wanyu/IteraTeR_full_sent huggingface dataset:
Original:  The attained validation set accuracies are as high as 99.12\% for the Inception version 3 network and 97.97\% for the Xception network. The presented results suggest that meaningful predictors composed of sMRI and network measures may offer the possibility for early detection of subjects in the early stages of AD .
Revised:  The attained validation set accuracies are as high as 99.12\% for the Inception version 3 network and 97.97\% for the transfer learning approaches exceed the performance of non-transfer learning based approaches demonstrating the effectiveness of these approaches for the binary AD classification task .
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Original: Tumor stromal interactions have been shown to be the driving force behind the poor prognosis associated with aggressive breast tumors. These interactions, specifically between tumor and the surrounding ECM, and tumor and vascular endothelium, promote tumor formation, angiogenesis, and metastasis .
Revised: Inflammatory breast cancer (IBC), a rare form of breast cancer associated with increased angiogenesis and metastasis, is largely driven by tumor-stromal interactions with the vasculature and the extracellular matrix (ECM). However, there is currently a lack of understanding of the role these interactions play in initiation and progression of the disease .
Edit intent: clarity
Original:  In this study, we develop an in vitrovascularized tumor platform that allows for investigation of tumor-stromal interactions in three breast tumor derived cell lines of varying aggressiveness: MDA-IBC3, SUM149, and  MDA-MB-231 .
Revised:  In this study, we developed the first three-dimensional, in vitro, vascularized, breast tumor platform to quantify the spatial and temporal dynamics of tumor-vasculature and MDA-MB-231 .
Edit intent: clarity
Original:  In this study, we develop an in vitrovascularized tumor platform that allows for investigation of tumor-stromal interactions in three breast tumor derived cell lines of varying aggressiveness: MDA-IBC3, SUM149, and  MDA-MB-231 .
Revised:  In this study, we develop an in vitrovascularized tumor platform that allows for investigation of tumor-stromal interactions in three breast tumor derived cell lines of varying aggressiveness: MDA-IBC3, SUM149, and tumor-ECM interactions specific to IBC. Platforms consisting of collagen type 1 ECM with an endothelialized blood vessel were cultured with IBC cells, MDA-IBC3 (HER2+) or SUM149 (triple negative), and for comparison to non-IBC cells, MDA-MB-231 .
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Original:  In this study, we develop an in vitrovascularized tumor platform that allows for investigation of tumor-stromal interactions in three breast tumor derived cell lines of varying aggressiveness: MDA-IBC3, SUM149, and  MDA-MB-231 . The platform recreates key features of breast tumors, including increased vascular permeability, vessel sprouting, and ECM remodeling. Morphological and quantitative analysis reveals differential effects from each tumor cell type on endothelial coverage, permeability, expression of VEGF, and collagen remodeling. Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage  compared to the control TIME only platform.
Revised:  In this study, we develop an in vitrovascularized tumor platform that allows for investigation of tumor-stromal interactions in three breast tumor derived cell lines of varying aggressiveness: MDA-IBC3, SUM149, and MDA-MB-231 (triple negative). An acellular collagen platform with an endothelial blood vessel served as control. SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage compared to the control TIME only platform.
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Original:  Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage  compared to the control TIME only platform.
Revised:  Triple negative tumors, SUM149 and MDA-MB-231 platforms exhibited a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage compared to the control TIME only platform.
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Original:  Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage  compared to the control TIME only platform.
Revised:  Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher vessel permeability and decreased endothelial coverage compared to the control TIME only platform.
Edit intent: clarity
Original:  Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage  compared to the control TIME only platform.
Revised:  Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage of the vessel lumen compared to the control TIME only platform.
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Original:  Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage  compared to the control TIME only platform.
Revised:  Triple negative tumors, SUM149 and MDA-MB-321, resulted in a significantly (p<0.05) higher endothelial permeability and decreased endothelial coverage compared to the control . Both IBC platforms, MDA-IBC3 and
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Original:  SUM149 /TIME platformswere 1.3 fold lower (p<0.05) , and MDA-MB-231 /TIME platforms were 1.5 fold lower (p< 0.01) in endothelial coverage compared to the control TIME only platform.
