Stabilization mechanisms of soil organic matter: Implications for C-saturation of soils

The relationship between soil structure and the ability of soil to stabilize soil organic matter (SOM) is a key element in soil C dynamics that has either been overlooked or treated in a cursory fashion when developing SOM models. The purpose of this paper is to review current knowledge of SOM dynamics within the framework of a newly proposed soil C saturation concept. Initially, we distinguish SOM that is protected against decomposition by various mechanisms from that which is not protected from decomposition. Methods of quantification and characteristics of three SOM pools defined as protected are discussed. Soil organic matter can be: (1) physically stabilized, or protected from decomposition, through microaggregation, or (2) intimate association with silt and clay particles, and (3) can be biochemically stabilized through the formation of recalcitrant SOM compounds. In addition to behavior of each SOM pool, we discuss implications of changes in land management on processes by which SOM compounds undergo protection and release. The characteristics and responses to changes in land use or land management are described for the light fraction (LF) and particulate organic matter (POM). We defined the LF and POM not occluded within microaggregates (53-250 mum sized aggregates as unprotected. Our conclusions are illustrated in a new conceptual SOM model that differs from most SOM models in that the model state variables are measurable SOM pools. We suggest that physicochemical characteristics inherent to soils define the maximum protective capacity of these pools, which limits increases in SOM (i.e. C sequestration) with increased organic residue inputs.

On the feasibility of using servo-mechanisms in wireless multimedia sensor network deployments

This paper considers the use of servo-mechanisms as part of a tightly integrated homogeneous Wireless Multi- media Sensor Network (WMSN). We describe the design of our second generation WMSN node platform, which has increased image resolution, in-built audio sensors, PIR sensors, and servo- mechanisms. These devices have a wide disparity in their energy consumption and in the information quality they return. As a result, we propose a framework that establishes a hierarchy of devices (sensors and actuators) within the node and uses frequent sampling of cheaper devices to trigger the activation of more energy-hungry devices. Within this framework, we consider the suitability of servos for WMSNs by examining the functional characteristics and by measuring the energy consumption of 2 analog and 2 digital servos, in order to determine their impact on overall node energy cost. We also implement a simple version of our hierarchical sampling framework to evaluate the energy consumption of servos relative to other node components. The evaluation results show that: (1) the energy consumption of servos is small relative to audio/image signal processing energy cost in WMSN nodes; (2) digital servos do not necessarily consume as much energy as is currently believed; and (3) the energy cost per degree panning is lower for larger panning angles.

Gender inequality and the spread of HIV-AIDS in India

Purpose The purpose of the paper is to analyze the low status of women as being a major contributor for the observed gender inequality in the spread of HIV/AIDS in India. Design/methodology/approach The paper uses data from National Aids Control Organization (NACO), National Family Health Survey (NFHS 3), and the Directorate of Economics and Statistics. Findings This study highlights the problems facing women in deterring the spread of HIV/AIDS in India. The status and empowerment of women are important variables in combating the disease among both men and women in India. Literacy, education, exposure to the media, labor market participation, awareness of HIV/AIDS, and economic independence are important considerations in improving the status of women in India. Policymakers need to focus on gender inequality in order to combat the spread of HIV/AIDS in India. Originality/value While absolute figures indicate men are more likely to be infected with HIV/AIDS, the rate of decline is higher for men compared to women in India. We explore several plausible explanations for such observed inequality in the spread of HIV/AIDS across gender. In particular, a potentially important factor - the low status of women in society is attributable as an impediment to the spread of the disease. A case study of the relationship between gender empowerment and the spread of HIV/AIDS in the state with the highest concentration, Manipur, provides more insight to the difficulties faced by women in combating HIV/AIDS in India.

Positive design and construction of mechanisms for the sustainable development in microenterprises in Africa

Enterprise development and its contribution to societal and economic outcomes are well known. However, limited research into microenterprises and the practices of microfinance and microcredit in developing countries has been carried out. This chapter presents the findings of research based on six years of engagement with the microentrepreneurs of Beira in Mozambique and suggests a model for responsible and sustainable support for enterprise development in developing economies. Building on semistructured interviews, observation, and participatory action research, this research project articulates a new approach supportive of enterprise development, as a process of cocreation with local people and based on sustainability principles. These findings are part of a longitudinal study of the successes and failures of small enterprises and their impact on social and economic activity.

