949 resultados para proteins model
Resumo:
In the past two decades there has been increasing interest in branding tourism destinations in an effort to meaningfully differentiate against a myriad of competing places that offer similar attractions and facilities. The academic literature relating to destination branding commenced only as recently as 1998, and there remains a dearth of empirical data that tests the effectiveness of brand campaigns, particularly in terms of enhancing destination loyalty. This paper reports the results of an investigation into destination brand loyalty for Australia as a long haul destination in a South American market. In spite of the high level of academic interest in the measurement of perceptions of destinations since the 1970s, few previous studies have examined perceptions held by South American consumers. Drawing on a model of consumer-based brand equity (CBBE), antecedents of destination brand loyalty was tested with data from a large Chilean sample of travelers, comprising a mix of previous visitors and non-visitors to Australia. Findings suggest that destination brand awareness, brand image, and brand value are positively related to brand loyalty for a long-haul destination. However, destination brand quality was not significantly related. The results also indicate that Australia is a more compelling destination brand for previous visitors compared to non-visitors.
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While Business Process Management (BPM) is an established discipline, the increased adoption of BPM technology in recent years has introduced new challenges. One challenge concerns dealing with the ever-growing complexity of business process models. Mechanisms for dealing with this complexity can be classified into two categories: 1) those that are solely concerned with the visual representation of the model and 2) those that change its inner structure. While significant attention is paid to the latter category in the BPM literature, this paper focuses on the former category. It presents a collection of patterns that generalize and conceptualize various existing mechanisms to change the visual representation of a process model. Next, it provides a detailed analysis of the degree of support for these patterns in a number of state-of-the-art languages and tools. This paper concludes with the results of a usability evaluation of the patterns conducted with BPM practitioners.
Resumo:
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.
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Erythromycin is the standard antibiotic used for treatment of Ureaplasma species during 3 pregnancy; however, maternally administered erythromycin may be ineffective at eliminating 4 intra-amniotic ureaplasma infections. We asked if erythromycin would eradicate intra-amniotic 5 ureaplasma infections in pregnant sheep. At 50 days of gestation (d, term=150d) pregnant ewes 6 received intra-amniotic injections of erythromycin-sensitive U. parvum serovar 3 (n=16) or 10B 7 medium (n=16). At 100d, amniocentesis was performed; five fetal losses (ureaplasma group: 8 n=4; 10B group: n=1) had occurred by this time. Remaining ewes were allocated into treatment 9 subgroups: medium only (M, n=7); medium and erythromycin (M/E, n=8); ureaplasma only (Up, 10 n=6) or ureaplasma and erythromycin (Up/E, n=6). Erythromycin was administered intra11 muscularly (500 mg), eight-hourly for four days (100d-104d). Amniotic fluid samples were 12 collected at 105d. At 125d preterm fetuses were surgically delivered and specimens were 13 collected for culture and histology. Erythromycin was quantified in amniotic fluid by liquid 14 chromatography-mass spectrometry. Ureaplasmas were isolated from the amniotic fluid, 15 chorioamnion and fetal lung of animals from the Up and Up/E groups, however, the numbers of 16 U. parvum recovered were not different between these groups. Inflammation in the 17 chorioamnion, cord and fetal lung was increased in ureaplasma-exposed animals compared to 18 controls, but was not different between the Up and Up/E groups. Erythromycin was detected in 19 amniotic fluid samples, although concentrations were low (<10-76 ng/mL). This study 20 demonstrates that maternally administered erythromycin does not eradicate chronic, intra- amniotic ureaplasma infections or improve fetal outcomes in an ovine model, potentially due to 22 the poor placental passage of erythromycin.
