Consistent, accurate and timely data are essential to the functioning of a modern organization. Managing the integrity of an organization’s data assets in a systematic manner is a challenging task in the face of continuous update, transformation and processing to support business operations. Classic approaches to constraint-based integrity focus on logical consistency within a database and reject any transaction that violates consistency, but leave unresolved how to fix or manage violations. More ad hoc approaches focus on the accuracy of the data and attempt to clean data assets after the fact, using queries to flag records with potential violations and using manual efforts to repair. Neither approach satisfactorily addresses the problem from an organizational point of view. In this thesis, we provide a conceptual model of constraint-based integrity management (CBIM) that flexibly combines both approaches in a systematic manner to provide improved integrity management. We perform a gap analysis that examines the criteria that are desirable for efficient management of data integrity. Our approach involves creating a Data Integrity Zone and an On Deck Zone in the database for separating the clean data from data that violates integrity constraints. We provide tool support for specifying constraints in a tabular form and generating triggers that flag violations of dependencies. We validate this by performing case studies on two systems used to manage healthcare data: PAL-IS and iMED-Learn. Our case studies show that using views to implement the zones does not cause any significant increase in the running time of a process.

Software maintenance is considered to be among the most difficult, lengthy and costly parts of a software application's life-cycle. Regardless of the nature of the software application and the software engineering efforts to reduce component coupling to minimum, dependencies between software components in applications will always exist and initiate software maintenance operations as they tend to threaten the "health" of the software system during the evolution of particular components. The situation is more serious with modern technologies and development paradigms, such as Service Oriented Architecture Systems and Cloud Computing that introduce larger software systems that consist of a substantial number of components which demonstrate numerous types of dependencies with each other. This work proposes a reference architecture and a corresponding software framework that can be used to model the dependencies between components in software systems and can support the verification of a set of policies that are derived from system dependencies and are relative to the software maintenance operations being applied. Dependency modelling is performed using configuration information from the system, as well as information harvested from component interface descriptions. The proposed approach has been applied to a medium scale SOA system, namely the SCA Travel Sample from Apache Software Foundation, and has been evaluated for performance in a configuration specification related to a simulated SOA system consisting to up to a thousand web services offered in a few hundred components.

Data quality problems such as duplicate records, missing values, and violation of integrity constrains frequently appear in real world applications. Such problems cost enterprises billions of dollars annually, and might have unpredictable consequences in mission-critical tasks. The process of data cleaning refers to detecting and correcting errors in data in order to improve the data quality. Numerous efforts have been taken towards improving the effectiveness and the efficiency of the data cleaning. A major challenge in the data cleaning process is the inherent uncertainty about the cleaning decisions that should be taken by the cleaning algorithms (e.g., deciding whether two records are duplicates or not). Existing data cleaning systems deal with the uncertainty in data cleaning decisions by selecting one alternative, based on some heuristics, while discarding (i.e., destroying) all other alternatives, which results in a false sense of certainty. Furthermore, because of the complex dependencies among cleaning decisions, it is difficult to reverse the process of destroying some alternatives (e.g., when new external information becomes available). In most cases, restarting the data cleaning from scratch is inevitable whenever we need to incorporate new evidence. To address the uncertainty in the data cleaning process, we propose a new approach, called probabilistic data cleaning, that views data cleaning as a random process whose possible outcomes are possible clean instances (i.e., repairs). Our approach generates multiple possible clean instances to avoid the destructive aspect of current cleaning systems. In this dissertation, we apply this approach in the context of two prominent data cleaning problems: duplicate elimination, and repairing violations of functional dependencies (FDs). First, we propose a probabilistic cleaning approach for the problem of duplicate elimination. We define a space of possible repairs that can be efficiently generated. To achieve this goal, we concentrate on a family of duplicate detection approaches that are based on parameterized hierarchical clustering algorithms. We propose a novel probabilistic data model that compactly encodes the defined space of possible repairs. We show how to efficiently answer relational queries using the set of possible repairs. We also define new types of queries that reason about the uncertainty in the duplicate elimination process. Second, in the context of repairing violations of FDs, we propose a novel data cleaning approach that allows sampling from a space of possible repairs. Initially, we contrast the existing definitions of possible repairs, and we propose a new definition of possible repairs that can be sampled efficiently. We present an algorithm that randomly samples from this space, and we present multiple optimizations to improve the performance of the sampling algorithm. Third, we show how to apply our probabilistic data cleaning approach in scenarios where both data and FDs are unclean (e.g., due to data evolution or inaccurate understanding of the data semantics). We propose a framework that simultaneously modifies the data and the FDs while satisfying multiple objectives, such as consistency of the resulting data with respect to the resulting FDs, (approximate) minimality of changes of data and FDs, and leveraging the trade-off between trusting the data and trusting the FDs. In presence of uncertainty in the relative trust in data versus FDs, we show how to extend our cleaning algorithm to efficiently generate multiple possible repairs, each of which corresponds to a different level of relative trust.

