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Quantitative Analysis and Modeling of Earth and Environmental Data: Space-Time and Spacetime Data Considerations introduces the notion of chronotopologic data analysis that offers a systematic, quantitative analysis of multi-sourced data and provides information about the spatial distribution and temporal dynamics of natural attributes (physical, biological, health, social). It includes models and techniques for handling data that may vary by space and/or time, and aims to improve understanding of the physical laws of change underlying the available numerical datasets, while taking into consideration the in-situ uncertainties and relevant measurement errors (conceptual, technical, computational). It considers the synthesis of scientific theory-based methods (stochastic modeling, modern geostatistics) and data-driven techniques (machine learning, artificial neural networks) so that their individual strengths are combined by acting symbiotically and complementing each other. The notions and methods presented in Quantitative Analysis and Modeling of Earth and Environmental Data: Space-Time and Spacetime Data Considerations cover a wide range of data in various forms and sources, including hard measurements, soft observations, secondary information and auxiliary variables (ground-level measurements, satellite observations, scientific instruments and records, protocols and surveys, empirical models and charts). Including real-world practical applications as well as practice exercises, this book is a comprehensive step-by-step tutorial of theory-based and data-driven techniques that will help students and researchers master data analysis and modeling in earth and environmental sciences (including environmental health and human exposure applications). Explores the analysis and processing of chronotopologic (i.e., space-time and spacetime) data that varies spatially and/or temporally, which is the case with the majority of data in scientific and engineering disciplines Stud

Quantitative Analysis and Modeling of Earth and Environmental Data: Space-Time and Spacetime Data Considerations introduces the notion of chronotopologic data analysis that offers a systematic, quantitative analysis of multi-sourced data and provides information about the spatial distribution and temporal dynamics of natural attributes (physical, biological, health, social). It includes models and techniques for handling data that may vary by space and/or time, and aims to improve understanding of the physical laws of change underlying the available numerical datasets, while taking into consideration the in-situ uncertainties and relevant measurement errors (conceptual, technical, computational). It considers the synthesis of scientific theory-based methods (stochastic modeling, modern geostatistics) and data-driven techniques (machine learning, artificial neural networks) so that their individual strengths are combined by acting symbiotically and complementing each other. The notions and methods presented in Quantitative Analysis and Modeling of Earth and Environmental Data: Space-Time and Spacetime Data Considerations cover a wide range of data in various forms and sources, including hard measurements, soft observations, secondary information and auxiliary variables (ground-level measurements, satellite observations, scientific instruments and records, protocols and surveys, empirical models and charts). Including real-world practical applications as well as practice exercises, this book is a comprehensive step-by-step tutorial of theory-based and data-driven techniques that will help students and researchers master data analysis and modeling in earth and environmental sciences (including environmental health and human exposure applications). Explores the analysis and processing of chronotopologic (i.e., space-time and spacetime) data that varies spatially and/or temporally, which is the case with the majority of data in scientific and engineering disciplines Stud

Quantitative Analysis and Modeling of Earth and Environmental Data: Space-Time and Spacetime Data Considerations introduces the notion of chronotopologic data analysis that offers a systematic, quantitative analysis of multi-sourced data and provides information about the spatial distribution and temporal dynamics of natural attributes (physical, biological, health, social). It includes models and techniques for handling data that may vary by space and/or time, and aims to improve understanding of the physical laws of change underlying the available numerical datasets, while taking into consideration the in-situ uncertainties and relevant measurement errors (conceptual, technical, computational). It considers the synthesis of scientific theory-based methods (stochastic modeling, modern geostatistics) and data-driven techniques (machine learning, artificial neural networks) so that their individual strengths are combined by acting symbiotically and complementing each other. The notions and methods presented in Quantitative Analysis and Modeling of Earth and Environmental Data: Space-Time and Spacetime Data Considerations cover a wide range of data in various forms and sources, including hard measurements, soft observations, secondary information and auxiliary variables (ground-level measurements, satellite observations, scientific instruments and records, protocols and surveys, empirical models and charts). Including real-world practical applications as well as practice exercises, this book is a comprehensive step-by-step tutorial of theory-based and data-driven techniques that will help students and researchers master data analysis and modeling in earth and environmental sciences (including environmental health and human exposure applications). Explores the analysis and processing of chronotopologic (i.e., space-time and spacetime) data that varies spatially and/or temporally, which is the case with the majority of data in scientific and engineering disciplines Stud

