title: Racing committees for large datasets

authors: Frank, Eibe

subjects: Science & Technology

abstract: This paper proposes a method for generating classifiers from large datasets by building a committee of simple base classifiers using a standard boosting algorithm. It permits the processing of large datasets even if the underlying base learning algorithm cannot efficiently do so. The basic idea is to split incoming data into chunks and build a committee based on classifiers built from these individual chunks. Our method extends earlier work by introducing a method for adaptively pruning the committee. This is essential when applying the algorithm in practice because it dramatically reduces the algorithm’s running time and memory consumption. It also makes it possible to efficiently “race” committees corresponding to different chunk sizes. This is important because our empirical results show that the accuracy of the resulting committee can vary significantly with the chunk size. They also show that pruning is indeed crucial to make the method practical for large datasets in terms of running time and memory requirements. Surprisingly, the results demonstrate that pruning can also improve accuracy.

text: Racing committees for large datasets This paper proposes a method for generating classifiers from large datasets by building a committee of simple base classifiers using a standard boosting algorithm. It permits the processing of large datasets even if the underlying base learning algorithm cannot efficiently do so. The basic idea is to split incoming data into chunks and build a committee based on classifiers built from these individual chunks. Our method extends earlier work by introducing a method for adaptively pruning the committee. This is essential when applying the algorithm in practice because it dramatically reduces the algorithm’s running time and memory consumption. It also makes it possible to efficiently “race” committees corresponding to different chunk sizes. This is important because our empirical results show that the accuracy of the resulting committee can vary significantly with the chunk size. They also show that pruning is indeed crucial to make the method practical for large datasets in terms of running time and memory requirements. Surprisingly, the results demonstrate that pruning can also improve accuracy.

year: 2002-01-01

title: The genetic structure of New Zealand's coastal benthos: using the estuarine clam Austrovenus stutchburyi, to determine rates of gene flow and population connectivity

authors: Ross, Philip M.

subjects: cockle

abstract: For many benthic marine taxa, dispersal over large distances is dependent on a pelagic larval phase. It is through the dispersal process that benthic taxa can found new populations, colonise disturbed or degraded habitats and achieve genetic exchange between geographically separated subpopulations. While it is widely accepted that the dispersal process is important in determining the dynamics of many marine communities, difficulties associated with the direct measurement of larval dispersal mean that detailed knowledge of the mechanisms controlling larval transport has been elusive. Consequently, indirect methods, such as population genetics, have been used to estimate dispersal pathways. This thesis examines the population genetic structure of New Zealand’s coastal benthos with the aim of enhancing our understanding of population connectivity, as well as identifying physical and biological processes that might influence population genetic structure.

The population genetic structure of New Zealand’s coastal benthos was examined in a quantitative literature review. Divergence between northern and southern populations was identified as the most frequently reported population genetic structure, with the divergence most often located in central New Zealand. Additional population structure although rare, was reported for a number of taxa, particularly those restricted to estuaries and with life history traits indicative of limited dispersal potential. A significant negative correlation between pelagic larval duration (PLD) and genetic divergence suggests that PLD may be a useful proxy for a species’ dispersal ability. However, variation in estimates of divergence for taxa with limited PLDs suggests that other factors may also influence dispersal potential. 
To determine whether populations of an estuarine organism with life history traits indicative of widespread dispersal are genetically subdivided, I examined the population genetic structure of the clam Austrovenus stutchburyi using the mitochondrial gene cytochrome oxidase c subunit I (COI). Analyses indicated that dispersal was limited and that gene flow was mostly occurring among estuaries in close proximity. Genetic boundaries were detected in central New Zealand, about the East and North Capes and in the south of the South Island. Similar boundaries have been reported for estuarine taxa lacking a dispersive larval phase suggesting that distribution and habitat requirements may influence patterns of gene flow. 
To further investigate gene flow among estuaries, I conducted a multi-scale genetic analysis of A. stutchburyi populations on New Zealand’s west coast Analyses of COI and microsatellite loci showed populations to be well connected within estuaries and at the regional sampling scale (≤ 156 km) although not at a national scale (≤ 1226 km). Distance among populations explained much of the observed genetic variation as did distance between estuaries. Long stretches of open coast appear to act as barriers to dispersal among A. stutchburyi populations. However, as long stretches of open coast also coincide with putative hydrodynamic dispersal barriers there is some uncertainty about the roles of barriers versus inter-estuary distance in generating the observed divergences. Within-estuary genetic differences were evident from COI analyses, but may result from local adaptation to within-estuary environmental gradients. 
I conclude that genetic connectivity among populations of New Zealand’s estuarine taxa is generally low relative to coastal species. The data presented here also suggest that migration among patchily distributed habitats, such as estuaries, will be dependent on the spatial arrangement of habitats. Consequently, patchily distributed taxa may experience low rates of ecologically meaningful connectivity, requiring relatively cautious management at small spatial scales to ensure the persistence of intact biological communities in the face of persistent anthropogenic and natural disturbances.

