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With the improvement of China’s living standards and the development of digital economy, consumers are not only pursuing simple material consumption, but also need to obtain psychological and spiritual needs of consumption. The marketing promotion model of co-branded cooperation between enterprises and IP has gradually developed and expanded while meeting the needs of consumers and has become a new way of win-win cooperation between enterprises. This paper aims to explore the connection between client buying intentions and their perception of the value of IP co-branded items. This paper collects sample data through network questionnaire survey and utilizes the statistical tool SPSS to verify and validate the info. The findings showcase that IP co-branded items boost client buying decision indirectly through how they view worth. Moreover, co-branded IP goods enhance client impressions of worth, which in turn boosts buyer intentions. Theoretically, this article presents the content of the research for elements changing consumer opinions regarding worth and plans to shop and provides reference value and enlightenment for enterprises in business cooperation.

Farnesoid X receptor (FXR) is a nuclear receptor known to play protective roles in anti-hepatocarcinogenesis and regulation of the basal metabolism of glucose, lipids, and bile acids. FXR expression is low or absent in HBV-associated hepatocarcinogenesis. Full-length HBx and HBx C-terminal truncation are frequently found in clinical HCC samples and play distinct roles in hepatocarcinogenesis by interacting with FXR or FXR signaling. However, the impact of C-terminal truncated HBx on the progression of hepatocarcinogenesis in the absence of FXR is unclear. In this study, we found that one known FXR binding protein, a C-terminal truncated X protein (HBx C40) enhanced obviously and promoted tumor cell proliferation and migration by altering cell cycle distribution and inducing apoptosis in the absence of FXR. HBx C40 enhanced the growth of FXR-deficient tumors in vivo. In addition, RNA-sequencing analysis showed that HBx C40 overexpression could affect energy metabolism. Overexpressed HSPB8 aggravated the metabolic reprogramming induced by down-regulating glucose metabolism-associated hexokinase 2 genes in HBx C40-induced hepatocarcinogenesis. Overall, our study suggests that C-terminal truncated HBx C40 synergizes with FXR deficiency by altering cell cycle distribution as well as disturbing glucose metabolism to promote HCC development.

Myocardial ischemia/reperfusion (I/R) injury is a potential complication of ischemic heart disease after recanalization. One of the primary reasons for I/R injury is the excessive accumulation of reactive oxygen species (ROS) in cardiomyocytes. Verapamil, a classic calcium channel blocker, has the potential to mitigate I/R-evoked oxidative stress. However, the underlying mechanisms have not been fully elucidated. SIRT1 is an essential regulator of I/R and offers resistance to oxidative stress arising from I/R. It is still inconclusive if verapamil can reduce myocardial I/R-triggered oxidative damage through modulating SIRT1 antioxidant signaling. To verify our hypothesis, the H9c2 cardiomyocytes and the mice were treated with verapamil and then exposed to hypoxia/reoxygenation (H/R) or I/R in the presence or absence of the SIRT1 inhibitor EX527. As expected, verapamil stimulated SIRT1 antioxidant signaling evidenced by upregulation of SIRT1, FoxO1, SOD2 expressions and downregulation of Ac-FoxO1 expression in vitro and in vivo . In addition, verapamil remarkably suppressed H/R and I/R-induced oxidative stress proven by declined ROS level and MDA content. The cardioprotective actions of verapamil via SIRT1 were further confirmed in the experiments with the presence of the specific SIRT1 inhibitor EX527. We demonstrated that verapamil alleviated myocardial I/R-evoked oxidative stress partially via activation of SIRT1 antioxidant signaling. Subsequently, verapamil protected against cardiac dysfunction and myocardial infarction accompanied by oxidative stress.

