title: Adaptive text mining: Inferring structure from sequences

authors: Witten, Ian H.

subjects: computer science

abstract: Text mining is about inferring structure from sequences representing natural language text, and may be defined as the process of analyzing text to extract information that is useful for particular purposes. Although hand-crafted heuristics are a common practical approach for extracting information from text, a general, and generalizable, approach requires adaptive techniques. This paper studies the way in which the adaptive techniques used in text compression can be applied to text mining. It develops several examples: extraction of hierarchical phrase structures from text, identification of keyphrases in documents, locating proper names and quantities of interest in a piece of text, text categorization, word segmentation, acronym extraction, and structure recognition. We conclude that compression forms a sound unifying principle that allows many text mining problems to be tacked adaptively.

text: Adaptive text mining: Inferring structure from sequences Text mining is about inferring structure from sequences representing natural language text, and may be defined as the process of analyzing text to extract information that is useful for particular purposes. Although hand-crafted heuristics are a common practical approach for extracting information from text, a general, and generalizable, approach requires adaptive techniques. This paper studies the way in which the adaptive techniques used in text compression can be applied to text mining. It develops several examples: extraction of hierarchical phrase structures from text, identification of keyphrases in documents, locating proper names and quantities of interest in a piece of text, text categorization, word segmentation, acronym extraction, and structure recognition. We conclude that compression forms a sound unifying principle that allows many text mining problems to be tacked adaptively.

year: 2004

title: Investigation of host cell wall degrading strategies of Pseudomonas syringae pv. actinidiae (Psa)

authors: Subasinghe, Rasika

subjects: Psa

abstract: Kiwifruit (Actinidia deliciosa and Actinidia chinensis) is cultivated in several countries including Italy, France, Chile, China, Japan, Korea and New Zealand and is an important income earner for a majority of these countries. In New Zealand, kiwifruit earns approximately USD 714 million per annum. In the recent past, the New Zealand kiwifruit industry was threatened by an outbreak of bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa). The invasion strategies and the mobility of Psa pathogen in the kiwifruit plant have not been fully described. Recent comparative genomic studies of Psa strains and other P. syringae pathovars that also infect woody hosts indicate similarities in genetic makeup among these pathovars. Interestingly, these pathovars contain genes capable of producing cell wall degrading enzymes, thus suggesting that Psa possesses the same capability. However, no previous research demonstrated that any P. syringae pathovar degrades the host’s cell walls or any cell wall component. This research investigated whether Psa produces xylanases to degrade cell wall material of kiwifruit stems and facilitate systemic mobility of the pathogen from the infection site. The research also investigates whether vessel anatomy and xylem architecture play a role in the systemic mobility of the pathogen within the plant.
Chapter Two of the thesis determines whether Psa is able to multiply and grow on kiwifruit wood-containing medium and whether Psa synthesises any xylanase to degrade cell wall material contained in the kiwifruit wood. For this purpose, the genome of Psa was analysed to ascertain whether sequences homologous to well-known cell wall degrading enzymes were present in the genome. The degree of similarity of the identified genes was compared to the cell wall degrading genes of other Pseudomonas woody host pathogens. Six genes encoding for well-known cell wall degrading enzymes were identified, with the degree of amino acid similarity varying between 58% and 98%. Patterns of Psa growth were examined in three media: standard nutrient broth, xylan and casein media and minimal media supplemented with kiwifruit cell wall material, called kiwifruit xylem medium. Growth of the bacterium was observed in the kiwifruit xylem