Refine
Year of publication
- 2015 (32) (remove)
Document Type
- Article (32) (remove)
Language
- English (32)
Has Fulltext
- yes (32)
Is part of the Bibliography
- no (32)
Keywords
- Hadron-Hadron Scattering (3)
- Charm physics (2)
- Heavy Ions (2)
- ALICE experiment (1)
- Acute coronary syndrome (1)
- Anti-kaon–nucleon physics (1)
- Atrial fibrillation (1)
- Bcr-Abl (1)
- Cardiac troponin (1)
- Elliptic flow (1)
- Heavy ions (1)
- Heavy-flavour decay muons (1)
- Heavy-ion collision (1)
- Jak2(V617F) (1)
- Kaonic nuclei (1)
- LHC (1)
- Low energy QCD (1)
- Myocardial infarction (1)
- Partial wave analysis (1)
- Pb–Pb collisions (1)
- QCD (1)
- Quark gluon plasma (1)
- RNA interference (RNAi) (1)
- Relativistic heavy ion physics (1)
- canonical/non-canonical (1)
- chronic myeloid leukemia (CML) (1)
- human erythroid leukemia (HEL) (1)
- peptide aptamer (PA) (1)
- ppK − (1)
- protein/lentiviral transduction (1)
- signal transducer and activator of transcription 5 (Stat5) (1)
Institute
- Physik (27)
- Frankfurt Institute for Advanced Studies (FIAS) (20)
- Informatik (20)
- Medizin (4)
- Biochemie und Chemie (1)
- Georg-Speyer-Haus (1)
The elliptic flow, v2, of muons from heavy-flavour hadron decays at forward rapidity (2.5<y<4) is measured in Pb–Pb collisions at √sNN=2.76 TeV with the ALICE detector at the LHC. The scalar product, two- and four-particle Q cumulants and Lee–Yang zeros methods are used. The dependence of the v2 of muons from heavy-flavour hadron decays on the collision centrality, in the range 0–40%, and on transverse momentum, pT, is studied in the interval 3<pT<10 GeV/c. A positive v2 is observed with the scalar product and two-particle Q cumulants in semi-central collisions (10–20% and 20–40% centrality classes) for the pT interval from 3 to about 5 GeV/c with a significance larger than 3σ, based on the combination of statistical and systematic uncertainties. The v2 magnitude tends to decrease towards more central collisions and with increasing pT. It becomes compatible with zero in the interval 6<pT<10 GeV/c. The results are compared to models describing the interaction of heavy quarks and open heavy-flavour hadrons with the high-density medium formed in high-energy heavy-ion collisions.
We present results of a search for two hypothetical strange dibaryon states, i.e. the H-dibaryon and the possible Λn‾ bound state. The search is performed with the ALICE detector in central (0–10%) Pb–Pb collisions at √sNN=2.76 TeV, by invariant mass analysis in the decay modes Λn‾→d‾π+ and H-dibaryon →Λpπ−. No evidence for these bound states is observed. Upper limits are determined at 99% confidence level for a wide range of lifetimes and for the full range of branching ratios. The results are compared to thermal, coalescence and hybrid UrQMD model expectations, which describe correctly the production of other loosely bound states, like the deuteron and the hypertriton.
Two-particle angular correlations between trigger particles in the forward pseudorapidity range (2.5<|η|<4.0) and associated particles in the central range (|η|<1.0) are measured with the ALICE detector in p-Pb collisions at a nucleon-nucleon centre-of-mass energy of 5.02 TeV. The trigger particles are reconstructed using the muon spectrometer, and the associated particles by the central barrel tracking detectors. In high-multiplicity events, the double-ridge structure, previously discovered in two-particle angular correlations at midrapidity, is found to persist to the pseudorapidity ranges studied in this Letter. The second-order Fourier coefficients for muons in high-multiplicity events are extracted after jet-like correlations from low-multiplicity events have been subtracted. The coefficients are found to have a similar transverse momentum (pT) dependence in p-going (p-Pb) and Pb-going (Pb-p) configurations, with the Pb-going coefficients larger by about 16±6%, rather independent of pT within the uncertainties of the measurement. The data are compared with calculations using the AMPT model, which predicts a different pT and η dependence than observed in the data. The results are sensitive to the parent particle v2 and composition of reconstructed muon tracks, where the contribution from heavy flavour decays are expected to dominate at pT>2 GeV/c.
