9 resultados para Central giant cell lesion

em Indian Institute of Science - Bangalore - Índia


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The effect of turbulence on the nonaxisymmetric flux rings of equipartition field strength in bipolar magnetic regions is studied on the basis of the small-scale momentum exchange mechanism and the giant cell drag combined with the Kelvin-Helmholtz drag mechanism. It is shown that the giant cell drag and small-scale momentum exchange mechanism can make equipartition flux loops emerge at low latitudes, in addition to making them exhibit the observed tilts. However, the sizes of the flux tubes have to be restricted to a couple of hundred kilometers. An ad hoc constraint on the footpoints of the flux loops is introduced by not letting them move in the phi direction, and it is found that equipartition fields of any size can be made to emerge at sunspot latitudes with the observed tilts by suitably adjusting the footpoint separations.

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Coherently moving flocks of birds, beasts, or bacteria are examples of living matter with spontaneous orientational order. How do these systems differ from thermal equilibrium systems with such liquid crystalline order? Working with a fluidized monolayer of macroscopic rods in the nematic liquid crystalline phase, we find giant number fluctuations consistent with a standard deviation growing linearly with the mean, in contrast to any situation where the central limit theorem applies. These fluctuations are long-lived, decaying only as a logarithmic function of time. This shows that flocking, coherent motion, and large-scale inhomogeneity can appear in a system in which particles do not communicate except by contact.

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We study giant magnons in the the D1-D5 system from both the boundary CFT and as classical solutions of the string sigma model in AdS(3) x S-3 x T-4. Re-examining earlier studies of the symmetric product conformal field theory we argue that giant magnons in the symmetric product are BPS states in a centrally extended SU(1 vertical bar 1) x SU(1 vertical bar 1) superalgebra with two more additional central charges. The magnons carry these additional central charges locally but globally they vanish. Using a spin chain description of these magnons and the extended superalgebra we show that these magnons obey a dispersion relation which is periodic in momentum. We then identify these states on the string theory side and show that here too they are BPS in the same centrally extended algebra and obey the same dispersion relation which is periodic in momentum. This dispersion relation arises as the BPS condition for the extended algebra and is similar to that of magnons in N = 4 Yang-Mills Yang-Mills.

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As with 1,2-diphenylethane (dpe), X-ray crystallographic methods measure the central bond in meso-3,4-diphenylhexane-2,5-done (dphd) as significantly shorter than normal for an sp(3)-sp(3) bond. The same methods measure the benzylic (ethane C-Ph) bonds in dphd as unusually long for sp(3)-sp(2) liaisons. Torsional motions of the phenyl rings about the C-Ph bonds have been proposed as the artifacts behind the result of a 'short' central bond in dpe. While a similar explanation can, presumably, hold for the even 'shorter' central bond in dphd, it cannot account for the 'long' C-Ph bonds. The phenyl groups, departing much from regular hexagonal shape, adopt highly skewed conformations with respect to the plane constituted by the four central atoms. It is thought that-the thermal motions of the phenyl rings, conditioned by the potential wells in which they are ensconced in the unit cell, are largely libratory around their normal axes. In what appears to be a straightforward explanation under the 'rigid-body' concept, it appears that these libratory motions of the phenyl rings, that account, at the same time, for the 'short' central bond, are the artifacts behind the 'long' measurement of the C-Ph bonds. These motions could be superimposed on torsional motions analogous to those proposed in the case of dpe. An inspection of the ORTEP diagram from the 298 K data on dphd clearly suggests these possibilities. Supportive evidence for these qualitative explanations from an analysis of the differences between the mean square displacements of C(1) and C(7)/C(1a) and C(7a) based on the 'rigid-body model' is discussed. (C) 2002 Elsevier Science B.V. All rights reserved.

