In this book, we consider the problem of achieving the maximum throughput and utility in a class of networks with resource-sharing constraints. This is a classical problem of great importance. In the context of wireless networks, we first propose a fully distributed scheduling algorithm that achieves the maximum throughput. Inspired by CSMA (Carrier Sense Multiple Access), which is widely deployed in today's wireless networks, our algorithm is simple, asynchronous, and easy to implement. Second, using a novel maximal-entropy technique, we combine the CSMA scheduling algorithm with congestion control to approach the maximum utility. Also, we further show that CSMA scheduling is a modular MAC-layer algorithm that can work with other protocols in the transport layer and network layer. Third, for wireless networks where packet collisions are unavoidable, we establish a general analytical model and extend the above algorithms to that case. Stochastic Processing Networks (SPNs) model manufacturing, communication, and service systems. In manufacturing networks, for example, tasks require parts and resources to produce other parts. SPNs are more general than queueing networks and pose novel challenges to throughput-optimum scheduling. We proposes a "deficit maximum weight" (DMW) algorithm to achieve throughput optimality and maximize the net utility of the production in SPNs. Table of Contents: Introduction / Overview / Scheduling in Wireless Networks / Utility Maximization in Wireless Networks / Distributed CSMA Scheduling with Collisions / Stochastic Processing networks

Scheduling and Congestion Control for Wireless and Processing Networks (Synthesis Lectures on Communication Networks, 6)

Computers & Technology

Libin, Jiang

Jean, Walrand

Networking & Cloud Computing

Morgan & Claypool Life Sciences

Histologically, muscle is conveniently divided into two groups, striated and nonstriated, based on whether the cells exhibit cross-striations in the light microscope (Figure 3). Smooth muscle is involuntary: its contraction is controlled by the autonomic nervous system. Striated muscle includes both cardiac (involuntary) and skeletal (voluntary). The former is innervated by visceral efferent fibers of the autonomic nervous system, whereas the latter is innervated by somatic efferent fibers, most of which have their cell bodies in the ventral, motor horn of the spinal cord. Smooth muscle is designed to have slow, relatively sustained contractions, while striated muscle contracts rapidly and usually phasically. Both cardiac and smooth muscle cells are mononucleated, whereas skeletal muscle cells (fibers) are multinucleated. [In aging hearts or hypertrophied hearts, cardiac muscle cells are often binucleated.] Multinucleation of skeletal muscle arises during development by the cytoplasmic fusion of muscle precursor cells, myoblasts. Adult skeletal muscle cells do not divide; that is also true of most cardiac myocytes. However, skeletal muscle exhibits a considerable amount of regeneration after injury. This is because adult skeletal muscle contains a stem cell, the satellite cell, which lies beneath the basement membrane surrounding the muscle fibers. [The multinucleation of cardiac muscle arises from karyokinesis without cytokinesis.] A diagrammatic series of enlargements of skeletal muscle are shown in Figure 4. A bundle of muscle fibers (fasciculus) is cut from the deltoid muscle. Each muscle cell is termed a myofiber or muscle fiber. Each muscle fiber contains contractile organelles termed myofibrils, which contain the contractile units of muscle termed sarcomeres. The sarcomeres are composed of myofilaments, which in turn are composed of contractile proteins. Muscle connective tissue layers are organized in concentric layers that are important in the entry and exit of vessels and nerves to and from the tissue. These are shown in Figure 5. The outermost layer is the epimysium or muscle sheath. Connective tissue septae (perimysium) run radially into the muscle tissue, dividing it into muscle fascicles. The deepest layer, surrounding each of the muscle fibers is the endomysium. The endomysium is in direct contact with a basal lamina that ensheathes each muscle fiber. It surrounds the plasma membrane of the muscle fiber termed the sarcolemma. Table of Contents: The Muscle Cell (Myofiber) / The Sarcomere / The Myosin Molecule / Regulation of Muscle Contraction / The Sarcoplasmic Reticulum / Muscle Fiber Types / The Myotendon Junction / The Satellite Cell / Muscular Dystrophy / Recommended Readings

Skeletal Muscle & Muscular Dystrophy (Colloquium Series on the Cell Biology of Medicine/ Morgan & Claypool Life Science Series, 2)