Revised:  SUM149 , expressed higher levels of VEGF (p<0.05) , and MDA-MB-231 /TIME platforms were 1.5 fold lower (p< 0.01) in endothelial coverage compared to the control TIME only platform.
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Original:  SUM149 /TIME platformswere 1.3 fold lower (p<0.05) , and MDA-MB-231 /TIME platforms were 1.5 fold lower (p< 0.01) in endothelial coverage compared to the control TIME only platform.
Revised:  SUM149 /TIME platformswere 1.3 fold lower (p<0.05) and increased collagen ECM porosity compared to non-IBC MDA-MB-231 /TIME platforms were 1.5 fold lower (p< 0.01) in endothelial coverage compared to the control TIME only platform.
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Original:  SUM149 /TIME platformswere 1.3 fold lower (p<0.05) , and MDA-MB-231 /TIME platforms were 1.5 fold lower (p< 0.01) in endothelial coverage compared to the control TIME only platform.
Revised:  SUM149 /TIME platformswere 1.3 fold lower (p<0.05) , and MDA-MB-231 (p< 0.01) in endothelial coverage compared to the control TIME only platform.
Edit intent: clarity
Original:  SUM149 /TIME platformswere 1.3 fold lower (p<0.05) , and MDA-MB-231 /TIME platforms were 1.5 fold lower (p< 0.01) in endothelial coverage compared to the control TIME only platform. HER2+ MDA-IBC3 tumor cells expressed high levels of VEGF (p<0.01) and induced vessel sprouting.
Revised:  SUM149 /TIME platformswere 1.3 fold lower (p<0.05) , and MDA-MB-231 /TIME platforms were 1.5 fold lower (p< 0.05) and control (p<0.01) and induced vessel sprouting.
Edit intent: clarity
Original:  HER2+ MDA-IBC3 tumor cells expressed high levels of VEGF (p<0.01) and induced vessel sprouting. Vessels sprouting was tracked for 3 weeks and with increasing time exhibited formation of multiple vessel sprouts that invaded into the ECM and surrounded clusters of MDA-IBC3 cells . Both IBC cell lines, SUM149 and MDA-IBC3, resulted in a collagen ECM with significantly greater porosity with 1.6 and 1.1 fold higher compared to control, p<0.01.
Revised:  HER2+ MDA-IBC3 tumor cells expressed high levels of VEGF (p<0.01) platforms. Additionally, unique to the MDA-IBC3 platform, we observed progressive sprouting of the endothelium over time resulting in viable vessels with lumen. The newly sprouted vessels encircled clusters of MDA-IBC3 cells . Both IBC cell lines, SUM149 and MDA-IBC3, resulted in a collagen ECM with significantly greater porosity with 1.6 and 1.1 fold higher compared to control, p<0.01.
Edit intent: clarity
Original:  Vessels sprouting was tracked for 3 weeks and with increasing time exhibited formation of multiple vessel sprouts that invaded into the ECM and surrounded clusters of MDA-IBC3 cells . Both IBC cell lines, SUM149 and MDA-IBC3, resulted in a collagen ECM with significantly greater porosity with 1.6 and 1.1 fold higher compared to control, p<0.01. The breast cancer in vitro vascularized platforms introduced in this paper are an adaptable, high throughout tool for unearthing tumor-stromal mechanisms and dynamics behind tumor progressionand may prove essential in developing effective targeted therapeutics .
Revised:  Vessels sprouting was tracked for 3 weeks and with increasing time exhibited formation of multiple vessel sprouts that invaded into the ECM and surrounded clusters of MDA-IBC3 cells replicating a feature of in vivo IBC. The IBC in vitro vascularized platforms introduced in this paper are an adaptable, high throughout tool for unearthing tumor-stromal mechanisms and dynamics behind tumor progressionand may prove essential in developing effective targeted therapeutics .
