TikTalk: A Video-Based Dialogue Dataset for Multi-Modal Chitchat in Real World

To facilitate the research on intelligent and human-like chatbots with multi-modal context, we introduce a new video-based multi-modal dialogue dataset, called TikTalk. We collect 38K videos from a popular video-sharing platform, along with 367K conversations posted by users beneath them. Users engage in spontaneous conversations based on their multi-modal experiences from watching videos, which helps recreate real-world chitchat context. Compared to previous multi-modal dialogue datasets, the richer context types in TikTalk lead to more diverse conversations, but also increase the difficulty in capturing human interests from intricate multi-modal information to generate personalized responses. Moreover, external knowledge is more frequently evoked in our dataset. These facts reveal new challenges for multi-modal dialogue models. We quantitatively demonstrate the characteristics of TikTalk, propose a video-based multi-modal chitchat task, and evaluate several dialogue baselines. Experimental results indicate that the models incorporating large language models (LLM) can generate more diverse responses, while the model utilizing knowledge graphs to introduce external knowledge performs the best overall. Furthermore, no existing model can solve all the above challenges well. There is still a large room for future improvements, even for LLM with visual extensions. Our dataset is available at \url{https://ruc-aimind.github.io/projects/TikTalk/}.Comment: Accepted to ACM Multimedia 202

Comprehensive investigation into the influence of glycosylation on head and neck squamous cell carcinoma and development of a prognostic model for risk assessment and anticipating immunotherapy

BackgroundIt has been well established that glycosylation plays a pivotal role in initiation, progression, and therapy resistance of several cancers. However, the correlations between glycosylation and head and neck squamous cell carcinoma (HNSCC) have not been elucidated in detail.MethodsThe paramount genes governing glycosylation were discerned via the utilization of the Protein-Protein Interaction (PPI) network and correlation analysis, coupled with single-cell RNA sequencing (scRNA-seq) analysis. To construct risk models exhibiting heightened predictive efficacy, cox- and lasso-regression methodologies were employed, and the veracity of these models was substantiated across both internal and external datasets. Subsequently, an exploration into the distinctions within the tumor microenvironment (TME), immunotherapy responses, and enriched pathways among disparate risk cohorts ensued. Ultimately, cell experiments were conducted to validate the consequential impact of SMS in Head and Neck Squamous Cell Carcinoma (HNSCC).ResultsA total of 184 genes orchestrating glycosylation were delineated for subsequent scrutiny. Employing cox- and lasso-regression methodologies, we fashioned a 3-gene signature, proficient in prognosticating the outcomes for patients afflicted with HNSCC. Noteworthy observations encompassed distinctions in the Tumor Microenvironment (TME), levels of immune cell infiltration, and the presence of immune checkpoint markers among divergent risk cohorts, holding potentially consequential implications for the clinical management of HNSCC patients.ConclusionThe prognosis of HNSCC can be proficiently anticipated through risk signatures based on Glycosylation-related genes (GRGs). A thorough delineation of the GRGs signature in HNSCC holds the potential to facilitate the interpretation of HNSCC’s responsiveness to immunotherapy and provide innovative strategies for cancer treatment

Liposomal Packaging Generates Wnt Protein with In Vivo Biological Activity

Wnt signals exercise strong cell-biological and regenerative effects of considerable therapeutic value. There are, however, no specific Wnt agonists and no method for in vivo delivery of purified Wnt proteins. Wnts contain lipid adducts that are required for activity and we exploited this lipophilicity by packaging purified Wnt3a protein into lipid vesicles. Rather than being encapsulated, Wnts are tethered to the liposomal surface, where they enhance and sustain Wnt signaling in vitro. Molecules that effectively antagonize soluble Wnt3a protein but are ineffective against the Wnt3a signal presented by a cell in a paracrine or autocrine manner are also unable to block liposomal Wnt3a activity, suggesting that liposomal packaging mimics the biological state of active Wnts. When delivered subcutaneously, Wnt3a liposomes induce hair follicle neogenesis, demonstrating their robust biological activity in a regenerative context

Nitric Oxide Negatively Regulates the Rapid Formation of <i>Pleurotus ostreatus</i> Primordia by Inhibiting the Mitochondrial <i>aco</i> Gene

