Remaining Useful Life Estimation Based on Detection of Explosive Changes: Analysis of Bearing Vibration

The monitoring of condition variables for maintenance purposes is a growing trend amongst researchers and practitioners where decisions are based on degradation levels. The two approaches in Condition-Based Maintenance (CBM) are diagnosing the level of degradation (diagnostics) or predicting when a certain level of degradation will be reached (prognostics). Using diagnostics determines when it is necessary to perform maintenance, but it rarely allows for estimation of future degradation. In the second case, prognostics does allow for degradation and failure prediction, however, its major drawback lies in when to perform the analysis, and exactly what information should be used for predictions. This encumbrance is due to previous studies that have shown that degradation variable could undergo a change that misleads these calculations. This paper addresses the issue of identifying explosive changes in condition variables, using Control Charts, to determine when to perform a new model fitting in order to obtain more accurate Remaining Useful Life (RUL) estimations. The diagnostic-prognostic methodology allows for discarding pre-change observations to avoid contamination in condition prediction. In addition the performance of the integration methodology is compared against adaptive autoregressive (AR) models. Results show that using only the observations acquired after the out-of-control signal produces more accurate RUL estimations

FAP-overexpressing fibroblasts produce an extracellular matrix that enhances invasive velocity and directionality of pancreatic cancer cells

<p>Abstract</p> <p>Background</p> <p>Alterations towards a permissive stromal microenvironment provide important cues for tumor growth, invasion, and metastasis. In this study, Fibroblast activation protein (FAP), a serine protease selectively produced by tumor-associated fibroblasts in over 90% of epithelial tumors, was used as a platform for studying tumor-stromal interactions.</p> <p>We tested the hypothesis that FAP enzymatic activity locally modifies stromal ECM (extracellular matrix) components thus facilitating the formation of a permissive microenvironment promoting tumor invasion in human pancreatic cancer.</p> <p>Methods</p> <p>We generated a tetracycline-inducible FAP overexpressing fibroblastic cell line to synthesize an <it>in vivo</it>-like 3-dimensional (3D) matrix system which was utilized as a stromal landscape for studying matrix-induced cancer cell behaviors. A FAP-dependent topographical and compositional alteration of the ECM was characterized by measuring the relative orientation angles of fibronectin fibers and by Western blot analyses. The role of FAP in the matrix-induced permissive tumor behavior was assessed in Panc-1 cells in assorted matrices by time-lapse acquisition assays. Also, FAP⁺matrix-induced regulatory molecules in cancer cells were determined by Western blot analyses.</p> <p>Results</p> <p>We observed that FAP remodels the ECM through modulating protein levels, as well as through increasing levels of fibronectin and collagen fiber organization. FAP-dependent architectural/compositional alterations of the ECM promote tumor invasion along characteristic parallel fiber orientations, as demonstrated by enhanced directionality and velocity of pancreatic cancer cells on FAP⁺matrices. This phenotype can be reversed by inhibition of FAP enzymatic activity during matrix production resulting in the disorganization of the ECM and impeded tumor invasion. We also report that the FAP⁺ matrix-induced tumor invasion phenotype is β₁-integrin/FAK mediated.</p> <p>Conclusion</p> <p>Cancer cell invasiveness can be affected by alterations in the tumor microenvironment. Disruption of FAP activity and β₁-integrins may abrogate the invasive capabilities of pancreatic and other tumors by disrupting the FAP-directed organization of stromal ECM and blocking β₁-integrin dependent cell-matrix interactions. This provides a novel preclinical rationale for therapeutics aimed at interfering with the architectural organization of tumor-associated ECM. Better understanding of the stromal influences that fuel progressive tumorigenic behaviors may allow the effective future use of targeted therapeutics aimed at disrupting specific tumor-stromal interactions.</p

Efecto Inhibitorio de Extractos Hidroalcoholicos de Larrea Tridentata Sobre Saprolegnia Sp