In recent years, deep convolutional neural network-based segmentation methods have achieved state-of-the-art performance for many medical analysis tasks. However, most of these approaches rely on optimizing the U-Net structure or adding new functional modules, which overlooks the complementation and fusion of coarse-grained and fine-grained semantic information. To address these issues, we propose a 2D medical image segmentation framework called Progressive Learning Network (PL-Net), which comprises Internal Progressive Learning (IPL) and External Progressive Learning (EPL). PL-Net offers the following advantages: 1) IPL divides feature extraction into two steps, allowing for the mixing of different size receptive fields and capturing semantic information from coarse to fine granularity without introducing additional parameters; 2) EPL divides the training process into two stages to optimize parameters and facilitate the fusion of coarse-grained information in the first stage and fine-grained information in the second stage. We conducted comprehensive evaluations of our proposed method on five medical image segmentation datasets, and the experimental results demonstrate that PL-Net achieves competitive segmentation performance. It is worth noting that PL-Net does not introduce any additional learnable parameters compared to other U-Net variants.

Hepatocellular carcinoma (HCC) is one of the most common malignancies around the world. Among the risk factors involved in liver carcinogenesis, hepatitis B virus (HBV) X protein (HBx) is considered to be a key regulator in hepatocarcinogenesis. Whether HBx promotes or protects against HCC remains controversial, therefore exploring new HBx-associated genes is still important. HBx was overexpressed in HepG2, HepG2.2.15 and SMMC-7721 cell lines, primary mouse hepatocytes and livers of C57BL/6N mice. High-throughput RNA sequencing profiling of HepG2 cells with HBx overexpression and related differentially-expressed genes (DEGs), pathway enrichment analysis, protein-protein interaction networks (PPIs), overlapping analysis were conducted. In addition, Gene Expression Omnibus (GEO) and proteomic datasets of HBV-positive HCC datasets were used to verify the expression and prognosis of selected DEGs. Finally, we also evaluated the known oncogenic role of HBx by oncogenic array analysis. A total of 523 DEGs were obtained from HBx-overexpressing HepG2 cells. Twelve DEGs were identified and validated in cells transiently transfected with HBx and three datasets of HBV-positive HCC transcription profiles. In addition, using the Kaplan-Meier plotter database, the expression levels of the twelve different genes were further analyzed to predict patient outcomes. Among the 12 identified HBx-associated hub genes, HBV-positive HCC patients expressing and showed a good overall survival (OS) and relapse-free survival (RFS). Thus, and expression could be potential prognostic markers.

Background Cervical cancer is the second most common cancer among women living in developing countries. Farnesoid X receptor (FXR) is a member of the nuclear receptor family, which regulates the development and proliferation of cancer. However, the role of and molecular mechanism by which FXR acts in cervical cancer are still unknown. Methods and results The relationship between FXR and the proliferation of cervical cancer cell lines was detected by MTT and colony formation assays. Immunohistochemistry was used to detect the expression of FXR in cervical cancer tissue slides. Western blotting was used to detect the expression of p14 ARF , mouse double minute 2 (MDM2) and p53 when FXR was overexpressed or siRNA was applied. Western blotting was used to detect the expression of MDM2 and p53 when pifithrin-α (PFT-α) was applied. FXR activation inhibited the proliferation of cervical cancer cell lines. FXR was significantly decreased in cervical squamous cell carcinoma, which was correlated with TNM stage, but not with metastasis. Overexpression of FXR activated the p14 ARF -MDM2-p53 pathway. As a p53 inhibitor, PFT-α increased MDM2 in Lenti-vector cells, but had no effect on MDM2 in Lenti-FXR cells. Conclusions FXR inhibits cervical cancer by upregulating the p14 ARF -MDM2-p53 pathway. Activation of FXR may be a potential strategy for the treatment of cervical cancer.