Science & Math

Fischman, Donald A

Biological Sciences

The Hepatic circulation is unique among vascular beds. The most obvious unique features include the dual vascular supply; the mechanism of intrinsic regulation of the hepatic artery (the hepatic arterial buffer response); the fact that portal blood flow, supplying two thirds of liver blood flow, is not controlled directly by the liver; the fact that 20% of the cardiac output rushes through the most vascularized organ in the body, driven by a pressure gradient of only a few millimeters of mercury; the extremely distensible capacitance and venous resistance sites; the unidirectional acinar blood flow that regulates parenchymal cell metabolic specialization; and the high concentration of macrophagic (Kupffer) cells filtering the blood. The liver is the only organ reported to have regional blood flow monitored by the autonomic nervous system. This mechanism, when dysfunctional, accounts for the hepatorenal syndrome and offers a mechanistic therapeutic target to treat this syndrome. The trigger for liver regeneration is dependent on hepatic hemodynamics so that chronic liver blood flow regulates liver cell mass. In severe liver disease, the whole body circulation is reorganized, by forming portacaval shunts, to accommodate the increased intrahepatic venous resistance. These shunts protect the venous drainage of the splanchnic organs but lead to loss of major regulatory roles of the liver. The development of knowledge of the hepatic vasculature is presented from a historical perspective with modern concepts summarized based on the perspective of the author's four decades of devotion to this most marvelous of organs.

Hepatic Circulation: Physiology and Pathophysiology (Colloquium Series on Integrated Systems Physiology: From Molecule to Function, 1)

Lautt, W. Wayne

Although cardiac output is measured as the flow of blood from the left ventricle into the aorta, the system that controls cardiac output includes many other components besides the heart itself. The heart's rate of output cannot exceed the rate of venous return to it, and therefore, the factors governing venous return are primarily responsible for control of output from the heart. Venous return is affected by its pressure gradient and resistance to flow throughout the vascular system. The pressure gradient for venous return is a function of several factors including the blood volume flowing through the system, the unstressed vascular volume of the circulatory system, its capacitance, mean systemic pressure, and right atrial pressure. Resistance to venous return is the sum of total vascular resistance from the aortic valve to the right atrium. The sympathetic nervous system and vasoactive circulating hormones affect short-term resistance, whereas local tissue blood flow autoregulatory mechanisms are the dominant determinants of long-term resistance to venous return. The strength of contraction of the heart responds to changes in atrial pressure driven by changes in venous return, with small changes in atrial pressure eliciting large changes in strength of contraction, as described by the Frank-Starling mechanism. In addition, the autonomic nervous system input to the heart alters myocardial pumping ability in response to cardiovascular challenges. The function of the cardiovascular system is strongly affected by the operation of the renal sodium excretion-body fluid volume-arterial pressure negative feedback system that maintains arterial blood pressure at a controlled value over long periods. The intent of this volume is to integrate the basic knowledge of these cardiovascular system components into an understanding of cardiac output regulation.

Control of Cardiac Output (Colloquium Series on the Cell Biology of Medicine)

Young, David B.

The partition of fluid between the vascular and interstitial compartments is regulated by forces (hydrostatic and oncotic) operating across the microvascular walls and the surface areas of permeable structures comprising the endothelial barrier to fluid and solute exchange, as well as within the extracellular matrix and lymphatics. In addition to its role in the regulation of vascular volume, transcapillary fluid filtration also allows for continuous turnover of water bathing tissue cells, providing the medium for diffusional flux of oxygen and nutrients required for cellular metabolism and removal of metabolic byproducts. Transendothelial volume flow has also been shown to influence vascular smooth muscle tone in arterioles, hydraulic conductivity in capillaries, and neutrophil transmigration across postcapillary venules, while the flow of this filtrate through the interstitial spaces functions to modify the activities of parenchymal, resident tissue, and metastasizing tumor cells. Likewise, the flow of lymph, which is driven by capillary filtration, is important for the transport of immune and tumor cells, antigen delivery to lymph nodes, and for return of filtered fluid and extravasated proteins to the blood. Given this background, the aims of this treatise are to summarize our current understanding of the factors involved in the regulation of transcapillary fluid movement, how fluid movements across the endothelial barrier and through the interstitium and lymphatic vessels influence cell function and behavior, and the pathophysiology of edema formation. Table of Contents: Fluid Movement Across the Endothelial Barrier / The Interstitium / The Lymphatic Vasculature / Pathophysiology of Edema Formation

Capillary Fluid Exchange: Regulation, Functions, and Pathology (Colloquium Series on Integrated Systems Physiology: From Mol)

Korthuis, Ronald J.

Scallan, Joshua

Huxley, Virginia H.

