39 resultados para Jung, C. G. (Carl Gustav), 1875-1961

em Queensland University of Technology - ePrints Archive


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Caulfield, Harold William; p.131 Cowan, Alexander; p.164 Cowley, Ebenezer; p.164 East Talgai Station; p.193 Eaves, S.H.; p.193-194 Edgar, J.S.; p.196 Everist, Selwyn; p.206 Experimental Farms and Gardens; pp.207-208 Government Houses - Queensland; pp.267-268

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In this paper I integrate the work of a number of philosophers to clarify some psychological issues that can arise in human existence when a conflict of intrapersonal or interpersonal desires arises. This paper utilises the work of Deleuze, Freud, Jung, Heidegger, Hegel and Nietzsche to provide a conceptual framework as to how mental disturbances can arise if unconscious desires cannot be satisfied due to the experience of a resistance from a conflicting or opposing desire. This paper argues that the phenomenal experience of a conflict of desires can be unconcealed in moments of un-readiness-to-hand and from the awareness of the psychophysiological experience of stress or angst. The work that is presented, results in the conclusion that it is fundamentally necessary to embrace Nietzsche’s idea of the ‘will to power’ to overcome these difficulties and to achieve personal individuation and authentic wellbeing. This advice is in contrast to an inauthentic choice of depending on the use of Freudian defence mechanisms to conceal a conflict of desires from consciousness. A detailed theoretical example of the process involved in the resolution of a conflict of desires through self-transcendence is specifically informed by the ideas of Nietzsche and Jung.

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To identify new susceptibility loci for psoriasis, we undertOk a genome-wide asociation study of 594,224 SNPs in 2,622 individuals with psoriasis and 5,667 controls. We identified asociations at eight previously unreported genomic loci. Seven loci harbored genes with recognized iMune functions (IL28RA, REL, IFIH1, ERAP1, TRAF3IP2, NFKBIA and TYK2). These asociations were replicated in 9,079 European samples (six loci with a combined P < 5-10 -8 and two loci with a combined P < 5-10-7). We also report compeLing evidence for an interaction betwEn the HLA-C and ERAP1 loci (combined P = 6.95-10-6). ERAP1 plays an important role in MHC claS I peptide proceSing. ERAP1 variants only influenced psoriasis susceptibility in individuals carrying the HLA-C risk aLele. Our findings implicate pathways that integrate epidermal barrier dysfunction with iNate and adaptive iMune dysregulation in psoriasis pathogenesis.

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Dolomite mineral samples having white and light green colours of Indian origin have been characterized by EPR, optical and NIR spectroscopy. The optical spectrum exhibits a number of electronic bands due to presence of Fe(III) ions in the mineral. From EPR studies, the parameters of g for Fe(III) and g, A and D for Mn(II) are evaluated and the data confirm that the ions are in distorted octahedron. Optical absorption studies reveal that Fe(III) is in distorted octahedron. The bands in NIR spectra are due to the overtones and combinations of water molecules. Thus EPR and optical absorption spectral studies have proven useful for the study of the chemistry of dolomite.

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EPR study of both blue and green sapphire samples confirms the presence of Cr(III) in four different octahedral sites. The g (1.98) value is the same but D values differ for the two the samples. The EPR spectra suggest that the blue sapphire contains more chromium than the green sapphire. No Fe(III) impurity was noted in the EPR spectrum.

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Knowledge of the regulation of food intake is crucial to an understanding of body weight and obesity. Strictly speaking, we should refer to the control of food intake whose expression is modulated in the interests of the regulation of body weight. Food intake is controlled, body weight is regulated. However, this semantic distinction only serves to emphasize the importance of food intake. Traditionally food intake has been researched within the homeostatic approach to physiological systems pioneered by Claude Bernard, Walter Cannon and others; and because feeding is a form of behaviour, it forms part of what Curt Richter referred to as the behavioural regulation of body weight (or behavioural homeostasis). This approach views food intake as the vehicle for energy supply whose expression is modulated by a metabolic drive generated in response to a requirement for energy. The idea was that eating behaviour is stimulated and inhibited by internal signalling systems (for the drive and suppression of eating respectively) in order to regulate the internal environment (energy stores, tissue needs).

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The CDKN2 gene, encoding the cyclin dependent kinase inhibitor p16, is a tumour suppressor gene involved in melanoma and maps to chromosome band 9p22. Mutations or interstitial deletions of this gene have been found both in the germline of familial melanoma cases and somatically in melanoma cell lines. Previous mutation analyses of melanoma cell lines have indicated a high frequency of C:G to T:A transitions, with all of these mutations occurring at dipyrimidine sites. Including three melanoma cell lines carrying tandem CC to TT mutations, the spectrum of mutations so far reported indicates a possible role for u.v. radiation in the mutagenesis of this gene in some tumours. To further examine this hypothesis we have characterised mutations of the CDKN2 gene in 30 melanoma cell lines. Nineteen lines carried complete or partial homozygous deletions of the gene. Of the remaining cell lines, eight were shown by direct sequencing of PCR products from exon 1 and exon 2 to carry a total of nine different mutations of CDKN2. Two cell lines carried tandem CC to TT mutations and a high rate of C:G to T:A transitions was observed. This study provides further evidence for the role of u.v. light in the genesis of melanoma, with one target being the CDKN2 tumour suppressor gene.

