wanyu/IteraTeR_full_sent huggingface dataset:
Original:  Duffie, Kapadia and Saita The Journal of Finance, 2007%DIFDELCMD < ]{%%% DasDuffie2007 and Duffie, Eckner, Horel and Saita%DIFDELCMD < [%%% The Journal of Finance, 2009 duffieEHS2009%DIFDELCMD < } %%% demonstrate the presence of frailty correlated default and the incapability of doubly stochastic assumption to capture default contagion or frailty (unobservable explanatory variables that are correlated across firms) .
Revised:  Duffie, Kapadia and Saita The Journal of Finance, 2007%DIFDELCMD < ]{%%% DasDuffie2007 and Duffie, Eckner, Horel and Saita%DIFDELCMD < [%%% duffieEHS2009%DIFDELCMD < } %%% demonstrate the presence of frailty correlated default and the incapability of doubly stochastic assumption to capture default contagion or frailty (unobservable explanatory variables that are correlated across firms) .
Edit intent: coherence
Original:  Duffie, Kapadia and Saita The Journal of Finance, 2007%DIFDELCMD < ]{%%% DasDuffie2007 and Duffie, Eckner, Horel and Saita%DIFDELCMD < [%%% The Journal of Finance, 2009 duffieEHS2009%DIFDELCMD < } %%% demonstrate the presence of frailty correlated default and the incapability of doubly stochastic assumption to capture default contagion or frailty (unobservable explanatory variables that are correlated across firms) .
Revised:  Duffie, Kapadia and Saita The Journal of Finance, 2007%DIFDELCMD < ]{%%% DasDuffie2007 and Duffie, Eckner, Horel and Saita%DIFDELCMD < [%%% The Journal of Finance, 2009 %DIFDELCMD < } %%% demonstrate the presence of frailty correlated default and the incapability of doubly stochastic assumption to capture default contagion or frailty (unobservable explanatory variables that are correlated across firms) .
Edit intent: clarity
Original:  Duffie, Kapadia and Saita The Journal of Finance, 2007%DIFDELCMD < ]{%%% DasDuffie2007 and Duffie, Eckner, Horel and Saita%DIFDELCMD < [%%% The Journal of Finance, 2009 duffieEHS2009%DIFDELCMD < } %%% demonstrate the presence of frailty correlated default and the incapability of doubly stochastic assumption to capture default contagion or frailty (unobservable explanatory variables that are correlated across firms) .
Revised:  Duffie, Kapadia and Saita The Journal of Finance, 2007%DIFDELCMD < ]{%%% DasDuffie2007 and Duffie, Eckner, Horel and Saita%DIFDELCMD < [%%% The Journal of Finance, 2009 duffieEHS2009%DIFDELCMD < } %%% .
Edit intent: meaning-changed
Original:  We investigated nine widely-used benchmarks for virtual screening and QSAR , and show that the amount of AVE bias strongly correlates with the performance of ligand-based predictive methods irrespective of the predicted property, chemical fingerprint, similarity measure, or previously-applied unbiasing techniques.
Revised:  We investigated seven widely-used benchmarks for virtual screening and QSAR , and show that the amount of AVE bias strongly correlates with the performance of ligand-based predictive methods irrespective of the predicted property, chemical fingerprint, similarity measure, or previously-applied unbiasing techniques.
Edit intent: meaning-changed
Original:  We investigated nine widely-used benchmarks for virtual screening and QSAR , and show that the amount of AVE bias strongly correlates with the performance of ligand-based predictive methods irrespective of the predicted property, chemical fingerprint, similarity measure, or previously-applied unbiasing techniques.
Revised:  We investigated nine widely-used benchmarks for virtual screening and classification , and show that the amount of AVE bias strongly correlates with the performance of ligand-based predictive methods irrespective of the predicted property, chemical fingerprint, similarity measure, or previously-applied unbiasing techniques.
