Cyberbullying

Cyberbullying is any bullying through technology, usually using mobile phones and the Internet or combinations of these. Methods used to bully include texting degoratory messages on mobile phones with young people showing them to their friends before sending to the victim; slagging or excluding someone in a chat room; inviting comments on nasty blogs or placing embarrassing or bullying videos on YouTube. It is important to distinguish if it is bullying or fighting using technology because that determines how it is best handled. Just because young people send a nasty text or use instant messaging to berate someone, it could be fighting between equals and not the intentional, aggressive, repeated acts of someone with more power which defines bullying.

The red mist? red shirts, success and team sports

Baron von Richthofen (the Red Baron) arguably the most famous fighter pilot of all time painted his plane the vividest of red hues, making it visible and identifiable at great distance, showing an aggressive pronouncement of dominance to other pilots. Can colour affect aggression and performance and if so is it observable within team sports? This study explores the effect of red on sporting performances within a team sports arena, through empirical analysis of match results from the Australian Rugby League spanning a period of 30 years. Both the descriptive analysis and the multivariate analysis report a positive relationship. Nevertheless, more evidence is required to better understand whether teams in red do enjoy greater success controlling explicitly in a multivariate analysis for many factors that simultaneously affect performance.

The effects of lane-changing on the immediate follower : anticipation, relaxation, and change in driver characteristics

This paper investigates the effects of lane-changing in driver behavior by measuring (i) the induced transient behavior and (ii) the change in driver characteristics, i.e., changes in driver response time and minimum spacing. We find that the transition largely consists of a pre-insertion transition and a relaxation process. These two processes are different but can be reasonably captured with a single model. The findings also suggest that lane-changing induces a regressive effect on driver characteristics: a timid driver (characterized by larger response time and minimum spacing) tends to become less timid and an aggressive driver less aggressive. We offer an extension to Newell’s car-following model to describe this regressive effect and verify it using vehicle trajectory data.

Do drivers respond emotionally and behaviourally differently to an intentionally anger provoking driving situation than to an ambiguous, but potentially provocative, one? Results of a self-report survey.

Aggressive driving is considered an important road-safety concern for drivers in highly motorised countries. However, understanding of the causes and maintenance factors fundamental to aggressive driving is limited. In keeping with theoretical advances from general aggression research such as the General Aggression Model (GAM), research has begun to examine the emotional and cognitive antecedents of aggressive driving in order to better understand the underlying processes motivating aggressive driving. Early findings in the driving area have suggested that greater levels of aggression are elicited in response to an intentionally aggressive on-road event. In contrast, general aggression research suggests that greater levels of aggression are elicited in response to an ambiguous event. The current study examined emotional and cognitive responses to two hypothetical driving scenarios with differing levels of aggressive intent (intentional versus ambiguous). There was also an interest in whether factors influencing responses were different for hostile aggression (that is, where the action is intended to harm the other) versus instrumental aggression (that is, where the action is motivated by an intention to remove an impediment or attain a goal). Results were that significantly stronger negative emotion and negative attributions, as well as greater levels of threat were reported in response to the scenario which was designed to appear intentional in nature. In addition, participants were more likely to endorse an aggressive behavioural response to a situation that appeared deliberately aggressive than to one where the intention was ambiguous. Analyses to determine if greater levels of negative emotions and cognitions are able to predict aggressive responses provided different patterns of results for instrumental aggression from those for hostile aggression. Specifically, for instrumental aggression, negative emotions and negative attributions were significant predictors for both the intentional and the ambiguous scenarios. In addition, perceived threat was also a significant predictor where the other driver’s intent was clearly aggressive. However, lower rather than higher, levels of perceived threat were associated with greater endorsement of an aggressive response. For hostile aggressive behavioural responses, trait aggression was the strongest predictor for both situations. Overall the results suggest that in the driving context, instrumental aggression is likely to be a much more common response than hostile aggression. Moreover, aggressive responses are more likely in situations where another driver’s behaviour is clearly intentional rather than ambiguous. The results also support the conclusion that there may be different underlying mechanisms motivating an instrumental aggressive response to those motivating a hostile one. In addition, understanding the emotions and cognitions underlying aggressive driving responses may be helpful in predicting and intervening to reduce driving aggression. The finding that drivers appear to regard tailgating as an instrumental response is of concern since this behaviour has the potential to result in crashes.