medium, however, the increase in CFU (Colony Forming Units) counts in kiwifruit xylem medium was low compared to that in the other two media. A characteristic bacterial growth pattern was observed in the standard nutrient broth media. In the kiwifruit xylem media, bacteria counts declined initially, then briefly recovered. In vitro enzyme assays were conducted for Psa in the kiwifruit xylem medium to determine the activity of xylanase enzyme. Two types of assays were conducted: 3,5-Dinitrosalicylic acid (DNSA) and Remazol Brilliant Blue (RBB). A significant xylanase activity was detected only in the Psa cultured in minimal medium supplemented with 0.5% kiwifruit xylem using the DNSA assay. However, no xylanase activity was detected using the RBB. It was concluded that Psa is capable of producing an active xylanase enzyme, and that synthesis of the enzyme is induced under low nutrient conditions and in the presence of kiwifruit xylem cell wall material.
Chapter Three describes investigations of xylanase activity in planta. Twenty mature Actinidia chinensis Planch. var. chinensis ‘Hort16A’ plants were used. Ten plants were left un-inoculated and ten plants were inoculated with Psa. Disease symptoms appeared in the inoculated plants after which both inoculated and non-inoculated shoots were harvested. Psa was re-isolated from infected plants and duplex PCRs were conducted to confirm that symptoms were due to Psa infection. RBB and DNSA assays were conducted on ground kiwifruit stem pieces to ascertain putative xylanase activity. The RBB assay indicated xylanase activity in inoculated kiwifruit stem pieces. RBB assay parameters were varied to ascertain whether the xylanase activity in infected tissues was consistent with enzymatic activity. Strength tests were conducted on infected and non-infected kiwifruit shoots to determine whether infection affected stem structural integrity. The average strength per mm thickness of non-infected kiwifruit xylem was significantly higher than that of infected xylem. RNA was extracted from both inoculated and non-inoculated stems and PCR conducted with primers specific to the xylanase genes identified in the Psa genome. One bacterial xylanase gene was expressed during infection of the kiwifruit stems. The observed reduction in stem strength was consistent with the xylanase activity detected using the RBB assay and the expression of the bacterial xylanase gene during infection.
Chapter Four investigated kiwifruit vessel lengths, the frequency of open vessel connections between kiwifruit stems and leaves, and the potential for movement of Psa from leaf inoculation sites into the supporting stem. Silicone injection was used to document xylem vessel length distribution within mature one-year-old stems of three kiwifruit cultivars that differ in Psa susceptibility.  There was no correlation between average vessel lengths and susceptibility. The air injection technique was used to estimate maximum vessel lengths in Hort16A seedlings and vessel connections from leaf to stem. It was observed that the maximum xylem vessel length of Hort16A kiwifruit seedlings was 345 mm, that 71% of leaves had an open vessel from the stem to the leaf blade, and that 79% of leaves had an open vessel from stem to the petiole. The average maximum vessel length and plant height were positively correlated. A negative correlation was observed between height of the plant and the number of nodes with vessels extending into leaves. Psa was observed to move in both basipetal and acropetal directions when the leaf blade of Hort16A seedlings was inoculated, and in the majority of leaves was detected in the petiole or stem when either the tip or base of the leaf lamina was inoculated. Psa movement exceeded the boundaries of known open vessel connections between stem and leaf, suggesting that if Psa was mobile in the xylem, then vessel end walls were not a significant barrier to movement. This finding supports the conclusion that Psa has the ability to overcome plant cell wall barriers to movement.
The overall findings of this thesis are that Psa does actively produce at least one cell wall degrading enzyme during infection of kiwifruit tissue, and that cell wall degrading enzymes contribute to an active invasion mechanism by this pathogen. For this reason Psa movement within the plant is not limited by cell wall barriers or the architecture of the xylem vascular system.

