Extending the task of diarization to speaker attribution

In this paper we extend the concept of speaker annotation within a single-recording, or speaker diarization, to a collection wide approach we call speaker attribution. Accordingly, speaker attribution is the task of clustering expectantly homogenous intersession clusters obtained using diarization according to common cross-recording identities. The result of attribution is a collection of spoken audio across multiple recordings attributed to speaker identities. In this paper, an attribution system is proposed using mean-only MAP adaptation of a combined-gender UBM to model clusters from a perfect diarization system, as well as a JFA-based system with session variability compensation. The normalized cross-likelihood ratio is calculated for each pair of clusters to construct an attribution matrix and the complete linkage algorithm is employed to conduct clustering of the inter-session clusters. A matched cluster purity and coverage of 87.1% was obtained on the NIST 2008 SRE corpus.

From Greek temple to bird's nest : mapping, assessing and understanding national integrity systems

In this paper, I would like to outline the approach we have taken to mapping and assessing integrity systems and how this has led us to see integrity systems in a new light. Indeed, it has led us to a new visual metaphor for integrity systems – a bird’s nest rather than a Greek temple. This was the result of a pair of major research projects completed in partnership with Transparency International (TI). One worked on refining and extending the measurement of corruption. This, the second, looked at what was then the emerging institutional means for reducing corruption – ‘national integrity systems’

Use of virtual index for measuring efficiency of innovation systems : a cross-country study

In this study we propose a virtual index for measuring the relative innovativeness of countries. Using a multistage virtual benchmarking process, the best and rational benchmark is extracted for inefficient ISs. Furthermore, Tobit and Ordinary Least Squares (OLS) regression models are used to investigate the likelihood of changes in inefficiencies by investigating country-specific factors. The empirical results relating to the virtual benchmarking process suggest that the OLS regression model would better explain changes in the performance of innovation- inefficient countries.

Deceit and Bruno Taut's Glashaus

The historical context surrounding Bruno Taut's Glashaus has been established through work of authors like Reyner Banham, Dennis Sharp and Ian Boyd-Whyte. However, these English language translations, are mostly derived from secondary sources such as Adolf Behne and Paul Scheerbart. Surprisingly, Taut's own writings largely do not feature in this prevailing account of his work. Since 1990, strong doubts have arisen about this conventional picture of Taut's Glashaus. Manfred spiedel, for instance, minimizes Paul Scheerbart's contribution to the design by arguing that Scheerbart met Taut only a few months before the construction of the Glashaus, that is, after Taut had finished his preliminary sketches. Kurt Junghanns goes further and asserts that the Glashaus design was complete beefore Taut and Scheerbart ever met. In 2005, Kai Gutschow published The Culture of Criticism: Adolf Behne and the Development of Modern Architecture in Germany, 1910 - 1914. Most startling, Gutschow asserts that Behne acts as the propagandist for the Glashaus by fabricating its link with Expressionism. This is particularly troubling because nobody contributed more to establishing the link between the Glashaus, Bruno Taut and Expressionism than Behne. As a result of this new evidence, this paper concurs that the established historical understanding of the Glashaus is flawed. By returning to Taut's own writings, a reinterpretation can be offered that strongly links the Glashaus to the Victoria regia lily and Strasbourg Cathedral. The significance of this approach is that it re-establishes Taut's own rational behind the design of the Glashaus, and thus contributes to the re-evaluation of the generally accepted histories of the Modern movement.

Learning the kernel matrix with semidefinite programming

Kernel-based learning algorithms work by embedding the data into a Euclidean space, and then searching for linear relations among the embedded data points. The embedding is performed implicitly, by specifying the inner products between each pair of points in the embedding space. This information is contained in the so-called kernel matrix, a symmetric and positive semidefinite matrix that encodes the relative positions of all points. Specifying this matrix amounts to specifying the geometry of the embedding space and inducing a notion of similarity in the input space - classical model selection problems in machine learning. In this paper we show how the kernel matrix can be learned from data via semidefinite programming (SDP) techniques. When applied to a kernel matrix associated with both training and test data this gives a powerful transductive algorithm -using the labeled part of the data one can learn an embedding also for the unlabeled part. The similarity between test points is inferred from training points and their labels. Importantly, these learning problems are convex, so we obtain a method for learning both the model class and the function without local minima. Furthermore, this approach leads directly to a convex method for learning the 2-norm soft margin parameter in support vector machines, solving an important open problem.