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.

Expression of PTRF in PC3 cells modulates cholesterol dynamics and the actin cytoskeleton impacting secretion pathways

Expression of caveolin-1 is up-regulated in prostate cancer metastasis and is associated with aggressive recurrence of the disease. Intriguingly, caveolin-1 is also secreted from prostate cancer cell lines and has been identified in secreted prostasomes. Caveolin-1 is the major structural component of the plasma membrane invaginations called caveolae. Co-expression of the coat protein Polymerase I and transcript release factor (PTRF) is required for caveolae formation. We recently found that expression of caveolin-1 in the aggressive prostate cancer cell line PC-3 is not accompanied by PTRF, leading to noncaveolar caveolin-1 lipid rafts. Moreover, ectopic expression of PTRF in PC-3 cells sequesters caveolin-1 into caveolae. Here we quantitatively analyzed the effect of PTRF expression on the PC-3 proteome using stable isotope labeling by amino acids in culture and subcellular proteomics. We show that PTRF reduced the secretion of a subset of proteins including secreted proteases, cytokines, and growth regulatory proteins, partly via a reduction in prostasome secretion. To determine the cellular mechanism accounting for the observed reduction in secreted proteins we analyzed total membrane and the detergent-resistant membrane fractions. Our data show that PTRF expression selectively impaired the recruitment of actin cytoskeletal proteins to the detergent-resistant membrane, which correlated with altered cholesterol distribution in PC-3 cells expressing PTRF. Consistent with this, modulating cellular cholesterol altered the actin cytoskeleton and protein secretion in PC-3 cells. Intriguingly, several proteins that function in ER to Golgi trafficking were reduced by PTRF expression. Taken together, these results suggest that the noncaveolar caveolin-1 found in prostate cancer cells generates a lipid raft microenvironment that accentuates secretion pathways, possibly at the step of ER sorting/exit. Importantly, these effects could be modulated by PTRF expression.

International tax cooperation in the Post-GFC era

Over the last five years we have observed the fallout from the global financial crisis (GFC). International cooperation and jointly adopted policies have dominated many of the solutions to the problems which have arisen. Initially, many nations in response to the GFC, implemented a two pronged short term solution by undertaking fiscal intervention and delivering rescue packages aimed at first, bailing out financial institutions and second, preventing or minimising the impact of a recession. Both programs involved large amounts of domestic spending. It was difficult in early 2007 to foresee the reduction that nations were about the face in domestic revenue collected. Five years on, not only have the first line effects of the GFC reduced the revenue raised by governments around the world, but the consequential costs associated with the rescue packages have also depleted domestic revenue bases. The response by stakeholders has been to attempt to secure domestic revenue bases through fiscally sustainable measures. Domestic sovereignty allows the levying of taxes as a nation chooses. However, rather than raise domestic taxes, revenue may also be increased by stemming the flow of income and capital to low and no-tax jurisdictions. The intervening five-year period since the GFC allows a unique insight into the response by nations and international organisations to tax evasion, tax avoidance and aggressive tax competition through the cross border flows of capital and the resulting affect that the GFC has had on international tax cooperation. By investigating the change in the international tax landscape over the last five years, which reveals the work done by stakeholders in developing fiscally responsible responses to the problems that have arisen, it may be possible to predict the trajectory of the international tax landscape over the next five years.

Australia leads with process bus

Powerlink Queensland has undertaken an aggressive program of research, development and implementation of IEC 61850-based system solutions. The intent is to move towards an IEC 61850 process bus using a two-step approach.

Psychosocial experience of cancer : surpassing mere survival and recognising the potential for posttraumatic growth as well as distress.

