\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"7007",leadTitle:null,fullTitle:"Biosensors for Environmental Monitoring",title:"Biosensors for Environmental Monitoring",subtitle:null,reviewType:"peer-reviewed",abstract:"Real-time and reliable detection of molecular compounds and bacteria is essential in modern environmental monitoring. For rapid analyses, biosensing devices combining high selectivity of biomolecular recognition and sensitivity of modern signal-detection technologies offer a promising platform. 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She received\nher PhD degree in chemistry in 2000 from the same university\nfor her studies on modeling and calibration of biosensors. She\nhas also pursued and completed professional self-improvement\nin Uppsala (Sweden) and Gröningen (the Netherlands). Dr.\nRinken’s research focuses on the design and development of biosensing systems for\nautomatic monitoring, and the study of signal rising, modeling, and calibration of\nbiosensor-based analytical systems.",institutionString:"University of Tartu",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"5",totalChapterViews:"0",totalEditedBooks:"5",institution:{name:"University of Tartu",institutionURL:null,country:{name:"Estonia"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:{id:"174179",title:"Dr.",name:"Kairi",middleName:null,surname:"Kivirand",slug:"kairi-kivirand",fullName:"Kairi Kivirand",profilePictureURL:"https://mts.intechopen.com/storage/users/174179/images/system/174179.png",biography:"Dr. Kairi Kivirand is a researcher at the University of Tartu,\nEstonia, and at the Tallinn University of Technology, Estonia.\nShe received a PhD in environmental chemistry in 2011 for her\nstudies of biosensors for biogenic amines. 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\r\n\tPalm oil is an edible vegetable oil extracted from the mesocarp of the oil palm fruit, mainly the Elaeis guineensis African oil palm and to a lesser degree, from the American oil palm Elaeis oleifera and the maripa palm Attalea maripa. Oil palm is the most profitable crop of vegetable oil per unit area and is important to economy of developing countries such as Malaysia and Indonesia. However, due to the impact it has on biodiversity, it is also extremely controversial. The expansion of oil palm plantations in Malaysia and Indonesia, includes the conversion of forests, and other forms of land in the landscapes that provide the livelihoods of clan members. The way this expansion takes place makes it important to understand the variables associated with why businesses are looking for frontier lands and what externalities are created during both the periods of land acquisition and plantation growth. We find that investors are encouraged to profit from timber harvested from plantation land clearing, an operation promoted by the local government. Also land acquisition and plantation growth have resulted in externalities to indigenous landowners in the form of time and money wasted. The reduced health of people due to the loss of livelihoods and the effect on food security are other externalities.
\r\n\r\n\tPalm oil, like all fats, is composed of fatty acids, esterified with glycerol. Palm oil has an especially high concentration of saturated fat, specifically the 16-carbon saturated fatty acid, palmitic acid, to which it gives its name. Monounsaturated oleic acid is also a major constituent of palm oil. Unrefined palm oil is a significant source of tocotrienol, part of the vitamin E family. Palm oil sludge or palm oil mill effluent (POME) is wastewater generated by processing oil palm and consists of various suspended materials. POME has a very high biochemical oxygen demand (BOD) and chemical oxygen demand (COD), which is 100 times higher than municipal sewage. The effluent also contains a high concentration of organic nitrogen, phosphorus, and other nutrient contents. POME is a colloidal suspension consisting of 95–96% water, 0.6–0.7% oil and 4–5% total solids, including 2–4% suspended solids originating from a mixture of sterilizer condensate, separator sludge and hydrocyclone wastewater.
\r\n\r\n\tIn terms of production, export, trade, and consumption, palm oil is the leading edible oil globally. With the bulk of palm oil used in foods, its role is well known in human nutrition. In addition to being a source of calories, the oil palm is a source of useful micronutrients, including β-carotene and tocotrienols (vitamin E isomers), due to its position as dietary fat. Energy-efficient usage is the key issue for our low-carbon society in future. The importance of the development of innovative energy materials and processes were well recognized for efficient energy systems. These, after extraction, have been extensively studied. In addition, to tackle vitamin A deficiency, unrefined "red palm oil" has been used. A water-soluble fraction of palm oil that is phenolic-rich has been available over the last decade and has also been the subject of more recent studies
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Dr. Hesam Kamyab was awarded the Young Water Professional Awards by International Water Association in 2014 in Taipei, Taiwan.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"225957",title:"Dr.",name:"Hesam",middleName:null,surname:"Kamyab",slug:"hesam-kamyab",fullName:"Hesam Kamyab",profilePictureURL:"https://mts.intechopen.com/storage/users/225957/images/system/225957.jpg",biography:"Dr.Hesam Kamyab is a Visiting Researcher Scholar at Universiti Teknologi Malaysia (UTM) in 2020. Dr. Kamyab was a Postdoctoral Research Fellow for 3 years in the Department of Engineering at UTM in 2017. He was appointed as a visiting researcher from the University of Illinois Chicago (UIC) in 2016. He obtained a Master of Bioscience and Bioengineering (Biotechnology) at Universiti Teknologi Malaysia (UTM). He earned PhD in Civil Engineering in the field of Environmental Engineering at Universiti Teknologi Malaysia (UTM). He was awarded the Young Water Professional Awards by International Water Association (IWA-YWP) in 2014 at Taipei, Taiwan. Moreover, He received an outstanding Reviewer Award in the Journal of Cleaner Production (Elsevier) and Clean Technologies Environmental Policy (Springer) in 2017. He was appointed as the Junior Board Member in the Journal of Cleaner Production, Elsevier (IF: 7.246) following his active paper review role. Also, he was appointed as managing guest editor in Energy Journal, Elsevier (IF: 6.082). He has a chair in IWA Emerging Water Leader (EWL). 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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"}}]},chapter:{item:{type:"chapter",id:"46781",title:"Mechanisms of Peripheral Nerve Injury – What to Treat, When to Treat",doi:"10.5772/58421",slug:"mechanisms-of-peripheral-nerve-injury-what-to-treat-when-to-treat",body:'Peripheral nerve injury, sometimes referred to as acquired nerve injury, is a catastrophic injury that imposes a number of negative outcomes that usually inflict one or more adverse health conditions or disabilities on its victims. These adverse health conditions and disabilities frequently place both short-term and long-term burdens on individuals, families, communities, the workplace, the health care system and economies in general. Considerable money and effort have been expended on attempts to lessen, prevent or ameliorate the effects of trauma on peripheral nerves.
There are many outcomes of neuropathy of peripheral nerves. Neuropathic pain is perhaps the best documented, largely because of the enormous impact of chronic neuropathic pain on individuals and the fact that it tends to be refractory to medical treatment [1, 2]. However, other outcomes of secondary injury to peripheral nerves include, in terms of sensory disturbance, numbness, dysesthesia (an unpleasant abnormal sensation, whether spontaneous or evoked), paresthesia (an abnormal sensation, such as tingling, whether spontaneous or evoked), hypoesthesia (decreased sensitivity to stimulation, excluding the special senses) and loss of proprioception (possibly contributing to altered gait and to falls). In terms of motor control, peripheral neuropathy can lead to weakness, loss of movement, loss of corrective motor control and loss of muscle mass. Neuropathy of the autonomic nervous system can be manifest as orthostatic hypotension, dysautonomia, altered sudomotor function, and the like. Injury or damage to nerves or nerve cells can be the result of factors or events that are unanticipated or unexpected, such as an accident, while other factors or events can be anticipated, such as a result of chemotherapy or even surgical intervention.