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Review of Coping with Choices to Die, by C. G. Prado. Cambridge: Cambridge University Press, 2011.

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The present study examined experimentally the phenological responses of a range of plant species to rises in temperature. We used the climate-change field protocol of the International Tundra Experiment (ITEX), which measures plant responses to warming of 1 to 2°C inside small open-topped chambers. The field study was established on the Bogong High Plains, Australia, in subalpine open heathlands; the most common treeless plant community on the Bogong High Plains. The study included areas burnt by fire in 2003, and therefore considers the interactive effects of warming and fire, which have rarely been studied in high mountain environments. From November 2003 to March 2006, various phenological phases were monitored inside and outside chambers during the snow-free periods. Warming resulted in earlier occurrence of key phenological events in 7 of the 14 species studied. Burning altered phenology in 9 of 10 species studied, with both earlier and later phenological changes depending on the species. There were no common phenological responses to warming or burning among species of the same family, growth form or flowering type (i.e. early or late-flowering species), when all phenological events were examined. The proportion of plants that formed flower buds was influenced by fire in half of the species studied. The findings support previous findings of ITEX and other warming experiments; that is, species respond individualistically to experimental warming. The inter-year variation in phenological response, the idiosyncratic nature of the responses to experimental warming among species, and an inherent resilience to fire, may result in community resilience to short-term climate change. In the first 3 years of experimental warming, phenological responses do not appear to be driving community-level change. Our findings emphasise the value of examining multiple species in climate-change studies.

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Recombinant human papillomavirus (HPV) virus-like particles (VLPs) made from the major capsid protein L1 are promising vaccine candidates for use as vaccines against genital and other HPV infections, and particularly against HPV-16. However, HPV-16 genotype variants have different binding affinities for neutralising mouse Mabs raised against HPV-16 L1 VLPs. This paper analyses, using a panel of well-characterised Mabs, the effects on the antigenicity of various C- and N-terminal deletants of HPV-16 L1 made in insect cells via recombinant baculovirus, of an A → T mutation at residue 266 (A266T), and of a C G mutation at conserved position 428 (C428G). The effects of these changes on assembly of the variant L1s were studied by electron microscopy. Binding of Mab H16:E70 to A266T was reduced by almost half in comparison to wild type L1. Retention of the C-terminal region 428-483 was critical for the binding of conformation-specific Mabs (H16:V5, H16:E70, H16:U4 and H16:9A) whereas deletion of the nuclear localisation signal (NLS) or the C428G mutation or an N-terminal deletion (residues 2-9) did not affect the antigenicity. The N-terminal deletion resulted in a mixed population of 30 and 55 nm VLPs, which differs from the same construct expressed in Escherichia coli, whereas pentamer aggregates resulted from deletion of the 428-465 region or the C428G mutation. The results have implications both for considering use of single-genotype HPV vaccines, and for design of novel second-generation vaccines. © 2006 Elsevier B.V. All rights reserved.

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Background Post traumatic stress disorder (PTSD) and depressive disorder are over represented in combat veterans. Veterans with both disorders have an increased risk of suicide. The nitric oxide synthase 1 adaptor protein (NOS1AP) gene, which modulates stress-evoked N-methyl-D-aspartate (NMDA) activity, was investigated in combat veterans. Methods A comprehensive genetic analysis of NOS1AP and its association with PTSD was investigated in Vietnam combat veterans with PTSD (n=121) and a group of healthy control individuals (n=237). PTSD patients were assessed for symptom severity and level of depression using the Mississippi Scale for Combat-Related PTSD and the Beck Depression Inventory-II (BDI). Results The G allele of NOS1AP SNP rs386231 was significantly associated with PTSD (p = 0.002). Analysis of variance revealed significant differences in BDI-II and Mississippi scores between genotypes for rs386231 with the GG genotype associated with increased severity of depression (p = 0.002 F = 6.839) and higher Mississippi Scale for Combat-Related PTSD scores (p = 0.033). Haplotype analysis revealed that the C/G haplotype (rs451275/rs386231) was significantly associated with PTSD (p = 0.001). Limitations The sample sizes in our study were not sufficient to detect SNP associations with very small effects. In addition the study was limited by its cross sectional design. Conclusions This is the first study reporting that a variant of the NOS1AP gene is associated with PTSD. Our data also suggest that a genetic variant in NOS1AP may increase the susceptibility to severe depression in patients with PTSD and increased risk for suicide.