Blue Carbon (BC) strategy refers to the approaches that mitigate and adapt to climate change through the conservation and restoration of seagrass, saltmarsh and mangrove ecosystems and, in some BC programs, also through the expansion of seaweed aquaculture. The major losses of coastal habitats in combination with the commitments of China under the Paris Agreement provide unique opportunity and necessity to develop a strong Chinese BC program. Here, we (1) characterize China's BC habitats, examine their changes since 1950 along with the drivers of changes; (2) consider the expansion of seaweed aquaculture and how this may be managed to become an emerging BC resource in China, along with the engineering solutions required to enhance its potential; and (3) provide the rationale and elements for BC program in China. We find China currently has 1326–2149 km2 wild and 2–15 km2 created mangrove, saltmarsh and seagrass habitats, while 9236–10059 km2 (77–87%) has been lost since 1950, mainly due to land reclamation. The current area of farmed seaweed habitat is 1252–1265 km2, which is close to the area of wild mangrove, saltmarsh and seagrass habitats. We conclude that BC strategies have potentials yet to be fully developed in China, particularly through climate change adaptation benefits such as coastal protection and eco-environmental co-benefits of seaweed farming such as habitat creation for fish and other biota, alleviation of eutrophication, hypoxia and acidification, and the generation of direct and value added products with lower environmental impact relative to land-based production. On this basis, we provide a roadmap for BC strategies adjusted to the unique characteristics and capacities of China.

Ce projet de maîtrise présente l’étude du comportement en fatigue d’un matériau composite tissé, qui utilise la technique d’émission acoustique (EA) pour la détection de l’initiation des dommages de fatigue. Ce travail fait partie du projet de recherche CRIAQ-COMP 407 dont le but est de développer une approche de prédiction de l’initiation de l’endommagement dans les composites tissés qui sont soumis à des chargements cycliques. Une méthode de localisation par émission acoustique a été introduite pour localiser les sources d’ondes de contraintes émettant dans la zone autour d’un défaut artificiel inséré préalablement dans l’échantillon. Les essais de fatigue ont été réalisés sous différentes conditions environnementales et la détection des seuils d’initiation des endommagements a permis de générer des courbes de durée de vie (courbes S-N). La comparaison des courbes S-N entre elles a permis d’évaluer l’influence de chacune de ces conditions sur la durée de vie en fatigue. Par la suite, une méthode de classification a été développée en combinant la carte de Kohonen et la méthode des k-moyennes. Cette approche a permis d’établir une corrélation entre les différents endommagements et les signaux acoustiques détectés. Ce mémoire est organisé en quatre chapitres: le premier chapitre présente l’état de l’art de l’application des matériaux composites, l’importance de la caractérisation de son comportement en fatigue, et le contexte général du projet de recherche. Dans le chapitre II, une revue exhaustive de la littérature est présentée. Les travaux de recherche traitant du comportement des composites tissés sous chargement statique et en fatigue ont été synthétisés. Ce chapitre contient aussi une revue sur les techniques d’analyse et de traitement des signaux d’émission acoustique utilisés pour suivre les modes d’endommagement en fatigue et pour reconnaitre les différentes classes des endommagements de fatigue. Le chapitre III présente les essais expérimentaux, les traitem