Edit intent: clarity
Original:  The breast cancer in vitro vascularized platforms introduced in this paper are an adaptable, high throughout tool for unearthing tumor-stromal mechanisms and dynamics behind tumor progressionand may prove essential in developing effective targeted therapeutics .
Revised:  The breast cancer in vitro vascularized platforms introduced in this study model well-described in vivo and clinical IBC phenotypes and provide an adaptable, high throughout tool for unearthing tumor-stromal mechanisms and dynamics behind tumor progressionand may prove essential in developing effective targeted therapeutics .
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Original:  The breast cancer in vitro vascularized platforms introduced in this paper are an adaptable, high throughout tool for unearthing tumor-stromal mechanisms and dynamics behind tumor progressionand may prove essential in developing effective targeted therapeutics .
Revised:  The breast cancer in vitro vascularized platforms introduced in this paper are an adaptable, high throughout tool for systematically and quantitatively investigating tumor-stromal mechanisms and dynamics behind tumor progressionand may prove essential in developing effective targeted therapeutics .
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Original:  The breast cancer in vitro vascularized platforms introduced in this paper are an adaptable, high throughout tool for unearthing tumor-stromal mechanisms and dynamics behind tumor progressionand may prove essential in developing effective targeted therapeutics .
Revised:  The breast cancer in vitro vascularized platforms introduced in this paper are an adaptable, high throughout tool for unearthing tumor-stromal mechanisms and dynamics of tumor progression .
Edit intent: clarity
Original:  In their celebrated (p,q) theorem from 1992, Alon and Kleitman proved the conjecture but did not obtain effective bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' . Ever since, obtaining such bounds is a major open problem in convexity theory .
Revised:  In a celebrated result from 1992, Alon and Kleitman proved the conjecture but did not obtain effective bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' . Ever since, obtaining such bounds is a major open problem in convexity theory .
Edit intent: clarity
Original:  In their celebrated (p,q) theorem from 1992, Alon and Kleitman proved the conjecture but did not obtain effective bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' . Ever since, obtaining such bounds is a major open problem in convexity theory .
Revised:  In their celebrated (p,q) theorem from 1992, Alon and Kleitman proved the conjecture . However, obtaining sharp bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' . Ever since, obtaining such bounds is a major open problem in convexity theory .
Edit intent: meaning-changed
Original:  In their celebrated (p,q) theorem from 1992, Alon and Kleitman proved the conjecture but did not obtain effective bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' . Ever since, obtaining such bounds is a major open problem in convexity theory .
Revised:  In their celebrated (p,q) theorem from 1992, Alon and Kleitman proved the conjecture but did not obtain effective bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' , is still a major open problem in convexity theory .
Edit intent: clarity
Original:  In their celebrated (p,q) theorem from 1992, Alon and Kleitman proved the conjecture but did not obtain effective bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' . Ever since, obtaining such bounds is a major open problem in convexity theory .
Revised:  In their celebrated (p,q) theorem from 1992, Alon and Kleitman proved the conjecture but did not obtain effective bounds on c_d(p,q), called `the Hadwiger-Debrunner numbers' . Ever since, obtaining such bounds is a major open problem in discrete and computational geometry .
Edit intent: meaning-changed
Original:  The best currently known asymptotic lower bound on the Hadwiger-Debrunner numbers in the plane is c_2(p,q) = \Omega( p{q}\log(p{q}))  . In this paper we present the significantly stronger lower bound c_2(p,q) \geq p^{1+\Omega(1/q)}.
Revised:  The best currently known lower bound on the Hadwiger-Debrunner numbers in the plane is c_2(p,q) = \Omega( p{q}\log(p{q})) . In this paper we present the significantly stronger lower bound c_2(p,q) \geq p^{1+\Omega(1/q)}.
Edit intent: clarity
Original:  The best currently known asymptotic lower bound on the Hadwiger-Debrunner numbers in the plane is c_2(p,q) = \Omega( p{q}\log(p{q}))  . In this paper we present the significantly stronger lower bound c_2(p,q) \geq p^{1+\Omega(1/q)}.
