889 resultados para Molecule manipulation


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Appendices : A. Electricity. B. Tables. C. Physical laboratories. Books of reference. Additional experimenrts.

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Mode of access: Internet.

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Includes bibliographical references (p. 27).

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Thesis (Ph.D.)--University of Washington, 2016-06

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Frequency of exposure to very low- and high-frequency words was manipulated in a three-phase (familiarisation, study, and test) design. During familiarisation, words were presented with their definition (once, four times, or not presented). One week (Experiment 1) or one day (Experiment 2) later, participants studied a list of homogeneous pairs (i.e., pair members were matched on background and familiarisation frequency). Item and associative recognition of high- and very low-frequency words presented in intact, rearranged, old-new, or new-new pairs were tested in Experiment 1. Associative recognition of very low-frequency words was tested in Experiment 2. Results showed that prior familiaris ation improved associative recognition of very low-frequency pairs, but had no effect on high-frequency pairs. The role of meaning in the formation of item-to-item and item-to-context associations and the implications for current models of memory are discussed.

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0We study the exact solution for a two-mode model describing coherent coupling between atomic and molecular Bose-Einstein condensates (BEC), in the context of the Bethe ansatz. By combining an asymptotic and numerical analysis, we identify the scaling behaviour of the model and determine the zero temperature expectation value for the coherence and average atomic occupation. The threshold coupling for production of the molecular BEC is identified as the point at which the energy gap is minimum. Our numerical results indicate a parity effect for the energy gap between ground and first excited state depending on whether the total atomic number is odd or even. The numerical calculations for the quantum dynamics reveals a smooth transition from the atomic to the molecular BEC.

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Clustering of the T cell integrin, LFA-1, at specialized regions of intercellular contact initiates integrin-mediated adhesion and downstream signaling, events that are necessary for a successful immunological response. But how clustering is achieved and sustained is not known. Here we establish that an LFA-1-associated molecule, PTA-1, is localized to membrane rafts and binds the carboxyl-terminal domain of isoforms of the actin-binding protein 4.1G. Protein 4.1 is known to associate with the membrane-associated guanylate kinase homologue, human discs large. We show that the carboxyl-terminal peptide of PTA-1 also can bind human discs large and that the presence or absence of this peptide greatly influences binding between PTA-1 and different isoforms of 4.1G. T cell stimulation with phorbol ester or PTA-1 cross-linking induces PTA-1 and 4.1G to associate tightly with the cytoskeleton, and the PTA-1 from such activated cells now can bind to the amino-terminal region of 4.1G. We propose that these dynamic associations provide the structural basis for a regulated molecular adhesive complex that serves to cluster and transport LFA-1 and associated molecules.

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Early pregnancy factor (EPF) is a secreted protein with immunosuppressive and growth factor properties. It has been shown to suppress the delayed-type hypersensitivity response in mice as well as acute and chronic forms of experimental autommume encephalomyelitis in rats and mice, respectively. In previous studies, we have demonstrated that EPF binds to a population of lymphocytes and we hypothesized that it mediates its suppressive effects by binding to CD4(+) T cells. In the present study, we isolated monocytes and subpopulations of lymphocytes and labelled them with fluoresceinated EPF in order to determine which populations bind EPF. We demonstrated that EPF binds specifically to CD4(+), CD8(+), CD14(+) (monocytes) and CD56(+) NK cells but not to CD19(+) B cells. The identity of the molecule(s) on the cell surface that is targeted by EPF is unknown, but as EPF is an extracellular homologue of the intracellular protein chaperonin 10 (Cpn 10), we examined the possibility that the EPF receptor is a membrane-associated form of chaperonin 60 (Cpn60), the functional associate of Cpn 10 within the cell. The EPF target molecule on lymphocytes was visualized by chemical cross-linking of exogenous iodinated Cpn10 to cells and probed with anti-Cpn60. The effect of anti-Cpn60 on activity in the EPF bioassay, the rosette inhibition test, was also examined. In both instances, no specific interaction of this antibody and the putative receptor was observed. It was concluded that the cell surface molecule targeted by EPF is unlikely to be a homologue of Cpn60.

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We report on the trapping, rotation, and in-situ growth of birefringent tetragonal lysozyme crystals in optical tweezers operating at a wavelength of 1070 nm. Variation of the pH and lysozyme concentration of the solution during growth was used to alter the length to width ratio of the crystals, and hence their orientation in the tweezers. Crystals with the optical axis skewed or perpendicular to the trapping-beam axis could be rotated by changing the orientation of linearly polarized light. We observed spontaneous spinning of some asymmetric crystals in the presence of linearly polarized light, due to radiation pressure effects. Addition of protein to the solution in the tweezers permitted real-time observation of crystal growth. (C) 2004 Optical Society of America.

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At autopsy, Alzheimer's disease is characterised by the presence of amyloid plaques and neurofibrillary tangles, made up of two peptide sequences, amyloid-beta(1-40) (A beta 40) and amyloid-beta(1-42) (A beta 42). In Tyrode's solution (2 mM Ca2+), 10 mu M A beta 42 peptide almost immediately aggregates and eventually forms p-sheets. This aggregation can be inhibited with 4,5-dianilinophthalimide (DAPH). Ca2+-permeant AMPA receptors are involved in the neuronal Ca2+ influx (neurotoxicity) induced by the A beta 42 peptide in cultured neuronal cells. The Ca2+ influx observed with pre-incubated A beta 42 peptide was inhibited by DAPH. DAPH also inhibits epidermal growth factor receptor kinase, and this will prevent its development for use in Alzheimer's disease. The potential of DAPH as a small-molecule lead compound for the treatment of Alzheimer's disease next requires the separation of the structural requirements that reverse fibril formation and inhibit epidermal growth factor receptor kinase.