Factors influencing poultry meat color [58].
\r\n\tThis book will consist of chapters that are an elegant mix of reviews and current developments on the subject that will be useful both to an expert on the subject as well as a newcomer to this area of research.
",isbn:"978-1-83969-076-1",printIsbn:"978-1-83969-075-4",pdfIsbn:"978-1-83969-092-1",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,isSalesforceBook:!1,isNomenclature:!1,hash:"8a2fd9bbbbae283bf115881d9d5cc47a",bookSignature:"Dr. Ashim Kumar Dutta",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/11857.jpg",keywords:"Frenkel Excitons, Wannier-Mott Excitons, Low Dimensional Solids, Molecular Crystals and Aggregates, Exciton Diffusion and Hopping, Exciton–Exciton Annihilation, Dynamics, Scaling Laws, Photoluminescence, Exciton Lifetime, Energy Harvesting, Semiconductors",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"April 19th 2022",dateEndSecondStepPublish:"June 23rd 2022",dateEndThirdStepPublish:"August 22nd 2022",dateEndFourthStepPublish:"November 10th 2022",dateEndFifthStepPublish:"January 9th 2023",dateConfirmationOfParticipation:null,remainingDaysToSecondStep:"5 days",secondStepPassed:!0,areRegistrationsClosed:!1,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"Dr. Ashim Kumar Dutta received his Ph.D. in physical chemistry from the Indian Association for the Cultivation of Science (IACS). He has worked on various international post-doctoral fellowships in Japan, Canada, and USA. Dr. Dutta has worked as head of research and product development in several companies, and presently works as vice-president for India Glycols Limited. He has authored/co-authored 36 articles in international journals and 21 patents.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"277477",title:"Dr.",name:"Ashim",middleName:"Kumar",surname:"Dutta",slug:"ashim-dutta",fullName:"Ashim Dutta",profilePictureURL:"https://mts.intechopen.com/storage/users/277477/images/system/277477.jpg",biography:"Dr. Ashim Kumar Dutta presently works as the vice president (R&D) with India Glycols Limited, one of the largest manufacturers of Green Surfactants in South East Asia. Earlier, he had worked with Unilever as a senior researcher and product development manager in their Home and Personal Care Category, with United Phosphorus Limited and Indofil as their global head for agrochemical formulations. He has authored/co-authored 36 articles in international journals and 19 patents. He received his Ph.D in physical chemistry from Indian Association for the Cultivation of Science (IACS) – a premiere research institute in India in 1993. Dr. Dutta has worked on various international post-doctoral fellowships in Japan, Canada and USA. His research interests include supramolecular assemblies, ultrathin nanostructured films, nanoparticles, novel surfactants, surfactant-polymer interactions, bio-membranes and spectroscopy of Langmuir-Blodgett films, tribology and rheology of complex systems.",institutionString:"India Glycols Limited",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"1",institution:null}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"20",title:"Physics",slug:"physics"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"440204",firstName:"Ana",lastName:"Cink",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/440204/images/20006_n.jpg",email:"ana.c@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:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1373",title:"Ionic Liquids",subtitle:"Applications and Perspectives",isOpenForSubmission:!1,hash:"5e9ae5ae9167cde4b344e499a792c41c",slug:"ionic-liquids-applications-and-perspectives",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"2270",title:"Fourier Transform",subtitle:"Materials Analysis",isOpenForSubmission:!1,hash:"5e094b066da527193e878e160b4772af",slug:"fourier-transform-materials-analysis",bookSignature:"Salih Mohammed Salih",coverURL:"https://cdn.intechopen.com/books/images_new/2270.jpg",editedByType:"Edited by",editors:[{id:"111691",title:"Dr.Ing.",name:"Salih",surname:"Salih",slug:"salih-salih",fullName:"Salih Salih"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"63256",title:"Novel Mechanism of Nonalcoholic Lipid Accumulation Promoting Malignant Transformation of Hepatocytes",doi:"10.5772/intechopen.77400",slug:"novel-mechanism-of-nonalcoholic-lipid-accumulation-promoting-malignant-transformation-of-hepatocytes",body:'Hepatocellular carcinoma (HCC) is one of the fifth most common malignant tumors, the third most frequent cause of cancer mortality worldwide [1, 2], and ranks the second in China among all malignancies with its mortality almost equal to its morbidity, especially in the inshore area of the Yangtze River [3, 4]. The principal treatment of HCC patient is surgical resection or liver transplantation, depending on whether the patient is a suitable transplant candidate [5, 6]. However, in most HCC patients with diagnosis at early stage is very difficult, thereby excluding the patients from definitive surgical resection. Sorafenib, the most commonly used systemic therapy, has shown to only minimally impact on patient survival by several months. Besides, neither chemotherapy nor radiotherapy are generally effective. Due to the poor prognosis of HCC patients, the early diagnosis and effective therapy of HCC are needed with several being in development, either in preclinical or clinical studies [7, 8].
