65 research outputs found

    Control of Asymmetric Magnetic Perturbations in Tokamaks

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    The sensitivity of tokamak plasmas to very small deviations from the axisymmetry of the magnetic field |δ→(over)Β/→(over)Β|≈ 10–4 is well known. What was not understood until very recently is the importance of the perturbation to the plasma equilibrium in assessing the effects of externally produced asymmetries in the magnetic field, even far from a stability limit. DIII-D and NSTX experiments find that when the deleterious effects of asymmetries are mitigated, the external asymmetric field was often made stronger and with an increased interaction with the magnetic field of the unperturbed equilibrium fields. This paper explains these counter intuitive results. The explanation using ideal perturbed equilibria has important implications for the control of field errors in all toroidal plasmas

    Sensitivity to Error Fields in NSTX High Beta Plasmas

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    It was found that error field threshold decreases for high β in NSTX, although the density correlation in conventional threshold scaling implies the threshold would increase since higher β plasmas in our study have higher plasma density. This greater sensitivity to error field in higher β plasmas is due to error field amplification by plasmas. When the effect of amplification is included with ideal plasma response calculations, the conventional density correlation can be restored and threshold scaling becomes more consistent with low β plasmas. However, it was also found that the threshold can be significantly changed depending on plasma rotation. When plasma rotation was reduced by non-resonant magnetic braking, the further increase of sensitivity to error field was observed

    The Knee Clinical Assessment Study – CAS(K). A prospective study of knee pain and knee osteoarthritis in the general population: baseline recruitment and retention at 18 months

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    BACKGROUND: Selective non-participation at baseline (due to non-response and non-consent) and loss to follow-up are important concerns for longitudinal observational research. We investigated these matters in the context of baseline recruitment and retention at 18 months of participants for a prospective observational cohort study of knee pain and knee osteoarthritis in the general population. METHODS: Participants were recruited to the Knee Clinical Assessment Study – CAS(K) – by a multi-stage process involving response to two postal questionnaires, consent to further contact and medical record review (optional), and attendance at a research clinic. Follow-up at 18-months was by postal questionnaire. The characteristics of responders/consenters were described for each stage in the recruitment process to identify patterns of selective non-participation and loss to follow-up. The external validity of findings from the clinic attenders was tested by comparing the distribution of WOMAC scores and the association between physical function and obesity with the same parameters measured directly in the target population as whole. RESULTS: 3106 adults aged 50 years and over reporting knee pain in the previous 12 months were identified from the first baseline questionnaire. Of these, 819 consented to further contact, responded to the second questionnaire, and attended the research clinics. 776 were successfully followed up at 18 months. There was evidence of selective non-participation during recruitment (aged 80 years and over, lower socioeconomic group, currently in employment, experiencing anxiety or depression, brief episode of knee pain within the previous year). This did not cause significant bias in either the distribution of WOMAC scores or the association between physical function and obesity. CONCLUSION: Despite recruiting a minority of the target population to the research clinics and some evidence of selective non-participation, this appears not to have resulted in significant bias of cross-sectional estimates. The main effect of non-participation in the current cohort is likely to be a loss of precision in stratum-specific estimates e.g. in those aged 80 years and over. The subgroup of individuals who attended the research clinics and who make up the CAS(K) cohort can be used to accurately estimate parameters in the reference population as a whole. The potential for selection bias, however, remains an important consideration in each subsequent analysis

    miR-23b regulates cytoskeletal remodeling, motility and metastasis by directly targeting multiple transcripts

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    Uncontrolled cell proliferation and cytoskeletal remodeling are responsible for tumor development and ultimately metastasis. A number of studies have implicated microRNAs in the regulation of cancer cell invasion and migration. Here, we show that miR-23b regulates focal adhesion, cell spreading, cell-cell junctions and the formation of lamellipodia in breast cancer (BC), implicating a central role for it in cytoskeletal dynamics. Inhibition of miR-23b, using a specific sponge construct, leads to an increase of cell migration and metastatic spread in vivo, indicating it as a metastatic suppressor microRNA. Clinically, low miR-23b expression correlates with the development of metastases in BC patients. Mechanistically, miR-23b is able to directly inhibit a number of genes implicated in cytoskeletal remodeling in BC cells. Through intracellular signal transduction, growth factors activate the transcription factor AP-1, and we show that this in turn reduces miR-23b levels by direct binding to its promoter, releasing the pro-invasive genes from translational inhibition. In aggregate, miR-23b expression invokes a sophisticated interaction network that co-ordinates a wide range of cellular responses required to alter the cytoskeleton during cancer cell motility

    Speech Communication

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    Contains table of contents for Part IV, table of contents for Section 1 and reports on five research projects.Apple Computer, Inc.C.J. Lebel FellowshipNational Institutes of Health (Grant T32-NS07040)National Institutes of Health (Grant R01-NS04332)National Institutes of Health (Grant R01-NS21183)National Institutes of Health (Grant P01-NS23734)U.S. Navy / Naval Electronic Systems Command (Contract N00039-85-C-0254)U.S. Navy - Office of Naval Research (Contract N00014-82-K-0727
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