spatial-temporal-control-murine-melanoma-initiation-from-mutant

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Cutaneous melanoma is well known as the most aggressive skin cancer. Although the risk factors and major genetic alterations continue to be documented ...

Cornell University

We conduct a comprehensive study of three different magnetic semiconductors, CrI, CrBr, and CrCl, by incorporating both few-layer and bilayer samples in van der Waals tunnel junctions. We find that the interlayer magnetic ordering, exchange gap, magnetic anisotropy, and magnon excitations evolve systematically with changing halogen atom. By fitting to a spin wave theory that accounts for nearest-neighbor exchange interactions, we are able to further determine a simple spin Hamiltonian describing all three systems. These results extend the 2D magnetism platform to Ising, Heisenberg, and XY spin classes in a single material family. Using magneto-optical measurements, we additionally demonstrate that ferromagnetism can be stabilized down to monolayer in more isotropic CrBr, with transition temperature still close to that of the bulk.

Evolution of interlayer and intralayer magnetism in three atomically thin chromium trihalides.

Consumption of a high-energy Western diet triggers mild adaptive β cell proliferation to compensate for peripheral insulin resistance; however, the underlying molecular mechanism remains unclear. In the present study we show that the toll-like receptors TLR2 and TLR4 inhibited the diet-induced replication of β cells in mice and humans. The combined, but not the individual, loss of TLR2 and TLR4 increased the replication of β cells, but not that of α cells, leading to enlarged β cell area and hyperinsulinemia in diet-induced obesity. Loss of TLR2 and TLR4 increased the nuclear abundance of the cell cycle regulators cyclin D2 and Cdk4 in a manner dependent on the signaling mediator Erk. These data reveal a regulatory mechanism controlling the proliferation of β cells in diet-induced obesity and suggest that selective targeting of the TLR2/TLR4 pathways may reverse β cell failure in patients with diabetes.

Toll-like receptors TLR2 and TLR4 block the replication of pancreatic β cells in diet-induced obesity.

The CuO antiferromagnetic insulator is transformed by hole-doping into an exotic quantum fluid usually referred to as the pseudogap (PG) phase. Its defining characteristic is a strong suppression of the electronic density-of-states () for energies || < [Formula: see text], where [Formula: see text] is the PG energy. Unanticipated broken-symmetry phases have been detected by a wide variety of techniques in the PG regime, most significantly a finite- density-wave (DW) state and a  = 0 nematic (NE) state. Sublattice-phase-resolved imaging of electronic structure allows the doping and energy dependence of these distinct broken-symmetry states to be visualized simultaneously. Using this approach, we show that even though their reported ordering temperatures  and  are unrelated to each other, both the DW and NE states always exhibit their maximum spectral intensity at the same energy, and using independent measurements that this is the PG energy [Formula: see text] Moreover, no new energy-gap opening coincides with the appearance of the DW state (which should theoretically open an energy gap on the Fermi surface), while the observed PG opening coincides with the appearance of the NE state (which should theoretically be incapable of opening a Fermi-surface gap). We demonstrate how this perplexing phenomenology of thermal transitions and energy-gap opening at the breaking of two highly distinct symmetries may be understood as the natural consequence of a vestigial nematic state within the pseudogap phase of BiSrCaCuO.

Dahihm Kim

Department of Biomedical Sciences

Cornell University

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Dahihm Kim

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Biomedical Sciences

Cornell University

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Department of Biomedical Sciences