The development of HCC is a complex multi-step process involved multiple genes. Major risk factors of HCC include hepatitis B virus (HBV) or hepatitis C virus (HCV) infection, alcoholic or nonalcoholic fatty liver disease, nitrosamines, aflatoxin, and other harmful substances [9, 10, 11, 12]. Chronic persistent infection of nonalcoholic is still the main pathological factor of inducing cirrhosis and HCC. However, with the changes of people’s dietary structure and lifestyle, the incidence of fatty liver disease (FLD) also rose sharply [13, 14, 15]. A median prevalence of alcoholic fatty liver disease (AFLD) and nonalcoholic fatty liver disease (NAFLD) is 4.5 and 15.0%, respectively [16, 17]. It is worrying that if no interference is conducted in the treatment, nonalcoholic steatohepatitis (NASH) or alcoholic hepatitis can also be developed for liver fibrosis, cirrhosis and liver cancer (Figure 1), and its exact mechanism is worth exploring. However, the underlying molecular mechanisms that lead to malignant transformation of infected liver cells still remain to be explored. Most of HCC patients died quickly because of the rapid tumor growth, and surgical operation or liver transplantation still is the only effective treatment for HCC [18, 19]. This article summarizes new advances on relationship between NAFLD and hepatocytes malignant transformation.
NAFLD progression and clinical diagnosis. ALT: alanine aminotransferase, NAFLD: non-alcoholic fatty liver disease, NAFL: nonalcoholic fatty liver, NASH: non-alcoholic steatohepatitis, HCC: hepatocellular carcinoma, HBsAg: hepatitis B surface antigen, HCV: hepatitis C virus, ANA: antinuclear antibody.
Liver is one of the most important organs in human for maintaining energy supply and lipid metabolism [20, 21]. The peroxisomal compartment in hepatocytes hosts several essential metabolic conversions. Upon nutrient deprivation, cells metabolize fatty acids (FAs) in mitochondria to supply energy. FAs mobilization depends on triacylglycerol lipolysis, whereas autophagy feeds the lipid droplet pool for continued fueling of mitochondria. Proteome imbalance of mitochondrial electron transport chain in brown adipocytes leads to metabolic benefits [22]. Lipid metabolism are defective in peroxisomal disorders that are either caused by failure to import the enzymes such as carnitine palmitoyltransferase (CPT) in the organelle or by mutations in the enzymes or in transporters needed to transfer the substrates across the peroxisomal membrane (Figure 2). Hepatocytes specific differences have been confirmed in mitochondrial DNA maintenance and expression [23]. Hepatic pathology is one of the cardinal features in disorders of peroxisome biogenesis and peroxisomal β-oxidation, although it rarely determines the clinical fate. Besides of the morphological changes, the impact of peroxisome malfunctions on other cellular compartments includes thermal instability of carnitine palmitoyltransferase II (CPT-II) variants in mitochondria and endoplasmic reticulum (ER) [24, 25, 26]. Proteomics analysis revealed numerous enzymes expression involved with the electron transport system, the tricarboxylic acid cycle, as well as lipid and amino acid metabolism in response to anoxia exposure [27].
