of B→K^*(892)γ Branching Fractions and CP and Isospin Asymmetries

We present an analysis of the decays B^0→K^(*0)(892)γ and B^+→K^(*+)(892)γ using a sample of about 383×10^6 BB̅ events collected with the BABAR detector at the PEP-II asymmetric energy B factory. We measure the branching fractions B(B^0→K^(*0)γ)=(4.47±0.10±0.16)×10^(-5) and B(B^+→K^(*+)γ)=(4.22±0.14±0.16)×10^(-5). We constrain the direct CP asymmetry to be -0.033<A(B→K^*γ)<0.028 and the isospin asymmetry to be 0.017<Δ_(0-)<0.116, where the limits are determined by the 90% confidence interval and include both the statistical and systematic uncertainties

Evidence for X(3872) → Ψ (2S)y in B^± → X(3872)K^± Decays and a Study of B → ccyK

In a search for B → ccyK decays with the BABAR detector, where cc includes J/Ψ and Ψ (2S), and K includes K^±, K^0_S , and K^*(892), we find evidence for X(3872) → J/Ψy and X(3872) → Ψ (2S) with 3:6σ and 3:5σ significance, respectively. We measure the product of branching fractions B(B^± → X(3872)K^±)B(X(3872) → J/Ψy)= [2:8 ± 0:8(stat) ± 0:1(syst)]X 10^(-6) and B(B^± → X(3872)K^±) X B(X(3872) → Ψ (2S)y) = [9:5 ± 2:7(stat) ± 0:6(syst)] X 10^(-6)

Measurements of [script B]([overline B]^0 → Λ_c^+[overline p]) and [script B](B^- → Λ_c^+[overline p]π^-) and studies of Λ_c^+π^- resonances

We present an investigation of the decays [overline B]^0 → Λ_c^+[overline p] and B^- → Λ_c^+[overline p]π^- based on 383×10^6 γ(4S) → B[overline B] decays recorded with the BABAR detector. We measure the branching fractions of these decays; their ratio is [script B](B^- → Λ_c^+[overline p]π^-)/[script B]([overline B]^0 → Λ_c^+[overline p])=15.4 ± 1.8 ± 0.3. The B^- → Λ_c^+[overline p]π^- process exhibits an enhancement at the Λ_c^+[overline p] threshold and is a laboratory for searches for excited charm baryon states. We observe the resonant decays B^- → ∑_c(2455)^0[overline p] and B^- → ∑_c(2800)^0[overline p] but see no evidence for B^- → ∑_c(2520)^0[overline p]. This is the first observation of the decay B^- → ∑_c(2800)^0[overline p]; however, the mass of the observed excited ∑_c^0 state is (2846 ± 8 ± 10) MeV/c^2, which is somewhat inconsistent with previous measurements. Finally, we examine the angular distribution of the B^- → ∑_c(2455)^0[overline p] decays and measure the spin of the ∑_c(2455)^0 baryon to be 1/2, as predicted by the quark model

Evidence for B^+ → [overline K]^(*0)K^(*+)

We present measurements of the branching fraction and fraction of longitudinal polarization for the decay B^+ K^(*0)K^(*+) with a sample of (467±5)×10^6 BB pairs collected with the BABAR detector at the PEP-II asymmetric-energy e^+e^- collider at the SLAC National Accelerator Laboratory. We obtain the branching fraction B(B^+ K^(*0)K^(*+))=(1.2±0.5±0.1)×10^(-6) with a significance of 3.7 standard deviations including systematic uncertainties. We measure the fraction of longitudinal polarization f_L=0.75_(-0.26)^(+0.16)±0.03. The first error quoted is statistical and the second is systematic

G3 Hedonic olfaction in huntington’s disease

Background Huntington’s disease (HD) features a broad range of neuropsychiatric symptoms. In particular depression, apathy, and anhedonia are frequently present in HD. Anhedonia and apathy are observed as core symptoms of depression in HD but also as distinct features of HD independent from major depression. Therefore, methods helping to dissociate these symptoms are an important need for a precise diagnostic workup. Assessing anhedonia by focusing on hedonic perception of a sensory stimulus may be particularly helpful in HD. Aims In this study, we examine anhedonia by measuring the perception of pleasantness of odours in HD patients compared to controls. Methods By using the “Sniffin’Sticks®” odour identification test we assess hyposmia. In order to dissociate hedonia and olfaction we use additional olfactory sticks with 22 odours assessing intensity and pleasantness of odours. Pleasantness of odours is measured on a visual 9-point scale. For the assessment of hedonia and apathy the Snaith-Hamilton-Pleasure-Scale (SHAPS) and the Starkstein scale are applied respectively. Depression is measured using the Zung Self-Rating Depression Scale and the Beck Depression Inventory II. Perspective The hypothesis of this study is that the assessment of hedonic olfaction in HD allows discriminating anhedonia and apathy from depression. To test our hypothesis we will compare the hedonic perception of odours between HD patients and age and gender matched controls. Furthermore, we will correlate hedonic olfaction with the questionnaire-based assessment of depression, apathy and anhedonia. These data will be compared to our previously published findings that have shown reduced hedonic olfaction in Parkinson’s disease