The field of endocrine disruption has been the focus of increasing attention from scientists and the general public in the past 30 years, amidst concerns that exposure to environmental chemicals with the potential to alter endocrine system function, known as endocrine disrupting chemicals (EDCs), may be contributing to an overall decline in wildlife populations and the reproductive health of humans. These concerns are based on observations of adverse effects of EDCs on marine and land animals, an increased incidence of reproductive and endocrine disease in humans, epidemiological evidence for links between body burden and disease, and endocrine disruption in laboratory animals following exposure to EDCs. Owing to its role in regulation of endocrine function as well as its responsiveness to hormones, the developing brain is an especially vulnerable target for many classes of EDCs. This book will address the evidence for EDC action on the developing brain, organized into 7 chapters. Topics covered include background about EDCs, evidence for exposures, concerns about EDC effects in the developing organism, and particularly on the developing nervous system, how EDCs perturb the brain's neuroendocrine systems, transgenerational epigenetic effects of EDCs, EDC effects on non-reproductive behaviors, and future perspectives. This is the first book completely dedicated to understanding links between EDCs and the developing brain, an area of emerging importance for human health.  Table of Contents: What Are Environmental Endocrine-Disrupting Chemicals (EDCs)? / EDC Exposures / EDCs and Development / EDCs and the Developing Brain / EDCs and Neuroendocrine Systems / Epigenetic Effects of EDCs / EDCs, the Brain, and the Future / Acknowledgments / References / Author Biographies

Endocrine Disruptors and The Developing Brain (Colloquium Series on the Developing Brain)

Andrea Gore

Sarah Dickerson

The microcirculation of the gastrointestinal tract is under the control of both myogenic and metabolic regulatory systems. The myogenic mechanism contributes to basal vascular tone and the regulation of transmural pressure, while the metabolic mechanism is responsible for maintaining an appropriate balance between O2 demand and O2 delivery. In the postprandial state, hydrolytic products of food digestion elicit a hyperemia, which serves to meet the increased O2 demand of nutrient assimilation. Metabolically linked factors (e.g., tissue pO2, adenosine) are primarily responsible for this functional hyperemia. The fenestrated capillaries of the gastrointestinal mucosa are relatively permeable to small hydrolytic products of food digestion (e.g., glucose), yet restrict the transcapillary movement of larger molecules (e.g., albumin). This allows for the absorption of hydrolytic products of food digestion without compromising the oncotic pressure gradient governing transcapillary fluid movement and edema formation. The gastrointestinal microcirculation is also an important component of the mucosal defense system whose function is to prevent (and rapidly repair) inadvertent epithelial injury by potentially noxious constituents of chyme. Two pathological conditions in which the gastrointestinal circulation plays an important role are ischemia/reperfusion and chronic portal hypertension. Ischemia/reperfusion results in mucosal edema and disruption of the epithelium due, in part, to an inflammatory response (e.g., increase in capillary permeability to macromolecules and neutrophil infiltration). Chronic portal hypertension results in an increase in gastrointestinal blood flow due to an imbalance in vasodilator and vasoconstrictor influences on the microcirculation.

The Gastrointestinal Circulation (Integrated Systems Physiology: From Molecule to Function)

Kvietys, Peter R.

The vascular endothelium lining the inner surface of blood vessels serves as the first interface for circulating blood components to interact with cells of the vascular wall and surrounding extravascular tissues. In addition to regulating blood delivery and perfusion, a major function of vascular endothelia, especially those in exchange microvessels (capillaries and postcapillary venules), is to provide a semipermeable barrier that controls blood–tissue exchange of fluids, nutrients, and metabolic wastes while preventing pathogens or harmful materials in the circulation from entering into tissues. During host defense against infection or tissue injury, endothelial barrier dysfunction occurs as a consequence as well as cause of inflammatory responses. Plasma leakage disturbs fluid homeostasis and impairs tissue oxygenation, a pathophysiological process contributing to multiple organ dysfunction associated with trauma, infection, metabolic disorder, and other forms of disease. In this book, we provide an updated overview of microvascular endothelial barrier structure and function in health and disease. The discussion is initiated with the basic physiological principles of fluid and solute transport across microvascular endothelium, followed by detailed information on endothelial cell–cell and cell–matrix interactions and the experimental techniques that are employed to measure endothelial permeability. Further discussion focuses on the signaling and molecular mechanisms of endothelial barrier responses to various stimulations or drugs, as well as their relevance to several common clinical conditions. Taken together, this book provides a comprehensive analysis of microvascular endothelial cell and molecular pathophysiology. Such information will assist scientists and clinicians in advanced basic and clinical research for improved health care. Table of Contents: Acknowledgments / Introduction / Structure and Function of Exchange Microvessels / Methods for Measuring Permeability / The Endothelial Barrier / Signaling Mechanisms in the Regulation of Endothelial Permeability / Endothelial Barrier Protectors / Pathophysiology and Clinical Relevance / Conclusion / References

