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The image of a refugee camp is often portrayed as a suspended space of exception, an inhospitable environment where refugees live in limbo-like states disconnected from the rest of the world. Acknowledging the exceptionality of camps, I argue that a top-down institutional approach only illuminates half the story and neglects the multi-faceted spatial dynamics of everyday refugee life. Through an ethnographic lens that draws from two years of fieldwork and includes the voices of 40 participants, I explore the everyday identities and belongings of encamped Karen living in protracted displacement along the Thai-Myanmar border. By examining refugee presence in the 'lived' material space and the 'lived' mediated space, I attempt to unpack themes of stuckness, transcendence, bare life, and ordinariness. To explore how offline life intertwines with online life, I take a socio-technical approach and ask: how, if at all, encamped Karen articulate their everyday lives, identities, and sense of belonging within the material space of Mae La? To what extent are media technologies used by inhabitants and their role in expressing everyday identities and belongings? To what extent, if at all, do new media technologies, mediated communication practices, and mediated environments interweave into everyday encamped life? In the context of Mae La, I found that refugees live in many different spaces where multiple identities coexist and circulate simultaneously. Although I recognise Mae La's exceptionality, I observe that life is not only lived in a state of suspension but is rich with an abundance of stories, memories, contradictions, and ambiguity. Participants demonstrated resistance to their prolonged encampment through practices such as music, rituals, and selfies. Mae La is evolving, and contrary to the past, inhabitants with access to new media technologies and mediated spaces take control of their representation and offer an account of their lives.

Idiopathic pulmonary fibrosis (IPF) is a type of chronic, interstitial lung disease, characterised by aberrant extracellular matrix (ECM) deposition. It is an ageing-associated disease, with a poor prognosis and limited treatments are available. Epithelial-mesenchymal transition (EMT) is a biological process where epithelial cells lose cell polarity and cell junctions, gaining a mesenchymal phenotype. The role of EMT, in the generation of fibroblasts in IPF, is controversial, with studies now suggesting that EMT contributes indirectly. Here, we utilised bioinformatic analysis to evaluate IPF microarray datasets. We showed that the epidermal growth factor receptor-mitogen-activated protein kinase (EGFR-MAPK) pathway and EMT could both be involved in the pathogenesis of IPF. These findings were validated with proteomic analysis of RAS-activated alveolar type II epithelial (ATIIER:KRASV 12) cells, where EMT was identified as a top process. In vitro studies of ATIIER:KRASV 12 cells were used to dissect the mechanisms underlying these processes. We found that RAS-activated EMT was induced via the EGFR-RAS-ERK-ZEB1 axis, but it was insufficient to induce the expression of ECM components in IPF. Autophagy was shown to be reduced in IPF. As autophagy and EMT have a complicated relationship, we explored this in IPF. Using ATII cells, we showed that autophagy inhibition induced EMT via the p62/NF-κB/Snail2 axis. In a similar manner to RAS-induced EMT, autophagy inhibition-induced EMT was insufficient to produce ECM components, however it did mediate secreted factors which were able to augment fibrosis via Snail2. Together, these findings demonstrate the importance of the EGFR-RAS signalling pathway and autophagy in the pathogenesis of IPF. EMT was induced in ATII cells, but was not sufficient to augment fibrosis directly. We demonstrate that secreted factors, induced by EMT, promote fibrosis. This thesis advances the understanding of the mechanisms underlying the activation of EMT in the fibrotic lung, but also, how this can indirectly result in fibrosis by paracrine signalling mechanisms.

This thesis examines changes in medium secure care over the past two decades in the context of developments in legislation and the forensic care pathway. Chapter two provides a baseline of medium secure care between 1997/98 based on an existing cohort of 958 patients across England and Wales and enables comparisons with later chapters. A secondary analysis was conducted to show the relationship between patient characteristics with medium secure service provision and reconviction up to six years following discharge. A logistic regression revealed that criminogenic factors strongly predicted reconviction without improvement with the addition of clinical and social factors, although the criminogenic profile of patients was not associated with decisions regarding the discharge pathway or allocation of restriction orders for patients. All remaining empirical chapters include longitudinal, retrospective studies that investigated a cohort of 285 forensic patients discharged from a Welsh medium secure hospital between 1999 and 2017. Chapter three presents a study that revealed changes in medium secure care over time that included: more high-risk patients with experiences of social deprivation admitted to medium security, an increase in restrictive practice and greater recovery outcomes for patients. Chapter four includes astudy that explored the factors that navigated the clinical decision-making of where patients were discharged from medium security and included: self-care and activities of daily living, engagement with family and social networks, the leave status of patients and a diagnosis of a psychotic related disorder. Chapter five presents a study that showed no significant change in the readmission rate(up to six years)following discharge from medium secure care between 1999 and 2017. Logistic regression showed that the number of previous psychiatric admissions was a hazard of readmission. A discussion of each empirical chapter and an integration of the findings concludes the thesis.