Learning the Kernel Matrix with Semi-Definite Programming

Kernel-based learning algorithms work by embedding the data into a Euclidean space, and then searching for linear relations among the embedded data points. The embedding is performed implicitly, by specifying the inner products between each pair of points in the embedding space. This information is contained in the so-called kernel matrix, a symmetric and positive definite matrix that encodes the relative positions of all points. Specifying this matrix amounts to specifying the geometry of the embedding space and inducing a notion of similarity in the input space -- classical model selection problems in machine learning. In this paper we show how the kernel matrix can be learned from data via semi-definite programming (SDP) techniques. When applied to a kernel matrix associated with both training and test data this gives a powerful transductive algorithm -- using the labelled part of the data one can learn an embedding also for the unlabelled part. The similarity between test points is inferred from training points and their labels. Importantly, these learning problems are convex, so we obtain a method for learning both the model class and the function without local minima. Furthermore, this approach leads directly to a convex method to learn the 2-norm soft margin parameter in support vector machines, solving another important open problem. Finally, the novel approach presented in the paper is supported by positive empirical results.

Parent decisions regarding paid work and care of the child

Australia has witnessed a continual increase in maternal employment over the past two decades, which has placed focus on child care- its effects on the child and on early childhood education and care policy and provision. The engagement of women in the paid workforce contributes to national economic development, and is recognised in government policy incentives such as cash subsidies and tax relief for child care fees. These incentives are targeted towards mothers, to encourage them to engage in paid work. Making a contribution to the family’s economy and to a mother’s economic self sufficiency are two key drivers for women’s engagement in satisfying paid work. Many women also seek to maintain a personal investment in the development of their career, simultaneously ensuring that the child is experiencing suitable care. Policies that support women’s choices for satisfying workforce engagement and care arrangements are prudent for ensuring productivity of the economy as well as for enhancing the wellbeing of parents and children (OECD, 2007). Policies that provide family friendly employment arrangements, paid parental leave, and child care support, directly affect maternal employment decisions. Availability of family friendly employment policies is viewed as one way to not only promote gender equity in employment opportunities but also support the wellbeing of children and families (OECD, 2007). Yet there are not comprehensive and coherent policies on work and family in Australia. Australia is due to implement its first paid parental leave scheme in January, 2011. At the time of the data collection of this research, June 2007 to December 2008, Australia had no statutory provision for paid parental leave. To date, most research has focused on the consequences of paid work and care decisions made by women. Far less is known about the processes of decision-making and reasons underlying women’s choices. Investigation of what is most salient for women as they make decisions regarding engagement in paid work, and care for their child is important in order to inform policy and practices related to parental leave, family friendly employment and care for the child. This prospective longitudinal research was of 124 Australian expectant first-time mothers who completed questionnaires in their third trimester of pregnancy, and again at six and twelve months postpartum. First-time expectant mothers' decisions regarding engaging in paid work and selecting care for their child represent those of a group who are invested in motherhood and have usually had direct experience of engaging in paid work. They therefore provide an important insight into society’s idealised views about motherhood and the emotional and social uncertainty of making personal decisions where the consequences of such decisions are unknown. These decisions reflect public beliefs about the role of women in contributing to the country’s productivity and decisions about providing for the economic and emotional care needs of their family. As so little is known about the reasoning and processes of decision-making of women’s choices regarding paid work and care of the child this research was designed to capture expectant first-time mother’s preferred options for engaging in paid work and the care of their child, and investigate their actual decisions made at six and 12 months postpartum. To capture preferred options, decisions and outcomes of decisions regarding paid work and care of the child a prospective longitudinal research design was utilised. This design had three important components that addressed key limitations in the extant literature. First the research commenced in pregnancy in order to investigate preferences