Neural networks in injection moulding: A new technique for quality control

Only a few quality control systems for moulded plastics products are based on the automatic online measurement and testing of products. Quality oriented production is thus seldom achieved in practice. With the aid of Neural Networks (NN) it is possible to have an understanding of the relationship between the process characteristics and product quality

Neuronale Netze beim Spritzgießen: Ein neuer Weg zur Qualitätssicherung

Prozeßnahe Qualitätsprüfung von Spritzgießprodukten direkt an der Spritzgießmaschine mit Hilfe automatischer Meß- und Prüfeinrichtungen ist bisher nur in geringem Maße realisiert. Mit Hilfe Neuronaler Netze (NN) ist es möglich, aus den Prozeßsignalverläufen während der Produktion auf die Produktqualität zu schließen. Neuronale Netze lernen dafür selbständig die Zusammenhänge zwischen Prozeßgrößen und Teilequalität. Only a few quality control systems for moulded plastics products are based on the automatic online measurement and testing of products. Quality oriented production is thus seldom achieved in practice. With the aid of Neural Networks (NN) it is possible to have an understanding of the relationship between the process characteristics and product quality

Paxillin Binding Is Not the Sole Determinant of Focal Adhesion Localization or Dominant-Negative Activity of Focal Adhesion Kinase/Focal Adhesion Kinase-related Nonkinase

The carboxy-terminal 150 residues of the focal adhesion kinase (FAK) comprise the focal adhesion-targeting sequence, which is responsible for its subcellular localization. The mechanism of focal adhesion targeting has not been fully elucidated. We describe a mutational analysis of the focal adhesion-targeting sequence of FAK to further examine the mechanism of focal adhesion targeting and explore additional functions encoded by the carboxy-terminus of FAK. The results demonstrate that paxillin binding is dispensable for focal adhesion targeting of FAK. Cell adhesion-dependent tyrosine phosphorylation strictly correlated with the ability of mutants to target to focal adhesions. Focal adhesion targeting was also a requirement for maximal FAK-dependent tyrosine phosphorylation of paxillin and FAK-related nonkinase (FRNK)–dependent inhibition of endogenous FAK function. However, there were additional requirements for these latter functions because we identified mutants that target to focal adhesions, yet are defective for the induction of paxillin phosphorylation or the dominant-negative function of FRNK. Furthermore, the paxillin-binding activity of FRNK mutants did not correlate with their ability to inhibit FAK, suggesting that FRNK has other targets in addition to paxillin

Instruction of haematopoietic lineage choices, evolution of transcriptional landscapes and cancer stem cell hierarchies derived from an AML1-ETO mouse model.

The t(8;21) chromosomal translocation activates aberrant expression of the AML1-ETO (AE) fusion protein and is commonly associated with core binding factor acute myeloid leukaemia (CBF AML). Combining a conditional mouse model that closely resembles the slow evolution and the mosaic AE expression pattern of human t(8;21) CBF AML with global transcriptome sequencing, we find that disease progression was characterized by two principal pathogenic mechanisms. Initially, AE expression modified the lineage potential of haematopoietic stem cells (HSCs), resulting in the selective expansion of the myeloid compartment at the expense of normal erythro- and lymphopoiesis. This lineage skewing was followed by a second substantial rewiring of transcriptional networks occurring in the trajectory to manifest leukaemia. We also find that both HSC and lineage-restricted granulocyte macrophage progenitors (GMPs) acquired leukaemic stem cell (LSC) potential being capable of initiating and maintaining the disease. Finally, our data demonstrate that long-term expression of AE induces an indolent myeloproliferative disease (MPD)-like myeloid leukaemia phenotype with complete penetrance and that acute inactivation of AE function is a potential novel therapeutic option