Retail centres are a visible sign of developed capitalist societies and make an appreciable contribution to these economies. For the firms involved in supplying air conditioning maintenance to retail centres, governance structures (that incorporate the make-or-buy decision and the decision concerning the nature of the exchange relationship) are fundamental business decisions. The absence of literature in this area creates a research opportunity to undertake a theoretical and empirical investigation into the determinants of the governance of air conditioning maintenance in Australian retail centres. The research objectives revolve around a microeconomic theory (Transaction Cost Economics) and two related theories – one from strategic management (Resource-Based Theory) and one from a power-based perspective (Resource Dependency Theory). In terms of the make-or-buy decision, an integrative framework of vertical integration is developed that aims to create a clearer understanding of the conditions under which Transaction Cost Economics (TCE) and Resource-Based Theory (RBT) are dominant. This approach is encouraged by the similarity of the assumptions made in TCE and RBT concerning rationality and which envisage a short term approach to profits. If a wider view is taken, that includes supply chains in which firms take a longer term approach to profits, then Resource Dependency Theory (RDT) can also be considered as a complementary theory to TCE. In order to test TCE on the issue of the nature of the exchange relationship, TCE's contractual schema is developed, along with a new type of asset specificity (Ongoing Asset Specificity). Case studies and a nationwide postal survey are used to collect data from multiple sources, comprising 51 interviews, the collection of documentary information, as well as 18 completed case study questionnaires and 205 useable survey questionnaires. Multiple research methods allow the relative strengths of different methods to be combined to more effectively test the hypotheses. Pattern matching and regression analysis are the main techniques used to analyse the data. The results provide a successful testing of the integrative framework of vertical integration. That is, this framework is shown to be more powerful in accounting for the make-or-buy decisions in the supply chains in this thesis, than the singular deployment of either TCE or RBT. With regard to the nature of the exchange relationship decision, the results also support the development of TCE's contractual schema and Ongoing Asset Specificity. Through the incorporation of these developments, TCE outperforms RDT across all of the internal and external exchanges in the supply chains in this thesis. In total, it is concluded that transaction costs and production costs can both be key determinants of the governance of air conditioning maintenance in the chain that supplies this activity to Australian retail centres. Moreover, and in this chain, upstream exchange relationships are not determined by downstream external exchange relationships. The implications of the results for practice - in more mainstream construction, and concerning the make-or-buy decision, particularly concern trades in close physical and intellectual proximity to the main contractor’s key activity of planning and coordinating site activity. Here, the results indicate that main contractors would benefit from focusing on the possibility of hold-up and not production cost improvements. With respect to external relationships, the results show that even when clients have an ongoing requirement for an activity, a discrete exchange can be both economical and effective. This suggests that calls by some government sponsored reports for all clients buying services from main contractors to seek a relational exchange are not justified. In terms of the firm's internal relationships and upstream external relationships, the evidence from this thesis is that these relationships should not necessarily be determined by the firm’s downstream external relationships. Here, for example, main contractors might not allow their exchanges with their staff and subcontractors to be determined by exchanges with their clients. More specifically, this thesis suggests that main contractors can prosper from developing relational exchanges with their staff, core subcontractors and suppliers despite engaging in discrete and arms-length exchanges with their clients. This finding may encourage main contractors to help move mainstream construction away from any "command and control" image.