Ce projet de maîtrise présente l’étude du comportement en fatigue d’un matériau composite tissé, qui utilise la technique d’émission acoustique (EA) pour la détection de l’initiation des dommages de fatigue. Ce travail fait partie du projet de recherche CRIAQ-COMP 407 dont le but est de développer une approche de prédiction de l’initiation de l’endommagement dans les composites tissés qui sont soumis à des chargements cycliques. Une méthode de localisation par émission acoustique a été introduite pour localiser les sources d’ondes de contraintes émettant dans la zone autour d’un défaut artificiel inséré préalablement dans l’échantillon. Les essais de fatigue ont été réalisés sous différentes conditions environnementales et la détection des seuils d’initiation des endommagements a permis de générer des courbes de durée de vie (courbes S-N). La comparaison des courbes S-N entre elles a permis d’évaluer l’influence de chacune de ces conditions sur la durée de vie en fatigue. Par la suite, une méthode de classification a été développée en combinant la carte de Kohonen et la méthode des k-moyennes. Cette approche a permis d’établir une corrélation entre les différents endommagements et les signaux acoustiques détectés. Ce mémoire est organisé en quatre chapitres: le premier chapitre présente l’état de l’art de l’application des matériaux composites, l’importance de la caractérisation de son comportement en fatigue, et le contexte général du projet de recherche. Dans le chapitre II, une revue exhaustive de la littérature est présentée. Les travaux de recherche traitant du comportement des composites tissés sous chargement statique et en fatigue ont été synthétisés. Ce chapitre contient aussi une revue sur les techniques d’analyse et de traitement des signaux d’émission acoustique utilisés pour suivre les modes d’endommagement en fatigue et pour reconnaitre les différentes classes des endommagements de fatigue. Le chapitre III présente les essais expérimentaux, les traitem

OBJECTIVE: Capillary network formation represents a specialized endothelial cell function and is a prerequisite to establish a continuous vessel lumen. Formation of endothelial cell connections that form the vascular structure is regulated, at least in part, at the transcriptional level. We report here that related transcription enhancer factor-1 (RTEF-1) plays an important role in vascular structure formation. METHODS AND RESULTS: Knockdown of RTEF-1 by small interfering RNA or blockage of RTEF-1 function by the transcription enhancer activators domain decreased endothelial connections in a Matrigel assay, whereas overexpression of RTEF-1 in endothelial cells resulted in a significant increase in cell connections and aggregation. In a model of oxygen-induced retinopathy, endothelial-specific RTEF-1 overexpressing mice had enhanced angiogenic sprouting and vascular structure remodeling, resulting in the formation of a denser and more highly interconnected superficial capillary plexus. Mechanistic studies revealed that RTEF-1 induced the expression of functional gap junction proteins including connexin 43, connexin 40, and connexin 37. Blocking connexin 43 function inhibited RTEF-1-induced endothelial cell connections and aggregation. CONCLUSIONS: These findings provide novel insights into the transcriptional control of endothelial function in the coordination of cell-cell connections.

OBJECTIVE: Capillary network formation represents a specialized endothelial cell function and is a prerequisite to establish a continuous vessel lumen. Formation of endothelial cell connections that form the vascular structure is regulated, at least in part, at the transcriptional level. We report here that related transcription enhancer factor-1 (RTEF-1) plays an important role in vascular structure formation. METHODS AND RESULTS: Knockdown of RTEF-1 by small interfering RNA or blockage of RTEF-1 function by the transcription enhancer activators domain decreased endothelial connections in a Matrigel assay, whereas overexpression of RTEF-1 in endothelial cells resulted in a significant increase in cell connections and aggregation. In a model of oxygen-induced retinopathy, endothelial-specific RTEF-1 overexpressing mice had enhanced angiogenic sprouting and vascular structure remodeling, resulting in the formation of a denser and more highly interconnected superficial capillary plexus. Mechanistic studies revealed that RTEF-1 induced the expression of functional gap junction proteins including connexin 43, connexin 40, and connexin 37. Blocking connexin 43 function inhibited RTEF-1-induced endothelial cell connections and aggregation. CONCLUSIONS: These findings provide novel insights into the transcriptional control of endothelial function in the coordination of cell-cell connections.

