58 research outputs found

    Ursolic Acid Inhibits Proliferation and Induces Apoptosis of Cancer Cells In Vitro and In Vivo

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    The aims of the study are to explore the effect of ursolic acid (UA) on the growth of gastric cancer cell line BGC-803 and hepatocellular cancer cell H22 xenograft and to understand the mechanism. UA inhibits growth of BGC-803 cells in vitro in dose-dependent and time-dependent manner. Treated with UA in vivo, tumor cells can be arrested to G0/G1 stage. The apoptotic rate was significantly increased in tumor cells treated with UA both in vitro and in vivo. DNA fragmentation was found in BGC-803 cells exposed to UA. UA activated caspase-3, -8, and -9 and down regulated expression of Bcl-2 in BGC-803 cells. The expression of caspase-3 and -8 was elevated in tumor cells from xenograft treated with UA. 18F-FLT PET-CT imaging confirmed tumor model and UA effectiveness. Our results indicated that UA inhibits growth of tumor cells both in vitro and in vivo by decreasing proliferation of cells and inducing apoptosis

    Regulatory mechanism of circular RNA involvement in osteoarthritis

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    Osteoarthritis (OA) causes joint pain, stiffness, and dysfunction in middle-aged and older adults; however, its pathogenesis remains unclear. Circular RNAs (circRNAs) are differentially expressed in patients with OA and participate in a multigene, multitarget regulatory network. CircRNAs are involved in the development of OA through inflammatory responses, including proliferation, apoptosis, autophagy, differentiation, oxidative stress, and mechanical stress. Most circRNAs are used as intracellular miRNA sponges in chondrocytes, endplate chondrocytes, mesenchymal stem cells, synoviocytes, and macrophages to promote the progression of OA. However, a small portion of circRNAs participates in the pathogenesis of OA by intracellular mechanisms, such as protein binding, methylation, or intercellular exosome pathways. In this sense, circRNAs might serve as potential novel biomarkers and therapeutic targets for OA

    The relationship between the interactive behavior of industry–university–research subjects and the cooperative innovation performance: The mediating role of knowledge absorptive capacity

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    IntroductionIndustry–university–research cooperation innovation, which is often characterized by resource complementarity and the sharing technology, has become one of the most preferred innovation cooperation methods for enterprises. However, various problems still occur in the process of industry–university–research cooperations, such as poor innovation performance and difficulty in sustaining cooperation. Existing studies mostly focus on the macroscopic perspectives of geographic location, cooperation scale, concentration, and diversification of industry–university–research cooperation subjects, and fail to explore the microscopic behavioral mechanisms.MethodsTherefore, this paper establishes the interactive behavior of industry–university–research subjects and defines its concepts and dimensions in an attempt to provide a mechanism for improving the cooperative innovation performance of industry–university–research from the micro-behavioral perspective. On the basis of theoretical analysis, this paper develops a model of the relationship between cooperative trust, cooperative communication, and cooperative innovation performance for interactive behavior, while exploring the mediating role of knowledge absorptive capacity. The model was validated by stepwise regression using data from 325 questionnaires.ResultsThe paper found that cooperative trust and cooperative communication in the cooperative interactive behavior of industry–university–research positively contribute to the improvement of cooperative innovation performance. Knowledge absorptive capacity plays a partially mediating role between the interactive behaviors and cooperative innovation performance. More specifically, knowledge absorptive capacity partially mediates cooperative communication in cooperative innovation performance and completely mediates cooperative trust in cooperative innovation performance. The results are largely consistent with the results of the heterogeneity analysis of the sample.DiscussionThis paper not only explains why the cooperative innovation performance of industry–university–research is poor from the perspective of interactive behavior, but also enriches the research perspective of industry–university–research and provides theoretical support for enterprises to optimize the relationship between industry, university, and research institutes

    The FilZ protein contains a single PilZ domain and facilitates the swarming motility of pseudoalteromonas sp. SM9913