Edit intent: clarity
Original:  RESULTS: Experiments on simulated phenotypic signals and SNP replication show that this approach offers a substantial gain in statistical power for cardiac genotype-phenotype associations while providing good control of the false discovery rate.
Revised:  Experiments on simulated phenotypic signals and SNP replication show that this approach offers a substantial gain in statistical power for cardiac genotype-phenotype associations while providing good control of the false discovery rate.
Edit intent: coherence
Original: In this paper, we introduce a new problem called Tree-Residue Vertex-Breaking (TRVB): given a multigraph G some of whose vertices are marked "breakable," is it possible to convert G into a tree via a sequence of "vertex-breaking" operations ( disconnecting the edges at a degree-k breakable vertex by replacing that vertex with k degree-1 vertices  )?
Revised: In this paper, we introduce a new problem called Tree-Residue Vertex-Breaking (TRVB): given a multigraph G some of whose vertices are marked "breakable," is it possible to convert G into a tree via a sequence of "vertex-breaking" operations ( replacing a degree-k breakable vertex by replacing that vertex with k degree-1 vertices )?
Edit intent: meaning-changed
Original: In this paper, we introduce a new problem called Tree-Residue Vertex-Breaking (TRVB): given a multigraph G some of whose vertices are marked "breakable," is it possible to convert G into a tree via a sequence of "vertex-breaking" operations ( disconnecting the edges at a degree-k breakable vertex by replacing that vertex with k degree-1 vertices  )?
Revised: In this paper, we introduce a new problem called Tree-Residue Vertex-Breaking (TRVB): given a multigraph G some of whose vertices are marked "breakable," is it possible to convert G into a tree via a sequence of "vertex-breaking" operations ( disconnecting the edges at a degree-k breakable vertex by k degree-1 vertices )?
Edit intent: clarity
Original: In this paper, we introduce a new problem called Tree-Residue Vertex-Breaking (TRVB): given a multigraph G some of whose vertices are marked "breakable," is it possible to convert G into a tree via a sequence of "vertex-breaking" operations ( disconnecting the edges at a degree-k breakable vertex by replacing that vertex with k degree-1 vertices  )?
Revised: In this paper, we introduce a new problem called Tree-Residue Vertex-Breaking (TRVB): given a multigraph G some of whose vertices are marked "breakable," is it possible to convert G into a tree via a sequence of "vertex-breaking" operations ( disconnecting the edges at a degree-k breakable vertex by replacing that vertex with k degree-1 vertices , disconnecting the k incident edges )?
Edit intent: meaning-changed
Original:  We consider the special cases of TRVB with any combination of the following additional constraints: G must be planar, G must be a simple graph, the degree of every breakable vertex must belong to an allowed list B, and the degree of every unbreakable vertex must belong to an allowed list U.
Revised:  We characterize the computational complexity of TRVB with any combination of the following additional constraints: G must be planar, G must be a simple graph, the degree of every breakable vertex must belong to an allowed list B, and the degree of every unbreakable vertex must belong to an allowed list U.
Edit intent: meaning-changed
Original:  To demonstrate the use of TRVB, we give a simple proof of the known result that Hamiltonicity in max-degree-3 square grid graphs is NP-hard \ge  .
Revised:  To demonstrate the use of TRVB, we give a simple proof of the known result that Hamiltonicity in max-degree-3 square grid graphs is NP-hard . We also demonstrate a connection between TRVB and the Hypergraph Spanning Tree problem. This connection allows us to show that the Hypergraph Spanning Tree problem in k-uniform 2-regular hypergraphs is NP-complete for any k\ge .
Edit intent: meaning-changed
Original:  To demonstrate the use of TRVB, we give a simple proof of the known result that Hamiltonicity in max-degree-3 square grid graphs is NP-hard \ge  .