and beliefs about paid work and care and to examine baseline data that may influence decisions made as the women returned to paid work. Second the research involved longitudinal tracking from the antenatal time point to six and 12 months postpartum in order to identify the influences on decisions made. Third the research measured outcomes of the decisions made at each time point. This research examined the intentions, preferences, beliefs, influences, and outcomes of the decisions about engagement in paid work and choice of care. The analyses examined factors predicting return to paid work, the timing of return and extent of engagement in paid work; the care for the child; satisfaction with paid work; satisfaction with care for the child, motherhood and fulfilment; and maternal wellbeing at six and 12 months postpartum. The factors of interest were both rational/economic (availability and extent of paid and unpaid maternity leave; flexible work patterns) and emotional/affective (career satisfaction, investment in motherhood, and concern with quality of care for the child). Results indicated a group preference, and realisation for, return to paid work within the first year after the birth of a child but with reduction in hours to part-time. Most women saw paid work not only as a source of income but also as source of personal satisfaction. There were four key themes arising from this research. First, the women strived to feel emotionally secure when deciding about engaging in paid work and care of the child. To achieve emotional security women made their decisions for paid work and care of the child differently. A woman’s decision for maternal employment is a function of her personal beliefs, preferences and context regarding paid work and care of the child. She adjusts her established work identity with her new identity as a mother. The second key theme from this research is that the women made their decisions for maternal employment in response to their personal context and there were different levels of opportunities between the women’s choices. There is inequity of entitlement regarding work conditions associated with a woman’s education level. This has implications for the woman’s engagement in paid work, and her child’s health and wellbeing. The third key theme is that the quality of the child’s care mattered to the women in the research. They preferred care provided by parents and/or relatives more than any other types of care. The fourth key theme identified that satisfaction and wellbeing outcomes experienced as a result of maternal employment decisions were a complex interaction between multiple factors that change across time with the ongoing development of the mother’s identity, and the development of the child. The implications for policy within Australia are that the employment of mothers in the workforce necessitates that non-parental care becomes a public concern, where there is universal access to good quality affordable care for every child, not just for those who can afford it. This is equitable and represents real choice while supporting the rights of the child (Thorpe, Cloney & Tayler, 2010), protecting and promoting the public interest (Cleveland & Krashinsky, 2010). Children’s health and wellbeing will be supported (Moore & Oberklaid, 2010) while children are in non-parental care, and they will be exposed to environments and experiences that support their learning and development. The significant design of the research enabled the trajectories of first-time expectant women to be tracked from the antenatal point to 12 months postpartum. But there were limitations: the small sample size, the over-representation of the sample being highly educated and the nature of a longitudinal research that is set within the economic, social and political context at that time. These limitations are discussed in relation to suggestions for future research.

Association between polymorphisms in the progesterone receptor gene and endometriosis

The progesterone receptor (PR) is a candidate gene for the development of endometriosis, a complex disease with strong hormonal features, common in women of reproductive age. We typed the 306 base pair Alu insertion (AluIns) polymorphism in intron G of PR in 101 individuals, estimated linkage disequilibrium (LD) between five single-nucleotide polymorphisms (SNPs) across the PR locus in 980 Australian triads (endometriosis case and two parents) and used transmission disequilibrium testing (TDT) for association with endometriosis. The five SNPs showed strong pairwise LD, and the AluIns was highly correlated with proximal SNPs rs1042839 (Δ2 = 0.877, D9 = 1.00, P < 0.0001) and rs500760 (Δ2 = 0.438, D9 = 0.942, P < 0.0001). TDT showed weak evidence of allelic association between endometriosis and rs500760 (P = 0.027) but not in the expected direction. We identified a common susceptibility haplotype GGGCA across the five SNPs (P = 0.0167) in the whole sample, but likelihood ratio testing of haplotype transmission and non-transmission of the AluIns and flanking SNPs showed no significant pattern. Further, analysis of our results pooled with those from two previous studies suggested that neither the T2 allele of the AluIns nor the T1/T2 genotype was associated with endometriosis.

