Origin of Hilbert space quantum scars in unconstrained models

Quantum many-body scar is a recently discovered phenomenon weakly violating eigenstate thermalization hypothesis, and it has been extensively studied across various models. However, experimental realizations are mainly based on constrained models such as the $PXP$ model. Inspired by recent experimental observations on the superconducting platform in Refs.~[Nat. Phys. 19, 120 (2022)] and [arXiv:2211.05803], we study a distinct class of quantum many-body scars based on a half-filling hard-core Bose-Hubbard model, which is generic to describe in many experimental platforms. It is the so-called Hilbert space quantum scar as it originates from a subspace with a hypercube geometry weakly connecting to other thermalization regions in Hilbert space. Within the hypercube, a pair of collective Fock states do not directly connect to the thermalization region, resulting in slow thermalization dynamics with remarkable fidelity revivals with distinct differences from dynamics of other initial states. This mechanism is generic in various real-space lattice configurations, including one-dimensional Su-Schrieffer-Heeger chain, comb lattice, and even random dimer clusters consisting of dimers. In addition, we develop a toy model based on Hilbert hypercube decay approximation, to explain the spectrum overlap between the collective states and all eigenstates. Furthermore, we explore the Hilbert space quantum scar in two- and three-dimensional Su-Schrieffer-Heeger many-body systems, consisting of tetramers or octamers, respectively. This study makes quantum many-body scar state more realistic in applications such as quantum sensing and quantum metrology

Group DETR v2: Strong Object Detector with Encoder-Decoder Pretraining

We present a strong object detector with encoder-decoder pretraining and finetuning. Our method, called Group DETR v2, is built upon a vision transformer encoder ViT-Huge~\cite{dosovitskiy2020image}, a DETR variant DINO~\cite{zhang2022dino}, and an efficient DETR training method Group DETR~\cite{chen2022group}. The training process consists of self-supervised pretraining and finetuning a ViT-Huge encoder on ImageNet-1K, pretraining the detector on Object365, and finally finetuning it on COCO. Group DETR v2 achieves $\textbf{64.5}$ mAP on COCO test-dev, and establishes a new SoTA on the COCO leaderboard https://paperswithcode.com/sota/object-detection-on-cocoComment: Tech report, 3 pages. We establishes a new SoTA (64.5 mAP) on the COCO test-de

Anatomical factors influencing temporomandibular joint clicking in young adults: temporomandibular joint structure disorder or lateral pterygoid muscle dysfunction?

Objective: This study aimed to investigate the selected anatomical factors that can potentially influence temporomandibular joint (TMJ) clicking in young adults by assessing TMJ structures and lateral pterygoid muscle (LPM) function using magnetic resonance imaging (MRI).Methods: The patients were divided into four groups: the healthy control group; the clicking on mouth opening group; the clicking on mouth closing group; and the clicking on mouth opening and closing group. Additionally, we used clinical palpation to evaluate the masticatory muscles' functional state and employed MRI using the OCOR-T1WI-FSE-CLOSED, OSAG-PDW-FSE-CLOSED, and OSAG-PDW-FSE-OPEN sequences to analyze the texture of the lateral pterygoid muscle (LPM).Results: The proportion of any articular disc or condylar morphology class did not differ significantly between the TMJ clicking and HC groups. The articular disc position did not differ significantly between the TMJ clicking and HC groups. In the TMJ clicking group, the presence of masticatory muscle dysfunction differed significantly between the clicking and non-clicking sides. Moreover, the LPM accounted for the highest proportion among masticatory muscles with tenderness in all TMJ clicking subgroups (77.78%–100%). Therefore, in the TMJ clicking group, the LPM texture was less defined, more uniform in gray scale, and more similar to local texture (p < 0.0001).Conclusion: The occurrence of TMJ clicking in young adults is unrelated to the TMJ structure but related to the function of masticatory muscles, particularly the LPM

Effect and Mechanism of Armillaria mellea 07-22 Fermentation on the Degradation of Zearalenone

This study used Armillaria mellea 07-22 as the experimental strain to degrade zearalenone (ZEN) by fungal biological fermentation. The degradation effects of Armillaria mellea on ZEN were studied, including the degradation effects of different concentrations of ZEN by the strain and the effects of different culture time, culture temperature, initial pH value and inoculation amount on the degradation of ZEN by the strain. Then the degradation mechanism was explored, the degradation effects of mycelium, fermentation supernatant and cell contents on ZEN were analyzed, and the effects of different fermentation time, pH values, and metal ions on degradation of ZEN by fermentation supernatant were studied, and the correlation between degradation effect and laccase production activity of the strain was illustrated. The results showed that Armillaria mellea 07-22 had a good degradation effect on ZEN. When the ZEN concentration was 5 μg/mL, the optimal degradation conditions were culture time of 8 days, culture temperature of 27 ℃, initial pH of 7.0, and inoculation amount of 10%. At this time, the degradation rate of ZEN was 78.72%. The degradation rates of ZEN by mycelium, fermentation supernatant and cell contents were 47.42%, 37.05% and 13.08% respectively. The extracellular enzymes secreted by Am-07-22 were the main way to degrade ZEN, and the mycelium cells also had a certain adsorption effect on ZEN. In addition, the correlation between the degradation rate of ZEN by fermentation supernatant and laccase activity was 0.973, and Cu2+ had the best promoting effect on the degradation of ZEN by fermentation supernatant

Autoantibodies from patients with kidney allograft vasculopathy stimulate a proinflammatory switch in endothelial cells and monocytes mediated via GPCR-directed PAR1-TNF-α signaling

Non-HLA-directed regulatory autoantibodies (RABs) are known to target G-protein coupled receptors (GPCRs) and thereby contribute to kidney transplant vasculopathy and failure. However, the detailed underlying signaling mechanisms in human microvascular endothelial cells (HMECs) and immune cells need to be clarified in more detail. In this study, we compared the immune stimulatory effects and concomitant intracellular and extracellular signaling mechanisms of immunoglobulin G (IgG)-fractions from kidney transplant patients with allograft vasculopathy (KTx-IgG), to that from patients without vasculopathy, or matched healthy controls (Con-IgG). We found that KTx-IgG from patients with vasculopathy, but not KTx-IgG from patients without vasculopathy or Con-IgG, elicits HMEC activation and subsequent upregulation and secretion of tumor necrosis factor alpha (TNF-alpha) from HMECs, which was amplified in the presence of the protease-activated thrombin receptor 1 (PAR1) activator thrombin, but could be omitted by selectively blocking the PAR1 receptor. The amount and activity of the TNF-alpha secreted by HMECs stimulated with KTx-IgG from patients with vasculopathy was sufficient to induce subsequent THP-1 monocytic cell activation. Furthermore, AP-1/c-FOS, was identified as crucial transcription factor complex controlling the KTx-IgG-induced endothelial TNF-alpha synthesis, and mircoRNA-let-7f-5p as a regulatory element in modulating the underlying signaling cascade. In conclusion, exposure of HMECs to KTx-IgG from patients with allograft vasculopathy, but not KTx-IgG from patients without vasculopathy or healthy Con-IgG, triggers signaling through the PAR1-AP-1/c-FOS-miRNA-let7-axis, to control TNF-alpha gene transcription and TNF-alpha-induced monocyte activation. These observations offer a greater mechanistic understanding of endothelial cells and subsequent immune cell activation in the clinical setting of transplant vasculopathy that can eventually lead to transplant failure, irrespective of alloantigen-directed responses