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Abstract We propose a new measurement of the ratio of positron-proton to electron-proton elastic scattering at DESY. The purpose is to determine the contributions beyond single-photon exchange, which are essential for the Quantum Electrodynamic (QED) description of the most fundamental process in hadronic physics. By utilizing a 20 cm long liquid hydrogen target in conjunction with the extracted beam from the DESY synchrotron, we can achieve an average luminosity of$$2.12\times 10^{35}$$ $2.12\times {10}^{35}$ cm$$^{-2}\cdot $$ ${}^{-2}·$s$$^{-1}$$ ${}^{-1}$ ($$\approx 200$$ $\approx 200$times the luminosity achieved by OLYMPUS). The proposed two-photon exchange experiment (TPEX) entails a commissioning run at a beam energy of 2 GeV, followed by measurements at 3 GeV, thereby providing new data up to$$Q^2=4.6$$ $Q^2=4.6$ (GeV/c)$$^2$$ ${}^2$(twice the range of current measurements). We present and discuss the proposed experimental setup, run plan, and expectations. 

Abstract The search for a dark photon holds considerable interest in the physics community. Such a force carrier would begin to illuminate the dark sector. Many experiments have searched for such a particle, but so far it has proven elusive. In recent years the concept of a low mass dark photon has gained popularity in the physics community. Of particular recent interest is the 8 Be and 4 He anomaly, which could be explained by a new fifth force carrier with a mass of 17 MeV/ c 2 . The proposed Darklight experiment would search for this potential low mass force carrier at ARIEL in the 10-20 MeV/ c 2 e + e − invariant mass range. This proceeding will focus on the experimental design and physics case of the Darklight experiment. 

There is a critical need for adjuvants that can safely elicit potent and durable T cell-based immunity to intracellular pathogens. Here, we report that parenteral vaccination with a carbomer-based adjuvant, Adjuplex (ADJ), stimulated robust CD8 T-cell responses to subunit antigens and afforded effective immunity against respiratory challenge with a virus and a systemic intracellular bacterial infection. Studies to understand the metabolic and molecular basis for ADJ’s effect on antigen cross-presentation by dendritic cells (DCs) revealed several unique and distinctive mechanisms. ADJ-stimulated DCs produced IL-1β and IL-18, suggestive of inflammasome activation, but in vivo activation of CD8 T cells was unaffected in caspase 1-deficient mice. Cross-presentation induced by TLR agonists requires a critical switch to anabolic metabolism, but ADJ enhanced cross presentation without this metabolic switch in DCs. Instead, ADJ induced in DCs, an unique metabolic state, typified by dampened oxidative phosphorylation and basal levels of glycolysis. In the absence of increased glycolytic flux, ADJ modulated multiple steps in the cytosolic pathway of cross-presentation by enabling accumulation of degraded antigen, reducing endosomal acidity and promoting antigen localization to early endosomes. Further, by increasing ROS production and lipid peroxidation, ADJ promoted antigen escape from endosomes to the cytosol for degradation by proteasomes into peptides for MHC I loading by TAP-dependent pathways. Furthermore, we found that induction of lipid bodies (LBs) and alterations in LB composition mediated by ADJ were also critical for DC cross-presentation. Collectively, our model challenges the prevailing metabolic paradigm by suggesting that DCs can perform effective DC cross-presentation, independent of glycolysis to induce robust T cell-dependent protective immunity to intracellular pathogens. These findings have strong implications in the rational development of safe and effective immune adjuvants to potentiate robust T-cell based immunity.