999 resultados para Pauli-like contributions


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Voluminous (≥3·9 × 105 km3), prolonged (∼18 Myr) explosive silicic volcanism makes the mid-Tertiary Sierra Madre Occidental province of Mexico one of the largest intact silicic volcanic provinces known. Previous models have proposed an assimilation–fractional crystallization origin for the rhyolites involving closed-system fractional crystallization from crustally contaminated andesitic parental magmas, with <20% crustal contributions. The lack of isotopic variation among the lower crustal xenoliths inferred to represent the crustal contaminants and coeval Sierra Madre Occidental rhyolite and basaltic andesite to andesite volcanic rocks has constrained interpretations for larger crustal contributions. Here, we use zircon age populations as probes to assess crustal involvement in Sierra Madre Occidental silicic magmatism. Laser ablation-inductively coupled plasma-mass spectrometry analyses of zircons from rhyolitic ignimbrites from the northeastern and southwestern sectors of the province yield U–Pb ages that show significant age discrepancies of 1–4 Myr compared with previously determined K/Ar and 40Ar/39Ar ages from the same ignimbrites; the age differences are greater than the errors attributable to analytical uncertainty. Zircon xenocrysts with new overgrowths in the Late Eocene to earliest Oligocene rhyolite ignimbrites from the northeastern sector provide direct evidence for some involvement of Proterozoic crustal materials, and, potentially more importantly, the derivation of zircon from Mesozoic and Eocene age, isotopically primitive, subduction-related igneous basement. The youngest rhyolitic ignimbrites from the southwestern sector show even stronger evidence for inheritance in the age spectra, but lack old inherited zircon (i.e. Eocene or older). Instead, these Early Miocene ignimbrites are dominated by antecrystic zircons, representing >33 to ∼100% of the dated population; most antecrysts range in age between ∼20 and 32 Ma. A sub-population of the antecrystic zircons is chemically distinct in terms of their high U (>1000 ppm to 1·3 wt %) and heavy REE contents; these are not present in the Oligocene ignimbrites in the northeastern sector of the Sierra Madre Occidental. The combination of antecryst zircon U–Pb ages and chemistry suggests that much of the zircon in the youngest rhyolites was derived by remelting of partially molten to solidified igneous rocks formed during preceding phases of Sierra Madre Occidental volcanism. Strong Zr undersaturation, and estimations for very rapid dissolution rates of entrained zircons, preclude coeval mafic magmas being parental to the rhyolite magmas by a process of lower crustal assimilation followed by closed-system crystal fractionation as interpreted in previous studies of the Sierra Madre Occidental rhyolites. Mafic magmas were more probably important in providing a long-lived heat and material flux into the crust, resulting in the remelting and recycling of older crust and newly formed igneous materials related to Sierra Madre Occidental magmatism.

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Recent studies have demonstrated that IGF-I associates with VN through IGF-binding proteins (IGFBP) which in turn modulate IGF-stimulated biological functions such as cell proliferation, attachment and migration. Since IGFs play important roles in transformation and progression of breast tumours, we aimed to describe the effects of IGF-I:IGFBP:VN complexes on breast cell function and to dissect mechanisms underlying these responses. In this study we demonstrate that substrate-bound IGF-I:IGFBP:VN complexes are potent stimulators of MCF-7 breast cell survival, which is mediated by a transient activation of ERK/MAPK and sustained activation of PI3-K/AKT pathways. Furthermore, use of pharmacological inhibitors of the MAPK and PI3-K pathways confirms that both pathways are involved in IGF-I:IGFBP:VN complex-mediated increased cell survival. Microarray analysis of cells stimulated to migrate in response to IGF-I:IGFBP:VN complexes identified differential expression of genes with previously reported roles in migration, invasion and survival (Ephrin-B2, Sharp-2, Tissue-factor, Stratifin, PAI-1, IRS-1). These changes were not detected when the IGF-I analogue (\[L24]\[A31]-IGF-I), which fails to bind to the IGF-I receptor, was substituted; confirming the IGF-I-dependent differential expression of genes associated with enhanced cell migration. Taken together, these studies have established that IGF-I:IGFBP:VN complexes enhance breast cell migration and survival, processes central to facilitating metastasis. This study highlights the interdependence of ECM and growth factor interactions in biological functions critical for metastasis and identifies potential novel therapeutic targets directed at preventing breast cancer progression.