It is the thesis of the present overview that many of the negative outcomes and disabilities of peripheral nerve injury can be reduced in severity, or prevented altogether, by early intervention with the appropriate methods, procedures and pharmaceutical formulations, continued for a medically-beneficial period of time.
While there are currently practices and interventions to treat, manage or diminish the negative outcomes of peripheral nerve injury once they have been established, immediate or early preventive approaches targeted at the development phase of these outcomes are nonexistent, few or ineffective. That is, at the time of a traumatic event medical attention focuses on treatment of immediate symptoms such as bleeding or to avoid infection, but medical attention does not typically address treatment to prevent the cascade of restorative, or adaptive, and degenerative, or maladaptive, metabolic and biochemical processes that result from peripheral nerve injury and that lead to prolonged or permanent adverse health conditions and disability.
Peripheral nerve injury or damage is not only to nerves or nerve cells, but can include damage to neural support cells, such as satellite cells and myelin cells, and also local circulation. In the context of the present overview the term "neural support cell" is any cell that supports or could be considered to support the health, normal function and survival of nerves and nerve cells, and include myelin cells and satellite cells, astroglia, oligodendrocytes, Schwann cells, vascular endothelial cells, and the like. Further, the term "neural support tissue" is any tissue that supports or could be considered to support the health, normal function, phenotype, gene expression or survival of nerves, nerve cells or support cells, and include the vasculature or microvasculature, particularly the endothelial cells that prevent blood from leaking into peripheral nerve tissue and that provide the selective blood-nerve barrier that allows the passage of certain supportive chemicals into nerve tissue as well as the passage of nerve tissue wastes out of nerve tissue.
Degeneration of axons or of neural support cells triggers a cascade of activated chemical pathways that lead to injury to otherwise intact nerve cells, Schwann cells, local vasculature and even more remote nerve cells by entry of degradation products into the blood circulation.
Trauma can be of many different types. For example, physical trauma can occur in vehicle accidents, in workplace accidents, sports accidents, on the battlefield, from falls, from assaults, from landmines and from explosive or other blasts, and the like, but can also occur as a result of surgical or other medical procedures.
Chemical trauma to nerves or nerve cells or neural support cells or neural support tissues can occur, from alcohol overdose, drug abuse, stimulant drugs such as pentylenetetrazol, carbon dioxide poisoning, acrylamide and related chemicals, overexposure to certain environmental chemicals such as copper or natural hazards such as scorpion venom toxin, herbicides, agricultural insecticides such as lindane, many industrial chemicals, neurotoxin bioterrorism chemicals such as soman and sarin, as well as radiation bioterrorism chemicals such as polonium and strontium.
Medically-induced trauma to nerves or nerve cells or neural support cells or neural support tissues can occur as a result of surgery, amputation, injections, laparoscopy, implants, during a medical procedure that reduces or impedes the blood supply to any tissue containing nerve cells for any period of time as described herein, chemotherapy (for example from methotrexate, cisplatin, cytosine arabinose, carmustine, thiotepa among others), radiation therapy, immunosuppressants (such as tacrolimus).
Surgery in and of itself can produce other types of trauma that are injurious to nerves, nerve cells and nerve support cells and neural support tissues. For example, the life-saving benefits of cardiac surgery are frequently followed by manifestations of damage to peripheral nerves and chronic neuropathic pain, which remains a significant complication of cardiac surgery and occurs with an incidence of 15% [3]. In a ten-year overview it was reported that chronic post-surgical pain constitutes a significant medical need that may be amenable to be reduced or prevented [4]. The incidence of persisting pain following amputation is 50-85%, that of intrathoracic surgery is 30-55%, mastectomy is 20-50%. Persisting pain after even simple procedures such as hernia repair and cholecystectomy are reported to be 5-35% and 5-50%, respectively. Post-sternectomy pain has been reported to be as high as 28% [5], hysterectomy as high as 32% [6], caesarean section as high as 12-18% [7, 8]. These are all astounding numbers, especially given the position taken here that the persisting pain may be reduced or prevented by appropriate and timely pharmaceutical intervention.
Similarly to medical surgical procedures, the incidence of peripheral nerve injury resulting from medical chemotherapy procedures has been underappreciated. A recent systematic review [9] has calculated that the prevalence of patients with neuropathic pain as a result of chemotherapy varies between 19% and 39%. Neuropathology-inducing chemotherapy drugs include paclitaxel, bortezomib, ixabepiline and oxaliplatin, as examples.
Broader than chemotherapy, peripheral neuropathy resulting from medications and toxic chemicals may also be preventable. Drugs that can trigger peripheral neuropathy include some antibiotics, as well as drugs for other disorders, including infliximab, etanercept, leflunomide, linezolid, statins, dichloroacetate and others [10-12]. A number of industrial chemicals also have the potential to induce peripheral neuropathy [12, 13]. Based on available knowledge, these types of peripheral neuropathy can be reduced or prevented if the appropriate medical intervention is applied early.
Peripheral nerve injury generally consists of two related processes, the initial injury and a secondary injury [14] that results from cascades of self-propagating metabolic and biochemical processes that lead to loss of cell function and cell death. Disability occurs to a large extent from the secondary injury that is triggered by the primary injury. Whether the numbers are large, as in the case of battlefield peripheral nerve injury, or small, as with falls in the elderly, peripheral nerve injury can be devastating to the individual. Whether the numbers are large, as those resulting from car accidents, or small, such as those resulting from laparoscopic surgery, the result of peripheral nerve injury can be a future of constant burning, debilitating neuropathic pain and other adverse health conditions.
In the context of the present overview the term "secondary injury" or "secondary damage", terms that can be used interchangeably for the present context, means any damage, injury, harm, loss, change in structure, change in phenotype, change in gene expression or change in function or survival of nerves, nerve cells, neural support cells or neural support tissue that occurs after a traumatic event and develops over the seconds, minutes, hours, days, weeks or even months following such an event. Secondary injury or secondary damage is usually considered to result from consecutive or parallel biochemical cascades of cellular and metabolic processes that are activated or triggered by the trauma-induced direct tissue damage to a peripheral nerve. Secondary injury or secondary damage is usually considered to involve endogenous processes or biosynthetic pathways that govern, regulate or influence the structure, health, function, gene expression or survival of nerves or nerve cells, or cells or tissues upon which nerves or nerve cells depend to maintain health and function, such as neural support cells and neural support tissues often with delayed clinical presentation [14]. Whereas a primary injury is irreversible [15], this secondary injury is salvageable [14]. This secondary injury is a neuropathology that can be reduced or prevented by appropriate and timely intervention.
Neuropathic pain is defined as pain caused by damage, lesion, disease or altered function of the peripheral somatosensory nervous system and is characterized as a constant burning pain accompanied by hyperesthesia (increased sensitivity to stimulation, excluding the special senses). Hyperesthesia is usually clarified in clinical use as either hyperalgesia (increased pain from a stimulus that normally provokes pain) or allodynia (pain due to a stimulus that does not normally provoke pain). Neuropathic pain may also include periodic attacks of pain that feel like electric shocks or shooting pain.
In understanding mechanisms of peripheral neuropathic pain it is important to distinguish this type of pain from nociceptive pain and inflammatory pain. Nociceptive pain is pain that arises from actual or potential damage to non-neural tissue and is due to the activation of nociceptors in these tissues. Nociceptive pain functions to protect from potential tissue damage or from further tissue damage, and triggers physiological and behavioural reflexes to avert damage. Inflammatory pain is pain that is triggered by inflammation and serves to aid in healing and repair of injured non-neural tissue. Each of nociceptive and inflammatory pain is brought about by a specific set of mechanisms and each has a specific treatment algorithm. Neuropathic pain is different, not only with respect to underlying mechanisms and treatments [16], but it is considered to be a maladaptive pain, as this type of pain neither protects nor supports healing and repair.
