Numerical investigation of the influence of topography on simulated downburst wind fields

A, dry, non-hydrostatic sub-cloud model is used to simulate an isolated stationary downburst wind event to study the influence topographic features have on the near-ground wind structure of these storms. It was generally found that storm maximum wind speeds could be increased by up to 30% because of the presence of a topographic feature at the location of maximum wind speeds. Comparing predicted velocity profile amplification with that of a steady flow impinging jet, similar results were found despite the simplifications made in the impinging jet model. Comparison of these amplification profiles with those found in the simulated boundary layer winds reveal reductions of up to 30% in the downburst cases. Downburst and boundary layer amplification profiles were shown to become more similar as the topographic feature height was reduced with respect to the outflow depth.

Influence of tilt and surface roughness on the outflow wind field of an impinging jet

A physical and numerical steady flow impinging jet has been used to simulate the bulk characteristics of a downburst-like wind field. The influence of downdraft tilt and surface roughness on the ensuing wall jet flow has been investigated. It was found that a simulated downdraft impinging the surface at a non-normal angle has the potential for causing larger structural loads than the normal impingement case. It was also found that for the current impinging jet simulations, surface roughness played a minor role in determining the storm maximum wind structure, but this influence increased as the wall jet diverged. However, through comparison with previous research it was found that the influence of surface roughness is Reynolds number dependent and therefore may differ from that reported herein for full-scale downburst cases. Using the current experimental results an empirical model has been developed for laboratory-scale impinging jet velocity structure that includes the influence of both jet tilt and surface roughness.

What aspects of demographic, personality, attitudes, and perceptions of law enforcement influence self-reported likelihood of drink driving?

The aim of the current study was to examine the associations between a number of individual factors (demographic factors (age and gender), personality factors, risk-taking propensity, attitudes towards drink driving, and perceived legitimacy of drink driving enforcement) and how they influence the self-reported likelihood of drink driving. The second aim of this study was to examine the potential of attitudes mediating the relationship between risk-taking and self-reported likelihood of drink driving. In total, 293 Queensland drivers volunteered to participate in an online survey that assessed their self-reported likelihood to drink drive in the next month, demographics, traffic-related demographics, personality factors, risk-taking propensity, attitudes towards drink driving, and perceived legitimacy of drink driving enforcement. An ordered logistic regression analysis was utilised to evaluate the first aim of the study; at the first step the demographic variables were entered; at step two the personality and risk-taking were entered; at the third step, the attitudes and perceptions of legitimacy variables were entered. Being a younger driver and having a high risk-taking propensity were related to self-reported likelihood of drink driving. However, when the attitudes variable was entered, these individual factors were no longer significant; with attitudes being the most important predictor of self-reported drink driving likelihood. A significant mediation model was found with the second aim of the study, such that attitudes mediated the relationship between risk-taking and self-reported likelihood of drink driving. Considerable effort and resources are utilised by traffic authorities to reducing drink driving on the Australian road network. Notwithstanding these efforts, some participants still had some positive attitudes towards drink driving and reported that they were likely to drink drive in the future. These findings suggest that more work is needed to address attitudes regarding the dangerousness of drink driving.

Do sex and atopy influence cough outcome measurements in children?

Background Despite the commonality of cough and its burden, there are no published data on the relationship between atopy or sex on objectively measured cough frequency or subjective cough scores in children. In 202 children with and without cough, we determined the effect of sex and atopy on validated cough outcome measurements (cough receptor sensitivity [CRS], objective cough counts, and cough scores). We hypothesized that in contrast to adult data, sex does not influence cough outcome measures, and atopy is not a determinant of these cough measurements. Methods We combined data from four previous studies. Atopy (skin prick test), the concentration of capsaicin causing two and five or more coughs (C2 and C5, respectively), objectively measured cough frequency, and cough scores were determined and their relationship explored. The children’s (93 girls, 109 boys) mean age was 10.6 years (SD 2.9), and 56% had atopy. Results In multivariate analysis, CRS was influenced by age (C2 coefficient, 5.9; P = .034; C5 coefficient, 29.1; P = .0001). Atopy and sex did not significantly influence any of the cough outcomes (cough counts, C2, C5, cough score) in control subjects and children with cough. Conclusions Atopy does not influence important cough outcome measures in children with and without chronic cough. However, age, but not sex, influences CRS in children. Unlike adult data, sex does not affect objective counts or cough score in children with and without chronic cough. Studies on cough in children should be age matched, but matching for atopic status and sex is less important.

