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Background. Mindfulness-based Cognitive Therapy (MBCT) is a relapse-prevention treatment for people in remission from major depression (rMDD). The neuropsychological mechanisms of MBCT are largely unknown. The key theoretical mechanisms of MBCT include self-compassion and rumination, with other mindfulness-based studies suggesting mechanisms across domains of attention, emotional processing, and cognitive flexibility. The aims of this thesis were to investigate the neuropsychological and neuroimaging mechanisms of MBCT in rMDD and to investigate relationships with relapse six months beyond MBCT. Paper One. 40 MBCT, 33 Treatment As Usual (TAU), and 42 healthy volunteers (HVs) took part. Experimental tasks for self-compassion and rumination were completed at baseline and post-session, alongside self-report questionnaires. Results showed increases for self-compassion following MBCT, with non-specific reductions for rumination. Paper Two. 40 MBCT, 33 TAU, and 42 HV participants took part. Tasks of attention, emotional processing, and cognitive flexibility were completed at baseline and post-session. Results showed increases in positive emotions post-MBCT, with non-specific changes for face emotion recognition and affective attentional bias tasks both post-MBCT and TAU. There were no changes over time for sustained attention or cognitive flexibility. Paper Three. 16 rMDD participants completed baseline and post-MBCT fMRI tasks of sustained attention and self-blame. Results showed reduced activation over time in the bilateral dACC in self-blame contrasts but no activation changes for sustained attention. Paper Four. 69 rMDD participants (38 MBCT & 31 TAU) completed task-based and self-report assessments up to six months follow-up. Non-relapsing MBCT participants showed increased self-compassion post-session which was maintained in follow-up. MBCT non-relapsing and TAU participants showed reduced rumination post-session and in follow-up. Conclusions. MBCT encourages a move towards more self-compassionate, positive processing but does not alter more automatic, bottom-up levels of processing. MBCT initiates a process for change beyond the course, particularly for self-compassion. Findings have theoretical and clinical implications and extend our understanding of the mechanisms of MBCT in rMDD participants.

Protein deposition in the form of amyloid fibrils is the hallmark of more than 40 human pathologies, including Alzheimer's disease (AD) and Parkinson's disease (PD). Misfolded protein oligomers formed as intermediates during the aggregation process have been strongly implicated in the onset and progression of these diseases. In this thesis, I describe our efforts to uncover molecular agents that can reduce the toxicity caused by protein aggregation via targeting the generation, the physiochemical properties or the membrane affinity of oligomeric species. We employed an integrative approach combining in vitro techniques, including chemical kinetics, atomic force microscopy, and biophysical measurements, and in vivo methods, including neuroblastoma cells and C. elegans models of AD and PD, to identify a range of small molecules and antibodies that can suppress the toxicity related to protein aggregation through a variety of mechanisms. In Chapter 3, we show that the deleterious effects of protein aggregation can be suppressed in AD and PD worms by interfering with the aggregation rates of the amyloid-β peptide (Aβ) and the α-synuclein protein (αS). In Chapter 4, we resolve the mechanism of action for a molecule that enhances the rate of Aβ42 aggregation in AD worms with the result that toxicity is reduced, and find that it potentiates the secondary nucleation microscopic step in vitro. In Chapter 5, we characterize molecules and antibodies that modify the physiochemical properties and self-association of oligomers comprised of several proteins into clusters with reduced diffusibility. In Chapter 6, we classify a family of molecules that protect the cell by displacing several types of oligomeric species from the membrane through a generic mechanism. These results demonstrate strategies by which one can target the aggregation process to alter its resulting toxicity, provide insight into modifying the properties of the most deleterious species associated with protein aggregation and suggest that the protection of the cell from the oligomer-induced cytotoxicity associated with numerous protein misfolding diseases is a promising strategy to combat protein misfolding diseases.

This survey study evaluates the incidence of tanning in adults who use indoor gyms.

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Loneliness is a risk factor for premature mortality but the mechanics of this relationship remain obscure. A potential mechanism is sleep disturbance. The present study aimed to examine the association between loneliness and sleep disturbance, evaluate loneliness as a risk factor for sleep disturbance and vice-versa, model effects between loneliness and sleep disturbance over time, and evaluate a mediation model of loneliness, sleep disturbance, and health. Data came from the 2006-2012 waves of the Health and Retirement Study, a nationally-representative study of older Americans; participants > 65 were included (n=11,400). Analyses included (i) linear regressions accounting for complex sampling and (ii) path analysis (cross-lagged panel and mediation models). Loneliness and sleep disturbance were correlated and were risk factors for one another. Cross-lagged panel models showed reciprocal effects between loneliness and sleep disturbance. Cross-lagged mediation models showed that loneliness predicted subsequent sleep disturbance, which in turn predicted poor self-reported health. Moreover, there was evidence of a direct and indirect effect of loneliness on sleep disturbance. All associations were weakened— but remained—when accounting for demographics, isolation, and depression. Collectively, these findings are consistent with the theory that sleep disturbance is a mechanism through which loneliness damages health. However, effects between loneliness and sleep are reciprocal, rather than unidirectional. Moreover, longitudinal effects were very small. Further research is necessary to speak to causality, assess daily associations between loneliness and sleep, assess a comprehensive model of the mechanics of loneliness and health, and examine loneliness and sleep in the context of other factors.

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Origami-adapted mechanisms form the basis of an increasing number of engineered systems. As most of these systems require the use of non-paper materials, various methods for accommodating thickness have been developed. These methods have opened new avenues for origami-based design. This work introduces approaches for the design of two new classes of thick-origami systems and demonstrates the approaches in hardware. One type of system, called "conceal-and-reveal,'' is introduced, and a method of designing these mechanisms is developed. Techniques are also developed for designing folding printed circuit boards which are fabricated from a single sheet of material. This enables areas of regional flexibility, leaving other areas stiff. This allows components to be attached to stiff regions and folding to occur at flexible regions. An optimization method is presented to design the geometry of surrogate hinges to aid in monolithic origami-based mechanisms such as flexible PCBs. Examples are shown which demonstrate each of these new techniques.