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Objective: This study documents the mental health status of people from Burmese refugee backgrounds, recently arrived in Australia; then examines the contributions of gender, premigration and postmigration factors in predicting mental health. Method: Structured interviews, including a demographic questionnaire, the Harvard Trauma Questionnaire, Postmigration Living Difficulties Checklist and Hopkins Symptom Checklist assessed premigration trauma, postmigration living difficulties, depression, anxiety, somatisation and traumatisation symptoms in a sample of 70 adults across five Burmese ethnic groups. Results: Substantial proportions of participants reported psychological distress in symptomatic ranges including: posttraumatic stress disorder (9%); anxiety (20%), and; depression (36%), as well as significant symptoms of somatisation (37%). Participants reported multiple and severe premigration traumas. Postmigration living difficulties of greatest concern included communication problems and worry about family not in Australia. Gender did not predict mental health. Level of exposure to traumatic events and postmigration living difficulties each made unique and relatively equal contributions to traumatisation symptoms. Postmigration living difficulties made unique contributions to depression, anxiety and somatisation symptoms. Conclusions: While exposure to traumatic events impacted on participants’ mental wellbeing, postmigration living difficulties had greater salience in predicting mental health outcomes of people from Burmese refugee backgrounds. Reported rates of posttraumatic stress disorder symptoms were consistent with a large review of adults across seven western countries. High levels of somatisation pointed to a nuanced expression of distress. Findings have implications for service provision in terms of implementing appropriate interventions to effectively meet the needs of this newly arrived group in Australia.

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Shelton, E.M. (p.548); Sherwood Arboretum (p.550); Soutter, William (pp.563-4); Styles (pp.575-6); Summer-House (579-580); Trapnell, W.G. (p.602); Tropical Gardens (pp.604-5);Verandah Gardening (p.614); Wickham Park (p.642); Wijaya, Made (p.642); Williams, George (p.644); Williams Keith A (p.644).

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This paper explores how visibly transgressing heteronormativity shapes police interactions with LGBT young people. While research evidences how sexually and gender diverse bodies can be abused in schools, policing is overlooked. Interviews with 35 LGBT young people demonstrate how bodies transgressing heteronormativity (that is, non-heteronormative bodies) mediate their policing experiences in Queensland, Australia. Drawing on Foucault, Butler, and others, the paper suggests police interactions and use of discretion with LGBT young people was informed by non-heteronormative bodies discursively performing queerness in ways read by police. The paper concludes noting tensions produced for youthful LGBT bodies in public spaces.

