975 resultados para DEPENDENT QUANTUM PROBLEMS


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Decoherence of quantum entangled particles is observed in most systems, and is usually caused by system-environment interactions. Disentangling two subsystems A and B of a quantum systemAB is tantamount to erasure of quantum phase relations between A and B. It is widely believed that this erasure is an innocuous process, which e.g. does not affect the energies of A and B. Surprisingly, recent theoretical investigations by different groups showed that disentangling two systems, i.e. their decoherence, can cause an increase of their energies. Applying this result to the context of neutronCompton scattering from H2 molecules, we provide for the first time experimental evidence which supports this prediction. The results reveal that the neutron-proton collision leading to the cleavage of the H-H bond in the sub-femtosecond timescale is accompanied by larger energy transfer (by about 3%) than conventional theory predicts. It is proposed to interpreted the results by considering the neutron-proton collisional system as an entangled open quantum system being subject to decoherence owing to the interactions with the “environment” (i.e., two electrons plus second proton of H2).

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This chapter outlines specific issues relating to behavioural and emotional problems in Aboriginal and Torres Strait Islander young people. It describes the most common disorders and their consequences, and how young Aboriginal people are at higher risk for developing such problems than other young Australians. The chapter also discusses the importance of psychosocial, cultural and environmental issues that need to be recognised in assessing and treating Aboriginal young people with behavioural and emotional problems. Issues concerning the delivery of both universal and culturally responsive prevention and intervention programs to address social and emotional wellbeing and mental health are discussed and possible interventions to enhance student engagement at school are provided. Finally, a range of mental health services for Aboriginal families which offer a culturally responsive approach to mental health treatment are listed.

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Various studies have been conducted to investigate the effects of impact loading on cartilage damage and chondrocyte death. These have shown that the rate and magnitude of the applied strain significantly influence chondrocyte death, and that cell death occurred mostly in the superficial zone of cartilage suggesting the need to further understand the fundamental mechanisms underlying the chondrocytes death induced at certain levels of strain-rate. To date there is no comprehensive study providing insight on this phenomenon. The aim of this study is to examine the strain-rate dependent behavior of a single chondrocyte using a computational approach based on Finite Element Method (FEM). An FEM model was developed using various mechanical models, which were Standard Neo-Hookean Solid (SnHS), porohyperelastic (PHE) and poroviscohyperelastic (PVHE) to simulate Atomic Force Microscopy (AFM) experiments of chondrocyte. The PVHE showed, it can capture both relaxation and loading rate dependent behaviors of chondrocytes, accurately compared to other models.

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We study two problems of online learning under restricted information access. In the first problem, prediction with limited advice, we consider a game of prediction with expert advice, where on each round of the game we query the advice of a subset of M out of N experts. We present an algorithm that achieves O(√(N/M)TlnN ) regret on T rounds of this game. The second problem, the multiarmed bandit with paid observations, is a variant of the adversarial N-armed bandit game, where on round t of the game we can observe the reward of any number of arms, but each observation has a cost c. We present an algorithm that achieves O((cNlnN) 1/3 T2/3+√TlnN ) regret on T rounds of this game in the worst case. Furthermore, we present a number of refinements that treat arm- and time-dependent observation costs and achieve lower regret under benign conditions. We present lower bounds that show that, apart from the logarithmic factors, the worst-case regret bounds cannot be improved.

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The effect of two different DNA minor groove binding molecules, Hoechst 33258 and distamycin A, on the binding kinetics of NF-κB p50 to three different specific DNA sequences was studied at various salt concentrations. Distamycin A was shown to significantly increase the dissociation rate constant of p50 from the sequences PRDII (5′-GGGAAATTCC-3′) and Ig-κ B (5′-GGGACTTTCC-3′) but had a negligible effect on the dissociation from the palindromic target-κB binding site (5′-GGGAATTCCC-3′). By comparison, the effect of Hoechst 33258 on binding of p50 to each sequence was found to be minimal. The dissociation rates for the protein–DNA complexes increased at higher potassium chloride concentrations for the PRDII and Ig-κB binding motifs and this effect was magnified by distamycin A. In contrast, p50 bound to the palindromic target-κB site with a much higher intrinsic affinity and exhibited a significantly reduced salt dependence of binding over the ionic strength range studied, retaining a KD of less than 10 pM at 150 mM KCl. Our results demonstrate that the DNA binding kinetics of p50 and their salt dependence is strongly sequence-dependent and, in addition, that the binding of p50 to DNA can be influenced by the addition of minor groove-binding drugs in a sequence-dependent manner.

