985 resultados para Cities. Sociabilities. Squares. Fear. Violence


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Rises recorded for girls’ violence in countries like Australia, Canada, United Kingdom and United States have been hotly contested. One view is these rising rates of violence are an artefact of new forms of policy, policing, criminalisation and social control over young women. Another view is that young women may indeed have become more violent as they have increasingly participated in youth subcultural activities involving gangs and drugs, and cyber‐cultural activities that incite and reward girls’ violence. Any comprehensive explanation will need to address how a complex interplay of cultural, social, behavioural, and policy responses contribute to these rises. This article argues that there is no singular cause, explanation or theory that accounts for the rises in adolescent female violence, and that many of the simple explanations circulating in popular culture are driven by an anti‐feminist ideology. By concentrating on females as victims of violence and very rarely as perpetrators, feminist criminology has for the most part ducked the thorny issue of female violence, leaving a discursive space for anti‐feminist sentiment to reign. The article concludes by arguing the case for developing a feminist theory of female violence.

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Objective Describe the characteristics of patients presenting to Emergency Departments (EDs) within Queensland, Australia with injuries due to assault with a glass implement (‘glassing’) and to set this within the broader context of presentations due to alcohol-related violence. Methods Analysis of prospectively collected ED injury surveillance data collated by the Queensland Injury Surveillance Unit (QISU) between 1999 and 2011. Cases of injury due to alcohol-related violence were identified and analysed using coded fields supplemented with qualitative data contained within the injury description text. Descriptive statistics were used to assess the characteristics of injury presentations due to alcohol-related violence. Violence included interpersonal violence and aggression (verbal aggression and object violence). Results A total of 4629 cases were studied. The study population was predominantly male (72%) and aged 18 to 24 (36%), with males in this age group comprising more than a quarter of the study population (28%). Nine percent of alcohol-related assault injuries were a consequence of ‘glassing’. The home was the most common location for alcohol-related violence (31%) and alcohol-related ‘glassings’ (33%). Overall, the most common glass object involved was a bottle (75%), however, within licensed venues an even mix of a drinking glass (44%) and glass bottle (45%) were identified. Conclusions Contrary to public perception generated by media, ‘glassing’ incidents, particularly at licensed venues, constitute a relatively small proportion of all alcohol-related violence. The current study highlights the predominance of young men injured following alcohol-related violence, demonstrating a key focus area within the population for aiming prevention strategies.

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Purpose A knowledge-based urban development needs to be sustainable and, therefore, requires ecological planning strategies to ensure a better quality of its services. The purpose of this paper is to present an innovative approach for monitoring the sustainability of urban services and help the policy-making authorities to revise the current planning and development practices for more effective solutions. The paper introduces a new assessment tool–Micro-level Urban-ecosystem Sustainability IndeX (MUSIX) – that provides a quantitative measure of urban sustainability in a local context. Design/methodology/approach A multi-method research approach was employed in the construction of the MUSIX. A qualitative research was conducted through an interpretive and critical literature review in developing a theoretical framework and indicator selection. A quantitative research was conducted through statistical and spatial analyses in data collection, processing and model application. Findings/results MUSIX was tested in a pilot study site and provided information referring to the main environmental impacts arising from rapid urban development and population growth. Related to that, some key ecological planning strategies were recommended to guide the preparation and assessment of development and local area plans. Research limitations/implications This study provided fundamental information that assists developers, planners and policy-makers to investigate the multidimensional nature of sustainability at the local level by capturing the environmental pressures and their driving forces in highly developed urban areas. Originality/value This study measures the sustainability of urban development plans through providing data analysis and interpretation of results in a new spatial data unit.

