wanyu/IteraTeR_full_sent huggingface dataset:
Original:  While this discussion has mainly focused on the dichotomy between Value at Risk (VaR) - a quantile - and Expected Shortfall (ES) - a tail expectation , this paper is concerned with Range Value at Risk (RVaR) . RVaR can be regarded as an interpolation of VaR and ES , which constitutes a tradeoff between the sensitivity of the latter and the robustness of the former . Recalling that RVaR is not elicitable , we show that a triplet of RVaR with two VaR components at different levels is elicitable.
Revised:  While this discussion has mainly focused on the dichotomy between Value at Risk (VaR) - a quantile - and Expected Shortfall (ES) - a tail expectation , this paper is concerned with Range Value at Risk (RVaR) . RVaR can be regarded as an interpolation of VaR and ES , which constitutes a tradeoff between the sensitivity of the latter and the robustness of the former , turning it into a practically relevant risk measure on its own. As such, there is a need to statistically validate RVaR forecasts and to compare and rank the performance of different RVaR models, tasks subsumed under the term 'backtesting' in finance. The predictive performance is best evaluated and compared in terms of strictly consistent loss or scoring functions. That is, functions which are minimised in expectation by the correct RVaR forecast. Much like ES, it has been shown recently that RVaR does not admit strictly consistent scoring functions, i.e., it is not elicitable , we show that a triplet of RVaR with two VaR components at different levels is elicitable.
Edit intent: meaning-changed
Original:  While this discussion has mainly focused on the dichotomy between Value at Risk (VaR) - a quantile - and Expected Shortfall (ES) - a tail expectation , this paper is concerned with Range Value at Risk (RVaR) . RVaR can be regarded as an interpolation of VaR and ES , which constitutes a tradeoff between the sensitivity of the latter and the robustness of the former . Recalling that RVaR is not elicitable , we show that a triplet of RVaR with two VaR components at different levels is elicitable.
Revised:  While this discussion has mainly focused on the dichotomy between Value at Risk (VaR) - a quantile - and Expected Shortfall (ES) - a tail expectation , this paper is concerned with Range Value at Risk (RVaR) . RVaR can be regarded as an interpolation of VaR and ES , which constitutes a tradeoff between the sensitivity of the latter and the robustness of the former . Recalling that RVaR is not elicitable . Mitigating this negative result, this paper shows that a triplet of RVaR with two VaR components at different levels is elicitable.
Edit intent: meaning-changed
Original:  Information feeds reported different prices for the same equity---violating the commonly-supposed economic behavior of a unified price for an indistinguishable product---more than 120 million times, with "actionable" latency arbitrage opportunities totaling almost 64 million  . During this period, roughly 22\% of all trades occurred while the SIP and aggregated direct feeds were dislocated.
Revised:  Information feeds reported different prices for the same equity more than 120 million times, with "actionable" latency arbitrage opportunities totaling almost 64 million . During this period, roughly 22\% of all trades occurred while the SIP and aggregated direct feeds were dislocated.
Edit intent: clarity
Original:  Information feeds reported different prices for the same equity---violating the commonly-supposed economic behavior of a unified price for an indistinguishable product---more than 120 million times, with "actionable" latency arbitrage opportunities totaling almost 64 million  . During this period, roughly 22\% of all trades occurred while the SIP and aggregated direct feeds were dislocated.
Revised:  Information feeds reported different prices for the same equity---violating the commonly-supposed economic behavior of a unified price for an indistinguishable product---more than 120 million times, with almost 64 million . During this period, roughly 22\% of all trades occurred while the SIP and aggregated direct feeds were dislocated.
Edit intent: clarity
Original:  Information feeds reported different prices for the same equity---violating the commonly-supposed economic behavior of a unified price for an indistinguishable product---more than 120 million times, with "actionable" latency arbitrage opportunities totaling almost 64 million  . During this period, roughly 22\% of all trades occurred while the SIP and aggregated direct feeds were dislocated.
