Reduction of anxiety in college students with Asperger\u27s disorder using behavioral relaxation training

The purpose of this study was to reduce levels of anxiety in college students with Asperger\u27s Disorder. Two students from Rowan University were taught Behavioral Relaxation Training over a period of four weeks. Measurements of anxiety and relaxation were gathered during biweekly sessions and those results were graphed. Results showed that a) behavioral relaxation training was quickly learned by participants and b) anxiety levels decreased on some measures with the use of behavioral relaxation. Issues facing those with Asperger\u27s Disorder were discussed as well as the wide variety of populations that have demonstrated positive change with behavioral relaxation training

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The design, synthesis and evaluation of Nrf2-Keap1 PPI inhibitors: a modular, virtual screening-led approach

Nrf2 (nuclear factor erythroid 2-related factor 2) is a cap’n’collar bZIP transcription factor and is the main activator of the transcription of over 100 genes that play roles in responses to oxidative stress and detoxifying xenobiotics. The main control of Nrf2 levels is exercised by Keap1 (Kelchlike ECH-associated protein 1) which facilitates the ubiquitination of Nrf2 and therefore its degradation. Keap1 is oxidation-sensitive and upon exposure to oxidants, it changes its conformation and binds Nrf2 tightly. Consequently, de novo-synthesised Nrf2 can accumulate. Following its discovery, Nrf2 received most attention in relation to cancer. Over the time, however, its implication in other pathologies have been more and more acknowledged, namely in inflammation and most importantly in neurodegenerative diseases. Especially Parkinson’s disease (PD), which is the second most common neurodegenerative disease, caused by the progressive loss of dopaminergic neurons in the substantia nigra, has been linked to oxidative stress. The role Nrf2 plays has been demonstrated in animal models of α-synuclein aggregation or chemically induced parkinsonism, where an increase in Nrf2 expression provided neuroprotection and a slowing of disease progression. Therefore, the inhibition of Keap1- mediated Nrf2 degradation presents a promising strategy for the mechanistic study and the therapy of PD. Several structures showing high potency towards Keap1 inhibition have been described, with activities in the nanomolar range. However, these compounds are large, or hydrophilic and charged. In order to develop new scaffolds, extensive virtual screening assays have been conducted which resulted in hits with promising molecular scaffolds. At the same time, chemical modifications on a known triazole structure have been performed in order to elucidate structure-activity relationships. In this thesis, the molecular modelling lead, as well the synthetic approach to both project components are described. Finally, the results of a competitive fluorescence polarisation (FP) assay for the second set of compounds are presented

Exploring the function of factor XIII free B subunit: Interactions with complement factors and a novel approach to identify potential binding partners.

Background The factor XIII (FXIII)-B subunit has a critical function as a carrier protein to stabilize FXIII-A in plasma and supply it to its main substrate, fibrinogen. However, the function of the excess free FXIII-B circulating in plasma is still elusive. Objectives In the present study, we explored potential interactions of free FXIII-B with complement factors and searched for novel binding partners. Methods We tested for cofactor activity in the degradation of complement C3b and C4b and used ELISA- and surface plasmon resonance-based binding assays to investigate interactions between FXIII-B and complement components. We performed immunoprecipitation and mass spectrometry analysis to identify potential binding partners of free FXIII-B in freshly drawn plasma samples. Results FXIII-B did not exhibit cofactor activity in the degradation of C3b and C4b similar to factor H and C4b-binding protein, nor did it bind to complement factors to a relevant extent. Identification of proteins potentially binding to free FXIII-B revealed high interindividual variation. We confirmed α2-macroglobulin (α2MG) as a candidate, although direct interactions or functional effects remain to be validated. Conclusions Our study reveals that free FXIII-B has no direct role in regulating the complement system, despite a structural similarity to major complement regulators. Further studies are needed to validate α2MG as a binding partner and explore potential functional consequences of this binding