Ansätze für die Verbesserung von PPS-Systemen durch Fuzzy-Logik

Ziel dieses Arbeitsberichts ist es, die Teilbereiche von Produktionsplanungs- und -steuerungssystemen (PPS-Systemen) zu identifizieren, die unter Beachtung der Interdependenzen zu anderen Teilbereichen mit einem Fuzzy-Ansatz modelliert und dadurch in ihrer Effizienz gesteigert werden können. Nach einer kurzen Einführung in die Fuzzy-Logik werden zunächst Ansätze für den Einsatz der Fuzzy-Logik innerhalb der Datenstrukturen der Produktionsplanung und -steuerung dargestellt. Danach werden die Funktionen von PPS-Systemen systematisch auf diesbezügliche Potentiale untersucht, wobei zwischen originärer und derivativer Verwendung der Fuzzy-Logik unterschieden wird, und Nutzeffekte sinnvoller 'Verunschärfungen' aufgezeigt werden. Der Arbeitsbericht schließt mit einem Ausblick

Endothelial MAPKs Direct ICAM-1 Signaling to Divergent Inflammatory Functions.

Lymphocyte transendothelial migration (TEM) is critically dependent on intraendothelial signaling triggered by adhesion to ICAM-1. Here we show that endothelial MAPKs ERK, p38, and JNK mediate diapedesis-related and diapedesis-unrelated functions of ICAM-1 in cerebral and dermal microvascular endothelial cells (MVECs). All three MAPKs were activated by ICAM-1 engagement, either through lymphocyte adhesion or Ab-mediated clustering. MAPKs were involved in ICAM-1-dependent expression of TNF-α in cerebral and dermal MVECs, and CXCL8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs. Endothelial JNK and to a much lesser degree p38 were the principal MAPKs involved in facilitating diapedesis of CD4(+) lymphocytes across both types of MVECs, whereas ERK was additionally required for TEM across dermal MVECs. JNK activity was critical for ICAM-1-induced F-actin rearrangements. Furthermore, activation of endothelial ICAM-1/JNK led to phosphorylation of paxillin, its association with VE-cadherin, and internalization of the latter. Importantly ICAM-1-induced phosphorylation of paxillin was required for lymphocyte TEM and converged functionally with VE-cadherin phosphorylation. Taken together we conclude that during lymphocyte TEM, ICAM-1 signaling diverges into pathways regulating lymphocyte diapedesis, and other pathways modulating gene expression thereby contributing to the long-term inflammatory response of the endothelium

Common Data Acquisition Systems (DAS) Software Development for Rocket Propulsion Test (RPT) Test Facilities

The advent of the commercial space launch industry and NASA's more recent resumption of operation of Stennis Space Center's large test facilities after thirty years of contractor control resulted in a need for a non-proprietary data acquisition systems (DAS) software to support government and commercial testing. The software is designed for modularity and adaptability to minimize the software development effort for current and future data systems. An additional benefit of the software's architecture is its ability to easily migrate to other testing facilities thus providing future commonality across Stennis. Adapting the software to other Rocket Propulsion Test (RPT) Centers such as MSFC, White Sands, and Plumbrook Station would provide additional commonality and help reduce testing costs for NASA. Ultimately, the software provides the government with unlimited rights and guarantees privacy of data to commercial entities. The project engaged all RPT Centers and NASA's Independent Verification & Validation facility to enhance product quality. The design consists of a translation layer which provides the transparency of the software application layers to underlying hardware regardless of test facility location and a flexible and easily accessible database. This presentation addresses system technical design, issues encountered, and the status of Stennis development and deployment

Common Data Acquisition Systems (DAS) Software Development for Rocket Propulsion Test (RPT) Test Facilities - A General Overview

The advent of the commercial space launch industry and NASA's more recent resumption of operation of Stennis Space Center's large test facilities after thirty years of contractor control resulted in a need for a non-proprietary data acquisition system (DAS) software to support government and commercial testing. The software is designed for modularity and adaptability to minimize the software development effort for current and future data systems. An additional benefit of the software's architecture is its ability to easily migrate to other testing facilities thus providing future commonality across Stennis. Adapting the software to other Rocket Propulsion Test (RPT) Centers such as MSFC, White Sands, and Plumbrook Station would provide additional commonality and help reduce testing costs for NASA. Ultimately, the software provides the government with unlimited rights and guarantees privacy of data to commercial entities. The project engaged all RPT Centers and NASA's Independent Verification & Validation facility to enhance product quality. The design consists of a translation layer which provides the transparency of the software application layers to underlying hardware regardless of test facility location and a flexible and easily accessible database. This presentation addresses system technical design, issues encountered, and the status of Stennis' development and deployment

AMP-activated protein kinase is a key regulator of acute neurovascular permeability

