184 resultados para mutualism disruption
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Introduction: Mothers’ sleep during the postpartum period is commonly characterised by bouts of sleep across the night, resulting in low sleep efficiency and daytime sleepiness. Understanding of the nature of mothers’ sleep disruption needs to incorporate indices of both sleep quantity and sleep quality, but objective assessment of sleep disturbance experienced during the first postpartum months has not been investigated in great detail. This longitudinal study aimed to objectively measure mothers’ sleep during the first 18 weeks postpartum, to ascertain the level of sleep disturbance experienced. Method: Eleven mothers (Mean age = 29.82, SD = 4.45) from Australia wore Actiwatch-2 devices for up to 7 days and nights at 6, 12 and 18 weeks postpartum. For each night of recording, a number of sleep bouts were identified. Total sleep time (TST) was calculated as the total number of minutes across the night within these bouts. Sleep efficiency was calculated as the percentage of minutes across the night classified as being part of a sleep bout, with higher scores indicating higher efficiency. Sleep quality captured the efficiency of sleep within sleep bouts, and was calculated as the percentage of epochs classified as sleep within sleep bouts, with higher scores indicating higher sleep quality. Results: At 6 weeks postpartum, mean total sleep time was 420.22 minutes (SD = 50.61). Total sleep time did not significantly differ across the assessment; however there was a trend towards an increase over time. Sleep efficiency increased across the time periods (F(2,10) = 10.30, p = .001), with a significant increase between week 12 and week 18. At 6 weeks postpartum, mean sleep quality was 93.15% (SD = 2.68) and scores did not significantly change across the assessment periods. While there was no relationship between sleep efficiency and sleep quality during weeks 6 and 12, a significant positive relationship was observed at week 18, r2 = .52, p = .013. Conclusions: Within this sample, a low level of disruption was consistently shown within the mothers’ night time sleep bouts. However, overall sleep efficiency suggested a significant proportion of time spent awake between sleep bouts. While TST remained stable over time, overall sleep efficiency improved, suggesting the mothers’ sleep was becoming more consolidated. A single sleep bout a night was not often experienced.
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Exogenous prostacyclin is effective in reducing pulmonary vascular resistance in some forms of human pulmonary hypertension (PH). To explore whether endogenous prostaglandins played a similar role in pulmonary hypertension, we examined the effect of deleting cyclooxygenase (COX)-gene isoforms in a chronic hypoxia model of PH. Pulmonary hypertension, examined by direct measurement of right ventricular end systolic pressure (RVESP), right ventricular hypertrophy (n = 8), and hematocrit (n = 3), was induced by 3 weeks of hypobarichypoxia in wild-type and COX-knockout (KO) mice. RVESP was increased in wild-type hypoxic mice compared with normoxic controls (24.4 ± 1.4 versus 13.8 ± 1.9 mm Hg; n = 8; p < 0.05). COX-2 KO mice showed a greater increase in RVESP following hypoxia (36.8 ± 2.7 mm Hg; p < 0.05). Urinary thromboxane (TX)B2 excretion increased following hypoxia (44.6 ± 11.1 versus 14.7 ± 1.8 ng/ml; n = 6; p < 0.05), an effect that was exacerbated by COX-2 gene disruption (54.5 ± 10.8 ng/ml; n = 6). In contrast, the increase in 6-keto-prostacyclin1α excretion following hypoxia was reduced by COX-2 gene disruption (29 ± 3 versus 52 ± 4.6 ng/ml; p < 0.01). Tail cut bleed times were lower following hypoxia, and there was evidence of intravascular thrombosis in lung vessels that was exacerbated by disruption of COX-2 and reduced by deletion of COX-1. The TXA2/endoperoxide receptor antagonist ifetroban (50 mg/kg/day) offset the effect of deleting the COX-2 gene, attenuating the hypoxia-induced rise in RVESP and intravascular thrombosis. COX-2 gene deletion exacerbates pulmonary hypertension, enhances sensitivity to TXA2, and induces intravascular thrombosis in response to hypoxia. The data provide evidence that endogenous prostaglandins modulate the pulmonary response to hypoxia. Copyright © 2008 by The American Society for Pharmacology and Experimental Therapeutics.
