82 research outputs found

    Impurity transport in FM-1

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    Toroidal plasma rotation in the PLT tokamak with neutral-beam injection

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    Toroidal plasma rotation in the Princeton Large Torus, PLT, has been measured for various plasma and neutral beam injection conditions. Measurements of the plasma rotational velocities were made from Doppler shifts of appropriate spectral lines and include data from both hydrogen and deuterium beams and co- and counter-injection at several electron densities. Without injection, a small but consistent toroidal rotation exists in a direction opposite to the plasma current (counter-direction) in the plasma center but parallel to the current (co-direction) in the plasma periphery. Using these measured velocities and the plasma density and temperature gradients, radial electron fields can be determined from theory, giving E/sub r / approx. = 40 V/cm near the plasma center and E/sub r/ approx. = 10 V/cm near the plasma edge. Insertion of a local, 2.5 percent magnetic well produced no observable effect on the beam driven rotation. Modeling of the time evolution and radial distribution of the rotation allows one to deduce an effective viscosity of the order of (1 to 5) x 10/sup 4/ cm/sup 2//sec

    Satellite spectra for helium-like titanium. Part II

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    K/sup ..cap alpha../ x-ray spectra of helium-like titanium, Ti XXI, from Tokamak Fusion Test Reactor (TFTR) plasmas have been observed with a high resolution crystal spectrometer and have been used as a diagnostic of central plasma parameters. The data allow detailed comparison with recent theoretical predictions for the Ti XXI helium-like lines and the associated satellite spectrum in the wavelength range from 2.6000 to 2.6400 A. Improved values for the excitation rate coefficients of the Ti XXI resonance line, the intercombination lines and the forbidden line, and new theoretical results on the wavelengths and transition probabilities for beryllium-like satellites due to transitions of the type 1s/sup 2/ 2lnl' - 1s2p2l'' nl'' with n = 2-4 have been calculated

    Replication and Virus-Induced Transcriptome of HAdV-5 in Normal Host Cells versus Cancer Cells - Differences of Relevance for Adenoviral Oncolysis

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    Adenoviruses (Ads), especially HAdV-5, have been genetically equipped with tumor-restricted replication potential to enable applications in oncolytic cancer therapy. Such oncolytic adenoviruses have been well tolerated in cancer patients, but their anti-tumor efficacy needs to be enhanced. In this regard, it should be considered that cancer cells, dependent on their tissue of origin, can differ substantially from the normal host cells to which Ads are adapted by complex virus-host interactions. Consequently, viral replication efficiency, a key determinant of oncolytic activity, might be suboptimal in cancer cells. Therefore, we have analyzed both the replication kinetics of HAdV-5 and the virus-induced transcriptome in human bronchial epithelial cells (HBEC) in comparison to cancer cells. This is the first report on genome-wide expression profiling of Ads in their native host cells. We found that E1A expression and onset of viral genome replication are most rapid in HBEC and considerably delayed in melanoma cells. In squamous cell lung carcinoma cells, we observed intermediate HAdV-5 replication kinetics. Infectious particle production, viral spread and lytic activity of HAdV-5 were attenuated in melanoma cells versus HBEC. Expression profiling at the onset of viral genome replication revealed that HAdV-5 induced the strongest changes in the cellular transcriptome in HBEC, followed by lung cancer and melanoma cells. We identified prominent regulation of genes involved in cell cycle and DNA metabolism, replication and packaging in HBEC, which is in accord with the necessity to induce S phase for viral replication. Strikingly, in melanoma cells HAdV-5 triggered opposing regulation of said genes and, in contrast to lung cancer cells, no weak S phase induction was detected when using the E2F promoter as reporter. Our results provide a rationale for improving oncolytic adenoviruses either by adaptation of viral infection to target tumor cells or by modulating tumor cell functions to better support viral replication

    Fiber Mediated Receptor Masking in Non-Infected Bystander Cells Restricts Adenovirus Cell Killing Effect but Promotes Adenovirus Host Co-Existence

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    The basic concept of conditionally replicating adenoviruses (CRAD) as oncolytic agents is that progenies generated from each round of infection will disperse, infect and kill new cancer cells. However, CRAD has only inhibited, but not eradicated tumor growth in xenograft tumor therapy, and CRAD therapy has had only marginal clinical benefit to cancer patients. Here, we found that CRAD propagation and cancer cell survival co-existed for long periods of time when infection was initiated at low multiplicity of infection (MOI), and cancer cell killing was inefficient and slow compared to the assumed cell killing effect upon infection at high MOI. Excessive production of fiber molecules from initial CRAD infection of only 1 to 2% cancer cells and their release prior to the viral particle itself caused a tropism-specific receptor masking in both infected and non-infected bystander cells. Consequently, the non-infected bystander cells were inefficiently bound and infected by CRAD progenies. Further, fiber overproduction with concomitant restriction of adenovirus spread was observed in xenograft cancer therapy models. Besides the CAR-binding Ad4, Ad5, and Ad37, infection with CD46-binding Ad35 and Ad11 also caused receptor masking. Fiber overproduction and its resulting receptor masking thus play a key role in limiting CRAD functionality, but potentially promote adenovirus and host cell co-existence. These findings also give important clues for understanding mechanisms underlying the natural infection course of various adenoviruses

    Some effects of parallel energy propagation on the structure of dissipative trapped electron modes

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    The limitation of ballooning by parallel energy propagation is investigated for the dissipative trapped electron mode, wherein the local energy influx is proportional to the poloidally dependent trapped particle fraction. For small energetic asymmetries [mg less than 2.5 (OmegaOmega/sub i/a/c/sub s/) (a/R/ sup sup3sup 3/sub4sub 4/] the structure along the field line is predominantly a phase shift, dictated by the condition that the asymmetric energy input be compensated by parallel energy flow. For large asymmetry, mode number, and parallel arc length, the phase and amplitude variations necessitate an integral equation treatment. (auth
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