The purpose of Language Identification (LID) is to identify a specific language from a spoken utterance, automatically. Language-specific characteristics are always associated with different languages. Most existing LID approaches utilise a statistical modelling process with common acoustic/phonotactic features to model specific languages while avoiding any language-specific knowledge. Great successes have been achieved in this area over past decades. However, there is still a huge gap between these languageindependent methods and the actual language-specific patterns. It is extremely useful to address these specific acoustic or semantic construction patterns, without spending huge labour on annotation which requires language-specific knowledge. Inspired by this goal, this research focuses on the language-feature dependency. Several practical methods have been proposed. Various features and modelling techniques have been studied in this research. Some of them carry out additional language-specific information without manual labelling, such as a novel duration modelling method based on articulatory features, and a novel Frequency-Modulation (FM) based feature. The performance of each individual feature is studied for each of the language-pair combinations. The similarity between languages and the contribution in identifying a language by using a particular feature are defined for the first time, in a quantitative style. These distance measures and languagedependent contributions become the foundations of the later-presented frameworks ?? language-dependent weighting and hierarchical language identification. The latter particularly provides remarkable flexibility and enhancement when identifying a relatively large number of languages and accents, due to the fact that the most discriminative feature or feature-combination is used when separating each of the languages. The proposed systems are evaluated in various corpora and task contexts including NIST language recognition evaluation tasks. The performances have been improved in various degrees. The key techniques developed for this work have also been applied to solve a different problem other than LID ?? speech-based cognitive load monitoring.

Alcohol and tobacco are drugs of abuse which are legal to sell and consume in most western societies. Addiction to these two substances has major social and health implications worldwide. The brain structure known to mediate addictive behaviour is the dopaminergic mesocorticolimbic system. Dopaminegic neurons arise from the ventral tegmental area, project to the nucleus accumbens and interact with the amygdala and the prefrontal cortex. Chronic alcoholism elicits marked damage in the prefrontal cortex with significant loss of neurons and glia. The key components of addiction, tolerance and dependence, are thought to be the result of semipermanent adaptive changes in gene expression. Gene expression profiling of the mesocorticolimbic system from human alcoholics and alcohol-dependent animals has revealed highly region-specific alterations. How these molecular changes result in the development of alcohol dependence in humans is not fully understood. Complicating factors in human alcoholism include a high comorbidity with smoking, socioeconomic factors and the prevalence of underlying psychological pathologies. Gene expression profiling of the prefrontal cortex of six alcoholics and six controls resulted in the identification of functional gene groups sensitive to alcoholism. Mitochondrial function was found down regulated while mRNA levels of genes involved in stress response and cell protection were elevated. These results correlate with the pathology of the prefrontal cortex in chronic alcoholism. Some of the control cases used for gene expression profiling were later identified as chronic smokers, while all of the alcoholics were heavy smokers. To date the heavy co-morbidity of alcoholism with smoking has not been taken into account. Thus the expression of selected genes were investigated by realtime PCR in an extended case set of non-smoking alcoholics, smoking alcoholics, smoking non-alcoholics and non-smoking, non-alcoholics. This study revealed that alcoholism itself had a significant impact on the expression of midkine, the high affinity glial glutamate transporter, member 1 and the tissue inhibitor of the metalloproteinase 3. Heavy smoking itself led to a small but significant elevation of MDK mRNA levels as well as an increase in variation of excitatory amino acid transporter 1 and metalloproteinase inhibitor, member 3 expression. Apolipoprotein D however was induced by chronic smoking but not by alcohol dependence. These results highlight the need of careful case selection in future studies on gene expression in the human alcoholic brain. Peptide antibodies were produced to midkine and a polyclonal antibody against the excitatory amino acid transporter 1 was obtained from a collaborating laboratory. Western blots utilizing these antibodies revealed a marked increase in midkine and excitatory amino acid transporter 1 protein in alcoholics compared to non-smoking and non-drinking controls. In coronal sections of human prefrontal cortex of alcoholics and non-smoking non-drinking controls, immunofluorescence of midkine was obtained from nuclei throughout the layers of the cortex and from the cell bodies of a distinct set of astrocytes in cortical layer II. Double staining with glial fibrillary acidic protein revealed that a portion of midkine-positive nuclei were localised in glial cells. There was no difference in immunostaining of alcohol and control sections with midkine. In summary these results indicate that midkine protein is induced in the prefrontal cortex of the chronic alcoholic. However, this increase in protein may not be strong enough to be visualised by immunohistochemistry. Midkine induction may be reflective of reparative processes in the prefrontal cortex of the chronic alcoholic. Excitatory amino acid transporter 1 staining in non-alcoholic, non-smoking control cases were obtained as a confluent band in cortical layer II and sparsely in deeper cortical layers. Excitatory amino acid transporter 1 immunoreactivity overlapped partially with glial fibrillary acidic protein labelling. In chronic alcoholics, excitatory amino acid transporter 1 staining in the area between the cortical layer II and VI was significantly increased. At withdrawal, glutamate levels may reach toxic levels in the cortex. The increase in cells expressing excitatory amino acid transporter 1 throughout the cortical layers may indicate a protective measure of this brain region in the chronic alcoholic. Additionally, layer specific expression of midkine and excitatory amino acid transporter 1 in the prefrontal cortex of the healthy individual may implicate a specialised role of these astrocytes.

