Clones and Macro co-changes

Ideally, any change that modifies the similar parts of a cloned code snippet should be propagated to all its duplicates. In practice however, consistent propagation of changes in clones does not always happen. Current evidence indicates that clone families have a 50% chance of having consistent changes. This paper measures cloning and co-changes at file level as a proxy to assess the frequency of consistent changes. Given that changes to a clone group are not necessarily propagated in the same commit transaction (i.e., late propagations), our analysis uses macro co-changes instead of the traditional definition of co-changes. Macro changes group bursts of changes that are closer among themselves than to other changes, regardless of author or message. Then, macro co-changes are sets of files that change in the same macro changes. Each cloned file is tagged depending on whether any of the files with which it macro co-changes is cloned with it (during the macro change) or not. Contrary to previous results, we discovered that most of the cloned files macro co-change only with files with which they share clones. Thus providing evidence that macro changes are appropriate to study the conjecture of clones requiring co-changes, and indicating that consistent changes might be the norm in cloned code

Clones and Macro-Co-Changes

Ideally, any change that modifies the similar parts of a cloned code snippet should be propagated to all its duplicates. In practice however, consistent propagation of changes in clones does not always happen. Current evidence indicates that clone families have a 50% chance of having consistent changes. This paper measures cloning and co-changes at file level as a proxy to assess the frequency of consistent changes. Given that changes to a clone group are not necessarily propagated in the same commit transaction (i.e., late propagations), our analysis uses macro co-changes instead of the traditional definition of co-changes. Macro changes group bursts of changes that are closer among themselves than to other changes, regardless of author or message. Then, macro co-changes are sets of files that change in the same macro changes. Each cloned file is tagged depending on whether any of the files with which it macro co-changes is cloned with it (during the macro change) or not. Contrary to previous results, we discovered that most of the cloned files macro co-change only with files with which they share clones. Thus providing evidence that macro changes are appropriate to study the conjecture of clones requiring co-changes, and indicating that consistent changes might be the norm in cloned code

A Novel Family of Mobile Genetic Elements Is Limited to the Germline Genome in \u3cem\u3eTetrahymena Thermophila\u3c/em\u3e

In the ciliated protozoan Tetrahymena thermophila, extensive DNA elimination is associated with differentiation of the somatic macronucleus from the germline micronucleus. This study describes the isolation and complete characterization of Tlr elements, a family of approximately 30 micronuclear DNA sequences that are efficiently eliminated from the developing macronucleus. The data indicate that Tlr elements are comprised of an ~22 kb internal region flanked by complex and variable termini. The Tlr internal region is highly conserved among family members and contains 15 open reading frames, some of which resemble genes encoded by transposons and viruses. The Tlr termini appear to be long inverted repeats consisting of (i) a variable region containing multiple direct repeats which differ in number and sequence from element to element and (ii) a conserved terminal 47 bp sequence. Taken together, these results suggest that Tlr elements comprise a novel family of mobile genetic elements that are confined to the Tetrahymena germline genome. Possible mechanisms of developmentally programmed Tlr elimination are discussed

Cellular Automata Model of Macroevolution

In this paper I describe a cellular automaton model of a multi-species ecosystem, suitable for the study of emergent properties of macroevolution. Unlike majority of ecological models, the number of coexisting species is not fixed. Starting from one common ancestor they appear by "mutations" of existent species, and then survive or extinct depending on the balance of local ecological interactions. Monte-Carlo numerical simulations show that this model is able to qualitatively reproduce phenomena that have been observed in other models and in nature.Comment: 8 pages, 3 figures, Fourteenth National Conference on Application of Mathematics in Biology and Medicine, Leszno 2008 (POLAND

Cnemidophorus laredoensis

Number of Pages: 5Integrative BiologyGeological Science

A quantitative assay for transformation of bone marrow cells by Abelson murine leukemia virus

A quantitative Abelson murine leukemia virus (A-MuLV) lymphoid cell transformation assay has been developed using a semisolid agarose culture system. Under these conditions lymphoid cell transformation was shown to vary linearly with the dose of A-MuLV used. The susceptibility of bone marrow cells from different strains of mice to A-MuLV-induced transformation can be estimated using the agarose assay. Strains with bone marrow cells of high, medium, and low susceptibility to A-MuLV can be identified. The assay has been used to study the susceptibility of cells from lymphoid organs of fetal and adult mice to A-MuLV. Cell suspensions from fetal liver, adult bone marrow, and adult spleen are susceptible to A-MuLV, while thymocytes are resistant to A-MuLV-induced transformation. Bovine serum albumin gradient fractionation of bone marrow cells before infection with A-MuLV demonstrates that the majority of A-MuLV-sensitive cells are recovered in a broad band partially overlapping the majority of the nucleated cells. The agarose assay system allows study of A-MuLV-lymphoid cell interaction at the level of single cell-single virus particle interaction

Structured Review of Code Clone Literature

This report presents the results of a structured review of code clone literature. The aim of the review is to assemble a conceptual model of clone-related concepts which helps us to reason about clones. This conceptual model unifies clone concepts from a wide range of literature, so that findings about clones can be compared with each other

The Glial Regenerative Response to Central Nervous System Injury Is Enabled by Pros-Notch and Pros-NFκB Feedback

Organisms are structurally robust, as cells accommodate changes preserving structural integrity and function. The molecular mechanisms underlying structural robustness and plasticity are poorly understood, but can be investigated by probing how cells respond to injury. Injury to the CNS induces proliferation of enwrapping glia, leading to axonal re-enwrapment and partial functional recovery. This glial regenerative response is found across species, and may reflect a common underlying genetic mechanism. Here, we show that injury to the Drosophila larval CNS induces glial proliferation, and we uncover a gene network controlling this response. It consists of the mutual maintenance between the cell cycle inhibitor Prospero (Pros) and the cell cycle activators Notch and NFκB. Together they maintain glia in the brink of dividing, they enable glial proliferation following injury, and subsequently they exert negative feedback on cell division restoring cell cycle arrest. Pros also promotes glial differentiation, resolving vacuolization, enabling debris clearance and axonal enwrapment. Disruption of this gene network prevents repair and induces tumourigenesis. Using wound area measurements across genotypes and time-lapse recordings we show that when glial proliferation and glial differentiation are abolished, both the size of the glial wound and neuropile vacuolization increase. When glial proliferation and differentiation are enabled, glial wound size decreases and injury-induced apoptosis and vacuolization are prevented. The uncovered gene network promotes regeneration of the glial lesion and neuropile repair. In the unharmed animal, it is most likely a homeostatic mechanism for structural robustness. This gene network may be of relevance to mammalian glia to promote repair upon CNS injury or disease