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In recent years, with the impact of global knowledge economy, a more comprehensive development approach has gained significant popularity. This new development approach, so called ‘knowledge-based urban development’, is different from its traditional predecessor. With a much more balanced focus on all of the four key development domains – economic, spatial, institutional, and socio-cultural – this contemporary approach, aims to bring economic prosperity, environmental sustainability and local institutional competence with a just socio-spatial order to our cities and regions. The ultimate goal of knowledgebased urban development is to produce a city purposefully designed to encourage the continuous production, circulation and commercialization of social and scientific knowledge – this will in turn establish a ‘knowledge city’. A city following the ‘knowledge city’ concept embarks on a strategic mission to firmly encourage and nurture locally focused innovation, science and creativity within the context of an expanding knowledge economy and society. In this regard a ‘knowledge city’ can be seen as an integrated city, which physically and institutionally combines the functions of a science and technology park with civic and residential functions and urban amenities. It also offers one of the effective paradigms for the sustainable cities of our time. This sixth edition of KCWS – The 6th Knowledge Cities World Summit 2013 – makes an important reminder that the ‘knowledge city’ concept is a key notion in the 21st Century development. Considering this notion, the Summit sheds light on the multifaceted dimensions and various scales of building a ‘knowledge city’ via ‘knowledge-based urban development’ paradigm by particularly focusing on the overall Summit theme of ‘Establishing Bridges’. At this summit, the theoretical and practical maturing of knowledge-based development paradigms are advanced through the interplay between the world’s leading academics’ theories and the practical models and strategies of practitioners’ and policy makers’ drawn from around the world. This summit proceeding is compiled in order to disseminate the knowledge generated and shared in KCWS 2013 with the wider research, governance, and practice communities the knowledge co-created in this summit. All papers of this proceeding have gone through a double-blind peer review process and been reviewed by our summit editorial review and advisory board members. We, organizers of the summit, cordially thank the members of the Summit Proceeding Editorial Review and Advisory Board for their diligent work in the review of the papers. Also we thank Prof.Dr. Ahmet Ademoğlu, Rector of İstanbul Şehir University, for providing all the support for the Summit. We hope the papers in this proceeding will inspire and make a significant contribution to the research, governance, and practice circles.

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Current approaches to airport development and land use sit at odds with the tradition of airports as spaces for aviation (Stevens et a/. 2010). While airports remain the primary interface between air transport and society, the functions they include within their boundaries have expanded well beyond the provision of infrastructure for aviation and logistics. Shopping malls, commercial office space, hotels, golf courses and conference facilities arc increasingly normal uses of land within airport boundaries (Kasarda 2008), and enhance the role of airports from transport infrastructure to a new form of economic infrastructure (Freestone 2009). However, the expanding role of airports, and the resulting diversification in airport land uses, has not been without opposition.

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Facial cues of racial outgroup or anger mediate fear learning that is resistant to extinction. Whether this resistance is potentiated if fear is conditioned to angry, other race faces has not been established. Two groups of Caucasian participants were conditioned with two happy and two angry face conditional stimuli (CSs). During acquisition, one happy and one angry face were paired with an aversive unconditional stimulus whereas the second happy and angry faces were presented alone. CS face race (Caucasian, African American) was varied between groups. During habituation, electrodermal responses were larger to angry faces regardless of race and declined less to other race faces. Extinction was immediate for Caucasian happy faces, delayed for angry faces regardless of race, and slowest for happy racial outgroup faces. Combining the facial cues of other race and anger does not enhance resistance to extinction of fear.

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Despite plentiful efforts to identify perpetrator, victim, and incident characteristics correlated with reporting violence against women to police, few studies have addressed the contexts that shape such reporting. Even fewer have examined variations in these contexts across geographic areas. Drawing upon National Crime Victimization Survey data from 1992 through 2009, this paper uses conjunctive analysis of case configurations to identify and investigate the dominant situational contexts of reporting of violence against women to police across rural, suburban, and urban areas. Our findings show that context matters and the importance of incident, perpetrator, and victim characteristics vary across geographic areas.

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Individual variability in the acquisition, consolidation and extinction of conditioned fear potentially contributes to the development of fear pathology including posttraumatic stress disorder (PTSD). Pavlovian fear conditioning is a key tool for the study of fundamental aspects of fear learning. Here, we used a selected mouse line of High and Low Pavlovian conditioned fear created from an advanced intercrossed line (AIL) in order to begin to identify the cellular basis of phenotypic divergence in Pavlovian fear conditioning. We investigated whether phosphorylated MAPK (p44/42 ERK/MAPK), a protein kinase required in the amygdala for the acquisition and consolidation of Pavlovian fear memory, is differentially expressed following Pavlovian fear learning in the High and Low fear lines. We found that following Pavlovian auditory fear conditioning, High and Low line mice differ in the number of pMAPK-expressing neurons in the dorsal sub nucleus of the lateral amygdala (LAd). In contrast, this difference was not detected in the ventral medial (LAvm) or ventral lateral (LAvl) amygdala sub nuclei or in control animals. We propose that this apparent increase in plasticity at a known locus of fear memory acquisition and consolidation relates to intrinsic differences between the two fear phenotypes. These data provide important insights into the micronetwork mechanisms encoding phenotypic differences in fear. Understanding the circuit level cellular and molecular mechanisms that underlie individual variability in fear learning is critical for the development of effective treatment of fear-related illnesses such as PTSD.

