Radio emission of highly inclined cosmic ray air showers measured with LOPES

LOPES-10 (the first phase of LOPES, consisting of 10 antennas) detected a significant number of cosmic ray air showers with a zenith angle larger than 50$^{\circ}$, and many of these have very high radio field strengths. The most inclined event that has been detected with LOPES-10 has a zenith angle of almost 80$^{\circ}$. This is proof that the new technique is also applicable for cosmic ray air showers with high inclinations, which in the case that they are initiated close to the ground, can be a signature of neutrino events.Our results indicate that arrays of simple radio antennas can be used for the detection of highly inclined air showers, which might be triggered by neutrinos. In addition, we found that the radio pulse height (normalized with the muon number) for highly inclined events increases with the geomagnetic angle, which confirms the geomagnetic origin of radio emission in cosmic ray air showers.Comment: A&A accepte

Results from the KASCADE, KASCADE-Grande, and LOPES experiments

The origin of high-energy cosmic rays in the energy range from 10^14 to 10^18 eV is explored with the KASCADE and KASCADE-Grande experiments. Radio signals from air showers are measured with the LOPES experiment. An overview on results is given.Comment: Talk at The ninth International Conference on Topics in Astroparticle and Underground Physics, TAUP 2005, Zaragoza, September 10-14, 200

Optimized Trigger for Ultra-High-Energy Cosmic-Ray and Neutrino Observations with the Low Frequency Radio Array

When an ultra-high energy neutrino or cosmic ray strikes the Lunar surface a radio-frequency pulse is emitted. We plan to use the LOFAR radio telescope to detect these pulses. In this work we propose an efficient trigger implementation for LOFAR optimized for the observation of short radio pulses.Comment: Submitted to Nuclear Instruments and Methods in Physics Research Section

Detection of motor changes in huntington's disease using dynamic causal modeling

Deficits in motor functioning are one of the hallmarks of Huntington's disease (HD), a genetically caused neurodegenerative disorder. We applied functional magnetic resonance imaging (fMRI) and dynamic causal modeling (DCM) to assess changes that occur with disease progression in the neural circuitry of key areas associated with executive and cognitive aspects of motor control. Seventy-seven healthy controls, 62 pre-symptomatic HD gene carriers (preHD), and 16 patients with manifest HD symptoms (earlyHD) performed a motor finger-tapping fMRI task with systematically varying speed and complexity. DCM was used to assess the causal interactions among seven pre-defined regions of interest, comprising primary motor cortex, supplementary motor area (SMA), dorsal premotor cortex, and superior parietal cortex. To capture heterogeneity among HD gene carriers, DCM parameters were entered into a hierarchical cluster analysis using Ward's method and squared Euclidian distance as a measure of similarity. After applying Bonferroni correction for the number of tests, DCM analysis revealed a group difference that was not present in the conventional fMRI analysis. We found an inhibitory effect of complexity on the connection from parietal to premotor areas in preHD, which became excitatory in earlyHD and correlated with putamen atrophy. While speed of finger movements did not modulate the connection from caudal to pre-SMA in controls and preHD, this connection became strongly negative in earlyHD. This second effect did not survive correction for multiple comparisons. Hierarchical clustering separated the gene mutation carriers into three clusters that also differed significantly between these two connections and thereby confirmed their relevance. DCM proved useful in identifying group differences that would have remained undetected by standard analyses and may aid in the investigation of between-subject heterogeneity

Combined LOPES and KASCADE-Grande Data Analysis

First analyses of coincident data of the LOPES (LOfar PrototypE Station) radio antennas with the particle air shower experiment KASCADE-Grande show basic correlations in the observed shower parameters, like the strength of the radio signal and the particle number, or comparing the estimated shower directions. In addition, an improvement of the experimental resolution of the shower parameters reconstructed by KASCADE-Grande can be obtained by including the data of the radio antennas. This important feature will be shown in this article explicitely by an example event.Comment: 5 pages, Proceedings of International Workshop on Acoustic and Radio EeV Neutrino detection Activities: ARENA, May 17-19, 2005, DESY Zeuthe

Brain regions showing white matter loss in Huntington's Disease are enriched for synaptic and metabolic genes

Background The earliest white matter changes in Huntington’s disease are seen before disease onset in the premanifest stage around the striatum, within the corpus callosum, and in posterior white matter tracts. While experimental evidence suggests that these changes may be related to abnormal gene transcription, we lack an understanding of the biological processes driving this regional vulnerability. Methods Here, we investigate the relationship between regional transcription in the healthy brain, using the Allen Institute for Brain Science transcriptome atlas, and regional white matter connectivity loss at three time points over 24 months in subjects with premanifest Huntington’s disease relative to control participants. The baseline cohort included 72 premanifest Huntington’s disease participants and 85 healthy control participants. Results We show that loss of corticostriatal, interhemispheric, and intrahemispheric white matter connections at baseline and over 24 months in premanifest Huntington’s disease is associated with gene expression profiles enriched for synaptic genes and metabolic genes. Corticostriatal gene expression profiles are predominately associated with motor, parietal, and occipital regions, while interhemispheric expression profiles are associated with frontotemporal regions. We also show that genes with known abnormal transcription in human Huntington’s disease and animal models are overrepresented in synaptic gene expression profiles, but not in metabolic gene expression profiles. Conclusions These findings suggest a dual mechanism of white matter vulnerability in Huntington’s disease, in which abnormal transcription of synaptic genes and metabolic disturbance not related to transcription may drive white matter loss