1,212 research outputs found
Acoustic resonances in microfluidic chips: full-image micro-PIV experiments and numerical simulations
We show that full-image micro-PIV analysis in combination with images of
transient particle motion is a powerful tool for experimental studies of
acoustic radiation forces and acoustic streaming in microfluidic chambers under
piezo-actuation in the MHz range. The measured steady-state motion of both
large 5 um and small 1 um particles can be understood in terms of the acoustic
eigenmodes or standing ultra-sound waves in the given experimental
microsystems. This interpretation is supported by numerical solutions of the
corresponding acoustic wave equation.Comment: RevTex, 10 pages, 9 eps figures; NOTE first authors changed his name
to S. Melker Hagsater in the published versio
Correlation studies of fission fragment neutron multiplicities
We calculate neutron multiplicities from fission fragments with specified
mass numbers for events having a specified total fragment kinetic energy. The
shape evolution from the initial compound nucleus to the scission
configurations is obtained with the Metropolis walk method on the
five-dimensional potential-energy landscape, calculated with the
macroscopic-microscopic method for the three-quadratic-surface shape family.
Shape-dependent microscopic level densities are used to guide the random walk,
to partition the intrinsic excitation energy between the two proto-fragments at
scission, and to determine the spectrum of the neutrons evaporated from the
fragments. The contributions to the total excitation energy of the resulting
fragments from statistical excitation and shape distortion at scission is
studied. Good agreement is obtained with available experimental data on neutron
multiplicities in correlation with fission fragments from U(n,f). At higher neutron energies a superlong fission mode appears which
affects the dependence of the observables on the total fragment kinetic energy.Comment: 12 pages, 10 figure
N=2 Boundary conditions for non-linear sigma models and Landau-Ginzburg models
We study N=2 nonlinear two dimensional sigma models with boundaries and their
massive generalizations (the Landau-Ginzburg models). These models are defined
over either Kahler or bihermitian target space manifolds. We determine the most
general local N=2 superconformal boundary conditions (D-branes) for these sigma
models. In the Kahler case we reproduce the known results in a systematic
fashion including interesting results concerning the coisotropic A-type branes.
We further analyse the N=2 superconformal boundary conditions for sigma models
defined over a bihermitian manifold with torsion. We interpret the boundary
conditions in terms of different types of submanifolds of the target space. We
point out how the open sigma models correspond to new types of target space
geometry. For the massive Landau-Ginzburg models (both Kahler and bihermitian)
we discuss an important class of supersymmetric boundary conditions which
admits a nice geometrical interpretation.Comment: 48 pages, latex, references and minor comments added, the version to
appear in JHE
T-duality for the sigma model with boundaries
We derive the most general local boundary conditions necessary for T-duality
to be compatible with superconformal invariance of the two-dimensional N=1
supersymmetric nonlinear sigma model with boundaries. To this end, we construct
a consistent gauge invariant parent action by gauging a U(1) isometry, with and
without boundary interactions. We investigate the behaviour of the boundary
conditions under T-duality, and interpret the results in terms of D-branes.Comment: 48 pages, LaTeX, v2: typos corrected, references adde
The Response of the Tracheal Epithelium to Concomitant Cis-Diamminedichloroplatinum (II) and Radiation. An Electron Microscopic Study in Rabbits
The ciliated epithelium of the rabbit trachea was irradiated with daily fractions of 2 Gy up to an accumulated dose of 20 Gy (total dose: 2, 6, 10, 16, or 20 Gy). Fifteen to forty-five minutes before the start of each irradiation 0.3 mg Cis-diamminedichloroplatinum (cis-DDP) was given by intraperitoneal injection to each rabbit. Examinations were carried out 1-10 days after each fractionation schedule, when specimens were taken for morphological investigations.
Scanning electron microscope (SEM) examination showed a gradual development of ciliary damage, from blebs on the cilia to swollen tips, broken and bent cilia and finally an epithelial injury with areas free from cilia, and a surface covered with microvilli-like structures. SEM also showed cell loss, and remnants of dead cells on the surface together with detritus. By transmission electron microscopy (TEM), ciliary damage, cell death and cell loss of the ciliated cell layer, as well as exfoliation of portions of goblet-like cells on the surface, could be confirmed. Scoring of SEM and TEM micro graphs showed that for the tracheal part treated with cis-DDP and radiation, the maximal damage was expressed in the dose group 10 Gy, and above this no further increase in the average reaction occurred. For the part of the trachea only exposed to cis-DDP, the damage increased with the dose. The difference observed speaks for an accelerated proliferation exerted by the radiation
The Influence of 5-Fluorouracil on the Endothelium in Small Arteries. An Electron Microscopic Study in Rabbits
5-Fluorouracil (5-FU) is a widely used antineoplastic agent. 5-FU induced cardiotoxicity is a still relatively unknown side-effect of this drug. This phenomenon could be due to a direct cytotoxic effect on the endothelial cells. We tested this hypothesis in an experimental study in rabbits, by scanning or transmission electron microscopic evaluation of endothelium in small arteries (the central artery of the ear) after in vivo treatment with 5-FU. Both local and systemic effects of 5-FU on endothelium were studied 15, 30, 60 and 120 minutes after intra-arterial or intraperitoneal treatment. Perfusion fixation at physiological pressure and temperature was used in order to minimize damage to the endothelium during the preparation procedure. Eighteen rabbits weighing 2.5-3.0 kg were used, and 6 animals served as controls. The following parameters were evaluated: vessel wall and endothelial cell contraction, cell edema, cytolysis, occurrence of denuded areas, platelet adhesion/aggregation and fibrin formation. For the description of each parameter a scale of negative points was used. Irreversible cell damage was observed in 5-FU treated animals: disruption of the endothelial sheet and patchy exposure of the subendothelium, sometimes as a focus for thrombus formation. Our findings support the hypothesis that the thrombogenic effect of 5-FU secondary to its direct cytotoxic effect on endothelium might be one of the pathophysiological mechanisms behind 5-FU induced cardiotoxicity
The Appearance of Endothelium in Small Arteries After Treatment with 5-Fluorouracil. An Electron Microscopic Study of Late Effects in Rabbits
Cardiotoxicity is an unexplained toxic manifestation of 5-fluorouracil (5-FU). Its possible mechanism could be a direct cytotoxic effect on the vascular endothelium. We have tested this hypothesis in an experimental study in rabbits, using scanning and transmission electron microscopic evaluation of endothelium in small arteries (the central artery of the ear). The perfusion fixation method at physiological pressure and temperature was used. Both local and systemic effects of 5-FU on endothelium were studied 1, 3, 7, 14 and 30 days after in vivo treatment with 5-FU. Fifteen rabbits were used and five additional animals served as controls. The following parameters were evaluated: vessel wall and endothelial cell contraction, cell oedema, cytolysis, occurrence of denuded areas, platelet adhesion/aggregation and fibrin formation. For the description of each parameter, a scale of negative points (0.0-3.0) was used. We found severe cell damage with accompanying thrombus formation. The findings support the hypothesis that the thrombogenic effect of 5-FU, secondary to its direct cytotoxic effect on endothelium, is the pathophysiological mechanism behind 5-FU cardiotoxicity
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