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Intrinsically photosensitive retinal ganglion cells (ipRGCs) in the eye transmit the environmental light level, projecting to the suprachiasmatic nucleus (SCN) (Berson, Dunn & Takao, 2002; Hattar, Liao, Takao, Berson & Yau, 2002), the location of the circadian biological clock, and the olivary pretectal nucleus (OPN) of the pretectum, the start of the pupil reflex pathway (Hattar, Liao, Takao, Berson & Yau, 2002; Dacey, Liao, Peterson, Robinson, Smith, Pokorny, Yau & Gamlin, 2005). The SCN synchronizes the circadian rhythm, a cycle of biological processes coordinated to the solar day, and drives the sleep/wake cycle by controlling the release of melatonin from the pineal gland (Claustrat, Brun & Chazot, 2005). Encoded photic input from ipRGCs to the OPN also contributes to the pupil light reflex (PLR), the constriction and recovery of the pupil in response to light. IpRGCs control the post-illumination component of the PLR, the partial pupil constriction maintained for > 30 sec after a stimulus offset (Gamlin, McDougal, Pokorny, Smith, Yau & Dacey, 2007; Kankipati, Girkin & Gamlin, 2010; Markwell, Feigl & Zele, 2010). It is unknown if intrinsic ipRGC and cone-mediated inputs to ipRGCs show circadian variation in their photon-counting activity under constant illumination. If ipRGCs demonstrate circadian variation of the pupil response under constant illumination in vivo, when in vitro ipRGC activity does not (Weng, Wong & Berson, 2009), this would support central control of the ipRGC circadian activity. A preliminary experiment was conducted to determine the spectral sensitivity of the ipRGC post-illumination pupil response under the experimental conditions, confirming the successful isolation of the ipRGC response (Gamlin, et al., 2007) for the circadian experiment. In this main experiment, we demonstrate that ipRGC photon-counting activity has a circadian rhythm under constant experimental conditions, while direct rod and cone contributions to the PLR do not. Intrinsic ipRGC contributions to the post-illumination pupil response decreased 2:46 h prior to melatonin onset for our group model, with the peak ipRGC attenuation occurring 1:25 h after melatonin onset. Our results suggest a centrally controlled evening decrease in ipRGC activity, independent of environmental light, which is temporally synchronized (demonstrates a temporal phase-advanced relationship) to the SCN mediated release of melatonin. In the future the ipRGC post-illumination pupil response could be developed as a fast, non-invasive measure of circadian rhythm. This study establishes a basis for future investigation of cortical feedback mechanisms that modulate ipRGC activity.

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Objectives The p38 mitogen-activated protein kinase (MAPK) signal transduction pathway is involved in a variety of inflammatory responses, including cytokine generation, cell differentiation proliferation and apoptosis. Here, we examined the effects of systemic p38 MAPK inhibition on cartilage cells and osteoarthritis (OA) disease progression by both in vitro and in vivo approaches. Methods p38 kinase activity was evaluated in normal and OA cartilage cells by measuring the amount of phosphorylated protein. To examine the function of p38 signaling pathway in vitro, normal chondrocytes were isolated and differentiated in the presence or absence of p38 inhibitor; SB203580 and analysed for chondrogenic phenotype. Effect of systemic p38 MAPK inhibition in normal and OA (induced by menisectomy) rats were analysed by treating animals with vehicle alone (DMS0) or p38 inhibitor (SB203580). Damage to the femur and tibial plateau was evaluated by modified Mankin score, histology and immunohistochemistry. Results Our in vitro studies have revealed that a down-regulation of chondrogenic and increase of hypertrophic gene expression occurs in the normal chondrocytes, when p38 is neutralized by a pharmacological inhibitor. We further observed that the basal levels of p38 phosphorylation were decreased in OA chondrocytes compared with normal chondrocytes. These findings together indicate the importance of this pathway in the regulation of cartilage physiology and its relevance to OA pathogenesis. At in vivo level, systematic administration of a specific p38 MAPK inhibitor, SB203580, continuously for over a month led to a significant loss of proteoglycan; aggrecan and cartilage thickness. On the other hand, SB203580 treated normal rats showed a significant increase in TUNEL positive cells, cartilage hypertrophy markers such as Type 10 collagen, Runt-related transcription factor and Matrix metalloproteinase-13 and substantially induced OA like phenotypic changes in the normal rats. In addition, menisectomy induced OA rat models that were treated with p38 inhibitor showed aggravation of cartilage damage. Conclusions In summary, this study has provided evidence that the component of the p38 MAPK pathway is important to maintain the cartilage health and its inhibition can lead to severe cartilage degenerative changes. The observations in this study highlight the possibility of using activators of the p38 pathway as an alternative approach in the treatment of OA.