Использование двигателя-маховика для создания управляющих моментов космического аппарата

In this article we present a comprehensive study of microcrystalline silicon (PC-Si:H) p-i-n solar cells prepared by using plasma-enhanced chemical vapor deposition (PECVD) at 13.56 MHz excitation frequency. In the first step the cell development was performed in a small area PECVD reactor showing the relationship between the deposition process parameters and the resulting solar cell performance. Subsequent up-scaling to a substrate area of 30 X 30 cm confirmed the scalability of optimized deposition parameters to large area reactors. We investigated the deposition regime of high rf power P (rf) (0.25-0.7 W/cm(2)) and high deposition pressure P (dep) (1 - 11 Torr) for the muc-Si:H i layer. Furthermore, the influence of silane concentration and deposition temperature was studied. A transition between amorphous and microcrystalline growth could be achieved by a variation of either deposition pressure, plasma power, or silane concentration. The best microcrystalline silicon solar cells were prepared close to the transition to amorphous growth. A high deposition pressure was a prerequisite for obtaining, high quality material at a high growth rate. The best solar cell efficiencies achieved so far are 8.1% and 6.6% at i-layer growth rates of 5 and 10 Angstrom/s, respectively, for muc-Si:H single junction cells. Applied in a-Si:H/muc-Si:H tandem cells a stabilized efficiency of 10.0% was achieved. (C) 2002 American Vacuum Society

hMYH and hMTH1 cooperate for survival in mismatch repair defective T-cell acute lymphoblastic leukemia

hMTH1 is an 8-oxodGTPase that prevents mis-incorporation of free oxidized nucleotides into genomic DNA. Base excision and mismatch repair pathways also restrict the accumulation of oxidized lesions in DNA by removing the mis-inserted 8-oxo-7,8-dihydro-2'-deoxyguanosines (8-oxodGs). In this study, we aimed to investigate the interplay between hMYH DNA glycosylase and hMTH1 for cancer cell survival by using mismatch repair defective T-cell acute lymphoblastic leukemia (T-ALL) cells. To this end, MYH and MTH1 were silenced individually or simultaneously using small hairpin RNAs. Increased sub-G1 population and apoptotic cells were observed upon concurrent depletion of both enzymes. Elevated cell death was consistent with cleaved caspase 3 accumulation in double knockdown cells. Importantly, overexpression of the nuclear isoform of hMYH could remove the G1 arrest and partially rescue the toxicity observed in hMTH1-depleted cells. In addition, expression profiles of human DNA glycosylases were generated using quantitative reverse transcriptase–PCR in MTH1 and/or MYH knockdown cells. NEIL1 DNA glycosylase, involved in repair of oxidized nucleosides, was found to be significantly downregulated as a cellular response to MTH1–MYH co-suppression. Overall, the results suggest that hMYH and hMTH1 functionally cooperate for effective repair and survival in mismatch repair defective T-ALL Jurkat A3 cells