Male germ cell apoptosis has been extensively explored in rodents. In contrast, very little is known about the susceptibility of developing germ cells to apoptosis in response to busulfan treatment. Spontaneous apoptosis of germ cells is rarely observed in the adult mouse testis, but under the experimental conditions described here, busulfan-treated mice exhibited a marked increase in apoptosis and a decrease in testis weight. TdT-mediated dUTP-X nicked end labeling analysis indicates that at one week following busulfan treatment, apoptosis was confined mainly to spermatogonia, with lesser effects on spermatocytes. The percentage of apoptosis-positive tubules and the apoptotic cell index increased in a time-dependent manner. An immediate effect was observed in spermatogonia within one week of treatment, and in the following week, secondary effects were observed in spermatocytes. RT-PCR analysis showed that expression of the spermatogonia-specific markers c-kit and Stra 8 was reduced but that Gli I gene expression remained constant, which is indicative of primary apoptosis of differentiating type A spermatogonia. Three and four weeks after busulfan treatment, RAD51 and FasL expression decreased to nearly undetectable levels, indicating that meiotic spematocytes and post-meiotic cells, respectively, were lost. The period of germ cell depletion did not coincide with increased p53 or Fas/FasL expression in the busulfan-treated testis, although p110Rb phosphorylation and PCNA expression were inhibited. These data suggest that increased depletion of male germ cells in the busulfan-treated mouse is mediated by loss of c-kit/SCF signaling but not by p53-or Fas/FasL-dependent mechanisms. Spermatogonial stem cells may be protected from cell death by modulating cell cycle signaling such that E2F-dependent protein expression, which is critical for G1 phase progression, is inhibited.
SUMMARYWe consider the physical layer error performance parameters and design criteria for digital satellite systems established by ITU-R Recommendation S.1062, where the performance objectives are given in terms of the bit error rate (BER) divided by the average number of errors within a cluster. It is well known that errors on satellite links employing forward error correction (FEC) schemes tend to occur in clusters. The resulting block error rate is the same as if it was caused by randomly occurring bit errors with an error-event ratio of BER/a, where a is the average number of errors within a cluster. The factor, a, accounts for the burstiness of the errors and also represents the ratio between the BER and the error-event ratio. This paper proposes theoretical methods to estimate the factor, a. Using the weight distributions of the FEC codes, we derive a set of expressions for the factor, a, as well as their compact lower bounds. We present lower bounds for various FEC schemes including binary BCH codes, block turbo codes, convolutional codes, and turbo codes. The simulation results show that the proposed lower bounds are good estimates in the high signalto-noise ratio region.
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