993 resultados para 1056 C.c.Q.


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Mode of access: Internet.

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Mode of access: Internet.

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Addenda (p. 61-72): Public meeting of the Georgia bar association, Illinois state bar association.

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This paper concerns the spaces of compact operators kappa(E,F), where E and F are Banach spaces C([1, xi], X) of all continuous X-valued functions defined on the interval of ordinals [1, xi] and equipped with the supremun norm. We provide sufficient conditions on X, Y, alpha, beta, xi and eta, with omega <= alpha <= beta < omega 1 for the following equivalence: (a) kappa(C([1, xi], X), C([1, alpha], Y)) is isomorphic to kappa(C([1,eta], X), C([1, beta], Y)), (b) beta < alpha(omega). In this way, we unify and extend results due to Bessaga and Pelczynski (1960) and C. Samuel (2009). Our result covers the case of the classical spaces X = l(p) and Y = l(q) with 1 < p, q < infinity.

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The present work evaluates both in vitro and in vivo antitumor activity of BPB-modified BthTX-I and its cationic synthetic peptide derived from the 115-129 C-terminal region. BPB-BthTX-1 presented cytotoxicity of 10-40% on different tumor cell lines, which were also susceptible to the lytic action of the synthetic peptide. Injection of the modified protein or the peptide in mice, 5 days after transplantation of S 180 tumor cells, reduced 30 and 36% of the tumor size on day 14th and 76 and 79% on day 60th, respectively, when compared to the untreated control group. Thus, these antitumor properties might be of interest in the development of therapeutic strategies against cancer. (C) 2009 The International Association for Biologicals. Published by Elsevier Ltd. All rights reserved.

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The structure constants of quantum Lie algebras depend on a quantum deformation parameter q and they reduce to the classical structure constants of a Lie algebra at q = 1. We explain the relationship between the structure constants of quantum Lie algebras and quantum Clebsch-Gordan coefficients for adjoint x adjoint --> adjoint We present a practical method for the determination of these quantum Clebsch-Gordan coefficients and are thus able to give explicit expressions for the structure constants of the quantum Lie algebras associated to the classical Lie algebras B-l, C-l and D-l. In the quantum case the structure constants of the Cartan subalgebra are non-zero and we observe that they are determined in terms of the simple quantum roots. We introduce an invariant Killing form on the quantum Lie algebras and find that it takes values which are simple q-deformations of the classical ones.

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Hepatitis C virus (HCV) is a major cause of hepatic disease and of liver transplantation worldwide. Mannan-binding lectin (MBL), encoded by the MBL2 gene, can have an important role as an opsonin and complement activating molecule in HCV persistence and liver injury. We assessed the MBL2 polymorphism in 102 Euro-Brazilian patients with moderate and severe chronic hepatitis C, paired for gender and age with 102 HCV seronegative healthy individuals. Six common single nucleotide polymorphisms in the MBL2 gene, three in the promoter (H/L, X/Y and P/Q) and three in exon 1 (A, the wild-type, and B, C or D also known as O) were evaluated using real-time polymerase chain reaction with fluorescent hybridization probes. The concentration of MBL in plasma was measured by enzyme-linked immunosorbent assay. The frequency of the YA/YO genotype was significantly higher in the HCV patients compared with the controls (P = 0.022). On the other hand, the genotypes associated with low levels of MBL (XA/XA, XA/YO and YO/YO) were decreased significantly in the patients with severe fibrosis (stage F4), when compared with the patients with moderate fibrosis (stage F2) (P = 0.04) and to the control group (P = 0.011). Furthermore, MBL2 genotypes containing X or O mutations were found to be associated with non-responsiveness to pginterferon and ribavirin treatment (P = 0.023). MBL2 polymorphisms may therefore be associated not only with the development of chronic hepatitis C, but also with its clinical evolution and response to treatment.

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Design Fifty out of 336 postmenopausal patients with chronic infection with the hepatitis C virus were selected. The non-inclusion criteria were other chronic or systemic liver diseases, severe vascular diseases, autoimmune diseases or malignant tumors. The patients were randomized into two groups: the HT group with 25 patients to be given transdermal hormone therapy (50 mu g estradiol plus 170 mu g norethisterone/day) and the control group with the other 25 patients (no medication). Hepatic tests (alanine aminotransferase, aspartate aminotransferase, gamma glutamyltransferase, total alkaline phosphatase, albumin, serum bilirubin) and hemostatic parameters (prothrombin time, factor V, fibrinogen) were evaluated at baseline and at 1, 4, 7 and 9 months of treatment. Results No significant changes in parameters were found in the comparison between the treated group and the controls, except for a decrease in total alkaline phosphatase (p = 0.002), presumably due to changes in bone remodelling. Conclusions There were no changes in liver function after a 9-month treatment with transdermal estradiol plus norethisterone in symptomatic postmenopausal patients with hepatitis C.

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The polyphase evolution of the Serido Belt (NE-Brazil) includes D, crust formation at 2.3-2.1 Ga, D-2 thrust tectonics at 1.9 Ga and crustal reworking by D-3 strike-slip shear zones at 600 Ma. Microstructural investigations within mylonites associated with D-2 and D-3 events were used to constrain the tectono-thermal evolution of the belt. D-2 shear zones commenced at deeper crustal levels and high amphibolite facies conditions (600-650 degreesC) through grain boundary migration, subgrain rotation and operation of quartz Q-prism slip. Continued shearing and exhumation of the terrain forced the re-equilibration of high-T fabrics and the switching of slip systems from (c)-prism to positive and negative (a)-rhombs. During D-3, enhancement of ductility by dissipation of heat that came from syn-D-3 granites developed wide belts of amphibolite facies mylonites. Continued shearing, uplift and cooling of the region induced D-3 shear zones to act in ductile-brittle regimes, marked by fracturing and development of thinner belts of greenschist facies mylonites. During this event, switching from (a)-prism to a basal slip indicates a thermal path from 600 to 350 degreesC. Therefore, microstructures and quartz c-axis fabrics in polydeformed rocks from the Serido Belt preserve the record of two major events, which includes contrasting deformation mechanisms and thermal paths. (C) 2003 Elsevier Ltd. All rights reserved.

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Humans and mice lacking functional caspase-8 in T cells manifest a profound immunodeficiency syndrome due to defective T cell antigen receptor (TCR)-induced NF-kappaB signaling and proliferation. It is unknown how caspase-8 is activated following T cell stimulation, and what is the caspase-8 substrate(s) that is necessary to initiate T cell cycling. We observe that following TCR ligation, a small portion of total cellular caspase-8 and c-FLIP(L) rapidly migrate to lipid rafts where they associate in an active caspase complex. Activation of caspase-8 in lipid rafts is followed by rapid cleavage of c-FLIP(L) at a known caspase-8 cleavage site. The active caspase.c-FLIP complex forms in the absence of Fas (CD95/APO1) and associates with the NF-kappaB signaling molecules RIP1, TRAF2, and TRAF6, as well as upstream NF-kappaB regulators PKC theta, CARMA1, Bcl-10, and MALT1, which connect to the TCR. The lack of caspase-8 results in the absence of MALT1 and Bcl-10 in the active caspase complex. Consistent with this observation, inhibition of caspase activity attenuates NF-kappaB activation. The current findings define a link among TCR, caspases, and the NF-kappaB pathway that occurs in a sequestered lipid raft environment in T cells.