Vulnerability assessment of reinforced concrete columns subjected to vehicular impacts

Columns are one of the key load bearing elements that are highly susceptible to vehicle impacts. The resulting severe damages to columns may leads to failures of the supporting structure that are catastrophic in nature. However, the columns in existing structures are seldom designed for impact due to inadequacies of design guidelines. The impact behaviour of columns designed for gravity loads and actions other than impact is, therefore, of an interest. A comprehensive investigation is conducted on reinforced concrete column with a particular focus on investigating the vulnerability of the exposed columns and to implement mitigation techniques under low to medium velocity car and truck impacts. The investigation is based on non-linear explicit computer simulations of impacted columns followed by a comprehensive validation process. The impact is simulated using force pulses generated from full scale vehicle impact tests. A material model capable of simulating triaxial loading conditions is used in the analyses. Circular columns adequate in capacity for five to twenty story buildings, designed according to Australian standards are considered in the investigation. The crucial parameters associated with the routine column designs and the different load combinations applied at the serviceability stage on the typical columns are considered in detail. Axially loaded columns are examined at the initial stage and the investigation is extended to analyse the impact behaviour under single axis bending and biaxial bending. The impact capacity reduction under varying axial loads is also investigated. Effects of the various load combinations are quantified and residual capacity of the impacted columns based on the status of the damage and mitigation techniques are also presented. In addition, the contribution of the individual parameter to the failure load is scrutinized and analytical equations are developed to identify the critical impulses in terms of the geometrical and material properties of the impacted column. In particular, an innovative technique was developed and introduced to improve the accuracy of the equations where the other techniques are failed due to the shape of the error distribution. Above all, the equations can be used to quantify the critical impulse for three consecutive points (load combinations) located on the interaction diagram for one particular column. Consequently, linear interpolation can be used to quantify the critical impulse for the loading points that are located in-between on the interaction diagram. Having provided a known force and impulse pair for an average impact duration, this method can be extended to assess the vulnerability of columns for a general vehicle population based on an analytical method that can be used to quantify the critical peak forces under different impact durations. Therefore the contribution of this research is not only limited to produce simplified yet rational design guidelines and equations, but also provides a comprehensive solution to quantify the impact capacity while delivering new insight to the scientific community for dealing with impacts.

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.

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.

Pedagogy of introductory computer programming : a people-first approach

Students struggle with learning to program. In recent years, not only has there been a dramatic drop in the number of students enrolling in IT and Computer Science courses, but attrition from these courses continues to be significant. Introductory programming subjects traditionally have high failure rates and as they tend to be core to IT and Computer Science courses can be a road block for many students to their university studies. Is programming really that difficult — or are there other barriers to learning that have a serious and detrimental effect on student progression? In-class experiments were conducted in introductory programming units to confirm our hypothesis that that pair-programming would benefit students' learning to program. We investigated the social and cultural barriers to learning programming by questioning students' perceptions of confidence, difficulty and enjoyment of programming. The results of paired and non-paired students were compared to determine the effect of pair-programming on learning outcomes. Both the empirical and anecdotal results of our experiments strongly supported our hypothesis.

An exploration of the technical, social and macro-societal pressures influencing the adoption of online social networking services by organisations

