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For an increasing number of older individuals over 50, entrepreneurship is becoming a means of finding new opportunities, fulfilling long held ambitions or, of augmenting retirement income. Yet, despite its potential benefits to individuals and the economy, understanding of later-life entrepreneurship is often only limited to describing this phenomenon as unnuanced and uniform, while ignoring substantial gendered heterogeneity in decisions about later-life entrepreneurship. This doctoral thesis extends the current view of later-life entrepreneurship to a nuanced, interconnected process. A qualitative research methodology is selected, underpinned by interpretative philosophy. To improve understanding of the gendered aspects of why and how later-life entrepreneurship is ignited, semi-structured interviews were conducted with 32 individuals over the age of 50 living in the United Kingdom. The analysed data informed an emergent, dynamic model that conceptualises the gendered aspects of acquiring age capital for venture creation in later life. The model captures the triggers, conflicting drivers, enablers, and barriers associated with this phenomenon. It illuminates laterlife entrepreneurship not as a simple action, but as a dynamic, complex process and explains the gendered complexities of motivational triggers, the conflicting drivers of the normative environment and the process of accumulating different forms of capital for venture creation. A key contribution of this research is extending the use of three theoretical lenses (one lead theory and two supporting theories), which highlights the limitations of being guided by only one theory, and the explanatory power offered by applying aspects of several theoretical frameworks. With regard the contribution to knowledge of the empirical findings, a nuanced, gendered perspective identified from the findings, contributes towards creating distinctive challenges for policy makers and other stakeholders designing business support.

Despite major advances in techniques of imaging the human brain, there is still uncertainty about the exact time at which many fetal and neonatal brain lesions occur. Pathological appearances do not always help owing to the difficulty in establishing the exact sequence of the tissue response to brain injury. In the first part of the present study, 179 post-mortem human brains from fetal, neonatal and infant cases (varying in age from the first trimester of gestation to children of 7 years of age) were examined macroscopically and by light microscopy. Of these brains, 69 showed no pathological abnormality, 98 had hypoxic/ischaemic lesions, 5 displayed congenital abnormalities and 4 brains showed venous infarcts. Hypoxic/ischaemic brain damage was the most common lesion in this series and affected fetuses from 16 weeks of gestation to term and infants who had survived to 19 months of age. This group was ideal for studying the glial, inflammatory and blood vessel responses to brain damage in fetal and early postnatal life. Light microscopical studies included immunocytochemistry for Glial Fibrillary Acidic Protein (GFAP) - an astrocyte marker, S-100 protein - a glial marker, fibronectin - a marker for the connective tissue in blood vessel walls, factor VIII Related Antigen - an endothelial cell marker and S22 - a macrophage marker. The expression of these markers was also assessed in the normal developing human brain. The second part of the study was designed to test the hypothesis that GFAP could be induced by injury to the fetal brain before the time at which it appears during normal fetal development. Cold lesions were inflicted upon fetal and neonatal rat brains and the glial response was examined by the immunoperoxidase staining technique. The expression of glial and mesenchymal cell markers in developing uninjured fetal and neonatal animals was also assessed. The results of this combined human and experimental study suggest that: a) The expression of GFAP by developing astrocytes can be induced by injury to the CNS in an area and at a time at which it is not observed in the normal developing brain b) In the human brain, formation of glial scar tissue occurs as early as 22 weeks of gestation in fetuses with hypoxic/ischaemic brain damage c) After 22 weeks gestation in man and 16 day gestation in the rat, the formation of glial scar tissue depends on the period elapsing from the time of injury to the moment of death, irrespective of age. d) The glial response is similar in different types of injury and in brains injured in utero or in postnatal life. Following this study a more logical approach has been adopted for the assessment of fetal and neonatal brain damage.