935 resultados para UBP domain


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We develop a covariant quantum theory of fluctuations on vacuum domain walls and strings. The fluctuations are described by a scalar field defined on the classical world sheet of the defects. We consider the following cases: straight strings and planar walls in flat space, true vacuum bubbles nucleating in false vacuum, and strings and walls nucleating during inflation. The quantum state for the perturbations is constructed so that it respects the original symmetries of the classical solution. In particular, for the case of vacuum bubbles and nucleating strings and walls, the geometry of the world sheet is that of a lower-dimensional de Sitter space, and the problem reduces to the quantization of a scalar field of tachyonic mass in de Sitter space. In all cases, the root-mean-squared fluctuation is evaluated in detail, and the physical implications are briefly discussed.

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In this paper we present a new method to track bonemovements in stereoscopic X-ray image series of the kneejoint. The method is based on two different X-ray imagesets: a rotational series of acquisitions of the stillsubject knee that will allow the tomographicreconstruction of the three-dimensional volume (model),and a stereoscopic image series of orthogonal projectionsas the subject performs movements. Tracking the movementsof bones throughout the stereoscopic image series meansto determine, for each frame, the best pose of everymoving element (bone) previously identified in the 3Dreconstructed model. The quality of a pose is reflectedin the similarity between its simulated projections andthe actual radiographs. We use direct Fourierreconstruction to approximate the three-dimensionalvolume of the knee joint. Then, to avoid the expensivecomputation of digitally rendered radiographs (DRR) forpose recovery, we reformulate the tracking problem in theFourier domain. Under the hypothesis of parallel X-raybeams, we use the central-slice-projection theorem toreplace the heavy 2D-to-3D registration of projections inthe signal domain by efficient slice-to-volumeregistration in the Fourier domain. Focusing onrotational movements, the translation-relevant phaseinformation can be discarded and we only consider scalarFourier amplitudes. The core of our motion trackingalgorithm can be implemented as a classical frame-wiseslice-to-volume registration task. Preliminary results onboth synthetic and real images confirm the validity ofour approach.

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In the search for high efficiency in root studies, computational systems have been developed to analyze digital images. ImageJ and Safira are public-domain systems that may be used for image analysis of washed roots. However, differences in root properties measured using ImageJ and Safira are supposed. This study compared values of root length and surface area obtained with public-domain systems with values obtained by a reference method. Root samples were collected in a banana plantation in an area of a shallower Typic Carbonatic Haplic Cambisol (CXk), and an area of a deeper Typic Haplic Ta Eutrophic Cambisol (CXve), at six depths in five replications. Root images were digitized and the systems ImageJ and Safira used to determine root length and surface area. The line-intersect method modified by Tennant was used as reference; values of root length and surface area measured with the different systems were analyzed by Pearson's correlation coefficient and compared by the confidence interval and t-test. Both systems ImageJ and Safira had positive correlation coefficients with the reference method for root length and surface area data in CXk and CXve. The correlation coefficient ranged from 0.54 to 0.80, with lowest value observed for ImageJ in the measurement of surface area of roots sampled in CXve. The IC (95 %) revealed that root length measurements with Safira did not differ from that with the reference method in CXk (-77.3 to 244.0 mm). Regarding surface area measurements, Safira did not differ from the reference method for samples collected in CXk (-530.6 to 565.8 mm²) as well as in CXve (-4231 to 612.1 mm²). However, measurements with ImageJ were different from those obtained by the reference method, underestimating length and surface area in samples collected in CXk and CXve. Both ImageJ and Safira allow an identification of increases or decreases in root length and surface area. However, Safira results for root length and surface area are closer to the results obtained with the reference method.

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We present a study of the magnetic relaxation of several ferrofluids composed of particles of about 40 Å in diameter (Fe3O4FeC, CoFe2O4). Our key observation is a nonthermal character of the relaxation below 3 K for the CoFe2O4 ferrofluid and below 1 K for the FeC ferrofluid. The crossover temperature from thermal to nonthermal (quantum) regime is in accordance with theoretical suggestions of macroscopic quantum tunneling of magnetization in single doma in particles

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We present a theoretical study of the quantum depinning of domain walls. Our approach extends earlier work by Stamp and confirms his suggestion that quantum tunneling of domain walls in ferromagnets may reveal itself at a macroscopic level in a manner similar to the Josephson effect in superconductors. The rate of tunneling of a domain wall through a barrier formed by a planar defect is calculated in terms of macroscopic parameters of the ferromagnet. A universal behavior of the WKB exponent in the limit of small barriers is demonstrated. The effect of dissipation on the tunneling rate is studied. It is argued that quantum diffusion of domain walls apparently explains a nonthermal magnetic relaxation observed in some materials at low temperatures.