Fatty acid oxidation and ATP production in mitochondria. The distribution of mitochondrial CPT-I or CPT-II with regulation plays important roles in fatty acid metabolism. Fatty acid (FA) β-oxidation requires successive carnitine acyltransferases to translocate acyl-coenzyme As (acyl-CoAs) from the cytoplasm into matrix. As initial and rate-limiting CPT-I generates acylcarnitines that traverse mitochondrial membranes via specific transporters into matrix, CPT-II produces acyl-CoAs from acylcarnitines for FA β-oxidation to acetyl-CoA. Then carnitine crosses the inner membrane, binds with the endogenous or exogenous acyl CoA to prevent acyl CoA accumulation causing poisoning. ACC: acetyl CoA carboxylase, CoA: coenzyme A, TCA: tricarboxylic acid cycle, UCP: uncoupling protein, I II III IV
Carnitine is a physiological substance that is essential for the proper metabolism of fat and energy production that actually transports both long and medium fatty acid chains. L-carnitine attracts long and medium fatty acid chains, breaks them down, and carries them to the mitochondria of the cells where they are metabolized (burned). The L-carnitine plays important roles in the catabolism of long-chain fatty acids in the mitochondria, not only due to increased mitochondrial fatty acid oxidation reflected by increased mitochondrial biogenesis, but also to changes in plasma clearance and reduced triacylglycerol (TAG) biosynthesis [28]. The ultimate result is that you burn more fats, and in the process give your body more natural energy. In the previous study, the increasing liver weight with lipid accumulation was discovered during the course of the wild-type mice (Figure 3) in circulating carnitine analogues [3-(2,2,2-trimethyl hydrazinium) propionate dihydrate, THP] [29, 30].
Liver lipid accumulation and liver weight tissues in mice models after carnitine analogues. A–D, the mice liver tissues with Oil red O staining: A & B, the control livers; C & D, the experimental livers; E, the alterations of different tissue weight after the experimental mice with carnitine analogues [
Hepatic CPT-II is a mitochondrial protein which is transported to mitochondrial inner membrane. It together with CPT-I oxidizes long-chain fatty acids in mitochondria. Defects or mutation of this gene are associated with mitochondrial long-chain fatty-acid oxidation disorders. Decreasing of its activity is a disorder of mitochondrial fatty acid oxidation with autosomal recessive mode of inheritance. The variants exert a dominant-negative effect on the homotetrameric protein of the enzyme (Figure 4), with reduced activities, thermal instability, fatty acid β-oxidation decreased to 30–59%, intracellular ATP to 48–79%, a significantly decreasing of mitochondrial membrane potential with increasing temperature at 41°C, and shortening half-lives of CPT-II, and the enzyme variant proteins were polyubiquitinated and rapidly degraded by a lactacystin-sensitive proteasome pathway [24]. The very unstable CPT II variants with decreased enzymatic activities may bring mitochondrial fuel utilization below the phenotypic threshold during high fever in humans with hepatitis virus infection, and thus might be as novel potential mechanisms for NAFLD formation [31, 32].
