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An iodine-catalyzed methyl azaarene sp3 C–H functionalization has been developed for the synthesis of pyrazolooxepinopyrazolones. This method has wide range of substrates, low catalyst loading, good functional group tolerance and metal-free conditions.

Background: Osteoarthritis (OA) is a common type of degenerative joint diseases that is regulated by a combination of complex intercellular signals and modulators, including non-coding RNAs. Mounting evidence suggests that miR-31-5p is physiologically involved in the regulation of chondrocytes, but the mechanism remains unclear. Methods: Expression levels of miR-31-5p and SOX4 in OA cartilage tissues and in IL-1β-stimulated chondrocytes were examined by quantification polymerase chain reaction (q-PCR) or immunohistochemistry assays. Cell proliferation and apoptosis were detected by Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. Expression of LC3 was detected using immunofluorescence staining. Expressions of autophagy-related proteins and extracellular regulated protein kinase (ERK)/mechanical target of rapamycin kinase (mTORC1) signal-related proteins were measured by Western blot analysis. Molecular interaction was validated by dual luciferase reporter assay. Results: Downregulation of miR-31-5p and upregulation of SOX4 were observed in both OA patients and OA chondrocytes. Mechanistic experiments revealed that miR-31-5p negatively modulated SOX4 expression by directly targeting its 3′- untranslated region. Moreover, overexpression of miR-31-5p suppressed the activation of mTORC1 in an ERK-dependent manner by inhibiting SOX4. Further functional experiments demonstrated that overexpressing miR-31-5p in OA chondrocytes markedly promoted its proliferation and autophagy while inhibiting apoptosis. However, these effects were abolished by overexpression of SOX4 or treatment with 3BDO, an mTOR activator. Conclusion: These results demonstrated that miR-31-5p enhanced survival and autophagy of OA chondrocytes through inactivation of mTORC1 via directly targeting SOX4, suggesting that miR-31-5p may play a protective role in OA progression.

Background: Ischemia-reperfusion (I/R) injury is the main cause of acute kidney injury (AKI), and its incidence and mortality increase year by year in the population. Dexmedetomidine (DEX) can improve AKI by regulating inflammation and oxidative stress, but its mechanism is still unclear. Methods: A hypoxia/reoxygenation (H/R) model of HK-2 cells and a kidney I/R model of C57BL/6J mice were established. In the experiment, cells were transfected with sh-PGC-1α to inhibit PGC-1α expression. The changes of ROS level and mitochondrial membrane potential (MMP) were analyzed. HE staining was used to assess kidney damage in mice. Concentration of kidney injury markers serum creatinine and blood urea nitrogen and expression of inflammatory factors were detected by ELISA. qPCR analysis was used to detect mRNA levels of related proteins in cells and mouse kidney tissues. The protein intracellular content and phosphorylation levels were determined by Western blotting. Result: The production of inflammatory factors and ROS was increased in HK-2 cells treated with H/R, while MMP, cell viability, and mitochondrial-related protein levels were decreased. DEX attenuated pathological changes induced by H/R, while knockdown of PGC-1α eliminated the mitigation effect. DEX inhibited the damage of I/R to the kidneys of mice and increased the expression of mitochondrial-related proteins and PGC-1α in the kidneys, while inhibiting the phosphorylation of STAT1 and the expression of IRF-1. Conclusions: DEX appears to inhibit mitochondrial damage and cellular inflammation by upregulating PGC-1α to affect STAT1 phosphorylation level and IRF-1 expression, thereby preventing AKI.

An iodine-catalyzed methyl azaarene sp

To investigate the expression level of microRNA-101-3p (miR-101-3p) and its possible association with progression, prognosis and chemotherapy in patients with non-small cell lung cancer (NSCLC), the Gene Expression Omnibus (GEO) database was used. Quantitative polymerase chain reaction was used to verify the expression in 327 NSCLC and 42 adjacent normal lung tissues, of which 42 viable tissues were paired with nearby normal lung tissues. Based on the Cox regression model, univariate and multivariate analyses were used to address the factors that had effects on overall survival (OS) and disease-free survival (DFS) rate. Data from the GEO database demonstrated that the miR-101-3p expression in NSCLC was downregulated, compared with normal lung cancer. Survival analysis through univariate and multivariate models indicated that the miR-101-3p expression level was a crucial risk factor for OS and DFS in patients with NSCLC. A number of clinical parameters were determined to be associated with miR-101-3p expression, including tumor diameter, lymph node metastasis and tumor-node-metastasis stage. Adjuvant chemotherapy with high expression of miR-101-3p was determined to increase OS and DFS in patients with NSCLC, compared with patients with de novo or low expression of miR-101-3p. The present results demonstrated that miR-101-3p expression levels were associated with NSCLC progression and prognosis, which indicated that miR-101-3p may serve as a biomarker for patients with NSCLC who have received adjuvant chemotherapy.

