\r\n\t
",isbn:"978-1-83881-922-4",printIsbn:"978-1-83881-921-7",pdfIsbn:"978-1-83881-923-1",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"dcfc52d92f694b0848977a3c11c13d00",bookSignature:"Dr. Fiaz Ahmad and Prof. Muhammad Sultan",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10454.jpg",keywords:"Agricultural Engineering, Technologies, Application, Sustainable Agriculture, Information Technology in Agriculture, Food Security, Renewable Energies, Precision Farming, Smart Agriculture, Farm Mechanization, Robotics, Post Harvest Technologies",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"November 25th 2020",dateEndSecondStepPublish:"December 23rd 2020",dateEndThirdStepPublish:"February 21st 2021",dateEndFourthStepPublish:"May 12th 2021",dateEndFifthStepPublish:"July 11th 2021",remainingDaysToSecondStep:"a month",secondStepPassed:!0,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"Dr. Ahmad is a researcher in the field of agricultural mechanization and agricultural equipment engineering, in-charge of Farm Machinery Design Laboratory at Bahauddin Zakariya University, with expertise in modeling and simulation. He applied for two patents at the national level.",coeditorOneBiosketch:"Renowned researcher with a focus on developing energy-efficient heat- and/or water-driven temperature and humidity control systems for agricultural storage, greenhouse, agricultural livestock and poultry applications including HVAC, desiccant air-conditioning, adsorption, Maisotsenko cycle (M-cycle), and adsorption desalination.",coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"338219",title:"Dr.",name:"Fiaz",middleName:null,surname:"Ahmad",slug:"fiaz-ahmad",fullName:"Fiaz Ahmad",profilePictureURL:"https://mts.intechopen.com/storage/users/338219/images/system/338219.jpg",biography:"Fiaz Ahmad obtained his Ph.D. (2015) from Nanjing Agriculture University China in the field of Agricultural Bioenvironmental and Energy Engineering and Postdoc (2020) from Jiangsu University China in the field of Plant protection Engineering. He got the Higher Education Commission, Pakistan Scholarship for Ph.D. studies, and Post-Doctoral Fellowship from Jiangsu Government, China. During postdoctoral studies, he worked on the application of unmanned aerial vehicle sprayers for agrochemical applications to control pests and weeds. He passed the B.S. and M.S. degrees in agricultural engineering from the University of Agriculture Faisalabad, Pakistan in 2007. From 2007 to 2008, he was a Lecturer in the Department of Agricultural Engineering, Bahauddin Zakariya University, Multan-Pakistan. Since 2009, he has been an Assistant Professor in the Department of Agricultural Engineering, BZ University Multan, Pakistan. He is the author of 33 journal articles. He also supervised 6 master students and is currently supervising 5 master and 2 Ph.D. students. In addition, Dr. Ahmad completed three university-funded projects. His research interests include the design of agricultural machinery, artificial intelligence, and plant protection environment.",institutionString:"Bahauddin Zakariya University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Bahauddin Zakariya University",institutionURL:null,country:{name:"Pakistan"}}}],coeditorOne:{id:"199381",title:"Prof.",name:"Muhammad",middleName:null,surname:"Sultan",slug:"muhammad-sultan",fullName:"Muhammad Sultan",profilePictureURL:"https://mts.intechopen.com/storage/users/199381/images/system/199381.jpeg",biography:"Muhammad Sultan completed his Ph.D. (2015) and Postdoc (2017) from Kyushu University (Japan) in the field of Energy and Environmental Engineering. He was an awardee of MEXT and JASSO fellowships (from the Japanese Government) during Ph.D. and Postdoc studies, respectively. In 2019, he did Postdoc as a Canadian Queen Elizabeth Advanced Scholar at Simon Fraser University (Canada) in the field of Mechatronic Systems Engineering. He received his Master\\'s in Environmental Engineering (2010) and Bachelor in Agricultural Engineering (2008) with distinctions, from the University of Agriculture, Faisalabad. He worked for Kyushu University International Institute for Carbon-Neutral Energy Research (WPI-I2CNER) for two years. Currently, he is working as an Assistant Professor at the Department of Agricultural Engineering, Bahauddin Zakariya University (Pakistan). He has supervised 10+ M.Eng./Ph.D. students so far and 10+ M.Eng./Ph.D. students are currently working under his supervision. He has published more than 70+ journal articles, 70+ conference articles, and a few magazine articles, with the addition of 2 book chapters and 2 edited/co-edited books. Dr. Sultan is serving as a Leading Guest Editor of a special issue in the Sustainability (MDPI) journal (IF 2.58). In addition, he is appointed as a Regional Editor for the Evergreen Journal of Kyushu University. His research is focused on developing energy-efficient heat- and/or water-driven temperature and humidity control systems for agricultural storage, greenhouse, livestock, and poultry applications. His research keywords include HVAC, desiccant air-conditioning, evaporative cooling, adsorption cooling, energy recovery ventilator, adsorption heat pump, Maisotsenko cycle (M-cycle), wastewater, energy recovery ventilators; adsorption desalination; and agricultural, poultry and livestock applications.",institutionString:"Bahauddin Zakariya University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Bahauddin Zakariya University",institutionURL:null,country:{name:"Pakistan"}}},coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"8",title:"Chemistry",slug:"chemistry"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"252211",firstName:"Sara",lastName:"Debeuc",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/252211/images/7239_n.png",email:"sara.d@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3621",title:"Silver Nanoparticles",subtitle:null,isOpenForSubmission:!1,hash:null,slug:"silver-nanoparticles",bookSignature:"David Pozo Perez",coverURL:"https://cdn.intechopen.com/books/images_new/3621.jpg",editedByType:"Edited by",editors:[{id:"6667",title:"Dr.",name:"David",surname:"Pozo",slug:"david-pozo",fullName:"David Pozo"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"44779",title:"Sympathovagal Imbalance in Type 2 Diabetes — Role of Brainstem Thyrotropin-Releasing Hormone",doi:"10.5772/56541",slug:"sympathovagal-imbalance-in-type-2-diabetes-role-of-brainstem-thyrotropin-releasing-hormone",body:'\nType 2 diabetes (T2D) is the world’s fastest growing disease with high morbidity and mortality rates. The potential to develop effective therapies is severely limited by poor understanding of mechanisms underlying the etiology and progression of T2D.
\nIncreasing evidence suggests that the brain plays a key role in regulating metabolism [1, 2]. In particular, the exquisitely precise adjustments in the sympathetic and parasympathetic outflow by the brain are critical for maintaining metabolic homeostasis. Enhanced sympathetic drive and impaired vagal efferent function contribute to multisystemic pathophysiology of T2D, including reduced insulin secretion, gastroparesis, hypertension, and high cardiovascular mortality [3-6]. The aim of this chapter is to emphasize the importance of the brainstem, which contains sympathovagal regulatory nuclei, in the regulation of metabolism, especially in T2D conditions. I focus on the role of b ainstem thyrotropin-releasing hormone (TRH) in the physiology of autonomic control of metabolism and the pathophysiology of autonomic dysfunction in T2D. TRH is a three amino acid neuropeptide originally discovered in the hypothalamic paraventricular nucleus. Brainstem raphe nuclei are another major locus of TRH neurons, which send TRH-containing projections to innervate brainstem and spinal sympathetic and vagal motor/premotor nuclei. TRH acts at these nuclei to control sympathetic and vagal descending pathways involved in regulating food intake, blood pressure, heart beat, pancreatic insulin secretion, and gastrointestinal secretion/motility. Our studies found an impaired brainstem TRH action on the vagal efferent control in a T2D rat model. Understanding brainstem disorders responsible for the sympathovagal imbalance in T2D is fundamental for revealing the mechanism of T2D development. Targeting on restoring a balanced sympathetic-vagal regulatory function of brainstem TRH could be a new direction for the prevention and therapy of T2D.
\nThe sympathetic and parasympathetic nerves are the two functionally opposite branches innervating visceral organs to mediate and integrate the central control of body metabolism. While numerous studies have well established the metabolic regulatory center of the hypothalamus, more and more recent studies revealed the importance of the brainstem in the neuroanatomically distributed control of energy balance [7]. Studies by Grill et al using the chronically decerebrate rat models demonstrated that the brainstem, also called hindbrain, contains an essential mechanism detecting metabolic need and exhibiting autonomic response to the metabolic challenge [7-9]. The brainstem is sufficient to mediate many aspects of the energetic response to starvation and maintain the normal glucose levels [10]. Indeed, the brainstem contains neural circuits receiving and sensing peripheral neural, nutritional and hormonal signals, and more importantly, including sympathovagal motor neurons and premotor neurons responding to these signals.
\nThe DVC is composed of the dorsal motor nucleus of the vagus (DMV) and the nucleus tractus solitarii (NTS) (Fig.1), which respectively contains somata of parasympathetic efferents projecting to the visceral organs [11-13] and neurons receiving vagal afferent input from the viscera [14]. The nearby area postrema (AP) and portions of the NTS, where the blood-brain barrier is incomplete, can be the portal of entry for circulating hormones entering the brain [15]. The Amb contains vagal motor neurons projecting to the thoracic organs as well as the upper gastrointestinal (GI) tract and the pancreas (Fig. 1).
\nThe DMV receives powerful influence from higher brain levels. Stimulation of the neurons in the paraventricular nucleus of the hypothalamus (PVN) activates DMV neurons projecting to the gut [16,17]. The ventromedial hypothalamic nucleus (VMH), which contains glucose sensitive neurons, also has direct connections with DMV and NTS [18,19]. In addition, the DMV receives descending connections from the locus coeruleus (LC), which is the origin of the noradrenergic innervation of the preganglionic autonomic nuclei in the medulla oblongata [20].
\nVagal afferent fibers arise from neurons in the nodose ganglia and their central and peripheral terminals are located respectively in the NTS and visceral organs. A number of NTS neurons directly, or indirectly via interneurons, connect with vagal motor neurons in the DMV, forming vago-vagal reflex, which may result in increased or decreased vagal efferent activity, and thus is an important component in the brainstem circuits controlling the vagal efferent function, independent of the higher brain [21-23].
\nAcetylcholine is the major transmitter of vagal preganglionic motoneurons in the DMV, which contains intense choline acetyltransferase (ChAT) [24]. By retrograde tracing of subdiaphragmatic vagus, the majority (52%) of labeled DMV cells is ChAT positive [25]. Nitric oxide (NO)-synthesizing neurons are identified in the DMV as vagal motoneurons projecting to the GI tract and also in the NTS [26,27]. These neurons are involved in the gastric receptive relaxation reflex [26]. The catecholaminergic NTS neurons are tyrosine hydroxylase (TH) positive that relay the signals received by the NTS to other brain structures [28].