We present a measurement of inclusive J/ψ production in p-Pb collisions at sNN−−−√ = 5.02 TeV as a function of the centrality of the collision, as estimated from the energy deposited in the Zero Degree Calorimeters. The measurement is performed with the ALICE detector down to zero transverse momentum, pT, in the backward (−4.46<ycms<−2.96) and forward (2.03<ycms<3.53) rapidity intervals in the dimuon decay channel and in the mid-rapidity region (−1.37<ycms<0.43) in the dielectron decay channel. The backward and forward rapidity intervals correspond to the Pb-going and p-going direction, respectively. The pT-differential J/ψ production cross section at backward and forward rapidity is measured for several centrality classes, together with the corresponding average pT and p2T values. The nuclear modification factor, QpPb, is presented as a function of centrality for the three rapidity intervals, and, additionally, at backward and forward rapidity, as a function of pT for several centrality classes. At mid- and forward rapidity, the J/ψ yield is suppressed up to 40% compared to that in pp interactions scaled by the number of binary collisions. The degree of suppression increases towards central p-Pb collisions at forward rapidity, and with decreasing pT of the J/ψ. At backward rapidity, the QpPb is compatible with unity within the total uncertainties, with an increasing trend from peripheral to central p-Pb collisions.
Two-particle angular correlations between unidentified charged trigger and associated particles are measured by the ALICE detector in p–Pb collisions at a nucleon–nucleon centre-of-mass energy of 5.02 TeV. The transverse-momentum range 0.7 < pT,assoc < pT,trig < 5.0 GeV/c is examined, to include correlations induced by jets originating from low momentum-transfer scatterings (minijets). The correlations expressed as associated yield per trigger particle are obtained in the pseudorapidity range |η| < 0.9. The near-side long-range pseudorapidity correlations observed in high-multiplicity p–Pb collisions are subtracted from both near-side short-range and away-side correlations in order to remove the non-jet-like components. The yields in the jet-like peaks are found to be invariant with event multiplicity with the exception of events with low multiplicity. This invariance is consistent with the particles being produced via the incoherent fragmentation of multiple parton–parton scatterings, while the yield related to the previously observed ridge structures is not jet-related. The number of uncorrelated sources of particle production is found to increase linearly with multiplicity, suggesting no saturation of the number of multi-parton interactions even in the highest multiplicity p–Pb collisions. Further, the number scales only in the intermediate multiplicity region with the number of binary nucleon–nucleon collisions estimated with a Glauber Monte-Carlo simulation.
The pT-differential production cross section of electrons from semileptonic decays of heavy-flavor hadrons has been measured at mid-rapidity in proton-proton collisions at s√=2.76 TeV in the transverse momentum range 0.5 < pT < 12 GeV/c with the ALICE detector at the LHC. The analysis was performed using minimum bias events and events triggered by the electromagnetic calorimeter. Predictions from perturbative QCD calculations agree with the data within the theoretical and experimental uncertainties.
Partial wave analysis of the reaction p(3.5 GeV) + p → pK +Λ to search for the "ppK−" bound state
(2015)
Employing the Bonn–Gatchina partial wave analysis framework (PWA), we have analyzed HADES data of the reaction p(3.5 GeV) + p → pK +Λ. This reaction might contain information about the kaonic cluster “ppK −” (with quantum numbers J P = 0− and total isospin I = 1/2) via its decay into pΛ. Due to interference effects in our coherent description of the data, a hypothetical KNN (or, specifically “ppK −”) cluster signal need not necessarily show up as a pronounced feature (e.g. a peak) in an invariant mass spectrum like pΛ. Our PWA analysis includes a variety of resonant and non-resonant intermediate states and delivers a good description of our data (various angular distributions and two-hadron invariant mass spectra) without a contribution of a KNN cluster. At a confidence level of CLs = 95% such a cluster cannot contribute more than 2–12% to the total cross section with a pK +Λ final state, which translates into a production cross-section between 0.7 μb and 4.2 μb, respectively. The range of the upper limit depends on the assumed cluster mass, width and production process.
Genetic generalised epilepsy (GGE) is the most common form of genetic epilepsy, accounting for 20% of all epilepsies. Genomic copy number variations (CNVs) constitute important genetic risk factors of common GGE syndromes. In our present genome-wide burden analysis, large (≥ 400 kb) and rare (< 1%) autosomal microdeletions with high calling confidence (≥ 200 markers) were assessed by the Affymetrix SNP 6.0 array in European case-control cohorts of 1,366 GGE patients and 5,234 ancestry-matched controls. We aimed to: 1) assess the microdeletion burden in common GGE syndromes, 2) estimate the relative contribution of recurrent microdeletions at genomic rearrangement hotspots and non-recurrent microdeletions, and 3) identify potential candidate genes for GGE. We found a significant excess of microdeletions in 7.3% of GGE patients compared to 4.0% in controls (P = 1.8 x 10-7; OR = 1.9). Recurrent microdeletions at seven known genomic hotspots accounted for 36.9% of all microdeletions identified in the GGE cohort and showed a 7.5-fold increased burden (P = 2.6 x 10-17) relative to controls. Microdeletions affecting either a gene previously implicated in neurodevelopmental disorders (P = 8.0 x 10-18, OR = 4.6) or an evolutionarily conserved brain-expressed gene related to autism spectrum disorder (P = 1.3 x 10-12, OR = 4.1) were significantly enriched in the GGE patients. Microdeletions found only in GGE patients harboured a high proportion of genes previously associated with epilepsy and neuropsychiatric disorders (NRXN1, RBFOX1, PCDH7, KCNA2, EPM2A, RORB, PLCB1). Our results demonstrate that the significantly increased burden of large and rare microdeletions in GGE patients is largely confined to recurrent hotspot microdeletions and microdeletions affecting neurodevelopmental genes, suggesting a strong impact of fundamental neurodevelopmental processes in the pathogenesis of common GGE syndromes.
