A two-stage strategy for the optimal layout of manufacturing cells

La disposición de los equipos en una planta, denominada simplificadamente 'layout', resulta de sumo interés cuando se desea alcanzar metas específicas relativas a inventario en proceso, almacenamiento, fallas o interrupciones del proceso productivo, ordenamiento en la distribución de tareas, de recursos y del tráfico de operarios y dispositivos de traslado, defectos en la calidad, costos de manipulación de materiales, etc. En este trabajo se propone un algoritmo para la determinación de celdas y el 'layout' óptimo de las mismas que consiste en dos etapas bien diferenciadas: primero se obtienen los grupos o celdas de máquinas (de equipos o, en forma más general, de elementos a ser agrupados) de manera tal que el costo del manejo de materiales inter-celdas sea mínimo y, en segundo lugar, teniendo como datos los grupos formados, se busca la mejor disposición de ellos entre sí y de las máquinas dentro de cada una de las celdas que haga más bajos tanto el costo de manipulación inter-celular como el intra-celular. Se presenta un estudio de caso a los efectos de comparación, comprobando así la eficiencia de la nueva propuesta.Plant layout becomes especially interesting when specific goals relative to work -in- process, storage, machine failures or production process halting, tasks or resources distribution, manpower movement, quality problems, material handling costs and so on should be reached . In this work an algorithm for determining the cells and the optimal layout inside and between them is provided. The procedure consists of two stages: firstly, groups (cells) of machines are formed through a kind of quadratic assignment model in a way that minimizes the intercellular movement of parts. With the determination of groups in hand, the second stage seeks for the optimal layout design considering both within each cell and between cells costs of transportation of the parts (intra- and inter-cellular material handling costs, respectively). A case study is presented so as to compare previous results to those of the new proposal, just to prove the efficiency of the latter.Fil: Camussi, Nelida Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Santa Fe. Instituto de Desarrollo Tecnológico para la Industria Química (i); Argentina. Universidad Nacional del Litoral; Argentin

Unravelling the enigma of proteinuria in burn patients

Hu and coworkers in the previous issue of Critical Care provide evidence for the clinical relevance of proteinuria in the outcome of burn patients. Proteinuria is a common finding after severe burns, appears within a short period and is detectable for several weeks. Proteinuria ranging from 0.5 to 3 to 4 g/day is initially of mixed type, then, after a week, gradually changes to tubular proteinuria. The clinical role of proteinuria is still unclear, mainly due to a lack of data on its pathogenesis. Recent studies have demonstrated an association between proteinuria and incidence of inhalation injury, sepsis, acute kidney injury and mortality rate. Proteinuria is considered the mirror of increased systemic capillary permeability, and possibly a direct marker of glomerular and tubular injury. Circulating plasma inflammatory mediators and pro-apoptotic factors reflecting burn injury, sepsis and acute kidney injury can affect the viability and function of tubular cells and podocytes. These studies highlight that proteinuria in burn patients should receive due consideration

Cytochalasin B-induced membrane vesicles convey angiogenic activity of parental cells

Naturally occurring extracellular vesicles (EVs) play essential roles in intracellular communication and delivery of bioactive molecules. Therefore it has been suggested that EVs could be used for delivery of therapeutics. However, to date the therapeutic application of EVs has been limited by number of factors, including limited yield and full understanding of their biological activities. To address these issues, we analyzed the morphology, molecular composition, fusion capacity and biological activity of Cytochalasin B-induced membrane vesicles (CIMVs). The size of these vesicles was comparable to that of naturally occurring EVs. In addition, we have shown that CIMVs from human SH-SY5Y cells contain elevated levels of VEGF as compared to the parental cells, and stimulate angiogenesis in vitro and in vivo

Synthesis and release of platelet-activating factor by human vascular endothelial cells treated with tumor necrosis factor or interleukin 1 alpha.