Revised:  Information feeds reported different prices for the same equity---violating the commonly-supposed economic behavior of a unified price for an indistinguishable product---more than 120 million times, with "actionable" latency arbitrage opportunities totaling almost 64 million dislocation segments featuring meaningfully longer duration and higher magnitude . During this period, roughly 22\% of all trades occurred while the SIP and aggregated direct feeds were dislocated.
Edit intent: meaning-changed
Original: Using the most comprehensive, commercially-available dataset of trading activity in U.S. equity markets, we catalog and analyze latency arbitrage opportunities and realized opportunity costs (ROC) incurred by market participants. We find that latency arbitrage opportunities are common, observing a total of over 3.1 billion latency arbitrage opportunities in the Russell 3000 during trading in 2016, or roughly 525 per second of trading.
Revised: Using the most comprehensive, commercially-available dataset of trading activity in U.S. equity markets, we catalog and analyze quote dislocations between the SIP National Best Bid and Offer (NBBO) and a synthetic BBO constructed from direct feeds. We observe a total of over 3.1 billion latency arbitrage opportunities in the Russell 3000 during trading in 2016, or roughly 525 per second of trading.
Edit intent: meaning-changed
Original:  We find that latency arbitrage opportunities are common, observing a total of over 3.1 billion latency arbitrage opportunities in the Russell 3000 during trading in 2016, or roughly 525 per second of trading.
Revised:  We find that latency arbitrage opportunities are common, observing a total of over 3.1 billion dislocation segments in the Russell 3000 during trading in 2016, or roughly 525 per second of trading.
Edit intent: meaning-changed
Original:  We find that latency arbitrage opportunities are common, observing a total of over 3.1 billion latency arbitrage opportunities in the Russell 3000 during trading in 2016, or roughly 525 per second of trading.
Revised:  We find that latency arbitrage opportunities are common, observing a total of over 3.1 billion latency arbitrage opportunities in the Russell 3000 during trading in 2016, roughly 525 per second of trading.
Edit intent: clarity
Original:  Up to 23\% of observed trades may have contributed the the measured inefficiencies , leading to a ROC greater than 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of ROC and may drive inefficiencies in other stocks.
Revised:  However, these dislocations do not occur uniformly throughout the trading day. We identify a characteristic structure that features more dislocations near the open and close. Additionally, around 23\% of observed trades may have contributed the the measured inefficiencies , leading to a ROC greater than 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of ROC and may drive inefficiencies in other stocks.
Edit intent: meaning-changed
Original:  Up to 23\% of observed trades may have contributed the the measured inefficiencies , leading to a ROC greater than 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of ROC and may drive inefficiencies in other stocks.
Revised:  Up to 23\% of observed trades executed during dislocations. These trades may have been impacted by stale information , leading to a ROC greater than 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of ROC and may drive inefficiencies in other stocks.
Edit intent: meaning-changed
Original:  Up to 23\% of observed trades may have contributed the the measured inefficiencies , leading to a ROC greater than 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of ROC and may drive inefficiencies in other stocks.
Revised:  Up to 23\% of observed trades may have contributed the the measured inefficiencies , leading to estimated opportunity costs on the order of 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of ROC and may drive inefficiencies in other stocks.
Edit intent: clarity
Original:  Up to 23\% of observed trades may have contributed the the measured inefficiencies , leading to a ROC greater than 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of ROC and may drive inefficiencies in other stocks.
Revised:  Up to 23\% of observed trades may have contributed the the measured inefficiencies , leading to a ROC greater than 2 billion USD. A subset of the constituents of the S&P 500 index experience the greatest amount of opportunity cost and appear to drive inefficiencies in other stocks.
Edit intent: clarity
Original:  Here we investigate possible reasons for this discrepancy. Rod-shaped fission yeast Schizosaccharomyces pombe cells  divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the  sizer value of zero.