Nitric oxide (NO) is as a signaling molecule that participates in the regulation of plant development and in a number of physiological processes. However, the function and regulatory pathway of NO in the growth and development of edible mushrooms are still unknown. This study found that NO played a negative role in the transformation of Pleurotus ostreatus from vegetative growth to reproductive growth by the exogenous addition of NO donors and scavengers. Further studies showed that NO can inhibit the gene expression and enzyme activity of aconitase (ACO). Moreover, the overexpression (OE) of mitochondrial aco and RNA interference (RNAi) confirmed that ACO participates in the regulation of the primordia formation rate. The effects of aco OE and RNAi on the tricarboxylic acid (TCA) cycle and energy metabolism were further measured. The results showed that RNAi-aco mutant strains can affect the enzyme activities of isocitrate dehydrogenase of mitochondria (ICDHm) and α-ketoglutarate dehydrogenase (α-KGDH) in the TCA cycle, thereby reducing the production of nicotinamide adenine dinucleotide (NADH) in the TCA cycle, decreasing the contents of adenosine triphosphate (ATP) and hydrogen peroxide (H2O2), and negatively regulating the rapid formation of primordia. In addition, H2O2 was significantly increased during the transformation from vegetative growth to reproductive growth of P. ostreatus. Additionally, the exogenous addition of H2O2 and its scavengers further confirmed the positive regulation by H2O2 in primordia formation. This study shows that during the growth and development of P. ostreatus, NO can inhibit the expression of the mitochondrial aco gene and ACO protein in the TCA cycle, reduce the production of ATP and H2O2 in the respiratory chain, and negatively regulate the rate of primordia formation

Self-renewing diploid Axin2(+) cells fuel homeostatic renewal of the liver.

The source of new hepatocytes in the uninjured liver has remained an open question. By lineage tracing using the Wnt-responsive gene Axin2 in mice, we identify a population of proliferating and self-renewing cells adjacent to the central vein in the liver lobule. These pericentral cells express the early liver progenitor marker Tbx3, are diploid, and thereby differ from mature hepatocytes, which are mostly polyploid. The descendants of pericentral cells differentiate into Tbx3-negative, polyploid hepatocytes, and can replace all hepatocytes along the liver lobule during homeostatic renewal. Adjacent central vein endothelial cells provide Wnt signals that maintain the pericentral cells, thereby constituting the niche. Thus, we identify a cell population in the liver that subserves homeostatic hepatocyte renewal, characterize its anatomical niche, and identify molecular signals that regulate its activity

LINC01128 - miR-16 interaction regulates the migration and invasion of human chorionic trophoblast cells

Objective: Pre-eclampsia (PE) is a major complication of pregnancy, but its pathogenesis is unclear. This study explored the role of LINC01128 in the progression of PE, and its interaction with miR-16 on the behaviors of trophoblasts. Methods: The mRNA levels of LINC01128 and miR-16 in placental tissues and HTR-8/SVneo cells were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit (CCK)-8, wound healing assay and transwell assay were used to detect proliferation, migration and invasion. E-Cadherin, Vimentin, Matrix metalloproteinase 2 (MMP2) and MMP9 protein expressions were detected by Western blot. The correlation between LINC01128 and miR-16 was determined and verified by starBase and dual-luciferase assay. Results: The expression of LINC01128 was downregulated in PE. Overexpression of LINC01128 promoted LINC01128 expression, cell proliferation, migration, invasion and the expressions of Vimentin, MMP2 and MMP9, but inhibited the expression of E-Cadherin. SiLINC01128 showed opposite effects. MiR-16 interacted with LINC01128, and miR-16 was high-expressed in PE placentae. MiR-16 inhibitor promoted cell proliferation, migration, invasion and related protein expressions, but inhibited the expression of E-Cadherin. However, siLINC01128 inhibited the regulatory effect of miR-16 inhibitor on HTR-8/Svneo cells. Conclusion: LINC01128/miR-16 is involved in HTR-8/SVneo cells by regulating the migration and invasion of human chorionic trophoblast cells

Self-renewing diploid Axin2(+) cells fuel homeostatic renewal of the liver.