Cell invasion with proliferation mechanisms motivated by time-lapse data

Cell invasion involves a population of cells which are motile and proliferative. Traditional discrete models of proliferation involve agents depositing daughter agents on nearest- neighbor lattice sites. Motivated by time-lapse images of cell invasion, we propose and analyze two new discrete proliferation models in the context of an exclusion process with an undirected motility mechanism. These discrete models are related to a family of reaction- diffusion equations and can be used to make predictions over a range of scales appropriate for interpreting experimental data. The new proliferation mechanisms are biologically relevant and mathematically convenient as the continuum-discrete relationship is more robust for the new proliferation mechanisms relative to traditional approaches.

Development of a 3-dimensional human skin equivalent wound model for investigating novel wound healing therapies

Numerous difficulties are associated with the conduct of preclinical studies related to skin and wound repair. Use of small animal models such as rodents is not optimal because of their physiological differences to human skin and mode of wound healing. Although pigs have previously been used because of their human-like mode of healing, the expense and logistics related to their use also renders them suboptimal. In view of this, alternatives are urgently required to advance the field. The experiments reported herein were aimed at developing and validating a simple, reproducible, three-dimensional ex vivo de-epidermised dermis human skin equivalent wound model for the preclinical evaluation of novel wound therapies. Having established that the human skin equivalent wound model does in fact “heal," we tested the effect of two novel wound healing therapies. We also examined the utility of the model for studies exploring the mechanisms underpinning these therapies. Taken together the data demonstrate that these new models will have wide-spread application for the generation of fundamental new information on wound healing processes and also hold potential in facilitating preclinical optimization of dosage, duration of therapies, and treatment strategies prior to clinical trials.

Effects of opening in the cross girders of the flat bottom rail wagons to the load transferring mechanisms when used as road bridge deck

A Flat Bed Rail Wagon (FBRW) has been proposed as an alternative solution for replacing bridges on low traffic volume roads. The subject matter for this paper is to investigate the impediment to load transfer from cross girders to main girder, through visually identifiable structural flaws. Namely, the effect of having large openings at close proximity to the connection of the main girder to the cross girder of a FBRW was examined. It was clear that openings locally reduce the section modulus of the secondary members; however it was unclear how these reductions would affect the load transfer to the main girder. The results are presented through modeling grillage action for which the loads applied onto the FBRW were distributed through cross girders to the main girder.

Increased Langerhan cell density and corneal nerve damage in diabetic patients : role of immune mechanisms in human diabetic neuropathy

Aim/hypothesis Immune mechanisms have been proposed to play a role in the development of diabetic neuropathy. We employed in vivo corneal confocal microscopy (CCM) to quantify the presence and density of Langerhans cells (LCs) in relation to the extent of corneal nerve damage in Bowman's layer of the cornea in diabetic patients. Methods 128 diabetic patients aged 58±1 yrs with a differing severity of neuropathy based on Neuropathy Deficit Score (NDS—4.7±0.28) and 26 control subjects aged 53±3 yrs were examined. Subjects underwent a full neurological evaluation, evaluation of corneal sensation with non-contact corneal aesthesiometry (NCCA) and corneal nerve morphology using corneal confocal microscopy (CCM). Results The proportion of individuals with LCs was significantly increased in diabetic patients (73.8%) compared to control subjects (46.1%), P=0.001. Furthermore, LC density (no/mm2) was significantly increased in diabetic patients (17.73±1.45) compared to control subjects (6.94±1.58), P=0.001 and there was a significant correlation with age (r=0.162, P=0.047) and severity of neuropathy (r=−0.202, P=0.02). There was a progressive decrease in corneal sensation with increasing severity of neuropathy assessed using NDS in the diabetic patients (r=0.414, P=0.000). Corneal nerve fibre density (P<0.001), branch density (P<0.001) and length (P<0.001) were significantly decreased whilst tortuosity (P<0.01) was increased in diabetic patients with increasing severity of diabetic neuropathy. Conclusion Utilising in vivo corneal confocal microscopy we have demonstrated increased LCs in diabetic patients particularly in the earlier phases of corneal nerve damage suggestive of an immune mediated contribution to corneal nerve damage in diabetes.