Revised:  The best currently known asymptotic lower bound on the Hadwiger-Debrunner numbers in the plane is c_2(p,q) = \Omega( p{q}\log(p{q})) while the best known upper bound is O(p^{(1.5+\delta)(1+\frac{1 . In this paper we present the significantly stronger lower bound c_2(p,q) \geq p^{1+\Omega(1/q)}.
Edit intent: meaning-changed
Original:  The best currently known asymptotic lower bound on the Hadwiger-Debrunner numbers in the plane is c_2(p,q) = \Omega( p{q}\log(p{q}))  . In this paper we present the significantly stronger lower bound c_2(p,q) \geq p^{1+\Omega(1/q)}.
Revised:  The best currently known asymptotic lower bound on the Hadwiger-Debrunner numbers in the plane is c_2(p,q) = \Omega( p{q}\log(p{q})) . In this paper we improve the lower bound significantly by showing that c_2(p,q) \geq p^{1+\Omega(1/q)}.
Edit intent: clarity
Original: Sample entropy (SampEn) has been accepted as an alternate, and sometimes a replacement, measure to approximate entropy ( ApEn) for characterizing temporal complexity of time series .
Revised: Sample entropy (SampEn) has been accepted as an alternate, and sometimes a replacement, measure to approximate entropy ( ApEn) and sample entropy (SampEn) are widely used for temporal complexity analysis of real-world phenomena .
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Original:  However, it still suffers from issues such as inconsistency over short-length signals and its tolerance parameter r, susceptibility to signal amplitude changes and insensitivity to self-similarity of time series.
Revised:  However, their relationship with the Hurst exponent as a measure of self-similarity has not been deeply studied. Also, they still suffer from susceptibility to signal amplitude changes and insensitivity to self-similarity of time series.
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Original:  However, it still suffers from issues such as inconsistency over short-length signals and its tolerance parameter r, susceptibility to signal amplitude changes and insensitivity to self-similarity of time series. We propose modifications to the ApEn and SampEn measures which are defined for 0<r<1, are more robust to signal amplitude changes and sensitive to self-similarity property of time series. We modified ApEn and SampEn by redefining the distance function used originally in their definitions.
Revised:  However, it still suffers from issues such as inconsistency over short-length signals and its tolerance parameter r, susceptibility to signal amplitude changes . A common practice for addressing this issue is to correct their input signal amplitude by its standard deviation. In this study, we first show using simulations that ApEn and SampEn by redefining the distance function used originally in their definitions.
Edit intent: coherence
Original:  We modified ApEn and SampEn by redefining the distance function used originally in their definitions. We then evaluated the new entropy measures, called range entropies (RangeEn) using different random processes and nonlinear deterministic signals. We further applied the proposed entropies to normal and epileptic electroencephalographic (EEG) signals under different states. Our results suggest that, unlike ApEn and SampEn , RangeEnmeasures are robust to stationary and nonstationary signal amplitude variations and that their trajectories in the tolerance r-plane are constrained between 0 (maximum entropy) and 1 (minimum entropy)  .
Revised:  We modified ApEn and SampEn are related to the Hurst exponent through their tolerance and embedding dimension parameters. We then propose a modification to ApEn and SampEn , RangeEnmeasures are robust to stationary and nonstationary signal amplitude variations and that their trajectories in the tolerance r-plane are constrained between 0 (maximum entropy) and 1 (minimum entropy) .
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Original:  Our results suggest that, unlike ApEn and SampEn , RangeEnmeasures are robust to stationary and nonstationary signal amplitude variations and that their trajectories in the tolerance r-plane are constrained between 0 (maximum entropy) and 1 (minimum entropy)  .
Revised:  Our results suggest that, unlike ApEn and SampEn called Range entropy or RangeEn. RangeEn measures represent a better robustness to nonstationary changes in signals and a more linear link to the Hurst exponent compared to ApEn and SampEn. They are always bounded in the tolerance r-plane are constrained between 0 (maximum entropy) and 1 (minimum entropy) .