text: Investigation of host cell wall degrading strategies of Pseudomonas syringae pv. actinidiae (Psa) Kiwifruit (Actinidia deliciosa and Actinidia chinensis) is cultivated in several countries including Italy, France, Chile, China, Japan, Korea and New Zealand and is an important income earner for a majority of these countries. In New Zealand, kiwifruit earns approximately USD 714 million per annum. In the recent past, the New Zealand kiwifruit industry was threatened by an outbreak of bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa). The invasion strategies and the mobility of Psa pathogen in the kiwifruit plant have not been fully described. Recent comparative genomic studies of Psa strains and other P. syringae pathovars that also infect woody hosts indicate similarities in genetic makeup among these pathovars. Interestingly, these pathovars contain genes capable of producing cell wall degrading enzymes, thus suggesting that Psa possesses the same capability. However, no previous research demonstrated that any P. syringae pathovar degrades the host’s cell walls or any cell wall component. This research investigated whether Psa produces xylanases to degrade cell wall material of kiwifruit stems and facilitate systemic mobility of the pathogen from the infection site. The research also investigates whether vessel anatomy and xylem architecture play a role in the systemic mobility of the pathogen within the plant.
Chapter Two of the thesis determines whether Psa is able to multiply and grow on kiwifruit wood-containing medium and whether Psa synthesises any xylanase to degrade cell wall material contained in the kiwifruit wood. For this purpose, the genome of Psa was analysed to ascertain whether sequences homologous to well-known cell wall degrading enzymes were present in the genome. The degree of similarity of the identified genes was compared to the cell wall degrading genes of other Pseudomonas woody host pathogens. Six genes encoding for well-known cell wall degrading enzymes were identified, with the degree of amino acid similarity varying between 58% and 98%. Patterns of Psa growth were examined in three media: standard nutrient broth, xylan and casein media and minimal media supplemented with kiwifruit cell wall material, called kiwifruit xylem medium. Growth of the bacterium was observed in the kiwifruit xylem medium, however, the increase in CFU (Colony Forming Units) counts in kiwifruit xylem medium was low compared to that in the other two media. A characteristic bacterial growth pattern was observed in the standard nutrient broth media. In the kiwifruit xylem media, bacteria counts declined initially, then briefly recovered. In vitro enzyme assays were conducted for Psa in the kiwifruit xylem medium to determine the activity of xylanase enzyme. Two types of assays were conducted: 3,5-Dinitrosalicylic acid (DNSA) and Remazol Brilliant Blue (RBB). A significant xylanase activity was detected only in the Psa cultured in minimal medium supplemented with 0.5% kiwifruit xylem using the DNSA assay. However, no xylanase activity was detected using the RBB. It was concluded that Psa is capable of producing an active xylanase enzyme, and that synthesis of the enzyme is induced under low nutrient conditions and in the presence of kiwifruit xylem cell wall material.
Chapter Three describes investigations of xylanase activity in planta. Twenty mature Actinidia chinensis Planch. var. chinensis ‘Hort16A’ plants were used. Ten plants were left un-inoculated and ten plants were inoculated with Psa. Disease symptoms appeared in the inoculated plants after which both inoculated and non-inoculated shoots were harvested. Psa was re-isolated from infected plants and duplex PCRs were conducted to confirm that symptoms were due to Psa infection. RBB and DNSA assays were conducted on ground kiwifruit stem pieces to ascertain putative xylanase activity. The RBB assay indicated xylanase activity in inoculated kiwifruit stem pieces. RBB assay parameters were varied to ascertain whether the xylanase activity in infected tissues was consistent with enzymatic activity. Strength tests were conducted on infected and non-infected kiwifruit shoots to determine whether infection affected stem structural integrity. The average strength per mm thickness of non-infected kiwifruit xylem was significantly higher than that of infected xylem. RNA was extracted from both inoculated and non-inoculated stems and PCR conducted with primers specific to the xylanase genes identified in the Psa genome. One bacterial xylanase gene was expressed during infection of the kiwifruit stems. The observed reduction in stem strength was consistent with the xylanase activity detected using the RBB assay and the expression of the bacterial xylanase gene during infection.
Chapter Four investigated kiwifruit vessel lengths, the frequency of open vessel connections between kiwifruit stems and leaves, and the potential for movement of Psa from leaf inoculation sites into the supporting stem. Silicone injection was used to document xylem vessel length distribution within mature one-year-old stems of three kiwifruit cultivars that differ in Psa susceptibility.  There was no correlation between average vessel lengths and susceptibility. The air injection technique was used to estimate maximum vessel lengths in Hort16A seedlings and vessel connections from leaf to stem. It was observed that the maximum xylem vessel length of Hort16A kiwifruit seedlings was 345 mm, that 71% of leaves had an open vessel from the stem to the leaf blade, and that 79% of leaves had an open vessel from stem to the petiole. The average maximum vessel length and plant height were positively correlated. A negative correlation was observed between height of the plant and the number of nodes with vessels extending into leaves. Psa was observed to move in both basipetal and acropetal directions when the leaf blade of Hort16A seedlings was inoculated, and in the majority of leaves was detected in the petiole or stem when either the tip or base of the leaf lamina was inoculated. Psa movement exceeded the boundaries of known open vessel connections between stem and leaf, suggesting that if Psa was mobile in the xylem, then vessel end walls were not a significant barrier to movement. This finding supports the conclusion that Psa has the ability to overcome plant cell wall barriers to movement.
The overall findings of this thesis are that Psa does actively produce at least one cell wall degrading enzyme during infection of kiwifruit tissue, and that cell wall degrading enzymes contribute to an active invasion mechanism by this pathogen. For this reason Psa movement within the plant is not limited by cell wall barriers or the architecture of the xylem vascular system.

