Boundedness in a taxis-consumption system involving signal-dependent motilities and concurrent enhancement of density-determined diffusion and cross-diffusion

This paper is concerned with the migration-consumption taxis system involving signal-dependent motilities $$\left\{ \begin{array}{l} u_t = \Delta \big(u^m\phi(v)\big), \\[1mm] v_t = \Delta v-uv, \end{array} \right. \qquad \qquad (\star)$$ in smoothly bounded domains $\Omega\subset\mathbb{R}^n$, where $m>1$ and $n\ge2$. It is shown that if $\phi\in C^3([0,\infty))$ is strictly positive on $[0,\infty)$, for all suitably regular initial data an associated no-flux type initial-boundary value problem possesses a globally defined bounded weak solution, provided $m>\frac{n}{2}$, which is consistent with the restriction imposed on $m$ in corresponding signal production counterparts of $(\star)$ so as to establish the similar result.Comment: 19 pages, 0 figure

Paxion: Patching Action Knowledge in Video-Language Foundation Models

Action knowledge involves the understanding of textual, visual, and temporal aspects of actions. We introduce the Action Dynamics Benchmark (ActionBench) containing two carefully designed probing tasks: Action Antonym and Video Reversal, which targets multimodal alignment capabilities and temporal understanding skills of the model, respectively. Despite recent video-language models' (VidLM) impressive performance on various benchmark tasks, our diagnostic tasks reveal their surprising deficiency (near-random performance) in action knowledge, suggesting that current models rely on object recognition abilities as a shortcut for action understanding. To remedy this, we propose a novel framework, Paxion, along with a new Discriminative Video Dynamics Modeling (DVDM) objective. The Paxion framework utilizes a Knowledge Patcher network to encode new action knowledge and a Knowledge Fuser component to integrate the Patcher into frozen VidLMs without compromising their existing capabilities. Due to limitations of the widely-used Video-Text Contrastive (VTC) loss for learning action knowledge, we introduce the DVDM objective to train the Knowledge Patcher. DVDM forces the model to encode the correlation between the action text and the correct ordering of video frames. Our extensive analyses show that Paxion and DVDM together effectively fill the gap in action knowledge understanding (~50% to 80%), while maintaining or improving performance on a wide spectrum of both object- and action-centric downstream tasks. The code and data will be made publicly available for research purposes at https://github.com/MikeWangWZHL/Paxion.git.Comment: NeurIPS 2023 spotligh

MicroRNA-197 Promotes Metastasis of Hepatocellular Carcinoma by Activating Wnt/β-Catenin Signaling

Background/Aims: MicroRNA-197 (miR-197) has been shown to play roles in epithelialmesenchymal transition (EMT) and metastasis. The Wnt/β-catenin pathway is associated with EMT, but whether miR-197 regulatesWnt/β-catenin remains unclear. This study was to demonstrate the role of miR-197 on the Wnt/β-catenin pathway in hepatocellular carcinoma (HCC). Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-197 in 105 HCC specimens and 15 HCC cell lines. We tested the predicted target gene of miR-197 using a genetic report system. The role of miR-197 in HCC cell invasion and migration (wound healingand cell invasion and migrationby Transwell assays) and in an HCC xenograft modelwas analyzed. Results: Using a miRNA microarray analysis of HCC specimens and compared with non-metastatic HCC, miR-197 was identified as one of the most upregulated miRNAs in metastatic HCC. miR-197 expression was positively associated with the invasiveness of HCC cell lines. Metastatic HCC cells with high miR-197 expression had Wnt/β-catenin signaling activation. High levels of miR-197 expression also promoted EMT and invasionHCC cells in vitro and in vivo. miR-197 directly targeted Axin-2, Naked cuticle 1 (NKD1), and Dickkopf-related protein 2 (DKK2), leading to inhibition of Wnt/β-catenin signaling. High miR-197 expression was found in HCC specimens from patients with portal vein metastasis;high miR-197 expression correlated to the expression of Axin2, NKD1, and DKK2. Conclusion: miR-197 promotes HCC invasion and metastasis by activating Wnt/β-catenin signaling. miR-197 could possibly be used as a prognostic marker and therapeutic target for HCC

Reduced expression of PTPRD correlates with poor prognosis in gastric adenocarcinoma.