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Genetic variability in the strength and precision of fear memory is hypothesised to contribute to the etiology of anxiety disorders, including post-traumatic stress disorder. We generated fear-susceptible (F-S) or fear-resistant (F-R) phenotypes from an F8 advanced intercross line (AIL) of C57BL/6J and DBA/2J inbred mice by selective breeding. We identified specific traits underlying individual variability in Pavlovian conditioned fear learning and memory. Offspring of selected lines differed in the acquisition of conditioned fear. Furthermore, F-S mice showed greater cued fear memory and generalised fear in response to a novel context than F-R mice. F-S mice showed greater basal corticosterone levels and hypothalamic corticotrophin-releasing hormone (CRH) mRNA levels than F-R mice, consistent with higher hypothalamic-pituitary-adrenal (HPA) axis drive. Hypothalamic mineralocorticoid receptor and CRH receptor 1 mRNA levels were decreased in F-S mice as compared with F-R mice. Manganese-enhanced magnetic resonance imaging (MEMRI) was used to investigate basal levels of brain activity. MEMRI identified a pattern of increased brain activity in F-S mice that was driven primarily by the hippocampus and amygdala, indicating excessive limbic circuit activity in F-S mice as compared with F-R mice. Thus, selection pressure applied to the AIL population leads to the accumulation of heritable trait-relevant characteristics within each line, whereas non-behaviorally relevant traits remain distributed. Selected lines therefore minimise false-positive associations between behavioral phenotypes and physiology. We demonstrate that intrinsic differences in HPA axis function and limbic excitability contribute to phenotypic differences in the acquisition and consolidation of associative fear memory. Identification of system-wide traits predisposing to variability in fear memory may help in the direction of more targeted and efficacious treatments for fear-related pathology. Through short-term selection in a B6D2 advanced intercross line we created mouse populations divergent for the retention of Pavlovian fear memory. Trait distinctions in HPA-axis drive and fear network circuitry could be made between naïve animals in the two lines. These data demonstrate underlying physiological and neurological differences between Fear-Susceptible and Fear-Resistant animals in a natural population. F-S and F-R mice may therefore be relevant to a spectrum of disorders including depression, anxiety disorders and PTSD for which altered fear processing occurs.

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A key question in neuroscience is how memory is selectively allocated to neural networks in the brain. This question remains a significant research challenge, in both rodent models and humans alike, because of the inherent difficulty in tracking and deciphering large, highly dimensional neuronal ensembles that support memory (i.e., the engram). In a previous study we showed that consolidation of a new fear memory is allocated to a common topography of amygdala neurons. When a consolidated memory is retrieved, it may enter a labile state, requiring reconsolidation for it to persist. What is not known is whether the original spatial allocation of a consolidated memory changes during reconsolidation. Knowledge about the spatial allocation of a memory, during consolidation and reconsolidation, provides fundamental insight into its core physical structure (i.e., the engram). Using design-based stereology, we operationally define reconsolidation by showing a nearly identical quantity of neurons in the dorsolateral amygdala (LAd) that expressed a plasticity-related protein, phosphorylated mitogen-activated protein kinase, following both memory acquisition and retrieval. Next, we confirm that Pavlovian fear conditioning recruits a stable, topographically organized population of activated neurons in the LAd. When the stored fear memory was briefly reactivated in the presence of the relevant conditioned stimulus, a similar topography of activated neurons was uncovered. In addition, we found evidence for activated neurons allocated to new regions of the LAd. These findings provide the first insight into the spatial allocation of a fear engram in the LAd, during its consolidation and reconsolidation phase.

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Do different brains forming a specific memory allocate the same groups of neurons to encode it? One way to test this question is to map neurons encoding the same memory and quantitatively compare their locations across individual brains. In a previous study, we used this strategy to uncover a common topography of neurons in the dorsolateral amygdala (LAd) that expressed a learning-induced and plasticity-related kinase (p42/44 mitogen-activated protein kinase; pMAPK), following auditory Pavlovian fear conditioning. In this series of experiments, we extend our initial findings to ask to what extent this functional topography depends upon intrinsic neuronal structure. We first showed that the majority (87 %) of pMAPK expression in the lateral amygdala was restricted to principal-type neurons. Next, we verified a neuroanatomical reference point for amygdala alignment using in vivo magnetic resonance imaging and in vitro morphometrics. We then determined that the topography of neurons encoding auditory fear conditioning was not exclusively governed by principal neuron cytoarchitecture. These data suggest that functional patterning of neurons undergoing plasticity in the amygdala following Pavlovian fear conditioning is specific to memory formation itself. Further, the spatial allocation of activated neurons in the LAd was specific to cued (auditory), but not contextual, fear conditioning. Spatial analyses conducted at another coronal plane revealed another spatial map unique to fear conditioning, providing additional evidence that the functional topography of fear memory storing cells in the LAd is non-random and stable. Overall, these data provide evidence for a spatial organizing principle governing the functional allocation of fear memory in the amygdala.