Many neuronal and retinal disorders are associated with pathological hyperpermeability of the microvasculature. We have used explants of rodent retinae to study acute neurovascular permeability and signal transduction and the role of AMP-activated protein kinase (AMPK). Following stimulation with either vascular endothelial growth factor (VEGF-A) or bradykinin (BK), AMPK was rapidly and strongly phosphorylated and acted as a key mediator of permeability downstream of Ca2+ Accordingly, AMPK agonists potently induced acute retinal vascular leakage. AMPK activation led to phosphorylation of endothelial nitric oxide synthase (eNOS), which in turn increased VE-cadherin phosphorylation on Y685. In parallel, AMPK also mediated phosphorylation of p38 MAP kinase and HSP27, indicating that it regulated paracellular junctions and cellular contractility, both previously associated with endothelial permeability. Endothelial AMPK provided a missing link in neurovascular permeability, connecting Ca2+ transients to the activation of eNOS and p38, irrespective of the permeability-inducing factor used. Collectively, we find that, due to its compatibility with small molecule antagonists/agonists and siRNA, the ex-vivo retina model constitutes a reliable tool to identify and study regulators and mechanism of acute neurovascular permeability

AMP-activated protein kinase is a key regulator of acute neurovascular permeability

Many neuronal and retinal disorders are associated with pathological hyperpermeability of the microvasculature. We have used explants of rodent retinae to study acute neurovascular permeability and signal transduction and the role of AMP-activated protein kinase (AMPK). Following stimulation with either vascular endothelial growth factor (VEGF-A) or bradykinin (BK), AMPK was rapidly and strongly phosphorylated and acted as a key mediator of permeability downstream of Ca2+ Accordingly, AMPK agonists potently induced acute retinal vascular leakage. AMPK activation led to phosphorylation of endothelial nitric oxide synthase (eNOS), which in turn increased VE-cadherin phosphorylation on Y685. In parallel, AMPK also mediated phosphorylation of p38 MAP kinase and HSP27, indicating that it regulated paracellular junctions and cellular contractility, both previously associated with endothelial permeability. Endothelial AMPK provided a missing link in neurovascular permeability, connecting Ca2+ transients to the activation of eNOS and p38, irrespective of the permeability-inducing factor used. Collectively, we find that, due to its compatibility with small molecule antagonists/agonists and siRNA, the ex-vivo retina model constitutes a reliable tool to identify and study regulators and mechanism of acute neurovascular permeability

Measuring streambed morphology using range imaging

River engineeringInnovative field and laboratory instrumentatio

AMP-activated protein kinase is a key regulator of acute neurovascular permeability

Many neuronal and retinal disorders are associated with pathological hyperpermeability of the microvasculature. We have used explants of rodent retinae to study acute neurovascular permeability, signal transduction and the role of AMP-activated protein kinase (AMPK). Following stimulation with either vascular endothelial growth factor (VEGF-A) or bradykinin (BK), AMPK was rapidly and strongly phosphorylated and acted as a key mediator of permeability downstream of Ca2+. Accordingly, AMPK agonists potently induced acute retinal vascular leakage. AMPK activation led to phosphorylation of endothelial nitric oxide synthase (eNOS, also known as NOS3), which in turn increased VE-cadherin (CDH5) phosphorylation on Y685. In parallel, AMPK also mediated phosphorylation of p38 MAP kinases (hereafter p38) and HSP27 (HSPB1), indicating that it regulated paracellular junctions and cellular contractility, both previously associated with endothelial permeability. Endothelial AMPK provided a missing link in neurovascular permeability, connecting Ca2+ transients to the activation of eNOS and p38, irrespective of the permeability-inducing factor used. Collectively, we find that, due to its compatibility with small molecule antagonists and agonists, as well as siRNA, the ex vivo retina model constitutes a reliable tool to identify and study regulators and mechanisms of acute neurovascular permeability

Differential Apicobasal VEGF Signaling at Vascular Blood-Neural Barriers

The vascular endothelium operates in a highly polarized environment, but to date there has been little exploration of apicobasal polarization of its signaling. We show that VEGF-A, histamine, IGFBP3, and LPA trigger unequal endothelial responses when acting from the circulation or the parenchymal side at blood-neural barriers. For VEGF-A, highly polarized receptor distribution contributed to distinct signaling patterns: VEGFR2, which was found to be predominantly abluminal, mediated increased permeability via p38; in contrast, luminal VEGFR1 led to Akt activation and facilitated cytoprotection. Importantly, such differential apicobasal signaling and VEGFR distribution were found in the microvasculature of brain and retina but not lung, indicating that endothelial cells at blood-neural barriers possess specialized signaling compartments that assign different functions depending on whether an agonist is tissue or blood borne.</p

Morphological changes of the south-eastern wall of Askja caldera, Iceland over the past 80 years

Calderas are subcircular depressions with near-vertical walls, which are often gravitationally unstable and prone to mass movements that sequentially widen their basins. However, the details of these erosional changes are difficult to decipher due to short observational periods. Here, we use a photogrammetric dataset of nearly 80 years to study the landslide-prone south-eastern wall of Askja caldera (Iceland). We analyzed aerial data from 1945 and 1987, stereo satellite data from 2013 and 2022, and drone images acquired in 2019, 2022, and 2023. We developed an inventory of geomorphological features and identified types of slope instability. We describe over 700 features, including circa 500 fractures, 200 sinkholes, and four major landslides. We found that morphological changes were persistent over the observation period, accumulating in a sector that collapsed in 2014. We discuss various factors of slope instability at Askja including possible volcano-permafrost interaction, and other processes that could induce mass wasting