PTPRD, encoding protein tyrosine phosphatases receptor type D, is located at chromosome 9p23-24.1, a loci frequently lost in many types of tumors. Recently, PTPRD has been proposed to function as a tumor suppressor gene. The current study aimed to investigate PTPRD expression and its prognostic significance in primary gastric adenocarcinoma.Quantitative real time reverse transcription PCR (qRT-PCR) and western blotting were used to examine PTPRD expression in paired gastric tumourous and paracancerous tissues. Compared with the matched normal gastric mucosa tissues, both the mRNA (P = 0.0138) and protein (P = 0.0093) expression of PTPRD in fresh surgical specimens were significantly reduced. Clinicopathological and prognostic roles of PTPRD in gastric adenocarcinoma were investigated using immunohistochemistry with 513 paraffin-embedded gastric adenocarcinoma tissue blocks. Statistical analysis revealed that reduced PTPRD expression was significantly associated with T stage (P = 0.004), TNM stage (P<0.001) and tumor size (P = 0.003). Furthermore, Kaplan-Meier survival analysis revealed that low expression of PTPRD significantly correlated with poor survival of gastric cancer patients (P<0.001). Cox regression analysis confirmed PTPRD expression as independent predictor of the overall survival of gastric cancer patients. The MTT assay determined the effects of PTPRD on cell proliferation of MGC803 and GES1 cell lines. Restoring PTPRD expression in MGC803 cells significantly inhibited their growth rate. Silencing PTPRD expression by siRNA treatment in GES1 significantly enhanced cell proliferation compared with mock siRNA treatment. Methylation analysis of PTPRD promoter CpG island in 3 primary GC samples showed one case with partial methylation.These results indicated that PTPRD is a candidate tumour suppressor in gastric cancer. Thus, PTPRD may play an important role in gastric tumorigenesis and serve as a valuable prognostic marker of gastric adenocarcinoma

Correlation between <i>PTPRD</i> expression and clinicopathological parameters of 513 gastric adenocarcinoma cases.

a<p>^aNumbers of cases in each group. * Statistically significant (<i>P</i><0.05).</p><p>Correlation between <i>PTPRD</i> expression and clinicopathological parameters of 513 gastric adenocarcinoma cases.</p

The mRNA expression of <i>PTPRD</i> in human primary gastric adenocarcinoma surgical specimens was evaluated by qRT-PCR.

<p>The relative mRNA expression of <i>PTPRD</i> was significantly decreased in GC tissues compared with the matched adjacent noncancerous tissues (n = 42, P = 0.0138). Horizontal lines represent the mean.</p

<i>PTPRD</i> protein expression in gastric adenocarcinoma surgical specimens evaluated by immunohistochemistry.

<p>(A) Strong <i>PTPRD</i> staining was observed in noncancerous gastric mucosa. (B) Strong <i>PTPRD</i> staining in well-differentiated gastric cancer. (C) Weak <i>PTPRD</i> staining in moderately differentiated GC. (D) Negative <i>PTPRD</i> staining in poorly differentiated GC. (E) Immunostaining of GC and adjacent nontumorous tissues showing a sharp contrast of <i>PTPRD</i> staining intensity.</p

The growth suppressor role of <i>PTPRD</i> in cell proliferation and DNA methylation analysis of <i>PTPRD</i>.

<p>(A) Western blotting analysis of <i>PTPRD</i> overexpression in MGC803 cells. (B) Western blotting analysis of decreased <i>PTPRD</i> expression in GES1 cells. (C) Cell proliferation assay showing the suppressive effect of restoring <i>PTPRD</i> expression on the proliferation of MGC803 cell line. (D) Results showing significantly enhanced proliferation rate of <i>PTPRD</i>-silenced GES1 cells compared with mock siRNA treatment GES1 cells. (E) Methylation analysis of <i>PTPRD</i> promoter CpG island in primary GC tissues. Among 3 GC samples, one case showed partial methylation and 2 cases were unmethylated. *, P<0.05 versus the mock control; **, P<0.01 versus the mock control.</p