Signal transducers and activators of transcription (Stats) play central roles in the conversion of extracellular signals, e.g., cytokines, hormones and growth factors, into tissue and cell type specific gene expression patterns. In normal cells, their signaling potential is strictly limited in extent and duration. The persistent activation of Stat3 or Stat5 is found in many human tumor cells and contributes to their growth and survival. Stat5 activation plays a pivotal role in nearly all hematological malignancies and occurs downstream of oncogenic kinases, e.g., Bcr-Abl in chronic myeloid leukemias (CML) and Jak2(V617F) in other myeloproliferative diseases (MPD). We defined the mechanisms through which Stat5 affects growth and survival of K562 cells, representative of Bcr-Abl positive CML, and HEL cells, representative for Jak2(V617F) positive acute erythroid leukemia. In our experiments we suppressed the protein expression levels of Stat5a and Stat5b through shRNA mediated downregulation and demonstrated the dependence of cell survival on the presence of Stat5. Alternatively, we interfered with the functional capacities of the Stat5 protein through the interaction with a Stat5 specific peptide ligand. This ligand is a Stat5 specific peptide aptamer construct which comprises a 12mer peptide integrated into a modified thioredoxin scaffold, S5-DBD-PA. The peptide sequence specifically recognizes the DNA binding domain (DBD) of Stat5. Complex formation of S5-DBD-PA with Stat5 causes a strong reduction of P-Stat5 in the nuclear fraction of Bcr-Abl-transformed K562 cells and a suppression of Stat5 target genes. Distinct Stat5 mediated survival mechanisms were detected in K562 and Jak2(V617F)-transformed HEL cells. Stat5 is activated in the nuclear and cytosolic compartments of K562 cells and the S5-DBD-PA inhibitor most likely affects the viability of Bcr-Abl+ K562 cells through the inhibition of canonical Stat5 induced target gene transcription. In HEL cells, Stat5 is predominantly present in the cytoplasm and the survival of the Jak2(V617F)+ HEL cells is impeded through the inhibition of the cytoplasmic functions of Stat5.
Background: Chronic ethanol (EtOH) abuse worsens pathophysiological derangements after hemorrhagic shock and resuscitation (H/R) that induce hepatic injury and strong inflammatory changes via JNK and NF-κB activation. Inhibiting JNK with a cell-penetrating, protease-resistant peptide D-JNKI-1 after H/R in mice with healthy livers ameliorated these effects. Here, we studied if JNK inhibition by D-JNKI-1 in chronically EtOH-fed mice after hemorrhagic shock prior to the onset of resuscitation also confers protection.
Methods: Male mice were fed a Lieber-DeCarli diet containing EtOH or an isocaloric control (ctrl) diet for 4 weeks. Animals were hemorrhaged for 90 min (32 ± 2 mm Hg) and randomly received either D-JNKI-1 (11 mg/kg, intraperitoneally, i. p.) or sterile saline as vehicle (veh) immediately before the onset of resuscitation. Sham animals underwent surgical procedures without H/R and were either D-JNKI-1 or veh treated. Two hours after resuscitation, blood samples and liver tissue were harvested.
Results: H/R induced hepatic injury with increased systemic interleukin (IL)-6 levels, and enhanced local gene expression of NF-κB-controlled genes such as intercellular adhesion molecule (ICAM)-1 and matrix metallopeptidase (MMP)9. c-Jun and NF-κB phosphorylation were increased after H/R. These effects were further increased in EtOH-fed mice after H/R. D-JNKI-1 application inhibited the proinflammatory changes and reduced significantly hepatic injury after H/R in ctrl-fed mice. Moreover, D-JNKI-1 reduces in ctrl-fed mice the H/R-induced c-Jun and NF-κB phosphorylation. However, in chronically EtOH-fed mice, JNK inhibition did not prevent the H/R-induced hepatic damage and proinflammatory changes nor c-Jun and NF-κB phosphorylation after H/R.
Conclusions: These results indicate, that JNK inhibition is protective only in not pre-harmed liver after H/R. In contrast, the pronounced H/R-induced liver damage in mice being chronically fed with ethanol cannot be prevented by JNK inhibition after H/R and seems to be under the control of NF-κB.