This original book is a unique and original in-depth study on how, in the past decade, Chinese State-Owned Enterprises (SOEs) have achieved technological innovation in the large infrastructure sectors. It reveals a "new world" of Chinese innovation, showing that SOEs are willing to innovate and are also more than capable of doing so. Based on findings from first-hand data and years of observations, this book shows how the innovation ecosystem perspective incentivises and facilitates Chinese SOEs' innovation and highlights the entrepreneurial role of the government. Using the examples of UHV Power Transmission, mobile telecommunication standards, high-speed trains, and nuclear electric power, the book exhibits the complex determinants of SOEs' success in radical technological innovations within the large infrastructure sector. Chapters also demonstrate the innovation process of SOEs, the unique innovation model of China, as well as its advantages and disadvantages. Catch-Up and Radical Innovation in Chinese State-Owned Enterprises will be a useful resource for academics in research disciplines such as development studies, innovation and entrepreneurship, and Chinese studies. It will also aid entrepreneurs, businesses and managers who intend to collaborate with Chinese SOEs, to better understand the trends of SOEs' engagement in radical innovation and the potential opportunities for broadening their international collaborations.

This book covers the fundamental principles behind the design of ultra-low power radios and how they can form networks to facilitate a variety of applications within healthcare and environmental monitoring, since they may operate for years off a small battery or even harvest energy from the environment. These radios are distinct from conventional radios in that they must operate with very constrained resources and low overhead. This book provides a thorough discussion of the challenges associated with designing radios with such constrained resources, as well as fundamental design concepts and practical approaches to implementing working designs. Coverage includes integrated circuit design, timing and control considerations, fundamental theory behind low power and time domain operation, and network/communication protocol considerations.

Representation learning in heterogeneous graphs (HG) is intended to provide a meaningful vector representation for each node so as to facilitate downstream applications such as link prediction, personalized recommendation, node classification, etc. This task, however, is challenging not only because of the need to incorporate heterogeneous structural (graph) information consisting of multiple types of node and edge, but also the need to consider heterogeneous attributes or types of content (e.g. text or image) associated with each node. Although considerable advances have been made in homogeneous (and heterogeneous) graph embedding, attributed graph embedding and graph neural networks, few are capable of simultaneously and effectively taking into account heterogeneous structural (graph) information as well as the heterogeneous content information of each node. In this book, we provide a comprehensive survey of current developments in HG representation learning. More importantly, we present the state-of-the-art in this field, including theoretical models and real applications that have been showcased at the top conferences and journals, such as TKDE, KDD, WWW, IJCAI and AAAI. The book has two major objectives: (1) to provide researchers with an understanding of the fundamental issues and a good point of departure for working in this rapidly expanding field, and (2) to present the latest research on applying heterogeneous graphs to model real systems and learning structural features of interaction systems. To the best of our knowledge, it is the first book to summarize the latest developments and present cutting-edge research on heterogeneous graph representation learning. To gain the most from it, readers should have a basic grasp of computer science, data mining and machine learning.

Lung diseases are leading causes of death and disability globally, with about 65 million people suffering from COPD, and 334 million from asthma. Each year, tens of millions of people develop and can die from lung infections such as pneumonia and TB. Systemic inflammation may induce and exacerbate local inflammatory diseases in the lungs, and local inflammation can in turn cause systemic inflammation. There is increasing evidence of the coexistence of systemic and local inflammation in patients suffering from asthma, COPD, and other lung diseases, and the co-morbidity of two or more local inflammatory diseases often occurs. For example, rheumatoid arthritis frequently occurs together with, and promotes the development of, pulmonary hypertension. This co-morbidity significantly impacts quality of life, and can result in death for some patients. Current treatment options for lung disease are neither always effective, nor condition-specific; there is a desperate need for novel therapeutics in the field. Additionally, the molecular and physiological significance of most major lung diseases is not well understood, which further impedes development of new treatments, especially in the case of coexistent lung diseases with other inflammatory diseases. Great progress has been made in recent years in many areas of the field, particularly in understanding the molecular geneses, regulatory mechanisms, signalling pathways, and cellular processes within lung disease, as well as basic and clinical technology, drug discovery, diagnoses, treatment options, and predictive prognoses. This is the first text to aggregate these developments. In two comprehensive volumes, experts from all over the world present state-of-the-art advances in the study of lung inflammation in health and disease. Contributing authors cover well-known as well as emerging topics in basic, translational, and clinical research, with the aim of providing researchers, clinicians, professionals, and students with new perspectives and concepts. The editors hope these books will also help to direct future research in lung disease and other inflammatory diseases, and result in the development of novel therapeutics.