Cardiac microvascular endothelial cell (CMEC) dysfunction is considered as a major contributor to the cardiovascular complications in diabetes mellitus, with oxidative stress caused by hyperglycemia playing a critical role in the progression of CMEC dysfunction. Melatonin is a kind of hormone well known for its antioxidant properties, which has potential protective effects against diabetes mellitus and its complications. However, the role of melatonin on CMEC dysfunction caused by hyperglycemia and its molecular mechanisms underlying these effects has not been clarified. Herein, we investigate the protective effects of melatonin on high glucose- (HG-) evoked oxidative stress and apoptosis in CMECs and underlying mechanisms. Our results revealed that melatonin ameliorated the injury caused by HG in primary cultured rat CMECs. Injury can be accompanied by reduced reactive oxygen species (ROS) and malondialdehyde (MDA) production, and enhanced superoxide dismutase (SOD) activity. Meanwhile, melatonin treatment significantly inhibited HG-induced CMEC apoptosis. Moreover, melatonin increased the activity of the AMPK/SIRT1 signaling axis in CMECs under HG condition, whereas administration of the AMPK inhibitor compound C or SIRT1 silencing partially abrogated the beneficial effects of melatonin. In streptozotocin- (STZ-) evoked diabetic mice, melatonin notably ameliorated cardiac dysfunction and activated the AMPK/SIRT1 signaling. In conclusion, our findings revealed that melatonin attenuates HG-induced CMEC oxidant stress, apoptosis injury, and STZ-induced cardiac dysfunction through regulating the AMPK/SIRT1 signaling pathway.

Cervical cancer is the second most common cancer among women living in developing countries. Farnesoid X receptor (FXR) is a member of the nuclear receptor family, which regulates the development and proliferation of cancer. However, the role of and molecular mechanism by which FXR acts in cervical cancer are still unknown. The relationship between FXR and the proliferation of cervical cancer cell lines was detected by MTT and colony formation assays. Immunohistochemistry was used to detect the expression of FXR in cervical cancer tissue slides. Western blotting was used to detect the expression of p14 , mouse double minute 2 (MDM2) and p53 when FXR was overexpressed or siRNA was applied. Western blotting was used to detect the expression of MDM2 and p53 when pifithrin-α (PFT-α) was applied. FXR activation inhibited the proliferation of cervical cancer cell lines. FXR was significantly decreased in cervical squamous cell carcinoma, which was correlated with TNM stage, but not with metastasis. Overexpression of FXR activated the p14 -MDM2-p53 pathway. As a p53 inhibitor, PFT-α increased MDM2 in Lenti-vector cells, but had no effect on MDM2 in Lenti-FXR cells. FXR inhibits cervical cancer by upregulating the p14 -MDM2-p53 pathway. Activation of FXR may be a potential strategy for the treatment of cervical cancer.

[This corrects the article DOI: 10.1155/2021/8882130.].

Pim-1 is an oncogenic serine/threonine protein kinase that is involved in several different functions such as cytokine induced signal transductions, cell proliferation and differentiation, and in lymphomagenesis and leukemogenesis. The SOCS1 and SOCS3 suppressors of cytokine signaling were found to be two of the potential targets of the Pim-1 kinase. Pim-1 kinase can phosphorylate SOCS1 and SOCS3, which stabilizes them and potentiates their inhibitory effects of on the JAK/STAT signaling pathway. Two crystal structures of human Pim-1 protein kinase were determined, the apo structure and the binary complex with Mg2+-adenylyl imidodiphosphate (AMPPNP) both to a resolution of 2.45Å. The overall structure of Pim-1 is similar to those in the catalytic domains of other protein kinases. It consists of two subdomains joined by a hinge on one edge. The catalytic site is located in the cleft between the subdomains. The Pim-1 kinase is constitutively active without the need for an activating phosphorylation as is essential for many kinases. The binary complex structure exhibits a relatively closed conformation of the domains which is similar to that of cyclic-AMP dependent protein kinase (cAPK) complexed with ATP and inhibitor peptide substrates. In Pim-1, an aspartate residue replaces the phosphorylated residue that is located in the activation loop of many protein kinases. This activation aspartate interacts with a conserved arginine adjacent to the catalytic aspartate in a similar manner to the phosphorylated activation residue in other protein kinases.