Mutation of CPT-II gene and hepatic lipid accumulation. (A) The CPT-II gene exon 1–5. (B) The sequence fragments of CPT-II gene exon 4 were amplified on mitochondrial inner membrane. The mutation analysis of CPT-II gene exon-4 using the specific primers were designed by sequencing with 1974 nucleotides coded 658 amino acids. Compared with the original sequence from Genbank, the two substitution sites were found at 1618 (G→A) and 1858 (T→C), and code amino acids at V368I and F448L, respectively [
The dynamic alterations of hepatic CPT-II expression in the mitochondrial inner membrane were investigated during the malignant transformation of hepatocytes induced by abnormal fatty accumulation. After the male Sprague-Dawley (SD) rats were fed with control, high fat (HF), and HF containing 2-fluorenylaceta-mide (2-FAA) diet, respectively. The rats were divided into control, fatty liver, degeneration, pre-cancerous, and cancerous groups according to the hematoxylin and eosin staining (H&E) of liver pathological examination, hepatic lipids accumulation were confirmed with the Oil Red O staining. Massive lipid accumulation hepatocytes were seen in rats on HF and HF containing 2-FAA diets. The lipid levels in the control group were significantly lower than those in the fatty liver, degeneration, precancerous, and cancerous groups. The serum triglyceride and total cholesterol levels in the degeneration, precancerous, and cancerous groups were 2–3 times higher than those in the control group. The serum aspartate aminotransferase and alanine aminotransferase levels (Figure 5) in the degeneration, precancerous, and cancerous groups were significantly higher (4–8 times) than those in the control group. The specific concentration (μg/mg protein) of liver CPT-II expression was significantly reduced during hepatocyte malignant transformation, as confirmed by immunohistochemistry, with the CPT-II levels significantly lower in the cancerous group than in any of other groups, indicated that low hepatic CPT-II expression might lead to abnormal lipid accumulation in hepatocytes, which should promote the malignant transformation of hepatocytes [33, 34].
Rat liver tissues and their pathological examination. Liver alterations after the rats (from left to right: upper, A, B, C, D, and E; under A1, B2, C3, D4, and E5) were sacrificed at different time according to the plan schoule. (A) A representative liver from rat with normal diet; (B) a representative liver from the rat with high-fat diet (HFD) without 2-fluorenyl acetamide (2-FAA); (C) a representative liver from the rats with HFD containing 2-FAA at early stage; (D) a representative liver at interim stage; and (E) a representative liver at later stage. The liver sections were examined with hematoxylin and eosin staining and then divided into the control (A1), fatty liver (B1), degeneration (C1), precancerous (D1), and cancerous (E1) groups; A1-E1: The original magnification of the corresponding rat liver sections was ×200 [
Lipid accumulation in liver or HCC will cause tumor-associated molecular signaling alteration including NF-κB (nuclear factor-kappa B), JNK (c-Jun N-terminal kinase)/activation protein-1 activation, and alterations of HCC development-related genes, respectively. For example, liver unsaturated fatty acids (UFA) inhibit the expression of phosphatase and tensin homolog (PTEN) deleted on chromosome 10 (10q23.3) via activating NF-κB/mTOR (mammalian target of rapamycin) complex [35]. As a tumor suppressor gene PTEN regulates the PKB/akt (serine-threonine kinase protein kinase B) pathway, and PTEN deficiency induces the proliferation of hepatocytes by inhibiting cell apoptosis and promoting HCC formation confirmed in mice models with the PTEN deficiency in resembling non-alcoholic steatohepatitis (NASH) features with developing steatosis, and inflammation damages or fibrosis in liver tissues [36].
DNA injury affects hepatic lipid metabolism. Reactive oxygen species (ROS) is an important factor in carcinogenesis. It can be induced in NAFLD patients with contiguous DNA damage by some of hepatic inflammatory cytokines or hepatitis virus infection and react with polyunsaturated fatty acids derived from hepatocyte membrane phospholipids, and subsequently results in reactive aldehydes production as lipid oxidation (LPO) byproducts, for example, 4-hydroxynonenal (4 HNE) that can react with DNA to form mutagenic exocyclic etheno-DNA adducts. Importantly, they are preferably formed in codon 249 of TP53, resulting in inactivation of tumor suppressor p53 gene, secondary growth advantage, and anti-apoptosis [37].
