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Inspired by the recent experimental advances in cold atom quantum simulators, we explore the experimentally implemented bosonic t-t′-J model on the square lattice using large-scale density matrix renormalization group simulations. By tuning the doping level δ and hopping ratio t′/t, we uncover six distinct quantum phases, several of which go far beyond the conventional paradigm of phase-coherent superfluidity (SF) expected for bosonic systems. In particular, in the presence of antiferromagnetic (AFM) order, doped holes are tightly bound into pairs, giving rise to a pair density wave (PDW) phase at low doping and small |t′/t|, which is suppressed on the t′ < 0 side, resulting in a disordered PDW state that lacks coherence of either individual bosons or pairs. Upon further doping, bosons can regain phase coherence and form a SF* state, characterized by condensation at emergent incommensurate momenta concurrent with an incommensurate magnetic order. On the t′ > 0 side, the sign-induced kinetic frustration inherently disfavors local AFM correlations, leading to a phase separation in which doped holes cluster into ferromagnetic (FM) domains spatially separated by undoped AFM regions. Upon further doping, this inhomogeneous state evolves into a uniform SF + xy-FM phase. Finally, we propose a concrete experimental scheme to realize both signs of t′/t in Rydberg tweezer arrays, with an explicit mapping between model parameters and experimentally accessible regimes. Our results reveal competing and intertwined orders in doped antiferromagnets, which are relevant to central issues in high-Tc superconductivity, reflecting the frustrated interplay between doped holes and spin background. 

Abstract Strain modulation is a crucial way in engineering nanoscale materials. It is even more important for single photon emitters in layered materials, where strain can trap a delocalized exciton, leading to quantum emission. Herein, we apply strain by using the piezoelectric relaxor ferroelectric substrate. In addition to the strain-tuning of energy and polarization, we report on new observations, including the enhanced polarizability and tunable diamagnetic shift, from the charged localized excitons. As indicated from the polarization-resolved measurements, we attribute the formation of charged localized excitons to selenium vacancy defects. The shallow defect trap, supported by the value of g-factor, further allows for strain-modulation of the electron-hole overlap, hence resulting in the tunable diamagnetic shift. Our results provide a new perspective in integrating layered materials with functional substrates. The contrasting features observed from the charged localized excitons also signify the prospect of charged localized emitters for quantum science and technology. 

Efficient single instance segmentation is critical for unlocking features in on-the-fly mobile imaging applications, such as photo capture and editing. Existing mobile solutions often restrict segmentation to portraits or salient objects due to computational constraints. Recent advancements like the Segment Anything Model improve accuracy but remain computationally expensive for mobile, because it processes the entire image with heavy transformer backbones. To address this, we propose TraceNet, a one-click-driven single instance segmentation model. TraceNet segments a user-specified instance by back-tracing the receptive field of a ConvNet backbone, focusing computations on relevant regions and reducing inference cost and memory usage during mobile inference. Starting from user needs in real mobile applications, we define efficient single-instance segmentation tasks and introduce two novel metrics to evaluate both accuracy and robustness to low-quality input clicks. Extensive evaluations on the MS-COCO and LVIS datasets highlight TraceNet’s ability to generate high-quality instance masks efficiently and accurately while demonstrating robustness to imperfect user inputs. 

Bismuth selenide (Bi2Se3) is a binary compound displaying a strong spin−orbit coupling, resulting in a narrow bulk bandgap material with a gapless metallic surface. By shrinking the size of Bi2Se3 within the strong confinement regime, its optoelectronic properties changed drastically. To achieve this goal, strongly confined Bi2Se3 quantum dots (QDs) were produced by pulsed laser ablation in liquids (PLAL). The laser used for the synthesis was a nanosecond Nd/YAG laser emitting at 1064 nm and pulsing at∼13mJ/pulse. The irradiation of the bulk target was performed at 1kHz in acetone and lasted 5 min. Finally, the Bi2Se3 QDs were spherical in shape with a diameter around 7±3 nm and displaying an energy bandgap of 1.97±0.19eV. 

Red-shifted and broadened Raman peaks of MoS₂reveal the strain and doping effects from Ti₃C₂MXene as a substrate. 

Abstract Heat shock factor 1 (HSF1) is a stress-responsive transcription factor that promotes cancer cell malignancy. To provide a better understanding of the biological processes regulated by HSF1, here we developed an HSF1 activity signature (HAS) and found that it was negatively associated with antitumor immune cells in breast tumors. Knockdown of HSF1 decreased breast tumor size and caused an influx of several antitumor immune cells, most notably CD8+ T cells. Depletion of CD8+ T cells rescued the reduction in growth of HSF1-deficient tumors, suggesting HSF1 prevents CD8+ T-cell influx to avoid immune-mediated tumor killing. HSF1 suppressed expression of CCL5, a chemokine for CD8+ T cells, and upregulation of CCL5 upon HSF1 loss significantly contributed to the recruitment of CD8+ T cells. These findings indicate that HSF1 suppresses antitumor immune activity by reducing CCL5 to limit CD8+ T-cell homing to breast tumors and prevent immune-mediated destruction, which has implications for the lack of success of immune modulatory therapies in breast cancer. Significance:The stress-responsive transcription factor HSF1 reduces CD8+ T-cell infiltration in breast tumors to prevent immune-mediated killing, indicating that cellular stress responses affect tumor-immune interactions and that targeting HSF1 could improve immunotherapies.