Efficient Bundle Sorting

This is the published version. Copyright © 2006 Society for Industrial and Applied MathematicsMany data sets to be sorted consist of a limited number of distinct keys. Sorting such data sets can be thought of as bundling together identical keys and having the bundles placed in order; we therefore denote this as bundle sorting. We describe an efficient algorithm for bundle sorting in external memory, which requires at most c(N/B) logM/Bk disk accesses, where N is the number of keys, M is the size of internal memory, k is the number of distinct keys, B is the transfer block size, and 2 < c < 4. For moderately sized k, this bound circumvents the Theta((N/B) logM/B (N/B)) I/O lower bound known for general sorting. We show that our algorithm is optimal by proving a matching lower bound for bundle sorting. The improved running time of bundle sorting over general sorting can be significant in practice, as demonstrated by experimentation. An important feature of the new algorithm is that it is executed "in-place," requiring no additional disk space

Efficient Bundle Sorting

AMS subject classification. 68W01 DOI. 10.1137/S0097539704446554Many data sets to be sorted consist of a limited number of distinct keys. Sorting such data sets can be thought of as bundling together identical keys and having the bundles placed in order; we therefore denote this as bundle sorting. We describe an efficient algorithm for bundle sorting in external memory, which requires at most c(N/B) logM/B k disk accesses, where N is the number of keys, M is the size of internal memory, k is the number of distinct keys, B is the transfer block size, and 2 < c < 4. For moderately sized k, this bound circumvents the Θ((N/B) logM/B(N/B)) I/O lower bound known for general sorting. We show that our algorithm is optimal by proving a matching lower bound for bundle sorting. The improved running time of bundle sorting over general sorting can be significant in practice, as demonstrated by experimentation. An important feature of the new algorithm is that it is executed “in-place,” requiring no additional disk space

InSite: a computational method for identifying protein-protein interaction binding sites on a proteome-wide scale

InSite is a computational method that integrates high-throughput protein and sequence data to infer the specific binding regions of interacting protein pairs

A Transcriptional Program Mediating Entry into Cellular Quiescence

The balance of quiescence and cell division is critical for tissue homeostasis and organismal health. Serum stimulation of fibroblasts is well studied as a classic model of entry into the cell division cycle, but the induction of cellular quiescence, such as by serum deprivation (SD), is much less understood. Here we show that SS and SD activate distinct early transcriptional responses genome-wide that converge on a late symmetric transcriptional program. Several serum deprivation early response genes (SDERGs), including the putative tumor suppressor genes SALL2 and MXI1, are required for cessation of DNA synthesis in response to SD and induction of additional SD genes. SDERGs are coordinately repressed in many types of human cancers compared to their normal counterparts, and repression of SDERGs predicts increased risk of cancer progression and death in human breast cancers. These results identify a gene expression program uniquely responsive to loss of growth factor signaling; members of SDERGs may constitute novel growth inhibitors that prevent cancer

Module Map of Stem Cell Genes Guides Creation of Epithelial Cancer Stem Cells

SummarySelf-renewal is a hallmark of stem cells and cancer, but existence of a shared stemness program remains controversial. Here, we construct a gene module map to systematically relate transcriptional programs in embryonic stem cells (ESCs), adult tissue stem cells, and human cancers. This map reveals two predominant gene modules that distinguish ESCs and adult tissue stem cells. The ESC-like transcriptional program is activated in diverse human epithelial cancers and strongly predicts metastasis and death. c-Myc, but not other oncogenes, is sufficient to reactivate the ESC-like program in normal and cancer cells. In primary human keratinocytes transformed by Ras and IκBα, c-Myc increases the fraction of tumor-initiating cells by 150-fold, enabling tumor formation and serial propagation with as few as 500 cells. c-Myc-enhanced tumor initiation is cell-autonomous and independent of genomic instability. Thus, activation of an ESC-like transcriptional program in differentiated adult cells may induce pathologic self-renewal characteristic of cancer stem cells