The publication of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 1994) introduced the notion that a life-threatening illness can be a stressor and catalyst for Posttraumatic Stress Disorder (PTSD). Since then a solid body of research has been established investigating the post-diagnosis experience of cancer. These studies have identified a number of short and long-term life changes resulting from a diagnosis of cancer and associated treatments. In this chapter, we discuss the psychosocial response to the cancer experience and the potential for cancer-related distress. Cancer can represent a life-threatening diagnosis that may be associated with aggressive treatments and result in physical and psychological changes. The potential for future trauma through the lasting effects of the disease and treatment, and the possibility of recurrence, can be a source of continued psychological distress. In addition to the documented adverse repercussions of cancer, we also outline the recent shift that has occurred in the psycho-oncology literature regarding positive life change or posttraumatic growth that is commonly reported after a diagnosis of cancer. Adopting a salutogenic framework acknowledges that the cancer experience is a dynamic psychosocial process with both negative and positive repercussions. Next, we describe the situational and individual factors that are associated with posttraumatic growth and the types of positive life change that are prevalent in this context. Finally, we discuss the implications of this research in a therapeutic context and the directions of future posttraumatic growth research with cancer survivors. This chapter will present both quantitative and qualitative research that indicates the potential for personal growth from adversity rather than just mere survival and return to pre-diagnosis functioning. It is important to emphasise however, that the presence of growth and prevalence of resilience does not negate the extremely distressing nature of a cancer diagnosis for the patient and their families and the suffering that can accompany treatment regimes. Indeed, it will be explained that for growth to occur, the experience must be one that quite literally shatters previously held schemas in order to act as a catalyst for change.

Subacute effects of ecstasy on mood : an exploration of associated risk factors

Ecstasy use may result in lowered mood, anxiety or aggression in the days following use. Yet, few studies have investigated what factors increase the risk of experiencing such symptoms. Ecstasy users (at least once in the last 12 months) who subsequently took ecstasy (n=35) over the next week, were compared on measures of mood, sleep, stress and drug use, with those who abstained (n=21) that week. Measures were administered the week prior to ecstasy use and 1 and 3 days following use, or the equivalent day for abstainers. Mood symptoms were assessed using the Kessler-10 self-report psychological distress scale, a subjective mood rating (1-10), and the depression, anxiety and hostility items of the clinician-rated Brief Psychiatric Rating Scale. Timeline followback methods were used to collect information on drug use and life stress in the past month. Self-reported sleep quality was also assessed. Ecstasy use was not associated with subacute depressive, anxiety or aggressive symptoms. Rather, lowered mood and increased psychological distress were associated with self-reported hours and quality of sleep obtained during the 3-day follow up. These findings highlight the importance of considering sleep disruption in understanding the short-term mood effects of ecstasy use.

FOXC2 expression links epithelial-mesenchymal transition and stem cell properties in breast cancer

Resistance to chemotherapy and metastases are the major causes of breast cancer-related mortality. Moreover, cancer stem cells (CSC) play critical roles in cancer progression and treatment resistance. Previously, it was found that CSC-like cells can be generated by aberrant activation of epithelial–mesenchymal transition (EMT), thereby making anti-EMT strategies a novel therapeutic option for treatment of aggressive breast cancers. Here, we report that the transcription factor FOXC2 induced in response to multiple EMT signaling pathways as well as elevated in stem cell-enriched factions is a critical determinant of mesenchymal and stem cell properties, in cells induced to undergo EMT- and CSC-enriched breast cancer cell lines. More specifically, attenuation of FOXC2 expression using lentiviral short hairpin RNA led to inhibition of the mesenchymal phenotype and associated invasive and stem cell properties, which included reduced mammosphere-forming ability and tumor initiation. Whereas, overexpression of FOXC2 was sufficient to induce CSC properties and spontaneous metastasis in transformed human mammary epithelial cells. Furthermore, a FOXC2-induced gene expression signature was enriched in the claudin-low/basal B breast tumor subtype that contains EMT and CSC features. Having identified PDGFR-β to be regulated by FOXC2, we show that the U.S. Food and Drug Administration-approved PDGFR inhibitor, sunitinib, targets FOXC2-expressing tumor cells leading to reduced CSC and metastatic properties. Thus, FOXC2 or its associated gene expression program may provide an effective target for anti-EMT-based therapies for the treatment of claudin-low/basal B breast tumors or other EMT-/CSC-enriched tumors.

