Dispersion aspects of periodically amplified soliton transmission systems

This thesis presents improvements to optical transmission systems through the use of optical solitons as a digital transmission format, both theoretically and experimentally. An introduction to the main concepts and impairments of optical fibre on pulse transmission is included before introducing the concept of solitons in optically amplified communications and the problems of soliton system design. The theoretical work studies two fibre dispersion profiling schemes and a soliton launch improvement. The first provides superior pulse transmission by optimally tailoring the fibre dispersion to better follow the power, and hence nonlinearity, decay and thus allow soliton transmission for longer amplifier spacings and shorter pulse widths than normally possible. The second profiling scheme examines the use of dispersion compensating fibre in the context of soliton transmission over existing, standard fibre systems. The limits for solitons in uncompensated standard fibre are assessed, before the potential benefits of dispersion compensating fibre included as part of each amplifier are shown. The third theoretical investigation provides a simple improvement to the propagation of solitons in a highly perturbed system. By introducing a section of fibre of the correct length prior to the first system amplifier span, the soliton shape can be better coupled into the system thus providing an improved "average soliton" propagation model. The experimental work covers two areas. An important issue for soliton systems is pulse sources. Three potential lasers are studied, two ring laser configurations and one semiconductor device with external pulse shaping. The second area studies soliton transmission using a recalculating loop, reviewing the advantages and draw-backs of such an experiment in system testing and design. One particular example of employing the recirculating loop is also examined, using a novel method of pulse shape stabilisation over long distances with low jitter. The future for nonlinear optical communications is considered with the thesis conclusions.

The impact of the CACNA1C gene polymorphism on frontolimbic function in bipolar disorder

Genome-wide association studies in bipolar disorder (BD)1 have implicated a single-nucleotide polymorphism (rs1006737, G right arrow A) in the CACNA1C gene, which encodes for the alpha 1c (CAV1.2) subunit of the voltage-gated, L-type calcium channel. Neuroimaging studies of healthy individuals report that this risk allele modulates brain function within limbic (amygdala, anterior cingulate gyrus) and hippocampal regions during tasks of reward processing2, 3 and episodic memory. Moreover, animal studies suggest that the CaV1.2 L-type calcium channels influence emotional behaviour through enhanced neurotransmission via the lateral amygdala pathway. On the basis of this evidence, we tested the hypotheses that the CACNA1C rs1006737 risk allele will modulate neural responses within predefined prefrontal and subcortical regions of interest during emotional face processing and that this effect would be amplified in BD patients.

The upstream Variable Number Tandem Repeat polymorphism of the monoamine oxidase type A gene influences trigeminal pain-related evoked responses

Monoamines have an important role in neural plasticity, a key factor in cortical pain processing that promotes changes in neuronal network connectivity. Monoamine oxidase type A (MAOA) is an enzyme that, due to its modulating role in monoaminergic activity, could play a role in cortical pain processing. The X-linked MAOA gene is characterized by an allelic variant of length, the MAOA upstream Variable Number Tandem Repeat (MAOA-uVNTR) region polymorphism. Two allelic variants of this gene are known, the high-activity MAOA (HAM) and low-activity MAOA (LAM). We investigated the role of MAOA-uVNTR in cortical pain processing in a group of healthy individuals measured by the trigeminal electric pain-related evoked potential (tPREP) elicited by repeated painful stimulation. A group of healthy volunteers was genotyped to detect MAOA-uVNTR polymorphism. Electrical tPREPs were recorded by stimulating the right supraorbital nerve with a concentric electrode. The N2 and P2 component amplitude and latency as well as the N2-P2 inter-peak amplitude were measured. The recording was divided into three blocks, each containing 10 consecutive stimuli and the N2-P2 amplitude was compared between blocks. Of the 67 volunteers, 37 were HAM and 30 were LAM. HAM subjects differed from LAM subjects in terms of amplitude of the grand-averaged and first-block N2-P2 responses (HAM>LAM). The N2-P2 amplitude decreased between the first and third block in HAM subjects but not LAM subjects. The MAOA-uVNTR polymorphism seemed to influence the brain response in a repeated tPREP paradigm and suggested a role of the MAOA as a modulator of neural plasticity related to cortical pain processing. Monoamines have an important role in neural plasticity, a key factor in cortical pain processing that promotes changes in neuronal network connectivity. Monoamine oxidase type A (MAOA) is an enzyme that, due to its modulating role in monoaminergic activity, could play a role in cortical pain processing. © 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.