Trauma to a peripheral nerve has effects on sensory neurons, on motor neurons controlling skeletal muscle and on autonomic efferent neurons controlling the cardiovascular system and organs. This accounts for the range of outcomes of peripheral nerve trauma indicated above. As much of the research in this area is focussed on symptoms, available knowledge tends to be clearly fractionated into the bases of sensory loss, motor loss or autonomic dysfunction.
The overriding research on sensory loss pertains to peripheral neuropathic pain, which will be surveyed here to exemplify the pathophysiological changes that occur in peripheral nerves more generally. Even here, though, much attention is focused on changes in the central nervous system [17], particularly at the level of the first sensory synapse in the spinal cord and in the brain stem [18, 19]. As a result, treatment options tend to focus on targets within the central nervous system [20-22]. Research also tends to focus on the incidence of neuropathic pain rather than on underlying neuropathological processes [18]. Notwithstanding this orientation, the first step here will be to examine the changes in peripheral nerves that result from injury.
Understanding pathophysiology arising from peripheral nerve trauma is further complicated by the various types of trauma, which consist largely of a total cut of a peripheral nerve, a partial cut, an event-triggered compression, a slowly-developing compression (such as from a tumour), and a degeneration of nerve cells or of neural support cells and neural support tissues. Total and partial cuts as well as event-triggered compression can occur as a result of an accident, a violent act or surgery. Degeneration can be induced, for example, by chemotherapy. Physical, surgical and chemical events provide a start time for medical care [4, 12, 23]. As post-herpetic neuralgia is associated with a time-locked event, which is the start of the symptoms of shingles, this type of neuropathic pain is included in this overview [24-26], as would be any other infection-or inflammation-induced neuropathy that is time-locked.
Multiple pathophysiological, neurochemical, and anatomical changes are triggered by peripheral nerve injury, whereby a simple focal peripheral nerve injury unleashes a range of peripheral as well as central nervous system processes that contribute to persistent pain and abnormal sensation. Repair mechanisms of neural tissues in response to injury, and the reaction of adjacent tissues to injury lead to a state of hyperexcitability in primary afferent nociceptors [27], a phenomenon termed peripheral sensitization. In turn, central neurons innervated by such nociceptors undergo dramatic functional changes including a state of hyperexcitability termed central sensitization [28].
Normally these sensitization phenomena extinguish as the tissue heals and inflammation subsides. However, when primary afferent function is altered in an enduring way by injury or disease of the peripheral nerves, these processes persist, become chronic and may be highly resistant to treatment.
Much of what has been learned regarding the pathophysiology of injury causing neuropathic pain has come from animal studies. Human laboratory studies, although limited in number, support the idea that the pathophysiological mechanisms discovered in animal models are valuable and relevant to our understanding of human neuropathic pain [29, 30]. There are several animal models of peripheral neuropathic pain, largely based on the types of primary injury or trauma that lead to peripheral neuropathic pain in humans [31-39].
Effects of peripheral nerve injury in these models include major changes in the properties of nerve cells and their support cells, particularly the Schwann cells. Changes in sensory nerve cells include spontaneous ectopic action potential generation, persisting sensitization of sensory nerve cell peripheral terminals, and increased release of excitatory neurotransmitters from their central nerve terminals [27, 40-42]. Other changes in sensory nerve cells include a change in function [43], changes in the expression of cell constituents such as sodium channels [44] and changes in the expression of neurotransmitters [45, 46], including de novo expression of substance P in large fibre, non-nociceptive sensory neurons [40]. While there is currently no universally effective treatment for peripheral neuropathic pain, one that is included in the algorithm of treatment regimens is gabapentin [16, 21], which it thought to act by reducing the release of excitatory neurotransmitters from the central terminals of sensory neurons [47, 48]; this action is thought to occur through inhibition of the influx of calcium into the nerve terminals, which is necessary for synaptic release mechanisms [49].
Two major hypotheses have been put forward to explain the role of sensory neurons in the generation of neuropathic pain [27]. One is the classic “excitable nociceptor hypothesis”, which implicates a reduced response threshold in nociceptive small C-fibre sensory neurons. Another hypothesis suggests ectopic impulse activity is generated in low threshold mechanoreceptor large fibre Aβ sensory neurons and that this activity is abnormally “amplified” in the spinal cord by central sensitization [27, 50]. The hypothesis implicating C-fibre sensory neurons in causing neuropathic pain is mainly based on the abnormal spontaneous activity observed in these neurons. However, several studies have shown that large fibre sensory neurons undergo significant changes in their electrophysiological properties as well as other phenotypic changes, such as the expression of substance P [51-53]. Further studies have shown that large fibre Aβ neurons, not the small C-fibre sensory neurons might be the major drivers of stimulus-evoked neuropathic pain and tactile allodynia [54].
Irrespective of these outcomes of peripheral nerve injury, which manifest in established neuropathic pain, the focus of the present overview is on the mechanisms and processes that lead to these outcomes. A consensus is that once these processes are set in place the resulting neuropathic pain is relatively refractory to medical treatment. The present overview therefore addresses the initial changes in peripheral nerve cells, neural support cells and neural support tissues that lead to long-term or permanent pathology, adverse health outcomes or disability.
Specific mechanisms triggered by injury to sensory nerve cells vary depending on the site of the trauma and the type of trauma [55]. There is also a reported difference in the restorative and degenerative processes activated between immature and mature rat models [56].
A cut to an axon induces an immediate influx of calcium, which disrupts the ionic balance of the nerve cell and initiates transport of a number of intracellular and extracellular chemicals to the nerve cell body in the dorsal root ganglion [57], contributing to spontaneous ectopic activity in small diameter normally nociceptive neurons and/or in the large diameter normally non-nociceptive neurons (summarized in [18, 27, 58]). Other changes are also induced in nerve cell bodies in the dorsal root ganglia when injury occurs to the axons, including chromatolysis, displacement of the cell nucleus, cell shrinkage and a decrease in axonal transport [59].
Abrupt non-cutting trauma can also cause injury to axons, which then begin to degenerate over the next several days [60, 61], leading to cell death in a delayed, progressive process [62]. Degeneration of the central and peripheral terminal projections of the damaged and dying nerve cells leads to sprouting of the terminal projections of neighbouring undamaged nerve cells, constituting a morphological reorganization of the spinal cord neuronal circuitry [63] and perhaps also of the peripheral innervations of tissues.
Trauma to the axon also alters the normal flow of proteins orthogradely toward the cell body in the dorsal root ganglion, and retrogradely toward the peripheral terminal along intracellular filaments. This alters the information arriving to the protein assembly mechanisms in the cell body and this leads to changes gene expression of proteins. Changes in gene expression follow a temporally specific pattern [64], indicating that different cellular contents are produced at varying times following trauma to a peripheral nerve. In addition to changes in the expression of proteins there are also changes in the cellular distribution of these proteins, particularly of sodium and calcium channels [65], which are critically involved in neuronal excitability and conduction. Changes in gene expression and generation of specific proteins are particularly relevant to secondary injury including changes in the expression of neurotransmitters, such as substance P, of trophic factors such as brain-derived neurotrophic factor and other factors, as well as kinases and other degradative enzymes [45, 66].