Respiratory diseases are leading causes of death and disability globally, with about 65 million people suffering from COPD, and 334 million from asthma, the most common chronic disease. Each year, tens of millions of people develop and can die from from respiratory infections such as pneumonia and TB. Systemic inflammation may induce and exacerbate local inflammatory diseases in the lungs, and local inflammation can in turn cause systemic inflammation. There is increasing evidence of the coexistence of systemic and local inflammation in patients suffering from asthma, COPD, and other lung diseases, and the co-morbidity of two or more local inflammatory diseases often occurs. For example, rheumatoid arthritis frequently occurs together with, and promotes the development of, pulmonary hypertension. This co-morbidity significantly impacts quality of life, and can result in death for those affected. Current treatment options for lung disease are neither effective, nor condition-specific; there is a desperate need for novel therapeutics in the field. Additionally, the molecular and physiological significance of most major lung diseases is not well understood, which further impedes development of new treatments, especially in the case of coexistent lung diseases with other inflammatory diseases. Great progress has been made in recent years in many areas of the field, particularly in understanding the molecular geneses, regulatory mechanisms, signalling pathways, and cellular processes within lung disease, as well as basic and clinical technology, drug discovery, diagnoses, treatment options, and predictive prognoses. This is the first text to aggregate these developments. In two comprehensive volumes, experts from all over the world present state-of-the-art advances in the study of lung inflammation in health and disease. Contributing authors cover well-known as well as emerging topics in basic, translational, and clinical research, with the aim of providing researchers, clinicians, professionals, and students with new perspectives and concepts. The editors hope these books will also help to direct future research in lung disease and other inflammatory diseases, and result in the development of novel therapeutics.

The main goal of this book is to form a high-quality platform in which well-known and emerging pioneering basic, translational and clinical scientists can present their latest, exciting findings in the studies of redox signaling in the pulmonary vasculature. Content from outstanding investigators with unique expertise and skills of molecular and cell biology, biochemistry, physiology, pharmacology, biophysics, biotechnology and medicine will update our current out-of-date concepts with new knowledge. Rapidly increasing scientific studies have gathered a large volume of novel and important information on redox signaling in healthy and diseased pulmonary vasculature. This volume covers the need for a cohesive book to display state-of-the-art advances in the field. The second major aim of this book is to help direct future research. Redox signaling is a major molecular process involved in almost every physiologic cellular response in the pulmonary vasculature including energy metabolism, host defense, gene expression, contraction, proliferation, and migration. Aberrancy in this important signaling pathway leads to a critical role in the development of nearly all pulmonary diseases, such as pulmonary hypertension, cor pulmonale, pulmonary edema, and vasculitis, among others.

This book covers the fundamental principles behind the design of ultra-low power radios and how they can form networks to facilitate a variety of applications within healthcare and environmental monitoring, since they may operate for years off a small battery or even harvest energy from the environment. These radios are distinct from conventional radios in that they must operate with very constrained resources and low overhead. This book provides a thorough discussion of the challenges associated with designing radios with such constrained resources, as well as fundamental design concepts and practical approaches to implementing working designs. Coverage includes integrated circuit design, timing and control considerations, fundamental theory behind low power and time domain operation, and network/communication protocol considerations.