Revised:  For example, rod-shaped fission yeast Schizosaccharomyces pombe cells divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the sizer value of zero.
Edit intent: clarity
Original:  Rod-shaped fission yeast Schizosaccharomyces pombe cells  divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the  sizer value of zero.
Revised:  Rod-shaped fission yeast Schizosaccharomyces pombe cells , which divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the sizer value of zero.
Edit intent: clarity
Original:  Rod-shaped fission yeast Schizosaccharomyces pombe cells  divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the  sizer value of zero.
Revised:  Rod-shaped fission yeast Schizosaccharomyces pombe cells divide at a fixed surface area [5, 6], exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the sizer value of zero.
Edit intent: coherence
Original:  Rod-shaped fission yeast Schizosaccharomyces pombe cells  divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the  sizer value of zero.
Revised:  Rod-shaped fission yeast Schizosaccharomyces pombe cells divide at a fixed surface area [5, 6], and exhibit a division-birth slope for cell lengths of 0.25 \pm0 .04 , significantly different from the sizer value of zero.
Edit intent: meaning-changed
Original:  Rod-shaped fission yeast Schizosaccharomyces pombe cells  divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the  sizer value of zero.
Revised:  Rod-shaped fission yeast Schizosaccharomyces pombe cells divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .02 , significantly different from the sizer value of zero.
Edit intent: meaning-changed
Original:  Rod-shaped fission yeast Schizosaccharomyces pombe cells  divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the  sizer value of zero.
Revised:  Rod-shaped fission yeast Schizosaccharomyces pombe cells divide at a fixed surface area [5, 6], and exhibit a division-birth slope of 0.23 \pm0 .04 , significantly different from the expected sizer value of zero.
Edit intent: clarity
Original:  To understand whether fission yeast uses a mix of sizer and adder control, or whether size sensing is simply imprecise, we developed a mathematical model of sizer control , including the relevant sources of variation.
Revised:  To understand whether fission yeast uses a mix of sizer and adder control, or whether size sensing is simply imprecise, we developed a mathematical model of sizer control including the relevant sources of variation.
Edit intent: fluency
Original:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat release of calcium through ryanodine receptors (RyRs) for cellular contraction, inositol 1,4,5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Revised:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction, inositol 1,4,5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Edit intent: clarity
Original:  Here we present a mathematical model of  RyR and IP3R channel interaction which demonstrates that cytosolic IP3 is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Revised:  Here we present a mathematical model of functional interactions between RyR and IP3R channel interaction which demonstrates that cytosolic IP3 is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Edit intent: meaning-changed
Original:  Here we present a mathematical model of  RyR and IP3R channel interaction which demonstrates that cytosolic IP3 is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Revised:  Here we present a mathematical model of RyR and IP3R channels which demonstrates that cytosolic IP3 is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Edit intent: clarity
Original:  Here we present a mathematical model of  RyR and IP3R channel interaction which demonstrates that cytosolic IP3 is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Revised:  Here we present a mathematical model of RyR and IP3R channel interaction which demonstrates that IP3-mediated Ca2+release in the cytosol is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Edit intent: meaning-changed
Original:  Through comparison with published experimental results we demonstrate the importance of appropriately representing IP3R gating, verify that our model is capable of reproducing known disease phenotypes in the calcium transient through alteration of channel proportions , and examine how sensitive the cardiac cell is to IP3.
Revised:  Through comparison with published experimental results we demonstrate the importance of appropriately representing IP3R gating, verify that our model is capable of reproducing known disease phenotypes in the calcium transient through alteration of channel properties , and examine how sensitive the cardiac cell is to IP3.