Changes in expression and distribution of calcium channels have received particular attention. Expression of the α-2-δ subunit of voltage-gated calcium channels is increased in neuropathic pain models and this increase correlates with the onset and duration of pain scores [67]. The anticonvulsant, gabapentin, and its derivative, pregabalin, are both reported to bind to the α-2-δ subunit of voltage-gated calcium channels and inhibit transport of this subunit to nerve terminals [68]. Gabapentin and pregabalin have both shown clinical efficacy for treating chronic neuropathic pain in humans [16, 69, 70].
Changes also occur in Schwann cells. Any changes in the supporting Schwann cells are important to understand because of their pivotal role in sustaining the physiological properties of peripheral nerve cells and because they are involved in a degenerative process termed \'Wallerian degeneration\' [71]. Schwann cells are the glial cells of the peripheral nervous system, and include myelinating cells and non-myelinating satellite cells. Dysfunction of Schwann cells is at the basis of several peripheral nerve disorders, such as Guillain-Barré disease and Charcot-Marie-Tooth disease [72-74]. As the Schwann cells decompose so do the myelin sheaths. The products of this decomposition trigger proliferation of new undifferentiated Schwann cells that align along the Bungner\'s bands that constitute the tubes within which the nerve bundles are contained, along with their support cells. Toll-like receptors are strongly induced by axotomy, they are critically involved in degeneration [75.76] and they lie at the crossroads of peripheral nerve pathology and pain [77].
Changes also occur in other non-neuronal cells, affected by axonal degeneration and Wallerian degeneration of axons. Macrophages and lymphocytes as well as immune cells from the blood infiltrate dorsal root ganglion cells and are attracted to the site of nerve damage [71, 78]. This chemical milieu contains many components that impact on all cell types, including neurotrophic factors such as brain-derived neurotrophic factor, glial-derived neurotrophic factor, nerve growth factor and neurotrophin-3 [79-82], pro-and anti-inflammatory cytokines such as tumor necrosis factor (TNF-α), interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10) and leukemia inhibitory factor [83, 84] and the chemokine monocyte chemoattractant protein-1 [85]. Axon-promoting chemicals are thought to provide support for regrowing axons [83]. Some components are thought to cause increased excitability of undamaged axons as a cause of neuropathic pain [86]. Even cutting ventral roots has been shown to lead to neuropathic pain behaviour in rats [87], presumably due to the migration of chemicals from degenerating nerve and neural support cells associated with motor control to intact neighbouring sensory neurons [88-90].
Peripheral nerves travel alongside blood vessels and trauma to the nerve often physically disrupts the blood-nerve barrier, allowing the milieu of chemicals produced by axon and Schwann cell degeneration to enter the bloodstream, which then carries these chemicals to remote parts of the body, including direct access to uninjured dorsal root ganglia, the enteric nervous system and the central nervous system [91]. This tends to carry peripheral nerve injury to remote sites beyond the site of a primary injury.
Although the focus of the present overview is on peripheral nerve injury, changes in sensory nerve cells produce changes in spinal cord nerve cells, glial cells and other neural support cells, and it is generally held that some of the outcomes of peripheral nerve injury may be brought about as a result of changes in the spinal cord. For example, peripheral nerve injury produces excessive excitation and activation of sensory neurons, which causes excessive release of glutamate, substance P and other neurotransmitters from their central terminals in the spinal cord and brain stem. Besides leading to central sensitization, released neuropeptides regulate gene expression and therefore the phenotype of neurons in the spinal cord and brain stem [92]. Outcomes of peripheral nerve injury in animal models have been reported to include major changes in the properties of spinal neurons and spinal neural support cells and neural support tissues [93-95]. Peripheral nerve injury has also been reported to produce changes in the processing of sensory information at the spinal and supraspinal levels [96-101].
As a result of acute peripheral nerve injury, discharge from both damaged and adjacent intact primary afferent fibres becomes abnormal. This modified afferent drive in turn has been reported to elevate the excitability and discharge of dorsal horn neurons [43, 102] and to induce changes in sensory processing at the level of the spinal dorsal horn including altered calcium-dependent signal transduction mechanisms [103], a shift in anion gradient [104], microglial activation [105], decreased inhibitory mechanisms [58], apoptosis [106] and others. It is thought that this modified sensory processing at the level of the spinal dorsal horn, termed central sensitization [50, 107, 108] or long term potentiation [109], contributes to neuropathic pain by exacerbating excitatory transmission to supraspinal structures.
In view of the evidence that central sensitization in humans is maintained by a constant barrage of synaptic activity from primary afferent nerve cells [58, 110] it is important in understanding mechanisms of neuropathic pain to understand the properties of primary sensory neurons and how they adapt to or change in response to nerve injury. It is at these properties, particularly at the processes that are involved in the initial stages of neuropathology, that early pharmaceutical intervention can be aimed.
For complete cut of a peripheral nerve a standard procedure is nerve repair or nerve grafting, but this approach remains suboptimal and is usually performed long after the cut has occurred. Axons have the capacity to regrow, but this is often incomplete or the regeneration misses the original tissue target. As a result there has been a wealth of research on mechanisms of regeneration and respective treatment modalities. Yet, outcome generally remains poor.
To make matters worse, leaders in the field of pain have suggested that "there is little evidence that chronic postsurgical pain can be prevented" and they cite papers such as those by Kehlet et al. [23], Gartner et al. [111] and Katz and Seltzer [112]. In fact, this assessment might just be correct, as the concept of \'prevention\' of postsurgical chronic pain is usually embedded in the concept of peri-surgical anaesthesia [113-115] rather than control of the degenerative processes that lead to secondary injury to nerve cells and Schwann cells in peripheral nerves. This latter approach is not included in steps to prevent postsurgical pain, let alone a rationalized, combination therapy based on a timed sequence of pharmaceutical interventions aimed at reducing or preventing the processes involved in secondary injury to these cells. The consensus therefore teaches away from this rationalized approach toward techniques that have been proven by evidence to be relatively ineffective, condemning multiples of thousands each year to a life of unending refractory pain.
Numerous efforts have been made to develop new and effective drugs and other approaches to treat neuropathic pain. Some treatments have been found to have beneficial effects. These include treatment with multimodal analgesics [116], anticonvulsants [16, 21], botulinum toxin [117, 118], peripheral nerve electrical stimulation [119, 120], as have invasive approaches such as spinal cord stimulation [121] and administration of stem cells [122]. However, these are aimed at treating existing pain. What are not being explored are new treatments to prevent the onset of neuropathic pain or any other of the sensory, motor of autonomic adverse sequelae of peripheral nerve injury.
Trauma to peripheral nerves is not considered life threatening, whether physical, chemical, metabolic or surgical. As a result there is limited incentive to pursue medical interventions, methods and procedures to reduce or prevent secondary peripheral nerve injury that results from trauma. For example, there is no appreciation of immediacy in medical intervention. Research on medical intervention for neuropathic pain focuses on treatment of an existing condition, once a complete diagnosis has been made. Complete or correct diagnosis can take weeks, months or even years. Standard treatment following peripheral nerve trauma typically involves drugs that reduce the pain intensity. Thus, in the pursuit of new drugs, neuropathic pain resulting from peripheral nerve trauma is becoming understood in terms of a static, or an established, condition. The processes that are involved in the initial pathophysiology of peripheral nerve injury remain poorly understood and few efforts are being made to understand or to intervene in these processes.
