Meson Photo-Couplings From Lattice Quantum Chromodynamics

We explore the calculation of three-point functions featuring a vector current insertion in lattice Quantum Chromodynamics. These three-point functions, in general, contain information about many radiative transition matrix elements simultaneously. We develop and implement the technology necessary to isolate a single matrix element via the use of optimized operators, operators designed to interpolate a single meson eigenstate, which are constructed as variationally optimized linear combination of meson interpolating fields within a large basis. In order to frame the results we also explore some well known phenomenology arising within the context of the constituent quark model before transitioning to a lattice calculation of the spectrum of isovector mesons in a version of QCD featuring three flavors of quarks all tuned to approximately the physical strange quark mass. We then proceed to calculate radiative transition matrix elements for the lightest few isovector pseudoscalar and vector particles. The dependence of these form factors and transitions on the photon virtuality is extracted and some model intuitions are explored

The ππ→πγ⋆\pi\pi\to\pi\gamma^\star amplitude and the resonant ρ→πγ⋆\rho\to\pi\gamma^\star transition from lattice QCD

We present a determination of the $P$-wave $\pi\pi\to\pi\gamma^\star$ transition amplitude from lattice quantum chromodynamics. Matrix elements of the vector current in a finite-volume are extracted from three-point correlation functions, and from these we determine the infinite-volume amplitude using a generalization of the Lellouch-L\"uscher formalism. We determine the amplitude for a range of discrete values of the $\pi\pi$ energy and virtuality of the photon, and observe the expected dynamical enhancement due to the $\rho$ resonance. Describing the energy dependence of the amplitude, we are able to analytically continue into the complex energy plane and from the residue at the $\rho$ pole extract the $\rho\to \pi \gamma^\star$ transition form factor. This calculation, at $m_\pi\approx 400$ MeV, is the first to determine the form factor of an unstable hadron within a first principles approach to QCD.Comment: 20 pages, 16 figures, 3 table

Resonant ⁺ → ⁺⁰ Amplitude from Quantum Chromodynamics

We present the first ab initio calculation of a radiative transition of a hadronic resonance within quantum chromodynamics (QCD). We compute the amplitude for →⋆, as a function of the energy of the pair and the virtuality of the photon, in the kinematic regime where couples strongly to the unstable ρ resonance. This exploratory calculation is performed using a lattice discretization of QCD with quark masses corresponding to mπ ≈ 400  MeV. We obtain a description of the energy dependence of the transition amplitude, constrained at 48 kinematic points, that we can analytically continue to the ρ pole and identify from its residue the ρ→⋆ form factor

→ * Amplitude and the Resonant → * Transition from Lattice QCD

We present a determination of the P-wave → ⋆ transition amplitude from lattice quantum chromodynamics. Matrix elements of the vector current in a finite volume are extracted from three-point correlation functions, and from these we determine the infinite-volume amplitude using a generalization of the Lellouch-Lüscher formalism. We determine the amplitude for a range of discrete values of the energy and virtuality of the photon and observe the expected dynamical enhancement due to the ρ resonance. Describing the energy dependence of the amplitude, we are able to analytically continue into the complex energy plane and from the residue at the ρ pole extract the ρ → ⋆ transition form factor. This calculation, at m ≈ 400  MeV, is the first to determine the form factor of an unstable hadron within a first principles approach to QCD

Resonant ⁺ → ⁺⁰ Amplitude from Quantum Chromodynamics

We present the first ab initio calculation of a radiative transition of a hadronic resonance within quantum chromodynamics (QCD). We compute the amplitude for →⋆, as a function of the energy of the pair and the virtuality of the photon, in the kinematic regime where couples strongly to the unstable ρ resonance. This exploratory calculation is performed using a lattice discretization of QCD with quark masses corresponding to mπ ≈ 400  MeV. We obtain a description of the energy dependence of the transition amplitude, constrained at 48 kinematic points, that we can analytically continue to the ρ pole and identify from its residue the ρ→⋆ form factor