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The magnetic properties of BaFe12O19 and BaFe10.2Sn0.74Co0.66O19 single crystals have been investigated in the temperature range (1.8 to 320 K) with a varying field from -5 to +5 T applied parallel and perpendicular to the c axis. Low-temperature magnetic relaxation, which is ascribed to the domain-wall motion, was performed between 1.8 and 15 K. The relaxation of magnetization exhibits a linear dependence on logarithmic time. The magnetic viscosity extracted from the relaxation data, decreases linearly as temperature goes down, which may correspond to the thermal depinning of domain walls. Below 2.5 K, the viscosity begins to deviate from the linear dependence on temperature, tending to be temperature independent. The near temperature independence of viscosity suggests the existence of quantum tunneling of antiferromagnetic domain wall in this temperature range.

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PURPOSE: To analyze in vivo the function of chicken acidic leucine-rich epidermal growth factor-like domain containing brain protein/Neuroglycan C (gene symbol: Cspg5) during retinal degeneration in the Rpe65⁻/⁻ mouse model of Leber congenital amaurosis. METHODS: We resorted to mice with targeted deletions in the Cspg5 and retinal pigment epithelium protein of 65 kDa (Rpe65) genes (Cspg5⁻/⁻/Rpe65⁻/⁻). Cone degeneration was assessed with cone-specific peanut agglutinin staining. Transcriptional expression of rhodopsin (Rho), S-opsin (Opn1sw), M-opsin (Opn1mw), rod transducin α subunit (Gnat1), and cone transducin α subunit (Gnat2) genes was assessed with quantitative PCR from 2 weeks to 12 months. The retinal pigment epithelium (RPE) was analyzed at P14 with immunodetection of the retinol-binding protein membrane receptor Stra6. RESULTS: No differences in the progression of retinal degeneration were observed between the Rpe65⁻/⁻ and Cspg5⁻/⁻/Rpe65⁻/⁻ mice. No retinal phenotype was detected in the late postnatal and adult Cspg5⁻/⁻ mice, when compared to the wild-type mice. CONCLUSIONS: Despite the previously reported upregulation of Cspg5 during retinal degeneration in Rpe65⁻/⁻ mice, no protective effect or any involvement of Cspg5 in disease progression was identified.

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It is very well known that the first succesful valuation of a stock option was done by solving a deterministic partial differential equation (PDE) of the parabolic type with some complementary conditions specific for the option. In this approach, the randomness in the option value process is eliminated through a no-arbitrage argument. An alternative approach is to construct a replicating portfolio for the option. From this viewpoint the payoff function for the option is a random process which, under a new probabilistic measure, turns out to be of a special type, a martingale. Accordingly, the value of the replicating portfolio (equivalently, of the option) is calculated as an expectation, with respect to this new measure, of the discounted value of the payoff function. Since the expectation is, by definition, an integral, its calculation can be made simpler by resorting to powerful methods already available in the theory of analytic functions. In this paper we use precisely two of those techniques to find the well-known value of a European call

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α-Synuclein aggregation and accumulation in Lewy bodies are implicated in progressive loss of dopaminergic neurons in Parkinson disease and related disorders. In neurons, the Hsp70s and their Hsp40-like J-domain co-chaperones are the only known components of chaperone network that can use ATP to convert cytotoxic protein aggregates into harmless natively refolded polypeptides. Here we developed a protocol for preparing a homogeneous population of highly stable β-sheet enriched toroid-shaped α-Syn oligomers with a diameter typical of toxic pore-forming oligomers. These oligomers were partially resistant to in vitro unfolding by the bacterial Hsp70 chaperone system (DnaK, DnaJ, GrpE). Moreover, both bacterial and human Hsp70/Hsp40 unfolding/refolding activities of model chaperone substrates were strongly inhibited by the oligomers but, remarkably, not by unstructured α-Syn monomers even in large excess. The oligomers acted as a specific competitive inhibitor of the J-domain co-chaperones, indicating that J-domain co-chaperones may preferably bind to exposed bulky misfolded structures in misfolded proteins and, thus, complement Hsp70s that bind to extended segments. Together, our findings suggest that inhibition of the Hsp70/Hsp40 chaperone system by α-Syn oligomers may contribute to the disruption of protein homeostasis in dopaminergic neurons, leading to apoptosis and tissue loss in Parkinson disease and related neurodegenerative diseases.