A second limit to incentive to understanding the pathophysiology of peripheral nerves is that a major focus of research has been on the changes in the spinal cord and other central nervous system structures that result from peripheral nerve trauma [123]. As a result, much of the research on the pathophysiology of neurons and neural support cells in neuropathic pain has focused on changes in the spinal cord, where the predominant concepts are \'central sensitization\' or \'long-term potentiation\' [108, 124] and \'neuroplasticity\' [125], as mechanisms underlying the pain. While this is important, it has tended to shift focus away from the changes in peripheral nerves and the role of primary afferent drive in the mechanisms of neuropathic pain [27, 43, 102].
There is a rich literature pertaining to pharmacological treatments for peripheral neuropathic pain as an existing condition, summarized in a number of thorough reviews [16, 20-22, 126]. This abundant literature is largely due to the fact that neuropathic pain is a particularly debilitating type of chronic pain, yet it remains refractory to medical treatment in a large number of patients. Despite this huge medical need, there is little information or drive with regard to reducing or preventing the development of peripheral neuropathic pain, which is the focus of the present overview.
Despite abundant information regarding the processes and mechanisms of the changes in the periphery and in the spinal cord, there appears to be little effort being made to understand these processes and mechanisms or to develop new therapeutics to prevent trauma-induced secondary injury in peripheral nerves. Steps to reduce or to prevent the development of neuropathic pain are not generally considered in medical practice, other than steps to avoid traumatic events. Prevention, from a medical intervention standpoint, is not found in consensus statements.
Novel therapies under development retain the focus on treatment of an existing symptom. Steps to reduce or prevent secondary nerve injury following peripheral nerve trauma through immediate medical intervention do not appear in major national statements or reports, such as the US National Pain Care Policy Act of 2009, the 2011 Annual Report of the Chief Medical Officer of the United Kingdom, or the 2011 report of the US Institute of Medicine, "Relieving Pain in America. A Blueprint for Transforming Prevention, Care, Education and Research".
Given the enormous impact of trauma-induced peripheral neuropathology and its sequelae on individuals, on families, on the healthcare system and on the economy, and the enormous social impact specifically of abuse of pain-relieving drugs, this presents an opportunity to exploit the limited knowledge we have regarding mechanisms underlying the secondary injury to peripheral nerves following traumatic events, to develop effective medical intervention to reduce or prevent the secondary processes that lead to peripheral nerve pathology.
Some insights into possible therapeutic approaches have come from animal studies, which have shown that peripheral neuropathy resulting from physical trauma is preventable when immediate and appropriate therapy is introduced [127] but is not preventable when treatment is delayed [128-131]. There is limited evidence that immediate or at least early medical intervention may have beneficial effects on long-term outcome. For example, immediate but not prolonged treatment with either an NK-1 receptor antagonist [130] or with progesterone [129] has been shown to have long-term benefit in an animal model of peripheral nerve injury. In fact, a recent study on early treatment with peripheral nerve stimulation of soldiers on the battlefield has reported improved functionality and opioid use reduction [120], a point well made as extremity trauma is a relatively more common medical condition in battle now because of advances in body armour [132].
As described above, due to the plethora of mechanisms that are triggered by event-related trauma to peripheral nerves combinatorial approach to reducing or preventing secondary injury to peripheral nerves may be necessary. There is presently no therapeutic approach to prevent or reduce the adverse health conditions or disability that result from trauma-induced damage to peripheral nerve cells, peripheral neural support cells or peripheral neural support tissues. There is little research directed at translation of new discoveries from animal studies to preventing or reducing peripheral neuropathology in humans and, as a result, until this invention there is little evidence or indication that this medical need will be met.
If new, appropriate therapeutics are to be developed in order to prevent or limit the disability that ensues from peripheral nerve injury, such therapeutics will have to target the biochemical and metabolic processes triggered by trauma, and therefore research is needed to understand these processes beyond what has been described in this overview. Further, from this understanding novel targets need to be identified that offer opportunities to develop novel therapeutics.
Injury triggers cascades of cellular, biochemical and metabolic processes, some of which tend to return nerve cells, neural support cells and neural support tissues toward normal function and cell health. Some changes tend to drive nerve cells, neural support cells and neural support tissues toward loss of cell function or cell death. The former group of processes is considered to be restorative or adaptive processes. The latter group of processes is considered to be degenerative or maladaptive. The eventual outcome at the cellular and tissue levels is determined by or results from the balance of all the restorative and degenerative processes triggered by or resulting from the primary injury and its sequelae. Indeed, the damage caused by these secondary processes can be as serious and extensive as, or even more serious and extensive than, that caused by the primary trauma. Secondary processes also progress over time so that injury and damage can continue over the days, weeks and even months after the initial injury. Further, the secondary processes can also progress spatially so that injury and damage can spread spatially and manifest at sites remote from the site of the primary trauma to other peripheral nerves.
This balance can be tipped toward normal function and health by appropriate pharmaceutical intervention at the appropriate time. This can be achieved because of the chemical nature or basis of the restorative and degenerative processes occurring at the cellular, biochemical and metabolic levels.
As indicated above, there are many targets or points of entry for pharmaceutical promotion, facilitation or potentiation of restorative processes to tip this balance toward function and health, and there are many targets or points of entry for pharmaceutical inhibition, lessening or blocking of degenerative processes that tip this balance away from function and health toward loss of function, adverse health conditions or disability. It is recommended, then, that future research focus on understanding these mechanisms and identifying potential targets for development of new therapeutic approaches.
Conventional or standard treatment of trauma typically consists of minimizing the symptoms of the immediate, or primary, traumatic injury. With conventional or standard methods and treatments, attempts are made to minimize these immediate symptoms. Standard treatment for any persisting loss of function or disability that results from the initial trauma is typically treated by rehabilitation, which is usually initiated after there has been overt recovery from the traumatic event itself. Initiation of rehabilitation typically comes weeks or even months later, when the adverse health conditions or disability are clear and obvious.
In significant contrast, it is suggested here that in addition to standard emergency or critical care at the time of an accident or trauma specific actions be directed toward mitigating or ameliorating the sequelae of post-trauma effects that are an indirect result of a primary trauma and that are expressed as a result of the balance of restorative and degenerative processes.
Presently, there is a gap in medical care between standard practice to treat a primary injury or damage at the time of trauma, and standard practice to rehabilitate. The suggestion here is to address this gap by understanding and promoting processes that drive toward recovery and restoration of cell health and function and at the same time inhibiting processes that drive toward loss of cell function and cell death.
Significantly, the point of differentiation between conventional or standard methods and the present position is the difference between the treatment of the symptoms of the primary injury, and formulations, methods and procedures taken at or about the time of trauma to prevent or lessen damage from the secondary sequelae that may or are likely to occur.
The cascades of mechanisms leading to secondary injury are triggered within minutes to hours, yet continue to occur over the ensuing days and weeks. As a result, symptoms of secondary injury manifest over such periods, and the present position argues to reduce or prevent the manifestation or expression of these symptoms of secondary injury, which are known on the basis of incidence studies to occur.
There is a general acceptance that disability results from trauma. Incidence studies indicate that a certain number of people in a population will go on to develop disability following trauma of any given type. Medical attention has not typically been directed at reducing these numbers, or preventing them altogether. Instead, it tends to be directed at saving life and addressing the immediate condition and symptoms. Yet, much of the disability that ensues as a result of trauma is brought about by secondary injury processes, largely biochemical, which can be modified by appropriate pharmaceutical intervention. Trauma-induced disability can thus be considered an unaddressed medical need. The present position here is that the number of people who go on to develop disability following trauma can be reduced. Further, the severity of disability of those that develop a disability can be reduced. The scope and the spirit of the present overview are directed toward this unaddressed need, both by reducing the number of victims of trauma that go on to develop adverse health conditions and disability, as well as by reducing the severity of disability in those who are left with trauma-induced health conditions.