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The field of literacy studies has always been challenged by the changing technologies that humans have used to express, represent and communicate their feelings, ideas, understandings and knowledge. However, while the written word has remained central to literacy processes over a long period, it is generally accepted that there have been significant changes to what constitutes ‘literate’ practice. In particular, the status of the printed word has been challenged by the increasing dominance of the image, along with the multimodal meaning-making systems facilitated by digital media. For example, Gunther Kress and other members of the New London Group have argued that the second half of the twentieth century saw a significant cultural shift from the linguistic to the visual as the dominant semiotic mode. This in turn, they suggest, was accompanied by a cultural shift ‘from page to screen’ as a dominant space of representation (e.g. Cope & Kalantzis, 2000; Kress, 2003; New London Group, 1996). In a similar vein, Bill Green has noted that we have witnessed a shift from the regime of the print apparatus to a regime of the digital electronic apparatus (Lankshear, Snyder and Green, 2000). For these reasons, the field of literacy education has been challenged to find new ways to conceptualise what is meant by ‘literacy’ in the twenty first century and to rethink the conditions under which children might best be taught to be fully literate so that they can operate with agency in today’s world.
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In Australia as far back as 1993, researchers such as Baladin and Chapmen reported that "18% of the total Australian population and 51% of the population over 60 years of age were identified as having a disability" (2001; p38.2). Statistics such as these are not by any means astonishing, even to members of the general public, and it is widely understood that these are only to increase significantly in our near future. What is particularly surprising however is, in the face of such statistics, the lack of new and creative responses to this demographic shift, particularly by the architecture and construction industries. The common response from a range of sectors seems to be the repetition of a series of models which offer limited, and often undesirable, housing options. It is this against this backdrop, characterized by a lack of original options from mainstream practitioners and relevant government bodies, that the need has arisen to develop alternative models at grass-roots level. This paper reports primarily on the work of one group comprising a not-for-profit organization, a pro-bono design practice group and a local university working together to design a more holistic, emotionally sustainable independent living model of housing for families where a member of the family has a disability. This approach recognizes the limitations of universal design in that it often does not " ... meet all the housing needs that arise for people with moderate to severe disabilities" (Scotts, Margie et al, 2007; p.17). It is hoped that by examining the work of such a collective which is not driven by profit or policy, but rather born with the aim to address first and foremost individual and community need, that better insight can be gained into the real requirements of individuals and families as well as open up a view to new ways of fulfilling them.
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A Simulink Matlab control system of a heavy vehicle suspension has been developed. The aim of the exercise presented in this paper was to develop a Simulink Matlab control system of a heavy vehicle suspension. The objective facilitated by this outcome was the use of a working model of a heavy vehicle (HV) suspension that could be used for future research. A working computer model is easier and cheaper to re-configure than a HV axle group installed on a truck; it presents less risk should something go wrong and allows more scope for variation and sensitivity analysis before embarking on further "real-world" testing. Empirical data recorded as the input and output signals of a heavy vehicle (HV) suspension were used to develop the parameters for computer simulation of a linear time invariant system described by a second-order differential equation of the form: (i.e. a "2nd-order" system). Using the empirical data as an input to the computer model allowed validation of its output compared with the empirical data. The errors ranged from less than 1% to approximately 3% for any parameter, when comparing like-for-like inputs and outputs. The model is presented along with the results of the validation. This model will be used in future research in the QUT/Main Roads project Heavy vehicle suspensions – testing and analysis, particularly so for a theoretical model of a multi-axle HV suspension with varying values of dynamic load sharing. Allowance will need to be made for the errors noted when using the computer models in this future work.
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BACKGROUND: Grafting of autologous hyaline cartilage and bone for articular cartilage repair is a well-accepted technique. Although encouraging midterm clinical results have been reported, no information on the mechanical competence of the transplanted joint surface is available. HYPOTHESIS: The mechanical competence of osteochondral autografts is maintained after transplantation. STUDY DESIGN: Controlled laboratory study. METHODS: Osteochondral defects were filled with autografts (7.45 mm in diameter) in one femoral condyle in 12 mature sheep. The ipsilateral femoral condyle served as the donor site, and the resulting defect (8.3 mm in diameter) was left empty. The repair response was examined after 3 and 6 months with mechanical and histologic assessment and histomorphometric techniques. RESULTS: Good surface congruity and plug placement was achieved. The Young modulus of the grafted cartilage significantly dropped to 57.5% of healthy tissue after 3 months (P < .05) but then recovered to 82.2% after 6 months. The aggregate and dynamic moduli behaved similarly. The graft edges showed fibrillation and, in some cases (4 of 6), hypercellularity and chondrocyte clustering. Subchondral bone sclerosis was observed in 8 of 12 cases, and the amount of mineralized bone in the graft area increased from 40% to 61%. CONCLUSIONS: The mechanical quality of transplanted cartilage varies considerably over a short period of time, potentially reflecting both degenerative and regenerative processes, while histologically signs of both cartilage and bone degeneration occur. CLINICAL RELEVANCE: Both the mechanically degenerative and restorative processes illustrate the complex progression of regeneration after osteochondral transplantation. The histologic evidence raises doubts as to the long-term durability of the osteochondral repair.