This book explores the role calcium signaling plays in cellular responses in almost all types of cells including airway smooth muscle cells. This universal signaling may result from extracellular calcium influx and/or intracellular calcium release, which are precisely controlled and regulated by ion channels, exchangers and/or transporters on the plasmalemmal or sarcoplasmic reticulum membrane. First, several chapters detail calcium release channels (ryanodine receptors and inositol trisphosphate receptors), voltage-dependent potassium channels, transient receptor potential channels, Orai channels, calcium-activated potassium channels, and calcium-activated chloride channels. Well-characterized sodium-calcium exchangers, voltage-dependent calcium channels, and calcium pumps are described also in depth over many chapters.

Ca2+ signaling can be expressed in Ca2+ sparks, waves, oscillations, and global changes in intracellular Ca2+ concentration. Calcium in subcellular compartments (cytosol, sarcoplasmic reticulum, mitochondria, and caveolae) also exhibit dynamic crosstalk. Many molecules including FK506 binding proteins, cyclic adenosine diphosphate ribose, reactive oxygen species, RhoA kinases, caveolin and integrins can modify and induce spatial, temporal and compartmental variations of calcium signaling. In addition, calcium signaling can exhibit sex hormone- and age-dependent changes. A number of chapters are dedicated to covering these diverse formats, spatiotemporal characteristics, multifaceted network and mathematical modeling of Ca2+ signaling.

Neurotransmitters, hormones, growth factors, inflammatory cytokines, and other stimuli may lead to multiple cellular responses by inducing Ca2+ signaling in airway smooth muscle cells. Increasing evidence suggests that Ca2+ pumps and canonical transient receptor potential channels are essential for airway smooth muscle remodeling. Accordingly, several chapters summarize recent advances in the studies of the key role of calcium signaling in physiological cellular responses as well as the development of asthma, chronic obstructive pulmonary disease and other respiratory disorders.

Lung diseases are leading causes of death and disability globally, with about 65 million people suffering from COPD, and 334 million from asthma. Each year, tens of millions of people develop and can die from lung infections such as pneumonia and TB. Systemic inflammation may induce and exacerbate local inflammatory diseases in the lungs, and local inflammation can in turn cause systemic inflammation. There is increasing evidence of the coexistence of systemic and local inflammation in patients suffering from asthma, COPD, and other lung diseases, and the co-morbidity of two or more local inflammatory diseases often occurs. For example, rheumatoid arthritis frequently occurs together with, and promotes the development of, pulmonary hypertension. This co-morbidity significantly impacts quality of life, and can result in death for some patients. Current treatment options for lung disease are neither always effective, nor condition-specific; there is a desperate need for novel therapeutics in the field. Additionally, the molecular and physiological significance of most major lung diseases is not well understood, which further impedes development of new treatments, especially in the case of coexistent lung diseases with other inflammatory diseases. Great progress has been made in recent years in many areas of the field, particularly in understanding the molecular geneses, regulatory mechanisms, signalling pathways, and cellular processes within lung disease, as well as basic and clinical technology, drug discovery, diagnoses, treatment options, and predictive prognoses. This is the first text to aggregate these developments. In two comprehensive volumes, experts from all over the world present state-of-the-art advances in the study of lung inflammation in health and disease. Contributing authors cover well-known as well as emerging topics in basic, translational, and clinical research, with the aim of providing researchers, clinicians, professionals, and students with new perspectives and concepts. The editors hope these books will also help to direct future research in lung disease and other inflammatory diseases, and result in the development of novel therapeutics.

