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Purpose: This study aims to explore the potential application of blockchain technology in Lean Six Sigma (LSS) project through a proposed blockchain-LSS (BLSS) model. The proposed model can tackle real-time problems in information sharing, transparency and traceability in every stage of the LSS project. Design/methodology/approach: The scoping review approach is used to develop the integrated model of the BLSS approach for operational excellence. The proposed model is validated through expert's input, which is collected by a questionnaire survey method. Findings: The prime function of the proposed BLSS model is the information sharing among the project team and real-time monitoring, transparency, traceability and immutability in the Define-Measure-Analyze-Improve-Control phase. The proposed model also consists the information about the role of blockchain features at each phase of the LSS project. The project team and industry employees can trace the success of the project at every moment, resulting in trust buildup and the elimination of fake data. Moreover, there would be no disputes among various sections/shops of the plant and employees to share the real information. Practical implications: This paper provides guidelines to practitioners and managers for integrating the LSS approach and blockchain. The blockchain helps managers and practitioners in better data traceability and transparency, monitoring of data as well as more sustainable LSS project management. Originality/value: To the best of the authors' knowledge, this is the first research attempt that developed an integrated model of blockchain and LSS approach to maintaining the immutable records of assets in projects and targeted Industry 4.0. [ABSTRACT FROM AUTHOR]

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Exogenous ubiquitin (UB) plays a protective role in [beta]-adrenergic receptor-stimulated and ischemia/reperfusion (I/R)-induced myocardial remodeling. Here, we report that UB treatment inhibits hypoxia/reoxygenation (H/R)-induced apoptosis in adult rat ventricular myocytes (ARVMs). The activation of Akt was elevated, whereas the activation of glycogen synthase kinase-3[beta] was reduced in UB-treated cells post-H/R. The level of oxidative stress was lower, whereas the number of ARVMs with polarized mitochondria was significantly greater in the UB-treated samples. ARVMs express CXCR4 with majority of CXCR4 localized in the membrane fraction. CXCR4 antagonism using AMD3100, and siRNA-mediated knockdown of CXCR4 negated the protective effects of UB. Two mutated UB proteins (unable to bind CXCR4) had no effect on H/R-induced apoptosis, activation of Akt and GSK-3[beta], or oxidative stress. UB treatment enhanced mitochondrial biogenesis, and inhibition of mitochondrial fission using mdivi1 inhibited H/R-induced apoptosis. Ex vivo, UB treatment significantly decreased infarct size and improved functional recovery of the heart following global I/R. Activation of caspase-9, a key player of the mitochondrial death pathway, was significantly lower in UB-treated hearts post-I/R. UB, most likely acting via CXCR4, plays a protective role in H/R-induced myocyte apoptosis and myocardial I/R injury via modulation of mitochondrial homeostasis and the mitochondrial death pathway of apoptosis. Key words: apoptosis, CXCR4, heart, myocytes, ubiquitin. L'ubiquitine (UB) exogene joue un role protecteur dans le remodelage myocardique stimule par le [beta]-AR et induit par l'ischemie/reperfusion (I/R). Les auteurs rapportent ici qu'un traitement avec l'UB inhibe l'apoptose induite par l'hypoxie/reoxygenation (H/R) dans les myocytes ventriculaires de rats adultes (ARVM, adult rat ventricular myocytes). L'activation d'Akt etait plus elevee alors que l'activation de la GSK-3[beta] etait plus faible chez les cellules traitees a l'UB apres H/R. Le stress oxydant etait plus faible alors que le nombre d'ARVM a mitochondries polarisees etait significativement plus eleve dans les echantillons traites a l'UB. Les ARVM expriment le CXCR4, la majorite du CXCR4 etant localise dans la fraction membranaire. L'antagonisme du CXCR4 par l'AMD3100 et le knockdown de CXCR4 realise par un ARNsi annulaient les effets protecteurs de l'UB. Deux formes mutees de l'UB (incapables de se lier au CXCR4) n'avaient pas d'effet sur l'apoptose induite par H/R, l'activation d'Akt ou de la GSK-3[beta] ou le stress oxydant. Le traitement a l'UB augmentait la biogenese mitochondriale et l'inhibition de la fission mitochondriale par mdivi1 inhibait l'apoptose induite par H/R. Ex vivo, le traitement a l'UB reduisait significativement la taille de l'infarctus et ameliorait la recuperation fonctionnelle du cc[epsilon]ur a la suite d'une I/R globale. L'activation de la caspase-9, un acteur cle de la voie mitochondriale de mort cellulaire, etait significativement plus faible dans les cc[epsilon]urs traites a l'UB apres I/R. L'UB, qui agit fort probablement par l'intermediaire du CXCR4, joue un role protecteur dans l'apoptose des myocytes induite par H/R et dans le dommage d'I/R du myocarde, par la modulation de l'homeostasie mitochondriale et la voie mitochondriale de mort cellulaire par apoptose. Mots-cles: apoptose, CXCR4, cc[epsilon]ur, myocytes, ubiquitine., Introduction Coronary heart disease is a leading cause of death worldwide. The effects of coronary heart disease are generally correlated with myocardial ischemia/reperfusion (I/R) injury (Powers et al. 2007; Hausenloy [...]