Alcohol and tobacco are drugs of abuse which are legal to sell and consume in most western societies. Addiction to these two substances has major social and health implications worldwide. The brain structure known to mediate addictive behaviour is the dopaminergic mesocorticolimbic system. Dopaminegic neurons arise from the ventral tegmental area, project to the nucleus accumbens and interact with the amygdala and the prefrontal cortex. Chronic alcoholism elicits marked damage in the prefrontal cortex with significant loss of neurons and glia. The key components of addiction, tolerance and dependence, are thought to be the result of semipermanent adaptive changes in gene expression. Gene expression profiling of the mesocorticolimbic system from human alcoholics and alcohol-dependent animals has revealed highly region-specific alterations. How these molecular changes result in the development of alcohol dependence in humans is not fully understood. Complicating factors in human alcoholism include a high comorbidity with smoking, socioeconomic factors and the prevalence of underlying psychological pathologies. Gene expression profiling of the prefrontal cortex of six alcoholics and six controls resulted in the identification of functional gene groups sensitive to alcoholism. Mitochondrial function was found down regulated while mRNA levels of genes involved in stress response and cell protection were elevated. These results correlate with the pathology of the prefrontal cortex in chronic alcoholism. Some of the control cases used for gene expression profiling were later identified as chronic smokers, while all of the alcoholics were heavy smokers. To date the heavy co-morbidity of alcoholism with smoking has not been taken into account. Thus the expression of selected genes were investigated by realtime PCR in an extended case set of non-smoking alcoholics, smoking alcoholics, smoking non-alcoholics and non-smoking, non-alcoholics. This study revealed that alcoholism itself had a significant impact on the expression of midkine, the high affinity glial glutamate transporter, member 1 and the tissue inhibitor of the metalloproteinase 3. Heavy smoking itself led to a small but significant elevation of MDK mRNA levels as well as an increase in variation of excitatory amino acid transporter 1 and metalloproteinase inhibitor, member 3 expression. Apolipoprotein D however was induced by chronic smoking but not by alcohol dependence. These results highlight the need of careful case selection in future studies on gene expression in the human alcoholic brain. Peptide antibodies were produced to midkine and a polyclonal antibody against the excitatory amino acid transporter 1 was obtained from a collaborating laboratory. Western blots utilizing these antibodies revealed a marked increase in midkine and excitatory amino acid transporter 1 protein in alcoholics compared to non-smoking and non-drinking controls. In coronal sections of human prefrontal cortex of alcoholics and non-smoking non-drinking controls, immunofluorescence of midkine was obtained from nuclei throughout the layers of the cortex and from the cell bodies of a distinct set of astrocytes in cortical layer II. Double staining with glial fibrillary acidic protein revealed that a portion of midkine-positive nuclei were localised in glial cells. There was no difference in immunostaining of alcohol and control sections with midkine. In summary these results indicate that midkine protein is induced in the prefrontal cortex of the chronic alcoholic. However, this increase in protein may not be strong enough to be visualised by immunohistochemistry. Midkine induction may be reflective of reparative processes in the prefrontal cortex of the chronic alcoholic. Excitatory amino acid transporter 1 staining in non-alcoholic, non-smoking control cases were obtained as a confluent band in cortical layer II and sparsely in deeper cortical layers. Excitatory amino acid transporter 1 immunoreactivity overlapped partially with glial fibrillary acidic protein labelling. In chronic alcoholics, excitatory amino acid transporter 1 staining in the area between the cortical layer II and VI was significantly increased. At withdrawal, glutamate levels may reach toxic levels in the cortex. The increase in cells expressing excitatory amino acid transporter 1 throughout the cortical layers may indicate a protective measure of this brain region in the chronic alcoholic. Additionally, layer specific expression of midkine and excitatory amino acid transporter 1 in the prefrontal cortex of the healthy individual may implicate a specialised role of these astrocytes.