Respiratory diseases are leading causes of death and disability globally, with about 65 million people suffering from COPD, and 334 million from asthma, the most common chronic disease. Each year, tens of millions of people develop and can die from from respiratory infections such as pneumonia and TB. Systemic inflammation may induce and exacerbate local inflammatory diseases in the lungs, and local inflammation can in turn cause systemic inflammation. There is increasing evidence of the coexistence of systemic and local inflammation in patients suffering from asthma, COPD, and other lung diseases, and the co-morbidity of two or more local inflammatory diseases often occurs. For example, rheumatoid arthritis frequently occurs together with, and promotes the development of, pulmonary hypertension. This co-morbidity significantly impacts quality of life, and can result in death for those affected. Current treatment options for lung disease are neither effective, nor condition-specific; there is a desperate need for novel therapeutics in the field. Additionally, the molecular and physiological significance of most major lung diseases is not well understood, which further impedes development of new treatments, especially in the case of coexistent lung diseases with other inflammatory diseases. Great progress has been made in recent years in many areas of the field, particularly in understanding the molecular geneses, regulatory mechanisms, signalling pathways, and cellular processes within lung disease, as well as basic and clinical technology, drug discovery, diagnoses, treatment options, and predictive prognoses. This is the first text to aggregate these developments. In two comprehensive volumes, experts from all over the world present state-of-the-art advances in the study of lung inflammation in health and disease. Contributing authors cover well-known as well as emerging topics in basic, translational, and clinical research, with the aim of providing researchers, clinicians, professionals, and students with new perspectives and concepts. The editors hope these books will also help to direct future research in lung disease and other inflammatory diseases, and result in the development of novel therapeutics.

This book explores the role calcium signaling plays in cellular responses in almost all types of cells including airway smooth muscle cells. This universal signaling may result from extracellular calcium influx and/or intracellular calcium release, which are precisely controlled and regulated by ion channels, exchangers and/or transporters on the plasmalemmal or sarcoplasmic reticulum membrane. First, several chapters detail calcium release channels (ryanodine receptors and inositol trisphosphate receptors), voltage-dependent potassium channels, transient receptor potential channels, Orai channels, calcium-activated potassium channels, and calcium-activated chloride channels. Well-characterized sodium-calcium exchangers, voltage-dependent calcium channels, and calcium pumps are described also in depth over many chapters. Ca2+ signaling can be expressed in Ca2+ sparks, waves, oscillations, and global changes in intracellular Ca2+ concentration. Calcium in subcellular compartments (cytosol, sarcoplasmic reticulum, mitochondria, and caveolae) also exhibit dynamic crosstalk. Many molecules including FK506 binding proteins, cyclic adenosine diphosphate ribose, reactive oxygen species, RhoA kinases, caveolin and integrins can modify and induce spatial, temporal and compartmental variations of calcium signaling. In addition, calcium signaling can exhibit sex hormone- and age-dependent changes. A number of chapters are dedicated to covering these diverse formats, spatiotemporal characteristics, multifaceted network and mathematical modeling of Ca2+ signaling. Neurotransmitters, hormones, growth factors, inflammatory cytokines, and other stimuli may lead to multiple cellular responses by inducing Ca2+ signaling in airway smooth muscle cells. Increasing evidence suggests that Ca2+ pumps and canonical transient receptor potential channels are essential for airway smooth muscle remodeling. Accordingly, several chapters summarize recent advances in the studies of the key role of calcium signaling in physiological cellular responses as well as the development of asthma, chronic obstructive pulmonary disease and other respiratory disorders.

Lucid Nightmares is a collection of short stories by award winning novelist Daniel Xiao Wang. Beware dark hallways, shadows, deserted convenience store, coffee shops... cats. Make sure the doors are locked, pull up a warm blanket, and prepare to see the world around you in a new, darker way.

With the world s second largest economy, China has the capacity to engage in substantial programs of development assistance and government investment in any and all of the emerging-market countries. RAND researchers assessed the scale, trends, and composition of these programs in 93 countries in six regions: Africa, Latin America, the Middle East, South Asia, Central Asia, and East Asia.