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Credit unions are important community, co-operative financial service organisations, that provide personal loans and other financial products to their local communities. Credit unions operate in a competitive market and as a result innovation is important to their sustainability. Despite this, little is understood about innovation in the sector. To address the gap in the literature, this study aims to investigate innovation in credit unions. To achieve this aim, five objectives were set including defining innovation in context, identifying the form and extent of innovation, documenting the innovation process and the sources and determinants in credit unions. To investigate the objectives, a mixed-methods methodology was adopted including survey data from credit unions in four countries including Ghana, Northern Ireland, Scotland and the Republic of Ireland and semi-structured interviews with 12 credit unions from Northern Ireland and Ghana. The study makes a number of contributions to the literature. It is the first study to report on the range of product, service and process innovations in credit unions and to identify how these differ across countries at different stages of development. In particular, a number of 'frugal' innovations were noted, that are unique to the sector. It is the first study to explicitly define, measure and investigate the determinants of innovation in credit unions. Finally, it is also the first study to look inside the 'black box', to determine whether credit unions have a strategic approach to innovation. Consistent with ecological and stakeholder theory this study found that the regulatory environment and larger boards are determinants of innovation. In addition, size was positively associated with innovation. Therefore, this study provides support for 'new model' management, which advocates deregulation and mergers to achieve a large size, as this should provide additional stimulus for innovation. It also found that larger boards are more innovative; therefore, when regulators are preparing corporate governance guidance for credit unions, they should consider larger boards.

Helminth parasites promote the development of antigen-specific anergy and regulation which often limits pathology but allows parasite survival. Parasite effectors mediating this are the subject of intense study as they may be useful as future vaccine targets. Fasciola hepatica possesses a TGF-like molecule (FhTLM), part of a larger TGF family, which play an important role in regulating parasite development and modulating host immune responses. We hypothesized that F. hepatica may utilise FhTLM to down modulate host immune responses via induction of regulatory. Consequently, in this study, the immuno-modulatory properties of FhTLM with regards to its effect on T-cell mediated immunosuppression and modulation of host immune cells and signals to benefit parasite survival were studied. The in vitro effect of FhTLM on induction of FoxP3 T-regs cells and anergic markers, PD-1, PD-L1 and CTLA-4, was studied in murine splenic CD4 T-cells. FhTLM failed to upregulate FoxP3 T-reg cells and all investigated anergic T-cell markers. However, production of IL-10, a key immunomodulatory cytokine was significantly enhanced in response to FhTLM stimulation. The interaction of FhTLM with naïve CD4 T-cells also promoted the development of inflammatory responses evidenced by enhanced production of pro-inflammatory cytokines and chemokines (TNF-α, IL-12 P70, IL-1β, IP-10, TARC, MIP-1β, IL-1ra, RANTES and CXCL12). The chemokines induced by FhTLM were biologically functional as supernatants from FhTLM stimulated cells promoted in vitro migration of both activated CD4 T-cells and eosinophils. Lastly, immune signals generated from CD4 T-cells, eosinophils and monocytes failed to support enhanced survival of newly excysted juvenile (NEJs) flukes and this response was not affected by the presence FhTLM. Whilst FhTLM did not directly modulate immune cells to promote parasite survival, induction of pro-inflammatory responses as evidenced by production of cytokines; IL-6, TNF-α, RANTES, MCP-1, Lipocalin -2, Endocan, Pentraxin-3 and ICAM-1 by LPS or IL-4-stimulated monocytes was suppressed or inhibited in the presence of FhTLM. Taken together, our data highlight an indirect mechanism used by the parasite to benefit parasite persistence and also implicate a role for IL-10 in suppression of protective host immune response to F. hepatica infection. In addition, our data also indicates that FhTLM has an anti-inflammatory potential and may have implications in the treatment of allergic or pro-inflammatory diseases.