Revised:  To demonstrate the use of TRVB, we give a simple proof of the known result that Hamiltonicity in max-degree-3 square grid graphs is NP-hard \ge 4, even when the incidence graph of the hypergraph is planar .
Edit intent: meaning-changed
Original:  Through the calibration process, we quantified the removal of healthy red blood cells and  the preferential infection of reticulocytes during Plamodium cynomolgi infection of Macaca mulatta.
Revised:  Through the calibration process, we quantified the removal of healthy red blood cells and the the preferential infection of reticulocytes during Plamodium cynomolgi infection of Macaca mulatta.
Edit intent: fluency
Original: The aim of this short note is to fill in a gap in our earlier paper [ 7 ] on 2BSDEs with reflections, and to explain how to correct the subsequent results in the second paper [ 6 ].
Revised: The aim of this short note is to fill in a gap in our earlier paper [ 16 ] on 2BSDEs with reflections, and to explain how to correct the subsequent results in the second paper [ 6 ].
Edit intent: meaning-changed
Original: The aim of this short note is to fill in a gap in our earlier paper [ 7 ] on 2BSDEs with reflections, and to explain how to correct the subsequent results in the second paper [ 6 ].
Revised: The aim of this short note is to fill in a gap in our earlier paper [ 7 ] on 2BSDEs with reflections, and to explain how to correct the subsequent results in the second paper [ 15 ].
Edit intent: meaning-changed
Original:  In particular, we recover and extend the results that Bernstein et al. (2000) , developed in the context of manifold learning, and those of Karaman and Frazzoli (2011), developed in the context of robotics .
Revised:  In particular, we recover and extend the results of Bernstein et al. (2000) , developed in the context of manifold learning, and those of Karaman and Frazzoli (2011), developed in the context of robotics .
Edit intent: fluency
Original: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the  von Foerster equation  for predicting population growth and cell age distributions.
Revised: Many single-cell observables are highly heterogeneous. A part of this heterogeneity stems from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the von Foerster equation for predicting population growth and cell age distributions.
Edit intent: clarity
Original: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the  von Foerster equation  for predicting population growth and cell age distributions.
Revised: The identifcation and separation of intrinsic variability from age-related phenomena : the fact that there is a nonuniform distribution of cells with different ages. This has led to a renewed interest in traditional analytic methodologies including use of the von Foerster equation for predicting population growth and cell age distributions.
Edit intent: meaning-changed
Original: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the  von Foerster equation  for predicting population growth and cell age distributions.
Revised: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in analytic methodologies including use of the von Foerster equation for predicting population growth and cell age distributions.
Edit intent: clarity
Original: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the  von Foerster equation  for predicting population growth and cell age distributions.
Revised: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the " von Foerster equation for predicting population growth and cell age distributions.
Edit intent: fluency
Original: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the  von Foerster equation  for predicting population growth and cell age distributions.
Revised: The identifcation and separation of intrinsic variability from age-related phenomena has been the subject of a growing body of literature, supporting renewed interest in traditional analytic methodologies including use of the von Foerster equation " for predicting population growth and cell age distributions.
Edit intent: fluency
Original:  Here we discuss how some of the most popular implementations of this machinery assume a strong condition on the ergodicity of the cell cycle duration ensemble and that two common definitions for the term , ergodicity, while identical in an ensemble with a fixed number of individuals , are in fact unique constraints when the ensemble is growing.
Revised:  Here we discuss how some of the most popular implementations of this machinery assume a strong condition on the ergodicity of the cell cycle duration ensemble . We show that one common definition for the term , ergodicity, while identical in an ensemble with a fixed number of individuals , are in fact unique constraints when the ensemble is growing.
Edit intent: meaning-changed
Original:  Here we discuss how some of the most popular implementations of this machinery assume a strong condition on the ergodicity of the cell cycle duration ensemble and that two common definitions for the term , ergodicity, while identical in an ensemble with a fixed number of individuals , are in fact unique constraints when the ensemble is growing.
