An Application of Optimized Bistable Laminates as a Low Velocity, Low Impact Mechanical Deterrent

This research considers the problem of using bistable laminates as a mechanical deterrent to the impending impact of a particle. The structure will be controlled through an algorithm that will utilize piezoelectric devices to activate them in unison with the bistable laminate to successfully deter. A novel experimental setup will be constructed to ensure that the bistable laminate stays fixed when acting as a mechanical deterrent. Piezoelectricity is the main driving force of the bistable laminate to morph and this study will use a Macro Fiber Composite (MFC) actuator that contains piezoelectric ceramic rods in a patch to transfer electrical energy into mechanical action. The bistability of the composite laminate is the ability to morph between two stable forms of the stacked laminate that will act as the moving element to deflect the incoming particle. The bistable mechanism containing the piezoelectric patch and bistable composite will undergo an optimization algorithm to maximize the chances of a successful deflection event. Having greater distance between states increases the chances of ensuring proper contact with the particle. Optimization can be utilized to maximize the total deflection between states of the bistable composite structure while also maximizing the piezoelectric limits. Areas that influence the bistable laminate such as deformation amount, edge lengths, and MFC patch compatibility will be included in the optimization algorithm. The MFC patch will influence the mechanism based on its active lengths and free strain. For this application-based approach, three different sizes of MFC piezoelectric patches will be used. Based on the particle\u27s characteristics, the timing of the bistable composite mechanism with the MFC patch will be rigorously studied to ensure proper deflection or reduction of impact through a Data Acquisition System and High Voltage Amplifier

Numerical Solutions of Matrix Differential Models using Cubic Matrix Splines II

This paper presents the non-linear generalization of a previous work on matrix differential models. It focusses on the construction of approximate solutions of first-order matrix differential equations Y'(x)=f(x,Y(x)) using matrix-cubic splines. An estimation of the approximation error, an algorithm for its implementation and illustrative examples for Sylvester and Riccati matrix differential equations are given.Comment: 14 pages; submitted to Math. Comp. Modellin

Designing and analysing feasibility studies of complex interventions: challenges related to assessing stop/go criteria

Randomised controlled trials (RCTs) are time-consuming and costly so funders often require evidence of feasibility before they will fund large scale trials1. Feasibility studies can provide invaluable evidence relating to the practicalities of conducting large RCTs and can improve their likelihood of success. However, conducting feasibility studies of complex interventions and deciding whether or not to proceed to a full RCT, is not always straightforward. We will present the challenges encountered during the design and analysis of two feasibility studies: OBI (Optimised Behavioural Intervention for avoidant chronic low back pain patients) and MIDSHIPS (Multicentre Intervention Designed for Self-Harm using Interpersonal Problem Solving) and discuss the steps taken to overcome them. Recruiting and treating participants in a limited number of centres, with few therapists, is a complex challenge for both of these feasibility studies and crucial to determining their success; we will present the lessons learnt from our experience. We will also discuss the impact of missing data on our ability to assess stop/go criteria with respect to proof-of-concept. Estimating follow-up questionnaire response rates is an important objective in both studies, hence we will discuss the methods employed to maximise data collection and present our approach for providing robust estimates of response rates for the phase III trials

Tract-specific differences in white matter microstructure between young adult APOE ε4 carriers and non-carriers:A replication and extension study

The parahippocampal cingulum bundle (PHCB) interconnects regions known to be vulnerable to early Alzheimer's disease (AD) pathology, including posteromedial cortex and medial temporal lobe. While AD-related pathology has been robustly associated with alterations in PHCB microstructure, specifically lower fractional anisotropy (FA) and higher mean diffusivity (MD), emerging evidence indicates that the reverse pattern is evident in younger adults at increased risk of AD. In one such study, Hodgetts et al. (2019) reported that healthy young adult carriers of the apolipoprotein-E (APOE) ε4 allele – the strongest common genetic risk factor for AD – showed higher FA and lower MD in the PHCB but not the inferior longitudinal fasciculus (ILF). These results are consistent with proposals claiming that heightened neural activity and intrinsic connectivity play a significant role in increasing posteromedial cortex vulnerability to amyloid-β and tau spread beyond the medial temporal lobe. Given the implications for understanding AD risk, here we sought to replicate Hodgetts et al.‘s finding in a larger sample (N = 128; 40 APOE ε4 carriers, 88 APOE ε4 non-carriers) of young adults (age range = 19–33). Extending this work, we also conducted an exploratory analysis using a more advanced measure of white matter microstructure: hindrance modulated orientational anisotropy (HMOA). Contrary to the original study, we did not observe higher FA or lower MD in the PHCB of APOE ε4 carriers relative to non-carriers. Bayes factors (BFs) further revealed moderate-to-strong evidence in support of these null findings. In addition, we observed no APOE ε4-related differences in PHCB HMOA. Our findings indicate that young adult APOE ε4 carriers and non-carriers do not differ in PHCB microstructure, casting some doubt on the notion that early-life variation in PHCB tract microstructure might enhance vulnerability to amyloid-β accumulation and/or tau spread

Tract-specific differences in white matter microstructure between young adult APOE ε4 carriers and non-carriers: A replication and extension study

The parahippocampal cingulum bundle (PHCB) interconnects regions known to be vulnerable to early Alzheimer's disease (AD) pathology, including posteromedial cortex and medial temporal lobe. While AD-related pathology has been robustly associated with alterations in PHCB microstructure, specifically lower fractional anisotropy (FA) and higher mean diffusivity (MD), emerging evidence indicates that the reverse pattern is evident in younger adults at increased risk of AD. In one such study, Hodgetts et al. (2019) reported that healthy young adult carriers of the apolipoprotein-E (APOE) ε4 allele – the strongest common genetic risk factor for AD – showed higher FA and lower MD in the PHCB but not the inferior longitudinal fasciculus (ILF). These results are consistent with proposals claiming that heightened neural activity and intrinsic connectivity play a significant role in increasing posteromedial cortex vulnerability to amyloid-β and tau spread beyond the medial temporal lobe. Given the implications for understanding AD risk, here we sought to replicate Hodgetts et al.‘s finding in a larger sample (N = 128; 40 APOE ε4 carriers, 88 APOE ε4 non-carriers) of young adults (age range = 19–33). Extending this work, we also conducted an exploratory analysis using a more advanced measure of white matter microstructure: hindrance modulated orientational anisotropy (HMOA). Contrary to the original study, we did not observe higher FA or lower MD in the PHCB of APOE ε4 carriers relative to non-carriers. Bayes factors (BFs) further revealed moderate-to-strong evidence in support of these null findings. In addition, we observed no APOE ε4-related differences in PHCB HMOA. Our findings indicate that young adult APOE ε4 carriers and non-carriers do not differ in PHCB microstructure, casting some doubt on the notion that early-life variation in PHCB tract microstructure might enhance vulnerability to amyloid-β accumulation and/or tau spread