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Purpose: In animal models hemi-field deprivation results in localised, graded vitreous chamber elongation and presumably deprivation induced localised changes in retinal processing. The aim of this research was to determine if there are variations in ERG responses across the retina in normal chick eyes and to examine the effect of hemi-field and full-field deprivation on ERG responses across the retina and at earlier times than have previously been examined electrophysiologically. Methods: Chicks were either untreated, wore monocular full-diffusers or half-diffusers (depriving nasal retina) (n = 6-8 each group) from day 8. mfERG responses were measured using the VERIS mfERG system across the central 18.2º× 16.7º (H × V) field. The stimulus consisted of 61 unscaled hexagons with each hexagon modulated between black and white according to a pseudorandom binary m-sequence. The mfERG was measured on day 12 in untreated chicks, following 4 days of hemi-field diffuser wear, and 2, 48 and 96 h after application of full-field diffusers. Results: The ERG response of untreated chick eyes did not vary across the measured field; there was no effect of retinal location on the N1-P1 amplitude (p = 0.108) or on P1 implicit time (p > 0.05). This finding is consistent with retinal ganglion cell density of the chick varying by only a factor of two across the entire retina. Half-diffusers produced a ramped retina and a graded effect of negative lens correction (p < 0.0001); changes in retinal processing were localized. The untreated retina showed increasing complexity of the ERG waveform with development; form-deprivation prevented the increasing complexity of the response at the 2, 48 and 96 h measurement times and produced alterations in response timing. Conclusions: Form-deprivation and its concomitant loss of image contrast and high spatial frequency images prevented development of the ERG responses, consistent with a disruption of development of retinal feedback systems. The characterisation of ERG responses in normal and deprived chick eyes across the retina allows the assessment of concurrent visual and retinal manipulations in this model. (Ophthalmic & Physiological Optics © 2013 The College of Optometrists.)
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In recent times, technology has advanced in such a manner that the world can now communicate in means previously never thought possible. Transnational organised crime groups, who have exploited these new technologies as basis for their criminal success, however, have not overlooked this development, growth and globalisation. Law enforcement agencies have been confronted with an unremitting challenge as they endeavour to intercept, monitor and analyse these communications as a means of disrupting the activities of criminal enterprises. The challenge lies in the ability to recognise and change tactics to match an increasingly sophisticated adversary. The use of communication interception technology, such as phone taps or email interception, is a tactic that when used appropriately has the potential to cause serious disruption to criminal enterprises. Despite the research that exists on CIT and TOC, these two bodies of knowledge rarely intersect. This paper builds on current literature, drawing them together to provide a clearer picture of the use of CIT in an enforcement and intelligence capacity. It provides a review of the literature pertaining to TOC, the structure of criminal enterprises and the vulnerability of communication used by these crime groups. Identifying the current contemporary models of policing it reviews intelligence-led policing as the emerging framework for modern policing. Finally, it assesses the literature concerning CIT, its uses within Australia and the limitations and arguments that exist. In doing so, this paper provides practitioners with a clearer picture of the use, barriers and benefits of using CIT in the fight against TOC. It helps to bridge the current gaps in modern policing theory and offers a perspective that can help drive future research.
