EFFICACY OF A SLIDING BEAM AS A NONLINEAR VIBRATION ISOLATOR

ABSTRACT The influence of friction due to beam sliding at its supports on its dynamic behavior and its efficacy as a nonlinear isolator is studied numerically under sinusoidal and random excitation excitations. Under sinusoidal excitation, the equation of motion of the system is solved numerically and the solution is utilized to estimate the system transmissibility. It is found that when the excitation frequency is increased beyond resonance, the friction at the sliding supports serves to improve the transmissibility. The dependence of the response on initial conditions establishes the basins of attraction for different values of friction coefficient and excitation frequency and amplitude. Under random excitation, the system response statistics are estimated from Monte Carlo simulation results for different values of friction coefficient and excitation power spectral density level. The friction is found to result in a significant reduction of the system response mean square

Gemcitabine-Mediated Radiosensitization of Human Soft Tissue Sarcoma1

Background/Purpose: Local and systemic control of soft tissue sarcoma (STS) remains a clinical challenge, particularly for retroperitoneal, deep truncal, or advanced extremity disease. 2′,2′-Difluoro-2′-deoxycytidine (gemcitabine) is a potent radiosensitizer in many tumor types, but it has not been studied in human STS. The purpose of this study was to determine the radiosensitizing potential of gemcitabine in preclinical models of human STS. Materials and Methods: The in vitro radiosensitizing activity of gemcitabine was assessed with clonogenic survival assay on three human STS cell lines: SK-LMS-1 (leiomyosarcoma), SW-872 (liposarcoma), and HT-1080 (fibrosarcoma). Cell cycle distribution was determined using dual-channel flow cytometry. The in vivo radiosensitizing activity of gemcitabine was assessed with subcutaneous SK-LMS-1 nude mice xenografts. Tumor-bearing mice were treated with concurrent weekly gemcitabine and fractionated daily radiotherapy (RT) (2 Gy daily) for 3 weeks (a total dose of 30 Gy). Results: The 50% inhibitory concentration (IC50) of gemcitabine for the human STS cell lines ranged from 10 to 1000 nM. Significant in vitro radiosensitization was demonstrated in all three human STS cell lines using gemcitabine concentrations at and below the IC50. Maximal radiosensitization was associated with accumulation of cells in early S-phase. SK-LMS-1 xenografts displayed significant tumor growth delay with combined gemcitabine and RT compared to either treatment alone. Treatment related toxicity was greatest in the gemcitabine plus RT arm, but remained at an acceptable level. Conclusions: Gemcitabine is a potent radiosensitizer in preclinical models of human STS. Clinical trials combining gemcitabine and RT in human STS are warranted

CD1d structure and regulation on human thymocytes, peripheral blood T cells, B cells and monocytes

Human T cells expressing CD161 and an invariant T-cell receptor (TCR) α-chain (Vα24invt T cells) specifically recognize CD1d and appear to have immunoregulatory functions. However, the physiological target cells for this T-cell population, and whether alterations in CD1d expression contribute to the regulation of Vα24invt T-cell responses, remain to be determined. A series of antibodies were generated to assess CD1d expression, structure and regulation on human lymphoid and myeloid cells. CD1d was expressed at high levels by human cortical thymocytes and immunoprecipitation analyses showed it to be a 48 000-MW glycosylated protein. However, after solubilization, the majority of the thymocyte CD1d protein, but not CD1d expressed by transfected cells, lost reactivity with monoclonal antibodies (mAbs) against native CD1d, indicating that it was alternatively processed. Moreover, thymocytes were not recognized by CD1d-reactive Vα24invt T-cell clones. Medullary thymocytes and resting peripheral blood T cells were CD1d–, but low-level CD1d expression was induced on activated T cells. CD1d was expressed by B cells in peripheral blood and lymph node mantle zones, but germinal centres were CD1d–. Resting monocytes were CD1d+ but, in contrast to CD1a, b and c, their surface expression of CD1d was not up-regulated by granulocyte–macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4) activation. These results demonstrate constitutive CD1d expression by human professional antigen-presenting cells and that post-translational processing of CD1d may contribute to regulation of the activity of CD1d-specific T cells