Revised:  Here we discuss how some of the most popular implementations of this machinery assume a strong condition on the ergodicity of the cell cycle duration ensemble and that two common definitions for the term ergodicity, "a single individual observed over many generations recapitulates the behavior of the entire ensemble" is implied by the other, "the probability of observing any state is conserved across time and over all individuals" in an ensemble with a fixed number of individuals , are in fact unique constraints when the ensemble is growing.
Edit intent: meaning-changed
Original:  Here we discuss how some of the most popular implementations of this machinery assume a strong condition on the ergodicity of the cell cycle duration ensemble and that two common definitions for the term , ergodicity, while identical in an ensemble with a fixed number of individuals , are in fact unique constraints when the ensemble is growing.
Revised:  Here we discuss how some of the most popular implementations of this machinery assume a strong condition on the ergodicity of the cell cycle duration ensemble and that two common definitions for the term , ergodicity, while identical in an ensemble with a fixed number of individuals but that this is not true when the ensemble is growing.
Edit intent: coherence
Original: In this paper, we theoretically analyze the performance of vehicle-to-vehicle (V2V) broadcast communications at an intersection and provide tractable formulae of performance metrics to optimize them .
Revised: In this paper, we theoretically analyze the performance of vehicle-to-vehicle (V2V) broadcast communications at an intersection on the basis of theoretical analysis. We consider a model in which locations of vehicles are modeled separately as queuing and running segments and derive key performance metrics of V2V broadcast communications via a stochastic geometry approach. Since these theoretical expressions are mathematically intractable, we developed closed-form approximate formulae for them. Using them, we optimize the broadcast rate such that the mean number of successful receivers per unit time is maximized. Because of the closed form approximation, the optimal rate can be used as a guideline for a real-time control-method, which is not achieved through time-consuming simulations. We evaluated our method through numerical examples and demonstrated the effectiveness of our method .
Edit intent: meaning-changed
Original: Based on data on gene expression profiles from microarrays for E. Coli and tumor tissues, I show the existence of heavy tails in the gene expression distribution functions, related to a set of strongly over- and under-expressed genes .
Revised: Based on data on gene expression profiles from microarrays for E. Coli and tumor tissues, I show that the evolution for thousands of generations leads to a set of strongly over- and under-expressed genes .
Edit intent: clarity
Original: Based on data on gene expression profiles from microarrays for E. Coli and tumor tissues, I show the existence of heavy tails in the gene expression distribution functions, related to a set of strongly over- and under-expressed genes .
Revised: Based on data on gene expression profiles from microarrays for E. Coli and tumor tissues, I show the existence of heavy tails in the gene expression distribution functions, related to a set of strongly over- and under-expressed genes , as compared to the initial expression profile. This fact is manifested as heavy tails in the gene expression distribution functions.
Edit intent: meaning-changed
Original:  The tails are heavier -- i.e. the fraction of genes and the expression levels are much higher (lower) -- in tumors than in bacteria , presumably due to epigenetic factors . Different tissue tumors show remarkably similar tails, indicating a kind of universality in cancer phenomena.
Revised:  The tails are heavier -- i.e. the fraction of genes and the expression levels vary much more -- in tumors than in bacteria , presumably due to epigenetic factors . Different tissue tumors show remarkably similar tails, indicating a kind of universality in cancer phenomena.
Edit intent: clarity
Original:  The tails are heavier -- i.e. the fraction of genes and the expression levels are much higher (lower) -- in tumors than in bacteria , presumably due to epigenetic factors . Different tissue tumors show remarkably similar tails, indicating a kind of universality in cancer phenomena.
Revised:  The tails are heavier -- i.e. the fraction of genes and the expression levels are much higher (lower) -- in tumors than in bacteria . Different tissue tumors show remarkably similar tails, indicating a kind of universality in cancer phenomena.