Naphthoquinones and Anthraquinones from Scent Glands of a Dyspnoid Harvestman, Paranemastoma quadripunctatum

Extracts of Paranemastoma quadripunctatum (Opiliones, Dyspnoi, Nemastomatidae) contained seven components, all of which likely originated from the secretion of well-developed prosomal scent glands. The two main components (together accounting for more than 90% of the secretion) were identified as 1,4-naphthoquinone and 6-methyl-1,4-naphthoquinone. The minor components were 1,4-naphthalenediol, two methoxy-naphthoquinones (2-methoxy-1,4-naphthoquinone, and 2-methoxy-6-methyl-1,4-naphthoquinone) and two anthraquinones (2-methyl-9,10-anthraquinone and a dimethyl-9,10-anthraquinone). While some chemical data on scent gland secretions of the other suborders of Opiliones (Cyphophthalmi, palpatorean Eupnoi, and Laniatores) already exist, this is the first report on the scent gland chemistry in the Dyspnoi. Naphthoquinones are known scent gland exudates of Cyphophthalmi and certain Eupnoi, methoxy-naphthoquinones and anthraquinones are new for opilionid scent gland secretions

Precision mouse models with expanded tropism for human pathogens

A major limitation of current humanized mouse models is that they primarily enable the analysis of human-specific pathogens that infect hematopoietic cells. However, most human pathogens target other cell types, including epithelial, endothelial and mesenchymal cells. Here, we show that implantation of human lung tissue, which contains up to 40 cell types, including nonhematopoietic cells, into immunodeficient mice (lung-only mice) resulted in the development of a highly vascularized lung implant. We demonstrate that emerging and clinically relevant human pathogens such as Middle East respiratory syndrome coronavirus, Zika virus, respiratory syncytial virus and cytomegalovirus replicate in vivo in these lung implants. When incorporated into bone marrow/liver/thymus humanized mice, lung implants are repopulated with autologous human hematopoietic cells. We show robust antigen-specific humoral and T-cell responses following cytomegalovirus infection that control virus replication. Lung-only mice and bone marrow/liver/thymus-lung humanized mice substantially increase the number of human pathogens that can be studied in vivo, facilitating the in vivo testing of therapeutics

Leishmania major Infection in Humanized Mice Induces Systemic Infection and Provokes a Nonprotective Human Immune Response

Background Leishmania (L.) species are the causative agent of leishmaniasis. Due to the lack of efficient vaccine candidates, drug therapies are the only option to deal with cutaneous leishmaniasis. Unfortunately, chemotherapeutic interventions show high toxicity in addition to an increased risk of dissemination of drug-resistant parasites. An appropriate laboratory animal based model is still missing which allows testing of new drug strategies in the context of human immune cells in vivo. Methodology/Principal Findings Humanized mice were infected subcutaneously with stationary phase promastigote L. major into the footpad. The human immune response against the pathogen and the parasite host interactions were analyzed. In addition we proved the versatility of this new model to conduct drug research studies by the inclusion of orally given Miltefosine. We show that inflammatory human macrophages get infected with Leishmania parasites at the site of infection. Furthermore, a Leishmania-specific human-derived T cell response is initiated. However, the human immune system is not able to prevent systemic infection. Thus, we treated the mice with Miltefosine to reduce the parasitic load. Notably, this chemotherapy resulted in a reduction of the parasite load in distinct organs. Comparable to some Miltefosine treated patients, humanized mice developed severe side effects, which are not detectable in the classical murine model of experimental leishmaniasis. Conclusions/Significance This study describes for the first time L. major infection in humanized mice, characterizes the disease development, the induction of human adaptive and innate immune response including cytokine production and the efficiency of Miltefosine treatment in these animals. In summary, humanized mice might be beneficial for future preclinical chemotherapeutic studies in systemic (visceral) leishmaniasis allowing the investigation of human immune response, side effects of the drug due to cytokine production of activated humane immune cells and the efficiency of the treatment to eliminate also not replicating (“hiding”) parasites