\nThe sympathetic preganglionic motor neurons are located in the IML of the spinal cord. A group of brainstem neurons in the RVLM are sympathetic premotor neurons that project monosynaptically to the IML. Brainstem RVLM is the final common point of convergence of most brain pathways regulating sympathetic tone controlling functions of multisystemic visceral organs [29, 30]. The efferent projections of the catecholamine neurons in the C1 area of the RVLM display important central control of the cardiovascular regulation [31]. Transneuronal labeling studies also showed that the RVLM is a major brain region involved in sympathetic control of the pancreas [32].
\nCoronal barainstem section (interaural-4.68 mm) showing the location of THR neurons and THR terminals, and THR regulation of sympathovagal functions.
The autonomic nervous system plays a fundamental role in the brain regulation of metabolism, as this system innervates and tightly controls multisystemic organs involved in food intake and digestion, nutrition absorption, peripheral hormone secretion, blood circulation, and metabolic waste excretion. Here we focus on the pancreatic endocrine secretion and food intake.
\nThe central nervous system requires glucose as an essential source of energy. To maintain blood glucose levels within a narrow range, the brain regulates pancreatic endocrine secretion through rich innervation of vagal and sympathetic nerves in the islets [33]. In rats, three of the five vagal branches, the posterior gastric, anterior gastric, and the hepatic branches, mediate insulin secretion [34]. The direct sympathetic innervation of the pancreas comes from the sympathetic chains and splanchnic and celiac ganglia [35]. Insulin secretion is stimulated by vagal activation and inhibited by sympathetic-adrenal activation [36]. The integrity of vagus-cholinergic component plays an important role in pancreatic islet proliferation and insulin secretion of the cephalic phase and during the early absorption period, and is necessary to maintain normal glucose tolerance [33, 37-40]. Impairment in glucose tolerance is frequently observed in pancreas-transplanted patients due to denervation of the grafted pancreas. These patients have a high basal invariant insulin levels but a reduced insulin secretory capacity in response to glucose challenge; cephalic phase insulin release is absent [41-43]. Decreased β-cell mass was observed in dogs undergone pancreas-transplantation [44]. Acetylcholine is the major neurotransmitter of the vagus nervous and M3 receptor represents the major muscarinic receptor that is functional in pancreatic β-cells [36, 45, 46]. Mutant mice selectively lacking M3 receptor in pancreatic β-cells display impaired glucose tolerance and greatly reduced insulin release. In contrast, mice selectively overexpressing M3 receptors in β-cells show a profound increase in glucose tolerance and insulin release. Moreover, the β-cell M3-overexpressing mice are resistant to diet-induced glucose intolerance and hyperglycemia [47]. These findings indicate that autonomic nerves play a key role in maintaining proper insulin release and glucose homeostasis.
\nFood intake provides body energy. Autonomic innervation, especially cholinergic processes of the vagus control hunger, meal initiation, and food digestion. Vagal-cholinergic (muscarinic) activation regulates gastric ghrelin biosynthesis and secretion [48, 49]. Elevation of plasma ghrelin induced by food deprivation can be blocked by subdiaphragmatic vagotomy and atropine treatment [50]. Circulating ghrelin levels in humans are increased or reduced by cholinergic agonists or antagonists, respectively [51].
\nHypoglycemia is a well established central stimulus that enhances autonomic activities [52-55]. The neuronal activations in the PVN, DVC and other autonomic-regulatory nuclei are initiated when blood glucose levels are immediately below the normal range; the extent of neuronal activation negatively correlates with glucose levels [55]. Microinjection of glucose into the DVC prevents hypoglycemia-induced gastric motility response, indicating a direct influence of glucose concentration on the DVC neurons [56, 57]. Acute glucose deprivation by 2-deoxy-glucose induces Fos expression in NADPH-positive neurons in the NTS and DMV [58] and in catecholamine neurons in the RVLM [59]. Electrophysiological data suggest that some DMV neurons have an enteroceptor function detecting changes in glucose concentration in their environment [60]; however, another study found that glucose had no direct effect on DMV neurons, which appear to be affected by glucose action on NTS neurons [61]. The NTS neurons transmit information of local glucose availability and peripheral glucose metabolic signals received from the vagal afferents toward other brain areas, such as the nearby DMV, via circuits mediating vagal-vagal reflex, and the hypothalamus, including the PVN, via the ascending adrenergic and noradrenergic pathways [61-64]. The response of medullary vagal-regulatory circuits to altered blood glucose levels seems independent of the higher brain structures. In dogs, decerebration and mid-brain or pontine section did not prevent insulin-hypoglycemia-induced gastric acid secretion, which was drastically reduced after destruction of the DMV [65]. Beside the enhanced vagal efferent outflow, which mediates hypoglycemia induced food intake, neuronal activation in the RVLM by glucose deprivation increases sympathetic efferent activity [59], which is important for the liver to produce and release more glucose. These findings indicate that activating brainstem autonomic regulatory circuits is an important counterregulatory response for changed metabolic status.
\nTRH is a three amino acid neuropeptide originally discovered in the hypothalamic PVN, where it regulates pituitary thyrotropin release. Brainstem raphe nuclei, including the raphe pallidus (Rpa), raphe obscurus (Rob) and the parapyramidal regions (PPR) are among other major loci capable of TRH synthesis in the brain (Fig.1). Raphe nuclei project TRH-containing fibers to sympathetic and vagal motor neurons located respectively in the brainstem DVC, the RVLM, and the spinal IML, areas densely clustered with TRH-immunoreactive nerve terminals and TRH receptor 1 [66-69] (Figs.1,2). Electron microscopic studies revealed that TRH terminals make direct synaptic contacts with dendrites of neurons in medial NTS and vagal motoneurons throughout the DMV [68]. The direct effects of TRH are to excite DMV neurons and inhibit NTS neurons [70]. TRH-containing fibers also innervate sympathetic premotor loci, particularly the RVLM [69, 71, 72]. These TRH-containing brainstem-spinal circuits are important central components of autonomic regulation of visceral organ functions and in particular, the baroreflex pathways [73].
\nPreproTHR-containing fibres (green) and ChAT neurons (red) in the DMV and TH neurons (red) in the RLVM and NTS.
Studies in the 1980s by Amir S et al and others found that intracerebroventricular (icv) injection of TRH induces hyperglycemia through pathways involving the adrenal gland in rats, but prevents central and peripheral stimuli-induced hyperglycemia in mice through stimulating insulin release [74-78].
\nOur studies demonstrated that injection of TRH or its stable analog RX77368 into brain ventricles activates both sympathetic and vagal descending pathways, inducing sympathetically driven hyperglycemia, hypertension and tachycardia, and vagally mediated stimulation of gastric secretion/contractility, pancreatic insulin secretion, and ghrelin release [49, 69, 79-82]. The gastric myenteric plexus innervates smooth muscle and mucosal layers and receives dense and intricate network of vagal efferent axons [83-86]. Electrical stimulation of the rat cervical vagus nerve induces widespread Fos expression in the gastric myenteric plexus in rats [87, 88]. Similarly, intracisternal injection of TRH analog, known to activate vagal preganglionic neurons in the DMV and increase gastric vagal efferent discharges [80, 89,90], activates gastric myenteric neurons in rats [91]. Brainstem microinjection and intrathecal (it) injection studies revealed that pontine locus coeruleus, brainstem RVLM and spinal IML are TRH action sites for activating sympathetic efferent pathways [69, 79, 92, 93], whereas the DMV, the Amb, and the dorsal portion of the RVLM are among those responsible for the resulting stimulation of vagal efferent outflow [69, 94-96]. Substantial evidence shows that TRH is the only brain peptide fulfilling all of the criteria as a neurotransmitter and/or neuromodulator activating vagal motor neurons in the DMV [49, 69, 80, 82, 97]. TRH knockout mice are significantly hyperglycemic with impaired insulin secretion in response to glucose [98].
\nAutonomic response to external and internal environmental changes is associated with activation of brainstem TRH containing pathways. Brainstem TRH gene expression is upregulated by energy deficiency or increased energy demand, such as starvation, hypothermia, and hypothyroidism [49, 99, 100].
\nThe physiological role of brainstem TRH in regulating sympathovagal efferent activities responding to metabolic challenge was first evidenced in the animal model of cold exposure, which is wildly used to induce sympathetic-vagally mediated gastric ulceration [99, 101, 102]. Cold exposure activates not only TRH system in the hypothalamus but also TRH-containing Rpa/Rob/PPR-DVC pathways in the brainstem [99, 103]. The hypothermia resulting from cold exposure induces Fos expression in the Rpa, Rob, PPR and DVC neurons and enhances brainstem TRH gene expression, especially in the Rpa and Rob [99, 104, 105]. These brainstem changes are with strongly concomitant activation of gastric myenteric neurons through the excitement of vagal-nicotinic pathways and therefore responsible for the vagal-mediated increases of gastric acid secretion/motility and sympathetic-mediated decrease of mucosal blood flow, leading to gastric ulcer formation [102, 106-108]. Cold exposure induced gastric ulceration and increased gastric emptying were prevented by icv injection of TRH antiserum or antisense oligodeoxynucleotides of TRH receptor, respectively [109, 110].
\nBrainstem TRH gene expression is influenced by thyroid hormone levels in a feedback regulatory manner. Thyroidectomy increases TRH mRNA levels in the raphe nuclei and the effect is reversed by thyroid hormone replacement [100]. This finding indicates that abnormal brainstem TRH gene expression and altered TRH regulation of sympathovagal efferent outflow may be involved in the autonomic disorders observed in hypo- or hyperthyroidism.
\nOur recent studies demonstrated that brainstem TRH is involved in food intake regulation. Intracisternal injection of the stable TRH analog RX77368 (7.5-25 ng) dose-dependently stimulated solid food intake by 2.4- to 3-fold in freely fed rats, an effect that lasted for 3 hours. By contrast, RX77368 at 25 ng injected into the lateral ventricle induced a delayed and insignificant orexigenic effect only in the first hour. In pentobarbital-anesthetized rats, intracisternal injection of TRH analog (50 ng) induced a significant bi-peak increase in serum total ghrelin levels from the basal of 8.7 ± 1.7 ng/ml to 13.4 ± 2.4 ng/ml at 30 min and 14.5 ± 2.0 ng/ml at 90 min, which was prevented by either bilateral vagotomy (-60 min) or atropine pretreatment (2 mg/kg, -30 min) but magnified by bilateral adrenalectomy (-60 min). TRH analog induced food intake in freely fed rats was abolished by either peripheral atropine or ghrelin receptor antagonist (D-Lys-3)-GHRP-6 (10 μmol/kg), or intracisternal Y1 receptor antagonist 122PU91 (10 nmol/5 µl). Brainstem TRH mRNA and TRH receptor1 mRNA increased by 57-58% and 33-35% in 24-48 h fasted rats and returned to the fed levels after a 3 hour re-feeding. Natural food intake in overnight fasted rats was significantly reduced by intracisternal TRH antibody, Y1 antagonist, and peripheral atropine. These data establish a physiological role of brainstem TRH in vagal-ghrelin-mediated stimulation of food intake, which involves interaction with brainstem Y1 receptors [49].