The primary application of refrigeration system is to transfer heat from a lower temperature region to a higher temperature one. A refrigeration cycle consists of a source at low temperature, a sink at high temperature, and a device to produce the work done to transfer heat from the source to sink. For the complete circulation, the refrigeration cycle should have an expansion device to circulate the refrigerant to the source.
\nMajor refrigeration systems include vapor-compression refrigeration system (VCRS), heat pump (HP), gas refrigeration system (GRS), multi-pressure refrigeration systems (MPRS), and absorption refrigeration system (ARS), as presented in Figure 1. These systems are combined with renewable sources, such as geothermal, solar, and wind energy sources.
\nThe classifications of refrigeration systems and renewable sources.
The vapor-compression refrigeration cycle (VCRS) is the most widely used cycle for refrigerators, air-conditioning systems, and heat pumps [1, 2]. It consists of four processes, as shown in Figure 2:
1-2 Isentropic compression in a compressor
2-3 Constant-pressure heat rejection in a condenser
3-4 Throttling in an expansion device
4-1 Constant-pressure heat absorption in an evaporator
Schematic and T-s diagram for the ideal VCRS.
The refrigerant enters the compressor from state 1 at saturated vapor to be isentropically compressed from low pressure of state 1 to high pressure and temperature of state 2, which is at the superheated region. Then, the refrigerant of state 2 enters the condenser to reject heat to the warm environment and exits at the saturated liquid as state 3. The refrigerant enters an adiabatic throttling or expansion valve to drop the pressure, which equals the pressure at the compressor inlet of state 1. The refrigerant temperature at state 1 is very low so that it absorbs heat from the refrigerated space at the evaporator and heated to be saturated vapor again. The vapor refrigeration system is a closed cycle where it starts and ends at state 1. This type of refrigeration system can be used for refrigerators, inside the air conditioners as split air conditioners, and separate as in radiant cooling systems [3, 4] and air-to-air systems [1].
\nThe first and second law of Thermodynamics for steady-state flow is applied for each component and the whole system. They include the energy balance equation (EnBE) and exergy balance equation (ExBE) in this order. The energy balance equation considers the heat transfer and work produced or done crossing the control volume of a component or a system, while the exergy balance equation considers the irreversibilities of a process, which are described by the exergy destruction. For the given system of Figure 2. The refrigerant mass flow rate is constant through the cycle and denotes as \n
The power input to the compressor, \n
The heat rejection rate from the condenser, \n
The energy and exergy balance equations for the expansion valve can be expressed as Eqs. (10) and (11), respectively. The expansion valves are considered to be decreasing the pressure adiabatically and isentropically, which means no heat transfer and work done in the throttling process [6]:
\nThe energy balance for the entire refrigeration system can be given as [5]:
\nThe coefficient of performance (COP) of the refrigeration system is defined as the ratio of useful energy, which is the rate of heat removal by the evaporator to the required energy, which is the power required to operate the compressor. The COP is given as below [5]:
\nThe Carnot or reversible COP is defined as the maximum COP of a refrigeration cycle operating between temperature limits \n
An actual vapor-compression refrigeration cycle differs from the ideal one because of the irreversibilities that occur in various components, such as fluid friction (causes pressure drops) and heat transfer to or from the surroundings. The aim of exergy analysis is to determine the exergy destruction in each component of the system and to determine the exergy efficiency of the entire system. Exergy destruction in a component can be evaluated based on entropy generation and an exergy balance equation using Eq. (15) [6]:
\nwhere \n
The exergetic coefficient of performance (\n
by substituting \n
Since \n
Heat pump system (HP) is similar to VCRS since it consists of a compressor, expansion valve, and outdoor and indoor coils, which operate exchangeably as condenser and evaporator. The advantage of HP systems is the ability to provide cooling and heating for the desired space, especially for the long winter season as in Canada and north European countries. This can be achieved by adding a reversing valve, as shown in Figure 3. There are two essential modes: heating mode and cooling mode. The condenser and evaporator are exchanging during the cooling and heating season since the reversing valve is switching between two modes according to the weather condition.
\nA heat pump can be used to heat a house in winter and to cool it in summer.
The energy source for heat pump can be classified into air-source, water-source, and ground-source. The air-source system uses atmospheric air through the evaporator, while the water-source system uses well water of depth 80 m and operates from 5 to 18°C. The ground-source system uses long piping under the ground since the soil temperature is not affected by climate change. The capacity and efficiency of heat pump drop at low-temperature environment, and therefore, other auxiliary systems, such as heaters or furnaces, are used to provide sufficient heating load for residential buildings.
\nThe COP of a heat pump is defined as the ratio of the heat removed for cooling mode or added for a heating mode of the indoor coil to the compressor power. Therefore, the COPheating and COPcooling are given in Eq. (19). \n
The exergetic COP is defined as the ratio of thermal exergy rate divided by the compressor power. It is also given as the ratio of COP to the reversible COP for both heating and cooling mode. \n
The VCRS is known as a modified, reverse Rankine cycle, while the gas refrigeration system (GRS) is known as a reverse Brayton cycle using a noncondensing gas such as air. The main advantage of this system is the small size for achieving the desired cooling due to the lighter weight of air than other refrigerants. This system can be used in aircraft cabin cooling.
\nAs illustrated in Figure 4, the major elements of GRS are compressor to raise the pressure of gas from state 1 to 2, a rejecting heat exchanger (condenser), turbine or expander to decrease the gas pressure isentropically, and an absorbing heat exchanger (evaporator) to absorb the heat from the refrigerated space at constant pressure. A regenerator heat exchanger can be added to the system for heat recovery between the hot and cold paths of circulated gas. It can be located between the two heat exchangers. Air is a popular refrigerant of this system since it can be utilized as a refrigerant and air-conditioning medium in smaller equipment units as aircraft cooling systems.
\nSimple gas refrigeration cycle and T-s diagram.
The energy analysis of a gas refrigeration system is similar to that of the vapor refrigeration system except that the gaseous fluid is treated as an ideal gas. Therefore, the enthalpy and entropy equations are written as [5]:
\nwhere the subscripts i and e indicate inlet and exit states, respectively. Therefore, the energy and exergy analysis for each component of Figure 5 is listed below [5, 6].
\nA two-stage cascade refrigeration system with the same refrigerant in both stages.
Compressor:
\nHeat exchanger 2 (condenser):
\nTurbine (expander):
\nHeat exchanger 1 (evaporator):
\nFor the entire refrigeration system, the energy balance can be written as:
\nThe net power for the system becomes:
\nThe COP of the gas refrigeration system is given as:
\nThe total exergy destruction in the system can be calculated by adding exergy destructions of each component:
\nIt can also be expressed as:
\nThus, the minimum power input to accomplish the required refrigeration load \n
The VCRS is the most popular refrigeration cycle because it is simple, inexpensive, and reliable. However, the industrial refrigeration systems should be efficient by providing more refrigeration load. This can be achieved by modifying the simple VCRS into multi-pressure refrigeration systems (MPRS). The MPRS can be classified into cascade RS, multi-compression RS, and multipurpose RS.
