Non-Abelian Dark Sectors and Their Collider Signatures

Motivated by the recent proliferation of observed astrophysical anomalies, Arkani-Hamed et al. have proposed a model in which dark matter is charged under a non-abelian "dark" gauge symmetry that is broken at ~ 1 GeV. In this paper, we present a survey of concrete models realizing such a scenario, followed by a largely model-independent study of collider phenomenology relevant to the Tevatron and the LHC. We address some model building issues that are easily surmounted to accommodate the astrophysics. While SUSY is not necessary, we argue that it is theoretically well-motivated because the GeV scale is automatically generated. Specifically, we propose a novel mechanism by which mixed D-terms in the dark sector induce either SUSY breaking or a super-Higgs mechanism precisely at a GeV. Furthermore, we elaborate on the original proposal of Arkani-Hamed et al. in which the dark matter acts as a messenger of gauge mediation to the dark sector. In our collider analysis we present cross-sections for dominant production channels and lifetime estimates for primary decay modes. We find that dark gauge bosons can be produced at the Tevatron and the LHC, either through a process analogous to prompt photon production or through a rare Z decay channel. Dark gauge bosons will decay back to the SM via "lepton jets" which typically contain >2 and as many as 8 leptons, significantly improving their discovery potential. Since SUSY decays from the MSSM will eventually cascade down to these lepton jets, the discovery potential for direct electroweak-ino production may also be improved. Exploiting the unique kinematics, we find that it is possible to reconstruct the mass of the MSSM LSP. We also present decay channels with displaced vertices and multiple leptons with partially correlated impact parameters.Comment: 44 pages, 25 figures, version published in JHE

Status Report of the DPHEP Study Group: Towards a Global Effort for Sustainable Data Preservation in High Energy Physics

Data from high-energy physics (HEP) experiments are collected with significant financial and human effort and are mostly unique. An inter-experimental study group on HEP data preservation and long-term analysis was convened as a panel of the International Committee for Future Accelerators (ICFA). The group was formed by large collider-based experiments and investigated the technical and organisational aspects of HEP data preservation. An intermediate report was released in November 2009 addressing the general issues of data preservation in HEP. This paper includes and extends the intermediate report. It provides an analysis of the research case for data preservation and a detailed description of the various projects at experiment, laboratory and international levels. In addition, the paper provides a concrete proposal for an international organisation in charge of the data management and policies in high-energy physics

Evidence for ground-state electron capture of 40^{40}K

Potassium-40 is a widespread isotope whose radioactivity impacts estimated geological ages spanning billions of years, nuclear structure theory, and subatomic rare-event searches - including those for dark matter and neutrinoless double-beta decay. The decays of this long-lived isotope must be precisely known for its use as a geochronometer, and to account for its presence in low-background experiments. There are several known decay modes for $^{40}$K, but a predicted electron-capture decay directly to the ground state of argon-40 has never been observed, while theoretical predictions span an order of magnitude. The KDK Collaboration reports on the first observation of this rare decay, obtained using a novel combination of a low-threshold X-ray detector surrounded by a tonne-scale, high-efficiency $\gamma$-ray tagger at Oak Ridge National Laboratory. A blinded analysis reveals a distinctly nonzero ratio of intensities of ground-state electron-captures ($I_{\text{EC}^0}$) over excited-state ones ($I_{\text{EC}^*}$) of $I_{\text{EC}^0} / I_{\text{EC}^*}=0.0095\stackrel{\text{stat}}{\pm}0.0022\stackrel{\text{sys}}{\pm}0.0010$ (68% CL), with the null hypothesis rejected at 4$\sigma$ [Stukel et al., DOI:10.1103/PhysRevLett.131.052503]. This unambiguous signal yields a branching ratio of $I_{\text{EC}^0}=0.098\%\stackrel{\text{stat}}{\pm}0.023\%\stackrel{\text{sys}}{\pm}0.010$, roughly half of the commonly used prediction. This first observation of a third-forbidden unique electron capture improves understanding of low-energy backgrounds in dark-matter searches and has implications for nuclear-structure calculations. A shell-model based theoretical estimate for the $0\nu\beta\beta$ decay half-life of calcium-48 is increased by a factor of $7^{+3}_{-2}$. Our nonzero measurement shifts geochronological ages by up to a percent; implications are illustrated for Earth and solar system chronologies.Comment: This is a companion submission to Stukel et al (KDK collaboration) "Rare $^{40}$K decay with implications for fundamental physics and geochronology" [arXiv:2211.10319; DOI: 10.1103/PhysRevLett.131.052503]. As such, both texts share some figures and portions of text. This version updates the text following its review and production proces

A novel experimental system for the KDK measurement of the 40^{40}K decay scheme relevant for rare event searches

Potassium-40 ($^{40}$K) is a long-lived, naturally occurring radioactive isotope. The decay products are prominent backgrounds for many rare event searches, including those involving NaI-based scintillators. $^{40}$K also plays a role in geochronological dating techniques. The branching ratio of the electron capture directly to the ground state of argon-40 has never been measured, which can cause difficulty in interpreting certain results or can lead to lack of precision depending on the field and analysis technique. The KDK (Potassium (K) Decay (DK)) collaboration is measuring this decay. A composite method has a silicon drift detector with an enriched, thermally deposited $^{40}$K source inside the Modular Total Absorption Spectrometer. This setup has been characterized in terms of energy calibration, gamma tagging efficiency, live time and false negatives and positives. A complementary, homogeneous, method is also discussed; it employs a KSr$_2$I$_5$:Eu scintillator as source and detector.Comment: 20 pages, 24 figures, Submitted to NIM