\nThe TRH-synthesizing neurons in brainstem raphe nuclei contain other neuropeptides and neurotransmitters, such as substance P (SP) and serotonin (5-HT). These transmitters/peptides co-release with TRH in the raphe projections innervating the target autonomic-regulatory neurons. In the DVC, 5-HT potentiates and SP suppresses the vagal-activating action of TRH [111, 112].
\nThe upper gut mechano-/chemo- signals and their impact on ascending sympathetic-vagal afferents are crucial information for the brain to adjust sympathetic-vagal efferent functions involved in controlling glucose and energy homeostasis [113, 114]. GI peptides, such as cholecystokinin (CCK) and secretin, released from the proximal small intestine, and peptide YY (PYY) and glucagon-like peptide-1 (GLP-1), released from the hindgut, all appear to accomplish their gastric/pancreatic regulatory functions through both the humoral route and the vagus nerve [113]. These peptides modulate, mostly inhibit, efferent vagal outflow at least partly through brainstem vago-vagal reflexive neurocircuits that initiated with stimulating vagal afferent pathways, acting on either vagal afferent terminals in the GI enteric plexuses, vagal afferent neurons in the nodose ganglions that express all the relevant receptors for these gut hormones, or brainstem AP/NTS neurons, where receptors of these peptides are localized [113, 114]. Glucose itself is an activator of vagal afferents [114]. In addition, information of glucose metabolism in the liver is sent to the brainstem via the afferent fibers in the hepatic vagal branch. Sensors localized in the portal vein pass nutrition signals to the brain through sympathetic-spinal pathways [113, 114]. Of particular noticeable, the vagal-efferent activation by brainstem TRH is inhibited by these signals from proximal gut. We have found that intraduodenal infusion of lipid or intravenous infusion of glucose, CCK, secretin, or PYY inhibits intracisternal TRH-induced gastric acid secretion that is mediated by vagal efferent activation [115-117].
\nCollectively, research findings show that the TRH containing raphe-DVC pathways and raphe-IML pathways play important physiological roles in maintaining metabolic homeostasis, through balancing sympathovagal outflow that controls multisystemic visceral organs.
\nRelative to healthy peers, diabetic patients have increased sympathetic and decreased parasympathetic activity that appears to be present at early stages of metabolic impairment, regardless of the presence or absence of autonomic neuropathy [118-121]. T2D patients have higher resting muscle sympathetic nerve activity burst incidence and arterial norepinephrine levels, lower plasma norepinephrine clearance and reduced neuronal reuptake, compared with obese metabolic syndrome patients [122]. The progression from obesity to T2D is associated with increased central sympathetic drive, blunted sympathetic responsiveness, and altered norepinephrine disposition [122]. Unbalanced autonomic function leads to the development of diabetes and its complications, including hypertension [123], increased risk of cardiovascular events such as arrhythmia [4, 124, 125], enhanced activity of hypothalamus-pituitary-adrenal axis [126], potentiated hepatic glucose output [127], suppression of insulin release [128], insulin resistance [6], lipemia and increased visceral fat [129], chronic renal failure [130], reduced gastric secretion/motility and altered gut hormone secretion [131, 132]. Moreover, sympathetic overactivity may be a contributing factor to the development of T2D in non-obese men [133]. Vagal impairment contributes significantly to the predominance of sympathetic activity in T2D [4].
\nConverging evidence suggests that hyper- or hypoglycemia affects GI functions by influencing vagal-cholinergic outflow to the viscera. GI functions stimulated by vagal efferent activation, such as sham feeding-induced pancreatic polypeptide (PP) release and gastric acid secretion, were remarkably reduced in humans during hyperglycemia [134]. In the rat, experimental diabetes lowered gastric acid secretion, which did not decrease further after vagotomy [135]. Hyperglycemia induced by intravenous glucose infusion completely prevented the gastric acid secretion stimulated by intracisternal TRH analog [115]. In contrast to hyperglycemia, insulin-hypoglycemia induces central-vagal stimulus of upper GI functions and has been widely used to test vagus nerve integrity [136-139]. These findings establish the mediating role of the vagus nerve in GI functional alternations induced by altered glucose metabolism.
\nGastroparesis is a common complication of diabetes [140]. Gastric acid secretion is markedly lower and gastric emptying abnormalities occur in about 30-50% of diabetic patients [141-144]. Although morphological changes in the vagus nerve were identified in diabetic patients [145], many observations indicate that hyperglycemia itself may play a major role in the abnormal GI motility of T2D patients, in addition to the traditionally-attributed irreversible autonomic neuropathy [143, 146]. Acute hyperglycemia causes reversible motility impairment in the GI tract in both healthy subjects and in diabetic patients and animals [147-151]. Delay in gastric emptying is observed within one week after streptozotocin treatment in rats, when there is no autonomic neuropathy developed [152]. Even changes in blood glucose levels within the normal postprandial range significantly impact gastric emptying in both normal subjects and diabetic patients [153]. These observations show that hyperglycemia in diabetes can influence vagal-mediated visceral functions through functional alteration, in addition to morphological damage, of the vagus nerve.
\nT2D Patients frequently lose the first phase insulin release that is mainly triggered by vagal activation [154]. The vagal-mediated acute insulin response to glucose is absent in those with glucose levels above 115 mg/dL [155]. In fact, after intravenous glucose infusion, both the first and second phases of insulin secretion are impaired in T2D patients [156]. The impaired second phase insulin secretion may result from reduced incretin secretory response and the reduction of absolute incretin effect in T2D [156-158], both can be attributed to impaired vagal efferent activity [159]. The impaired vagal function reduces the proliferation of pancreatic islet β-cells, resulting in an approximately 60% reduction in β-cell mass in T2D patients [38, 160]. With increasing duration of T2D, the decrease of postprandial insulin secretion becomes more prominent [161]. The contribution of sympathetic overactivity to the inhibition of insulin secretion in T2D was evidenced in a patient, who underwent a spinal-sympathetic blockage for treating a disorder that was not directly related to diabetes but resulted in a dramatic 50% decrease in her insulin need [162]. Adrenalectomy increases basal insulin secretion in rats [82].
\nCardiovascular disease is the leading cause of mortality in patients with T2D. T2D patients have a high incidence of hypertension and nonischemic heart failure, and worse outcomes in acute cardiovascular events compared to non-diabetic controls [163, 164]. A key mechanism underlying cardiovascular disorders is an increase in sympathetic nerve activity [73, 165], in addition to pathological cardiovascular changes due to inflammation and over-activity of the renin-angiotensin system [164, 166-168], which are associated with altered sympathovagal function as well. The cardiac vagal and sympathetic nerve functions are both abnormal in T2D patients, but particularly shown as decreased cardiac vagal baroreflex sensitivity [169]. These autonomic dysregulation contribute to increased blood pressure (BP), cardiac arrhythmias and atrial fibrillation, and the resulting progression to heart failure [4, 118, 170-173]. The attenuated sympathetic response to hypotension may contribute directly to mortality in diabetes and cardiovascular disease [174]. Autonomic dysfunction has become one of the most powerful predictor of risk for cardiac mortality in T2D patients [169, 175].
\nOur lab in the last 10 years used a T2D rat model and combined systemic T2D pathophysiology and autonomic neuroscience to assess the role of brainstem TRH in the central mechanism responsible for the sympathovagal imbalance in T2D.
\nThe GK rat is an extensively studied polygenic model of non-obese T2D that was obtained by selective breeding of individuals with glucose intolerance from a non-diabetic Wistar rat colony [176,177]. GK rats are used to dissect genetic etiology of T2D [178,179], and exhibit well-characterized features typical of human T2D, such as fasting hyperglycemia, impaired insulin-secretory response to glucose, reduced β-cell mass, chronic inflammation, disruption of hepatic lipid metabolism, hypertension, and insulin resistance [97, 176, 178, 180, 181]. GK rats and human T2D share similar late complications, such as neuropathy, nephropathy, and cardiovascular disorders including heart failure [180, 182-184]. Glucose-stimulated insulin release was reduced by 90% in the first phase and by 75% in the second phase in GK rats [185]. Vagal-dependent increase of islet blood flow, which is required for glucose-induced insulin secretion, is diminished in GK rats [186]. Carbachol, an agonist for muscarinic acetylcholine receptors, fully normalizes insulin secretion in GK rats responding to 16.7 mmol/L glucose through an effect abolished by atropine [187].
\nHigher amounts of visceral fat is a sign of a high ratio of sympathetic vs parasympathetic reactivity [129]. We measured the lean and fat body mass quantities in awake rats by non-invasive magnetic resonance imaging. Compared to Wistar rats with same body weight, GK rats have doubled fat mass and significantly less lean mass. During rat growth from 285 g to 320 g, the increase in Wistar rats is mainly lean weight while that in GK rats is mainly fat weight. Coinciding with this finding, serum leptin levels elevated in GK rats in normally feed, fast, and refeed status. Hyperleptinemia is associated with increased sympathetic activity as leptin increases sympathetic nerve activity to influence cardiovascular, renal, muscle, endocrine, and adrenal gland functions [188, 189].
\nTRH is a physiological stimulator on DMV neurons to induce a vagally mediated excitation of gastric secretory/motility functions [80]. The well-known gastric acid-stimulatory effect of intracisternal injection of TRH analog was totally absent in T2D GK rats, indicating that TRH action in the DMV to activate vagal efferent outflow is severely damaged in GK rats.
\nTRH analog RX77368 (50 ng) injected intracisternally induced markedly greater hyperglycemic and weaker insulin responses in GK rats than in Wistar rats. Bilateral vagotomy blocked RX77368-induced insulin secretion while adrenalectomy abolished its hyperglycemic effect. In adrenalectomized GK but not Wistar rats, RX77368 dramatically increased serum insulin levels by 6.5-fold and decreased blood glucose levels from 154 to 98 mg%; these changes were prevented by simultaneous vagotomy. These results indicate that central-vagal activation-induced insulin secretion is susceptible in T2D GK rats and the dominant sympathetic-adrenal response to brainstem TRH plays a suppressing role on vagal-mediated insulin secretion. This unbalanced sympathovagal activation by medullary TRH may contribute to the impaired insulin secretion in T2D [82].
