77 research outputs found
Block Chain based Searchable Symmetric Encryption
The mechanism for traditional Searchable Symmetric Encryption is pay-then-use. That is to say, if a user wants to search some documents that contain special keywords, he needs to pay to the server firstly, then he can enjoy search service. Under this situation, these kinds of things will happen: After the user paying the service fees, the server may either disappear because of the poor management or returning nothing. As a result, the money that the user paid cannot be brought back quickly. Another case is that the server may return incorrect document sets to the user in order to save his own cost. Once such events happen, it needs the arbitration institution to mediate which will cost a long time. Besides, to settle the disputes the user has to pay to the arbitration institution. Ideally, we deeply hope that when the user realizes the server has a tendency to cheat in the task of searching, he can immediately and automatically withdraw his money to safeguard his right. However, the existing SSE protocols cannot satisfy this demand.
To solve this dilemma, we find a compromised method by introducing the block chain into SSE. Our scheme achieves three goals stated below. Firstly, when the server does not return any thing to user after he gets the search token, the user can get some compensation from the server, because the server can infer some important information from the Index and this token. Besides, the user also doesn\u27t pay the service charge. Secondly, if the documents that the server returns are false, the server cannot receive service fees, meanwhile, he will be punished. Lastly, when the user receives some bitcoin from server at the beginning, he may terminate the protocol. Under this situation, the server is a victim. In order to prevent such thing from happening, the server will broadcast a transaction to redeem his pledge after an appointed time
Preparation and enhanced properties of Fe3O4 nanoparticles reinforced polyimide nanocomposites
Polyimide (PI) nanocomposite reinforced with Fe3O4 nanoparticles (NPs) at various NPs loadings levels of 5.0, 10.0, 15.0, and 20.0 wt% were prepared. The chemical interactions of the Fe3O4 NPs/PI nanocomposites were characterized using Fourier Transform Infrared (FT-IR) spectroscopy. X-ray Diffraction (XRD) results revealed that the addition of NPs had a significant effect on the crystallization of PI. Scanning electron microscope (SEM) and the atomic force microscope (AFM) were used to characterize the dispersion and surface morphology of the Fe3O4 NPs and the PI nanocomposites. The obtained optical band gap of the nanocomposites characterized using Ultraviolet-Visible Diffuse Reflectance Spectroscopy (UV-Vis DRS) was decreased with increasing the Fe3O4 loading. Differential scanning calorimetry (DSC) results showed a continuous increase of Tg with increasing the Fe3O4 NPs loading. Some differences were observed in the onset decomposition temperature between the pure PI and nanocomposites since the NPs and the PI matrix were physically entangled together to form the nanocomposites. The contact angle of pure PI was larger than that of Fe3O4/PI nanocomposites films, and increased with increasing the loading of Fe3O4. The degree of swelling was increased with increasing the Fe3O4 loading and the swelling time. The dielectric properties of the nanocomposite were strongly related to the Fe3O4 loading levels. The Fe3O4/PI magnetic property also had been improved with increasing the loading of the magnetic nanoparticles
The Protective Effect of Magnesium Lithospermate B on Hepatic Ischemia/Reperfusion via Inhibiting the Jak2/Stat3 Signaling Pathway
Acute inflammation is an important component of the pathogenesis of hepatic ischemia/reperfusion injury (HIRI). Magnesium lithospermate B (MLB) has strong neuroprotective and cardioprotective effects. The purpose of this study was to determine whether MLB had underlying protective effects against hepatic I/R injury and to reveal the potential mechanisms related to the hepatoprotective effects. In this study, we first examined the protective effect of MLB on HIRI in mice that underwent 1 h ischemia followed by 6 h reperfusion. MLB pretreatment alleviated the abnormal liver function and hepatocyte damage induced by I/R injury. We found that serum inflammatory cytokines, including IL-6, IL-1ÎČ, and TNF-α, were significantly decreased by MLB during hepatic ischemia/reperfusion (I/R) injury, suggesting that MLB may alleviate hepatic I/R injury via inhibiting inflammatory signaling pathways. Second, we investigated the protein level of p-Jak2/Jak2 and p-Stat3/Stat3 using Western blotting and found that MLB could significantly inhibit the activation of the Jak2/Stat3 signaling pathway, which was further verified by AG490 in a mouse model. Finally, the effect of MLB on the Jak2/Stat3 pathway was further assessed in an in vitro model of RAW 264.7 cells; 1 ”g/ml LPS induced the secretion of inflammatory mediators, including IL-6, TNF-α, and activation of the Jak2/Stat3 signaling pathway. MLB significantly inhibited the abnormal secretion of inflammatory factors and the activation of the Jak2/Stat3 signaling pathway in RAW264.7 cells. In conclusion, MLB was found for the first time to reduce inflammation induced by hepatic I/R via suppressing the Jak2/Stat3 pathway
Effects of 6-Hydroxykaempferol: A Potential Natural Product for Amelioration of Tendon Impairment
Tendon impairment is a common injury associated with impairment of range of motion and pain. Currently, evidence has confirmed that natural herbs contribute to orthopedics and have shown excellent results in the clinical management of tendon impairment. Shujin Huoxue tablet (SHT) and its complex prescriptions are regularly used in tendon rupture therapy with positive results. This study aimed to discover the potential molecules that promote tendon healing. The Chinese traditional medicine system pharmacological database analysis platform (TCMSP) is the primary resource. The Traditional Chinese Medicine Integrated Database and Encyclopedia of Traditional Chinese Medicine database were used as secondary databases. The GeneCards database was used to search for reported tendinopathy-related genes by keywords. Functions of the targeted genes were analyzed using Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes. Proteinâprotein interaction information was extracted from the STRING database. Docking study, MTT assay, quantitative real-time PCR, and migration assays were performed to obtain a better understanding of the herbs according to cell function to test the basic pharmacological action in vitro. A total of 104 disease nodes, 496 target gene nodes, 35 ingredient nodes, and one drug node were extracted. According to the TCMSP database, 6-hydroxykaempferol, which reportedly promotes the proliferation of microvascular endothelial cells, is a molecule found in SHT. We found that it promoted the proliferation and migration of tendon fibroblasts and elevated tendon repair-related gene expression. Purified 6-hydroxykaempferol promoted the proliferation and migration of tendon fibroblasts and increased their mRNA expression in tendon proliferation
Resveratrol: A Multifunctional Compound Improving Endothelial Function: Editorial to: âResveratrol Supplementation Gender Independently Improves Endothelial Reactivity and Suppresses Superoxide Production in Healthy Ratsâ by S. Soylemez et al.
The red wine polyphenol resveratrol boosts endothelium-dependent and -independent vasorelaxations. The improvement of endothelial function by resveratrol is largely attributable to nitric oxide (NO) derived from endothelial NO synthase (eNOS). By stimulating eNOS expression, eNOS phosphorylation and eNOS deacetylation, resveratrol enhances endothelial NO production. By upregulating antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and suppressing the expression and activity of NADPH oxidases, resveratrol inhibits superoxide-mediated NO inactivation. Some resveratrol effects are mediated by sirtuin 1 (SIRT1) or estrogen receptors, respectively
3D structure of a heparin mimetic analogue of a FGF-1 activator. A NMR and molecular modelling study
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