Probing CP Violation with Neutrino Disappearance Alone.

The best way to probe CP violation in the lepton sector is with long-baseline accelerator neutrino experiments in the appearance mode: the appearance of ν_{e} in predominantly ν_{μ} beams. Here we show that it is possible to discover CP violation with disappearance experiments only, by combining JUNO for electron neutrinos and DUNE or Hyper-Kamiokande for muon neutrinos. While the maximum sensitivity to discover CP is quite modest (1.

Intersections of Climate Change with Food Systems, Nutrition, and Health: An Overview and Evidence Map.

Scientific research linking climate change to food systems, nutrition, and nutrition-related health (FSNH) has proliferated, showing bidirectional and compounding dependencies that create cascading risks for human and planetary health. Within this proliferation, it is unclear which evidence to prioritize for action and which research gaps, if filled, would catalyze the most impact. We systematically searched for synthesis literature (i.

TLR9 agonism differentially impacts human NK cell-mediated direct killing and antibody-dependent cell-mediated cytotoxicity.

There are two known mechanisms by which natural killer (NK) cells recognize and kill diseased targets: (i) direct killing and (ii) antibody-dependent cell-mediated cytotoxicity (ADCC). We investigated an indirect NK cell activation strategy for the enhancement of human NK cell killing function. We did this by leveraging the fact that toll-like receptor 9 (TLR9) agonism within pools of human peripheral blood mononuclear cells (PBMCs) results in a robust interferon signaling cascade that leads to NK cell activation.

BET inhibition reforms the immune microenvironment and alleviates T cell dysfunction in chronic lymphocytic leukemia.

Redundant tumor microenvironment (TME) immunosuppressive mechanisms and epigenetic maintenance of terminal T cell exhaustion greatly hinder functional antitumor immune responses in chronic lymphocytic leukemia (CLL). Bromodomain and extraterminal (BET) proteins regulate key pathways contributing to CLL pathogenesis and TME interactions, including T cell function and differentiation. Herein, we report that blocking BET protein function alleviates immunosuppressive networks in the CLL TME and repairs inherent CLL T cell defects.

Next-Generation Sequencing-Based Identification of as Causative Agent of High Mortality Disease in NOD.Cg-/SzJ (NSG) Mice.

NOD.Cg-/SzJ (NSG) mice, lacking many components of a mature immune system, are at increased risk of disease. General understanding of potential pathogens of these mice is limited.