Semantic service discovery in the service ecosystem

Electronic services are a leitmotif in ‘hot’ topics like Software as a Service, Service Oriented Architecture (SOA), Service oriented Computing, Cloud Computing, application markets and smart devices. We propose to consider these in what has been termed the Service Ecosystem (SES). The SES encompasses all levels of electronic services and their interaction, with human consumption and initiation on its periphery in much the same way the ‘Web’ describes a plethora of technologies that eventuate to connect information and expose it to humans. Presently, the SES is heterogeneous, fragmented and confined to semi-closed systems. A key issue hampering the emergence of an integrated SES is Service Discovery (SD). A SES will be dynamic with areas of structured and unstructured information within which service providers and ‘lay’ human consumers interact; until now the two are disjointed, e.g., SOA-enabled organisations, industries and domains are choreographed by domain experts or ‘hard-wired’ to smart device application markets and web applications. In a SES, services are accessible, comparable and exchangeable to human consumers closing the gap to the providers. This requires a new SD with which humans can discover services transparently and effectively without special knowledge or training. We propose two modes of discovery, directed search following an agenda and explorative search, which speculatively expands knowledge of an area of interest by means of categories. Inspired by conceptual space theory from cognitive science, we propose to implement the modes of discovery using concepts to map a lay consumer’s service need to terminologically sophisticated descriptions of services. To this end, we reframe SD as an information retrieval task on the information attached to services, such as, descriptions, reviews, documentation and web sites - the Service Information Shadow. The Semantic Space model transforms the shadow's unstructured semantic information into a geometric, concept-like representation. We introduce an improved and extended Semantic Space including categorization calling it the Semantic Service Discovery model. We evaluate our model with a highly relevant, service related corpus simulating a Service Information Shadow including manually constructed complex service agendas, as well as manual groupings of services. We compare our model against state-of-the-art information retrieval systems and clustering algorithms. By means of an extensive series of empirical evaluations, we establish optimal parameter settings for the semantic space model. The evaluations demonstrate the model’s effectiveness for SD in terms of retrieval precision over state-of-the-art information retrieval models (directed search) and the meaningful, automatic categorization of service related information, which shows potential to form the basis of a useful, cognitively motivated map of the SES for exploratory search.

Negative space and positive environment : mapping opportunities for urban resilience

Cities have long held a fascination for people – as they grow and develop, there is a desire to know and understand the intricate interplay of elements that makes cities ‘live’. In part, this is a need for even greater efficiency in urban centres, yet the underlying quest is for a sustainable urban form. In order to make sense of the complex entities that we recognise cities to be, they have been compared to buildings, organisms and more recently machines. However the search for better and more elegant urban centres is hardly new, healthier and more efficient settlements were the aim of Modernism’s rational sub-division of functions, which has been translated into horizontal distribution through zoning, or vertical organisation thought highrise developments. However both of these approaches have been found to be unsustainable, as too many resources are required to maintain this kind or urbanisation and social consequences of either horizontal or vertical isolation must also be considered. From being absolute consumers of resources, of energy and of technology, cities need to change, to become sustainable in order to be more resilient and more efficient in supporting culture, society as well as economy. Our urban centres need to be re-imagined, re-conceptualised and re-defined, to match our changing society. One approach is to re-examine the compartmentalised, mono-functional approach of urban Modernism and to begin to investigate cities like ecologies, where every element supports and incorporates another, fulfilling more than just one function. This manner of seeing the city suggests a framework to guide the re-mixing of urban settlements. Beginning to understand the relationships between supporting elements and the nature of the connecting ‘web’ offers an invitation to investigate the often ignored, remnant spaces of cities. This ‘negative space’ is the residual from which space and place are carved out in the Contemporary city, providing the link between elements of urban settlement. Like all successful ecosystems, cities need to evolve and change over time in order to effectively respond to different lifestyles, development in culture and society as well as to meet environmental challenges. This paper seeks to investigate the role that negative space could have in the reorganisation of the re-mixed city. The space ‘in-between’ is analysed as an opportunity for infill development or re-development which provides to the urban settlement the variety that is a pre-requisite for ecosystem resilience. An analysis of the urban form is suggested as an empirical tool to map the opportunities already present in the urban environment and negative space is evaluated as a key element in achieving a positive development able to distribute diverse environmental and social facilities in the city.