Evaluating a model of parental influence on youth physical activity

Objective To test a conceptual model linking parental physical activity orientations, parental support for physical activity, and children's self-efficacy perceptions with physical activity participation. Participants and setting The sample consisted of 380 students in grades 7 through 12 (mean age, 14.0±1.6 years) and their parents. Data collection took place during the fall of 1996. Main outcome measures Parents completed a questionnaire assessing their physical activity habits, enjoyment of physical activity, beliefs regarding the importance of physical activity, and supportive behaviors for their child's physical activity. Students completed a 46-item inventory assessing physical activity during the previous 7 days and a 5-item physical activity self-efficacy scale. The model was tested via observed variable path analysis using structural equation modeling techniques (AMOS 4.0). Results An initial model, in which parent physical activity orientations predicted child physical activity via parental support and child self-efficacy, did not provide an acceptable fit to the data. Inclusion of a direct path from parental support to child physical activity and deletion of a nonsignificant path from parental physical activity to child physical activity significantly improved model fit. Standardized path coefficients for the revised model ranged from 0.17 to 0.24, and all were significant at the p<0.0001 level. Conclusions Parental support was an important correlate of youth physical activity, acting directly or indirectly through its influence on self-efficacy. Physical activity interventions targeted at youth should include and evaluate the efficacy of individual-level and community-level strategies to increase parents’ capacity to provide instrumental and motivational support for their children's physical activity.

The stress-buffering effects of control on task satisfaction and perceived goal attainment : an experimental study of the moderating influence of desire for control

The purpose of the present study was to examine the extent to which Desire for Control (DFC) interacts with experimental manipulations of demand and control, and the consequences of these interactions on task satisfaction and perceived goal attainment (i.e. task performance and task mastery). It was expected that the proposed stress-buffering effects of control would be evident only for individuals high in DFC. Moreover, it was anticipated that control may have a stress-exacerbating effect for those low in DFC. These hypotheses were tested on a sample of 137 first year psychology students who participated in an in-basket activity under low and high conditions of demand and control. Results revealed that the proposed stress-buffering effect of control was found only for those high in DFC and a stress-exacerbating effect of increased control was evident for those low in DFC on task performance and task mastery perceptions. Future research directions and the implications of these findings to applied settings are discussed.

Differentiation state and invasiveness of human breast cancer cell lines

Eighteen breast cancer cell lines were examined for expression of markers of epithelial and fibroblastic differentiation: E-cadherin, desmoplakins, ZO- 1, vimentin, keratin and β1 and β4 integrins. The cell lines were distributed along a spectrum of differentiation from epithelial to fibroblastic phenotypes. The most well-differentiated, epithelioid cell lines contained proteins characteristic of desmosomal, adherens and tight junctions, were adherent to one another on plastic and in the basement membrane matrix Matrigel and were keratin-positive and vimentin-negative. These cell lines were all weakly invasive in an in vitro chemoinvasion assay. The most poorly-differentiated, fibroblastic cell lines were E-cadherin-, desmoplakin- and ZO-1-negative and formed branching structures in Matrigel. They were vimentin-positive, contained only low levels of keratins and were highly invasive in the in vitro chemoinvasion assay. Of all of the markers analyzed, vimentin expression correlated best with in vitro invasive ability and fibroblastic differentiation. In a cell line with unstable expression of vimentin, T47D(CO), the cells that were invasive were of the fibroblastic type. The differentiation markers described here may be useful for analysis of clinical specimens and could potentially provide a more precise measure of differentiation grade yielding more power for predicting prognosis.

When leadership meets organizational change : the influence of the top management team and supervisory leaders on change appraisals, change attitudes, and adjustment to change

Despite the importance of adaption and change for firm survival, the failure rate of organizational change efforts remains alarmingly high (Beer and Nohria, 2000; Kotter, 1995). In a recent global survey of over 3,000 executives,Meaney and Pung (2008) reported that two-thirds of executives indicated that their firm had failed to successfully implement organizational changes. Similarly, academic researchers have also concluded that difficulties in implementing and managing organizational change efforts often precipitate organizational crises (Probst and Raisch, 2005). As a result, attention has been directed to identify the factors that improve the likelihood of successfully implementing organizational change efforts. While there has been practitioner-oriented discussion around the pivotal role of workplace leaders in reducing resistance to change, only a limited number of empirical studies have examined relationships between leader behavior and employee change attitudes (e.g., Bommer, Rich, and Rubin, 2005; Herold, Caldwell, and Liu, 2008; Nemanich and Keller, 2007; Oreg and Berson, 2011). However...