Measuring the business value that Internet technologies deliver for organisations has proven to be a difficult and elusive task, given their complexity and increased embeddedness within the value chain. Yet, despite the lack of empirical evidence that links the adoption of Information Technology (IT) with increased financial performance, many organisations continue to adopt new technologies at a rapid rate. This is evident in the widespread adoption of Web 2.0 online Social Networking Services (SNSs) such as Facebook, Twitter and YouTube. These new Internet based technologies, widely used for social purposes, are being employed by organisations to enhance their business communication processes. However, their use is yet to be correlated with an increase in business performance. Owing to the conflicting empirical evidence that links prior IT applications with increased business performance, IT, Information Systems (IS), and E-Business Model (EBM) research has increasingly looked to broader social and environmental factors as a means for examining and understanding the broader influences shaping IT, IS and E-Business (EB) adoption behaviour. Findings from these studies suggest that organisations adopt new technologies as a result of strong external pressures, rather than a clear measure of enhanced business value. In order to ascertain if this is the case with the adoption of SNSs, this study explores how organisations are creating value (and measuring that value) with the use of SNSs for business purposes, and the external pressures influencing their adoption. In doing so, it seeks to address two research questions: 1. What are the external pressures influencing organisations to adopt SNSs for business communication purposes? 2. Are SNSs providing increased business value for organisations, and if so, how is that value being captured and measured? Informed by the background literature fields of IT, IS, EBM, and Web 2.0, a three-tiered theoretical framework is developed that combines macro-societal, social and technological perspectives as possible causal mechanisms influencing the SNS adoption event. The macro societal view draws on the concept of Castells. (1996) network society and the behaviour of crowds, herds and swarms, to formulate a new explanatory concept of the network vortex. The social perspective draws on key components of institutional theory (DiMaggio & Powell, 1983, 1991), and the technical view draws from the organising vision concept developed by Swanson and Ramiller (1997). The study takes a critical realist approach, and conducts four stages of data collection and one stage of data coding and analysis. Stage 1 consisted of content analysis of websites and SNSs of many organisations, to identify the types of business purposes SNSs are being used for. Stage 2 also involved content analysis of organisational websites, in order to identify suitable sample organisations in which to conduct telephone interviews. Stage 3 consisted of conducting 18 in-depth, semi-structured telephone interviews within eight Australian organisations from the Media/Publishing and Galleries, Libraries, Archives and Museum (GLAM) industries. These sample organisations were considered leaders in the use of SNSs technologies. Stage 4 involved an SNS activity count of the organisations interviewed in Stage 3, in order to rate them as either Advanced Innovator (AI) organisations, or Learning Focussed (LF) organisations. A fifth stage of data coding and analysis of all four data collection stages was conducted, based on the theoretical framework developed for the study, and using QSR NVivo 8 software. The findings from this study reveal that SNSs have been adopted by organisations for the purpose of increasing business value, and as a result of strong social and macro-societal pressures. SNSs offer organisations a wide range of value enhancing opportunities that have broader benefits for customers and society. However, measuring the increased business value is difficult with traditional Return On Investment (ROI) mechanisms, ascertaining the need for new value capture and measurement rationales, to support the accountability of SNS adoption practices. The study also identified the presence of technical, social and macro-societal pressures, all of which influenced SNS adoption by organisations. These findings contribute important theoretical insight into the increased complexity of pressures influencing technology adoption rationales by organisations, and have important practical implications for practice, by reflecting the expanded global online networks in which organisations now operate. The limitations of the study include the small number of sample organisations in which interviews were conducted, its limited generalisability, and the small range of SNSs selected for the study. However, these were compensated in part by the expertise of the interviewees, and the global significance of the SNSs that were chosen. Future research could replicate the study to a larger sample from different industries, sectors and countries. It could also explore the life cycle of SNSs in a longitudinal study, and map how the technical, social and macro-societal pressures are emphasised through stages of the life cycle. The theoretical framework could also be applied to other social fad technology adoption studies.

Lingodroids : studies in spatial cognition and language

The Lingodroids are a pair of mobile robots that evolve a language for places and relationships between places (based on distance and direction). Each robot in these studies has its own understanding of the layout of the world, based on its unique experiences and exploration of the environment. Despite having different internal representations of the world, the robots are able to develop a common lexicon for places, and then use simple sentences to explain and understand relationships between places even places that they could not physically experience, such as areas behind closed doors. By learning the language, the robots are able to develop representations for places that are inaccessible to them, and later, when the doors are opened, use those representations to perform goal-directed behavior.

Six degrees of cohesion in patent citation network

While the phrase “six degrees of separation” is widely used to characterize a variety of humanderived networks, in this study we show that in patent citation network, related patents are connected with an average distance of 6, whereas an average distance for a random pair of nodes in the graph is approximately 15. We use this information to improve the recall level in prior-art retrieval in the setting of blind relevance feedback without any textual knowledge.