text: The genetic structure of New Zealand's coastal benthos: using the estuarine clam Austrovenus stutchburyi, to determine rates of gene flow and population connectivity For many benthic marine taxa, dispersal over large distances is dependent on a pelagic larval phase. It is through the dispersal process that benthic taxa can found new populations, colonise disturbed or degraded habitats and achieve genetic exchange between geographically separated subpopulations. While it is widely accepted that the dispersal process is important in determining the dynamics of many marine communities, difficulties associated with the direct measurement of larval dispersal mean that detailed knowledge of the mechanisms controlling larval transport has been elusive. Consequently, indirect methods, such as population genetics, have been used to estimate dispersal pathways. This thesis examines the population genetic structure of New Zealand’s coastal benthos with the aim of enhancing our understanding of population connectivity, as well as identifying physical and biological processes that might influence population genetic structure.

The population genetic structure of New Zealand’s coastal benthos was examined in a quantitative literature review. Divergence between northern and southern populations was identified as the most frequently reported population genetic structure, with the divergence most often located in central New Zealand. Additional population structure although rare, was reported for a number of taxa, particularly those restricted to estuaries and with life history traits indicative of limited dispersal potential. A significant negative correlation between pelagic larval duration (PLD) and genetic divergence suggests that PLD may be a useful proxy for a species’ dispersal ability. However, variation in estimates of divergence for taxa with limited PLDs suggests that other factors may also influence dispersal potential. 
To determine whether populations of an estuarine organism with life history traits indicative of widespread dispersal are genetically subdivided, I examined the population genetic structure of the clam Austrovenus stutchburyi using the mitochondrial gene cytochrome oxidase c subunit I (COI). Analyses indicated that dispersal was limited and that gene flow was mostly occurring among estuaries in close proximity. Genetic boundaries were detected in central New Zealand, about the East and North Capes and in the south of the South Island. Similar boundaries have been reported for estuarine taxa lacking a dispersive larval phase suggesting that distribution and habitat requirements may influence patterns of gene flow. 
To further investigate gene flow among estuaries, I conducted a multi-scale genetic analysis of A. stutchburyi populations on New Zealand’s west coast Analyses of COI and microsatellite loci showed populations to be well connected within estuaries and at the regional sampling scale (≤ 156 km) although not at a national scale (≤ 1226 km). Distance among populations explained much of the observed genetic variation as did distance between estuaries. Long stretches of open coast appear to act as barriers to dispersal among A. stutchburyi populations. However, as long stretches of open coast also coincide with putative hydrodynamic dispersal barriers there is some uncertainty about the roles of barriers versus inter-estuary distance in generating the observed divergences. Within-estuary genetic differences were evident from COI analyses, but may result from local adaptation to within-estuary environmental gradients. 
I conclude that genetic connectivity among populations of New Zealand’s estuarine taxa is generally low relative to coastal species. The data presented here also suggest that migration among patchily distributed habitats, such as estuaries, will be dependent on the spatial arrangement of habitats. Consequently, patchily distributed taxa may experience low rates of ecologically meaningful connectivity, requiring relatively cautious management at small spatial scales to ensure the persistence of intact biological communities in the face of persistent anthropogenic and natural disturbances.

year: 2011

title: Association of Single Nucleotide Polymorphisms in Surfactant Protein A and D with Otitis Media.

authors: Barnett, Catherine Margaret Eleanor

subjects: otitis media

abstract: Otitis Media is one of the most common childhood diseases. Recurrent acute otitis media RAOM is characterized by repeated episodes of inflammation of the middle ear in conjunction with middle ear fluid, and often with an inflamed or bulging eardrum. Defective clearance by the Eustachian tube results in mucus build-up and is characteristic of otitis media with effusion (OME). Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, respiratory syncytial virus, and rhinovirus are the most common contributors to otitis media pathogenesis. In New Zealand, OME has been implicated with conductive hearing loss in childhood and has been shown to significantly impact on speech and language development. New Zealand Māori and Polynesian children have displayed significantly higher hearing test failure rates than European-Caucasian children.

The collectins, Surfactant Protein (SP)-A and -D are encoded by three genes (SP-A1, SP-A2, and SP-D) and are host defense proteins present in the middle ear and Eustachian tube. Single nucleotide polymorphisms (SNPs) in SP-A1 and SP-A2 have been associated with increased or decreased susceptibility to otitis media, meningococcal disease, and range of respiratory diseases. Using allele-specific primers and real-time PCR with SYBR  Green I melting curve analysis, four groups of individuals were genotyped for eleven SP-A1, SP-A2, and SP-D SNPs: European-Caucasian individuals with RAOM/OME; New Zealand Māori/Polynesian individuals with RAOM/OME; individuals with meningococcal disease; and a control group. The computer program, Haploview, was employed to perform χ2 analyses and identify statistically significant associations of alleles/haplotypes with RAOM/OME or meningococcal disease.