Stress-Induced Reinstatement of Drug Seeking: 20 Years of Progress

In human addicts, drug relapse and craving are often provoked by stress. Since 1995, this clinical scenario has been studied using a rat model of stress-induced reinstatement of drug seeking. Here, we first discuss the generality of stress-induced reinstatement to different drugs of abuse, different stressors, and different behavioral procedures. We also discuss neuropharmacological mechanisms, and brain areas and circuits controlling stress-induced reinstatement of drug seeking. We conclude by discussing results from translational human laboratory studies and clinical trials that were inspired by results from rat studies on stress-induced reinstatement. Our main conclusions are (1) The phenomenon of stress-induced reinstatement, first shown with an intermittent footshock stressor in rats trained to self-administer heroin, generalizes to other abused drugs, including cocaine, methamphetamine, nicotine, and alcohol, and is also observed in the conditioned place preference model in rats and mice. This phenomenon, however, is stressor specific and not all stressors induce reinstatement of drug seeking. (2) Neuropharmacological studies indicate the involvement of corticotropin-releasing factor (CRF), noradrenaline, dopamine, glutamate, kappa/dynorphin, and several other peptide and neurotransmitter systems in stress-induced reinstatement. Neuropharmacology and circuitry studies indicate the involvement of CRF and noradrenaline transmission in bed nucleus of stria terminalis and central amygdala, and dopamine, CRF, kappa/dynorphin, and glutamate transmission in other components of the mesocorticolimbic dopamine system (ventral tegmental area, medial prefrontal cortex, orbitofrontal cortex, and nucleus accumbens). (3) Translational human laboratory studies and a recent clinical trial study show the efficacy of alpha-2 adrenoceptor agonists in decreasing stress-induced drug craving and stress-induced initial heroin lapse

SV2 Mediates Entry of Tetanus Neurotoxin into Central Neurons

Tetanus neurotoxin causes the disease tetanus, which is characterized by rigid paralysis. The toxin acts by inhibiting the release of neurotransmitters from inhibitory neurons in the spinal cord that innervate motor neurons and is unique among the clostridial neurotoxins due to its ability to shuttle from the periphery to the central nervous system. Tetanus neurotoxin is thought to interact with a high affinity receptor complex that is composed of lipid and protein components; however, the identity of the protein receptor remains elusive. In the current study, we demonstrate that toxin binding, to dissociated hippocampal and spinal cord neurons, is greatly enhanced by driving synaptic vesicle exocytosis. Moreover, tetanus neurotoxin entry and subsequent cleavage of synaptobrevin II, the substrate for this toxin, was also dependent on synaptic vesicle recycling. Next, we identified the potential synaptic vesicle binding protein for the toxin and found that it corresponded to SV2; tetanus neurotoxin was unable to cleave synaptobrevin II in SV2 knockout neurons. Toxin entry into knockout neurons was rescued by infecting with viruses that express SV2A or SV2B. Tetanus toxin elicited the hyper excitability in dissociated spinal cord neurons - due to preferential loss of inhibitory transmission - that is characteristic of the disease. Surprisingly, in dissociated cortical cultures, low concentrations of the toxin preferentially acted on excitatory neurons. Further examination of the distribution of SV2A and SV2B in both spinal cord and cortical neurons revealed that SV2B is to a large extent localized to excitatory terminals, while SV2A is localized to inhibitory terminals. Therefore, the distinct effects of tetanus toxin on cortical and spinal cord neurons are not due to differential expression of SV2 isoforms. In summary, the findings reported here indicate that SV2A and SV2B mediate binding and entry of tetanus neurotoxin into central neurons

Platelet Activating Factor Blocks Interkinetic Nuclear Migration in Retinal Progenitors through an Arrest of the Cell Cycle at the S/G2 Transition

Nuclear migration is regulated by the LIS1 protein, which is the regulatory subunit of platelet activating factor (PAF) acetyl-hydrolase, an enzyme complex that inactivates the lipid mediator PAF. Among other functions, PAF modulates cell proliferation, but its effects upon mechanisms of the cell cycle are unknown. Here we show that PAF inhibited interkinetic nuclear migration (IKNM) in retinal proliferating progenitors. The lipid did not, however, affect the velocity of nuclear migration in cells that escaped IKNM blockade. The effect depended on the PAF receptor, Erk and p38 pathways and Chk1. PAF induced no cell death, nor a reduction in nucleotide incorporation, which rules out an intra-S checkpoint. Notwithstanding, the expected increase in cyclin B1 content during G2-phase was prevented in the proliferating cells. We conclude that PAF blocks interkinetic nuclear migration in retinal progenitor cells through an unusual arrest of the cell cycle at the transition from S to G2 phases. These data suggest the operation, in the developing retina, of a checkpoint that monitors the transition from S to G2 phases of the cell cycle