// Ying-Chun Song 1, * , Gai-Xia Lu 1, * , Hong-Wei Zhang 2, * , Xiao-Ming Zhong 3, * , Xian-Ling Cong 4, * , Shao-Bo Xue 1, * , Rui Kong 1, * , Dan Li 1 , Zheng-Yan Chang 5 , Xiao-Feng Wang 6 , Yun-Jie Zhang 6 , Ran Sun 4 , Li Chai 1 , Ru-Ting Xie 5 , Ming-Xiang Cai 1 , Ming Sun 1 , Wei-Qing Mao 1 , Hui-Qiong Yang 5 , Yun-Chao Shao 6 , Su-Yun Fan 1 , Ting-Miao Wu 1 , Qing Xia 6 , Zhong-Wei Lv 1 , David A. Fu 6 and Yu-Shui Ma 1, 7 1 Department of Nuclear Medicine, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China 2 Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China 3 Department of Radiology, Jiangxi Provincial Tumor Hospital/Ganzhou City People’s Hospital, Nanchang 330029, China 4 Department of Biobank, China-Japan Unoin Hospital, Jilin University, Changchun 130033, China 5 Department of Pathology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China 6 Department of Orthopedic Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China 7 Shanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, College of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China * These authors have contributed equally to this work Correspondence to: Zhong-Wei Lv, email: shtjnmd@163.com David A. Fu, email: 061101021@fudan.edu.cn Yu-Shui Ma, email: mayushui2015@126.com Keywords: GBM, glioma, proteomics analysis, gene expression analysis, Bioinformatics Analysis Received: May 24, 2017 Accepted: August 26, 2017 Published: October 19, 2017 ABSTRACT Glioblastoma multiforme (GBM), the most aggressive and lethal primary brain tumor, is characterized by very low life expectancy. Understanding the genomic and proteogenomic characteristics of GBM is essential for devising better therapeutic approaches.Here, we performed proteomic profiling of 8 GBM and paired normal brain tissues. In parallel, comprehensive integrative genomic analysis of GBM was performed in silico using mRNA microarray and sequencing data. Two whole transcript expression profiling cohorts were used - a set of 3 normal brain tissues and 22 glioma tissue samples and a cohort of 5 normal brain tissues and 49 glioma tissue samples. A validation cohort included 529 GBM patients from The Cancer Genome Atlas datasets. We identified 36 molecules commonly changed at the level of the gene and protein, including up-regulated TGFBI and NES and down-regulated SNCA and HSPA12A. Single amino acid variant analysis identified 200 proteins with high mutation rates in GBM samples. We further identified 14 differentially expressed genes with high-level protein modification, among which NES and TNC showed differential expression at the protein level. Moreover, higher expression of NES and TNC mRNAs correlated with shorter overall survival, suggesting that these genes constitute potential biomarkers for GBM.

Chitosan coated bentonite (CCB) was prepared by microwave irridiation, original bentonite as raw materials and chitosan as modifier. The adsorption performance in acid scarlet dye solution was discussed. Firstly the optimum adsorption conditions: concentration of chitosan of 35 g/L, bentonite quality and chitosan solution volume rate of 0.7(g/L), microwave time of 17 min, infilltration time of 50 min, deacetylation degree of chitosan of 85%, soil particle size of 15 mm, pH of 5, dosage of CCB of 20 g/g, stirring speed of 300 r/min, centrifugal time of 15 min, and stirring time of 35 min, were investigated by single factor experiment. And the maximum adsorption rate reached to 96.2%. Subsquently, all the effect tendencies of the physicochemical parameters of the preparation and adsorption were studied on the optium experimental condition, which would provide reference data for the subsequent pilot test. The results suggested that CCB was a promising sorbent to remove organic contaminants and might be utilized to purify water contaminated by organic compounds.

A new type of adsorbent which prepared with waste paper as raw material was applied in the treatment of dye wastewater, and studied the processing conditions on treatment effect. Batch adsorption study carried out as a function of the dosage, the stirring time, the stirring speed and the pH. The adsorption rate of newspaper adsorbent to basic blue dye simulated wastewater and alkaline yellow wastewater with an initial concentration of 80mg·L-1 can reach 98.56% and 92.23% at 4g·L-1 of the dosage of paper adsorbent, 15min of the stirring time and 150r·min-1of the stirring speed. The maximum adsorption were 233.1g·L-1 and 289.4g·L-1 respectively. The isothermal adsorption experiment was also studied and concluded that the adsorption equilibrium data fitted with the Langmuir isotherm. The characterization experiment showed that the modified paper adsorbent had stronger absorbability.

Assuming that road slope and landslide object are rigid, the landslide’s moving displacement was drawn based on their geometry shapes and the physi-mechanical features of materials, and the dynamic model of landslide was also set up, then DDOD(double difference observation data) was combined with the deformed monitoring point and the carrier phase observation data on base point, which can be used to monitor the landslide’s deformation rule from horizontal, vertical and directional view simultaneously. Observing equation was set up, which sufficiently reflects the activities of landslide in entire directions. Filter model includes some information such as mechanical state and GPS observing data by Kalman filter.

Organizational structure is a key factor which determine absorptive capacity and thus influence open innovation, the late studies ignored this. Open innovation requires enterprises to reconstruct the traditional hierarchy organization, achieve the knowledge and decision-making powers match, create a good organizational base and enhance the absorption capacity. Enterprises modular reconstruction whose main content is competency element modular and organizational structure modular, not only can give full play to core competencies and absorptive capacity embedded in each module, effectively acquire, accumulate, absorb and integrate the internal and external innovative resources, and can form a modular innovation networks, and then become a effective platform for open innovation to enhance its efficient.

The essence of the business competition is the competition of knowledge innovation, to maintain and enhance the competitive advantage of enterprises must be based on improving enterprise innovation capacity. Referring to the thought of material supply chain, building knowledge supply chain can effectively eliminate the gap between enterprises and universities and research institutions, optimize knowledge flow, enhance enterprise innovation ability in the process of the knowledge formation, development, transfer and application, so enterprises can maintain and enhance their competitive advantage.