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Reactive oxygen species (ROS) form as a natural by-product of the normal metabolism of oxygen and play important roles within the cell. Under normal circumstances the cell is able to maintain an adequate homeostasis between the formation of ROS and its removal through particular enzymatic pathways or via antioxidants. If however, this balance is disturbed a situation called oxidative stress occurs. Critically, oxidative stress plays important roles in the pathogenesis of many diseases, including cancer. Epigenetics is a process where gene expression is regulated by heritable mechanisms that do not cause any direct changes to the DNA sequence itself, and disruption of epigenetic mechanisms has important implications in disease. Evidence is emerging that histone deacetylases (HDACs) play decisive roles in regulating important cellular oxidative stress pathways including those involved with sensing oxidative stress and those involved with regulating the cellular response to oxidative stress. In particular aberrant regulation of these pathways by HDACs may play critical roles in cancer progression. In this review we discuss the current evidence linking epigenetics and oxidative stress and cancer, using chronic obstructive pulmonary disease and non-small cell lung cancer to illustrate the importance of epigenetics on these pathways within these disease settings. © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
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We found that procaspase 8 was overexpressed in non-small-cell lung cancers (NSCLCs) compared with matched normal tissues. The caspase 8 inhibitor FLICE-inhibitory protein (FLIP) was also overexpressed in the majority of NSCLCs. Silencing FLIP induced caspase 8 activation and apoptosis in NSCLC cell lines, but not in normal lung cell lines. Apoptosis induced by FLIP silencing was mediated by the TRAIL death receptors DR4 and DR5, but was not dependent on ligation of the receptors by TRAIL. Furthermore, the apoptosis induced by FLIP silencing was dependent on the overexpression of procaspase 8 in NSCLC cells. Moreover, in NSCLC cells, but not in normal cells, FLIP silencing induced co-localization of DR5 and ceramide, and disruption of this co-localization abrogated apoptosis. FLIP silencing supra-additively increased TRAIL-induced apoptosis of NSCLC cells; however, normal lung cells were resistant to TRAIL, even when FLIP was silenced. Importantly, FLIP silencing sensitized NSCLC cells but not normal cells to chemotherapy in vitro, and silencing FLIP in vivo retarded NSCLC xenograft growth and enhanced the anti-tumour effects of cisplatin. Collectively, our results suggest that due to frequent procaspase 8 overexpression, NSCLCs may be particularly sensitive to FLIP-targeted therapies.
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We report the first successful Agrobacterium-mediated transformation of Australian elite rice cultivars, Jarrah and Amaroo, using binary vectors with our improved promoters and selectable markers. Calli derived from mature embryos were used as target tissues. The binary vectors contained hph (encoding hygromycin resistance) or bar (encoding herbicide resistance) as the selectable marker gene and uidA (gus) or sgfpS65T as the reporter gene driven by different promoters. Use of Agrobacterium strain AGL1 carrying derivatives of an improved binary vector pWBVec8, wherein the CaMV35S driven hph gene is interrupted by the castor bean catalase 1 intron, produced a 4-fold higher number of independent transgenic lines compared to that produced with the use of strain EHA101 carrying the binary vector pIG121-Hm wherein the CaMV35S driven hph is intronless. The Ubiquitin promoter produced 30-fold higher β-glucuronidase (GUS) activity (derivatives of binary vector pWBVec8) in transgenic plants than the CaMV35S promoter (pIG121-Hm). The two modified SCSV promoters produced GUS activity comparable to that produced by the Ubiquitin promoter. Progeny analysis (R1) for hygromycin resistance and GUS activity with selected lines showed both Mendelian and non-Mendelian segregation. Lines showing very high levels of GUS activity in T0 showed a reduced level of GUS activity in their T1 progeny, while lines with moderate levels of GUS activity showed increased levels in T1 progeny. Stable heritable green fluorescent protein (GFP) expression was also observed in few transgenic plants produced with the binary vector pTO134 which had the CaMV35S promoter-driven selectable marker gene bar and a modified CaMV35S promoter-driven reporter gene sgfpS65T.
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Forming peer alliances to share and build knowledge is an important aspect of community arts practice, and these co-creation processes are increasingly being mediated by the internet. This paper offers guidance for practitioners who are interested in better utilising the internet to connect, share, and make new knowledge. It argues that new approaches are required to foster the organising activities that underpin online co-creation, building from the premise that people have become increasingly networked as individuals rather than in groups (Rainie and Wellman 2012: 6), and that these new ways of connecting enable new modes of peer-to-peer production and exchange. This position advocates that practitioners move beyond situating the internet as a platform for dissemination and a tool for co-creating media, to embrace its knowledge collaboration potential. Drawing on a design experiment I developed to promote online knowledge co-creation, this paper suggests three development phases – developing connections, developing ideas, and developing agility – to ground six methods. They are: switching and routing, engaging in small trades of ideas with networked individuals; organising, co-ordinating networked individuals and their data; beta-release, offering ‘beta’ artifacts as knowledge trades; beta-testing, trialing and modifying other peoples ‘beta’ ideas; adapting, responding to technological disruption; and, reconfiguring, embracing opportunities offered by technological disruption. These approaches position knowledge co-creation as another capability of the community artist, along with co-creating art and media.