In the European-Caucasian population, two SP-A1 alleles, one SP-A2 allele, and four haplotypes (CGAGC, 1A3, 1A9, and 1A10) were found to be associated with increased risk of RAOM/OME (P lt; 0.05). Conversely, haplotypes 6A2 and 1A2 were found to be protective against susceptibility to RAOM/OME (P lt; 0.05). In New Zealand Māori and Polynesian individuals, two SP-A1 alleles, three SP-A2 alleles, one SP-D allele, and four haplotypes (6A8, 6A10, 1A3, and 1A10) were found to be associated with increased risk of RAOM/OME (P lt; 0.05). An additional four haplotypes (6A2, 1A0, 1A2, and TA) were determined to be protective against susceptibility to RAOM/OME (P lt; 0.05). However, protective SPA1/SPA2/SPD haplotype 6A2-1A0-TA was significantly under-represented in the New Zealand Māori and Polynesian population (P lt; 0.05). A single allele and haplotype were associated with increased risk of meningococcal disease (P lt; 0.05).

The findings of this study confirm that specific genetic variants of SP-A and SP-D are associated with either increased or decreased risk of developing RAOM and/or OME. Furthermore, it was demonstrated that New Zealand Māori and Polynesian individuals appear to exhibit more haplotypes susceptible to RAOM/OME. This may provide a partial explanation for the higher RAOM/OME-related failure rates of hearing tests in New Zealand Māori and Polynesian children. However, there are numerous socio-economic and environmental factors that also contribute to otitis media pathogenesis which were not considered in this study. The effects of the SP-A1, SP-A2, and SP-D alleles and haplotypes on the bacterial/viral binding efficiencies of SP-A and SP-D need to be investigated by further research, using a large population, to confirm the association with susceptibility or resistance with RAOM/OME.

text: Association of Single Nucleotide Polymorphisms in Surfactant Protein A and D with Otitis Media. Otitis Media is one of the most common childhood diseases. Recurrent acute otitis media RAOM is characterized by repeated episodes of inflammation of the middle ear in conjunction with middle ear fluid, and often with an inflamed or bulging eardrum. Defective clearance by the Eustachian tube results in mucus build-up and is characteristic of otitis media with effusion (OME). Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, respiratory syncytial virus, and rhinovirus are the most common contributors to otitis media pathogenesis. In New Zealand, OME has been implicated with conductive hearing loss in childhood and has been shown to significantly impact on speech and language development. New Zealand Māori and Polynesian children have displayed significantly higher hearing test failure rates than European-Caucasian children.

The collectins, Surfactant Protein (SP)-A and -D are encoded by three genes (SP-A1, SP-A2, and SP-D) and are host defense proteins present in the middle ear and Eustachian tube. Single nucleotide polymorphisms (SNPs) in SP-A1 and SP-A2 have been associated with increased or decreased susceptibility to otitis media, meningococcal disease, and range of respiratory diseases. Using allele-specific primers and real-time PCR with SYBR  Green I melting curve analysis, four groups of individuals were genotyped for eleven SP-A1, SP-A2, and SP-D SNPs: European-Caucasian individuals with RAOM/OME; New Zealand Māori/Polynesian individuals with RAOM/OME; individuals with meningococcal disease; and a control group. The computer program, Haploview, was employed to perform χ2 analyses and identify statistically significant associations of alleles/haplotypes with RAOM/OME or meningococcal disease.

In the European-Caucasian population, two SP-A1 alleles, one SP-A2 allele, and four haplotypes (CGAGC, 1A3, 1A9, and 1A10) were found to be associated with increased risk of RAOM/OME (P lt; 0.05). Conversely, haplotypes 6A2 and 1A2 were found to be protective against susceptibility to RAOM/OME (P lt; 0.05). In New Zealand Māori and Polynesian individuals, two SP-A1 alleles, three SP-A2 alleles, one SP-D allele, and four haplotypes (6A8, 6A10, 1A3, and 1A10) were found to be associated with increased risk of RAOM/OME (P lt; 0.05). An additional four haplotypes (6A2, 1A0, 1A2, and TA) were determined to be protective against susceptibility to RAOM/OME (P lt; 0.05). However, protective SPA1/SPA2/SPD haplotype 6A2-1A0-TA was significantly under-represented in the New Zealand Māori and Polynesian population (P lt; 0.05). A single allele and haplotype were associated with increased risk of meningococcal disease (P lt; 0.05).

The findings of this study confirm that specific genetic variants of SP-A and SP-D are associated with either increased or decreased risk of developing RAOM and/or OME. Furthermore, it was demonstrated that New Zealand Māori and Polynesian individuals appear to exhibit more haplotypes susceptible to RAOM/OME. This may provide a partial explanation for the higher RAOM/OME-related failure rates of hearing tests in New Zealand Māori and Polynesian children. However, there are numerous socio-economic and environmental factors that also contribute to otitis media pathogenesis which were not considered in this study. The effects of the SP-A1, SP-A2, and SP-D alleles and haplotypes on the bacterial/viral binding efficiencies of SP-A and SP-D need to be investigated by further research, using a large population, to confirm the association with susceptibility or resistance with RAOM/OME.

year: 2007