OBJECTIVE: Capillary network formation represents a specialized endothelial cell function and is a prerequisite to establish a continuous vessel lumen. Formation of endothelial cell connections that form the vascular structure is regulated, at least in part, at the transcriptional level. We report here that related transcription enhancer factor-1 (RTEF-1) plays an important role in vascular structure formation. METHODS AND RESULTS: Knockdown of RTEF-1 by small interfering RNA or blockage of RTEF-1 function by the transcription enhancer activators domain decreased endothelial connections in a Matrigel assay, whereas overexpression of RTEF-1 in endothelial cells resulted in a significant increase in cell connections and aggregation. In a model of oxygen-induced retinopathy, endothelial-specific RTEF-1 overexpressing mice had enhanced angiogenic sprouting and vascular structure remodeling, resulting in the formation of a denser and more highly interconnected superficial capillary plexus. Mechanistic studies revealed that RTEF-1 induced the expression of functional gap junction proteins including connexin 43, connexin 40, and connexin 37. Blocking connexin 43 function inhibited RTEF-1-induced endothelial cell connections and aggregation. CONCLUSIONS: These findings provide novel insights into the transcriptional control of endothelial function in the coordination of cell-cell connections.

OBJECTIVE: Capillary network formation represents a specialized endothelial cell function and is a prerequisite to establish a continuous vessel lumen. Formation of endothelial cell connections that form the vascular structure is regulated, at least in part, at the transcriptional level. We report here that related transcription enhancer factor-1 (RTEF-1) plays an important role in vascular structure formation. METHODS AND RESULTS: Knockdown of RTEF-1 by small interfering RNA or blockage of RTEF-1 function by the transcription enhancer activators domain decreased endothelial connections in a Matrigel assay, whereas overexpression of RTEF-1 in endothelial cells resulted in a significant increase in cell connections and aggregation. In a model of oxygen-induced retinopathy, endothelial-specific RTEF-1 overexpressing mice had enhanced angiogenic sprouting and vascular structure remodeling, resulting in the formation of a denser and more highly interconnected superficial capillary plexus. Mechanistic studies revealed that RTEF-1 induced the expression of functional gap junction proteins including connexin 43, connexin 40, and connexin 37. Blocking connexin 43 function inhibited RTEF-1-induced endothelial cell connections and aggregation. CONCLUSIONS: These findings provide novel insights into the transcriptional control of endothelial function in the coordination of cell-cell connections.

OBJECTIVE: Capillary network formation represents a specialized endothelial cell function and is a prerequisite to establish a continuous vessel lumen. Formation of endothelial cell connections that form the vascular structure is regulated, at least in part, at the transcriptional level. We report here that related transcription enhancer factor-1 (RTEF-1) plays an important role in vascular structure formation. METHODS AND RESULTS: Knockdown of RTEF-1 by small interfering RNA or blockage of RTEF-1 function by the transcription enhancer activators domain decreased endothelial connections in a Matrigel assay, whereas overexpression of RTEF-1 in endothelial cells resulted in a significant increase in cell connections and aggregation. In a model of oxygen-induced retinopathy, endothelial-specific RTEF-1 overexpressing mice had enhanced angiogenic sprouting and vascular structure remodeling, resulting in the formation of a denser and more highly interconnected superficial capillary plexus. Mechanistic studies revealed that RTEF-1 induced the expression of functional gap junction proteins including connexin 43, connexin 40, and connexin 37. Blocking connexin 43 function inhibited RTEF-1-induced endothelial cell connections and aggregation. CONCLUSIONS: These findings provide novel insights into the transcriptional control of endothelial function in the coordination of cell-cell connections.