Alcohol and tobacco are drugs of abuse which are legal to sell and consume in most western societies. Addiction to these two substances has major social and health implications worldwide. The brain structure known to mediate addictive behaviour is the dopaminergic mesocorticolimbic system. Dopaminegic neurons arise from the ventral tegmental area, project to the nucleus accumbens and interact with the amygdala and the prefrontal cortex. Chronic alcoholism elicits marked damage in the prefrontal cortex with significant loss of neurons and glia. The key components of addiction, tolerance and dependence, are thought to be the result of semipermanent adaptive changes in gene expression. Gene expression profiling of the mesocorticolimbic system from human alcoholics and alcohol-dependent animals has revealed highly region-specific alterations. How these molecular changes result in the development of alcohol dependence in humans is not fully understood. Complicating factors in human alcoholism include a high comorbidity with smoking, socioeconomic factors and the prevalence of underlying psychological pathologies. Gene expression profiling of the prefrontal cortex of six alcoholics and six controls resulted in the identification of functional gene groups sensitive to alcoholism. Mitochondrial function was found down regulated while mRNA levels of genes involved in stress response and cell protection were elevated. These results correlate with the pathology of the prefrontal cortex in chronic alcoholism. Some of the control cases used for gene expression profiling were later identified as chronic smokers, while all of the alcoholics were heavy smokers. To date the heavy co-morbidity of alcoholism with smoking has not been taken into account. Thus the expression of selected genes were investigated by realtime PCR in an extended case set of non-smoking alcoholics, smoking alcoholics, smoking non-alcoholics and non-smoking, non-alcoholics. This study revealed that alcoholism itself had a significant impact on the expression of midkine, the high affinity glial glutamate transporter, member 1 and the tissue inhibitor of the metalloproteinase 3. Heavy smoking itself led to a small but significant elevation of MDK mRNA levels as well as an increase in variation of excitatory amino acid transporter 1 and metalloproteinase inhibitor, member 3 expression. Apolipoprotein D however was induced by chronic smoking but not by alcohol dependence. These results highlight the need of careful case selection in future studies on gene expression in the human alcoholic brain. Peptide antibodies were produced to midkine and a polyclonal antibody against the excitatory amino acid transporter 1 was obtained from a collaborating laboratory. Western blots utilizing these antibodies revealed a marked increase in midkine and excitatory amino acid transporter 1 protein in alcoholics compared to non-smoking and non-drinking controls. In coronal sections of human prefrontal cortex of alcoholics and non-smoking non-drinking controls, immunofluorescence of midkine was obtained from nuclei throughout the layers of the cortex and from the cell bodies of a distinct set of astrocytes in cortical layer II. Double staining with glial fibrillary acidic protein revealed that a portion of midkine-positive nuclei were localised in glial cells. There was no difference in immunostaining of alcohol and control sections with midkine. In summary these results indicate that midkine protein is induced in the prefrontal cortex of the chronic alcoholic. However, this increase in protein may not be strong enough to be visualised by immunohistochemistry. Midkine induction may be reflective of reparative processes in the prefrontal cortex of the chronic alcoholic. Excitatory amino acid transporter 1 staining in non-alcoholic, non-smoking control cases were obtained as a confluent band in cortical layer II and sparsely in deeper cortical layers. Excitatory amino acid transporter 1 immunoreactivity overlapped partially with glial fibrillary acidic protein labelling. In chronic alcoholics, excitatory amino acid transporter 1 staining in the area between the cortical layer II and VI was significantly increased. At withdrawal, glutamate levels may reach toxic levels in the cortex. The increase in cells expressing excitatory amino acid transporter 1 throughout the cortical layers may indicate a protective measure of this brain region in the chronic alcoholic. Additionally, layer specific expression of midkine and excitatory amino acid transporter 1 in the prefrontal cortex of the healthy individual may implicate a specialised role of these astrocytes.