Chemotaxis and chemokinesis of human prostate tumor cell lines in response to human prostate stromal cell secretory proteins containing a nerve growth factor-like protein

The migration of three human prostate tumor epithelial cell lines (TSU-pr1, PC-3, DU-145) in response to secreted protein from a human prostate stromal cell line was investigated by using the modified blind-well Boyden chamber assay. Migrated cells were quantified by spectrophotometrically measuring the concentration of crystal violet stain extracted from their nuclei. Cell number was correlated linearly with the concentration of extracted crystal violet stain. All three tumor cell lines showed intrinsic migratory ability in the absence of chemoattractants, such that approximately 1-7% of plated cells migrated across the filter of the Boyden chambers during a 5-h incubation period. Prostate tumor cell migration was significantly enhanced (3-13-fold) in response to stromal cell secretory protein in a dose-dependent manner, whereas bovine serum albumin had no effect on stimulating tumor cell migration. Immunoprecipitation of the stromal cell secreted protein with a nerve growth factor antibody partially and significantly reduced its stimulatory activity for tumor cell migration. A Zigmond-Hirsch matrix assay of tumor cell migration in response to various concentration gradients of stromal cell secreted protein demonstrated both chemotaxis and chemokinesis by all three cell lines. These results are consistent with the stromal cell secretory protein stimulation of chemokinetic tumor cell migration through the capsule of the prostate. Outside of the prostate gland metastasis of tumor cells may occur by chemotaxis to preferential sites containing chemoattractants similar to or related to maintenance factors that can substitute for components of stromal cell secretory protein.

SPARC/osteonectin induces matrix metalloproteinase 2 activation in human breast cancer cell lines

Activation of the matrix metalloproteinase 2 (MMP-2) has been shown to play a major role in the proteolysis of extracellular matrix (ECM) associated with tumor invasion. Although the precise mechanism of this activation remains elusive, levels of the membrane type 1-MMP (MT1-MMP) at the cell surface and of the tissue inhibitor of MMP-2 (TIMP-2) appear to be two important determinants. Induction of MMP-2 activation in cells cultivated on collagen type I gels indicated that the ECM is important in the regulation of this process. In this study, we show that SPARC/osteonectin, a small ECM- associated matricellular glycoprotein, can induce MMP-2 activation in two invasive breast cancer cell lines (MDA-MB-231 and BT549) but not in a noninvasive counterpart (MCF7), which lacks MT1-MMP. Using a set of peptides from different regions of SPARC, we found that peptide 1.1 (corresponding to the NH2-terminal region of the protein) contained the activity that induced NIMP-2 activation. Despite the requirement for MT1-MMP, seen in MCF-7 cells transfected with MT1-MMP, the activation of MMP-2 by SPARC peptide 1.1 was not associated with increased steady-state levels of MT1-MMP mRNA or protein in either MT1-MMP-transfected MCF-7 cells or constitutively expressing MDA- MB-231 and BT549 cells. We did, however, detect decreased levels of TIMP-2 protein in the media of cells incubated with peptide 1.1 or recombinant SPARC; thus, the induction of MMP-2 activation by SPARC might be due in part to a diminution of TIMP-2 protein. We conclude that SPARC, and specifically its NH2-terminal domain, regulates the activation of MMP-2 at the cell surface and is therefore likely to contribute to the proteolytic pathways associated with tumor invasion.

Loss of epithelial markers and acquisition of vimentin expression in adriamycin- and vinblastine-resistant human breast cancer cell lines

We have previously observed that breast cancer cell lines could exhibit either epithelial or fibroblastic phenotypes as reflected by their morphologies and intermediate filament protein expression (C. L. Sommers, D. Walker-Jones, S. E. Heckford, P. Worland, E. Valverius, R. Clark, M. Stampfer, and E. P. Gelmann, Cancer Res., 49: 4258-4263, 1989). Fibroblastoid, vimentin-expressing breast cancer cell lines are more invasive in vitro and in vivo (E. W. Thompson, S. Paik, N. Brunner, C. L. Sommers, G. Zugmaier, R. Clarke, T. B. Shima, J. Torri, S. Donahue, M. E. Lippman, G. R. Martin, and R. B. Dickson, J. Cell. Physiol., 150: 534-544, 1992). We hypothesized that a breast cancer cell with an epithelial phenotype could undergo a transition to a fibroblastic phenotype, possibly resulting in more invasive capacity. We now show that two Adriamycin-resistant MCF-7 cell lines and a vinblastine-resistant ZR-75-B cell line have undergone such a transition. Adriamycin-resistant MCF-7 cells express vimentin, have diminished keratin 19 expression, have lost cell adhesion molecule uvomorulin expression, and have reduced formation of desmosomes and tight junctions as determined by reduced immunodetection of their components desmoplakins I and II and zonula occludens (ZO)-1. Other MCF-7 cell lines selected for resistance to vinblastine and to Adriamycin and verapamil did not have these characteristics, indicating that drug selection does not invariably cause these phenotypic changes. In addition, to determine if vimentin expression in MCF-7 cells alone could manifest a fibroblastic phenotype, we transfected the full-length human vimentin complementary DNA into MCF-7 cells. Although vimentin expression was achieved in MCF-7 cells, it did not affect the phenotype of the cells in terms of the distribution of keratins, desmoplakins I and II, ZO-1, or uvomorulin or in terms of in vitro invasiveness. We conclude that vimentin expression is a marker for a fibroblastic and invasive phenotype in breast cancer cells but does not by itself give rise to this phenotype.