\nSome industrial applications require low temperature below −70°C with substantially large pressure and temperature difference (−70 to 100°C). VCRS cannot achieve these applications because it can operate within a temperature range of +10 to −30°C. Therefore, a modification of VCRS can be performed by using multiple refrigeration cycles operating in series, the so-called cascade refrigeration systems. The refrigerants of each cycle can be different. The evaporator of the first refrigeration cycle is connected to the condenser of the next refrigeration system forming an interchange heat exchanger between the 2 cycles, as shown in Figure 5. Cascade refrigeration systems are mainly used for liquefaction of natural gas, hydrogen, and other gases [7, 8, 9]. The major benefit of this system is decreasing the compressor power and increasing the refrigeration load compared with a VCRS with large temperature and pressure difference, as shown in the T-s diagram of cascade system in Figure 5. Therefore, reducing system components can be fulfilled in an appropriate way [2].
\nThe net compressor power can be determined by the summation of all compressor power in all cascaded refrigeration system and written as [2]:
\nThe refrigeration load can be described as:
\nThe heat exchanger that connects the 2 cycles together has an energy balance equation as follows [5]:
\nTherefore, the COP and exergetic COP of the cascade refrigeration system can be explained as the following [5, 6]:
\nSimilar to the cascade refrigeration system, multistage compression refrigeration system is used for applications below −30°C. This requires a large-pressure-ratio compressor and cannot be performed by one compressor because of the lack of efficiency and performance. Therefore, using multistage compressors connected in series can improve the performance of the refrigeration system by increasing the pressure ratio and increasing the refrigeration load. As shown in Figure 6, a two-stage compression refrigeration cycle consists of two compressors, a condenser, an evaporator, a flash intercooler, a mixer, and two throttling valves. The compressors. The upper compressor compresses the total refrigerant mass flow rate in a vapor form from the intermediate pressure of state 9 to the high pressure of state 4. The vapor refrigerant cools down in the condenser to saturated liquid at high pressure of state 5 and then passes through the upper expansion valve to reduce the pressure to intermediate pressure. The wet refrigerant passes through the flash intercooler to split the vapor and liquid phase. The vapor phase at state 3 enters the mixer to mix with the exit superheated refrigerant of the lower compressor at state 2. The liquid phase at state 7 is expanded by the lower throttling valve to state 8, which enters the lower pressure evaporator to absorb heat from the refrigerated space. The minimum temperature can be achieved by two-stage compression at −65°C, while the three-stage compression can attain about −100°C.
\nA two-stage compression refrigeration system with a flash chamber.
The heat transfer to the evaporator can be written, according to Figure 6, as [10]:
\nwhere \n
Therefore, the COP of this system can be determined as the following [10]:
\nThe second efficiency or the exergetic COP can be calculated as [6, 10]:
\nMultipurpose refrigeration systems are also considered as a branch of MPRS. This type of system accomplishes different refrigeration loads in one system. Therefore, a modification of VCRS can be done by using multiple evaporators at different low pressure and different refrigerant capacity. Also, this system can be operated using one compressor or multistage compressor.
\nThere are different configurations of multipurpose refrigeration systems [2], as shown in Figure 7. Firstly, a system of a single compressor and individual expansion valves consists of two evaporators and single compressor with individual expansion valves for each evaporator and one compressor, as shown in Figure 7a. Operation under these conditions means the dropping of pressure from high-pressure evaporators through back pressure valves to ensure the compression of the vapor from the higher temperature evaporators through a pressure ratio. Secondly, a system of a single compressor with multi-expansion valves consists of two evaporators and a compressor with multiple arrangements of expansion valves, as shown in Figure 7b. The only advantage of the arrangement is that the flashed vapor at the pressure of the high-temperature evaporator is not allowed to go to the lower-temperature evaporator, thus improving its efficiency. Finally, a system of individual compressors with multi-expansion valves consists of a compressor for each evaporator and multiple arrangements of expansion valves, as shown in Figure 7c, to reduce the total power requirement. This amounts to parallel operation of evaporators and is called sectionalizing. There may be a separate condenser for each compressor or a common condenser for the whole plant.
\nMultipurpose refrigeration system: (a) two evaporators with individual expansion valve, (b) two evaporators and multi-expansion valve, and (c) individual compressors and multi-expansion valve.
The heat transfer to the evaporators and the net compressor power of the multipurpose refrigeration system despite the system configuration can be evaluated as [2]:
\nwhere \n
Therefore, the COP of this system can be determined as the following [5]:
\nThe second efficiency or the exergetic COP can be calculated as [6]:
\nThe absorption refrigeration system (ARS) is similar to the VCRS except that the compressor of the vapor-compression system is replaced by three elements: an absorber, a solution pump, and a generator. The ABS medium is a mixture of a refrigerant and absorbent, such as ammonia-water system (NH3 + H2O) and water-lithium bromide (LiBr2 + H2O). The solubility of refrigerant (ammonia or lithium bromide) in the absorbent (water) is satisfactory, but the difference in boiling points is significant, which may affect the purity of vaporization. Thus, a purge unit or rectifier is used in the system. The refrigerant concentration in the mixture changes according to the pressure and temperature for each step. The ABS.
\nAs shown in Figure 8, the ARS consists of a condenser, an evaporator, an absorber, a regeneration heat exchanger (HX1), heat recovery heat exchanger (HX2), a generator, two expansion valves, and a solution pump. The system includes an analyzer and a rectifier to remove the water vapor that may have formed in the generator. Thus, only ammonia vapor goes to the condenser. This system utilizes the absorbent water to release and absorb ammonia as the refrigerant. Starting from state 3, the strong solution (a high concentration of ammonia refrigerant) is heated in the high-pressure generator. This produces refrigerant vapor off the solution at state 7. The hot pure ammonia vapor is cooled in the condenser at state 8 and condenses at state 9 by passing through the HX2 before entering a throttling valve into the low pressure at state 10. Then the refrigerant liquid passes through the evaporator to remove the heat from refrigerated medium and leaves at low-pressure vapor phase of state 11. The pure ammonia is heated by the HX2 to enter the absorber and mixed with the absorbent water. The weak solution (about 24% ammonia concentration) flows down from the generator at state 4 through the regeneration heat exchanger HX1 at state 5 through a throttling valve and enters the absorber at state 6. Therefore, the weak refrigerant is absorbed by the water because of the strong chemical affinity for each other. The absorber is cooled to produce a strong solution at low pressure at state 1. The strong solution is obtained and pumped by a solution pump to the generator passing through HX1, where it is again heated, and the cycle continues. Then, the water absorbs the ammonia in the absorber at the condenser temperature supplied by the circulating water or air, and hence a strong solution (about 38% ammonia concentration) occurs. For ammonia-water ARSs, the most suitable absorber is the film-type absorber because of high heat and mass transfer rates, enhanced overall performance, and large concentration rates [11].
\nAmmonia absorption refrigeration cycle.