\nTRH analog RX77368 injected intrathecally or microinjected into the RVLM, the TRH action sites for activating the sympathetic efferent function, induced a significantly potentiated hyperglycemic response and an impaired first hour insulin response in T2D GK rats, compared to Wistar rats, indicating a sympathetic overactivation together with an impaired vagal counterregulatory response to hyperglycemia in GK rats [69, 82].
\nIn comparison with Wistar rats, GK rats exhibited basal systolic hypertension (152 ± 2 mmHg) and a significantly potentiated, dose-related hypertensive response to intracisternal injection of TRH analog RX77368 (10-60 ng). In GK rats only, intracisternal RX77368 (30-60 ng) markedly increased heart rate (+88 bpm) and induced acute cardiac mortality (100%) resulting from congestive heart failure, concurrent with extreme hyperglycemia (>480 mg%), increased plasma H2O2 and 8-isoprostane, and increased heart mRNA levels of NADPH oxidase 4 and vascular cell adhesion molecule-1, which are the oxidative stress and inflammation markers. GK rats also had elevated basal levels of plasma epinephrine, higher adrenal gene expression of epinephrine-synthesizing enzymes tyrosine hydroxylase and dopamine β-hydroxylase, and greater responses of plasma catecholamines and the adrenal enzymes to intracisternal TRH analog, compared to Wistar rats. Pretreatment with the nicotine receptor blocker hexamethonium prevented intracisternal TRH analog induced hypertensive and tachycardic responses, and cardiac mortality in GK rats. The α-receptor blockage with phentolamine abolished the hypertensive response but enhanced tachycardia (+160 bpm), and reduced mortality by 50%. The angiotensin II type 1 receptor antagonist irbesartan prevented intracisternal RX77368-induced increases in blood pressure, heart rate, and mortality. These findings indicate that sympathetic overactivation triggered by brainstem TRH and the lack of effective vagal counterregulation contribute to the cardiovascular morbidity and mortality in T2D, which involves heightened cardiac inflammation and peripheral oxidative stress responses to the sympathetic drive and a mediating role of renin-angiotensin system [97]. The cardiovascular autonomic imbalance in GK rats further confirms a diminished vagal-activating function of brainstem TRH, which is responsible for the damaged vagal arm function in the baroreceptor reflex.
\nUsing the T2D GK rat model, we found a damaged brainstem TRH action on activating the vagal efferent functions, which contributes to reveal the central mechanism of the sympathovagal imbalance in T2D. Further studies are warranted to investigate in the cellular and molecular levels of the abnormal vagal motor neuronal functions in T2D, such as insulin and TRH signaling in the DVC neurons.
\nLiving kidney donation has successfully improved the lives of many patients worldwide for over half a century. Do we still have the same need for living donors in 2018? The answer is obviously yes and for many reasons. The first is organ shortage with a widening gap between renal supply and demand in all countries that increases every year despite the use of marginal deceased donors. Waiting lists are growing everywhere. The site of the US Government Information on Organ Donation and Transplantation,
Currently, 40% of kidney grafts in the United States are from living donors [1]. In Europe, the level is highly variable between countries, standing for approximately 10% in France and up to 60% in Norway and Sweden [2, 3]. Approximately, one in three kidney transplants performed in the UK are from living donors [4], and according to the Global Observatory on Donation and Transplantation (GODT), 84,347 kidney transplants were done worldwide in 2015, of which 41.8% were from living donors [5].
\nIn some countries, namely Middle Eastern and Eastern, kidney transplantation is relying only or mostly on living donors [6, 7]. Worldwide kidney transplant from living donors in 2017, based on the International Registry in Organ Donation and Transplantation, is shown in Figure 1 [8].
\nWorldwide kidney transplant from living donors in 2017. International Registry in Organ Donation and Transplantation.
Women traditionally outrank men in their enthusiasm to donate one of their kidneys. Although most recipients are male, women represented 63% of all living donations in 2016 [9].
\nIn regard to these facts, living donors have exceptional courage and nobility; they go through a major surgery, accepting all surgical and medical risks and of no medical and physical benefit for them. It is our vocation and duty to provide them a safe and good practice according to legal and ethical bylaws and to protect their health in the long term.
\nThe first true altruistic voluntary living donation happened in Paris at Necker Hospital on December 25, 1952, when a mother, Gilberte Renard, convinced the medical team to give her kidney to her son Marius, 16 years old, apprentice carpenter who had his right solitary kidney removed after falling from a scaffolding. Unfortunately, the graft remained functional for approximately 3 weeks despite the use of steroids and Marius died on January 27, 1953. His donating mother died in 1992 at age 85 [10, 11].
\nThe second important milestone happened 1 year later on December 23,1954 at Brigham Hospital in Boston USA, when Dr. Murray performed a successful renal transplantation on Richard Hersick, the donor being his monozygotic identical twin brother Ronald. The kidney was removed from Ronald by the urologist Harrison. No effort was made to preserve the isograft; but nonetheless, it functioned promptly despite 82 min of warm ischemia [12]. The graft remained functional for 8 years and was lost due to a recurrence of the renal disease and causing the death of Richard. His brother Ronald died in 2010 at age 79, after a cardiac surgery, just 4 days after the 56th anniversary of his pioneering kidney operation [11, 13].
\nThe next two following years, the Brigham team performed seven successful kidney transplants also between identical twins. The most famous was that of Edith Helm, the third case at Brigham, who got pregnant 2 years after her transplant and was the first kidney recipient to carry to term and give birth to a child. Edith Helm also holds the record of the best graft longevity of 55 years; she died in 2011 at age 76, with a functioning graft. Her donating identical twin sister, Wanda Foster, gave birth three times following her kidney donation and was still alive in 2016 [11, 14].
\nIn 1960, the first kidney transplantation between genetically nonrelated patients was performed using immunosuppression. Late in 1963, a conference near Washington DC was held to present the overall findings from 216 recipients of renal allografts. The results were not gratifying: 52% of all those receiving grafts from related donors had died, and 81% of those with kidneys from unrelated or cadaveric donors. Joseph Murray concluded at that time that “kidney transplantation is still highly experimental and not yet a therapeutic procedure.” By 1965, 1 year survival rates of allografted kidneys from living related donors were much better approaching 80%, due to better immunosuppression [12, 15].
\nIn 1987, Alexandre et al. in Belgium published a first series of ABO-incompatible (ABO-I) living donors using splenectomy and heavy immunosuppressive regimen in the recipient. Results were fairly optimal [16].
\nThen, since 1989 and due to organ shortage, most ABO-I kidney transplantations have taken place in Japan with recently published data showing an excellent long-term outcome. Currently, ABO-I reached approximately 30% of all living donor renal transplantation in Japan [17, 18].
\nFrom the surgical point of view, all donor nephrectomies were done by open techniques mostly using a lumbar retroperitoneal approach; and the first successful trial of removing a live donor kidney using a laparoscopic approach was in 1995 at John’s Hopkins hospital by Ratner et al. [19]. Since then, considerable numbers of transplant centers worldwide have adopted laparoscopic donor nephrectomy (LDN) which is now considered as the gold standard approach for kidney retrieval on live donors and has undoubtedly revolutionized kidney donation.
\nSuitability of the potential kidney recipient for transplantation must be established before starting donor assessment. There is a significant variability among transplant programs in the criteria used to evaluate donors. ABO blood grouping is an important early screening test. Initial assessment of donor and recipient histocompatibility status must be undertaken at an early stage in living donor kidney transplant workup to avoid unnecessary and invasive clinical investigation [4]. Although donors are not true patients, they must undergo a complete and extensive evaluation before considering kidney removal. This evaluation includes medical and surgical past history, risk factors like alcohol intake and smoking, family history (mainly renal disease, hypertension, and diabetes), renal, liver, and cardiopulmonary function. They should have no active malignancy or infection. The waiting period before transplant in recipients with a history of malignancy depends on the type, TNM stage and grade of the tumor, and recipient’s age and general health. Recipients with tumors that have a low recurrence rate can be considered for immediate transplantation after successful treatment. Active HBV and HCV are usually contraindications to living donor kidney donation; and HIV infection is an absolute contraindication. Screening of serum prostate-specific antigen (PSA) is mandatory in males above 54 years as also mammograms in women. A urine albumin/creatinine ratio done on a spot urine sample is a recommended screening test and it should be <30 mg/mmol. The presence of persistent microhematuria (two or more positive urine analysis) or recently called “persistent nonvisible hematuria,” with no evident explanation like stones, neoplasms, and infection, should be investigated with cystoscopy and renal biopsy. Assessment of renal function is based on serum creatinine and calculation of creatinine clearance. Differential kidney function, using DMSA isotope scanning, is recommended when there is >10% variation in kidney size or abnormal renal anatomy [4]. Donors with mild and well-controlled hypertension, on one or two antihypertensive drugs, and with no evidence of end organ damage (retinopathy, left ventricular hypertrophy, proteinuria), might be accepted [20]. Data regarding long-term safety of nephrectomy in hypertensive donors are modest; but small studies with short-term follow-up suggest no increase in the incidence of kidney disease or worsening of the control of hypertension in donors with a history of mild well-controlled hypertension [21]. The Amsterdam Forum consensus guidelines in 2004 stated that some patients (age > 50, GFR >80, and with low urine albumin excretion of <30 mg/d) with easily controlled hypertension can represent a low-risk group for the development of kidney disease but might be considered as donors [22]. A psychosocial assessment is recommended for all donors with appropriate referral to a mental health professional who can be a psychologist or a psychiatrist. This assessment also evaluates whether the decision to donate is free of constraint and other undue pressures. Donor age is suggested to be between 22 and 75 years; but the upper age limit can be beyond if the donor is in good health and with a normal range of age-related change in kidney function (e.g., advisory threshold GFR levels considered acceptable at age 80 years is 58 ml/min/1.73 m2 for males and 49 ml/min/1.73 m2 for females). A safe threshold level of predonation kidney function is one that leaves sufficient function after donation to maintain the donor in normal status without affecting lifespan [4]. Old donors (> 60 years) should be aware of a greater risk of pre- and postoperative complications. We are very cautious about young donors who are less than 30 years old because their absolute risk over a lifetime, particularly with additional risk factors for end-stage renal disease (like hypertension, obesity, and diabetes), is likely to be more significant [4]. Living donors should ideally have a body mass index (BMI) that is less than 30 kg/m2. Data on the safety of kidney donation in the very obese (BMI >35 kg/m2) are limited and donation should be discouraged. Morbid obesity increases the risk of hypertension, dyslipidemia, insulin resistance and diabetes, heart disease, stroke, sleep apnea, and certain cancers [23]. On the other hand, data suggest that laparoscopic living-donor nephrectomy (LLDN) is an increasingly safe procedure in the otherwise healthy obese kidney donor and does not result in a high rate of major perioperative complications [24, 25]. Also, transplantation from an old or obese donor is most probably better than dialysis or transplantation from a deceased donor [26]. Computed tomography and tomographic angiography are used to assess renal vascular anatomy (presence of accessory vessels, intervessel distance, distance from ostium to the first division, presence of atherosclerotic disease), renal dimensions, presence of stones, urinary tract anatomy, and the existence of any suspicious lesion not seen on ultrasound. Around 25% of will have multiple arteries to one kidney and 7% will have multiple vessels to both kidneys [27]. Renal pedicles with less than three arteries are accepted.
