Jung and Goddess: the significance of Jungian and post-Jungian theory to the development of the Western Goddess Movement

This study is concerned with the significance of Jungian and post-Jungian theory to the development of the contemporary Western Goddess Movement, which includes the various self-identified nature-based, Pagan, Goddess Feminism, Goddess Consciousness, Goddess Spirituality, Wicca, and Goddess-centred faith traditions that have seen a combined increase in Western adherents over the past five decades and share a common goal to claim Goddess as an active part of Western consciousness and faith traditions. The Western Goddess Movement has been strongly influenced by Jung’s thought, and by feminist revisions of Jungian Theory, sometimes interpreted idiosyncratically, but presented as a route to personal and spiritual transformation. The analysis examines ways in which women encounter Goddess through a process of Jungian Individuation and traces the development of Jungian and post-Jungian theories by identifying the key thinkers and central ideas that helped to shape the development of the Western Goddess Movement. It does so through a close reading and analysis of five biographical ‘rebirth’ memoirs published between 1981 and 1998: Christine Downing’s (1981) The Goddess: Mythological Images of the Feminine; Jean Shinoda Bolen’s (1994) Crossing to Avalon: A Woman’s Midlife Pilgrimage; Sue Monk Kidd’s (1996) The Dance of the Dissident Daughter: A Woman’s Journey from Christian Tradition to the Sacred Feminine; Margaret Starbird’s (1998) The Goddess in the Gospels: Reclaiming the Sacred Feminine; and Phyllis Curott’s (1998) Book of Shadows: A Modern Woman’s Journey into the Wisdom of Witchcraft and the Magic of the Goddess. These five memoirs reflect the diversity of the faith traditions in the Western Goddess Movement. The enquiry centres upon two parallel and complementary research threads: 1) critically examining the content of the memoirs in order to determine their contribution to the development of the Goddess Movement and 2) charting and sourcing the development of the major Jungian and post-Jungian theories championed in the memoirs in order to evaluate the significance of Jungian and post-Jungian thought in the Movement. The aim of this study was to gain a better understanding of the original research question: what is the significance of Jungian and post-Jungian theory for the development of the Western Goddess Movement? Each memoir is subjected to critical review of its intended audiences, its achievements, its functions and strengths, and its theoretical frameworks. Research results offered more than the experiences of five Western women, it also provided evidence to analyse the significance of Jungian and post-Jungian theory to the development of the Western Goddess Movement. The findings demonstrate the vital contributions of the analytical psychology of Carl Jung, and post-Jungians M Esther Harding, Erich Neumann, Christine Downing, E.C. Whitmont, and Jean Shinoda Bolen; the additional contributions of Sue Monk Kidd, Margaret Starbird, and Phyllis Curott, and exhibit Jungian and post-Jungian pathways to Goddess. Through a variety of approaches to Jungian categories, these memoirs constitute a literature of Individuation for the Western Goddess Movement.

Essays on cultural and institutional dynamics in economic development using spatial analysis

This thesis seeks to research patterns of economic growth and development from a number of perspectives often resonated in the growth literature. By addressing themes about history, geography, institutions and culture the thesis is able to bring to bear a wide range of inter-related literatures and methodologies within a single content. Additionally, by targeting different administrative levels in its research design and approach, this thesis is also able to provide a comprehensive treatment of the economic growth dilemma from both cross-national and sub-national perspectives. The three chapters herein discuss economic development from two broad dimensions. The first of these chapters takes on the economic growth inquiry by attempting to incorporate cultural geography within a cross-country formal spatial econometric growth framework. By introducing the global cultural dynamics of languages and ethnic groups as spatial network mechanisms, this chapter is able to distinguish economic growth effects accruing from own-country productive efforts from those accruing from interconnections within a global productive network chain. From this, discussions and deductions about the implications for both developed and developing countries are made as regards potentials for gains and losses from such types and levels of productive integration. The second and third chapters take a different spin to the economic development inquiry. They both focus on economic activity in Africa, tackling the relevant issues from a geo-intersected dimension involving historic regional tribal homelands and modern national and subnational administrative territories. The second chapter specifically focuses on attempting to adopt historical channels to investigate the connection between national institutional quality and economic development in demarcated tribal homelands at the fringes of national African borders. The third chapter on the other hand focuses on looking closer at the effects of demarcations on economic activity. It particularly probes how different kinds of demarcation warranted by two different but very relevant classes of politico-economic players have affected economic activity quite distinguishably within the resulting subnational regions in Africa.