In vitro and in vivo examination of the cell surface glycoprotein CDCP1

A number of reports have demonstrated the importance of the CUB domaincontaining protein 1 (CDCP1) in facilitating cancer progression in animal models and the potential of this protein as a prognostic marker in several malignancies. CDCP1 facilitates metastasis formation in animal models by negatively regulating anoikis, a type of apoptosis triggered by the loss of attachment signalling from cell-cell contacts or cell-extra cellular matrix (ECM) contacts. Due to the important role CDCP1 plays in cancer progression in model systems, it is considered a potential drug target to prevent the metastatic spread of cancers. CDCP1 is a highly glycosylated 836 amino acid cell surface protein. It has structural features potentially facilitating protein-protein interactions including 14 N-glycosylation sites, three CUB-like domains, 20 cysteine residues likely to be involved in disulfide bond formation and five intracellular tyrosine residues. CDCP1 interacts with a variety of proteins including Src family kinases (SFKs) and protein kinase C ä (PKCä). Efforts to understand the mechanisms regulating these interactions have largely focussed on three CDCP1 tyrosine residues Y734, Y743 and Y762. CDCP1-Y734 is the site where SFKs phosphorylate and bind to CDCP1 and mediate subsequent phosphorylation of CDCP1-Y743 and -Y762 which leads to binding of PKCä at CDCP1-Y762. The resulting trimeric protein complex of SFK•CDCP1•PKCä has been proposed to mediate an anti-apoptotic cell phenotype in vitro, and to promote metastasis in vivo. The effect of mutation of the three tyrosines on interactions of CDCP1 with SFKs and PKCä and the consequences on cell phenotype in vitro and in vivo have not been examined. CDCP1 has a predicted molecular weight of ~90 kDa but is usually detected as a protein which migrates at ~135 kDa by Western blot analysis due to its high degree of glycosylation. A low molecular weight form of CDCP1 (LMWCDCP1) of ~70 kDa has been found in a variety of cancer cell lines. The mechanisms leading to the generation of LMW-CDCP1 in vivo are not well understood but an involvement of proteases in this process has been proposed. Serine proteases including plasmin and trypsin are able to proteolytically process CDCP1. In addition, the recombinant protease domain of the serine protease matriptase is also able to cleave the recombinant extracellular portion of CDCP1. Whether matriptase is able to proteolytically process CDCP1 on the cell surface has not been examined. Importantly, proteolytic processing of CDCP1 by trypsin leads to phosphorylation of its cell surface-retained portion which suggests that this event leads to initiation of an intracellular signalling cascade. This project aimed to further examine the biology of CDCP1 with a main of focus on exploring the roles played by CDCP1 tyrosine residues. To achieve this HeLa cells stably expressing CDCP1 or the CDCP1 tyrosine mutants Y734F, Y743F and Y762F were generated. These cell lines were used to examine: • The roles of the tyrosine residues Y734, Y743 and Y762 in mediating interactions of CDCP1 with binding proteins and to examine the effect of the stable expression on HeLa cell morphology. • The ability of the serine protease matriptase to proteolytically process cell surface CDCP1 and to examine the consequences of this event on HeLa cell phenotype and cell signalling in vitro. • The importance of these residues in processes associated with cancer progression in vitro including adhesion, proliferation and migration. • The role of these residues on metastatic phenotype in vivo and the ability of a function-blocking anti-CDCP1 antibody to inhibit metastasis in the chicken embryo chorioallantoic membrane (CAM) assay. Interestingly, biochemical experiments carried out in this study revealed that mutation of certain CDCP1 tyrosine residues impacts on interactions of this protein with binding proteins. For example, binding of SFKs as well as PKCä to CDCP1 was markedly decreased in HeLa-CDCP1-Y734F cells, and binding of PKCä was also reduced in HeLa-CDCP1-Y762F cells. In contrast, HeLa-CDCP1-Y743F cells did not display altered interactions with CDCP1 binding proteins. Importantly, observed differences in interactions of CDCP1 with binding partners impacted on basal phosphorylation of CDCP1. It was found that HeLa-CDCP1, HeLa-CDCP1-Y743F and -Y762F displayed strong basal levels of CDCP1 phosphorylation. In contrast, HeLa-CDCP1-Y734F cells did not display CDCP1 phosphorylation but exhibited constitutive phosphorylation of focal adhesion kinase (FAK) at tyrosine 861. Significantly, subsequent investigations to examine this observation suggested that CDCP1-Y734 and FAK-Y861 are competitive substrates for SFK-mediated phosphorylation. It appeared that SFK-mediated phosphorylation of CDCP1- Y734 and FAK-Y861 is an equilibrium which shifts depending on the level of CDCP1 expression in HeLa cells. This suggests that the level of CDCP1 expression may act as a regulatory mechanism allowing cells to switch from a FAK-Y861 mediated pathway to a CDCP1-Y734 mediated pathway. This is the first time that a link between SFKs, CDCP1 and FAK has been demonstrated. One of the most interesting observations from this work was that CDCP1 altered HeLa cell morphology causing an elongated and fibroblastic-like appearance. Importantly, this morphological change depended on CDCP1- Y734. In addition, it was observed that this change in cell morphology was accompanied by increased phosphorylation of SFK-Y416. This suggests that interactions of SFKs with CDCP1-Y734 increases SFK activity since SFKY416 is critical in regulating kinase activity of these proteins. The essential role of SFKs in mediating CDCP1-induced HeLa cell morphological