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Antibodies can play a protective but non-essential role in natural chlamydial infections dependent on antigen specificity and antibody isotype. IgG is the dominant antibody in both male and female reproductive tract mucosal secretions, and is bi-directionally trafficked across epithelia by the neonatal Fc receptor (FcRn). Using physiologically relevant pH-polarized epididymal epithelia grown on Transwells®, IgG specifically targeting an extracellular chlamydial antigen; the Major Outer Membrane Protein (MOMP), enhanced uptake and translocation of infection at pH 6-6.5 but not at neutral pH. This was dependent on FcRn expression. Conversely, FcRn-mediated transport of IgG targeting the intracellular chlamydial inclusion membrane protein A (IncA), induced aberrant inclusion morphology, recruited autophagic proteins independent of lysosomes, and significantly reduced infection. Challenge of female mice with MOMP-specific IgG-opsonized C. muridarum delayed infection clearance but exacerbated oviduct occlusion. In male mice, MOMP-IgG elicited by immunization afforded no protection against testicular chlamydial infection, whereas; the transcytosis of IncA-IgG significantly reduced testicular chlamydial burden. Together these data show that the protective and pathological effects of IgG are dependent on FcRn-mediated transport as well as the specificity of IgG for intracellular or extracellular antigens.

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Most vaccines developed against Chlamydia using animal models provide partial protection against a genital tract infection. However, protection against the oviduct pathology associated with infertility is highly variable and often has no defining immunological correlate. When comparing two adjuvants (CTA1-DD and a combination of Cholera toxin plus CpG- oligodeoxynucleotide–CT/CpG) combined with the chlamydial major outer membrane protein (MOMP) antigen and delivered via the intranasal (IN), sublingual (SL) or transcutaneous (TC) routes, we identified two vaccine groups with contrasting outcomes following infection. SL immunization with MOMP/CTA1-DD induced a 70% reduction in the incidence of oviduct pathology, without significantly altering the course of infection. Conversely, IN immunization with MOMP/CT/CpG prevented an ascending infection, but not the oviduct pathology. This anomaly presented a unique opportunity to study the mechanisms by which vaccines can prevent oviduct pathology, other than by controlling the infection. The IL-17 signaling in the oviducts was found to associate with both the enhancement of immunity to infection and the development of oviduct pathology. This conflicting role of IL-17 may provide some explanation for the discordance in protection between infection and disease and suggests that controlling immunopathology, as opposed to the rapid eradication of the infection, may be essential for an effective human chlamydial vaccine that prevents infertility.

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In this work, 17-polychlorinated dibenzo-pdioxin/furan (PCDD/Fs) isomers were measured in ambient air at four urban sites in Seoul, Korea (from February to June 2009). The concentrations of their summed values RPCDD/Fs) across all four sites ranged from 1,947 (271 WHO05 TEQ) (Jong Ro) to 2,600 (349 WHO05 TEQ) fg/m3 (Yang Jae) with a mean of 2,125 ± 317) fg/m3 (292 WHO05 TEQ fg/m3). The sum values for the two isomer groups of RPCDD and RPCDF were 527 (30 WHO05 TEQ) and 1,598 (263 WHO05 TEQ) fg/m3, respectively. The concentration profile of individual species was dominated by the 2,3,4,7,8-PeCDF isomer, which contributed approximately 36 % of the RPCDD/Fs value. The observed temporal trends in PCDD/F concentrations were characterized by relative enhancement in the winter and spring. The relative contribution of different sources, when assessed by principal component analysis, is explained by the dominance of vehicular emissions along with coal (or gas) burning as the key source of ambient PCDD/Fs in the residential areas studied.

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Tobacco smoking, alcohol drinking, and occupational exposures to polycyclic aromatic hydrocarbons are the major proven risk factors for human head and neck squamous-cell cancer (HNSCC). Major research focus on gene-environment interactions concerning HNSCC has been on genes encoding enzymes of metabolism for tobacco smoke constituents and repair enzymes. To investigate the role of genetically determined individual predispositions in enzymes of xenobiotic metabolism and in repair enzymes under the exogenous risk factor tobacco smoke in the carcinogenesis of HNSCC, we conducted a case-control study on 312 cases and 300 noncancer controls. We focused on the impact of 22 sequence variations in CYP1A1, CYP1B1, CYP2E1, ERCC2/XPD, GSTM1, GSTP1, GSTT1, NAT2, NQO1, and XRCC1. To assess relevant main and interactive effects of polymorphic genes on the susceptibility to HNSCC we used statistical models such as logic regression and a Bayesian version of logic regression. In subgroup analysis of nonsmokers, main effects in ERCC2 (Lys751Gln) C/C genotype and combined ERCC2 (Arg156Arg) C/A and A/A genotypes were predominant. When stratifying for smokers, the data revealed main effects on combined CYP1B1 (Leu432Val) C/G and G/G genotypes, followed by CYP1B1 (Leu432Val) G/G genotype and CYP2E1 (-70G>T) G/T genotype. When fitting logistic regression models including relevant main effects and interactions in smokers, we found relevant associations of CYP1B1 (Leu432Val) C/G genotype and CYP2E1 (-70G>T) G/T genotype (OR, 10.84; 95% CI, 1.64-71.53) as well as CYP1B1 (Leu432Val) G/G genotype and GSTM1 null/null genotype (OR, 11.79; 95% CI, 2.18-63.77) with HNSCC. The findings underline the relevance of genotypes of polymorphic CYP1B1 combined with exposures to tobacco smoke.