\nThe presence of multiple renal cystic lesions in a potential living kidney donor requires careful evaluation and a detailed family history; in those with a family history of polycystic kidney disease under the age of 40 years, the presence of two or more cysts (unilateral or bilateral) indicates autosomal dominant polycystic disease (ADPKD) and exclude donation [28]. For those aged 40–59 years, the absence of at least two cysts in each kidney gives a 100% negative predictive value for ADPKD, while for those older, up to four cysts are acceptable in each kidney [4]. History or current presence of bilateral renal stones is a contra indication for donation; but in some centers, donors with a history of nephrolithiasis are accepted as long as stones are no longer present and metabolic studies are normal [29].
\nMultiple techniques have been described to harvest a kidney from a living donor. The old classic open surgery performed through a lumbar or subcostal incision is nowadays much less popular compared to mini-invasive approaches using laparoscopic extra corporeal manipulation and magnified ultrahigh definition view of the surgical field. But regardless of how minimally invasive laparoscopy can be, living donor nephrectomy remains a maximally invasive surgery because we are dealing with major vessels and consequently very serious and sometimes lethal hemorrhagic complications might occur. Highly qualified, competent, and well-trained surgeons are allowed to perform such techniques within a very well-equipped environment and with experienced surgical staff. A living donor program should undertake at least 30 cases per year to maintain adequate experience. Today, laparoscopy is by far the preferred procedure for kidney removal in live donors, offering a quick recovery, less pain, and a shorter hospital stay; and it will be the technique detailed in this chapter. A well-informed consent is obtained prior to surgery. The surgeon performing living donor nephrectomy has a particular responsibility to ensure that the donor fully understands the potential risks and long-term effects of the operation. Surgery must offer to the donor safety, low morbidity, and fast recovery; and must obtain a graft with adequate vessel length, short warm ischemia time, and well-preserved ureteral blood supply. A donor kidney with a single renal artery should, whenever possible, be chosen for transplantation to minimize the risk of vascular complications in the recipient procedure; similarly, single renal veins are usually preferred. Many transplant centers prefer the left kidney for LLDN because of the longer vein and perhaps an easier surgery on the left side; but with increasing experience, kidney side was not a real obstacle [30] although for some authors the right kidney was the only risk factor for early graft thrombosis [31, 32]. The answer to which kidney to take when facing a donor with two arteries on the left and a single artery on the right is based on the surgeon’s experience of laparoscopic right nephrectomy and his skills in reconstructing the vasculature of the graft. The presence of a retroaortic renal vein is of no problem with no increased complications; and it is even an easier case because of the large distance between the artery and the retroaortic vein which is in an inferior position (Figure 2). The most important criterion regarding the side to be chosen for retrieval is to keep the better kidney for the living donor.
\nRetroaortic vein (V). See the distance between the artery (A) and the vein (V). U = ureter.
There is variability among different centers on the choice of laparoscopic technique between only pure laparoscopy (transperitoneal versus retroperitoneal), only hand-assisted laparoscopy or a combination of both. Laparoendoscopic single-site surgery (LESS), natural orifice transluminal endoscopic surgery (NOTES), and robotic-assisted are other interesting techniques that still need to be evaluated. In our experience, we started our first 10 cases with hand assistance, given the increased security that it provides, and then switched to pure transperitoneal laparoscopic approach which will be detailed in this chapter.
\nLaparoscopic donor nephrectomy has had a big impact on anesthesia and recovery of this special category of patients. Intraoperative anesthesia for laparoscopic live donors follows the rules of laparoscopic kidney surgery as far as sedation and muscle relaxation but the concept of protection of the donor kidney is mandatory throughout the case, one among many disparities compared to other kidney surgeries [33]. Nowadays, two large-bore IV catheters are considered more than enough as far as vascular access and risk of bleeding. Arterial lines are not recommended and noninvasive blood pressure monitoring is a reasonable option [34]. After induction of anesthesia, classically with propofol and a neuromuscular blocking agent, maintenance of anesthesia has been the subject of many studies to evaluate the nephrotoxicity of various agents. While isoflurane and desflurane were considered safe and with the least toxicity on the kidney, this was not the case with sevoflurane that is associated with production of compound A in the circulation; a direct nephrotoxic substance [35]. Despite many works, the type of anesthetic agent was not shown to impact serum creatinine or GFR in transplanted grafts and it was concluded that toxicity, if any, was minimal. Nitrous oxide is one agent preferably avoided in laparoscopic surgery as it can cause bowel distention in more than 50% of cases and subsequent compromise of insufflation or surgical field exposure in near 25% of laparoscopic donor nephrectomy, increasing the need even more for neuromuscular blocking agents [36]. Mechanical ventilation settings are not different from other laparoscopic procedures. Special considerations for donor nephrectomy would include tolerance of mild hypercapnia to 45 mmHg since it helps better tissue perfusion and circulation in light of pneumoperitoneum. Positive-end expiratory pressure (PEEP) at 5–10 mmHg, a 20–30% increase in minute ventilation reflecting an increased respiratory rate with constant volumes, is similar to other laparoscopic procedures. The effects of pneumoperitoneum were explored by studies on rats demonstrating that abdominal insufflation with CO2 during laparoscopy in subjects with chronic renal function impairment should not be a contraindication to surgery [37]. Additionally, if insufflation had a substantial negative effect on kidney function, we would have expected this to have a great impact on kidney donors out of concern on the retained kidney, which has not been born out in the literature. IV hydration holds a crucial place in counteracting the notorious effects of pneumoperitoneum on tissue perfusion and renal plasma flow caused by an increased intraperitoneal pressure sometimes near 15 mmHg. Some studies emphasized the great effects of hydration on mean arterial pressure preservation and ensuring hemodynamic stability [38]. Whether this is realized by giving donors colloid boluses preoperatively or during surgery is based on institutional protocols and the team preferences. In general, a patient undergoing laparoscopic donor nephrectomy should get 4–6 L during the procedure to maintain at least a urine output >50 mL/h [38]. This will help avoid the use of any vasopressors or inotrope agents because of the associated deleterious renal vasoconstriction. If they become really needed, ephedrine is the best agent to start with, giving small boluses in order to attain the desired effects. IV fluids should be warmed and full measures should be taken to prevent hypothermia. There is a mounting evidence to suggest that 0.9% normal saline can be detrimental to patient outcome, and may indeed contribute to renal dysfunction, and therefore, the use of this solution in donors cannot be recommended; Ringer’s lactate solution is the intravenous fluid of choice [4]. The administration of mannitol 12–25 g once or twice, or furosemide at small doses during the case, is another example of common practice depending on departmental protocols, but they lack any definite data or evidence to support it.
\nWe routinely give antibiotic prophylaxis based on one single shot of cefazolin. After placement of a Foley catheter, the patient is put in a complete lateral decubitus position almost 90° to the table without any flexure or kidney rest; the belly being on the external border of the table. Arms and legs are well secured with pillows and gel pads to prevent any vascular or nerve compression. We start by doing the extraction site as a small transverse supra pubic incision 6–8 cm width, depending on donor kidney size, with opening of the peritoneum and insertion of a LapCap device (Applied Medical-Alexis Laparoscopic System with Kii® Fios® First Entry) (Figure 3 and Video 1 (
Left side: position of patient and 3 trocar placement: 5 mm subcostal, 10 mm umbilical or para umbilical (yellow dot) depending on obesity, and 12 mm left iliac fossa. LapCap device shown on the right.
Left kidney suspended with a 2/0 silk suture on the parietal wall.
As described in all transperitoneal approaches, we start by taking the colon off the kidney medially along the Toldt’s fascia from the iliac vessels up to the colonic angle (splenic flexure on the left and hepatic flexure on the right). Gerota’s fascia is left intact on the kidney (Figure 5). The lateral and parietal attachments of the kidney are left in place to prevent the kidney from slipping down and disturbing later the hilar dissection. We use from the start a LigaSure™ Maryland 5 mm (Covidien) sealing device. We then dissect and isolate the ureter inferiorly down to the iliac vessels with identification of the psoas muscle and the genital vessels. All periureteral and inferior renal pole fat must be well preserved to keep a well-vascularized ureter (Figure 6). Avoid any injury to the genitofemoral nerve and try to keep the psoas fascia in place. The gonadal vein can be divided proximally and distally and kept with the ureter in order to protect ureteric vascularity. This is thought to be the cause of postoperative ipsilateral orchialgia, which occurs in 6.2–9.6% of male donors [40, 41]. Large studies, however, have demonstrated that leaving the gonadal vein in situ does not lead to increased ureteric complications in the transplant recipient [42] and prevents orchialgia [40, 43].
\nLeft renal aspect after colon dissection. Gerota’s fascia is left intact.
Ureter with well-preserved periureteral fat and vasculature.
The ureter and its peri ureteral fat are lifted up to undertake an upper dissection along the genital vein until we reach the inferior border and the anterior aspect of the renal vein (Video 2 (
Spleen separated from the left renal upper pole.
The renal pedicle is now ready to be dissected. Before starting the hilar dissection, 12–25 mg of mannitol is administered. All lymphatics and autonomic nerve plexuses superior to the vein and around the renal artery are sealed and cut. Some small segments of these structures are sometimes difficult or possibly dangerous to access, and in such a case, they are quickly sealed and cut after the stapling of the renal pedicle. Very careful and minutious dissection is undertaken between the artery and vein to prepare a clear, precise, and secure positioning of the stapling device. The left renal artery is dissected at its aortic origin (Video 5 (
The ureter and its periureteral fat are again lifted up at the level of the iliac vessels and posterior dissection will start from here and go up to the whole posterior surface of the kidney. The ureter is isolated with a generous periureteric fat. After completing this posterior release, the kidney is completely lying medially and we can free the posterior aspect of the renal artery (Figure 8; Video 6 (
Laparoscopic view after posterior left renal dissection.
