Willingness to pay for change : the use of contingent valuation and choice experiments in the Trinidad and Tobago water services sector

Financing water infrastructure has been increasingly identified as a constraint to reaching the Millennium Development Goals for developing countries' water sectors and a significant area in which potential exists to develop sustainable financing is through the design of appropriate tariff policies.This thesis examines in detail the demand for water service improvements by analysing the willingness to pay for such improvements in Trinidad and Tobago. The basis for the work is a household sample survey conducted in 2003 which assessed the current quality of service and attitudes towards changing the status quo situation. The survey of 1419 households showed that services are poorer than officially stated, and that in response many households have opted for private coping solutions to mitigate the poor service levels of the utility.Choice experiments, which have only limited previous application in the sector, are employed to develop attribute based utility models describing the welfare effects of service level changes, in addition to the more commonly used contingent valuation method. A rigorous comparison of the two methods is developed. It provides evidence that the choice experiment methodology has benefits for policy analysis around the willingness to pay for service changes in the water sector.An analysis of proposed marginal cost based tariffs in Trinidad, as a part of wider sector reforms, is used as a case study for the policy applications of the choice experiment based willingness to pay data. Consumers are willing to pay for investments in water infrastructure, provided that they impact upon the actual service received. Marginal cost based tariffs might be socially unacceptable given that whilst significant, the willingness to pay, given likely service changes associated with planned investments by the Trinidadian water utility, for service changes is not sufficient to cover this economically efficient level of tariff

Biophysical Parameters Can Induce Epithelial-to-Mesenchymal Phenotypic and Genotypic Changes in HT-29 Cells: A Preliminary Study

Epithelial to mesenchymal transition (EMT) in cancer is the process described where cancer epithelial cells acquire mesenchymal properties which can lead to enhanced invasiveness. Three-dimensional cancer models often lack the relevant and biomimetic microenvironment parameters appropriate to the native tumour microenvironment thought to drive EMT. In this study, HT-29 epithelial colorectal cells were cultivated in different oxygen and collagen concentrations to investigate how these biophysical parameters influenced invasion patterns and EMT. Colorectal HT-29 cells were grown in physiological hypoxia (5% O2) and normoxia (21% O2) in 2D, 3D soft (60 Pa), and 3D stiff (4 kPa) collagen matrices. Physiological hypoxia was sufficient to trigger expression of markers of EMT in the HT-29 cells in 2D by day 7. This is in contrast to a control breast cancer cell line, MDA-MB-231, which expresses a mesenchymal phenotype regardless of the oxygen concentration. In 3D, HT-29 cells invaded more extensively in a stiff matrix environment with corresponding increases in the invasive genes MMP2 and RAE1. This demonstrates that the physiological environment can directly impact HT-29 cells in terms of EMT marker expression and invasion, compared to an established cell line, MDA-MB-231, which has already undergone EMT. This study highlights the importance of the biophysical microenvironment to cancer epithelial cells and how these factors can direct cell behaviour. In particular, that stiffness of the 3D matrix drives greater invasion in HT-29 cells regardless of hypoxia. It is also pertinent that some cell lines (already having undergone EMT) are not as sensitive to the biophysical features of their microenvironment

A deficiency of uPAR alters endothelial angiogenic function and cell morphology

The angiogenic potential of a cell requires dynamic reorganization of the cytoskeletal architecture that involves the interaction of urokinase-type plasminogen activator receptor (uPAR) with the extracellular matrix. This study focuses on the effect of uPAR deficiency (uPAR-/-) on angiogenic function and associated cytoskeletal organization. Utilizing murine endothelial cells, it was observed that adhesion, migration, proliferation, and capillary tube formation were altered in uPAR-/- cells compared to wild-type (WT) cells. On a vitronectin (Vn) matrix, uPAR-/- cells acquired a "fried egg" morphology characterized by circular actin organization and lack of lamellipodia formation. The up-regulation of β1 integrin, FAK(P-Tyr925), and paxillin (P-Tyr118), and decreased Rac1 activation, suggested increased focal adhesions, but delayed focal adhesion turnover in uPAR-/- cells. This accounted for the enhanced adhesion, but attenuated migration, on Vn. VEGF-enriched Matrigel implants from uPAR-/- mice demonstrated a lack of mature vessel formation compared to WT mice. Collectively, these results indicate that a uPAR deficiency leads to decreased angiogenic functions of endothelial cells

Valuing improvements in the water rights system in South Africa : a contingent ranking approach

In the context of increasing water scarcity, understanding is growing that irrigation water rights are important and that a lack of effective water rights systems constitute a major reason for inefficient water management. This study carried out a contingent ranking experiment to study how smallholder irrigators in South Africa would value potential changes in water rights. Three specific dimensions of water rights, relevant for the South African case, are considered: duration, quality of title and transferability. Results indicate that smallholder irrigators are prepared to pay considerably higher water prices if improvements are made in the water rights system. This implies that the proposed interventions in the water rights system would improve the efficiency and productivity of the small-scale irrigation sector. The increased willingness to pay could furthermore also assist South African government to reach the objective of increased cost recovery

High glucose environment inhibits cranial neural crest survival by activating excessive autophagy in the chick embryo

High glucose levels induced by maternal diabetes could lead to defects in neural crest development during embryogenesis, but the cellular mechanism is still not understood. In this study, we observed a defect in chick cranial skeleton, especially parietal bone development in the presence of high glucose levels, which is derived from cranial neural crest cells (CNCC). In early chick embryo, we found that inducing high glucose levels could inhibit the development of CNCC, however, cell proliferation was not significantly involved. Nevertheless, apoptotic CNCC increased in the presence of high levels of glucose. In addition, the expression of apoptosis and autophagy relevant genes were elevated by high glucose treatment. Next, the application of beads soaked in either an autophagy stimulator (Tunicamycin) or inhibitor (Hydroxychloroquine) functionally proved that autophagy was involved in regulating the production of CNCC in the presence of high glucose levels. Our observations suggest that the ERK pathway, rather than the mTOR pathway, most likely participates in mediating the autophagy induced by high glucose. Taken together, our observations indicated that exposure to high levels of glucose could inhibit the survival of CNCC by affecting cell apoptosis, which might result from the dysregulation of the autophagic process