Beam steering with high front-to-back ratio and high directivity on small platforms using decoupled antenna pairs

Beam steering with high front-to-back ratio and high directivity on a small platform is proposed. Two closely spaced antenna pairs with eigenmode port decoupling are used as the basic radiating elements. Two orthogonal radiation patterns are obtained for each antenna pair. High front-to-back ratio and high directivity are achieved by combining the two orthogonal radiation patterns. With an infinite groundplane, a front-to-back ratio of 21 dB with a directivity of 9.8 dB can be achieved. Beam steering, at the expense of a slight decrease in directivity, is achieved by placing the two antenna pairs 0.5λ apart. The simulated half power beamwidth is 58°. A prototype was designed and the 2-D radiation patterns were measured. The prototype supports three directions of beam steering. The half power beamwidth was measured as 46°, 48°, and 50° for the three respective beam directions. The measured front-to-back ratio in azimuth plane is 8.5 dB, 8.0 dB and 7.6 dB, respectively.

Compilation of somatic mutations of the CDKN2 gene in human cancers : non-random distribution of base substitutions

The CDKN2 gene, encoding the cyclin-dependent kinase inhibitor p16, is a tumour suppressor gene that maps to chromosome band 9p21-p22. The most common mechanism of inactivation of this gene in human cancers is through homozygous deletion; however, in a smaller proportion of tumours and tumour cell lines intragenic mutations occur. In this study we have compiled a database of over 120 published point mutations in the CDKN2 gene from a wide variety of tumour types. A further 50 deletions, insertions, and splice mutations in CDKN2 have also been compiled. Furthermore, we have standardised the numbering of all mutations according to the full-length 156 amino acid form of p16. From this study we are able to define several hot spots, some of which occur at conserved residues within the ankyrin domains of p16. While many of the hotspots are shared by a number of cancers, the relative importance of each position varies, possibly reflecting the role of different carcinogens in the development of certain tumours. As reported previously, the mutational spectrum of CDKN2 in melanomas differs from that of internal malignancies and supports the involvement of UV in melanoma tumorigenesis. Notably, 52% of all substitutions in melanoma-derived samples occurred at just six nucleotide positions. Nonsense mutations comprise a comparatively high proportion of mutations present in the CDKN2 gene, and possible explanations for this are discussed.

CDKN2A/p16 is inactivated in most melanoma cell lines

The CDKN2A gene maps to chromosome 9p21-22 and is responsible for melanoma susceptibility in some families. Its product, p16, binds specifically to CDK4 and CDK6 in vitro and in vivo, inhibiting their kinase activity. CDKN2A is homozygously deleted or mutated in a large proportion of tumor cell lines and some primary tumors, including melanomas. The aim of this study was to investigate the involvement of CDKN2A and elucidate the mechanisms of p16 inactivation in a panel of 60 cell lines derived from sporadic melanomas. Twenty-six (43%) of the melanoma lines were homozygously deleted for CDKN2A, and an additional 15 (25%) lines carried missense, nonsense, or frameshift mutations. All but one of the latter group were shown by microsatellite analysis to be hemizygous for the region of 9p surrounding CDKN2A. p16 was detected by Western blotting in only five of the cell lines carrying mutations. Immunoprecipitation of p16 in these lines, followed by Western blotting to detect the coprecipitation of CDK4 and CDK6, revealed that p16 was functionally compromised in all cell lines but the one that carried a heterozygous CDKN2A mutation. In the remaining 19 lines that carried wild-type CDKN2A alleles, Western blot analysis and immunoprecipitation indicated that 11 cell lines expressed a wild-type protein. Northern blotting was performed on the remaining eight cell lines and revealed that one cell line carried an aberrantly sized RNA transcript, and two other cell lines failed to express RNA. The promoter was found to be methylated in five cell lines that expressed CDKN2A transcript but not p16. Presumably, the message seen by Northern blotting in these cell lines is the result of cross-hybridization of the total cDNA probe with the exon 1beta transcript. Microsatellite analysis revealed that the majority of these cell lines were hemi/homozygous for the region surrounding CDKN2A, indicating that the wild-type allele had been lost. In the 11 cell lines that expressed functional p16, microsatellite analysis revealed loss of heterozygosity at the markers immediately surrounding CDKN2A in five cases, and the previously characterized R24C mutation of CDK4 was identified in one of the remaining 6 lines. These data indicate that 55 of 60 (92%) melanoma cell lines demonstrated some aberration of CDKN2A or CDK4, thus suggesting that this pathway is a primary genetic target in melanoma development.