Background: There have been many epidemiological studies into the influence of exposure to the most toxic elements on the risk of cancer in the workplace, mainly due to the exposure of certain occupational groups, or perhaps in populations near industrial sources. Toxic elements include arsenic, copper, nickel, and uranium; and many more of these elements have been shown to increase the risk of several different types of cancers in these highly-exposed groups. Many of these elements naturally exist in the soil, and the health impact of these levels of environmental exposures on the general population has received little attention to date possibly due to the belief that soil concentrations of these elements are too low to cause harm to the general population. Therefore, the long-term effect of such chronic exposure to metals in the soil remains unclear. Aims and objectives: The goals are to utilise a new resource known as THIN-GBASE for conducting a series of environmental epidemiological studies to test the hypothesis that BCC, lung and GIT cancers are associated with high exposure to certain low-level metals in soil. We sought to use this resource in determining which soil metals should be tested for predicting each of the cancer outcomes. Methods: For BCC, an ecological study was initially undertaken to assess the overall regional variation in BCC to provide national and contemporary breakdowns of incidence rates across the UK. The primary exposure of interest for BCC was low-level soil arsenic, and we therefore quantified soil arsenic exposure levels based on the UK national safety limits for arsenic [i.e. As-C4SLs = 35 mg/kg]. A population-based cohort study was conducted to quantify the risks associated between the development of BCC and increasing levels of exposure to soil arsenic. For lung cancer, a two-stage process was adopted: 1) data mining analysis using the correlation-based filter selection model was used to find the restricted set of soil metals were best predictors for lung cancer; and 2) a prospective cohort study was use where these sets of elements were fitted together (adjusted for confounding variables) in a multivariable Cox proportional-hazards model to determine the risks associated between the development of lung cancer, with increasing levels of exposure to each specific element. For GIT cancers, a three-stage process was adopted: stages 1 and 2 used a similar methodology for the lung cancer study. In stage 3, all GIT cancers were divided into three broader outcomes i.e. upper GIT (includes mouth & oesophagus), stomach (as standalone) and colorectal (includes small, large, rectum and anal canal) cancers. A multivariate competing risk survival model was adjusted for the three different GIT cancers as competing events to identify associations between any of the selected group of metals found in stage 1 and GIT-specific cancers. Results: For BCC, the findings for the ecological study show that overall EASRs & WASRs for BCC in the UK was 98.6 and 66.9 per 100,000 person-years, respectively. It indicates a large geographical variation in age-sex standardised incidence of BCC with the South East having the highest incidence of BCC (202.7/100,000 person-years), followed by South Central (193.5/100,000 person-years) and Wales (185.7/100,000 person-years). Incidence rates of BCC were substantially higher in the least socioeconomically deprived groups. It was observed that increasing levels of deprivation led to a decreased rate of BCC (p < 0.001). In terms of age groups, the largest annual increase was observed among those aged 30-49 years. Assessment for soil arsenic indicated that individuals living in areas with concentrations ≥35mg/kg significantly had an increased hazard of developing BCC (35-70mg/kg: adjusted HR 1.08, 95% CI: 1.02-1.14; ≥70mg/kg: adjusted HR 1.17, 95% CI: 1.09-1.28). Urban residents with the highest exposure of soil arsenic had the greatest risk of developing BCC (≥ 70.0 mg/kg: HR 1.18, 95% CI: 1.06-1.36). For lung cancer, the correlation-based filter selection model identified aluminium, lead and uranium as the appropriate set of exposures for modelling lung cancer risk. Complete adjustments of hazards model showed evidence of an increased risk of developing lung cancer with elevated concentrations for only soil aluminium at medium levels ranging between 47,000-61,600mg/kg. Urban residents with the highest exposure of soil aluminium had the greatest risk of developing lung cancer (≥ 61,600mg/kg: HR 1.12, 95% CI: 1.04-1.22). For GIT cancers, the correlation-based filter selection model identified seven elements i.e. aluminium, phosphorus, zinc, uranium, calcium, manganese, and lead, as the appropriate set of exposures for predicting GIT cancer risk. The complete adjustment for hazards model indicated that the risk of developing overall GIT cancers were significantly associated with elevated exposure levels of soil phosphorus only (873-1,127mg/kg: HR 1.08, 95% CI: 1.02-1.14; 1,127-1,456mg/kg: HR 1.07, 95% CI: 1.01-1.13; and ≥1,145mg/kg: HR 1.07, 95% CI: 1.01-1.13). There were no consistent relationships identified between any of the selected groups of elements and the GIT-specific cancer outcomes when adjusting for different GIT cancers as competing events. Conclusion: There appears to be slight evidence of BCC, respiratory and GIT cancer risk with elevated exposure to soil arsenic, aluminium and phosphorus, respectively. The series of investigations conducted for this research are one of the first, if not, contemporary UK-based study to present novel estimates for a group of ill-defined pollutants. This research demonstrates that linking geochemical data with electronic primary care medical records can be a valuable approach of proving whether long term exposure to low-level soil contaminants may have a health consequence in the population.