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The PAR-domain basic leucine zipper (PAR bZip) transcription factors DBP, TEF, and HLF accumulate in a highly circadian manner in several peripheral tissues, including liver and kidney. Mice devoid of all three of these proteins are born at expected Mendelian ratios, but are epilepsy prone, age at an accelerated rate, and die prematurely. In the hope of identifying PAR bZip target genes whose altered expression might contribute to the high morbidity and mortality of PAR bZip triple knockout mice, we compared the liver and kidney transcriptomes of these animals to those of wild-type or heterozygous mutant mice. These experiments revealed that PAR bZip proteins control the expression of many enzymes and regulators involved in detoxification and drug metabolism, such as cytochrome P450 enzymes, carboxylesterases, and constitutive androstane receptor (CAR). Indeed, PAR bZip triple knockout mice are hypersensitive to xenobiotic compounds, and the deficiency in detoxification may contribute to their early aging.

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We discuss the dynamics of the transient pattern formation process corresponding to the splay Fréedericksz transition. The emergence and subsequent evolution of the spatial periodicity is here described in terms of the temporal dependence of the wave numbers corresponding to the maxima of the structure factor. Situations of perpendicular as well as oblique field-induced stripes relative to the initial orientation of the director are both examined with explicit indications of the time scales needed for their appearance and posterior development.

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We study the dynamics of the late stages of the Fréedericksz transition in which a periodic transient pattern decays to a final homogeneous state. A stability analysis of an unstable stationary pattern is presented, and equations for the evolution of the domain walls are obtained. Using results of previous theories, we analyze the effect that the specific dynamics of the problem, incorporating hydrodynamic couplings, has on the expected logarithmic domain growth law.

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BACKGROUND: NR2E3 (PNR) is an orphan nuclear receptor essential for proper photoreceptor determination and differentiation. In humans, mutations in NR2E3 have been associated with the recessively inherited enhanced short wavelength sensitive (S-) cone syndrome (ESCS) and, more recently, with autosomal dominant retinitis pigmentosa (adRP). NR2E3 acts as a suppressor of the cone generation program in late mitotic retinal progenitor cells. In adult rod photoreceptors, NR2E3 represses cone-specific gene expression and acts in concert with the transcription factors CRX and NRL to activate rod-specific genes. NR2E3 and CRX have been shown to physically interact in vitro through their respective DNA-binding domains (DBD). The DBD also contributes to homo- and heterodimerization of nuclear receptors. METHODOLOGY/PRINCIPAL FINDINGS: We analyzed NR2E3 homodimerization and NR2E3/CRX complex formation in an in vivo situation by Bioluminescence Resonance Energy Transfer (BRET(2)). NR2E3 wild-type protein formed homodimers in transiently transfected HEK293T cells. NR2E3 homodimerization was impaired in presence of disease-causing mutations in the DBD, except for the p.R76Q and p.R104W mutant proteins. Strikingly, the adRP-linked p.G56R mutant protein interacted with CRX with a similar efficiency to that of NR2E3 wild-type and p.R311Q proteins. In contrast, all other NR2E3 DBD-mutant proteins did not interact with CRX. The p.G56R mutant protein was also more effective in abolishing the potentiation of rhodospin gene transactivation by the NR2E3 wild-type protein. In addition, the p.G56R mutant enhanced the transrepression of the M- and S-opsin promoter, while all other NR2E3 DBD-mutants did not. CONCLUSIONS/SIGNIFICANCE: These results suggest different disease mechanisms in adRP- and ESCS-patients carrying NR2E3 mutations. Titration of CRX by the p.G56R mutant protein acting as a repressor in trans may account for the severe clinical phenotype in adRP patients.