AIMS: Related transcription enhancer factor-1 (RTEF-1) has previously been demonstrated to play an important role in both endothelial cells and cardiomyocytes. However, the function of RTEF-1 in the communication between these two adjacent cell types has not been elucidated. METHODS AND RESULTS: We have found that endothelium-specific RTEF-1 transgenic mice (VE-Cad/RTEF-1) developed significant cardiac hypertrophy after transverse aortic constriction surgery, as evidenced by an increased ratio of heart weight to tibia length, enlarged cardiomyocyte size, thickened left ventricular wall and elevated expression of hypertrophic gene markers, with up-regulation of vascular endothelial growth factor B (VEGF-B). Additionally, VEGF-B was increased in endothelial cells from VE-Cad/RTEF-1 mice, as well as in endothelial cells with forced RTEF-1 expression (HMEC-1/RTEF-1), and coincidentally decreased when RTEF-1 was deficient in HMEC-1. Using chromatin immunoprecipitation and luciferase assays, we found that RTEF-1 increased VEGF-B promoter activity through a direct interaction. Hypertrophy-associated genes and protein synthesis were up-regulated in cardiomyocytes that were incubated with conditioned medium from HMEC-1/RTEF-1 and the endothelial cells of VE-Cad/RTEF-1 mice. This effect could be abrogated by treating the myocytes with VEGF-B small interfering RNA and extracellular signal-regulated kinase 1/2 inhibitor. CONCLUSION: Our data demonstrated that increased RTEF-1 in endothelial cells upregulates VEGF-B, which is able to stimulate hypertrophic genes in cardiomyocytes. These results suggest that the RTEF-1-driven increase of VEGF-B plays an important role in communication between the endothelium and myocardium.

The amount of available hypoxia-inducible factor (HIF)-1α has been considered to be largely a consequence of post-translational modification by multiple ubiquitin-proteasome pathways. However, the role of transcriptional regulation of HIF-1α is less certain, and the mechanisms of transcriptional regulation of HIF-1α require further investigation. Here we report that related transcriptional enhancer factor-1 (RTEF-1), a member of the TEF transcriptional factor family, transcriptionally regulates the HIF-1α gene under normoxic and hypoxic conditions. The expression of HIF-1α mRNA was decreased in endothelial cells in which RTEF-1 was knocked down with siRNA. Sequential deletional analysis of the HIF-1α promoter revealed that the MCAT-like element in the HIF-1α promoter was essential for HIF-1α transcription. Binding of RTEF-1 to the MCAT-like element was confirmed by ChIP. Treatment of endothelial cells with a HIF-1 inhibitor resulted in retardation of RTEF-1-induced proliferation and tube formation. Moreover, increased HIF-1α expression was observed in transgenic mice expressing RTEF-1 under the VE-cadherin promoter (VE-Cad/RTEF-1). VE-Cad/RTEF-1 mice subjected to hindlimb ischemia demonstrated increased levels of HIF-1α, accelerated recovery of blood flow, and increased capillary density compared with littermate controls. These results identify RTEF-1 as a regulator of HIF-1α transcription, which results in up-regulation of HIF-1α and acceleration of recovery from ischemia.

Endothelial cells rapidly respond to changes in oxygen homeostasis by regulating gene expression. Regulator of G protein signaling 5 (RGS5) is a negative regulator of G protein-mediated signaling that is strongly expressed in vessels during angiogenesis; however, the role of RGS5 in hypoxia has not been fully understood. Under hypoxic conditions, we found that the expression of RGS5, but not other RGS, was induced in human umbilical vein endothelial cells (HUVEC). RGS5 mRNA was increased when HUVEC were incubated with chemicals that stabilized hypoxia-inducible factor-1alpha (HIF-1alpha), whereas hypoxia-stimulated RGS5 promoter activity was absent in HIF-1beta(-/-) cells. Vascular endothelial growth factor (VEGF), which is regulated by HIF-1, did not appear to be involved in hypoxia-induced RGS5 expression; however, VEGF-mediated activation of p38 but not ERK1/2 was increased by RGS5. Overexpression of RGS5 in HUVEC exhibited a reduced growth rate without affecting the cell proliferation. Annexin V assay revealed that RGS5 induced apoptosis with significantly increased activation of caspase-3 and the Bax/Bcl-2 ratio. Small interfering RNA-specific for RGS5, caspase-3 inhibitor, and p38 inhibitor resulted in an attenuation of RGS5-stimulated apoptosis. Matrigel assay proved that RGS5 significantly impaired the angiogenic effect of VEGF and stimulated apoptosis in vivo. We concluded that RGS5 is a novel HIF-1-dependent, hypoxia-induced gene that is involved in the induction of endothelial apoptosis. Moreover, RGS5 antagonizes the angiogenic effect of VEGF by increasing the activation of p38 signaling, suggesting that RGS5 could be an important target for apoptotic therapy.