Originally, the artery was secured using locking polymer clips that are much cheaper than staples. On April 2006, the manufacturer of Weck Hem-o-lok ligating clips, Teleflex Medical, added a contraindication to the use of these clips on renal vessels in laparoscopic live donor nephrectomy, after receiving 15 medical device reports of 12 injuries and 3 deaths, all of which occurred between November 19, 2001 and March 20, 2005. All reports were associated with using the clips for ligation of the renal artery during LLDN [47, 48]. Clip dislodgement may occur several hours following the procedure resulting in fatal hemorrhage on the ward [49]. US Food and Drug Administration (FDA) issued on May 2011 a warning to healthcare providers that Weck Hem-o-Lok ligating clips should not be used for the ligation of the renal artery during LLDN because of serious risks and potential life-threatening complications to the donor [50]. On the other hand, surgeons must be aware that reported failure rates for staplers are 3.0% [51]. Stapler misfire rates can be reduced by avoiding the use of titanium and other clips around the hilar structures before securing the renal pedicle [46].
\nBefore ending the surgery, latero aortic and inter aorto caval lymphatics are clipped (Hem-o-lok clips) to prevent chylous leakage (Video 9 (
Left renal artery and vein stumps after stapling and kidney harvesting. Clips on lymphatics are placed after vascular stapling.
In some patients, the right side seems to be easier than the left. Steps are almost the same. Trocar placement has the same distribution as on the left except for an additional 5 mm trocar inserted at the xiphoid for liver retraction (Figure 10). Less right colon dissection is needed and careful duodenal displacement is performed to expose the inferior vena cava (IVC). Genital vein is usually kept in place. The renal upper pole is carefully separated from the adrenal as on the left side starting from the upper border of the right vein. Renal vessels are also approached from below after isolation of the ureter and periureteral fat and identification of the psoas muscle and lifting up the kidney. The right renal vein is exposed at its insertion into the IVC. Duplication of renal vein is more common on the right side and is reported in as much as 15% of potential renal donors [54] (Figure 11). The adrenal vein, gonadal vein, and retroperitoneal veins (lumbar, ascending lumbar, and hemiazygos) may drain into the right renal vein in 30, 7, and 3% of cases, respectively [55]. The IVC must be well dissected below and above the renal vein to permit later easy positioning of the stapler device. In usual anatomy, the renal artery is classically found just behind the vein and the space between artery and vein is normally easily created. Retrocaval area is a difficult area to work at during LLDN; therefore, the exact location of the first segmental branch of right renal artery with respect to the IVC should be clearly identified in the pretransplant angio CT scan. In some cases, posterior release of the artery behind the IVC is necessary to reach the main trunk (Video 10 (
Liver retracted through a 5-mm xiphoid trocar.
Laparoscopic view of right donor kidney with two veins (V) and one artery (A).
The early postoperative period after laparoscopic donor nephrectomy is a particular moment in the management of kidney donors. Extubation is done after normothermic state. Orogastric tube is removed prior to extubation. Hemoglobin measurement is realized every 6 h postsurgery, and if normal, it will be repeated the next morning with serum creatinine and electrolytes. Urine output is monitored. Shoulder tip discomfort and pain is a major complaint after LLDN perhaps from residual pneumoperitoneum. Epidural analgesia is ineffective for shoulder pain. There has been collective belief to aggressively minimize pain postoperatively in this special category of patients who are usually narcotics naïve. IV “patient-controlled analgesia” (PCA; fentanyl or morphine less commonly) was considered to be the modality of choice to achieve that. If PCA is not available, pain control is achieved with IV paracetamol and if needed ketoprofen or ketorolac over the first 24 h [57]. To reduce the risk of nephrotoxicity, the patient should be kept well hydrated. Opiates also have an effective role for breakthrough pain when opiate-sparing strategies have not been effective. Clear liquids are started on the day of surgery with increase of diet later. The emergence of enhanced recovery after surgery (ERAS) brought major changes to the traditional standard of care. Many centers across the USA have adopted the enhanced recovery programs that include intraoperative fluid restriction to 3 ml/kg/h preventing excessive third spacing and bowel edema, urine output of 0.5 ml/kg/h, use of local subfascial bupivacaine or other anesthetics as well as a postoperative narcotic-free pain control regimen, i.e., acetaminophen, ketorolac, etc. [58]. Novelties in this management were associated with reduced length of hospital stay, better pain control, and increased patient satisfaction. It has become evident that ERAS would potentially enhance the benefits of laparoscopic surgery for kidney donors [59].
\nFoley catheter is removed on the morning of day 1 and ambulation started as soon as possible either during the evening of day 0 or the next morning. Living kidney donors are classified as “medium risk” patients for deep venous thrombosis (DVT) and pulmonary embolism [4]. All living donors must have intra- and postoperative compression stockings and should receive adequate thromboprophylaxis with low-molecular weight-heparin and continuing for at least 1 week. Patient is discharged most frequently on day 2 and seen back 10 days later with a follow-up at 6 months, 1 year, and 2 years after donation. Donors must resume a normal lifestyle as soon as possible with regular surveillance of their blood pressure and their weight. They should be warned about avoiding nephrotoxic medications.
\nLLDN appears to be a safe procedure or at least as safe as the open one. But serious complications including death may occur. Overall mortality rate is approximately 0.03% [34] although some large series reported no mortality [60, 61, 62, 63]. Most of these deaths occurred in the postoperative period and were due to hemorrhage [47], CO2 gas embolism [64], and pulmonary embolism [34]. The risk of a major intraoperative hemorrhage during LLDN is between 0.6 and 1.6% [60, 63]. Conversion to open surgery has been reported to occur in 0 to 13% of cases, but in most large series, conversion rates of 1–2% are reported [4, 60, 61, 62, 63]. Other intraoperative complications are splenic or liver laceration, ureteral and intestinal injury, and pleural laceration. The total incidence of surgical complications is 5.46% [61]. All major complications occurred in the first 100 cases [62]. This raises the question of the learning curve and how many laparoscopic nephrectomies should be done before performing the first LLDN? There is no precise answer but a number between 50 and 100 seems to be convincing for this type of surgery to be learned.
\nPostoperative complications of LLDN are hematomas, fever, urinary tract infection, pneumonia, pulmonary embolism, wound infection, incisional hernias, prolonged ileus, chylous ascites, and left testicular pain perhaps due to gonadal vein division or extensive mobilization of the left colon which may damage the neural plexus supplying the testis and may also disrupt lymphatic drainage [65]. Chylous leakage is a rare complication of LLDN. Prevention is assured by doing a meticulous and extensive clipping of lymphatic channels along the dissection area [52, 66].
\nLong-term complications are arterial hypertension, renal failure, and proteinuria, particularly in more high-risk donors, such as those with obesity, old or young donors, hypertensive donors, and those with kidney stones [67, 68]. Following kidney donation, there is a compensatory increase in function in the remaining kidney. By 3 months, remnant kidney clearance increases to a mean GFR of around 65–75% of predonation renal function [4]. The average decrease in GFR after donation was 26 mL/min/1.73 m2 (range 8–50) [4, 69]. The incidence of end-stage renal disease (ESRD) in living kidney donors appears to be similar to or lower than that seen in the unselected general population despite a reduction in GFR [4, 24, 70]. The estimated lifetime risk of ESRD was 90 per 10,000 in donors, 326 per 10,000 in the general population, and 14 per 10,000 in matched healthy nondonor controls [71]. Live donor nephrectomy alone will not lead to renal failure [72].
\nConcerning hypertension, a large meta-analysis demonstrated that donors have an increased systolic blood pressure of 5 mmHg after 5–10 years from donation [73]. The rate of hypertension in donors was similar to that of the general population [74]. But it seems that there are no effects on kidney function and microalbuminuria at least in Caucasian population. Blacks and Hispanics may have higher risks of hypertension-associated kidney disease after donation [75, 76].
\nFinally, it is interesting to know that longevity of live donors remains greater compared to the general population [24, 72, 77].
\nLiving donation is a success story that saved many patients with end-stage renal disease from dialysis and offered them a better quality of life and longer life expectancy. Donor surgery has shifted from the old open technique to a mini-invasive approach that offers less pain to this category of people who are not true patients but true heroes full of courage and nobility. Ensuring the safety and excellent long-term outcomes of these donors is our duty, through all steps from preoperative workup, surgery, and postoperative care.
\nDonors must be aware of all potential complications before acceptance and should feel free to resign at any moment. Complications of LLDN are present and must be prevented by entrusting them to highly qualified and experienced surgeons.
\nIntechOpen aims to ensure that original material is published while at the same time giving significant freedom to our Authors. To that end we maintain a flexible Copyright Policy guaranteeing that there is no transfer of copyright to the publisher and Authors retain exclusive copyright to their Work.
',metaTitle:"Publication Agreement - Chapters",metaDescription:"IN TECH aims to guarantee that original material is published while at the same time giving significant freedom to our authors. For that matter, we uphold a flexible copyright policy meaning that there is no transfer of copyright to the publisher and authors retain exclusive copyright to their work.\n\nWhen submitting a manuscript the Corresponding Author is required to accept the terms and conditions set forth in our Publication Agreement as follows:",metaKeywords:null,canonicalURL:"/page/publication-agreement-chapters",contentRaw:'[{"type":"htmlEditorComponent","content":"The Corresponding Author (acting on behalf of all Authors) and INTECHOPEN LIMITED, incorporated and registered in England and Wales with company number 11086078 and a registered office at 5 Princes Gate Court, London, United Kingdom, SW7 2QJ conclude the following Agreement regarding the publication of a Book Chapter:
\\n\\n1. DEFINITIONS
\\n\\nCorresponding Author: The Author of the Chapter who serves as a Signatory to this Agreement. The Corresponding Author acts on behalf of any other Co-Author.
\\n\\nCo-Author: All other Authors of the Chapter besides the Corresponding Author.
\\n\\nIntechOpen: IntechOpen Ltd., the Publisher of the Book.
\\n\\nBook: The publication as a collection of chapters compiled by IntechOpen including the Chapter. Chapter: The original literary work created by Corresponding Author and any Co-Author that is the subject of this Agreement.
\\n\\n2. CORRESPONDING AUTHOR'S GRANT OF RIGHTS
\\n\\n2.1 Subject to the following Article, the Corresponding Author grants and shall ensure that each Co-Author grants, to IntechOpen, during the full term of copyright and any extensions or renewals of that term the following:
\\n\\nThe aforementioned licenses shall survive the expiry or termination of this Agreement for any reason.
\\n\\n2.2 The Corresponding Author (on their own behalf and on behalf of any Co-Author) reserves the following rights to the Chapter but agrees not to exercise them in such a way as to adversely affect IntechOpen's ability to utilize the full benefit of this Publication Agreement: (i) reprographic rights worldwide, other than those which subsist in the typographical arrangement of the Chapter as published by IntechOpen; and (ii) public lending rights arising under the Public Lending Right Act 1979, as amended from time to time, and any similar rights arising in any part of the world.
