Redundancy relations and robust failure detection

All failure detection methods are based on the use of redundancy, that is on (possible dynamic) relations among the measured variables. Consequently the robustness of the failure detection process depends to a great degree on the reliability of the redundancy relations given the inevitable presence of model uncertainties. The problem of determining redundancy relations which are optimally robust in a sense which includes the major issues of importance in practical failure detection is addressed. A significant amount of intuition concerning the geometry of robust failure detection is provided

Effect of moulting, eyestalk ablation, starvation and transportation on the immune response of the Indian spiny lobster, Panulirus homarus

The Indian spiny lobster, Panulirus homarus (Linnaeus 1758), is of great commercial importance and has a high demand in the internationalmarket.However, due to the lack of larval rearing technology, traders depend heavily on the wild-caught undersized lobsters that are normally maintained in impoundments for fattening. Overstocking and poormanagement of these holding and fattening systems can result in stress, which can eventually lead to disease outbreak. Crustaceans respond to these stress factors with their innate immune system, consisting of bothcellularand humoral factors

Model reduction for analysis of cascading failures in power systems

In this paper, we apply a principal-orthogonal decomposition based method to the model reduction of a hybrid, nonlinear model of a power network. The results demonstrate that the sequence of fault events can be evaluated and predicted without necessarily simulating the whole system

Primary cilia elongation in response to interleukin-1 mediates the inflammatory response

Primary cilia are singular, cytoskeletal organelles present in the majority of mammalian cell types where they function as coordinating centres for mechanotransduction, Wnt and hedgehog signalling. The length of the primary cilium is proposed to modulate cilia function, governed in part by the activity of intraflagellar transport (IFT). In articular cartilage, primary cilia length is increased and hedgehog signaling activated in osteoarthritis (OA). Here, we examine primary cilia length with exposure to the quintessential inflammatory cytokine interleukin-1 (IL-1), which is up-regulated in OA. We then test the hypothesis that the cilium is involved in mediating the downstream inflammatory response. Primary chondrocytes treated with IL-1 exhibited a 50 % increase in cilia length after 3 h exposure. IL-1-induced cilia elongation was also observed in human fibroblasts. In chondrocytes, this elongation occurred via a protein kinase A (PKA)-dependent mechanism. G-protein coupled adenylate cyclase also regulated the length of chondrocyte primary cilia but not downstream of IL-1. Chondrocytes treated with IL-1 exhibit a characteristic increase in the release of the inflammatory chemokines, nitric oxide and prostaglandin E2. However, in cells with a mutation in IFT88 whereby the cilia structure is lost, this response to IL-1 was significantly attenuated and, in the case of nitric oxide, completely abolished. Inhibition of IL-1-induced cilia elongation by PKA inhibition also attenuated the chemokine response. These results suggest that cilia assembly regulates the response to inflammatory cytokines. Therefore, the cilia proteome may provide a novel therapeutic target for the treatment of inflammatory pathologies, including OA

Syntheses, structure, reactivity and species recognition studies of oxo-vanadium(V) and -molybdenum(VI) complexes

Alkoxo-rich Schiff-bases of potentially tri-, tetra- and penta-dentate binding capacity, and their sodium tetrahydroborate-reduced derivatives, have been synthesized. Their oxo-vanadium(V) and -molybdenum(VI) complexes were synthesized and characterized using several analytical and spectral techniques including multinuclear NMR spectroscopy and single-crystal X-ray diffraction studies. Eight structurally different types of complexes possessing distorted square-pyramidal, trigonal-bipyramidal and octahedral geometries have been obtained. While (VO)-O-V exhibits dimeric Structures with 2-HOC6H4CH=NC(CH2OH)(3) and 2-HOC6H4CH2-NHC(CH2OH)(3) and related ligands through the formation of a symmetric V2O2 core as a result of bridging of one of the CH2O- groups, Mo O-VI gives only mononuclear complexes even when some unbound CH2OH groups are available and the metal center is co-ordinatively unsaturated. In all the complexes the nitrogen atom from a HC=N or H2CNH group of the ligand occupies a near trans position to the M=O bond. While the Schiff-base ligands act in a tri- and tetra-dentate manner in the vanadium(V) complexes, they are only tridentate in the molybdenum(VI) complexes. Proton NMR spectra in the region of bound CH, provides a signature that helps to differentiate dinuclear from mononuclear complexes. Carbon-13 NMR co-ordination induced shifts of the bound CH, group fit well with the charge on the oxometal species and the terminal or bridging nature of the ligand. The reactivity of the vanadium(V) complexes towards bromination of the dye xylene cyanole was studied. Transmetallation reactions of several preformed metal complexes of 2-HOC6H4CH=NC(CH2OH)(3) with VO3+ were demonstrated as was selective extraction of VO3+ from a mixture of VO(acac)(2)] and MoO2(acac)(2)] using this Schiff base. The unusual selectivity and that of related derivatives for VO3+ is supported by binding constants and the solubility of the final products, and was established through a.c. conductivity measurements. The cis-MoO22+ complexes with alkoxo binding showed an average Mo-O-alk distance of 1.926 Angstrom, a value that is close to that observed in the molybdenum(VI) enzyme dmso reductase (1.92 Angstrom). Several correlations have been drawn based on the data

In vivo measurement of apolipoprotein E from the brain interstitial fluid using microdialysis

BACKGROUND: The APOE4 allele variant is the strongest known genetic risk factor for developing late-onset Alzheimer’s disease. The link between apolipoprotein E (apoE) and Alzheimer’s disease is likely due in large part to the impact of apoE on the metabolism of amyloid β (Aβ) within the brain. Manipulation of apoE levels and lipidation within the brain has been proposed as a therapeutic target for the treatment of Alzheimer’s disease. However, we know little about the dynamic regulation of apoE levels and lipidation within the central nervous system. We have developed an assay to measure apoE levels in the brain interstitial fluid of awake and freely moving mice using large molecular weight cut-off microdialysis probes. RESULTS: We were able to recover apoE using microdialysis from human cerebrospinal fluid (CSF) in vitro and mouse brain parenchyma in vivo. Microdialysis probes were inserted into the hippocampus of wild-type mice and interstitial fluid was collected for 36 hours. Levels of apoE within the microdialysis samples were determined by ELISA. The levels of apoE were found to be relatively stable over 36 hours. No apoE was detected in microdialysis samples from apoE KO mice. Administration of the RXR agonist bexarotene increased ISF apoE levels while ISF Aβ levels were decreased. Extrapolation to zero-flow analysis allowed us to determine the absolute recoverable concentration of apoE3 in the brain ISF of apoE3 KI mice. Furthermore, analysis of microdialysis samples by non-denaturing gel electrophoresis determined lipidated apoE particles in microdialysis samples were consistent in size with apoE particles from CSF. Finally, we found that the concentration of apoE in the brain ISF was dependent upon apoE isoform in human apoE KI mice, following the pattern apoE2>apoE3>apoE4. CONCLUSIONS: We are able to collect lipidated apoE from the brain of awake and freely moving mice and monitor apoE levels over the course of several hours from a single mouse. Our technique enables assessment of brain apoE dynamics under physiological and pathophysiological conditions and in response to therapeutic interventions designed to affect apoE levels and lipidation within the brain