Epilepsy affects 50 million people worldwide and is characterised by spontaneous recurring seizures. Current anti-epileptic drugs (AEDs) control seizure activity, but are neither preventative nor curative. However, approximately one in three people with epilepsy do not have their seizures adequately controlled with currently available AEDs. Therefore, ongoing research into novel AEDs is still warranted. Research conducted at the University of Reading has demonstrated the non-psychoactive phytocannabinoids cannabidiol (CBD) and cannabidivarin (CBDV) to exert significant anti-epileptiform and anticonvulsant properties in vitro and in vivo. However, the mechanism/s by which CBD and CBDV mediate these effects are currently unknown. The aims of this research were to investigate the effects of CBD, and primarily CBDV, on synaptic transmission using extracellular and intracellular electrophysiological techniques in normal, healthy brain tissue and brain tissue from a rat model of temporal lobe epilepsy. Acute transverse hippocampal slices were taken from young (P24-28) control rats, rats with epilepsy (~P50-60) and age-matched (~P50-60) non-epileptic control rats. Pairs of evoked local field potentials were recorded from the CA1 region using multi-electrode arrays and the paired pulse ratio (PPR) was obtained. Whole cell patch clamp of CA1 pyramidal cells was used to record miniature and spontaneous inhibitory postsynaptic currents (mIPSCs and sIPSCs, respectively). Cumulative concentrations of CBD and CBDV significantly reduced the PPR in hippocampal slices from control rats and cumulative concentrations of CBDV significantly reduced the PPR in hippocampal slices from rats confirmed to have epilepsy. The effect of cumulative concentrations of CBDV on PPR in hippocampal slices from rats with epilepsy was stronger than that observed in slices from P50-60 control rats, as CBDV reduced the PPR across a greater range of inter-stimulus intervals. In hippocampal slices from CBDV-treated rats with epilepsy, application of acute CBDV was more effective at reducing the PPR across a wider range of inter­stimulus intervals and suggests that chronic treatment with CBDV may 'unmask' the effect of acute CBDV. In hippocampal slices from rats with epilepsy, mIPSC frequency was significantly reduced and indicates a deficit in the presynaptic quantal release of GABA neurotransmitter in the CA1 region. CBDV had no effect on mIPSC amplitude or frequency in hippocampal slices from both P24-28 control rats and rats with epilepsy, CBDV significantly reduced sIPSC frequency without affecting sIPSC amplitude in hippocampal slices from control rats. However, in hippocampal slices from rats with epilepsy, CBDV had no effect on sIPSC amplitude or frequency. The results of the patch clamp experiments are consistent with CBDV decreasing action potential-dependent presynaptic release of GABA from inhibitory interneurones in hippocampal slices from control rats, but not in rats with epilepsy. In conclusion, CBD and CBDV alter synaptic transmission in the CA1 region of the hippocampus to enhance glutamatergic signalling via a mechanism that is likely to be presynaptic in origin and may involve the modulation of [Ca2+] and a change in release probability of neurotransmitter. The effect of CBDV on the PPR was similar in hippocampal slices from both epileptic and non­epileptic rats, which suggests a common mechanism to alter synaptic transmission in both tissues. In addition, chronic CBDV-treatment may also increase the effectiveness of the mechanism by which CBDV reduces the PPR in hippocampal tissue from rats confirmed to have epilepsy. Finally, epilepsy altered inhibitory neurotransmission in the CA1 area, which is likely to be due to the reduction in quanta! release of GABA from interneurones that synapse onto CA1 pyramidal neurones. CBDV may have a disease-dependent effect on inhibitory neurotransmission in hippocampus CA1, as CBDV reduced the action-potential-dependent release of GABA in tissue from control rats, but had no effect in tissue from epileptic rats.