70 research outputs found

    Stress and efficiency studies in EFG

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    Stress and efficiency studies in EFG were carried out for silicon sheet growth. Methods were developed to quantify influence of dislocation electrical activity on bulk lifetime. A new creep law formulation for silicon stress was developed. Bulk lifetime degradation due to increase in doping levels was also examined

    Technical progress in silicon sheet growth under DOE/JPL FSA program, 1975-1986

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    The technical progress made in the Silicon Sheet Growth Program during its 11 years was reviewed. At present, in 1986, only two of the original 9 techniques have survived to the start-up, pilot-plant stage in industry. These two techniques are the edge-defined, film-fed growth (EFG) technique that produces closed shape polygons, and the WEB dendritic technique that produces single ribbons. Both the status and future concerns of the EFG and WEB techniques were discussed

    Large area silicon sheet by EFG

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    Work carried out on the JPL Flat Plate Solar Array Project, for the purpose of developing a method for silicon ribbon production by Edge-defined Film-fed Growth (EEG) for use as low-cost substrate material in terrestrial solar cell manufacture, is described. A multiple ribbon furnace unit that is designed to operate on a continuous basis for periods of at least one week, with melt replenishment and automatic ribbon width control, and to produce silicon sheet at a rate of one square meter per hour, was constructed. Program milestones set for single ribbon furnace operation to demonstrate basic EEG system capabilities with respect to growth speed, thickness and cell performance were achieved for 10 cm wide ribbon: steady-state growth at 4 cm/min and 200 micron thickness over periods of an hour and longer was made routine, and a small area cell efficiency of 13+% demonstrated. Large area cells of average efficiency of 10 to 11%, with peak values of 11 to 12% were also achieved. The integration of these individual performance levels into multiple ribbon furnace operation was not accomplished

    Hydrogenation of Si from SiNx(H) films: Characterization of H introduced into the Si

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    A promising method to introduce H into multicrystalline Si solar cells in order to passivate bulk defects is by the postdeposition annealing of a H-rich, SiNx surface layer. It has previously been difficult to characterize the small concentration of H that is introduced by this method. Infrared spectroscopy has been used together with marker impurities in the Si to determine the concentration and depth of H introduced into Si from an annealed SiNx film

    Hydrogenation of Si from SiN_x: H films: how much hydrogen is really in the Si?

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    A promising method to introduce H into Si solar cells in order to passivate bulk defects is by the post-deposition annealing of an H-rich, SiN_x surface layer. It previously has been difficult to characterize the small concentration of H that is introduced by this method. IR spectroscopy has been used together with marker impurities in the Si to determine the concentration and depth of H introduced into Si from an annealed SiN_x film

    Expression of Y-box-binding protein dbpC/contrin, a potentially new cancer/testis antigen

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    Y-box-binding proteins are members of the human cold-shock domain protein superfamily, which includes dbpA, dbpB/YB-1, and dbpC/contrin. dbpC/contrin is a germ cell-specific Y-box-binding protein and is suggested to function as a nuclear transcription factor and RNA-binding protein in the cytoplasm. Whereas ubiquitous dbpB/YB-1 expression has been well studied in various types of human carcinomas as a prognostic or predictive marker, the dbpC/contrin expression in human tumour cells has not been reported. In this report, we provide the first evidence showing that dbpC was highly expressed in human testicular seminoma and ovarian dysgerminomas, and in carcinomas in other tissues and that its expression in normal tissues is nearly restricted to germ cells and placental trophoblasts. These results indicate that dbpC/contrin would be a potentially novel cancer/testis antigen

    Mifepristone prevents repopulation of ovarian cancer cells escaping cisplatin-paclitaxel therapy

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    <p>Abstract</p> <p>Background</p> <p>Advanced ovarian cancer is treated with cytoreductive surgery and combination platinum- and taxane-based chemotherapy. Although most patients have acute clinical response to this strategy, the disease ultimately recurs. In this work we questioned whether the synthetic steroid mifepristone, which as monotherapy inhibits the growth of ovarian cancer cells, is capable of preventing repopulation of ovarian cancer cells if given after a round of lethal cisplatin-paclitaxel combination treatment.</p> <p>Methods</p> <p>We established an <it>in vitro</it> approach wherein ovarian cancer cells with various sensitivities to cisplatin or paclitaxel were exposed to a round of lethal doses of cisplatin for 1 h plus paclitaxel for 3 h. Thereafter, cells were maintained in media with or without mifepristone, and short- and long-term cytotoxicity was assessed.</p> <p>Results</p> <p>Four days after treatment the lethality of cisplatin-paclitaxel was evidenced by reduced number of cells, increased hypodiploid DNA content, morphological features of apoptosis, DNA fragmentation, and cleavage of caspase-3, and of its downstream substrate PARP. Short-term presence of mifepristone either enhanced or did not modify such acute lethality. Seven days after receiving cisplatin-paclitaxel, cultures showed signs of relapse with escaping colonies that repopulated the plate in a time-dependent manner. Conversely, cultures exposed to cisplatin-paclitaxel followed by mifepristone not only did not display signs of repopulation following initial chemotherapy, but they also had their clonogenic capacity drastically reduced when compared to cells repopulating after cisplatin-paclitaxel.</p> <p>Conclusions</p> <p>Cytostatic concentrations of mifepristone after exposure to lethal doses of cisplatin and paclitaxel in combination blocks repopulation of remnant cells surviving and escaping the cytotoxic drugs.</p
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