Companies have reacted to the opportunities and threats of globalization through numerous production practices that have increased supply chain complexity. One of the ways companies have been able to manage this increased level of complexity is by integrating their supply chains. Logistical capabilities at the company level play a key role in integrating global supply chains, but logistical capabilities need not be company specific. In this study we explore the role of a country's logistical capabilities in external supply chain integration. Our results indicate that plants situated in countries with superior levels of logistical capabilities adopt significantly lower levels of external supply chain integration. Additionally, plants situated in countries with superior logistical capabilities do not gain the same performance benefits from external integration as plants situated in countries with relatively low levels of logistical capabilities.

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Purpose-This study applies information-processing theory to empirically investigate the impact of complexity on the triple bottom line. Specifically, we assess the impact of internal manufacturing complexity on environmental, social, and financial performance. Furthermore, we assess the moderating role of connectivity and shared schema in reducing the potential negative impact of complexity on performance. Design/methodology/approach-Multi-country survey data collected through the Global Manufacturing Research Group (GMRG) was utilized to test our hypotheses. We used structural equation modeling to test our measurement and initial structural model. Furthermore, to test the proposed moderating hypotheses we applied the latent moderated structural equations approach. Findings-Results indicate that while complexity has a negative impact on environmental and social performance, it does not significantly affect financial performance. Furthermore, this negative impact can be reduced, to some extent, through connectivity, however shared schema does not significantly impact on the complexityperformance relationship. Originally/value-This study presents a comprehensive analysis of the impact of complexity on sustainability. Furthermore, it provides managerial applications as it proposes specific tools to deal with the potential negative influences of complexity.

Objective: Atherothrombosis occurs upon rupture of an atherosclerotic plaque and leads to the formation of a mural thrombus. Computational fluid dynamics and numerical models indicated that the mechanical stress applied to a thrombus increases dramatically as a thrombus grows, and that strong inter-platelet interactions are essential to maintain its stability. We investigated whether GPVI-mediated platelet activation helps to maintain thrombus stability by using real-time video-microscopy. Approach and Results: We showed that GPVI blockade with 2 distinct Fab fragments promoted efficient disaggregation of human thrombi preformed on collagen or on human atherosclerotic plaque material in the absence of thrombin. ACT017-induced disaggregation was achieved under arterial blood flow conditions, and its effect increased with wall shear rate. GPVI regulated platelet activation within a growing thrombus as evidenced by the loss in thrombus contraction when GPVI was blocked, and the absence of the disaggregating effect of an anti-GPVI agent when the thrombi were fully activated with soluble agonists. The GPVI-dependent thrombus stabilizing effect was further supported by the fact that inhibition of any of the 4 key immunoreceptor tyrosine-based motif signalling molecules, src-kinases, Syk, PI3Kβ, or phospholipase C, resulted in kinetics of thrombus disaggregation similar to ACT017. The absence of ACT017-induced disaggregation of thrombi from 2 afibrinogenemic patients suggests that the role of GPVI requires interaction with fibrinogen. Finally, platelet disaggregation of fibrin-rich thrombi was also promoted by ACT017 in combination with r-tPA (recombinant tissue-type plasminogen activator). Conclusions: This work identifies an unrecognized role for GPVI in maintaining thrombus stability and suggests that targeting GPVI could dissolve platelet aggregates with a poor fibrin content.