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Pavlovian fear conditioning is a robust technique for examining behavioral and cellular components of fear learning and memory. In fear conditioning, the subject learns to associate a previously neutral stimulus with an inherently noxious co-stimulus. The learned association is reflected in the subjects' behavior upon subsequent re-exposure to the previously neutral stimulus or the training environment. Using fear conditioning, investigators can obtain a large amount of data that describe multiple aspects of learning and memory. In a single test, researchers can evaluate functional integrity in fear circuitry, which is both well characterized and highly conserved across species. Additionally, the availability of sensitive and reliable automated scoring software makes fear conditioning amenable to high-throughput experimentation in the rodent model; thus, this model of learning and memory is particularly useful for pharmacological and toxicological screening. Due to the conserved nature of fear circuitry across species, data from Pavlovian fear conditioning are highly translatable to human models. We describe equipment and techniques needed to perform and analyze conditioned fear data. We provide two examples of fear conditioning experiments, one in rats and one in mice, and the types of data that can be collected in a single experiment. © 2012 Springer Science+Business Media, LLC.

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A growing body of evidence suggests that mitochondrial function may be important in brain development and psychiatric disorders. However, detailed expression profiles of those genes in human brain development and fear-related behavior remain unclear. Using microarray data available from the public domain and the Gene Ontology analysis, we identified the genes and the functional categories associated with chronological age in the prefrontal cortex (PFC) and the caudate nucleus (CN) of psychiatrically normal humans ranging in age from birth to 50 years. Among those, we found that a substantial number of genes in the PFC (115) and the CN (117) are associated with the GO term: mitochondrion (FDR qv <0.05). A greater number of the genes in the PFC (91%) than the genes in the CN (62%) showed a linear increase in expression during postnatal development. Using quantitative PCR, we validated the developmental expression pattern of four genes including monoamine oxidase B (MAOB), NADH dehydrogenase flavoprotein (NDUFV1), mitochondrial uncoupling protein 5 (SLC25A14) and tubulin beta-3 chain (TUBB3). In mice, overall developmental expression pattern of MAOB, SLC25A14 and TUBB3 in the PFC were comparable to the pattern observed in humans (p<0.05). However, mice selectively bred for high fear did not exhibit normal developmental changes of MAOB and TUBB3. These findings suggest that the genes associated with mitochondrial function in the PFC play a significant role in brain development and fear-related behavior.

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Although the endocannabinoid system (ECS) has been implicated in brain development and various psychiatric disorders, precise mechanisms of the ECS on mood and anxiety disorders remain unclear. Here, we have investigated developmental and disease-related expression pattern of the cannabinoid receptor 1 (CB1) and the cannabinoid receptor 2 (CB2) genes in the dorsolateral prefrontal cortex (PFC) of humans. Using mice selectively bred for high and low fear, we further investigated potential association between fear memory and the cannabinoid receptor expression in the brain. The CB1, not the CB2, mRNA levels in the PFC gradually decrease during postnatal development ranging in age from birth to 50 years (r 2 > 0.6 & adj. p < 0.05). The CB1 levels in the PFC of major depression patients were higher when compared to the age-matched controls (adj. p < 0.05). In mice, the CB1, not the CB2, levels in the PFC were positively correlated with freezing behavior in classical fear conditioning (p < 0.05). These results suggest that the CB1 in the PFC may play a significant role in regulating mood and anxiety symptoms. Our study demonstrates the advantage of utilizing data from postmortem brain tissue and a mouse model of fear to enhance our understanding of the role of the cannabinoid receptors in mood and anxiety disorders

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Pavlovian fear conditioning, also known as classical fear conditioning is an important model in the study of the neurobiology of normal and pathological fear. Progress in the neurobiology of Pavlovian fear also enhances our understanding of disorders such as posttraumatic stress disorder (PTSD) and with developing effective treatment strategies. Here we describe how Pavlovian fear conditioning is a key tool for understanding both the neurobiology of fear and the mechanisms underlying variations in fear memory strength observed across different phenotypes. First we discuss how Pavlovian fear models aspects of PTSD. Second, we describe the neural circuits of Pavlovian fear and the molecular mechanisms within these circuits that regulate fear memory. Finally, we show how fear memory strength is heritable; and describe genes which are specifically linked to both changes in Pavlovian fear behavior and to its underlying neural circuitry. These emerging data begin to define the essential genes, cells and circuits that contribute to normal and pathological fear.