This study recognised the quantification of biomass, C and nutrient stocks in cocoa systems of Ghana as an important step to producing a sustainable and carbon-friendly cocoa sector. Eight farms in Ghana were selected for sampling cocoa stands on the basis of three variables: region (Eastern region (ER), Western region (WR)), shade management (shaded, un shaded) and stand age «15, >15 years). All biometric data were collected within a plot area of 2700 m2 in each farm. Also two experiments, a l20-day dry matter loss and a l30-day carbon emission from litter decomposition and organic matter mineralization, were conducted concurrently. In these, single species leaf litters: cocoa (as in unshaded cocoa system), Newbouldia laevis (dominant shade tree in Eastern region) and Persea americana (dominant shade tree in Western region) and I: I mixed species leaf litters (mimicking shaded systems: cocoa + Newbouldia laevis and cocoa + Persea americana) were incubated to determine and predict the litter decomposition and nutrient dynamics in cocoa systems with or without the shade trees. Allometric equations were developed to estimate the biomass of live cocoa tree components (R2 = 0.79 - 0.95). Biomass of non-cocoa trees was estimated using an existing allometric equation developed by the Food and Agricultural Organization. In addition, the Water, Nutrient and Light Capture in Agroforestry Systems (WaNuLCAS) model was tested on hypothetical cocoa systems to assess its suitability to simulate biomass, C and nutrient stocks in the systems over time. Total ecosystem biomass ranged from 48.1 ± 6.5 to 101.6 ± 12.6 Mg I ha. The unshaded system had the lowest biomass production. Biomass production was higher in the Eastern than Western region and larger in > 15 years stands than < 15 years stands. While the C stock in biomass from shaded systems was twice that in unshaded systems, there was no significant difference in total ecosystem C stocks (biomass C + soil C to 60 cm depth) between the two systems due to a larger soil carbon stock in the latter.

One of the many benefits of cover crops (CCs) is nutrient provision, which can be optimized by synchronizing the nutrient release from residue decomposition with the demand for subsequent cash crops. This study is part of a multistate research (13 states) to measure cotton lint yield in response to cover cropping as a nutrient management strategy. This research-based information will help farmers optimize nitrogen (N) fertilization when integrating CCs into their production systems. A two-year field trial was conducted in 2021 and 2022 with four cover crop treatments (cereal rye, crimson clover, mixtures of cereal rye and crimson clover, and control) and five N rates (0, 45, 90, 135, and 180 kg N ha-1) in a cotton production system. Nutrient release patterns were determined with litter bag methods. Soil samples were collected and analyzed for physio-biogeochemical properties underlying soil functions. Cotton lint yield and nutrient use efficiency (NUE) were measured. Integrating cover crops did not change lint yield, while applying N rates at 90 and 45 kg N ha-1 increased the yield in 2021 and 2022, respectively, beyond which the yields did not change. However, the NUE decreased with increasing N rates. Planting crimson clover decreased the NUE in 2022, which was improved by incorporating cereal rye. These results indicate that maximum lint yield and NUE of dryland cotton could be achieved with a moderate N rate (45 kg N ha-1) under cover crop mixtures.