CDKN2A is not the principal target of deletions on the short arm of chromosome 9 in neuroendocrine (Merkel cell) carcinoma of the skin

The majority of small-cell lung cancers (SCLCs) express p16 but not pRb. Given our previous study showing loss of pRb in Merkel cell carcinoma (MCC)/neuroendocrine carcinoma of the skin and the clinicopathological similarities between SCLC and MCC, we wished to determine if this was also the case in MCC. Twenty-nine MCC specimens from 23 patients were examined for deletions at 10 loci on 9p and 1 on 9q. No loss of heterozygosity (LOH) was seen in 9 patients including 2 for which tumour and cell line DNAs were examined. Four patients had LOH for all informative loci on 9p. Ten tumours showed more limited regions of loss on 9p, and from these 2 common regions of deletion were determined. Half of all informative cases had LOH at D9S168, the most telomeric marker examined, and 3 specimens showed loss of only D9S168. A second region (IFNA-D9S126) showed LOH in 10 (44%) cases, and case MCC26 showed LOH for only D9S126, implicating genes centromeric of the CDKN2A locus. No mutations in the coding regions of p16 were seen in 7 cell lines tested, and reactivity to anti-p16 antibody was seen in all 11 tumour specimens examined and in 6 of 7 cell lines from 6 patients. Furthermore, all cell lines examined reacted with anti-p14(ARF) antibody. These results suggest that neither transcript of the CDKN2A locus is the target of deletions on 9p in MCC and imply the existence of tumour-suppressor genes mapping both centromeric and telomeric of this locus.

Evidence for three tumor suppressor loci on chromosome 9p involved in melanoma development

Cytogenetic and loss of heterozygosity (LOH) studies have long indicated the presence of a tumor suppressor gene (TSG) on 9p involved in the development of melanoma. Although LOH at 9p has been reported in approximately 60% of melanoma tumors, only 5-10% of these tumors have been shown to carry CDKN2A mutations, raising the possibility that another TSG involved in melanoma maps to chromosome 9p. To investigate this possibility, a panel of 37 melanomas derived from 35 individuals was analyzed for CDKN2A mutations by single-strand conformation polymorphism analysis and sequencing. The melanoma samples were then typed for 15 markers that map to 9p13-24 to investigate LOH trends in this region. In those tumors demonstrating retention of heterozygosity at markers flanking CDKN2A and LOH on one or both sides of the gene, multiplex microsatellite PCR was performed to rule out homozygous deletion of the region encompassing CDKN2A. CDKN2A mutations were found in tumors from 5 patients [5 (14%) of 35], 4 of which demonstrated LOH across the entire region examined. The remaining tumor with no observed LOH carried two point mutations, one on each allele. Although LOH was identified at one or more markers in 22 (59%) of 37 melanoma tumors corresponding to 20 (57%) of 35 individuals, only 11 tumors from 9 individuals [9 (26%) of 35] demonstrated LOH at D9S942 and D9S1748 the markers closest to CDKN2A. Of the remaining 11 tumors with LOH 9 demonstrated LOH at two or more contiguous markers either centromeric and/or telomeric to CDKN2A while retaining heterozygosity at several markers adjacent to CDKN2A. Multiplex PCR revealed one tumor carried a homozygous deletion extending from D9S1748 to the IFN-alpha locus. In the remaining eight tumors, multiplex PCR demonstrated that the observed heterozygosity was not attributable to homozygous deletion and stromal contamination at D9S1748, D9S942, or D9S974, as measured by comparative amplification strengths, which indicates that retention of heterozygosity with flanking LOH does not always indicate a homozygous deletion. This report supports the conclusions of previous studies that a least two TSGs involved in melanoma development in addition to CDKN2A may reside on chromosome 9p.