Loss of breast epithelial marker hCLCA2 promotes epithelial to mesenchymal transition and indicates higher risk of metastasis

Transition between epithelial and mesenchymal states is a feature of both normal development and tumor progression. We report that expression of chloride channel accessory protein hCLCA2 is a characteristic of epithelial differentiation in the immortalized MCF10A and HMLE models, while induction of epithelial-to-mesenchymal transition by cell dilution, TGFβ or mesenchymal transcription factors sharply reduces hCLCA2 levels. Attenuation of hCLCA2 expression by lentiviral small hairpin RNA caused cell overgrowth and focus formation, enhanced migration and invasion, and increased mammosphere formation in methylcellulose. These changes were accompanied by downregulation of E-cadherin and upregulation of mesenchymal markers such as vimentin and fibronectin. Moreover, hCLCA2 expression is greatly downregulated in breast cancer cells with a mesenchymal or claudin-low profile. These observations suggest that loss of hCLCA2 may promote metastasis. We find that higher-than-median expression of hCLCA2 is associated with a one-third lower rate of metastasis over an 18-year period among breast cancer patients compared with lower-than-median (n=344, unfiltered for subtype). Thus, hCLCA2 is required for epithelial differentiation, and its loss during tumor progression contributes to metastasis. Overexpression of hCLCA2 has been reported to inhibit cell proliferation and is accompanied by increases in chloride current at the plasma membrane and reduced intracellular pH (pHi). We found that knockdown cells have sharply reduced chloride current and higher pHi, both characteristics of tumor cells. These results suggest a mechanism for the effects on differentiation. Loss of hCLCA2 may allow escape from pHi homeostatic mechanisms, permitting the higher intracellular and lower extracellular pH that are characteristic of aggressive tumor cells.

Microscopic cooperative traffic based on NGSIM data

The deployment of new emerging technologies, such as cooperative systems, allows the traffic community to foresee relevant improvements in terms of traffic safety and efficiency. Vehicles are able to communicate on the local traffic state in real time, which could result in an automatic and therefore better reaction to the mechanism of traffic jam formation. An upstream single hop radio broadcast network can improve the perception of each cooperative driver within radio range and hence the traffic stability. The impact of a cooperative law on traffic congestion appearance is investigated, analytically and through simulation. Ngsim field data is used to calibrate the Optimal Velocity with Relative Velocity (OVRV) car following model and the MOBIL lane-changing model is implemented. Assuming that congestion can be triggered either by a perturbation in the instability domain or by a critical lane changing behavior, the calibrated car following behavior is used to assess the impact of a microscopic cooperative law on abnormal lane changing behavior. The cooperative law helps reduce and delay traffic congestion as it increases traffic flow stability.

Avoiding road rage

Road Rage describes a range of aggressive and dangerous driving behaviours directed at other road users. The phrase involves images of uncontrolled temper and the open display of anger and frustration. A common alternative term is “aggressive driving” with road rage seen to be a manifestation of extreme aggressive driving.

Genetic association of the KLK4 locus with risk of prostate cancer

The Kallikrein-related peptidase, KLK4, has been shown to be significantly overexpressed in prostate tumours in numerous studies and is suggested to be a potential biomarker for prostate cancer. KLK4 may also play a role in prostate cancer progression through its involvement in epithelial-mesenchymal transition, a more aggressive phenotype, and metastases to bone. It is well known that genetic variation has the potential to affect gene expression and/or various protein characteristics and hence we sought to investigate the possible role of single nucleotide polymorphisms (SNPs) in the KLK4 gene in prostate cancer. Assessment of 61 SNPs in the KLK4 locus (±10 kb) in approximately 1300 prostate cancer cases and 1300 male controls for associations with prostate cancer risk and/or prostate tumour aggressiveness (Gleason score <7 versus ≥7) revealed 7 SNPs to be associated with a decreased risk of prostate cancer at the Ptrend<0.05 significance level. Three of these SNPs, rs268923, rs56112930 and the HapMap tagSNP rs7248321, are located several kb upstream of KLK4; rs1654551 encodes a non-synonymous serine to alanine substitution at position 22 of the long isoform of the KLK4 protein, and the remaining 3 risk-associated SNPs, rs1701927, rs1090649 and rs806019, are located downstream of KLK4 and are in high linkage disequilibrium with each other (r2≥0.98). Our findings provide suggestive evidence of a role for genetic variation in the KLK4 locus in prostate cancer predisposition.