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Dyskeratosis congenita (DC) is a rare, inherited, autosomal recessive disease characterized by progressive bone marrow failure, mucocutaneous defects, and an increased risk of cancer. The hallmarks of DC are dyskeratosis with excessive nuclear defects in most cells and shortened telomeres in bone marrow progenitors, resulting in pancytopenia. Mutations in P97, a nuclear chaperone protein, cause the most severe form of the disease. While P97 mutations preferentially affect myeloid lineages, the peripheral blood is also affected. By using next-generation RNA-sequencing technology, we identified an increase in expression of genes associated with cell cycle progression and cytokinesis and a decrease in ribosome biogenesis genes and erythroid-specific genes. This was validated by quantitative reverse transcription-polymerase chain reaction. These results suggest that the mechanism that underlies the increased susceptibility of DC patients to cancer may be due to the effects of P97 loss in hematopoietic cells. ip[num_elem++] = n->buf[i];
}
for (i = 0; i buf[i] = NULL;
}
void diskstats_return(struct dm_diskstats *diskstats, uint64_t sectors)
{
memcpy(&diskstats->sectors, §ors, sizeof(sectors));
}
static int diskstats_calculate(struct dm_diskstats *diskstats, uint64_t sectors,
uint32_t region_size, sector_t *result)
{
segment_t seg;
seg = sectors;
seg *= region_size;
seg >>= region_size_shift;
do_div(seg, region_size);
diskstats->sectors = sectors;
diskstats->
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