This dissertation consists of three inter-related essays in applied economics, which delves deeper into different research questions with varying econometric models on the recent financial sector crisis in Ghana, sub-Saharan Africa. The emergence of financial institutions in recent times, coupled with lending models in the field of microfinance is celebrated as significant improvements, which further enhances the perceptive miracle of enabling previously un-bankable households by creating “safe nets” to replace the missing links that excluded them from access to more traditional forms of financial services like savings, credit, and investment. In recent times however, financial opportunists took advantage of the vulnerable households by creating unsustainable investments within Microfinance Institutions, Savings and Loans Companies, commercial banking institutions, and other financial houses that functioned as de facto ponzi schemes. Their ultimate goal was to exploit vulnerable households for selfish monetary advantage. The influx of these ponzi-financial institutions (PFI’s) has rendered Ghana’s financial sector unstable, leading to loss of confidence in the banking sub-sector. The government of Ghana and supervisory agency have done very little to safeguard depositor’s funds. Chapter 1 determines the impact of PFI’s on household savings, using a three-wave pooled cross-sectional dataset from World Bank’s Living Standards Measurement survey to analyse this impact by employing a difference-in-differences estimation strategy with regional and time fixed effects. The findings suggest that the activities of these PFI’s induced all households to increase their average savings by 502.00 Ghana cedis ($125). Further evidence shows that the non-poor income group also increased their average savings by 414.50 Ghana Cedis ($103.63). It is interesting to note that urban households increased their annual savings by an average of 914.30 Ghana Cedis ($228.57), relative to rural dwellers. The results in this chapter were further strengthened by a number of robustness checks. Elasticities of savings and investment in the post-closure of PFI’s would be negatively affected. In chapter 2, we employ a two-wave pooled cross-sectional dataset to investigate the post-closure of these PFI’s on household savings. We follow the approach adopted by Ravallion et al (2005) to execute a difference-in-difference-in-differences estimation strategy with geographical and time fixed effects. The findings adduced from this chapter suggests that post-closure of PFI’s led to a significant reduction in household savings among all households and the non-poor, consistent with previous findings. On the average, all households and non-poor households reduced their average savings by 788.70 Ghana cedis ($157.00) and 888.70 Ghana cedis ($222.18) respectively. Contrary to earlier narrative, previous period savings shows a negative relationship with household savings behavior. The results of this chapter were further strengthened by a number of robustness checks and falsification tests. And finally, chapter 3 examines the impact of PFI’s on household credit acquisition, by employing a Propensity Score Matching technique to test for and measure the treatment effect on the observations of interest. This is done by using the greedy matching approach to run through the list of treated units and select the closest eligible control unit to be paired with each treated unit. The results obtained from the analyses indicate that the presence of PFI’s (2006-2013) reduced credit acquisition on the average by a 3-percentage point among households, while the post-closure effect (2013-2017) increased credit acquisition on the average by a 2-percentage point. The combine effect shows that households reduced their credit acquisition on the average by a 2-percentage point between the period 2006-2017, which thus indicate that activities of PFI’s negatively impacted credit-acquisition.

Chlorine is a widely used toxic chemical that is considered a chemical threat agent. Chlorine inhalation injures airway epithelium, and efficient epithelial repair is necessary to restore normal lung structure and function. Regeneration of injured tissues typically proceeds through the proliferation and differentiation of stem or progenitor cells. Knowledge of underlying mechanisms that regulate these processes during airway epithelial repair is lacking. This dissertation characterizes respiratory epithelial repair after chlorine injury to investigate potential signaling pathways that could be manipulated to regulate stem/progenitor cells in airway repair. Repair of the pseudostratified tracheal epithelium after chlorine-induced injury was characterized in C57BL/6 mice by morphometric analysis of tracheal sections following standard histological staining and specific staining for proliferating cells and epithelial cell types. Surviving basal epithelial cells served as progenitor cells for tracheal epithelial regeneration after chlorine injury. In areas where repair was inefficient owing to few remaining basal cells, airway fibrosis was observed. To investigate potential signaling pathways that could be manipulated to facilitate epithelial repair after chlorine-induced injury, the low affinity nerve growth factor receptor (NGFR) and the Wnt/ß-catenin pathway were examined. Pharmacological treatment of isolated tracheal epithelial cells with NGFR ligands did not influence the growth of tracheal basal cells in vitro. Overexpression of nerve growth factor (NGF) in airway epithelium or mutation of NGFR increased the pool of stem cells that formed a differentiated pseudostratified epithelium in vitro. Treatment of chlorine-exposed mice with NGF did not impact epithelial repair in vivo. Minimal effect of NGF overexpression on epithelial repair in transgenic mice was observed. NGFR mutation resulted in increased sensitivity of mice to chlorine-induced airway injury, but unexpectedly protected mice from the development of fibrosis. Stimulation of Wnt/ß-catenin signaling with lithium chloride prevented the formation of pseudostratified epithelium in vitro. Chlorine inhalation in mice activated ß-catenin signaling in the tracheal epithelium. Treatment of mice with lithium chloride or the Wnt/ß-catenin signaling modulator ICG-001 reduced collagen content in the lung after chlorine exposure. This work highlights the potential contribution of NGFR and Wnt/ß-catenin signaling to airway epithelial repair and identifies potential therapeutic targets for inhibiting chlorine-induced airway fibrosis.