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The formation of new blood vessels is a prerequisite for bone healing. CYR61 (CCN1), an extracellular matrix-associated signaling protein, is a potent stimulator of angiogenesis and mesenchymal stem cell expansion and differentiation. A recent study showed that CYR61 is expressed during fracture healing and suggested that CYR61 plays a significant role in cartilage and bone formation. The hypothesis of the present study was that decreased fixation stability, which leads to a delay in healing, would lead to reduced CYR61 protein expression in fracture callus. The aim of the study was to quantitatively analyze CYR61 protein expression, vascularization, and tissue differentiation in the osteotomy gap and relate to the mechanical fixation stability during the course of healing. A mid-shaft osteotomy of the tibia was performed in two groups of sheep and stabilized with either a rigid or semirigid external fixator, each allowing different amounts of interfragmentary movement. The sheep were sacrificed at 2, 3, 6, and 9 weeks postoperatively. The tibiae were tested biomechanically and histological sections from the callus were analyzed immunohistochemically with regard to CYR61 protein expression and vascularization. Expression of CYR61 protein was upregulated at the early phase of fracture healing (2 weeks), decreasing over the healing time. Decreased fixation stability was associated with a reduced upregulation of the CYR61 protein expression and a reduced vascularization at 2 weeks leading to a slower healing. The maximum cartilage callus fraction in both groups was reached at 3 weeks. However, the semirigid fixator group showed a significantly lower CYR61 immunoreactivity in cartilage than the rigid fixator group at this time point. The fraction of cartilage in the semirigid fixator group was not replaced by bone as quickly as in the rigid fixator group leading to an inferior histological and mechanical callus quality at 6 weeks and therefore to a slower healing. The results supply further evidence that CYR61 may serve as an important regulator of bone healing.
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Although player enjoyment is central to computer games, there is currently no accepted model of player enjoyment in games. There are many heuristics in the literature, based on elements such as the game interface, mechanics, gameplay, and narrative. However, there is a need to integrate these heuristics into a validated model that can be used to design, evaluate, and understand enjoyment in games. We have drawn together the various heuristics into a concise model of enjoyment in games that is structured by flow. Flow, a widely accepted model of enjoyment, includes eight elements that, we found, encompass the various heuristics from the literature. Our new model, GameFlow, consists of eight elements -- concentration, challenge, skills, control, clear goals, feedback, immersion, and social interaction. Each element includes a set of criteria for achieving enjoyment in games. An initial investigation and validation of the GameFlow model was carried out by conducting expert reviews of two real-time strategy games, one high-rating and one low-rating, using the GameFlow criteria. The result was a deeper understanding of enjoyment in real-time strategy games and the identification of the strengths and weaknesses of the GameFlow model as an evaluation tool. The GameFlow criteria were able to successfully distinguish between the high-rated and low-rated games and identify why one succeeded and the other failed. We concluded that the GameFlow model can be used in its current form to review games; further work will provide tools for designing and evaluating enjoyment in games.
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A distinctive feature of Chinese test is that a Chinese document is a sequence of Chinese with no space or boundary between Chinese words. This feature makes Chinese information retrieval more difficult since a retrieved document which contains the query term as a sequence of Chinese characters may not be really relevant to the query since the query term (as a sequence Chinese characters) may not be a valid Chinese word in that documents. On the other hand, a document that is actually relevant may not be retrieved because it does not contain the query sequence but contains other relevant words. In this research, we propose a hybrid Chinese information retrieval model by incorporating word-based techniques with the traditional character-based techniques. The aim of this approach is to investigate the influence of Chinese segmentation on the performance of Chinese information retrieval. Two ranking methods are proposed to rank retrieved documents based on the relevancy to the query calculated by combining character-based ranking and word-based ranking. Our experimental results show that Chinese segmentation can improve the performance of Chinese information retrieval, but the improvement is not significant if it incorporates only Chinese segmentation with the traditional character-based approach.