Adipokine is a plethora of pro- and anti-inflammatory cytokines that secretes from adipose tissue with low-grade inflammation. Adiponectin and leptin have evolved as crucial signals in many obesity-related pathologies including (NAFLD) [38, 39, 40]. Adiponectin regulates the metabolism of blood glucose and hepatic fatty acid, and is decreased in NAFLD that might be critically involved in the pro-inflammatory state associated with obesity and related disorders, overproduction of leptin, a rather pro-inflammatory mediator, is considered of equal relevance [41, 42]. An imbalanced adipokine profile in obesity consecutively contributes to metabolic inflammation in NAFLD, which is also associated with a substantial risk for developing HCC in the non-cirrhotic stage of disease [43, 44]. Both related to liver tumorigenesis especially in preclinical models, especially in hepatic satellite cell activation with stimulating the tissue inhibitor of metalloproteinase 1 production via the JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway promoting fibrogenesis [45, 46], or angiogenesis or progression from NASH to HCC that has been confirmed in mice models [47, 48].
According to the data from animal models with HCC cell lines, adiponectin could increase JNK activation and induce cell apoptosis with AMPK alteration, which could inhibit mTOR phosphorylation, xenograft growth, tumor growth and metastasis by suppression of tumor angiogenesis in nude mice. However, lower circulating adiponectin favors tumorigenesis in NASH model [49]. Adipose-derived tumor necrosis factor is a potent activator of pro-oncogenic pathways involving in mTOR, JNK, NF-κB, and extra-cellular signal-regulated kinases; Interleukin-6 (IL-6) combining with its receptors on liver or non-parenchymal cells can promote signal-transmuting receptor (gp130) complex with IL-6R activating JAK1 signaling, and STAT3 activation or phosphorylation promotes the proliferation and anti-apoptosis of cancer cells [50], indicated that adiponectin coefficient action from adipose tissues and related- cytokines affect fatty acid metabolism and hepatocyte malignant transformation via many signal molecules.
Lipid reprogramming has been considered as a crucial characteristic in HCC initiation and progression. SREBPs are the key transcription regulators of hepatic lipogenesis, and activate hepatic steatosis at the early stage. Tat-interacting protein 30 (TIP30) is a tumor suppressor protein that has been found to be expressed in a wide variety of tumor tissues that is involved in the control of cell apoptosis, growth, metastasis, angiogenesis, DNA repair, and tumor cell metabolism. TIP30 regulates lipid metabolism in human HCC by regulating SREBP1 (sterol regulatory element-binding protein 1) through the Akt/mTOR signaling pathway [51, 52]. In human HCC tissues, SREBP1 could significantly induce lipogenesis and be associated with a poor prognosis [53].
SREBP1c gene at mRNA level was up-regulated in human HCC tissues and not in their adjacent non-cancerous or non-cancerous liver tissues. The inhibition of SREBP1 expression resulted in growth arrest and apoptosis of cancerous cells, and increased the cell proliferation ability. HBx (HBV protein X) expression induces lipid accumulation in hepatic cells mediated by the induction of SREBP1, a key regulator of lipogenic genes in the liver. HBx interacts with LXRalpha (liver X receptor alpha) and enhances the binding of LXRalpha to LXRE (LXR-response element), thereby resulting in the up-regulation of SREBP1 and fatty acid synthase, suggested that HBV infection can stimulate the SREBP1-mediated control of lipid accumulation [54].
Aberrantly high expression of TRIM24 occurs in human HCC clinical samples and positively correlated with HCC tumor grade. Its knockdown inhibits proliferation and migration in HCC cells
According to accumulating data, human liver OPN is a multifunctional protein involved in some pathological alterations including hepatic immunity, hepatocytes inflammation, liver fibrosis, and the development of HCC. Deficiency of OPN in obese mice fed with a high-fat diet reduced hepatic steatosis and inflammation, and liver cell ballooning, portal leukocyte infiltration and macrophage accumulation were attenuated. It is induced by Hedgehog signaling, may directly promote pro-fibrogenic responses in steatohepatitis, or act as a paracrine factor secreted by bile duct or natural killer T cells (NKT), and also can be as an autocrine factor promoting fibrosis in hepatic satellite cells (HSC) [59].