The energy and exergy analysis for each component is presented according to Figure 8. The partial mass balance (PMBE) is also included to determine the concentration mass of ammonia and water in the absorber and generator. That is because the ARS has two fluids as refrigerant and absorbent and their composition at different points is different, particularly in the absorber and generator. The exergy analysis of ammonia-water ARSs is to determine the exergy destruction of each component and to determine the overall exergy efficiency based on the second law of thermodynamics. The exergy analysis (ExBE) for each component is stated below [5, 6]:
\nAbsorber:
\nwhere \n
Solution pump:
\nRegeneration heat exchanger (HX1):
\nGenerator:
\nwhere \n
Condenser:
\nwhere \n
Heat recovery heat exchanger (HX2):
\nExpansion valves:
\nEvaporator:
\nwhere \n
For the entire system, the overall energy balance of the complete system can be written as follows, by considering that there is negligible heat loss to the environment:
\nThe COP of the system then becomes:
\nwhere \n
The ARS is a heat-driven system, which requires heat pump instead or required power by a compressor. That means the ARS is a combination of a heat pump and a refrigeration cycle without a compressor. Therefore, the maximum (reversible) of an ARS can be achieved by a reversible heat engine and a reversible refrigerator, as shown in Figure 9. A reversible heat pump is operating by absorbing the heat from a source at and rejecting heat to an environment of to produce a work output from the heat engine. This work is defined as the reversible efficiency of the heat pump multiplied by the heat absorber from the source, which is the heat transfer from the generator in the ARS. This work output is used by the reversible refrigerator to keep a refrigerated space at TL\n while rejecting heat to the environment at T0\n. Therefore, the reversible COP of ARS can be obtained by the thermal efficiency of a reversible heat engine and the COP of a reversible refrigerator as in Eq. (72) [10]:
\nThe maximum COP of an absorption refrigeration system.
The temperature of the heat source is taken as the average temperature of geothermal water. Then the second-law efficiency of this absorption system is determined to be [10]:
\nThe refrigeration systems require an input work to release the heat from the refrigerated space to the environment, which is called as a work-driven system. The absorption refrigeration system is based on external heat transfer from an external source, which can be classified as a heat-driven system. For industrial refrigeration systems, energy demand is high and should be provided in a secure and eco-friendly approach to reduce environmental pollution. This can be executed by fossil-based fuels such as oil, natural gas, and coal, which produce substantial carbon mono-oxide and dioxide emissions that affect global warming and climate change. Massive efforts point to renewable sources such as geothermal energy, solar energy, and wind energy, which promise a potential solution to provide the clean energy needed as work or heat to operate the refrigeration. Schematic diagram of Figure 10 shows possible ways of renewable sources for work-driven and heat-driven refrigeration system.
\nRenewable sources for refrigeration systems: (a) work-driven and (b) heat-driven source.
An integrated system of a concentrated solar power plant integrated with desalination process and absorption refrigeration cycle is utilized to supply power, freshwater, and refrigeration [12]. The system, as shown in Figure 11, consists of concentrated solar collectors connected with steam turbine power plant, a multi-effect desalination process with a parallel feed of seawater, and a single-stage ammonia-water absorption refrigeration system. The solar collectors provide thermal energy 21,030 kW to the steam power plant to deliver an electric power of 4632 kW. The refrigeration load from the absorption cooling system is 820.8 kW. The desalination system can also provide 22.79 kg/s freshwater. This cycle has obtained overall energy and exergy efficiencies to be 80.70% and 66.05%, respectively.
\nSchematic diagram of the integrated solar thermal power plant, absorption refrigeration system, and MED cycle (adopted from [12]).
Another example, a small-scale system, is designed to provide an electrical load to residential buildings [13]. This system utilizes, as shown in Figure 12, photovoltaic solar system (PV) to provide electrical power. This electric power is used for a water electrolyzer system to split the water electrochemically to produce hydrogen and oxygen gases. The hydrogen gas enters high-temperature solid oxide fuel cells (SOFC) to produce electricity and heat. The heat is transferred to an absorption cooling system by heat recovery generator. The PV system may generate excess electricity more than the demand during off-peak hours. This system is designed for a detached house in Toronto city, Canada. The PV solar system delivers maximum power of 3.35 kW. The water electrolyzer can produce 0.792 and 0.538 kg/day of gaseous hydrogen in summer and winter seasons. The SOFC fuel cell supplies 8.43 kWh per day in summer season. The maximum energy and exergy efficiencies of the photovoltaic system are 17 and 18.3%, respectively, while the maximum total energy and exergy efficiencies are obtained to be 55.7 and 49.0%, respectively.
\nSchematic of the photovoltaic-fuel cell CHIP system for residential applications (adopted from [13]).
In a similar study, a hybrid renewable system was designed to produce electricity and clean fuel such as hydrogen gas and provide cooling for a residential building in two locations Egypt and Saudi Arabia in summer season [14]. The cooling loads for a house are 18.06 and 19.3 kW in Egypt and Saudi Arabia, respectively. This system, as shown in Figure 13, depends on the photovoltaic solar system and wind turbines to provide excess electricity more than the electric grid. The excess electricity is delivered to a water electrolyzer to produce pure oxygen and hydrogen gases stored in tanks for clean fueling services. Part of the hydrogen gas is used for a proton-exchange membrane (PEM) fuel cell that can produce heat and electricity through an electrochemical process without any mechanical parts. The heat generated from the fuel cell can be utilized by a generator of an ammonia-water ARS to provide cooling. The hybrid renewable system can operate in a significant performance with water mass flow rate of 1.8 kg/s to produce hydrogen with a mass flow rate of 0.2 kg/s and ammonia mass flow rate of about 0.2 kg/s to produce cooling load between 40 and 120 kW more than the design cooling load of one house. The energy and exergy efficiencies are obtained to be about 67 and 68%, respectively. Therefore, this hybrid system can be sufficient for more than one house.
\nSchematic diagram of a hybrid renewable system (adopted from [14]).
A multigeneration system is designed by [15] and powered by geothermal energy assisted with solar energy to produce five outputs: heating air for residential building, hot domestic water, drying food, refrigeration for industry, and electricity. This multigeneration system, as shown in Figure 14, consists of a heat pump system, a single flash geothermal cycle, an absorption cooling system, thermal energy storage connected with auxiliary steam turbine and concentrated solar collectors, hot water system, and drying system. The system has achieved overall energy and exergy efficiencies to be 69.6 and 42.8%, respectively. The first and second steam turbines have the power of 10,043 and 9886 kW. The COP and COPex\n are 0.678 and 0.253 for the absorption cooling system and 2.029 and 0.1826 for heat pump system, respectively. The refrigeration load is 1787 kW. The overall energy and exergy efficiencies for the whole system are 69.6 and 42.8%, respectively.
\nSchematic diagram of the multigeneration system powered by the solar and geothermal energy (adopted from [15]).
A wind system is combined with a refrigeration system, as shown in Figure 15. Wind energy is coupled with compressed air energy storage (CAES) systems to store wind energy for long-term usage [16]. The integrated system consists of a combined gas power cycle, including compressors, intercooling heat exchangers, and gas turbine, an organic Rankine power cycle (ORC), and an absorption refrigeration system (ARS). The system objective is to provide electricity, domestic hot water, and cooling load. The system can generate electricity of 33.67 kW provided by wind turbines (83.24 kWh) and fuel combustion (258.97 kWh), cooling load of 2.56 kW, and mass flow rate of hot water of 1.82 ton per day hot. The energy efficiency of the system is achieved to be 53.94%.
\nSchematic diagram of gas power cycle with wind turbine, CAES, ORC, and ARS (adopted from [16]).
The refrigeration systems are applied in our life for preserving food, cooling air, and other industrial applications. Most refrigeration systems require external power or external heat to release the heat from the refrigerated space. Many industrial applications involve large cooling energy, which can be operated by multi-pressure refrigeration system, which requires a large amount of external power. The chapter has presented some applications with renewable sources to replace the fossil fuel-driven energy with an environmentally friendly energy source such as geothermal, solar, and wind energy so-called hybrid or integrated systems. In addition to cooling load, the hybrid systems can produce electricity, heating load, and clean fuel such as hydrogen fuel. The absorption refrigeration system is mostly-combined with hybrid system to use the heating load from solar or geothermal energy to produce cooling load.
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