Corneal nerve structure and function as markers of diabetic neuropathy

Diabetic neuropathy is a significant clinical problem that currently has no effective therapy, and in advanced cases, leads to foot ulceration and lower limb amputation. The accurate detection, characterisation and quantification of this condition are important in order to define at-risk patients, anticipate deterioration, monitor progression and assess new therapies. This thesis evaluates novel corneal methods of assessing diabetic neuropathy. Over the past several years two new non-invasive corneal markers have emerged, and in cross-sectional studies have demonstrated their ability to stratify the severity of this disease. Corneal confocal microscopy (CCM) allows quantification of corneal nerve parameters and non-contact corneal aesthesiometry (NCCA), the presumed functional correlate of corneal structure, assesses the sensitivity of the cornea. Both these techniques are quick to perform, produce little or no discomfort for the patient, and with automatic analysis paradigms developed, are suitable for clinical settings. Each has advantages and disadvantages over established techniques for assessing diabetic neuropathy. New information is presented regarding measurement bias of CCM images, and a unique sampling paradigm and associated accuracy determination method of combinations is described. A novel high-speed corneal nerve mapping procedure has been developed and application of this procedure in individuals with neuropathy has revealed regions of sub-basal nerve plexus that dictate further evaluation, as they appear to show earlier signs of damage than the central region of the cornea that has to date been examined. The discriminative capacity of corneal sensitivity measured by NCCA is revealed to have reasonable potential as a marker of diabetic neuropathy. Application of these new corneal markers for longitudinal evaluation of diabetic neuropathy has the potential to reduce dependence on more invasive, costly, and time-consuming assessments, such as skin biopsy.

Human proximal tubule epithelial cells modulate autologous dendritic cell function

Background We have previously demonstrated that human kidney proximal tubule epithelial cells (PTEC) are able to modulate autologous T and B lymphocyte responses. It is well established that dendritic cells (DC) are responsible for the initiation and direction of adaptive immune responses and that these cells occur in the renal interstitium in close apposition to PTEC under inflammatory disease settings. However, there is no information regarding the interaction of PTEC with DC in an autologous human context. Methods Human monocytes were differentiated into monocyte-derived DC (MoDC) in the absence or presence of primary autologous activated PTEC and matured with polyinosinic:polycytidylic acid [poly(I:C)], while purified, pre-formed myeloid blood DC (CD1c+ BDC) were cultured with autologous activated PTEC in the absence or presence of poly(I:C) stimulation. DC responses were monitored by surface antigen expression, cytokine secretion, antigen uptake capacity and allogeneic T-cell-stimulatory ability. Results The presence of autologous activated PTEC inhibited the differentiation of monocytes to MoDC. Furthermore, MoDC differentiated in the presence of PTEC displayed an immature surface phenotype, efficient phagocytic capacity and, upon poly(I:C) stimulation, secreted low levels of pro-inflammatory cytokine interleukin (IL)-12p70, high levels of anti-inflammatory cytokine IL-10 and induced weak Th1 responses. Similarly, pre-formed CD1c+ BDC matured in the presence of PTEC exhibited an immature tolerogenic surface phenotype, strong endocytic and phagocytic ability and stimulated significantly attenuated T-cell proliferative responses. Conclusions Our data suggest that activated PTEC regulate human autologous immunity via complex interactions with DC. The ability of PTEC to modulate autologous DC function has important implications for the dampening of pro-inflammatory immune responses within the tubulointerstitium in renal injuries. Further dissection of the mechanisms of PTEC modulation of autologous immune responses may offer targets for therapeutic intervention in renal medicine.

Delta opioid-receptor function in the dorsal striatum plays a role in high levels of ethanol consumption in rats

Binge-like patterns of excessive drinking during young adulthood increase the propensity for alcohol use disorders (AUDs) later in adult life; however, the mechanisms that drive this are not completely understood. Previous studies showed that the δ-opioid peptide receptor (DOP-R) is dynamically regulated by exposure to ethanol and that the DOP-R plays a role in ethanol-mediated behaviors. The aim of this study was to determine the role of the DOP-R in high ethanol consumption from young adulthood through to late adulthood by measuring DOP-R-mediated [(35)S]GTPγS binding in brain membranes and DOP-R-mediated analgesia using a rat model of high ethanol consumption in Long Evans rats. We show that DOP-R activity in the dorsal striatum and DOP-R-mediated analgesia changes during development, being highest during early adulthood and reduced in late adulthood. Intermittent access to ethanol but not continuous ethanol or water from young adulthood leads to an increase in DOP-R activity in the dorsal striatum and DOP-R-mediated analgesia into late adulthood. Multiple microinfusions of naltrindole into the dorsal striatum or multiple systemic administration of naltrindole reduces ethanol consumption, and following termination of treatment, DOP-R activity in the dorsal striatum is attenuated. These findings suggest that DOP-R activity in the dorsal striatum plays a role in high levels of ethanol consumption and suggest that targeting the DOP-R is an alternative strategy for the treatment of AUDs.

Planning for sustainable urban futures: an ecological approach to sustainable urban development

In recent years, cities have shown increasing signs of environmental problems due to the negative impacts of urban activities. The degradation and depletion of natural resources, climate change, and development pressure on green areas have become major concerns for cities. In response to these problems, urban planning policies have shifted to a sustainable focus and authorities have begun to develop new strategies for improving the quality of urban ecosystems. An extremely important function of an urban ecosystem is to provide healthy and sustainable environments for both natural systems and communities. Therefore, ecological planning is a functional requirement in the establishment of sustainable built environment. With ecological planning, human needs are supplied while natural resources are used in the most effective and sustainable manner and ecological balance is sustained. Protecting human and environmental health, having healthy ecosystems, reducing environmental pollution and providing green spaces are just a few of the many benefits of ecological planning. In this context, this chapter briefly presents a short overview of the importance of the implementation of ecological planning into sustainable urban development. Furthermore, it presents a conceptual framework for a new methodology for developing sustainable urban ecosystems through ecological planning approach.