BACKGROUND: Response gene to complement 32 (RGC-32) is induced by activation of complement and regulates cell proliferation. To determine the mechanism of RGC-32 in angiogenesis, we examined the role of RGC-32 in hypoxia-related endothelial cell function. METHODS AND RESULTS: Hypoxia/ischemia is able to stimulate both angiogenesis and apoptosis. Hypoxia-inducible factor-1/vascular endothelial growth factor is a key transcriptional regulatory pathway for angiogenesis during hypoxia. We demonstrated that the increased RGC-32 expression by hypoxia was via hypoxia-inducible factor-1/vascular endothelial growth factor induction in cultured endothelial cells. However, overexpression of RGC-32 reduced the proliferation and migration and destabilized vascular structure formation in vitro and inhibited angiogenesis in Matrigel assays in vivo. Silencing RGC-32 had an opposing, stimulatory effect. RGC-32 also stimulated apoptosis as shown by the increased apoptotic cells and caspase-3 cleavage. Mechanistic studies revealed that the effect of RGC-32 on the antiangiogenic response was via attenuating fibroblast growth factor 2 expression and further inhibiting expression of cyclin E without affecting vascular endothelial growth factor and fibroblast growth factor 2 signaling in endothelial cells. In the mouse hind-limb ischemia model, RGC-32 inhibited capillary density with a significant attenuation in blood flow. Additionally, treatment with RGC-32 in the xenograft tumor model resulted in reduced growth of blood vessels that is consistent with reduced colon tumor size. CONCLUSIONS: We provide the first direct evidence for RGC-32 as a hypoxia-inducible gene and antiangiogenic factor in endothelial cells. These data suggest that RGC-32 plays an important homeostatic role in that it contributes to differentiating the pathways for vascular endothelial growth factor and fibroblast growth factor 2 in angiogenesis and provides a new target for ischemic disorder and tumor therapies.

Competitive planning programmes for global integration have been created in cities throughout developed and developing countries during the past 2 decades. In China, global aspiration planning has been characterised by the establishment of Pudong New Area of Shanghai in 1990, with a group of foreign direct investment (FDI)-oriented themed zones targeting different types of global flows. Pudong very rapidly became a focus of FDI in the city, which extended to China as a whole in the 1990s, and now is further extended to playing a global role. However, spatial planning for the themed zones in Pudong has been limited in its scope to the physical design, land use, and the pattern of transport routes. This limited role of land use planning has been inadequate to coordinate the mutual engagement between global and local factors; however, an improved mechanism for coordinating planning has not yet emerged to replace it. The competitive and entrepreneurial approach of land management in conjunction with the imperatives of global firms has effectively diminished the original plan's intention that each zone should focus on particular industries, with each of them complementing the others.

Wu, J., Zhang, H., Pan, Y., Krause-Jensen, D., He, Z., Fan, W., ... & Rivkin, R. B. (2020). Opportunities for blue carbon strategies in China. Ocean & Coastal Management, 194, Article no. 105241. https://doi.org/10.1016/j.ocecoaman.2020.105241