changes was demonstrated using the SFK-selective inhibitor SU6656. This inhibitor caused reversion of HeLa-CDCP1 cell morphology to an epithelial appearance characteristic of HeLa-vector cells. Significantly, in vitro studies revealed that certain CDCP1-mediated cell phenotypes are mediated by cellular pathways dependent on CDCP1 tyrosine residues whereas others are independent of these sites. For example, CDCP1 expression caused a marked increase in HeLa cell motility that was independent of CDCP1 tyrosine residues. In contrast, CDCP1- induced decrease in HeLa cell proliferation was most prominent in HeLa- CDCP1-Y762F cells, potentially indicating a role for this site in regulating proliferation in HeLa cells. Another cellular event which was identified to require phosphorylation of a particular CDCP1 tyrosine residue is adhesion to fibronectin. It was observed that the CDCP1-mediated strong decrease in adhesion to fibronectin is mostly restored in HeLa-CDCP1-Y743F cells. This suggests a possible role for CDCP1-Y743 in causing a CDCP1-mediated decrease in adhesion. Data from in vivo experiments indicated that HeLa-CDCP1-Y734F cells are more metastic than HeLa-CDCP1 cells in vivo. This indicates that interaction of CDCP1 with SFKs and PKCä may not be required for CDCP1-mediated metastasis formation of HeLa cells in vivo. The metastatic phenotype of these cells may be caused by signalling involving FAK since HeLa-CDCP1- Y734F cells are the only CDCP1 expressing cells displaying constitutive phosphorylation of FAK-Y861. HeLa-CDCP1-Y762F cells displayed a very low metastatic ability which suggests that this CDCP1 tyrosine residue is important in mediating a pro-metastatic phenotype in HeLa cells. More detailed exploration of cellular events occurring downstream of CDCP1-Y734 and -Y762 may provide important insights into the mechanisms altering the metastatic ability of CDCP1 expressing HeLa cells. Complementing the in vivo studies, anti-CDCP1 antibodies were employed to assess whether these antibodies are able to inhibit metastasis of CDCP1 and CDCP1 tyrosine mutants expressing HeLa cells. It was found that HeLa- CDCP1-Y734F cells were the only cell line which was markedly reduced in the ability to metastasise. In contrast, the ability of HeLa-CDCP1, HeLa- CDCP1-Y743F and -Y762F cells to metastasise in vivo was not inhibited. These data suggest a possible role of interactions of CDCP1 with SFKs, occurring at CDCP1-Y734, in preventing an anti-metastatic effect of anti- CDCP1 antibodies in vivo. The proposal that SFKs may play a role in regulating anti-metastatic effects of anti-CDCP1 antibodies was supported by another experiment where differences between HeLa-CDCP1 cells and CDCP1 expressing HeLa cells (HeLa-CDCP1-S) from collaborators at the Scripps Research Institute were examined. It was found that HeLa-CDCP1-S cells express different SFKs than CDCP1 expressing HeLa cells generated for this study. This is important since HeLa-CDCP1-S cells can be inhibited in their metastatic ability using anti-CDCP1 antibodies in vivo. Importantly, these data suggest that further examinations of the roles of SFKs in facilitating anti-metastatic effects of anti-CDCP1 antibodies may give insights into how CDCP1 can be blocked to prevent metastasis in vivo. This project also explored the ability of the serine protease matriptase to proteolytically process cell surface localised CDCP1 because it is unknown whether matriptase can cleave cell surface CDCP1 as it has been reported for other proteases such as trypsin and plasmin. Furthermore, the consequences of matriptase-mediated proteolysis on cell phenotype in vitro and cell signalling were examined since recent reports suggested that proteolysis of CDCP1 leads to its phosphorylation and may initiate cell signalling and consequently alter cell phenotype. It was found that matriptase is able to proteolytically process cell surface CDCP1 at low nanomolar concentrations which suggests that cleavage of CDCP1 by matriptase may facilitate the generation of LWM-CDCP1 in vivo. To examine whether matriptase-mediated proteolysis induced cell signalling anti-phospho Erk 1/2 Western blot analysis was performed as this pathway has previously been examined to study signalling in response to proteolytic processing of cell surface proteins. It was found that matriptase-mediated proteolysis in CDCP1 expressing HeLa cells initiated intracellular signalling via Erk 1/2. Interestingly, this increase in phosphorylation of Erk 1/2 was also observed in HeLa-vector cells. This suggested that initiation of cell signalling via Erk 1/2 phosphorylation as a result of matriptase-mediated proteolysis occurs by pathways independent of CDCP1. Subsequent investigations measuring the flux of free calcium ions and by using a protease-activated receptor 2 (PAR2) agonist peptide confirmed this hypothesis. These data suggested that matriptase-mediated proteolysis results in cell signalling via a pathway induced by the activation of PAR2 rather than by CDCP1. This indicates that induction of cell signalling in HeLa cells as a consequence of matriptase-mediated proteolysis occurs via signalling pathways which do not involve phosphorylation of Erk 1/2. Consequently, it appears that future attempts should focus on the examination of cellular pathways other than Erk 1/2 to elucidate cell signalling initiated by matriptase-mediated proteolytic processing of CDCP1. The data presented in this thesis has explored in vitro and in vivo aspects of the biology of CDCP1. The observations summarised above will permit the design of future studies to more precisely determine the role of CDCP1 and its binding partners in processes relevant to cancer progression. This may contribute to further defining CDCP1 as a target for cancer treatment.

