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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.
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.
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 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.
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.
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.
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