year: 2018

title: Health reform and the impact on Mäori 1983-1997

authors: Ferguson, Lisa Arleen.

abstract: This study investigates the New Zealand health sector reforms from 1983 to 1997and examines whether the reform process has been consistent with the principles of the Treaty of Waitangi. It evaluates the impact of the reforms on Mäori from that perspective. 

The study introduces the health sector reforms generally and then their specific effects on Mäori. It draws on two research exercises undertaken by the author, being research for the Wai 692 Napier Hospital and Health Services claim to the Waitangi Tribunal and on improving Mäori Health outcomes for the National Health Committee. The methodologies used are those from the discipline of history.

The study outlines the argument for Crown responsibilities under the Treaty and draws out the distinctions between Article 2 and Article 3 of the Treaty. It provides a historical background to the place of the Treaty in the health sector, and forms the basis for a Treaty based analysis of the health reforms and their impact. 

The New Zealand health sector has undergone massive government initiated structural change throughout the period under study. During this time the neo-liberal reforms have had a key role in reshaping health service structures. The process of change, the international influences on the changes, and the resulting entities are described. An example from Tainui Iwi of the effect of structural health reform illustrates the changes in Mäori health service provision by Mäori.
Since 1983 successive governments have produced copious Mäori health policy. The key policy documents, and their recommendations, are identified, as is the degree to which they were implemented. The cyclical nature of such policy making suggests that it is not always followed by policy implementation. While Mäori are identified as a health gain priority, the evidence reviewed shows that the responsibility to implement and monitor the policy is diffuse and ineffective.

The Wai 692 claim provides a detailed look at the impact of the 1990s health reform for Mäori. The claim was precipitated by the threatened closure of Napier Hospital, but was broadened to include a wide-ranging look at the impact of health reform on Mäori. As a case study it provides a specific example of one Iwi’s experience of the reality of policy implementation at that time versus policy making.

Crown evaluation of the effectiveness of its own policies, and the extent to which its own agencies breach those policies is explored. The lack of control and accountability measures, plus the inability of the Crown to monitor (let alone sanction) success or failure, is highlighted. A contrast is drawn between the health and local government sectors, using the operation of the Resource Management Act (1991). 

The latest health sector reforms consequent on the 1999 Labour/Alliance coalition government are briefly considered, together with an overview of the Crown’s effectiveness in delivering improved Mäori health outcomes. The study suggests that the use of the Treaty as a cornerstone for Maori health policy formation and delivery may lead to more effective engagement between the Crown and Mäori in addressing Mäori health issues. The study concludes by asking the question, has the health sector reform process of the 1980s and 1990s itself been a Treaty breach?

A brief postscript considers the further reform of the health sector beyond the period of study.

text: Health reform and the impact on Mäori 1983-1997 This study investigates the New Zealand health sector reforms from 1983 to 1997and examines whether the reform process has been consistent with the principles of the Treaty of Waitangi. It evaluates the impact of the reforms on Mäori from that perspective. 

The study introduces the health sector reforms generally and then their specific effects on Mäori. It draws on two research exercises undertaken by the author, being research for the Wai 692 Napier Hospital and Health Services claim to the Waitangi Tribunal and on improving Mäori Health outcomes for the National Health Committee. The methodologies used are those from the discipline of history.

The study outlines the argument for Crown responsibilities under the Treaty and draws out the distinctions between Article 2 and Article 3 of the Treaty. It provides a historical background to the place of the Treaty in the health sector, and forms the basis for a Treaty based analysis of the health reforms and their impact. 

The New Zealand health sector has undergone massive government initiated structural change throughout the period under study. During this time the neo-liberal reforms have had a key role in reshaping health service structures. The process of change, the international influences on the changes, and the resulting entities are described. An example from Tainui Iwi of the effect of structural health reform illustrates the changes in Mäori health service provision by Mäori.
Since 1983 successive governments have produced copious Mäori health policy. The key policy documents, and their recommendations, are identified, as is the degree to which they were implemented. The cyclical nature of such policy making suggests that it is not always followed by policy implementation. While Mäori are identified as a health gain priority, the evidence reviewed shows that the responsibility to implement and monitor the policy is diffuse and ineffective.

The Wai 692 claim provides a detailed look at the impact of the 1990s health reform for Mäori. The claim was precipitated by the threatened closure of Napier Hospital, but was broadened to include a wide-ranging look at the impact of health reform on Mäori. As a case study it provides a specific example of one Iwi’s experience of the reality of policy implementation at that time versus policy making.

Crown evaluation of the effectiveness of its own policies, and the extent to which its own agencies breach those policies is explored. The lack of control and accountability measures, plus the inability of the Crown to monitor (let alone sanction) success or failure, is highlighted. A contrast is drawn between the health and local government sectors, using the operation of the Resource Management Act (1991). 

The latest health sector reforms consequent on the 1999 Labour/Alliance coalition government are briefly considered, together with an overview of the Crown’s effectiveness in delivering improved Mäori health outcomes. The study suggests that the use of the Treaty as a cornerstone for Maori health policy formation and delivery may lead to more effective engagement between the Crown and Mäori in addressing Mäori health issues. The study concludes by asking the question, has the health sector reform process of the 1980s and 1990s itself been a Treaty breach?

A brief postscript considers the further reform of the health sector beyond the period of study.

year: 2002