The role of non-coding RNA in the development of pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a progressive disease of the small pulmonary arteries, characterised by pulmonary vascular remodelling due to excessive proliferation and resistance to apoptosis of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs). The increased pulmonary vascular resistance and elevated pulmonary artery pressures result in right heart failure and premature death. Germline mutations of the bone morphogenetic protein receptor-2 (bmpr2) gene, a receptor of the transforming growth factor beta (TGF-β) superfamily, account for approximately 75%-80% of the cases of heritable form of PAH (HPAH) and 20% of sporadic cases or idiopathic PAH (IPAH). IPAH patients without known bmpr2 mutations show reduced expression of BMPR2. However only ~ 20% of bmpr2-mutation carriers will develop the disease, due to an incomplete penetrance, thus the need for a ‘second hit’ including other genetic and/or environmental factors is accepted. Diagnosis of PAH occurs most frequently when patients have reached an advanced stage of disease. Although modern PAH therapies can markedly improve a patient’s symptoms and slow the rate of clinical deterioration, the mortality rate from PAH remains unacceptably high. Therefore, the development of novel therapeutic approaches is required for the treatment of this multifaceted disease. Noncoding RNAs (ncRNAs) include microRNAs (miRNAs) and long noncoding RNAs (lncRNAs). MiRNAs are ~ 22 nucleotide long and act as negative regulators of gene ex-pression via degradation or translational inhibition of their target mRNAs. Previous studies showed extensive evidence for the role of miRNAs in the development of PAH. LncRNAs are transcribed RNA molecules greater than 200 nucleotides in length. Similar to classical mRNA, lncRNAs are translated by RNA polymerase II and are generally alternatively spliced and polyadenylated. LncRNAs are highly versatile and function to regulate gene expression by diverse mechanisms. Unlike miRNAs, which exhibit well-defined actions in negatively regulating gene expression via the 3’-UTR of mRNAs, lncRNAs play more diverse and unpredictable regulatory roles. Although a number of lncRNAs have been intensively investigated in the cancer field, studies of the role of lncRNAs in vascular diseases such as PAH are still at a very early stage. The aim of this study was to investigate the involvement of specific ncRNAs in the development of PAH using experimental animal models and cell culture. The first ncRNA we focused on was miR-143, which is up-regulated in the lung and right ventricle tissues of various animal models of PH, as well as in the lungs and PASMCs of PAH patients. We show that genetic ablation of miR-143 is protective against the development of chronic hypoxia induced PH in mice, assessed via measurement of right ventricular systolic pressure (RVSP), right ventricular hypertrophy (RVH) and pulmonary vascular remodelling. We further report that knockdown of miR-143-3p in WT mice via anti-miR-143-3p administration prior to exposure of mice to chronic hypoxia significantly decreases certain indices of PH (RVSP) although no significant changes in RVH and pulmo-nary vascular remodelling were observed. However, a reversal study using antimiR-143-3p treatment to modulate miR-143-3p demonstrated a protective effect on RVSP, RVH, and muscularisation of pulmonary arteries in the mouse chronic hypoxia induced PH model. In vitro experiments showed that miR-143-3p overexpression promotes PASMC migration and inhibits PASMC apoptosis, while knockdown miR-143-3p elicits the opposite effect, with no effects observed on cellular proliferation. Interestingly, miR-143-3p-enriched exosomes derived from PASMCs mediated cell-to-cell communication between PASMCs and PAECs, contributing to the pro-migratory and pro-angiogenic phenotype of PAECs that underlies the pathogenesis of PAH. Previous work has shown that miR-145-5p expression is upregulated in the chronic hypoxia induced mouse model of PH, as well as in PAH patients. Genetic ablation and pharmacological inhibition (subcutaneous injection) of miR-145-5p exert a protective against the de-velopment of PAH. In order to explore the potential for alternative, more lung targeted delivery strategies, miR-145-5p expression was inhibited in WT mice using intranasal-delivered antimiR-145-5p both prior to and post exposure to chronic hypoxia. The decreased expression of miR-145-5p in lung showed no beneficial effect on the development of PH compared with control antimiRNA treated mice exposed to chronic hypoxia. Thus, miR-143-3p modulated both cellular and exosome-mediated responses in pulmonary vascular cells, while the inhibition of miR-143-3p prevented the development of experimental pulmonary hypertension. We focused on two lncRNAs in this project: Myocardin-induced Smooth Muscle Long noncoding RNA, Inducer of Differentiation (MYOSLID) and non-annotated Myolnc16, which were identified from RNA sequencing studies in human coronary artery smooth muscle cells (HCASMCs) that overexpress myocardin. MYOSLID was significantly in-creased in PASMCs from patients with IPAH compared to healthy controls and increased in circulating endothelial progenitor cells (EPCs) from bmpr2 mutant PAH patients. Exposure of PASMCs to hypoxia in vitro led to a significant upregulation in MYOSLID expres-sion. MYOSLID expression was also induced by treatment of PASMC with BMP4, TGF-β and PDGF, which are known to be triggers of PAH in vitro. Small interfering RNA (siR-NA)-mediated knockdown MYOSLID inhibited migration and induced cell apoptosis without affecting cell proliferation and upregulated several genes in the BMP pathway in-cluding bmpr1α, bmpr2, id1, and id3. Modulation of MYOSLID also affected expression of BMPR2 at the protein level. In addition, MYOSLID knockdown affected the BMP-Smad and BMP-non-Smad signalling pathways in PASMCs assessed by phosphorylation of Smad1/5/9 and ERK1/2, respectively. In PAECs, MYOSLID expression was also induced by hypoxia exposure, VEGF and FGF2 treatment. In addition, MYOSLID knockdown sig-nificantly decreased the proliferation of PAECs. Thus, MYOSLID may be a novel modulator in pulmonary vascular cell functions, likely through the BMP-Smad and –non-Smad pathways. Treatment of PASMCs with inflammatory cytokines (IL-1 and TNF-α) significantly in-duced the expression of Myolnc16 at a very early time point. Knockdown of Myolnc16 in vitro decreased the expression of il-6, and upregulated the expression of il-1 and il-8 in PASMCs. Moreover, the expression levels of chemokines (cxcl1, cxcl6 and cxcl8) were sig-nificantly decreased with Myolnc16 knockdown. In addition, Myolnc16 knockdown decreased the MAP kinase signalling pathway assessed by phosphorylation of ERK1/2 and p38 MAPK and inhibited cell migration and proliferation in PASMCs. Thus, Myolnc16 may a novel modulator of PASMCs functions through anti-inflammatory signalling pathways. In summary, in this thesis we have demonstrated how miR-143-3p plays a protective role in the development of PH both in vivo animal models and patients, as well as in vitro cell cul-ture. Moreover, we have showed the role of two novel lncRNAs in pulmonary vascular cells. These ncRNAs represent potential novel therapeutic targets for the treatment of PAH with further work addressing to investigate the target genes, and the pathways modulated by these ncRNAs during the development of PAH.