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Social capital is regarded as the bedrock of innovation. However, inadequate efforts have been made to synthesize the way in which different components of social capital dynamically influence innovation. This paper reviews existing empirical studies on the relationship between social capital and innovation of the individual, team, organization, city and nation. Analyses were carried out to identify consensus, discordances and gaps in the social capital-innovation connection. The findings suggested that the structural components of social capital, including ego network size, structural holes, tie strength and centrality have a significant impact on innovation.Their impact, however, tends to be moderated by contextual and intellectual factors, such as the nature and type of innovation, internal vs external ties, costs of maintaining the ties and existing intellectual capital. The relational components of social capital, trust and cognitive norms, demonstrated a consistently positive relationship with innovation across contexts.The cognitive components of social capital have not sufficiently established their contribution to innovation apart from the other two dimensions. Several insights regarding the general literature on social capital and innovation were identified, including the conceptualization of social capital, measurement of innovation, and the causal relationship between social capital and innovation. Suggestions are offered for future research agenda. Implications for managerial practices based on the study findings are also drawn.

Antipsychotic polypharmacy in schizophrenia is much debated, since it is common and costly with unclear evidence for its efficacy and safety. We conducted a systematic literature search and a random effects meta-analysis of randomized trials comparing augmentation with a second antipsychotic vs. continued antipsychotic monotherapy in schizophrenia. Co-primary outcomes were total symptom reduction and study-defined response. Antipsychotic augmentation was superior to monotherapy regarding total symptom reduction (16 studies, N5694, standardized mean difference, SMD5-0.53, 95% CI: 20.87 to 20.19, p50.002). However, superiority was only apparent in open-label and low-quality trials (both p<0.001), but not in double-blind and high-quality ones (p50.120 and 0.226, respectively). Study-defined response was similar between antipsychotic augmentation and monotherapy (14 studies, N5938, risk ratio 5 1.19, 95% CI: 0.99 to 1.42, p50.061), being clearly non-significant in double-blind and high-quality studies (both p50.990). Findings were replicated in clozapine and nonclozapine augmentation studies. No differences emerged regarding all-cause/specific-cause discontinuation, global clinical impression, as well as positive, general and depressive symptoms. Negative symptoms improved more with augmentation treatment (18 studies, N5931, SMD5-0.38, 95% CI: 20.63 to 20.13, p<0.003), but only in studies augmenting with aripiprazole (8 studies, N5532, SMD5-0.41, 95% CI: 20.79 to 20.03, p50.036). Few adverse effect differences emerged: D2 antagonist augmentation was associated with less insomnia (p50.028), but more prolactin elevation (p50.015), while aripiprazole augmentation was associated with reduced prolactin levels (p<0.001) and body weight (p50.030). These data suggest that the common practice of antipsychotic augmentation in schizophrenia lacks double-blind/high-quality evidence for efficacy, except for negative symptom reduction with aripiprazole augmentation.

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Lung cancer remains as the leading cause of cancer-related death worldwide, and lung adenocarcinoma (LUAD) is the most common histological subtype. This study aims to investigate biomarkers associated with cancer progression and prognosis of LUAD. We integrated expression profiles of 668 lung cancer patients in five datasets from the Gene Expression Omnibus (GEO) and identified a panel of differentially expressed genes (DEGs). Function enrichment analysis highlighted that these genes were closely associated with the carcinogenesis of LUAD, such as cell cycle, ECM-receptor interaction and p53 signaling pathway. Cyclin-dependent kinase 1 (CDK1) and MAD2 mitotic arrest deficient-like 1 (MAD2L1), two critical mitotic checkpoint genes, were selected for further study. Elevated expression of CDK1 and MAD2L1 was validated in an independent LUAD cohort. Kaplan-Meier analysis revealed that CDK1 and MAD2L1 expression was negatively correlated with both overall survival (OS) and relapse-free survival (RFS). In conclusion, CDK1 and MAD2L1 were adverse prognostic biomarkers for LUAD whose increased expression could render patients with LUAD a high risk of cancer recurrence and poor survival, suggesting that they might be applied as potential targets for LUAD treatment.