The silencing OPN gene transcription by specific shRNA could result in increasing Bax, decreasing Bcl-2/Bcl-xL and X-linked inhibitor of apoptosis protein expression, and NF-κB activation, and induction of mitochondria-mediated apoptosis in HCCLM3 cells [19]. There were statistically significant differences in plasma OPN levels between the HCC group and the other groups. Regarding the validity of plasma OPN was a predictor of fatty change, with 50% diagnostic accuracy, 70% sensitivity, 45% specificity, 50% positive predictive value, and 75% negative predictive value at a cutoff value of 134 ng/mL. The data indicated that plasma OPN level could be of diagnostic potential value in NAFLD [60].
Human hepatic satellite cells (hHSC) in the perisinusoidal space between sinusoids and hepatocytes are the predominant fibrogenic cells in liver tissues, and activated by liver cell injury to transdifferentiate from a quiescent state to proliferate matrix producing myofibroblasts [61, 62, 63]. The excessive production of extra-cellular matrix might result in cirrhosis occurrence. Human amphiregulin could increase the cell proliferation via EGFR, PI3K, and p38 mitogenic signaling pathways, inducing significantly up-regulation of fibrogenic biomarkers, confirmed by the mice NASH model that exhibited rapid progression of advanced fibrosis and HCC, with mimics histological, immunological and transcriptomic features of NASH, and a useful tool for preclinical drug testing [64, 65]. In addition, fatty liver as a pro-metastasis microenvironment with hHSCs could promote HCC migration and proliferation. Fasting and specific microRNAs could inhibit hHSC activation or potentiate anti-cancer activity of Sorafenib in HCC [66, 67].
Activated immune cells interact with cells in tissues by metabolic stress will migrate to liver and drive the progression from NAFLD to HCC. The dysregulation of lipid metabolism in NAFLD from mice models or human samples causes a selective loss of intrahepatic CD4+ but not CD8+ T lymphocytes, leading to accelerated hepatocarcinogenesis via cross-talk with liver cells [68, 69]. The NKT cells primarily cause steatosis in liver tissues via secreted a type II trans-membrane protein (a TNF ligand super-family member, TNFSF14), and both of CD8+ and NKT cells cooperatively induce liver injury by feeding choline-deficient high-fat diet [70]. CD4+ T lymphocytes have greater mitochondrial mass than CD8+ T lymphocytes and generate higher levels of mitochondrially derived reactive oxygen species (ROS) [71].
Disruption of mitochondrial function by linoleic acid, a fatty acid accumulated in NAFLD, causes more oxidative damage than other free fatty acids such as palmitic acid, and mediates selective loss of intrahepatic CD4+ T lymphocytes. Hepatic immune cells recognize cell injury or pathogen invasion with intracellular or surface-expressed pattern recognition receptors, subsequently initiating signaling cascades that trigger the release of factors promoting inflammatory response during NAFLD progression, demonstrating that the transition from NASH to HCC through liver cell lymphotoxin-β receptor (LTβR) and NF-κB signaling.
Polyploidization is one of the most dramatic genomic changes with rarely reported. The physiological events occur in liver development or adult life. However, the pathological polyploidization takes place in NAFLD, a widespread metabolic disorder that maybe is a risk factor for HCC. The liver parenchyma in NAFLD models displayed the process alterations with a large ratio of highly polyploid mononuclear cells, but was not observed in normal liver parenchyma. Biopsies from NASH patients revealed the alterations in hepatocyte ploidy compared with tissue from controls. Hepatocytes from NAFLD mice revealed that progression through the S/G2 phases of the cell cycle was inefficient and associated with activation of a G2/M DNA damage checkpoint, which prevented activation of the cyclin B1/CDK1 complex. The oxidative stress promotes the highly polyploid cells, and antioxidant- treated NAFLD hepatocytes resumed normal cell division and returned to normal state of polyploidy, indicated that oxidative stress promote pathological polyploidization in NAFLD that might contribute to HCC [74].