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    Swarming regulation is complicated in flagellated bacteria, especially those possessing dual flagellar systems. It remains unclear whether and how the movement of the constitutive polar flagellum is regulated during swarming motility of these bacteria. Here, we report the downregulation of polar flagellar motility by the c-di-GMP effector FilZ in the marine sedimentary bacterium Pseudoalteromonas sp. SM9913. Strain SM9913 possesses two flagellar systems, and filZ is located in the lateral flagellar gene cluster. The function of FilZ is negatively controlled by intracellular c-di-GMP. Swarming in strain SM9913 consists of three periods. Deletion and overexpression of filZ revealed that, during the period when strain SM9913 expands quickly, FilZ facilitates swarming. In vitro pull-down and bacterial two-hybrid assays suggested that, in the absence of c-di-GMP, FilZ interacts with the CheW homolog A2230, which may be involved in the chemotactic signal transduction pathway to the polar flagellar motor protein FliMp, to interfere with polar flagellar motility. When bound to c-di-GMP, FilZ loses its ability to interact with A2230. Bioinformatic investigation indicated that filZ-like genes are present in many bacteria with dual flagellar systems. Our findings demonstrate a novel mode of regulation of bacterial swarming motility

    An Image Enhancement Method Using the Quantum-Behaved Particle Swarm Optimization with an Adaptive Strategy

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    Image enhancement techniques are very important to image processing, which are used to improve image quality or extract the fine details in degraded images. In this paper, two novel objective functions based on the normalized incomplete Beta transform function are proposed to evaluate the effectiveness of grayscale image enhancement and color image enhancement, respectively. Using these objective functions, the parameters of transform functions are estimated by the quantum-behaved particle swarm optimization (QPSO). We also propose an improved QPSO with an adaptive parameter control strategy. The QPSO and the AQPSO algorithms, along with genetic algorithm (GA) and particle swarm optimization (PSO), are tested on several benchmark grayscale and color images. The results show that the QPSO and AQPSO perform better than GA and PSO for the enhancement of these images, and the AQPSO has some advantages over QPSO due to its adaptive parameter control strategy

    Genetic variants of SLC12A3 modulate serum lipid profiles in a group of Mongolian pedigree population

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    Abstract Background The serum lipid profile, including LDL-C level, is associated with hypertension which is the major cause of cerebrovascular disease (CVD) amounting 30% of global death rate. Previous work also demonstrated important roles of genetic variants of SLC12A3 gene on human CVD, hypertension and other diseases in Mongolian population. However, the relationship between SLC12A3 gene polymorphisms on individuals’ lipid profile is still unknown. Methods A panel of 15 SNPs of SLC12A3 gene was genotyped within a 424 Mongolians pedigree cohort. The associations between SLC12A3 polymorphisms and four lipid profiles were analyzed by family-based association test (FBAT) and confirmed with haplotype analysis. Results From both single site and haplotype analyses, the results demonstrated a close relationship between SLC12A3 polymorphisms and LDL-C level. Two SNPs, rs5803 and rs711746 showed significant associations with individuals’ serum LDL-C level (z = − 2.08, P -e  = 0.038; z = 2.09, P -e  = 0.023, respectively), and distribution of haplotypes constructed by two SNPs also associated with participants’ serum LDL-C level, significantly (Global Chi 2 = 9.06 df = 3, P = 0.028). Conclusion Our results demonstrated the importance of SLC12A3 polymorphisms in individuals’ difference about their serum lipid profiles, thereby providing evidence that the genetic variants may contribute to CVD development via modulating person’s LDL-C level and blood pressure, in certain contexts

    Polymorphisms in the SLC12A3 Gene Encoding Sodium-Chloride Cotransporter are Associated with Hypertension: A Family-Based Study in the Mongolian Population

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    Background/Aims: Hypertension or persistent high blood pressure (BP) is a leading cause of death worldwide. Extensive evidence indicates that the thiazide-sensitive Na+-Cl- cotrans-porter (NCC) affects BP via regulation of renal sodium reabsorption. However, the relationship between genetic variants of the NCC-encoding SLC12A3 gene and hypertension in the Mongolian population is still ambiguous. In this study, we aimed to genotype an extended cohort of hypertensive Mongolian families for polymorphisms in the SLC12A3 locus. Methods: Eighty-eight families with a history of hypertension, including parents, offspring, and relatives underwent clinical testing. Family-based association tests and haplotype analysis were used to evaluate the association between hypertension and polymorphisms in the SLC12A3 locus. Results: We identified three single nucleotide polymorphisms (SNPs), one in the SLC12A3 coding region (p = 0.05) and two in the intron (p = 0.02 and p = 0.07), which were significantly associated with the hypertension phenotype. Haplotype-specific association tests confirmed the correlation of these SNPs with hypertension (p Conclusion: These results suggest that SNPs in the SLC12A3 gene confer susceptibility to hypertension in the Mongolian population. Further research is needed to validate the functional role of SLC12A3 polymorphisms in hypertension
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