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Effective social work practice with Aboriginal peoples and communities requires knowledge of operational communication skills and practice methods. In addition, there is also a need for practitioners to be aware of the history surrounding white engagement with Aboriginal communities and their cultures. Indeed, the Australian Association of Social Workers (AASW) acknowledges the importance of social workers practising cultural safety. Engendering knowledge of cultural safety for social work students is the opportunity to listen and talk with Aboriginal people who have experienced the destructive impacts of colonisation and the subsequent disruption to family and community. This article discusses the use of field experiences within a Masters of Social Work (Qualifying) Program (MSW) as an educational method aimed at increasing student awareness of contemporary Aboriginal issues and how to practice effectively and within a culturally safe manner.
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Most persistent organic pollutants (POPs) like polychlorinated biphenyls (PCBs), a range of polybrominated diphenyl ethers (PBDEs) and organochlorine pesticides (OCPs) are readily absorbed (via the ingestion and inhalation) and accumulate in fatty tissue, including adipose tissue and human milk [1]. Health effects related to exposure to these chemicals may include neurological effects, altered functioning of the nervous system and/or endocrine disruption [2-4]. The burden of environmental disease is recognized as much higher for children than adults, especially in young children under 5 years of age worldwide [5]. There is increased concern regarding the environmental impact on the health of children who have been disproportionately affected by environmental problems. For example they may be subjected to relatively higher exposure, have greater physiological susceptibility and/or suffer more extreme consequences due to growth [6-9]. It is therefore worthwhile to assess the correlation between burden of disease and exposure to xenobiotic chemical pollutants like POPs. Such assessment may provide guidance for legislative changes regarding chemical bans and give reliable advice to parents including lactating mothers.
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The advances made within the aviation industry over the past several decades have significantly improved the availability, affordability and convenience of air travel and have been greatly beneficial in both social and economic terms. Air transport has developed into an irreplaceable service being relied on by millions of people each day and as such airports have become critical elements of national infrastructure to facilitate the movement of people and goods. As components of critical infrastructure (CI), airports are integral parts of a national economy supporting regional as well as national trade, commercial activity and employment. Therefore, any disruption or crisis which impacts the continuity of operations at airports can have significant negative consequences for the airport as a business, for the local economy and other nodes of transport infrastructure as well as for society. Due to the highly dynamic and volatile environment in which airports operate in, the aviation industry has faced many different challenges over the years ranging from terrorist attacks such as September 11, to health crises such as the SARS epidemic to system breakdowns such as the recent computer system outage at Virgin Blue Airlines in Australia. All these events have highlighted the vulnerability of airport systems to a range of disturbances as well as the gravity and widespread impact of any kind of discontinuity in airport functions. Such incidents thus emphasise the need for increasing resilience and reliability of airports and ensuring business continuity in the event of a crisis...
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We previously showed that integrin alphavbeta3 overexpression and engagement by its ligand vitronectin increased adhesion, motility, and proliferation of human ovarian cancer cells. In search of differentially regulated genes involved in these tumor biological events, we previously identified the integrin-linked kinase (ILK) to be under control of alphavbeta3. In the present investigation we demonstrated significantly upregulated ILK protein as a function of alphavbeta3 in two ovarian cancer cell lines, OV-MZ-6 and OVCAR-3, and proved co-localization at the surface of alphavbeta3-overexpressing cells adherent to vitronectin. Increase of ILK protein was reflected by enhanced ILK promoter activity, an effect, which we further characterized with regard to transcriptional response elements involved. Abrogation of NF-kappaB/c-rel or p53 binding augmented ILK promoter activity and preserved induction by alphavbeta3. The AP1-mutant exhibited decreased promoter activity but was also still inducible by alphavbeta3. Disruption of the two DNA consensus motifs for Ets proteins led to divergent observations: mutation of the Ets motif at promoter position -462 bp did not significantly alter promoter activity but still allowed response to alphavbeta3. In contrast, disruption of the second Ets motif at position -85 bp did not only lead to slightly diminished promoter activity but also, in that case, abrogated ILK promoter induction by alphavbeta3. Subsequent co-transfection studies with ets-1 in the presence of the second Ets motif led to additional induction of ILK promoter activity. Taken together, these data suggest that ets-1 binding to the second Ets DNA motif strongly contributes to alphavbeta3-mediated ILK upregulation. By increasing ILK as an important integrin-proximal kinase, alphavbeta3 may promote its intracellular signaling and tumor biological processes arising thereof in favor of ovarian cancer metastasis.
