Emodin inhibits proliferation and invasion, and induces apoptosis in human esophageal cancer cell line ECA109

Purpose: To determine the anticancer effects of emodin in human esophageal carcinoma cell line ECA109.Methods: Cell viability was determined by MTT assay, while cell invasion and apoptosis were measured by Transwell assay and flow cytometry, respectively. Expression levels of MMP-2, Bax, Bcl-2 and caspase-3 proteins were determined by Western blot.Results: Flow cytometry data showed that the proportion of apoptotic cells was increased by emodin treatment. Apoptotic rates produced by 10, 20 and 50 μM emodin were 13.9 ± 3.8, 25.6 ± 6.2 and 39.8 ± 7.7 %, respectively. Transwell assay data revealed concentration-dependent suppression of the invasive rate of ECA109 cells by emodin (10, 20 and 50 μM) was 30.0 ± 4.5, 56.0 ± 6.8 and 69.0 ± 8.1 %, respectively. Furthermore, emodin treatment inhibited expressions of MMP-2 and Bcl-2 proteins, but induced the expression of Bax and caspase-3, when compared with control groups.Conclusion: These results suggest that emodin inhibits cell proliferation and cell invasion, but induces cell apoptosis in human esophageal cancer cell line ECA109. Thus, emodin is a potential candidate for development of an effective chemotherapeutic agent against esophageal cancer.Keywords: Emodin, Esophageal Cancer, Apoptosis, Cell invasion, Bax, Caspase-

The Influence of Deleterious Mutations on Adaptation in Asexual Populations

We study the dynamics of adaptation in asexual populations that undergo both beneficial and deleterious mutations. In particular, how the deleterious mutations affect the fixation of beneficial mutations was investigated. Using extensive Monte Carlo simulations, we find that in the “strong-selection weak mutation (SSWM)” regime or in the “clonal interference (CI)” regime, deleterious mutations rarely influence the distribution of “selection coefficients of the fixed mutations (SCFM)”; while in the “multiple mutations” regime, the accumulation of deleterious mutations would lead to a decrease in fitness significantly. We conclude that the effects of deleterious mutations on adaptation depend largely on the supply of beneficial mutations. And interestingly, the lowest adaptation rate occurs for a moderate value of selection coefficient of deleterious mutations

MonoHair: High-Fidelity Hair Modeling from a Monocular Video

Undoubtedly, high-fidelity 3D hair is crucial for achieving realism, artistic expression, and immersion in computer graphics. While existing 3D hair modeling methods have achieved impressive performance, the challenge of achieving high-quality hair reconstruction persists: they either require strict capture conditions, making practical applications difficult, or heavily rely on learned prior data, obscuring fine-grained details in images. To address these challenges, we propose MonoHair,a generic framework to achieve high-fidelity hair reconstruction from a monocular video, without specific requirements for environments. Our approach bifurcates the hair modeling process into two main stages: precise exterior reconstruction and interior structure inference. The exterior is meticulously crafted using our Patch-based Multi-View Optimization (PMVO). This method strategically collects and integrates hair information from multiple views, independent of prior data, to produce a high-fidelity exterior 3D line map. This map not only captures intricate details but also facilitates the inference of the hair's inner structure. For the interior, we employ a data-driven, multi-view 3D hair reconstruction method. This method utilizes 2D structural renderings derived from the reconstructed exterior, mirroring the synthetic 2D inputs used during training. This alignment effectively bridges the domain gap between our training data and real-world data, thereby enhancing the accuracy and reliability of our interior structure inference. Lastly, we generate a strand model and resolve the directional ambiguity by our hair growth algorithm. Our experiments demonstrate that our method exhibits robustness across diverse hairstyles and achieves state-of-the-art performance. For more results, please refer to our project page https://keyuwu-cs.github.io/MonoHair/.Comment: Accepted by IEEE CVPR 202

Anxiety Specific Response and Contribution of Active Hippocampal Neural Stem Cells to Chronic Pain Through Wnt/β-Catenin Signaling in Mice

Chronic pain usually results in persistent anxiety, which worsens the life quality of patients and complicates the treatment of pain. Hippocampus is one of the few brain regions in many mammalians species which harbors adult neural stem cells (NSCs), and plays a key role in the development and maintenance of chronic anxiety. Recent studies have suggested a potential involvement of hippocampal neurogenesis in modulating chronic pain. Whether and how hippocampal NSCs are involved in the pain-associated anxiety remains unclear. Here, we report that mice suffering persistent neuropathic pain showed a quick reduction of active NSCs in the ventral dentate gyrus (vDG), which was followed by the decrease of neurogenesis and appearance of anxiety. Wnt/β-catenin signaling, a key pathway in sustaining the active status of NSCs was suppressed in the vDG of mice suffering chronic pain. Depleting β-catenin by inducible Nestin-Cre significantly reduced the number of active NSCs and facilitated anxiety development, while expressing stabilized β-catenin amplified active NSCs and alleviated anxiety, indicating that Wnt activated NSCs is required for anxiety development under chronic pain. Treatment with Fluoxetine, the most widely used anxiolytic in clinic, significantly increased the proliferation of active NSCs and enhanced Wnt signaling. Interestingly, both β-catenin manipulation and Fluoxetine treatment had no significant effects on the pain thresholds. Therefore, our data demonstrated an anxiety-specific response and contribution of activated NSCs to chronic pain through Wnt/β-catenin signaling, which may be targeted for treating chronic pain- or other diseases-associated anxiety