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Signals from the tumor microenvironment trigger cancer cells to adopt an invasive phenotype through epithelial-mesenchymal transition (EMT). Relatively little is known regarding key signal transduction pathways that serve as cytosolic bridges between cell surface receptors and nuclear transcription factors to induce EMT. A better understanding of these early EMT events may identify potential targets for the control of metastasis. One rapid intracellular signaling pathway that has not yet been explored during EMT induction is calcium. Here we show that stimuli used to induce EMT produce a transient increase in cytosolic calcium levels in human breast cancer cells. Attenuation of the calcium signal by intracellular calcium chelation significantly reduced epidermal growth factor (EGF)- and hypoxia-induced EMT. Intracellular calcium chelation also inhibited EGF-induced activation of signal transducer and activator of transcription 3 (STAT3), while preserving other signal transduction pathways such as Akt and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. To identify calcium-permeable channels that may regulate EMT induction in breast cancer cells, we performed a targeted siRNA-based screen. We found that transient receptor potential-melastatin-like 7 (TRPM7) channel expression regulated EGF-induced STAT3 phosphorylation and expression of the EMT marker vimentin. Although intracellular calcium chelation almost completely blocked the induction of many EMT markers, including vimentin, Twist and N-cadherin, the effect of TRPM7 silencing was specific for vimentin protein expression and STAT3 phosphorylation. These results indicate that TRPM7 is a partial regulator of EMT in breast cancer cells, and that other calcium-permeable ion channels are also involved in calcium-dependent EMT induction. In summary, this work establishes an important role for the intracellular calcium signal in the induction of EMT in human breast cancer cells. Manipulation of calcium-signaling pathways controlling EMT induction in cancer cells may therefore be an important therapeutic strategy for preventing metastases.

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Based on the characterization by Atomic Force Microscopy (AFM), we report that the mechanical property of single chondrocytes has dependency on the strain-rates. By comparing the mechanical deformation responses and the Young’s moduli of living and fixed chondrocytes at four different strain-rates, we explore the deformation mechanisms underlying this dependency property. We found that the strain-rate-dependent mechanical property of living cells is governed by both of the cellular cytoskeleton (CSK) and the intracellular fluid when the fixed chondrocytes is mainly governed by their intracellular fluid which is called the consolidation-dependent deformation behavior. Finally, we report that the porohyperelastic (PHE) constitutive material model which can capture the consolidation-dependent behavior of both living and fixed chondrocytes is a potential candidature to study living cell biomechanics.

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This study investigated the relationship between psychosocial risk factors and (1) neck symptoms and (2) neck pain and disability as measured by the neck disability index (NDI). Female office workers employed in local private and public organizations were invited to participate, with 333 completing a questionnaire. Data were collected on various risk factors including age, negative affectivity, history of previous neck trauma, physical work environment, and task demands. Sixty-one percent of the sample reported neck symptoms lasting greater than 8 days in the last 12 months. The mean NDI of the sample was 15.5 out of 100, indicating mild neck pain and disability. In a hierarchical multivariate logistic regression, low supervisor support was the only psychosocial risk factor identified with the presence of neck symptoms. Similarly, low supervisor support was the only factor associated with the score on the NDI. These associations remained after adjustment for potential confounders of age, negative affectivity, and physical risk factors. The interaction of job demands, decision authority, and supervisor support was significantly associated with the NDI in the final model and this association increased when those with previous trauma were excluded. Interestingly, and somewhat contrary to initial expectations, as job demands increased, high decision authority had an increasing effect on the NDI when supervisor support was low.

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Epidermal growth factor receptor (EGFR) levels predict a poor outcome in human breast cancer and are most commonly associated with proliferative effects of epidermal growth factor (EGF), with little emphasis placed on motogenic responses to EGF. We found that MDA-MB-231 human breast cancer cells elicited a potent chemotactic response despite their complete lack of a proliferative response to EGF. Antagonists of EGFR ligation, the EGFR kinase, phosphatidylinositol 3'-kinase, and phospholipase C, but not the mitogen- activated protein kinases (extracellular signal-regulated protein kinase 1 and 2), blocked MDA-MB-231 chemotaxis. These findings suggest that EGF may influence human breast cancer progression via migratory pathways, the signaling for which appears to be dissociated, at least in part, from the proliferative pathways.