Ecological aspects of biosecurity surveillance design for the detection of multiple invasive animal species

Complex surveillance problems are common in biosecurity, such as prioritizing detection among multiple invasive species, specifying risk over a heterogeneous landscape, combining multiple sources of surveillance data, designing for specified power to detect, resource management, and collateral effects on the environment. Moreover, when designing for multiple target species, inherent biological differences among species result in different ecological models underpinning the individual surveillance systems for each. Species are likely to have different habitat requirements, different introduction mechanisms and locations, require different methods of detection, have different levels of detectability, and vary in rates of movement and spread. Often there is a further challenge of a lack of knowledge, literature, or data, for any number of the above problems. Even so, governments and industry need to proceed with surveillance programs which aim to detect incursions in order to meet environmental, social and political requirements. We present an approach taken to meet these challenges in one comprehensive and statistically powerful surveillance design for non-indigenous terrestrial vertebrates on Barrow Island, a high conservation nature reserve off the Western Australian coast. Here, the possibility of incursions is increased due to construction and expanding industry on the island. The design, which includes mammals, amphibians and reptiles, provides a complete surveillance program for most potential terrestrial vertebrate invaders. Individual surveillance systems were developed for various potential invaders, and then integrated into an overall surveillance system which meets the above challenges using a statistical model and expert elicitation. We discuss the ecological basis for the design, the flexibility of the surveillance scheme, how it meets the above challenges, design limitations, and how it can be updated as data are collected as a basis for adaptive management.

The Kinaesthetic Fusion Effect : mechanisms and extensions

This study investigated the Kinaesthetic Fusion Effect (KFE) that was first described by Craske and Kenny in 1981. It was reported that when, without vision, participants pressed a button that resulted in a probe simultaneously touching the contralateral limb at a displaced location, they perceived an apparent change in limb length. The current study did not fully replicate these earlier findings. Participants did not perceive any reduction in the sagittal separation of the button and probe following repeated exposure to the tactile stimuli that was present on both arms. However, a localised and partial medio-lateral fusion was observed, with the touched positions seeming closer together. In addition, tactile acuity was found to decrease progressively for distal positions of the upper limb and a foreshortening effect was found which may result from a line-of-sight judgment and represent a feature of the reporting method used. A number of years have elapsed since the description of the original KFE. Although frequently cited in the literature, there has been no further investigation into the mechanisms of action. The results of the current study are considered in light of more recent literature concerning intersensory integration. Future research should focus on further clarification for the specific conditions that must be present for a fusion effect to occur. Finally, this thesis will benefit future studies that require participants to report the perceived locations of the unseen limbs.