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PurposeBecause the mechanism of how knowledge sharing affects organizational innovation is still unclear, the study focuses on the relationship between knowledge sharing and organizational innovation performance, with a focus on mediating role of absorptive capacity and individual creativity.Design/methodology/approachOn the basis of the knowledge base view and organizational learning theory, the study propose a model to verify the impact of inbound and outbound knowledge sharing on organizational innovation performance based on previous research. It also analyzed how these effects were mediated by individual creativity and absorptive capacity. The study collected 166 samples to verify the theoretical model.FindingsResults corroborate that inbound knowledge sharing cannot directly promote organizational innovation performance, and absorptive capacity has a full mediation effect between inbound knowledge sharing and organizational innovation performance. Knowledge outbound sharing, individual creativity and absorptive capacity can improve innovation performance. In addition, absorptive capacity and individual creativity have direct and significant impacts on organizational innovation performance. Moreover, absorptive capacity plays a partial mediate role between individual creativity and innovation performance. Finally, this study discusses the policy implications of the study and describes possible future research directions.Originality/valueThe paper creatively divides knowledge sharing into inbound knowledge sharing and outbound knowledge sharing and verifies that knowledge sharing does not directly affect organizational innovation performance. The mediating role of absorptive capacity and individual creativity was analysis.

Aberrant methylation has been shown to trigger the inactivation of tumor suppressor genes during tumorigenesis. MicroRNAs (miRNAs) have been found deregulated in human colorectal cancer (CRC), and some of them may function as tumor suppressor genes. Here, we investigated CpG island promoter hypermethylation as a potential mechanism underlying miRNA disruption and identifed methylation-sensitive miRNAs that might repress CRC development. We compared differential expression of miRNAs after 5-aza-2'-deoxycitidine (5-aza-dC) treatment using microarrays. DNA methylation status of the candidate miRNA was analyzed. The candidate miRNA was transfected into CRC cells and growth-suppressive mechanisms were explored. Luciferase reporter assay and western blot were used to identify the target genes of the candidate miRNA. The expression of mir-345 was significantly increased after 5-aza-dC treatment. DNA methylation analyses of mir-345 showed high methylation levels in tumor versus normal tissues. Expression of mir-345 was significantly down-regulated in 51.6% of CRC tissues compared with corresponding non-cancerous tissues. Low expression of mir-345 was associated with lymph node metastasis and worse histological type. Increased mir-345 function was sufficient to suppress colon cancer cell proliferation and invasiveness in vitro. Furthermore, we identified BCL2-associated athanogene 3 (BAG3), an anti-apoptosis protein, to be a target of mir-345. These results suggested as a methylation-sensitive miRNA in CRC, mir-345 may play an important role of antineoplastic as a growth inhibitor in the development of CRC.

The prevalence of diabetes is steadily increasing in China. When diabetes is uncontrolled, it generates dire consequences for health and well-being. Numerous studies have shown that health outcomes were associated with social support and medication adherence. Previous study confirmed that social support was associated with medication adherence in patients with heart failure, HIV diseases, and first-episode psychosis. However, the relationship between social support and medication adherence in patients with type 2 diabetes mellitus (T2DM) is remains unclear. This study aims to examine whether social support is associated with medication adherence in patients with T2DM. This study was conducted in the First Affiliated Hospital of the General Hospital of the People’s Liberation Army (PLA). In Beijing, a systematic random sample of 412 patients with T2DM over 18 years was recruited at baseline, and demographic characteristics, clinical data and their assessment of social support were collected from medical records and self-reported questionnaires. 330 of these patients completed a self-report measure of medication adherence at the sixth month after baseline data collection. Regression analysis showed that social support presented a positive effect on medication adherence, additionally, support utilization and the subscale of social support exhibited a significantly strong influence on medication adherence in patients with T2DM. Although medication adherence was influenced by multiple factors, this finding confirmed that social support must be recognized as a core element in interventions aimed at improving in the management of patients with T2DM.

Protein tyrosine phosphatases (PTPs) are enzymes that remove phosphate from tyrosine residues in proteins. Recent whole-exome sequencing of human cancer genomes reveals that many PTPs are frequently mutated in a variety of cancers. Among these mutated PTPs, protein tyrosine phosphatase T (PTPRT) appears to be the most frequently mutated PTP in human cancers. Beside PTPN11 which functions as an oncogene in leukemia, genetic and functional studies indicate that most of mutant PTPs are tumor suppressor genes. Identification of the substrates and corresponding kinases of the mutant PTPs may provide novel therapeutic targets for cancers harboring these mutant PTPs.