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The magnetorotational instability (MRI) is a crucial mechanism of angular momentum transport in a variety of astrophysical accretion disks. In systems accreting at well below the Eddington rate, such as the central black hole in the Milky Way (Sgr A*), the plasma in the disk is essentially collisionless. We present a nonlinear study of the collisionless MRI using first-principles particle-in-cell plasma simulations. We focus on local two-dimensional (axisymmetric) simulations, deferring more realistic three-dimensional simulations to future work. For simulations with net vertical magnetic flux, the MRI continuously amplifies the magnetic field, B, until the Alfven velocity, v(A), is comparable to the speed of light, c (independent of the initial value of v(A)/c). This is consistent with the lack of saturation of MRI channel modes in analogous axisymmetric MHD simulations. The amplification of the magnetic field by the MRI generates a significant pressure anisotropy in the plasma (with the pressure perpendicular to B being larger than the parallel pressure). We find that this pressure anisotropy in turn excites mirror modes and that the volume-averaged pressure anisotropy remains near the threshold for mirror mode excitation. Particle energization is due to both reconnection and viscous heating associated with the pressure anisotropy. Reconnection produces a distinctive power-law component in the energy distribution function of the particles, indicating the likelihood of non-thermal ion and electron acceleration in collisionless accretion disks. This has important implications for interpreting the observed emission-from the radio to the gamma-rays-of systems such as Sgr A*.

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Background: Taxol (generic name paclitaxel), a plant-derived antineoplastic agent, used widely against breast, ovarian and lung cancer, was originally isolated from the bark of the Pacific yew, Taxus brevifolia. The limited supply of the drug has prompted efforts to find alternative sources, such as chemical synthesis, tissue and cell cultures of the Taxus species both of which are expensive and yield low levels. Fermentation processes with microorganisms would be the methods of choice to lower the costs and increase yields. Previously we have reported that F. solani isolated from T. celebica produced taxol and its precursor baccatin III in liquid grown cultures J Biosci 33: 259-67, 2008. This study was performed to evaluate the inhibition of proliferation and induction of apoptosis of cancer cell lines by the fungal taxol and fungal baccatin III of F. solani isolated from T. celebica. Methods: Cell lines such as HeLa, HepG2, Jurkat, Ovcar3 and T47D were cultured individually and treated with fungal taxol, baccatin III with or without caspase inhibitors according to experimental requirements. Their efficacy on apoptotic induction was examined. Results: Both fungal taxol and baccatin III inhibited cell proliferation of a number of cancer cell lines with IC50 ranging from 0.005 to 0.2 mu M for fungal taxol and 2 to 5 mu M for fungal baccatin III. They also induced apoptosis in JR4-Jurkat cells with a possible involvement of anti-apoptotic Bcl2 and loss in mitochondrial membrane potential, and was unaffected by inhibitors of caspase-9,-2 or -3 but was prevented in presence of caspase-10 inhibitor. DNA fragmentation was also observed in cells treated with fungal taxol and baccatin III. Conclusions: The cytotoxic activity exhibited by fungal taxol and baccatin III involves the same mechanism, dependent on caspase-10 and membrane potential loss of mitochondria, with taxol having far greater cytotoxic potential.

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In contemporary wideband orthogonal frequency division multiplexing (OFDM) systems, such as Long Term Evolution (LTE) and WiMAX, different subcarriers over which a codeword is transmitted may experience different signal-to-noise-ratios (SNRs). Thus, adaptive modulation and coding (AMC) in these systems is driven by a vector of subcarrier SNRs experienced by the codeword, and is more involved. Exponential effective SNR mapping (EESM) simplifies the problem by mapping this vector into a single equivalent fiat-fading SNR. Analysis of AMC using EESM is challenging owing to its non-linear nature and its dependence on the modulation and coding scheme. We first propose a novel statistical model for the EESM, which is based on the Beta distribution. It is motivated by the central limit approximation for random variables with a finite support. It is simpler and as accurate as the more involved ad hoc models proposed earlier. Using it, we develop novel expressions for the throughput of a point-to-point OFDM link with multi-antenna diversity that uses EESM for AMC. We then analyze a general, multi-cell OFDM deployment with co-channel interference for various frequency-domain schedulers. Extensive results based on LTE and WiMAX are presented to verify the model and analysis, and gain new insights.