\\n\\nThe Corresponding Author confirms that they (and any Co-Author) are and will remain a member of any applicable licensing and collecting society and any successor to that body responsible for administering royalties for the reprographic reproduction of copyright works.
\\n\\nSubject to the license granted above, copyright in the Chapter and all versions of it created during IntechOpen's editing process (including the published version) is retained by the Corresponding Author and any Co-Author.
\\n\\nSubject to the license granted above, the Corresponding Author and any Co-Author retains patent, trademark and other intellectual property rights to the Chapter.
\\n\\n2.3 All rights granted to IntechOpen in this Article are assignable, sublicensable or otherwise transferrable to third parties without the Corresponding Author's or any Co-Author’s specific approval.
\\n\\n2.4 The Corresponding Author (on their own behalf and on behalf of each Co-Author) will not assert any rights under the Copyright, Designs and Patents Act 1988 to object to derogatory treatment of the Chapter as a consequence of IntechOpen's changes to the Chapter arising from translation of it, corrections and edits for house style, removal of problematic material and other reasonable edits.
\\n\\n3. CORRESPONDING AUTHOR'S DUTIES
\\n\\n3.1 When distributing or re-publishing the Chapter, the Corresponding Author agrees to credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen. The Corresponding Author warrants that each Co-Author will also credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen, when they are distributing or re-publishing the Chapter.
\\n\\n3.2 When submitting the Chapter, the Corresponding Author agrees to:
\\n\\nThe Corresponding Author will be held responsible for the payment of the Open Access Publishing Fees.
\\n\\nAll payments shall be due 30 days from the date of the issued invoice. The Corresponding Author or the payer on the Corresponding Author's and Co-Authors' behalf will bear all banking and similar charges incurred.
\\n\\n3.3 The Corresponding Author shall obtain in writing all consents necessary for the reproduction of any material in which a third-party right exists, including quotations, photographs and illustrations, in all editions of the Chapter worldwide for the full term of the above licenses, and shall provide to IntechOpen upon request the original copies of such consents for inspection (at IntechOpen's option) or photocopies of such consents.
\\n\\nThe Corresponding Author shall obtain written informed consent for publication from people who might recognize themselves or be identified by others (e.g. from case reports or photographs).
\\n\\n3.4 The Corresponding Author and any Co-Author shall respect confidentiality rights during and after the termination of this Agreement. The information contained in all correspondence and documents as part of the publishing activity between IntechOpen and the Corresponding Author and any Co-Author are confidential and are intended only for the recipient. The contents may not be disclosed publicly and are not intended for unauthorized use or distribution. Any use, disclosure, copying, or distribution is prohibited and may be unlawful.
\\n\\n4. CORRESPONDING AUTHOR'S WARRANTY
\\n\\n4.1 The Corresponding Author represents and warrants that the Chapter does not and will not breach any applicable law or the rights of any third party and, specifically, that the Chapter contains no matter that is defamatory or that infringes any literary or proprietary rights, intellectual property rights, or any rights of privacy. The Corresponding Author warrants and represents that: (i) the Chapter is the original work of themselves and any Co-Author and is not copied wholly or substantially from any other work or material or any other source; (ii) the Chapter has not been formally published in any other peer-reviewed journal or in a book or edited collection, and is not under consideration for any such publication; (iii) they themselves and any Co-Author are qualifying persons under section 154 of the Copyright, Designs and Patents Act 1988; (iv) they themselves and any Co-Author have not assigned and will not during the term of this Publication Agreement purport to assign any of the rights granted to IntechOpen under this Publication Agreement; and (v) the rights granted by this Publication Agreement are free from any security interest, option, mortgage, charge or lien.
\\n\\nThe Corresponding Author also warrants and represents that: (i) they have the full power to enter into this Publication Agreement on their own behalf and on behalf of each Co-Author; and (ii) they have the necessary rights and/or title in and to the Chapter to grant IntechOpen, on behalf of themselves and any Co-Author, the rights and licenses expressed to be granted in this Publication Agreement. If the Chapter was prepared jointly by the Corresponding Author and any Co-Author, the Corresponding Author warrants and represents that: (i) each Co-Author agrees to the submission, license and publication of the Chapter on the terms of this Publication Agreement; and (ii) they have the authority to enter into this Publication Agreement on behalf of and bind each Co-Author. The Corresponding Author shall: (i) ensure each Co-Author complies with all relevant provisions of this Publication Agreement, including those relating to confidentiality, performance and standards, as if a party to this Publication Agreement; and (ii) remain primarily liable for all acts and/or omissions of each such Co-Author.
\\n\\nThe Corresponding Author agrees to indemnify and hold IntechOpen harmless against all liabilities, costs, expenses, damages and losses and all reasonable legal costs and expenses suffered or incurred by IntechOpen arising out of or in connection with any breach of the aforementioned representations and warranties. This indemnity shall not cover IntechOpen to the extent that a claim under it results from IntechOpen's negligence or willful misconduct.
\\n\\n4.2 Nothing in this Publication Agreement shall have the effect of excluding or limiting any liability for death or personal injury caused by negligence or any other liability that cannot be excluded or limited by applicable law.
\\n\\n5. TERMINATION
\\n\\n5.1 IntechOpen has a right to terminate this Publication Agreement for quality, program, technical or other reasons with immediate effect, including without limitation (i) if the Corresponding Author or any Co-Author commits a material breach of this Publication Agreement; (ii) if the Corresponding Author or any Co-Author (being an individual) is the subject of a bankruptcy petition, application or order; or (iii) if the Corresponding Author or any Co-Author (being a company) commences negotiations with all or any class of its creditors with a view to rescheduling any of its debts, or makes a proposal for or enters into any compromise or arrangement with any of its creditors.
\\n\\nIn case of termination, IntechOpen will notify the Corresponding Author, in writing, of the decision.
\\n\\n6. INTECHOPEN’S DUTIES AND RIGHTS
\\n\\n6.1 Unless prevented from doing so by events outside its reasonable control, IntechOpen, in its discretion, agrees to publish the Chapter attributing it to the Corresponding Author and any Co-Author.
\\n\\n6.2 IntechOpen has the right to use the Corresponding Author’s and any Co-Author’s names and likeness in connection with scientific dissemination, retrieval, archiving, web hosting and promotion and marketing of the Chapter and has the right to contact the Corresponding Author and any Co-Author until the Chapter is publicly available on any platform owned and/or operated by IntechOpen.
\\n\\n6.3 IntechOpen is granted the authority to enforce the rights from this Publication Agreement, on behalf of the Corresponding Author and any Co-Author, against third parties (for example in cases of plagiarism or copyright infringements). In respect of any such infringement or suspected infringement of the copyright in the Chapter, IntechOpen shall have absolute discretion in addressing any such infringement which is likely to affect IntechOpen's rights under this Publication Agreement, including issuing and conducting proceedings against the suspected infringer.
\\n\\n7. MISCELLANEOUS
\\n\\n7.1 Further Assurance: The Corresponding Author shall and will ensure that any relevant third party (including any Co-Author) shall, execute and deliver whatever further documents or deeds and perform such acts as IntechOpen reasonably requires from time to time for the purpose of giving IntechOpen the full benefit of the provisions of this Publication Agreement.
\\n\\n7.2 Third Party Rights: A person who is not a party to this Publication Agreement may not enforce any of its provisions under the Contracts (Rights of Third Parties) Act 1999.
\\n\\n7.3 Entire Agreement: This Publication Agreement constitutes the entire agreement between the parties in relation to its subject matter. It replaces and extinguishes all prior agreements, draft agreements, arrangements, collateral warranties, collateral contracts, statements, assurances, representations and undertakings of any nature made by or on behalf of the parties, whether oral or written, in relation to that subject matter. Each party acknowledges that in entering into this Publication Agreement it has not relied upon any oral or written statements, collateral or other warranties, assurances, representations or undertakings which were made by or on behalf of the other party in relation to the subject matter of this Publication Agreement at any time before its signature (together "Pre-Contractual Statements"), other than those which are set out in this Publication Agreement. Each party hereby waives all rights and remedies which might otherwise be available to it in relation to such Pre-Contractual Statements. Nothing in this clause shall exclude or restrict the liability of either party arising out of its pre-contract fraudulent misrepresentation or fraudulent concealment.
\\n\\n7.4 Waiver: No failure or delay by a party to exercise any right or remedy provided under this Publication Agreement or by law shall constitute a waiver of that or any other right or remedy, nor shall it preclude or restrict the further exercise of that or any other right or remedy. No single or partial exercise of such right or remedy shall preclude or restrict the further exercise of that or any other right or remedy.
\\n\\n7.5 Variation: No variation of this Publication Agreement shall be effective unless it is in writing and signed by the parties (or their duly authorized representatives).
\\n\\n7.6 Severance: If any provision or part-provision of this Publication Agreement is or becomes invalid, illegal or unenforceable, it shall be deemed modified to the minimum extent necessary to make it valid, legal and enforceable. If such modification is not possible, the relevant provision or part-provision shall be deemed deleted.
\\n\\nAny modification to or deletion of a provision or part-provision under this clause shall not affect the validity and enforceability of the rest of this Publication Agreement.
\\n\\n7.7 No partnership: Nothing in this Publication Agreement is intended to, or shall be deemed to, establish or create any partnership or joint venture or the relationship of principal and agent or employer and employee between IntechOpen and the Corresponding Author or any Co-Author, nor authorize any party to make or enter into any commitments for or on behalf of any other party.
\\n\\n7.8 Governing law: This Publication Agreement and any dispute or claim (including non-contractual disputes or claims) arising out of or in connection with it or its subject matter or formation shall be governed by and construed in accordance with the law of England and Wales. The parties submit to the exclusive jurisdiction of the English courts to settle any dispute or claim arising out of or in connection with this Publication Agreement (including any non-contractual disputes or claims).
\\n\\nLast updated: 2020-11-27
\\n\\n\\n\\n
\\n"}]'},components:[{type:"htmlEditorComponent",content:"
The Corresponding Author (acting on behalf of all Authors) and INTECHOPEN LIMITED, incorporated and registered in England and Wales with company number 11086078 and a registered office at 5 Princes Gate Court, London, United Kingdom, SW7 2QJ conclude the following Agreement regarding the publication of a Book Chapter:
\n\n1. DEFINITIONS
\n\nCorresponding Author: The Author of the Chapter who serves as a Signatory to this Agreement. The Corresponding Author acts on behalf of any other Co-Author.
\n\nCo-Author: All other Authors of the Chapter besides the Corresponding Author.
\n\nIntechOpen: IntechOpen Ltd., the Publisher of the Book.
