The HiSPARC experiment

The High School Project on Astrophysics Research with Cosmics (HiSPARC) is a large extensive air shower (EAS) array with detection stations throughout the Netherlands, United Kingdom, Denmark and Namibia. HiSPARC is a collaboration of universities, scientific institutes and high schools. The majority of detection stations is hosted by high schools. A HiSPARC station consists of two or four scintillators placed inside roof boxes on top of a building. The measured response of a detector to single incoming muons agrees well with GEANT4 simulations. The response of a station to EASs agrees with simulations as well. A four-scintillator station was integrated in the KASCADE experiment and was used to determine the accuracy of the shower direction reconstruction. Using simulations, the trigger efficiency of a station to detect a shower as function of both distance to the shower core and zenith angle was determined. The HiSPARC experiment is taking data since 2003. The number of stations (~140 in 2019) still increases. The project demonstrates that its approach is viable for educational purposes and that scientific data can be obtained in a collaboration with high school students and teachers.Comment: Accepted for publication in NIM

DNA damage in transcribed genes induces apoptosis via the JNK pathway and the JNK-phosphatase MKP-1

The nucleotide excision repair (NER) system consists of two subpathways, global genome repair (GGR) and transcription-coupled repair (TCR), which exhibit distinct functions in the cellular response to genotoxic stress. Defects in TCR result in prolonged UV light-induced stalling of RNA polymerase II and hypersensitivity to apoptosis induced by UV and certain chemotherapeutic drugs. Here, we show that low doses of UV trigger delayed activation of the stress-induced MAPkinase JNK and its proapoptotic targets c-Jun and ATF-3 in TCR-deficient primary human fibroblasts from Xeroderma Pigmentosum (XP) and Cockayne syndrome (CS) patients. This delayed activation of the JNK pathway is not observed in GGR-deficient TCR-proficient XP cells, is independent of functional p53, and is established through repression of the JNK-phosphatase MKP-1 rather than by activation of the JNK kinases MKK4 and 7. Enzymatic reversal of UV-induced cyclobutane pyrimidine dimers (CPDs) by CPD photolyase abrogated JNK activation, MKP-1 repression, and apoptosis in TCR-deficient XPA cells. Ectopic expression of MKP-1 inhibited DNA-damage-induced JNK activity and apoptosis. These results identify both MKP-1 and JNK as sensors and downstream effectors of persistent DNA damage in transcribed genes and suggest a link between the JNK pathway and UV-induced stalling of RNApol II.Oncogene advance online publication, 25 July 2005; doi:10.1038/sj.onc.1208875

Spin density matrix elements in exclusive ρ0\mathrm{\rho^0} electroproduction on 1H\mathrm{^1H} and 2H\mathrm{^2H} targets at 27.5 GeV beam energy

Spin Density Matrix Elements (SDMEs) describing the angular distribution of exclusive rho^0 electroproduction and decay are determined in the HERMES experiment with 27.6 GeV beam energy and unpolarized hydrogen and deuterium targets. Eight (fifteen) SDMEs that are related (unrelated) to the longitudinal polarization of the beam are extracted in the kinematic region 1 GeV^2 < Q^2 < 7 GeV^2, 3.0 GeV < W < 6.3 GeV, and -t < 0.4 GeV^2. Within the given experimental uncertainties, a hierarchy of relative sizes of helicity amplitudes is observed. Kinematic dependences of all SDMEs on Q^2 and t are presented, as well as the longitudinal-to-transverse rho^0 electroproduction cross section ratio as a function of Q^2. A small but statistically significant deviation from the hypothesis of s-channel helicity conservation is observed. An indication is seen of a contribution of unnatural-parity-exchange amplitudes; these amplitudes are naturally generated with a quark-exchange mechanism.Comment: 41 pages, 20 figures, 16 table; revised version corrects small typos, text clarified on 6 pages, two references added and new data added to figure 2