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The leaf surface usually stays flat, maintained by coordinated growth. Growth perturbation can introduce overall surface curvature, which can be negative, giving a saddle-shaped leaf, or positive, giving a cup-like leaf. Little is known about the molecular mechanisms that underlie leaf flatness, primarily because only a few mutants with altered surface curvature have been isolated and studied. Characterization of mutants of the CINCINNATA-like TCP genes in Antirrhinum and Arabidopsis have revealed that their products help maintain flatness by balancing the pattern of cell proliferation and surface expansion between the margin and the central zone during leaf morphogenesis. On the other hand, deletion of two homologous PEAPOD genes causes cup-shaped leaves in Arabidopsis due to excess division of dispersed meristemoid cells. Here, we report the isolation and characterization of an Arabidopsis mutant, tarani (tni), with enlarged, cup-shaped leaves. Morphometric analyses showed that the positive curvature of the tni leaf is linked to excess growth at the centre compared to the margin. By monitoring the dynamic pattern of CYCLIN D3;2 expression, we show that the shape of the primary arrest front is strongly convex in growing tni leaves, leading to excess mitotic expansion synchronized with excess cell proliferation at the centre. Reduction of cell proliferation and of endogenous gibberellic acid levels rescued the tni phenotype. Genetic interactions demonstrated that TNI maintains leaf flatness independent of TCPs and PEAPODs.

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Huntington's disease (HD) is an autosomal dominant disorder of central nervous system caused by expansion of CAG repeats in exon1 of the huntingtin gene (Htt). Among various dysfunctions originated from the mutation in Htt gene, transcriptional deregulation has been considered to be one of the most important abnormalities. Large numbers of investigations identified altered expressions of genes in brains of HD patients and many models of HD. In this study we employed 2D SDS-PAGE/MALDI-MS coupled with 2D-DIGE and real-time PCR experiments of an array of genes focused to HD pathway to determine altered protein and gene expressions in STHdh(Q111)/Hdh(Q111) cells, a cell model of HD and compared with STHdh(Q7)/Hdh(Q7) cells, its wild type counterpart. We annotated 76 proteins from these cells and observed differential expressions of 31 proteins (by 2D-DIGE) involved in processes like unfolded protein binding, negative regulation of neuron apoptosis, response to superoxides etc. Our PCR array experiments identified altered expressions of 47 genes. Altogether significant alteration of 77 genes/proteins could be identified in this HD cell line with potential relevance to HD biology. Biological significance: In this study we intended to find out differential proteomic and genomic profiles in HD condition. We used the STHdh cells, a cellular model for HD and control. These are mouse striatal neuronal cell lines harboring 7 and 111 knock -in CAG repeats in their two alleles. The 111Q containing cell line (STHdh(Q111)/Hdh(Q111)) mimics diseased condition, whereas the 7Q containing ones (STHdh(Q7)/Hdh(Q7)), serves as the proper control cell line. Proteomic experiments were performed earlier to obtain differential expressions of proteins in R6/2 mice models, Hdh(Q) knock -in mice and in plasma and CSF from HD patients. However, no earlier report on proteomic alterations in these two HD cell lines and control was available in literature. It was, therefore, an important objective to find out differential expressions of proteins in these two cell lines. In this study, we annotated 76 proteins from STHdh(Q7)/Hdh(Q7) and STHdh(Q111)/Hdh(Q111) cells using 2D-gel/mass spectrometry. Next, by performing 2D-DIGE, we observed differential expressions of 31 proteins (16 upregulated and 15 downregulated) between these two cell lines. We also performed customized qRT-PCR array focused to HD pathway and found differential expressions of 47 genes (8 gene exptessions increased and 39 genes were decreased significantly). A total of 77 genes/proteins (Htt downregulated in both the studies) were found to be significantly altered from both the experimental paradigms. We validated the differential expressions of Vim, Hypk, Ran, Dstn, Hspa5 and Sod2 either by qRT-PCR or Western blot analysis or both. Out of these 77, similar trends in alteration of 19 out of 31 and 38 out of 47 proteins/genes were reported in earlier studies. Thus our study confirmed earlier observations on differential gene/protein expressions in HD and are really useful. Additionally, we observed differential expression of some novel genes/proteins. One of this was Hypk, a Htt-interacting chaperone protein with the ability to solubilize mHtt aggregated structures in cell lines. We propose that downregulation of Hypk in STHdh-Qm (Q111)/Hdh(Q111) has a causal effect towards HD pathogenesis. Thus the novel findings from our study need further research and might be helpful to understand the molecular mechanism behind HD pathogenesis. (C) 2015 Elsevier B.V. All rights reserved.