Edit intent: clarity
Original: Calcium  plays a central role in mediating both contractile function and hypertrophicsignalling in cardiomyocytes. While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction,  inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Revised: Calcium plays a central role in mediating both contractile function and hypertrophic signalling in ventricular cardiomyocytes. L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction, inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Edit intent: clarity
Original:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction,  inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Revised:  While L-type Ca2+ channels trigger release of Ca2+ from ryanodine receptors (RyRs) for cellular contraction, inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Edit intent: clarity
Original:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction,  inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Revised:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction, while signalling downstream of Gq coupled receptors stimulates Ca2+ release via inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Edit intent: meaning-changed
Original:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction,  inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Revised:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction, inositol 1,4, 5-trisphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Edit intent: fluency
Original:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction,  inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Revised:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction, inositol 1,4, 5-triphosphate receptors (IP3Rs) , engaging hypertrophic signalling pathways. Modulation of the amplitude, duration, and duty cycle of the cytosolic Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy.
Edit intent: clarity
Original:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction,  inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ to modify beat-to-beat calcium to concurrently signal translocation of transcription factor NFAT into the nucleus to initiate hypertrophy. Details of both the generation and delivery of this translocation signalare unclear however. A recent study by Hannanta-anan and Chow has indicated that NFAT integrates the calcium signalover time. Their experiments revealed that an increase in the duration of elevated cytosolic calcium within each period of oscillation (increase in the duty cycle) increases NFAT-mediated gene transcription. However, it is not clear whether this mechanism exists in cardiac cells, or is even the mechanism underlying NFAT activation. Here we present a mathematical model of functional interactions between RyR and IP3R channels which demonstrates that IP3-mediated Ca2+ release in the cytosol is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Revised:  While L-type Ca2+ channels (LCCs) trigger beat-to-beat re-lease of calcium through ryanodine receptors (RyRs) for cellular contraction, inositol 1,4, 5-triphosphate receptors (IP3Rs) have been implicated in releasing Ca2+ contraction signal, and spatial localisation, have all been proposed to encode this hypertrophic signal. Given current knowledge of IP3Rs, we develop a model describing the effect of functional interaction (cross-talk) between RyR and IP3R channels which demonstrates that IP3-mediated Ca2+ release in the cytosol is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Edit intent: meaning-changed
Original:  Here we present a mathematical model of functional interactions between RyR and IP3R channels which demonstrates that IP3-mediated Ca2+ release in the cytosol is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Revised:  Here we present a mathematical model of functional interactions between RyR and IP3R channels on the Ca2+ release in the cytosol is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte.
Edit intent: clarity
Original:  Here we present a mathematical model of functional interactions between RyR and IP3R channels which demonstrates that IP3-mediated Ca2+ release in the cytosol is indeed capable of increasing the duty cycle of the calcium signal in the cardiomyocyte. Through comparison with published experimental results we demonstrate the importance of appropriately representing IP3R gating, verify that our model is capable of reproducing known disease phenotypes in the calcium transientthrough alteration of channel properties , and examine how sensitive the cardiac cell is to IP3 . A key result of our study is that increasing IP3 concentration increases calcium transient duration but may not always lead to positive inotropy.
Revised:  Here we present a mathematical model of functional interactions between RyR and IP3R channels which demonstrates that IP3-mediated Ca2+ transient , and examine how sensitive the cardiac cell is to IP3 . A key result of our study is that increasing IP3 concentration increases calcium transient duration but may not always lead to positive inotropy.
Edit intent: clarity
Original:  Through comparison with published experimental results we demonstrate the importance of appropriately representing IP3R gating, verify that our model is capable of reproducing known disease phenotypes in the calcium transientthrough alteration of channel properties , and examine how sensitive the cardiac cell is to IP3 . A key result of our study is that increasing IP3 concentration increases calcium transient duration but may not always lead to positive inotropy.
Revised:  Through comparison with published experimental results we demonstrate the importance of appropriately representing IP3R gating, verify that our model is capable of reproducing known disease phenotypes in the calcium transientthrough alteration of channel properties , and examine the sensitivity of the Ca2+ transient shape to properties of IP3R activation . A key result of our study is that increasing IP3 concentration increases calcium transient duration but may not always lead to positive inotropy.
Edit intent: clarity