Alcohol and tobacco are drugs of abuse which are legal to sell and consume in most western societies. Addiction to these two substances has major social and health implications worldwide. The brain structure known to mediate addictive behaviour is the dopaminergic mesocorticolimbic system. Dopaminegic neurons arise from the ventral tegmental area, project to the nucleus accumbens and interact with the amygdala and the prefrontal cortex. Chronic alcoholism elicits marked damage in the prefrontal cortex with significant loss of neurons and glia. The key components of addiction, tolerance and dependence, are thought to be the result of semipermanent adaptive changes in gene expression. Gene expression profiling of the mesocorticolimbic system from human alcoholics and alcohol-dependent animals has revealed highly region-specific alterations. How these molecular changes result in the development of alcohol dependence in humans is not fully understood. Complicating factors in human alcoholism include a high comorbidity with smoking, socioeconomic factors and the prevalence of underlying psychological pathologies. Gene expression profiling of the prefrontal cortex of six alcoholics and six controls resulted in the identification of functional gene groups sensitive to alcoholism. Mitochondrial function was found down regulated while mRNA levels of genes involved in stress response and cell protection were elevated. These results correlate with the pathology of the prefrontal cortex in chronic alcoholism. Some of the control cases used for gene expression profiling were later identified as chronic smokers, while all of the alcoholics were heavy smokers. To date the heavy co-morbidity of alcoholism with smoking has not been taken into account. Thus the expression of selected genes were investigated by realtime PCR in an extended case set of non-smoking alcoholics, smoking alcoholics, smoking non-alcoholics and non-smoking, non-alcoholics. This study revealed that alcoholism itself had a significant impact on the expression of midkine, the high affinity glial glutamate transporter, member 1 and the tissue inhibitor of the metalloproteinase 3. Heavy smoking itself led to a small but significant elevation of MDK mRNA levels as well as an increase in variation of excitatory amino acid transporter 1 and metalloproteinase inhibitor, member 3 expression. Apolipoprotein D however was induced by chronic smoking but not by alcohol dependence. These results highlight the need of careful case selection in future studies on gene expression in the human alcoholic brain. Peptide antibodies were produced to midkine and a polyclonal antibody against the excitatory amino acid transporter 1 was obtained from a collaborating laboratory. Western blots utilizing these antibodies revealed a marked increase in midkine and excitatory amino acid transporter 1 protein in alcoholics compared to non-smoking and non-drinking controls. In coronal sections of human prefrontal cortex of alcoholics and non-smoking non-drinking controls, immunofluorescence of midkine was obtained from nuclei throughout the layers of the cortex and from the cell bodies of a distinct set of astrocytes in cortical layer II. Double staining with glial fibrillary acidic protein revealed that a portion of midkine-positive nuclei were localised in glial cells. There was no difference in immunostaining of alcohol and control sections with midkine. In summary these results indicate that midkine protein is induced in the prefrontal cortex of the chronic alcoholic. However, this increase in protein may not be strong enough to be visualised by immunohistochemistry. Midkine induction may be reflective of reparative processes in the prefrontal cortex of the chronic alcoholic. Excitatory amino acid transporter 1 staining in non-alcoholic, non-smoking control cases were obtained as a confluent band in cortical layer II and sparsely in deeper cortical layers. Excitatory amino acid transporter 1 immunoreactivity overlapped partially with glial fibrillary acidic protein labelling. In chronic alcoholics, excitatory amino acid transporter 1 staining in the area between the cortical layer II and VI was significantly increased. At withdrawal, glutamate levels may reach toxic levels in the cortex. The increase in cells expressing excitatory amino acid transporter 1 throughout the cortical layers may indicate a protective measure of this brain region in the chronic alcoholic. Additionally, layer specific expression of midkine and excitatory amino acid transporter 1 in the prefrontal cortex of the healthy individual may implicate a specialised role of these astrocytes.

The purpose of this thesis is to explore the relationship between certain descriptive and prescriptive elements in Modernisation theory, and selected phases in Maori development in the nineteenth and twentieth centuries. This analysis also extends to consideration of the significance of intentional development, as defined by Michael Cowen and Robert Shenton (Cowen & Shenton, 1996), as the emerging basis for such development.The particular focus within the theoretical framework is on the characteristics and implications of social transformation that are said to accompany rapid economic development - particularly for non-Western peoples living within an emerging Western economic environment. As a corollary of this, consideration is given to the evident conversion from such transitions being unplanned consequences of the forces of economic development, to the increasingly conscious, planned bases for the processes of modernisation being applied to Maori development.This thesis concludes that there has been a discernable intensification in the forces of modernisation impacting on Maori, and that this has been complemented by more deliberate efforts - at a governmental level - to advance this process. One consequence of this trend has been that the alternative models for Maori development have been virtually excluded, even from consideration by successive Governments, and that a singular theoretical model has become the near-universal standard for governmental discourse about this area of indigenous development in New Zealand.