A locking-free discontinuous Galerkin method for linear elastic Steklov eigenvalue problem

In this paper, a discontinuous Galerkin finite element method of Nitsche's version for the Steklov eigenvalue problem in linear elasticity is presented. The a priori error estimates are analyzed under a low regularity condition, and the robustness with respect to nearly incompressible materials (locking-free) is proven. Furthermore, some numerical experiments are reported to show the effectiveness and robustness of the proposed method.Comment: 25 pages, 6 figure

Pre-training Multi-party Dialogue Models with Latent Discourse Inference

Multi-party dialogues are more difficult for models to understand than one-to-one two-party dialogues, since they involve multiple interlocutors, resulting in interweaving reply-to relations and information flows. To step over these obstacles, an effective way is to pre-train a model that understands the discourse structure of multi-party dialogues, namely, to whom each utterance is replying. However, due to the lack of explicitly annotated discourse labels in multi-party dialogue corpora, previous works fail to scale up the pre-training process by putting aside the unlabeled multi-party conversational data for nothing. To fully utilize the unlabeled data, we propose to treat the discourse structures as latent variables, then jointly infer them and pre-train the discourse-aware model by unsupervised latent variable inference methods. Experiments on multiple downstream tasks show that our pre-trained model outperforms strong baselines by large margins and achieves state-of-the-art (SOTA) results, justifying the effectiveness of our method. The official implementation of this paper is available at https://github.com/EricLee8/MPD_EMVI.Comment: Accepted by ACL 202

mGluR5 antagonism inhibits cocaine reinforcement and relapse by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.

Metabotropic glutamate receptor 5 (mGluR5) antagonism inhibits cocaine self-administration and reinstatement of drug-seeking behavior. However, the cellular and molecular mechanisms underlying this action are poorly understood. Here we report a presynaptic glutamate/cannabinoid mechanism that may underlie this action. Systemic or intra-nucleus accumbens (NAc) administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) dose-dependently reduced cocaine (and sucrose) self-administration and cocaine-induced reinstatement of drug-seeking behavior. The reduction in cocaine-taking and cocaine-seeking was associated with a reduction in cocaine-enhanced extracellular glutamate, but not cocaine-enhanced extracellular dopamine (DA) in the NAc. MPEP alone, when administered systemically or locally into the NAc, elevated extracellular glutamate, but not DA. Similarly, the cannabinoid CB1 receptor antagonist, rimonabant, elevated NAc glutamate, not DA. mGluR5s were found mainly in striatal medium-spiny neurons, not in astrocytes, and MPEP-enhanced extracellular glutamate was blocked by a NAc CB1 receptor antagonist or N-type Ca++ channel blocker, suggesting that a retrograde endocannabinoid-signaling mechanism underlies MPEP-induced glutamate release. This interpretation was further supported by our findings that genetic deletion of CB1 receptors in CB1-knockout mice blocked both MPEP-enhanced extracellular glutamate and MPEP-induced reductions in cocaine self-administration. Together, these results indicate that the therapeutic anti-cocaine effects of mGluR5 antagonists are mediated by elevation of extracellular glutamate in the NAc via an endocannabinoid-CB1 receptor disinhibition mechanism

Limited Genetic Connectivity Among Sargassum horneri (Phaeophyceae) Populations in the Chinese Marginal Seas Despite Their high Dispersal Capacity

Sargassum horneri is a habitat-forming species in the Northwest Pacific and an important contributor to seaweed rafts. In this study, 131 benthic samples and 156 floating samples were collected in the Yellow Sea and East China Sea (ECS) to test the effects of seaweed rafts on population structure and connectivity. Our results revealed high levels of genetic diversity in both benthic and floating samples based on concatenated mitochondrial markers (rpl5-rps3, rnl-atp9, and cob-cox2). Phylogenetic analyses consistently supported the existence of two lineages (lineages I and II), with divergence dating to c. 0.692 Mya (95% HPD: 0.255-1.841 Mya), indicating that long-term isolation may have occurred during the mid-Pleistocene (0.126-0.781 Mya). Extended Bayesian skyline plots demonstrated a constant population size over time in lineage I and slight demographic expansion in lineage II. Both lineages were found in each marginal sea (including both benthic and floating samples), but PCoA, F-ST, and AMOVA analyses consistently revealed deep genetic variation between regions. Highly structured phylogeographic pattern supports limited genetic connectivity between regions. IMA analyses demonstrated that asymmetric gene flow between benthic populations in the North Yellow Sea (NYS) and ECS was extremely low (ECS -> NYS, 2Nm = 0.6), implying that high dispersal capacity cannot be assumed to lead to widespread population connectivity, even without dispersal barriers. In addition, there were only a few shared haplotypes between benthic and floating samples, suggesting the existence of hidden donors for the floating masses in the Chinese marginal seas

TCF1 and LEF1 Control Treg Competitive Survival and Tfr Development to Prevent Autoimmune Diseases.

CD4+ Foxp3+ T regulatory (Treg) cells are key players in preventing lethal autoimmunity. Tregs undertake differentiation processes and acquire diverse functional properties. However, how Treg's differentiation and functional specification are regulated remains incompletely understood. Here, we report that gradient expression of TCF1 and LEF1 distinguishes Tregs into three distinct subpopulations, particularly highlighting a subset of activated Treg (aTreg) cells. Treg-specific ablation of TCF1 and LEF1 renders the mice susceptible to systemic autoimmunity. TCF1 and LEF1 are dispensable for Treg's suppressive capacity but essential for maintaining a normal aTreg pool and promoting Treg's competitive survival. As a consequence, the development of T follicular regulatory (Tfr) cells, which are a subset of aTreg, is abolished in TCF1/LEF1-conditional knockout mice, leading to unrestrained T follicular helper (Tfh) and germinal center B cell responses. Thus, TCF1 and LEF1 act redundantly to control the maintenance and functional specification of Treg subsets to prevent autoimmunity