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We introduce Claude Lévi Strauss' canonical formula (CF), an attempt to rigorously formalise the general narrative structure of myth. This formula utilises the Klein group as its basis, but a recent work draws attention to its natural quaternion form, which opens up the possibility that it may require a quantum inspired interpretation. We present the CF in a form that can be understood by a non-anthropological audience, using the formalisation of a key myth (that of Adonis) to draw attention to its mathematical structure. The future potential formalisation of mythological structure within a quantum inspired framework is proposed and discussed, with a probabilistic interpretation further generalising the formula

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Human skin fibroblasts were cultured long-term in the presence of ascorbic acid to allow formation of a three-dimensional collagen matrix, and the effects of this on activation of secreted matrix metalloproteinase-2 (MMP-2) were examined. Accumulation of collagen over time correlated with increased levels of both mature MMP-2 and cell-associated membrane type 1-MMP (MT1-MMP), and subsequently increased mRNA levels for MT1-MMP, providing temporal resolution of the "nontranscriptional" and "transcriptional" effects of collagen on MT-1MMP functionality. MMP-2 activation by these cultures was blocked by inhibitors of prolyl-4-hydroxylase, or when fibroblasts derived from the collagen α1(I) gene-deficient Mov-13 mouse were used. MMP-2 activation by the Mov-13 fibroblasts was rescued by transfection of a full-length α1(I) collagen cDNA, and to our surprise, also by transfection with an α1(I) collagen cDNA carrying a mutation at the C-proteinase cleavage, which almost abrogated fibrillogenesis. Although studies with ascorbate-cultured MT1-MMP-/- fibroblasts showed that MT1-MMP played a significant role in the collagen-induced MMP-2 activation, a residual MT1-MMP-independent activation of MMP-2 was seen which resembled the level of MMP-2 activation persisting when wild-type fibroblasts were cultured in the presence of both ascorbic acid and MMP inhibitors. We were also unable to block this residual activation with inhibitors specific for serinyl, aspartyl, or cysteinyl enzymes.

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While the Probability Ranking Principle for Information Retrieval provides the basis for formal models, it makes a very strong assumption regarding the dependence between documents. However, it has been observed that in real situations this assumption does not always hold. In this paper we propose a reformulation of the Probability Ranking Principle based on quantum theory. Quantum probability theory naturally includes interference effects between events. We posit that this interference captures the dependency between the judgement of document relevance. The outcome is a more sophisticated principle, the Quantum Probability Ranking Principle, that provides a more sensitive ranking which caters for interference/dependence between documents’ relevance.

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The decision of Wilson J in Calvert v Nickless Ltd [2004] QSC 449 involves significant questions of interpretation of sections 315 and 317 of the Workcover Queensland Act 1996 (Qld) relating to claims for damages for future economic loss and for gratuitous services.

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BACKGROUND Androgen-dependent prostate cancer (PrCa) xenograft models are required to study PrCa biology in the clinically relevant in vivo environment. METHODS Human PrCa tissue from a femoral bone metastasis biopsy (BM18) was grown and passaged subcutaneously through male severe combined immune-deficient (SCID) mice. Human mitochondria (hMt), prostate specific antigen (PSA), androgen receptor (AR), cytokeratin-18 (CK-18), pan-cytokeratin, and high molecular weight-cytokeratin (HMW-CK) were assessed using immunohistochemistry (IHC). Surgical castration was performed to examine androgen dependence. Serum was collected pre- and post-castration for monitoring of PSA levels. RESULTS: BM18 stained positively for hMt, PSA, AR, CK-18, pan keratin, and negatively for HMW-CK, consistent with the staining observed in the original patient material. Androgen-deprivation induced tumor regression in 10/10 castrated male SCID mice. Serum PSA levels positively correlated with BM18 tumor size. CONCLUSIONS BM18 expresses PSA and AR, and rapidly regresses in response to androgen withdrawal. This provides a new clinically significant PrCa model for the study of androgen-dependent growth.

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We have isolated a series of sublines of the hormone-dependent MCF-7 human breast cancer cell line after selection both in vivo and in vitro for growth in the presence of subphysiological concentrations of estrogens. These sublines represent a model system for study of the processes leading to hormonal autonomy. The cells form growing tumors in ovariectomized athymic nude mice in the absence of estrogen supplementation but retain some responsivity to estrogen as determined by stimulation of the rate of tumor growth in vivo and by induction of progesterone receptor. An ovarian-independent but hormone-responsive phenotype may occur early in the natural progression to hormone-independent and unresponsive growth in breast cancer. We observed no change in the affinity or decrease in the level of expression of estrogen receptors and progesterone receptors among the sublines and the parental cells. Epidermal growth factor receptors are not overexpressed in ovarian-independent cells. Thus, altered hormone receptor expression may be a late event in the acquisition of a hormone-independent and unresponsive phenotype. Sublines isolated by in vivo but not in vitro selection are more invasive than the parental cells both in vivo and across an artificial basement membrane in vitro. Thus, as yet unknown tumor-host interactions may be important in the development of an invasive phenotype. Furthermore, acquisition of the ovarian-independent and invasive phenotypes can occur independently.