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The term ‘‘new media’’ has been in play for decades now, and one might be forgiven for wondering how much longer digital forms and platforms can really be called ‘‘new,’’ or even what the scholarship of new media contributes to knowledge. Is it possible to say new things about new media? We think so. This Companion not only demonstrates the variety, salience, and importance of new media studies but also proposes a distinctive approach to the topic : an approach we call ‘‘new media dynamics.’’ In this view, what’s interesting about ‘‘new media’’ is not novelty as such but dynamism. Capitalism, technology, social networks, and media all evolve and change, sometimes to our delight, sometimes our dismay. This incessant process of disruption, renewal, and eventual (if often partial) replacement is now one of humanity’s central experiences. This cutting-edge collection brings together a stellar array of the world’s top researchers, cultural entrepreneurs, and emerging scholars to give the dynamics of new media their first full-length, multidisciplinary, historical, and critical treatment. Across 34 chapters, an international line-up of the very best authors reflects on the historical, technical, cultural, and political changes that underlie the emergence of new media, as existing patterns and assumptions are challenged by the forces of ‘‘creative destruction’’ and innovation, both economic and cultural. At the same time they show that familiar themes and problems carry through from ‘‘old’’media – questions of identity, sexuality, politics, relationships, and meaning.
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Upon overexpression of integrin αvβ3 and its engagement by vitronectin, we previously showed enhanced adhesion, proliferation, and motility of human ovarian cancer cells. By studying differential expression of genes possibly related to these tumor biological events, we identified the epidermal growth-factor receptor (EGF-R) to be under control of αvβ3 expression levels. Thus in the present study we characterized αvβ3-dependent changes of EGF-R and found significant upregulation of its expression and activity which was reflected by prominent changes of EGF-R promoter activity. Upon disruption of DNA-binding motifs for the transcription factors p53, ETF, the repressor ETR, p50, and c-rel, respectively, we sought to identify DNA elements contributing to αvβ3-mediated EGF-R promoter induction. Both, the p53- and ETF-mutant, while exhibiting considerably lower EGF-R promoter activity than the wild type promoter, retained inducibility by αvβ3. Mutation of the repressor motif ETR, as expected, enhanced EGF-R promoter activity with a further moderate increase upon αvβ3 elevation. The p50-mutant displayed EGF-R promoter activity almost comparable to that of the wild type promoter with no impairment of induction by αvβ3. However, the activity of an EGF-R promoter mutant displaying a disrupted c-rel-binding motif did not only prominently decline, but, moreover, was not longer responsive to enhanced αvβ3, involving this DNA element in αvβ3-dependent EGF-R upregulation. Moreover, αvβ3 did not only increase the EGF-R but, moreover, also led to obvious co-clustering on the cancer cell surface. By studying αvβ3/EGF-R-effects on the focal adhesion kinase (FAK) and the mitogen activated protein kinases (MAPK) p44/42 (erk−1/erk−2), having important functions in synergistic crosstalk between integrins and growth-factor receptors, we found for both significant enhancement of expression and activity upon αvβ3/VN interaction and cell stimulation by EGF. Upregulation of the EGF-R by integrin αvβ3, both receptor molecules with a well-defined role as targets for cancer treatment, might represent an additional mechanism to adapt synergistic receptor signaling and crosstalk in response to an altered tumor cell microenvironment during ovarian cancer progression.
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A total of 1,625 tornadoes occurred in the United States in 2011, resulting in economic losses that exceeded $25 billion. Two tornado outbreaks stand out because they caused more than half of those losses. The tornadoes that cut through Tuscaloosa, Alabama, on April 27 and Joplin, Missouri, on May 22 were responsible for a combined 223 fatalities and more than 13,000 damaged buildings in the two cities. Although the economic losses associated with tornado damage are well documented, the writers argue that the overall impact should encompass longer term, broader considerations such as the social disruption and psychological effects that impact communities. This paper examines observations by tornado damage assessment teams led by the first author in these two medium-sized cities and suggests that the evolution of building codes and past approaches to construction have led to conditions that made this extent of damage possible. The authors outline a multidisciplinary path forward that incorporates engineering research and social and economic studies into a new design paradigm leading to building code changes and social practices that will improve resistance and mitigate future losses at a community level from tornadoes.