Assessing the property market impact of stigma removal : high voltage overhead transmission lines removal in Wellington, NZ

This thesis advances the understanding of the impact of stigma on property values. A case study in Wellington, New Zealand, enabled hedonic modelling and an empirical analysis to determine the impact of the stigma from the high voltage transmission line structure and how long the stigma remained after removal. The results reveal a substantial difference between the discount applied to individual properties while the structure is in place, as compared to the overall increase in neighbourhood value once the structure, which created the stigma, is removed.

Epithelial mesenchymal transition traits in human breast cancer cell lines

Epithelial mesenchymal transition (EMT) has long been associated with breast cancer cell invasiveness and evidence of EMT processes in clinical samples is growing rapidly. Genome-wide transcriptional profiling of increasingly larger numbers of human breast cancer (HBC) cell lines have confirmed the existence of a subgroup of cell lines (termed Basal B/Mesenchymal) with enhanced invasive properties and a predominantly mesenchymal gene expression signature, distinct from subgroups with predominantly luminal (termed Luminal) or mixed basal/luminal (termed Basal A) features (Neve et al Cancer Cell 2006). Studies providing molecular and cellular analyses of EMT features in these cell lines are summarised, and the expression levels of EMT-associated factors in these cell lines are analysed. Recent clinical studies supporting the presence of EMT-like changes in vivo are summarised. Human breast cancer cell lines with mesenchymal properties continue to hold out the promise of directing us towards key mechanisms at play in the metastatic dissemination of breast cancer.

Expression of c-ets-1 mRNA is associated with an invasive, EMT-derived phenotype in breast carcinoma cell lines

We have previously observed in vitro that some stromal proteinases (MMP- 2, MT1-MMP) were expressed or activated by invasive carcinoma cell lines exhibiting mesenchymal features, presumably acquired through an epithelial to mesenchymal transition (EMT). To examine the potential contribution of c- ets-1 to this phenotype, we have compared here the expression of c-ets-1 with invasiveness in vitro and expression of vimentin, E-cadherin, uPA, MMP-1 and MMP-3 in a panel of human breast cancer cell lines. Our results clearly demonstrate an association between c-ets-1 expression and the invasive, EMT- derived phenotype, which is typified by the expression of vimentin and the lack of E-cadherin. While absent from the two non-invasive, vimentin-negative cell lines, c-ets-1 was abundantly expressed in all the four vimentin- positive lines. However, we could not find a clear quantitative or qualitative relationship between the expression of c-ets-1 and the three proteinases known to he regulated by c-ets-1, except that when they were expressed, it was only in the invasive c-ets-1-positive lines. UPA mRNAs were found in three of the four vimentin-positive lines, MMP-1 in two of the four, and MMP-3 could not be detected in any of the cell lines. Intriguingly, MDA- MB-435 cells, which exhibit the highest metastatic potential of these cell lines in nude mice, expressed vimentin and c-ets-1, but lacked expression of these three proteinases, at least under the culture conditions employed. Taken together, our results show that c-ets-1 expression is associated with an invasive, EMT-derived phenotype in breast cancer cells, although it is apparently not sufficient to ensure the expression of uPA, MMP-1 or MMP-3, in the vimentin-positive cells. Such proteases regulation is undoubtedly qualified by the cellular context. This study therefore advances our understanding of the molecular regulation of invasiveness in EMT-associated carcinoma progression, and suggests that c-ets-1 may contribute to the invasive phenotype in carcinoma cells.

LCC15-MB cells are MDA-MB-435 : a review of misidentified breast and prostate cell lines

Current stocks of the LCC15-MB cell line, which we originally isolated from a human breast-bone metastasis, were found to be genetically matched to the MDA-MB-435 cell line from the Lombardi Cancer Center (MDA-MB-435-LCC) using comparative genomic hybridisation, DNA microsatellite analysis and chromosomal number. LCC15-MB stocks used for our previously published studies as well as the earliest available LCC15-MB cells also showed identity to MDA-MB-435-LCC cells. The original karyotype reported for LCC15-MB cells was considerably different to that of MDA-MB-435 cells, indicating that the original LCC15-MB cells were lost to contamination by MDA-MB-435-LCC cells. Chromosome number is the simplest test to distinguish original LCC 15-MB cells (n ∼ 75) from MDA-MB-435 (n ∼ 52). Collectively, our results prove that LCC15-MB cells currently available are MDA-MB-435 cells and we suggest their re-designation as MDA-MB-435-LCC15 cells. We also review the known misclassification of breast and prostate cancer cell lines to date and have initiated a register maintained at http://www.svi.edu.au/cell_lines_registry.doc.