The source of new hepatocytes in the uninjured liver has remained an open question. By lineage tracing using the Wnt-responsive gene Axin2 in mice, we identify a population of proliferating and self-renewing cells adjacent to the central vein in the liver lobule. These pericentral cells express the early liver progenitor marker Tbx3, are diploid, and thereby differ from mature hepatocytes, which are mostly polyploid. The descendants of pericentral cells differentiate into Tbx3-negative, polyploid hepatocytes, and can replace all hepatocytes along the liver lobule during homeostatic renewal. Adjacent central vein endothelial cells provide Wnt signals that maintain the pericentral cells, thereby constituting the niche. Thus, we identify a cell population in the liver that subserves homeostatic hepatocyte renewal, characterize its anatomical niche, and identify molecular signals that regulate its activity

Tissue Repair in the Mouse Liver Following Acute Carbon Tetrachloride Depends on Injury‐Induced Wnt/β‐Catenin Signaling

In the liver, Wnt/β-catenin signaling is involved in regulating zonation and hepatocyte proliferation during homeostasis. We examined Wnt gene expression and signaling after injury, and we show by in situ hybridization that Wnts are activated by acute carbon tetrachloride (CCl4 ) toxicity. Following injury, peri-injury hepatocytes become Wnt-responsive, expressing the Wnt target gene axis inhibition protein 2 (Axin2). Lineage tracing of peri-injury Axin2+ hepatocytes shows that during recovery the injured parenchyma becomes repopulated and repaired by Axin2+ descendants. Using single-cell RNA sequencing, we show that endothelial cells are the major source of Wnts following acute CCl4 toxicity. Induced loss of β-catenin in peri-injury hepatocytes results in delayed repair and ultimately injury-induced lethality, while loss of Wnt production from endothelial cells leads to a delay in the proliferative response after injury. Conclusion: Our findings highlight the importance of the Wnt/β-catenin signaling pathway in restoring tissue integrity following acute liver toxicity and establish a role of endothelial cells as an important Wnt-producing regulator of liver tissue repair following localized liver injury

Prevalence of sarcopenic obesity in the older non-hospitalized population: a systematic review and meta-analysis

Abstract Background Sarcopenic obesity emerges as a risk factor for adverse clinical outcomes in non-hospitalized older adults, including physical disabilities, metabolic diseases, and even mortality. In this systematic review and meta-analysis, we investigated the overall SO prevalence in non-hospitalized adults aged ≥ 65 years and assessed the sociodemographic, clinicobiological, and lifestyle factors related to SO. Methods We searched the PubMed, Embase, Cochrane Library, and Web of Science databases for studies reporting the prevalence of SO from database inception to October 2023. Two researchers independently screened the literature, evaluated the study quality, and extracted the data. Both fixed- and random-effects models were used in the meta-analysis to estimate the pooled SO prevalence and perform subgroup analyses. Publication and sensitivity bias analyses were performed to test the robustness of the associations. Results Among 46 studies eligible for review and a total of 71,757 non-hospitalized older adults, the combined prevalence of SO was 14% (95% CI:11–17%, I2 = 99.5%, P < 0.01). Subgroup analysis according to lifestyle factors demonstrated that the SO prevalence was 17% (95% CI: 8–29%, I2 = 99.5%, P < 0.01) in older adults without exercise habits. Regarding clinicobiological factors, older adults with a history of falls (15% [95% CI: 10–22%, I2 = 82%, P < 0.01]), two or more chronic diseases (19% [95% CI: 10–29%, I2 = 97%, P < 0.01]), functional impairment (33% [95% CI: 29–37%, I2 = 0%, P = 0.95]), cognitive impairment (35% [95% CI: 9–65%, I2 = 83%, P = 0.02]), osteoporosis (20% [95% CI: 8–35%, I2 = 96%, P < 0.01]), high fasting glucose level (17% [95% CI: 1–49%, I2 = 98%, P < 0.01]), or the use of antipsychotics (13% [95% CI: 2–28%, I2 = 0%, P = 0.32]) exhibited a higher SO prevalence. Conclusion SO prevalence is high among non-hospitalized older adults, especially those with functional and cognitive impairments. Thus, SO is a potential problem for the aging population; implementation of planned interventions in the community is needed to reduce the prevalence and adverse outcomes of SO