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Australia’s efforts to transition to a low-emissions economy have stagnated following the successive defeats of the Carbon Pollution Reduction Scheme. This failure should not, however, be regarded as the end of Australia’s efforts to make this transition. In fact, the opportunity now exists for Australia to refine its existing arrangements to enable this transition to occur more effectively. The starting point for this analysis is the legal arrangements applying to the electricity generation sector, which is the largest sectoral emitter of anthropogenic greenhouse gas emissions in Australia. Without an effective strategy to mitigate this sector’s contribution to anthropogenic climate change, it is unlikely that Australia will be able to transition towards a low-emissions economy. It is on this basis that this article assesses the dominant national legal arrangement – the Renewable Energy Target – underpinning the electricity generation sector's efforts to become a low-emissions sector.
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Genetic variation is the resource animal breeders exploit in stock improvement programs. Both the process of selection and husbandry practices employed in aquaculture will erode genetic variation levels overtime, hence the critical resource can be lost and this may compromise future genetic gains in breeding programs. The amount of genetic variation in five lines of Sydney Rock Oyster (SRO) that had been selected for QX (Queensland unknown) disease resistance were examined and compared with that in a wild reference population using seven specific SRO microsatellite loci. The five selected lines had significantly lower levels of genetic diversity than did the wild reference population with allelic diversity declining approximately 80%, but impacts on heterozygosity per locus were less severe. Significant deficiencies in heterozygotes were detected at six of the seven loci in both mass selected lines and the wild reference population. Against this trend however, a significant excess of heterozygotes was recorded at three loci Sgo9, Sgo14 and Sgo21 in three QX disease resistant lines (#2, #5 and #13). All populations were significantly genetic differentiated from each other based on pairwise FST values. A neighbour joining tree based on DA genetic distances showed a clear separation between all culture and wild populations. Results of this study show clearly, that the impacts of the stock improvement program for SRO has significantly eroded natural levels of genetic variation in the culture lines. This could compromise long-term genetic gains and affect sustainability of the SRO breeding program over the long-term.
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The Texas Transportation Commission (“the Commission”) is responsible for planning and making policies for the location, construction, and maintenance of a comprehensive system of highways and public roads in Texas. In order for the Commission to carry out its legislative mandate, the Texas Constitution requires that most revenue generated by motor vehicle registration fees and motor fuel taxes be used for constructing and maintaining public roadways and other designated purposes. The Texas Department of Transportation (TxDOT) assists the Commission in executing state transportation policy. It is the responsibility of the legislature to appropriate money for TxDOT’s operation and maintenance expenses. All money authorized to be appropriated for TxDOT’s operations must come from the State Highway Fund (also known as Fund 6, Fund 006, or Fund 0006). The Commission can then use the balance in the fund to fulfill its responsibilities. However, the value of the revenue received in Fund 6 is not keeping pace with growing demand for transportation infrastructure in Texas. Additionally, diversion of revenue to nontransportation uses now exceeds $600 million per year. As shown in Figure 1.1, revenues and expenditures of the State Highway Fund per vehicle mile traveled (VMT) in Texas have remained almost flat since 1993. In the meantime, construction cost inflation has gone up more than 100%, effectively halving the value of expenditure.
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This research report documents work conducted by the Center for Transportation (CTR) at The University of Texas at Austin in analyzing the Joint Analysis using the Combined Knowledge (J.A.C.K.) program. This program was developed by the Texas Department of Transportation (TxDOT) to make projections of revenues and expenditures. This research effort was to span from September 2008 to August 2009, but the bulk of the work was completed and presented by December 2008. J.A.C.K. was subsequently renamed TRENDS, but for consistency with the scope of work, the original name is used throughout this report.