Regulation of Endothelial Barrier Function (Integrated Systems Physiology: From Molecule to Function to Disease, 12)

Yuan, Sarah Y.

Rigor, Robert R.

The secretions of the exocrine pancreas provide for digestion of a meal into components that are then available for processing and absorption by the intestinal epithelium. Without the exocrine pancreas, malabsorption and malnutrition result. This chapter describes the cellular participants responsible for the secretion of digestive enzymes and fluid that in combination provide a pancreatic secretion that accomplishes the digestive functions of the gland. Key cellular participants, the acinar cell and the duct cell, are responsible for digestive enzyme and fluid secretion, respectively, of the exocrine pancreas. This chapter describes the neurohumoral pathways that mediate the pancreatic response to a meal as well as details of the cellular mechanisms that are necessary for the organ responses, including protein synthesis and transport and ion transports, and the regulation of these responses by intracellular signaling systems. Examples of pancreatic diseases resulting from dysfunction in cellular mechanisms provide emphasis of the importance of the normal physiologic mechanisms. Table of Contents: Introduction / Anatomy / Pancreatic Embryology and Development / Digestive Enzymes / Water and Ion Secretion from the Pancreatic Ductal System / Regulation of Whole-Organ Pancreatic Secretion / Measurement of Exocrine Pancreatic Secretion in Humans / Clinical Application of Knowledge of Pancreatic Physiology / Summary / References

The Exocrine Pancreas (Integrated Systems Physiology: From Molecule to Function to Disease, 13)

Pandol, Stephen J.

In the intestine, a unique immunological system that is different from the systemic immune system exists to provide adaptive immunity in response to luminal bacteria and dietary antigens. There are many lymphoid cell aggregates called gut-associated lymphoid tissue (GALT) including Peyer’s patches (PPs), which function as important induction sites for the mucosal immune response. M-cells are present in the epithelium of PPs, having a specialized structure for uptake of macromolecules such as bacteria. In addition to GALT, there are abundant lymphoid cells in the intestinal lamina propria, where they mainly play a role as immune effector cells. 
 The intestinal mucosa thus shows a unique morphological structure with many immune cells being present under physiological conditions. This condition is known as "controlled inflammation." These abundant immune cells also have characteristic functions: they are "negatively regulated" and have been educated not to overreact unnecessarily to the intestinal luminal milieu. Main players that control inflammation of the intestinal mucosa include regulatory cytokines and regulatory T cells which induce oral tolerance to intestinal bacteria and food antigens, and the secretory IgA system. The maintenance of unique immunological activity in the intestine is also related to an organized, orchestrated lymphocyte migratory mechanism called the "common mucosal immune system." 
 These negative regulatory mechanisms of the intestinal immune system are disturbed in certain disease conditions, causing the immunocompetent cells to respond to food components and commensal bacteria by becoming activated and to overproduce inflammatory cytokines and chemokines. These disease conditions include food allergies, such as celiac disease, and the inflammatory bowel diseases, such as ulcerative colitis and Crohn’s disease, although their exact etiological mechanisms remain to be revealed. 
 Table of Contents: Introduction / GALT: Its Structure and Formation / Intestinal Epithelial Cells and Their Immune Function / Innate Immunity in the Intestinal Mucosa / Intraepithelial Lymphocytes (IELs) / Lymphoid Cell Trafficking in Intestinal Immunology / Site of Induction of Mucosal Immunity and Antigen Presentation by Dendritic Cells / Production of Secretory IgA (SIgA) / Effector Site of Acquired Immunity and T Helper Cell Subpopulation / Immune Regulatory System and Oral Tolerance / Food Allergy and Celiac Disease / Inflammatory Bowel Diseases / Enteric Infection with Pathogenic Microbes and Mucosal Immunity / References

Intestinal Immune System (Integrated Systems Physiology: From Molecule to Function to)

Miura, Soichiro

Hokari, Ryota

Komoto, Shunsuke

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