Exercise for health : a randomized, controlled trial evaluating impact of a pragmatic, translational exercise intervention on quality of life, function and treatment-related side effects following breast cancer

Purpose Exercise for Health was a randomized, controlled trial designed to evaluate two modes of delivering (face-to-face [FtF] and over-the-telephone [Tel]) an 8-month translational exercise intervention, commencing 6-weeks post-breast cancer surgery (PS). Methods Outcomes included quality of life (QoL), function (fitness and upper-body) and treatment-related side effects (fatigue, lymphoedema, body mass index, menopausal symptoms, anxiety, depression and pain). Generalised estimating equation modelling determined time (baseline [5-weeks PS], mid-intervention [6-months PS], post-intervention [12-months PS]), group (FtF, Tel, Usual Care [UC]) and time-by-group effects. 194 women representative of the breast cancer population were randomised to the FtF (n=67), Tel (n=67) and UC (n=60) groups. Results: There were significant (p<0.05) interaction effects on QoL, fitness and fatigue, with differences being observed between the treatment groups and the UC group. Trends observed for the treatment groups were similar. The treatment groups reported improved QoL, fitness and fatigue over time and changes observed between baseline and post-intervention were clinically relevant. In contrast, the UC group experienced no change, or worsening QoL, fitness and fatigue, mid-intervention. Although improvements in the UC group occurred by 12-months post-surgery, the change did not meet the clinically relevant threshold. There were no differences in other treatment-related side-effects between groups. Conclusion This translational intervention trial, delivered either face-to-face or over-the-telephone, supports exercise as a form of adjuvant breast cancer therapy that can prevent declines in fitness and function during treatment and optimise recovery post-treatment.

Evidence for a dual function of EphB4 as tumor promoter and suppressor regulated by the absence or presence of the ephrin-B2 ligand

Overexpression of the receptor tyrosine kinase EphB4 is common in epithelial cancers and linked to tumor progression by promoting angiogenesis, increasing survival and facilitating invasion and migration. However, other studies have reported loss of EphB4 suggesting a tumor suppressor function in some cancers. These opposing roles may be regulated by (i) the presence of the primary ligand ephrin-B2 that regulates pathways involved in tumor suppression or (ii) the absence of ephrin-B2 that allows EphB4 signaling via ligand-independent pathways that contribute to tumor promotion. To explore this theory, EphB4 was overexpressed in the prostate cancer cell line 22Rv1 and the mammary epithelial cell line MCF-10A. Overexpressed EphB4 localized to lipid-rich regions of the plasma membrane and confirmed to be ligand-responsive as demonstrated by increased phosphorylation of ERK1/2 and internalization. EphB4 overexpressing cells demonstrated enhanced anchorage-independent growth, migration and invasion, all characteristics associated with an aggressive phenotype, and therefore supporting the hypothesis that overexpressed EphB4 facilitates tumor promotion. Importantly, these effects were reversed in the presence of ephrin-B2 which led to a reduction in EphB4 protein levels, demonstrating that ligand-dependent signaling is tumor suppressive. Furthermore, extended ligand stimulation caused a significant decrease in proliferation that correlated with a rise in caspase-3/7 and -8 activities. Together, these results demonstrate that overexpression of EphB4 confers a transformed phenotype in the case of MCF-10A cells and an increased metastatic phenotype in the case of 22Rv1 cancer cells and that both phenotypes can be restrained by stimulation with ephrin-B2, in part by reducing EphB4 levels.

Relationship among CFH and ARMS2 genotypes, macular pigment optical density, and neuroretinal function in persons without age-related macular degeneration

Purpose: To determine whether there is a difference in neuroretinal function and in macular pigment optical density between persons with high- and low-risk gene variants for age-related macular degeneration (AMD) and no ophthalmoscopic signs of AMD, and to compare the results on neuroretinal function to patients with manifest early AMD. Methods and Participants: Neuroretinal function was assessed with the multifocal electroretinogram (mfERG) for 32 participants (22 healthy persons with no AMD and 10 early AMD patients). The 22 healthy participants with no AMD had high- or low-risk genotypes for either CFH (rs380390) and/or ARMS2 (rs10490924). Trough-to-peak response densities and peak-implicit times were analyzed in 5 concentric rings. Macular pigment optical densitometry was assessed by customized heterochromatic flicker photometry. Results: Trough-to-peak response densities for concentric rings 1 to 3 were, on average, significantly greater in participants with high-risk genotypes than in participants with low-risk genotypes and in persons with early AMD after correction for age and smoking (p<0.05). The group peak- implicit times for ring 1 were, on average, delayed in the patients with early AMD compared with the participants with high- or low-risk genotypes, although these differences were not significant. There was no significant correlation between genotypes and macular pigment optical density. Conclusion: Increased neuroretinal activity in persons who carry high-risk AMD genotypes may be due to genetically determined subclinical inflammatory and/or histological changes in the retina. Neuroretinal function in healthy persons genetically susceptible to AMD may be a useful additional early biomarker (in combination with genetics) before there is clinical manifestation.