Glycolysis mediates neuron specific histone acetylation in valproic acid-induced human excitatory neuron differentiation

Pregnancy exposure of valproic acid (VPA) is widely adopted as a model of environmental factor induced autism spectrum disorder (ASD). Increase of excitatory/inhibitory synaptic transmission ratio has been proposed as the mechanism of VPA induced ASD. How this happened, particularly at the level of excitatory neuron differentiation in human neural progenitor cells (NPCs) remains largely unclear. Here, we report that VPA exposure remarkably inhibited human NPC proliferation and induced excitatory neuronal differentiation without affecting inhibitory neurons. Following VPA treatment, mitochondrial dysfunction was observed before neuronal differentiation, as showed by ultrastructural changes, respiratory complex activity, mitochondrial membrane potential and oxidation levels. Meanwhile, extracellular acidification assay revealed an elevation of glycolysis by VPA stimulation. Interestingly, inhibiting glycolysis by 2-deoxy-d-glucose-6-phosphate (2-DG) efficiently blocked the excitatory neuronal differentiation of human NPCs induced by VPA. Furthermore, 2-DG treatment significantly compromised the VPA-induced expression of H3ac and H3K9ac, and the VPA-induced binding of H3K9ac on the promoter of Ngn2 and Mash1, two key transcription factors of excitatory neuron fate determination. These data, for the first time, demonstrated that VPA biased excitatory neuron differentiation by glycolysis-mediated histone acetylation of neuron specific transcription factors

α1A-Adrenergic Receptor Induces Activation of Extracellular Signal-Regulated Kinase 1/2 through Endocytic Pathway

G protein-coupled receptors (GPCRs) activate mitogen-activated protein kinases through a number of distinct pathways in cells. Increasing evidence has suggested that endosomal signaling has an important role in receptor signal transduction. Here we investigated the involvement of endocytosis in α1A-adrenergic receptor (α1A-AR)-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Agonist-mediated endocytic traffic of α1A-AR was assessed by real-time imaging of living, stably transfected human embryonic kidney 293A cells (HEK-293A). α1A-AR was internalized dynamically in cells with agonist stimulation, and actin filaments regulated the initial trafficking of α1A-AR. α1A-AR-induced activation of ERK1/2 but not p38 MAPK was sensitive to disruption of endocytosis, as demonstrated by 4°C chilling, dynamin mutation and treatment with cytochalasin D (actin depolymerizing agent). Activation of protein kinase C (PKC) and C-Raf by α1A-AR was not affected by 4°C chilling or cytochalasin D treatment. U73122 (a phospholipase C [PLC] inhibitor) and Ro 31–8220 (a PKC inhibitor) inhibited α1B-AR- but not α1A-AR-induced ERK1/2 activation. These data suggest that the endocytic pathway is involved in α1A-AR-induced ERK1/2 activation, which is independent of Gq/PLC/PKC signaling

Automatic 3D tooth segmentation using convolutional neural networks in harmonic parameter space

Automatic segmentation of 3D tooth models into individual teeth is an important step in orthodontic CAD systems. 3D tooth segmentation is a mesh instance segmentation task. Complex geometric features on the surface of 3D tooth models often lead to failure of tooth boundary detection, so it is difficult to achieve automatic and accurate segmentation by traditional mesh segmentation methods. We propose a novel solution to address this problem. We map a 3D tooth model isomorphically to a 2D harmonic parameter space and convert it into an image. This allows us to use a CNN to learn a highly robust image segmentation model to achieve automated and accurate segmentation of 3D tooth models. Finally, we map the image segmentation mask back to the 3D tooth model and refine the segmentation result using an improved Fuzzy Clustering-and-Cuts algorithm. Our method has been incorporated into an orthodontic CAD system, and performs well in practice

Corporate Inventory Adjustment and the Effectiveness of Fiscal Policy in China

For many years, China has been very much conservative in fiscal expansion. In this paper, we analyze the impact of economic policy uncertainty on the adjustment of corporate inventory holdings, as well as its intrinsic mechanism and economic consequences. The empirical results show that the increase in policy uncertainty has a significant and negative effect on the level of corporate inventories, and non-SOEs are affected more than SOEs. In addition, we find that the larger the financial constraints or the better the external governance, the greater the inhibitory effect of policy uncertain on inventory investment. In summary, policy uncertainty may lead to an increase in corporate cash holdings and a reduction in inventories through the deterioration of the financing environment and the increase of business risk. The main issues are examined with a view to providing policy recommendations that would allow to maintain robust growth in a sustainable manne