Human endothelial cells synthesize large amounts of platelet-activating factor (PAF) after 30-min treatment with recombinant tumor necrosis factor (TNF). Synthesis of PAF peaks at 4-6 h, whereas in endothelial cells treated with interleukin 1 alpha (IL-1) it peaks at 8-12 h. More than twice as much PAF is synthesized in response to optimal concentrations of TNF than in response to IL-1. However, PAF synthesis is stimulated by lower molar concentrations of IL-1 than TNF. About 30% of PAF produced in response to either TNF or IL-1 is released into the medium, whereas approximately 70% remains cell-associated. Experiments with labeled precursors show that PAF is synthesized de novo in response to TNF. This activity of TNF is inhibited by treating endothelial cells with the inhibitors of protein or RNA synthesis cycloheximide or actinomycin D. This finding may be explained by the observation that TNF induces in endothelial cells an acetyltransferase required for PAF synthesis. The induction of this enzymatic activity precedes the peak of PAF synthesis in TNF-treated cells. After prolonged incubation with either TNF or IL-1, endothelial cells no longer respond to the same monokine, but are still capable of producing PAF when treated with the other monokine. The finding that these monokines do not show reciprocal tachyphylaxis in endothelial cells may be explained by their binding to different receptors. In cells treated simultaneously with different concentrations of TNF and IL-1, PAF synthesis is stimulated in an additive rather than synergistic way. This suggests that PAF is synthesized by the same pathway in response to TNF or IL-1

Role of ncRNAs in modulation of liver fibrosis by extracellular vesicles

Abstract Extracellular vesicles (EVs) are small membrane vesicles carrying bioactive lipids, proteins and nucleic acids of the cell of origin. In particular, EVs carry non-coding RNAs (ncRNAs) and the vesicle membrane may protect them from degradation. Once released within the extracellular space, EVs can transfer their cargo, including ncRNAs, to neighboring or distant cells, thus inducing phenotypical and functional changes that may be relevant in several physio-pathological conditions. This review provides an overview of the role of EV-carried ncRNAs in the modulation of liver fibrosis. In particular, we focused on EV-associated microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) involved into the development of liver fibrosis and on the potential use of EV-associated ncRNAs as diagnostic and prognostic biomarkers of liver fibrosis

Extracellular vesicles: A therapeutic option for liver fibrosis

Extracellular vesicles (EVs) are a heterogeneous population of small membrane vesicles released by all types of cells in both physiological and pathological conditions. EVs shuttle different types of molecules and are able to modify the behavior of target cells by various mechanisms of action. In this review, we have summarized the papers present in the literature, to our acknowledge, that reported the EV effects on liver diseases. EVs purified from serum, stem cells, and hepatocytes were investigated in different experimental in vivo models of liver injury and in particular of liver fibrosis. Despite the different EV origin and the different types of injury (toxic, ischemic, diet induced, and so on), EVs showed an anti-fibrotic effect. In particular, EVs had the capacities to inhibit activation of hepatic stellate cells, one of the major players of liver fibrosis development; to reduce inflammation and apoptosis; to counteract the oxidative stress; and to increase hepatocyte proliferation, contributing to reducing fibrosis and ameliorating liver function and morphology

Resident Stem Cells and Renal Carcinoma

According to the cancer stem cell hypothesis tumors are maintained by a cancer stem cell population which is able to initiate and maintain tumors. Tumor-initiating stem cells display stem or progenitor cell properties such as self-renewal and capacity to re-establish tumors that recapitulate the tumor of origin. In this paper, we discuss data relative to the presence of cancer stem cells in human renal carcinoma and their possible origin from normal resident stem cells. The cancer stem cells identified in human renal carcinomas are not derived from the normal CD133+ progenitors of the kidney, but rather from a more undifferentiated population that retains a mesenchymal phenotype. This population is able to self-renewal, clonogenicity, and in vivo tumor initiation. Moreover, they retain pluripotent differentiation capability, as they can generate not only the epithelial component of the tumor, but also tumor endothelial cells. This suggests that renal cancer stem cells may contribute to the intratumor vasculogenesis