\n\nBook: The publication as a collection of chapters compiled by IntechOpen including the Chapter. Chapter: The original literary work created by Corresponding Author and any Co-Author that is the subject of this Agreement.
\n\n2. CORRESPONDING AUTHOR'S GRANT OF RIGHTS
\n\n2.1 Subject to the following Article, the Corresponding Author grants and shall ensure that each Co-Author grants, to IntechOpen, during the full term of copyright and any extensions or renewals of that term the following:
\n\nThe aforementioned licenses shall survive the expiry or termination of this Agreement for any reason.
\n\n2.2 The Corresponding Author (on their own behalf and on behalf of any Co-Author) reserves the following rights to the Chapter but agrees not to exercise them in such a way as to adversely affect IntechOpen's ability to utilize the full benefit of this Publication Agreement: (i) reprographic rights worldwide, other than those which subsist in the typographical arrangement of the Chapter as published by IntechOpen; and (ii) public lending rights arising under the Public Lending Right Act 1979, as amended from time to time, and any similar rights arising in any part of the world.
\n\nThe Corresponding Author confirms that they (and any Co-Author) are and will remain a member of any applicable licensing and collecting society and any successor to that body responsible for administering royalties for the reprographic reproduction of copyright works.
\n\nSubject to the license granted above, copyright in the Chapter and all versions of it created during IntechOpen's editing process (including the published version) is retained by the Corresponding Author and any Co-Author.
\n\nSubject to the license granted above, the Corresponding Author and any Co-Author retains patent, trademark and other intellectual property rights to the Chapter.
\n\n2.3 All rights granted to IntechOpen in this Article are assignable, sublicensable or otherwise transferrable to third parties without the Corresponding Author's or any Co-Author’s specific approval.
\n\n2.4 The Corresponding Author (on their own behalf and on behalf of each Co-Author) will not assert any rights under the Copyright, Designs and Patents Act 1988 to object to derogatory treatment of the Chapter as a consequence of IntechOpen's changes to the Chapter arising from translation of it, corrections and edits for house style, removal of problematic material and other reasonable edits.
\n\n3. CORRESPONDING AUTHOR'S DUTIES
\n\n3.1 When distributing or re-publishing the Chapter, the Corresponding Author agrees to credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen. The Corresponding Author warrants that each Co-Author will also credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen, when they are distributing or re-publishing the Chapter.
\n\n3.2 When submitting the Chapter, the Corresponding Author agrees to:
\n\nThe Corresponding Author will be held responsible for the payment of the Open Access Publishing Fees.
\n\nAll payments shall be due 30 days from the date of the issued invoice. The Corresponding Author or the payer on the Corresponding Author's and Co-Authors' behalf will bear all banking and similar charges incurred.
\n\n3.3 The Corresponding Author shall obtain in writing all consents necessary for the reproduction of any material in which a third-party right exists, including quotations, photographs and illustrations, in all editions of the Chapter worldwide for the full term of the above licenses, and shall provide to IntechOpen upon request the original copies of such consents for inspection (at IntechOpen's option) or photocopies of such consents.
\n\nThe Corresponding Author shall obtain written informed consent for publication from people who might recognize themselves or be identified by others (e.g. from case reports or photographs).
\n\n3.4 The Corresponding Author and any Co-Author shall respect confidentiality rights during and after the termination of this Agreement. The information contained in all correspondence and documents as part of the publishing activity between IntechOpen and the Corresponding Author and any Co-Author are confidential and are intended only for the recipient. The contents may not be disclosed publicly and are not intended for unauthorized use or distribution. Any use, disclosure, copying, or distribution is prohibited and may be unlawful.
\n\n4. CORRESPONDING AUTHOR'S WARRANTY
\n\n4.1 The Corresponding Author represents and warrants that the Chapter does not and will not breach any applicable law or the rights of any third party and, specifically, that the Chapter contains no matter that is defamatory or that infringes any literary or proprietary rights, intellectual property rights, or any rights of privacy. The Corresponding Author warrants and represents that: (i) the Chapter is the original work of themselves and any Co-Author and is not copied wholly or substantially from any other work or material or any other source; (ii) the Chapter has not been formally published in any other peer-reviewed journal or in a book or edited collection, and is not under consideration for any such publication; (iii) they themselves and any Co-Author are qualifying persons under section 154 of the Copyright, Designs and Patents Act 1988; (iv) they themselves and any Co-Author have not assigned and will not during the term of this Publication Agreement purport to assign any of the rights granted to IntechOpen under this Publication Agreement; and (v) the rights granted by this Publication Agreement are free from any security interest, option, mortgage, charge or lien.
\n\nThe Corresponding Author also warrants and represents that: (i) they have the full power to enter into this Publication Agreement on their own behalf and on behalf of each Co-Author; and (ii) they have the necessary rights and/or title in and to the Chapter to grant IntechOpen, on behalf of themselves and any Co-Author, the rights and licenses expressed to be granted in this Publication Agreement. If the Chapter was prepared jointly by the Corresponding Author and any Co-Author, the Corresponding Author warrants and represents that: (i) each Co-Author agrees to the submission, license and publication of the Chapter on the terms of this Publication Agreement; and (ii) they have the authority to enter into this Publication Agreement on behalf of and bind each Co-Author. The Corresponding Author shall: (i) ensure each Co-Author complies with all relevant provisions of this Publication Agreement, including those relating to confidentiality, performance and standards, as if a party to this Publication Agreement; and (ii) remain primarily liable for all acts and/or omissions of each such Co-Author.
\n\nThe Corresponding Author agrees to indemnify and hold IntechOpen harmless against all liabilities, costs, expenses, damages and losses and all reasonable legal costs and expenses suffered or incurred by IntechOpen arising out of or in connection with any breach of the aforementioned representations and warranties. This indemnity shall not cover IntechOpen to the extent that a claim under it results from IntechOpen's negligence or willful misconduct.
\n\n4.2 Nothing in this Publication Agreement shall have the effect of excluding or limiting any liability for death or personal injury caused by negligence or any other liability that cannot be excluded or limited by applicable law.
\n\n5. TERMINATION
\n\n5.1 IntechOpen has a right to terminate this Publication Agreement for quality, program, technical or other reasons with immediate effect, including without limitation (i) if the Corresponding Author or any Co-Author commits a material breach of this Publication Agreement; (ii) if the Corresponding Author or any Co-Author (being an individual) is the subject of a bankruptcy petition, application or order; or (iii) if the Corresponding Author or any Co-Author (being a company) commences negotiations with all or any class of its creditors with a view to rescheduling any of its debts, or makes a proposal for or enters into any compromise or arrangement with any of its creditors.
\n\nIn case of termination, IntechOpen will notify the Corresponding Author, in writing, of the decision.
\n\n6. INTECHOPEN’S DUTIES AND RIGHTS
\n\n6.1 Unless prevented from doing so by events outside its reasonable control, IntechOpen, in its discretion, agrees to publish the Chapter attributing it to the Corresponding Author and any Co-Author.
\n\n6.2 IntechOpen has the right to use the Corresponding Author’s and any Co-Author’s names and likeness in connection with scientific dissemination, retrieval, archiving, web hosting and promotion and marketing of the Chapter and has the right to contact the Corresponding Author and any Co-Author until the Chapter is publicly available on any platform owned and/or operated by IntechOpen.
\n\n6.3 IntechOpen is granted the authority to enforce the rights from this Publication Agreement, on behalf of the Corresponding Author and any Co-Author, against third parties (for example in cases of plagiarism or copyright infringements). In respect of any such infringement or suspected infringement of the copyright in the Chapter, IntechOpen shall have absolute discretion in addressing any such infringement which is likely to affect IntechOpen's rights under this Publication Agreement, including issuing and conducting proceedings against the suspected infringer.
\n\n7. MISCELLANEOUS
\n\n7.1 Further Assurance: The Corresponding Author shall and will ensure that any relevant third party (including any Co-Author) shall, execute and deliver whatever further documents or deeds and perform such acts as IntechOpen reasonably requires from time to time for the purpose of giving IntechOpen the full benefit of the provisions of this Publication Agreement.
\n\n7.2 Third Party Rights: A person who is not a party to this Publication Agreement may not enforce any of its provisions under the Contracts (Rights of Third Parties) Act 1999.
\n\n7.3 Entire Agreement: This Publication Agreement constitutes the entire agreement between the parties in relation to its subject matter. It replaces and extinguishes all prior agreements, draft agreements, arrangements, collateral warranties, collateral contracts, statements, assurances, representations and undertakings of any nature made by or on behalf of the parties, whether oral or written, in relation to that subject matter. Each party acknowledges that in entering into this Publication Agreement it has not relied upon any oral or written statements, collateral or other warranties, assurances, representations or undertakings which were made by or on behalf of the other party in relation to the subject matter of this Publication Agreement at any time before its signature (together "Pre-Contractual Statements"), other than those which are set out in this Publication Agreement. Each party hereby waives all rights and remedies which might otherwise be available to it in relation to such Pre-Contractual Statements. Nothing in this clause shall exclude or restrict the liability of either party arising out of its pre-contract fraudulent misrepresentation or fraudulent concealment.
\n\n7.4 Waiver: No failure or delay by a party to exercise any right or remedy provided under this Publication Agreement or by law shall constitute a waiver of that or any other right or remedy, nor shall it preclude or restrict the further exercise of that or any other right or remedy. No single or partial exercise of such right or remedy shall preclude or restrict the further exercise of that or any other right or remedy.
\n\n7.5 Variation: No variation of this Publication Agreement shall be effective unless it is in writing and signed by the parties (or their duly authorized representatives).
\n\n7.6 Severance: If any provision or part-provision of this Publication Agreement is or becomes invalid, illegal or unenforceable, it shall be deemed modified to the minimum extent necessary to make it valid, legal and enforceable. If such modification is not possible, the relevant provision or part-provision shall be deemed deleted.
\n\nAny modification to or deletion of a provision or part-provision under this clause shall not affect the validity and enforceability of the rest of this Publication Agreement.
\n\n7.7 No partnership: Nothing in this Publication Agreement is intended to, or shall be deemed to, establish or create any partnership or joint venture or the relationship of principal and agent or employer and employee between IntechOpen and the Corresponding Author or any Co-Author, nor authorize any party to make or enter into any commitments for or on behalf of any other party.
\n\n7.8 Governing law: This Publication Agreement and any dispute or claim (including non-contractual disputes or claims) arising out of or in connection with it or its subject matter or formation shall be governed by and construed in accordance with the law of England and Wales. The parties submit to the exclusive jurisdiction of the English courts to settle any dispute or claim arising out of or in connection with this Publication Agreement (including any non-contractual disputes or claims).
\n\nLast updated: 2020-11-27
\n\n\n\n
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