Edit intent: clarity
Original: Based on data on gene expression profiles from microarrays for E. Coli and tumor tissues, I show that the evolution for thousands of generations leads to a set of strongly over- and under-expressed genes, as compared to the initial expression profile.
Revised: In many situations, the gene expression signature is a unique marker of the biological state. We study the modification of the gene expression distribution function when the biological state of a system experiences a change. This change may be the result of a selective pressure, as in the Long Term Evolution Experiment with E. Coli and tumor tissues, I show that the evolution for thousands of generations leads to a set of strongly over- and under-expressed genes, as compared to the initial expression profile.
Edit intent: meaning-changed
Original: Based on data on gene expression profiles from microarrays for E. Coli and tumor tissues, I show that the evolution for thousands of generations leads to a set of strongly over- and under-expressed genes, as compared to the initial expression profile. This fact is manifested as heavy tails in the gene expression distribution functions .
Revised: Based on data on gene expression profiles from microarrays for E. Coli populations, or the progression to Alzheimer disease in aged brains, or the progression from a normal tissue to the cancer state. The first two cases seem to belong to a class of transitions, where the initial and final states are relatively close to each other, and the distribution function for the differential expressions is short ranged, with a tail of only a few dozens of strongly varying genes. In the latter case, cancer, the initial and final states are far apart and separated by a low-fitness barrier. The distribution function shows a very heavy tail, with thousands of silenced and over-expressed genes. We characterize the biological states by means of their principal component representations, and the expression distribution functions .
Edit intent: meaning-changed
Original:  This fact is manifested as heavy tails in the gene expression distribution functions . The tails are heavier -- i.e. the fraction of genes and the expression levels vary much more -- in tumors than in bacteria. Different tissue tumors show remarkably similar tails, indicating a kind of universality in cancer phenomena .
Revised:  This fact is manifested as heavy tails in the gene expression distribution functions by their maximal and minimal differential expression values and the exponents of the Pareto laws describing the tails .
Edit intent: meaning-changed
Original:  First we focus on the case where the set of possible distributions of a financial loss is given by the neighborhood of a given baseline distribution in the Wasserstein distance, or more generally, an optimal-transport distance.
Revised:  First we focus on the case where the uncertainty is modeled by a nonlinear expectation penalizing distributions that are "far" in terms of optimal-transport distance (Wasserstein distance for instance) from a given baseline distribution in the Wasserstein distance, or more generally, an optimal-transport distance.
Edit intent: meaning-changed
Original:  First we focus on the case where the set of possible distributions of a financial loss is given by the neighborhood of a given baseline distribution in the Wasserstein distance, or more generally, an optimal-transport distance. Here it turns out that the computation of the robust OCE reduces to a finite dimensional problem, which in some cases can even be solved explicitly.
Revised:  First we focus on the case where the set of possible distributions of a financial loss is given by the neighborhood of a given baseline distribution . It turns out that the computation of the robust OCE reduces to a finite dimensional problem, which in some cases can even be solved explicitly.
Edit intent: coherence
Original:   Further, we derive convex dual representations of the robust OCE for measurable claims without any assumptions on the set of distributions and finally give conditions on the latter set under which the robust average value-at-risk is a tail risk measure.
Revised:  This principle also applies to the shortfall risk measure as well as for the pricing of European options. Further, we derive convex dual representations of the robust OCE for measurable claims without any assumptions on the set of distributions and finally give conditions on the latter set under which the robust average value-at-risk is a tail risk measure.
Edit intent: meaning-changed
Original:   Further, we derive convex dual representations of the robust OCE for measurable claims without any assumptions on the set of distributions and finally give conditions on the latter set under which the robust average value-at-risk is a tail risk measure.
Revised:  Further, we derive convex dual representations of the robust OCE for measurable claims without any assumptions on the set of distributions . Finally, we give conditions on the latter set under which the robust average value-at-risk is a tail risk measure.
Edit intent: coherence