PTEN inactivation is rare in melanoma tumours but occurs frequently in melanoma cell lines

Deletions detected in cytogenetic and loss of heterozygosity (LOH) studies indicate that at least one tumour suppressor gene maps to the long arm of chromosome 10. Previous deletion mapping studies have observed LOH on 10q in about 30% of melanomas analysed. The PTEN gene, mapping to chromosome band 10q23.3, encodes a protein with both lipid and protein phosphatase activity. Somatic mutations and deletions in have been detected in a variety of cell lines and tumours, including melanoma samples. We performed mutation analyses and extensive allelic loss studies to investigate the role this gene plays in melanoma pathogenesis. We found that a total of 34 out of 57 (60%) melanoma cell lines carried hemizygous deletions of chromosome 10q encompassing the PTEN locus. A further three cell lines carried smaller deletions excluding PTEN. Inactivation of both PTEN alleles by exon-specific homozygous deletion or mutation was observed in 13 out of 57 (23%) melanoma cell lines. The mutation spectrum observed does not indicate an important role for ultraviolet radiation in the genesis of these mutations, and evidence from three cell lines supports the acquisition of PTEN aberrations in culture. Ten out of 49 (20%) matched melanoma tumour/normal samples harboured hemizygous deletions of either the whole chromosome or most of the long arm. Mutations within were detected in only one of the 10 tumours demonstrating LOH at 10q23 that were analysed. These results suggest that PTEN inactivation may be important for the propagation of melanoma cells in culture, and that another chromosome 10 tumour suppressor gene may be important for melanoma pathogenesis.

Deletion mapping suggests that the 1p22 melanoma susceptibility gene is a tumor suppressor localized to a 9-Mb interval

Loss of the short arm of chromosome 1 is frequently observed in many tumor types, including melanoma. We recently localized a third melanoma susceptibility locus to chromosome band 1p22. Critical recombinants in linked families localized the gene to a 15-Mb region between D1S430 and D1S2664. To map the locus more finely we have performed studies to assess allelic loss across the region in a panel of melanomas from 1p22-linked families, sporadic melanomas, and melanoma cell lines. Eighty percent of familial melanomas exhibited loss of heterozygosity (LOH) within the region, with a smallest region of overlapping deletions (SRO) of 9 Mb between D1S207 and D1S435. This high frequency of LOH makes it very likely that the susceptibility locus is a tumor suppressor. In sporadic tumors, four SROs were defined. SRO1 and SRO2 map within the critical recombinant and familial tumor region, indicating that one or the other is likely to harbor the susceptibility gene. However, SRO3 may also be significant because it overlaps with the markers with the highest 2-point LOD score (D1S2776), part of the linkage recombinant region, and the critical region defined in mesothelioma. The candidate genes PRKCL2 and GTF2B, within SRO2, and TGFBR3, CDC7, and EVI5, in a broad region encompassing SRO3, were screened in 1p22-linked melanoma kindreds, but no coding mutations were detected. Allelic loss in melanoma cell lines was significantly less frequent than in fresh tumors, indicating that this gene may not be involved late in progression, such as in overriding cellular senescence, necessary for the propagation of melanoma cells in culture.