Implementation of Industry 4.0 principles and tools: Simulation and case study in a manufacturing SME

Small and medium enterprises (SME) face various challenges in order to remain competitive in a global market. Industry 4.0 (I4.0) is increasingly presented as the new paradigm for improving productivity, ensuring economic growth, and guaranteeing the sustainability of manufacturing companies. However, SMEs are ill equipped and lack resources to undertake this digital shift. This paper presents the digital shift process of an SME in a personalized mass production context. Our work provides a better understanding of the interaction between Lean and I4.0. It contributes to the development of Lean 4.0 implementation strategies that are better adapted to manufacturing SMEs in a personalized mass production context. We also demonstrate the usefulness of simulation as a decision-making assistance tool when implementing I4.0. A practical case is documented to fill a gap in the scientific literature identified by several researchers

Agility and Industry 4.0 implementation strategy in a Quebec manufacturing SME

The emergence of new information technologies, market globalization, climate change, labor shortages, and changing consumer habits have led to dynamic demand and the need for customized mass production systems. This has forced companies, especially small- and medium-sized enterprises (SME), to rethink their product design, production, and marketing models to remain competitive by increasing their agility in the face of growing and changing demand. It becomes relevant to investigate how to move efficiently towards customized mass production in an Industry 4.0 (I4.0) environment. The objective of this research is to develop a strategy for implementing I4.0 in manufacturing SME, based on lean, agility, and intelligent modular product design. A literature review made it possible to target the following performance measures: reducing inventory, minimizing makespan, and reducing time to consumer (reaction time). A case study was conducted in an SME in the agri-food sector to validate the proposed strategy. Inventory levels were reduced by more than 70% and time was cut by almost 65%

Strategy using modularity tools to operationalize mass customization in manufacturing small and medium-sized enterprises

Abstract With the rise of technology, increasing competitiveness, market globalization and the fourth industrial revolution, companies are forced to rethink the way they do business to create or maintain a competitive advantage. Consumers, who are increasingly informed, demanding and concerned about sustainable development, are forcing companies to adapt to their needs to respond adequately to personalized demand. Small and medium-sized enterprises (SMEs) in the manufacturing sector must adjust to this new context. The move towards mass customization is one way of meeting customer requirements. However, no strategy for making this shift currently exists in the literature. The aim of this article is to present a strategy for operationalizing mass customization using modular tools. Action research is used to test the proposed strategy. The paper proposes 4 transformation axes to migrate towards mass customization: Modular product design, Modular process design, Technology use, Collaboration network. This article also highlights the need to tackle modular product design first to migrate to mass customization, by proposing a 3-stage strategy: modular product architecture, standardization of interfaces and definition of configuration rules. A case study is used to test the proposed strategy

The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

Type 2 innate lymphoid cells (ILC2s) both contribute to mucosal homeostasis and initiate pathologic inflammation in allergic asthma. However, the signals that direct ILC2s to promote homeostasis versus inflammation are unclear. To identify such molecular cues, we profiled mouse lung-resident ILCs using single-cell RNA sequencing at steady state and after in vivo stimulation with the alarmin cytokines IL-25 and IL-33. ILC2s were transcriptionally heterogeneous after activation, with subpopulations distinguished by expression of proliferative, homeostatic and effector genes. The neuropeptide receptor Nmur1 was preferentially expressed by ILC2s at steady state and after IL-25 stimulation. Neuromedin U (NMU), the ligand of NMUR1, activated ILC2s in vitro, and in vivo co-administration of NMU with IL-25 strongly amplified allergic inflammation. Loss of NMU-NMUR1 signalling reduced ILC2 frequency and effector function, and altered transcriptional programs following allergen challenge in vivo. Thus, NMUR1 signalling promotes inflammatory ILC2 responses, highlighting the importance of neuro-immune crosstalk in allergic inflammation at mucosal surfaces

Mitogen-Activated Protein Kinases Regulate Susceptibility to Ventilator-Induced Lung Injury

Background: Mechanical ventilation causes ventilator-induced lung injury in animals and humans. Mitogen-activated protein kinases have been implicated in ventilator-induced lung injury though their functional significance remains incomplete. We characterize the role of p38 mitogen-activated protein kinase/mitogen activated protein kinase kinase-3 and c-jun-NH2-terminal kinase-1 in ventilator-induced lung injury and investigate novel independent mechanisms contributing to lung injury during mechanical ventilation. Methodology and Principle Findings: C57/BL6 wild-type mice and mice genetically deleted for mitogen-activated protein kinase kinase-3 (mkk-3-/-) or c-Jun-NH2-terminal kinase-1 (jnk1-/-) were ventilated, and lung injury parameters were assessed. We demonstrate that mkk3-/- or jnk1-/- mice displayed significantly reduced inflammatory lung injury and apoptosis relative to wild-type mice. Since jnk1-/- mice were highly resistant to ventilator-induced lung injury, we performed comprehensive gene expression profiling of ventilated wild-type or jnk1-/- mice to identify novel candidate genes which may play critical roles in the pathogenesis of ventilator-induced lung injury. Microarray analysis revealed many novel genes differentially expressed by ventilation including matrix metalloproteinase-8 (MMP8) and GAFF45α. Functional characterization of MMP8 revealed that mmp8-/- mice were sensitized to ventilator-induced lung injury with increased lung vascular permeability. Conclusion: We demonstrate that mitogen-activated protein kinase pathways mediate inflammatory lung injury during ventilator-induced lung injury. C-Jun-NH2-terminal kinase was also involved in alveolo-capillary leakage and edema formation, whereas MMP8 inhibited alveolo-capillary protein leakage. © 2008 Dolinay et al