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Original:  Our results suggest that, unlike ApEn and SampEn , RangeEnmeasures are robust to stationary and nonstationary signal amplitude variations and that their trajectories in the tolerance r-plane are constrained between 0 (maximum entropy) and 1 (minimum entropy)  .
Revised:  Our results suggest that, unlike ApEn and SampEn , RangeEnmeasures are robust to stationary and nonstationary signal amplitude variations and that their trajectories in the tolerance r-plane between 0 (maximum entropy) and 1 (minimum entropy) .
Edit intent: clarity
Original:  Our results suggest that, unlike ApEn and SampEn , RangeEnmeasures are robust to stationary and nonstationary signal amplitude variations and that their trajectories in the tolerance r-plane are constrained between 0 (maximum entropy) and 1 (minimum entropy)  .
Revised:  Our results suggest that, unlike ApEn and SampEn , RangeEnmeasures are robust to stationary and nonstationary signal amplitude variations and that their trajectories in the tolerance r-plane are constrained between 0 (maximum entropy) and 1 (minimum entropy) and need no signal amplitude correction .
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Original:  suggesting that the new definitions are sensitive to self-similarity structures of signals. RangeEn analysis of epileptic EEG data showed distinct behaviours in the r-domain for extracranial versus intracranial recordings as well as different states of epileptic EEG data.
Revised:  suggesting that the new definitions are sensitive to self-similarity analyses on epileptic EEG data showed distinct behaviours in the r-domain for extracranial versus intracranial recordings as well as different states of epileptic EEG data.
Edit intent: clarity
Original:  RangeEn analysis of epileptic EEG data showed distinct behaviours in the r-domain for extracranial versus intracranial recordings as well as different states of epileptic EEG data. The constrained trajectory of RangeEn in the r-plane makes them a good candidate for studying complex biological signals such as EEG during seizure and non-seizure states. The Python package used to generate the results shown in this paper is publicly available at: URL
Revised:  RangeEn analysis of epileptic EEG data as a real-world example. Python implementation of this study is publicly available at: URL
Edit intent: clarity
Original: The dynamics associated with invasion and metastasis, which hallmarks of cancer , and involve collective cell migration by blood or interstitial flow, is poorly understood. ~In the present contribution, we describe a theory to the essence of fluid shear stress (FSS) driven collective motion using the stochastic quantization method . Long range hydrodynamic interactions between cells exhibit complex collective properties whose understanding may be crucial for describing metastasis.
Revised: The migration behaviors of cancer cells are known to be heterogeneous. However, the interplay between the adhesion interactions, dynamical shape changes and fluid flows in regulating cell migration heterogeneity and plasticity during cancer metastasis is still elusive. To further quantitative understanding of cell motility and morphology, we develop a theory using stochastic quantization method . Long range hydrodynamic interactions between cells exhibit complex collective properties whose understanding may be crucial for describing metastasis.
Edit intent: coherence
Original:  ~In the present contribution, we describe a theory to the essence of fluid shear stress (FSS) driven collective motion using the stochastic quantization method . Long range hydrodynamic interactions between cells exhibit complex collective properties whose understanding may be crucial for describing metastasis. ~Theory predicts a shear flow induced migrationof colony of cells characterized by super-diffusive motion.
Revised:  ~In the present contribution, we describe a theory to the essence of fluid shear stress (FSS) driven collective motion using the stochastic quantization method that describes the role of biophysical cues in regulating diverse cell motility. We show that the cumulative effect of time dependent adhesion interactions that determine the structural rearrangements and self-generated force due to actin remodeling, dictate the super-diffusive motion.
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Original:  ~Theory predicts a shear flow induced migrationof colony of cells characterized by super-diffusive motion.
Revised:  ~Theory predicts a shear flow induced migrationof colony of cells characterized by super-diffusive motion of mesenchymal phenotype in the absence of flow. Interstitial flows regulate cell motility phenotype and promote the amoeboid over mesenchymal motility through adhesion interactions. Cells exhibit a dynamical slowing down of collective migration, with a decreasing degree of super-diffusion.
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