In recent years, the aquaculture sector has undergone rapid growth owing to its significance in food production. Nonetheless, freshwater fish industries are encountering significant hurdles, including diseases caused by Oomycetes, like Saprolegniae. This research project evaluates the impact of Larrea tridentata extract on inhibiting Saprolegnia Sp. through an in vitro bioassay. Saprolegnia strains were procured from fish afflicted with this Oomycete. Morphological methods were employed to identify the fungus, resulting in the isolation of two strains - S. parasitica and S. Ferax - which were tested in the inhibitory assay. The yield was found to be 167.5 mg/mL in methanol and 113 mg/mL in ethanol. Phytochemical analysis revealed the presence of phenols, flavonoids and tannins, as well as intense antioxidant activity. Concentrations above 50 mg/mL exhibited complete inhibition of the Oomycete. This suggests that the utilization of an ethanolic extract presents a promising option for implementation in aquatic organisms.En los últimos años, el sector acuícola ha experimentado un rápido crecimiento debido a su relevancia en la producción alimentaria. No obstante, las industrias de peces de agua dulce se enfrentan a grandes desafíos, incluyendo enfermedades causadas por Oomicetos, como Saprolegniae. En este proyecto se evaluó el efecto del extracto de Larrea tridentata sobre la inhibición de Saprolegnia Sp. mediante un bioensayo in vitro. Las cepas de Saprolegnia fueron obtenidas &nbsp;de peces infectados con este Oomiceto. La identificación del hongo se realizo vía morfológica obteniéndose dos cepas S. parasítica y S. Ferax. Las cuales fueron usadas en el ensayo inhibitorio. El rendimiento fue de 167.5 mg/mL en metanol y 113 mg/mL en etanol, el análisis fitoquímico reveló la presencia de fenoles, flavonoides y taninos, así como una intensa actividad antioxidante. En cuanto a la inhibición del Oomiceto, se encontró que a una concentración arriba de 50 mg/mL presentaba una inhibición completa del microorganismo. Lo anterior permite concluir que el uso de extracto etanólico es una opción potencial para su uso en organismos acuáticos

The Interplay between Entamoeba and Enteropathogenic Bacteria Modulates Epithelial Cell Damage

In amoebiasis, a human disease that is a serious health problem in many developing countries, efforts have been made to identify responsible factors for the tissue damage inflicted by the parasite Entamoeba histolytica. This amoeba lives in the lumen of the colon without causing damage to the intestinal mucosa, but under unknown circumstances becomes invasive, destroying the intestinal tissue. Bacteria in the intestinal flora have been proposed as inducers of higher amoebic virulence, but the causes or mechanisms responsible for the induction are still undetermined. Mixed intestinal infections with Entamoeba histolytica and enteropathogenic bacteria, showing exacerbated manifestations of disease, are common in endemic countries. We implemented an experimental system to study amoebic virulence in the presence of pathogenic bacteria and its consequences on epithelial cells. Results showed that amoebae that ingested enteropathogenic bacteria became more virulent, causing more damage to epithelial cells. Bacteria induced release of inflammatory proteins by the epithelial cells that attracted amoebae, facilitating amoebic contact to the epithelial cells and higher damage. Our results, although a first approach to this complex problem, provide insights into amoebic infections, as interplay with other pathogens apparently influences the intestinal environment, the behavior of cells involved and the manifestations of the disease

Targeting SOX10-deficient cells to reduce the dormant-invasive phenotype state in melanoma

Cellular plasticity contributes to intra-tumoral heterogeneity and phenotype switching, which enable adaptation to metastatic microenvironments and resistance to therapies. Mechanisms underlying tumor cell plasticity remain poorly understood. SOX10, a neural crest lineage transcription factor, is heterogeneously expressed in melanomas. Loss of SOX10 reduces proliferation, leads to invasive properties, including the expression of mesenchymal genes and extracellular matrix, and promotes tolerance to BRAF and/or MEK inhibitors. We identify the class of cellular inhibitor of apoptosis protein-1/2 (cIAP1/2) inhibitors as inducing cell death selectively in SOX10-deficient cells. Targeted therapy selects for SOX10 knockout cells underscoring their drug tolerant properties. Combining cIAP1/2 inhibitor with BRAF/MEK inhibitors delays the onset of acquired resistance in melanomas in vivo. These data suggest that SOX10 mediates phenotypic switching in cutaneous melanoma to produce a targeted inhibitor tolerant state that is likely a prelude to the acquisition of resistance. Furthermore, we provide a therapeutic strategy to selectively eliminate SOX10-deficient cells