ECU-oriented models for NOx prediction. Part 1: a mean value engine model for NOx prediction

The implantation of nitrogen oxide sensors in diesel engines was proposed in order to track the emissions at the engine exhaust, with applications to the control and diagnosis of the after-treatment devices. However, the use of models is still necessary since the output from these sensors is delayed and filtered. The present paper deals with the problem of nitrogen oxide estimation in turbocharged diesel engines combining the information provided by both models and sensors. In Part 1 of this paper, a control-oriented nitrogen oxide model is designed. The model is based on the mapping of the nitrogen oxide output and a set of corrections which account for the variations in the intake and ambient conditions, and it is designed for implementation in commercial electronic control units. The model is sensitive to variations in the engine's air path, which is solved through the engine volumetric efficiency and the first-principle equations but disregards the effect of variation in the injection settings. In order to consider the effect of the thermal transients on the in-cylinder temperature, the model introduces a dynamic factor. The model behaves well in both steady-state operation and transient operation, achieving a mean average error of 7% in the steady state and lower than 10% in an exigent sportive driving mountain profile cycle. The relatively low calibration effort and the model accuracy show the feasibility of the model for exhaust gas recirculation control as well as onboard diagnosis of the nitrogen oxide emissions.Guardiola, C.; Pla Moreno, B.; Blanco-Rodriguez, D.; Calendini, PO. (2015). ECU-oriented models for NOx prediction. Part 1: a mean value engine model for NOx prediction. Proceedings of the Institution of Mechanical Engineers, Part D: Journal of Automobile Engineering. 229(8):992-1015. doi:10.1177/0954407014550191S9921015229

Maximum-Likelihood Parameter Estimation in Terahertz Time-Domain Spectroscopy

We present a maximum-likelihood method for parameter estimation in terahertz time-domain spectroscopy. We derive the likelihood function for a parameterized frequency response function, given a pair of time-domain waveforms with known time-dependent noise amplitudes. The method provides parameter estimates that are superior to other commonly used methods and provides a reliable measure of the goodness of fit. We also develop a simple noise model that is parameterized by three dominant sources and derive the likelihood function for their amplitudes in terms of a set of repeated waveform measurements. We demonstrate the method with applications to material characterization

Social Capital, Network Governance and Social Innovation: Towards a New Paradigm?

Limited knowledge and empirical evidence exist so far on how governance is related to social capital, and to comprehensively evaluate the effects of collaborative public-private partnerships in rural development actions, and whether these elements foster socially innovative actions. The book chapter begins to address these knowledge gaps. It highlights the conceptual framework linking social capital and network governance and identifies specific approaches to analysing governance. Moreover, it conceptually identifies the key elements for assessing governance mechanisms in the LEADER approach and explains its adoption in the evaluation method proposed in the book. The chapter concludes by outlining how social capital and governance may support social innovation, a topic which is developed more comprehensively in relation to LEADER's specific contribution in the final chapter of the same book

MAO-B Elevation in Mouse Brain Astrocytes Results in Parkinson's Pathology

Age-related increases in monoamine oxidase B (MAO-B) may contribute to neurodegeneration associated with Parkinson's disease (PD). The MAO-B inhibitor deprenyl, a long-standing antiparkinsonian therapy, is currently used clinically in concert with the dopamine precursor L-DOPA. Clinical studies suggesting that deprenyl treatment alone is not protective against PD associated mortality were targeted to symptomatic patients. However, dopamine loss is at least 60% by the time PD is symptomatically detectable, therefore lack of effect of MAO-B inhibition in these patients does not negate a role for MAO-B in pre-symptomatic dopaminergic loss. In order to directly evaluate the role of age-related elevations in astroglial MAO-B in the early initiation or progression of PD, we created genetically engineered transgenic mice in which MAO-B levels could be specifically induced within astroglia in adult animals. Elevated astrocytic MAO-B mimicking age related increase resulted in specific, selective and progressive loss of dopaminergic neurons in the substantia nigra (SN), the same subset of neurons primarily impacted in the human condition. This was accompanied by other PD-related alterations including selective decreases in mitochondrial complex I activity and increased mitochondrial oxidative stress. Along with a global astrogliosis, we observed local microglial activation within the SN. These pathologies correlated with decreased locomotor activity. Importantly, these events occurred even in the absence of the PD-inducing neurotoxin MPTP. Our data demonstrates that elevation of murine astrocytic MAO-B by itself can induce several phenotypes of PD, signifying that MAO-B could be directly involved in multiple aspects of disease neuropathology. Mechanistically this may involve increases in membrane permeant H2O2 which can oxidize dopamine within dopaminergic neurons to dopaminochrome which, via interaction with mitochondrial complex I, can result in increased mitochondrial superoxide. Our inducible astrocytic MAO-B transgenic provides a novel model for exploring pathways involved in initiation and progression of several key features associated with PD pathology and for therapeutic drug testing

Transient receptor potential canonical 4 and 5 proteins as targets in cancer therapeutics

Novel approaches towards cancer therapy are urgently needed. One approach might be to target ion channels mediating Ca²+ entry because of the critical roles played by Ca²+ in many cell types, including cancer cells. There are several types of these ion channels, but here we address those formed by assembly of transient receptor potential canonical (TRPC) proteins, particularly those which involve two closely related members of the family: TRPC4 and TRPC5. We focus on these proteins because recent studies point to roles in important aspects of cancer: drug resistance, transmission of drug resistance through extracellular vesicles, tumour vascularisation, and evoked cancer cell death by the TRPC4/5 channel activator (−)-englerin A. We conclude that further research is both justified and necessary before these proteins can be considered as strong targets for anti-cancer cell drug discovery programmes. It is nevertheless already apparent that inhibitors of the channels would be unlikely to cause significant adverse effects, but, rather, have other effects which may be beneficial in the context of cancer and chemotherapy, potentially including suppression of innate fear, visceral pain and pathological cardiac remodelling