In Peru, the Textile sector generates between 350 and 400 thousand direct jobs, representing 1.9% of Gross domestic product (GDP) and just over 10% of manufacturing. SMEs are characterized by being formed by family businesses, low levels of investment in new technologies and limited financial resources. This context has made SMEs are delayed compared to large companies in implementing Lean Manufacturing. Manufacturing textile companies that have problems with low productivity, excessive use of physical space, unnecessary movement and transport, use the tools of Lean Manufacturing and distribution plant for solving these problems. Many of the problems found in companies are related to the disorganization of processes, material flow and layout. Therefore, companies have seen the need to apply different strategic tools to help them increase the efficiency of their processes and become more competitive in their market. Among the strategic tools is the Lean Manufacturing. Several authors conclude that the plant distributions that SMEs have are not correct for increased productivity, however, the improvement models presenting lack information on how to create step by step a new layout of the company. Because of this, this article details the steps that SMEs can follow in search for a plant distribution model under the SLP tool.
The goal of this work was to elucidate the pathogenic mechanism of an ALS-associated missense mutation, p.Arg573Gly (R573G), in the TBK1 gene. In particular, we seek to analyze the influence of this variant on the cellular levels and the function of TBK1 in immortalized cells from an ALS patient. The patient (Code# E7) belonged to a Spanish family with autosomal dominant disease manifesting in the sixth decade as either dementia or ALS. Four control individuals without signs of neurological disease were also included in this study. Our results indicate that the R375G TBK1 mutation did not affect the levels of mRNA nor the total TBK1 content; however, we observed a significant decrease in the levels of TBK1 phosphorylation, which is essential for TBK1 activity, as well as a significant reduction in the phosphorylation of p62 and RIPK1, known substrates for TBK1. Lymphoblasts from the R573G TBK1 mutation carrier patient display pathological TDP-43 homeostasis, showing elevated levels of phosphorylated TDP-43 and accumulation of the protein in the cytosolic compartment. In addition, the functional decrease in TBK1 activity observed in the E7 patient did not alter the autophagy flux, but it seems to be enough to increase ROS levels as well as the expression of pro-inflammatory cytokine IL-6.
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