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This research charts the long cultural trajectory of albinism from early modern travel encounters and Enlightenment exhibitions to medical classification and biological experimentation. It argues the whiteness of albinism functioned as a visible provocation to thinkers involved in work crucial to major conceptual developments in western science and medicine. It stresses this rare complexion was a prism through which medical and scientific researchers studied human variation, disease and inheritance. It examines how albinism paralleled a broader historical production of modern racial and pathological identities. T¬his research traces medico-scientific discourses in order to understand their affect on people diagnosed with albinism. It commences with analysis of ‘unusually white’ people in travel narratives and Enlightenment ephemera between 1650-1799. It bridges plural representations of ‘unusual whiteness’ as sub-human or racially distinct with the crystallisation from the 1770s of a pathological definition for ‘leucoethiopia’. It demonstrates circulation of medical case studies and the formal classification of albinism as congenital disease by medical men in 1822 reflected a far-reaching revolution in medical thought and practice across Europe. It links this medical paradigm shift with the rise of heredity theory from the 1850s. It argues widespread experimentation with albino animals supported fierce early twentieth-century debates among biologists about Mendel’s laws of heredity. It concludes with analysis of the dialectic between medical knowledge about albinism and ‘albino’ identities. It argues people with albinism both internalised and camouflaged medical associations with defect through the adoption of class privilege and individual social tactics. Overall, this research makes a significant claim to rethink the histories of race, disability and medicine. It spotlights albinism as a critical nexus to understand the making of the normal and the pathological body, and it pinpoints the unstable relationship between medical diagnosis and individual agency.

This thesis concerns the application of electron diffraction to the problem of structure solution. The technique of precession electron diffraction, in particular, is discussed as a method to improve the applicability of methods borrowed from X-ray crystallography to intensities measured from electron diffraction. Simulations are presented which demonstrate that diffracted intensities with precession electron diffraction are less sensitive to the phases of structure factors compared to those recorded without, consistent with the intensities becoming “more kinematical” in nature. The technique of automated diffraction tomography is developed. Transformations are derived which map the positions of diffraction maxima into three-dimensional reciprocal space following an automated peak detection process. The factors which complicate the process of unit cell determination are discussed, and an algorithm designed for autoindexing “obstinate” lists of X-ray reflections was found to be able to determine the unit cells accurately. Intensity measurements from the tomographically acquired diffraction patterns were taken in an automated fashion using this method, and Patterson maps calculated which were comparable with maps calculated from zone-axis precession electron diffraction intensities or kinematical simulation. An algorithm for geometrical refinement of the unit cell and tilting geometry is proposed. Finally, the application of the technique of precession electron diffraction, combined with techniques developed in the course of this research, is described in the context of the partial solution of an unknown intermediate form of tin oxide. The results support a revised form of a structure recently proposed from ab-initio structure simulations, with a tin sublattice similar to a supercell of the rutile structure of SnO2. Some signs of oxygen atoms were found in the Fourier maps, but the results of a least-squares refinement were unsatisfactory.

The lateralisation of sensory processing provides a measure of efficiency of information processing in the human brain. Several event-related potential (ERP) studies have suggested that the lateralisation of somatosensory processing is disturbed in schizophrenia, with individuals with the disorder exhibiting a symmetrical response over both parietal cortices in contrast to the contralaterally dominant response observable in healthy adults (Jones and Miller, 1981; Cooper et ai., 1985; Andrews et al., 1986). This finding has, however, been disputed by several other studies (Shagass et al., 1983; Furlong et ai., 1990; Allen et ai., 1991). Recent changes in ERP acquisition and analysis procedures, coupled with the emergence of functional magnetic resonance imaging (fMRI), dictate further investigation of this phenomenon. 24 right-handed medicated individuals with schizophrenia, 23 right-handed healthy individuals and 10 non-right-handed healthy individuals were recruited for an ERP study, which used a piezoelectric device attached to the index finger to elicit a passive somatosensory response. Little evidence of abnormallateralisation of somatosensory processing at PI, N1 and P3 latencies was found in individuals with schizophrenia, despite several amplitude reductions in these ERP components. The same sample also took part in an extended experiment modified for fMRI. In this study the schizophrenia group exhibited significantly diminished lateralisation of the primary somatosensory cortex (SI) response when compared to the healthy right-handed group (p=0.029) and a borderline reduction when compared to the healthy non-right-handed group (p=0.059). Furthermore, the contralateral SI response was shown to be significantly less focal in the schizophrenia group when compared to both healthy groups. Symptom analysis showed that high scores in the disorganisation syndrome were associated with loss of SI focalisation, in accord with Spitzer's cortical spreading hypothesis of disorganisation (Spitzer et ai., 1993; Spitzer et al., 1994; Spitzer, 1997). Given the disturbances observed in inter-hemispheric lateralisation and intra-hemispheric focalisation, it is likely that there is a generalised problem of cortical recruitment in schizophrenia. Anterior cingulate cortex (ACe) activity was compared between the study groups in light of the proposed roles of ACC in cortical recruitment and cerebral coordination. Our findings of reduced ACC activity in the schizophrenia group provide some support for the hypothesis that ACC dysfunction underlies the disturbances of lateralisation and focalisation reported in schizophrenia.