NAFLD is characterized by excess lipids in hepatocytes, due to excessive fatty acid influx from adipose tissue, de novo hepatic lipogenesis, in addition to excessive dietary fat and carbohydrate intake [44, 19]. Serious imbalance was found between limited antioxidant defenses and excessive formation of reactive species produced by liver oxidative stress such as ROS or RNS (reactive nitrogen species). Obese persons could increase free fatty acids uptake, stimulates FA oxidation for compensating excessive liver fat storage, and accelerate β-oxidation leads to increased production of ROS that damage mitochondrial membrane and DNA [75, 37].
Chronic lipid overload in hepatocytes induces mitochondrial oxidative stress or hepatocytes damage leading the NAFLD developing into a more severe liver disease condition, NASH, cirrhosis or HCC. Oxidative stress may induce endoplasmic reticulum (ER) dysfunction for liver malignancy. ER plays an important role in NAFLD pathogenesis, and consecutive increasing oxidative stress, inflammation and activation of NF-κB and JNK signaling pathways lead to the accumulation of intracellular lipids [76]. Extra-cellular signal-regulated protein kinase (ERK) is highly expressed in HCC via PIK13 activation. Among others, copper is one of the main bio-metals required for the preponderance of the enzymes involved in physiological redox reactions, which primarily occurs during mitochondrial respiration. Antioxidant food agents recognized to improve NAFLD and its complications have been described in the copper-related literatures [77, 78].
NAFLD is associated with insulin resistance (IR) leading to a resistance in the antilipolytic effect of insulin in adipose tissue with an increase of FFAs. The increase of FFAs induces mitochondrial dysfunction and lipotoxicity [79]. Liver steatosis defined as lipid accumulation in hepatocytes is very frequently found in adults and obese adolescents. Etiologically, obesity and IR or excess alcohol intake are the most frequent causes of liver steatosis. Insulin as a key hormone regulates lipogenesis and lipolysis in adipose depots. The adipose tissue becomes resistant to the antilipolytic effect of insulin and FA release is increased with lipolysis or lipid intake, promoting triglyceride synthesis with lipid accumulation occurrence in livers [80, 81].
Liver lipid accumulation causes IR by the activation of NF-κB pathway and leads to hyperinsulinemia to activate phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway, implicated the malignant transformation of hepatocytes or in hepatocarcinogenesis [82]. Hyperinsulinemia up-regulates insulin-like growth factor-1 that stimulates cell proliferation and inhibits cell apoptosis [83]. Insulin activates insulin receptor substrate-1 (IRS-1) with up-regulating expression in HCC [84]. The IRS-1-mediated related-signaling molecules may act as survival factors, promote liver cell proliferation via mitogen-activated protein kinase and PI3K, and protect against transforming growth factor β1-induced apoptosis in HCC progression [85, 86].
Liver is the main storage site for iron in the body because of its rich reticuloendothelial system [87]. Acquired hepatic iron overload is seen in a number of NAFLD patients. The dietary iron supplementation enhances experimental steatohepatitis induced by long-term high-fat diet feeding rats [88]. Excess liver iron may increase NASH risk and its progression to HCC [89, 90]. Abnormal iron deposition in liver is more frequent in NASH patients, in which necroinflammation may be the driving factor. Iron and the coexistence of hyperinsulinemia are risk factors for NASH development and together they may contribute to insulin resistance, disease progression and HCC. Iron reduction has been proposed as treatment for dysmetabolic iron overload syndrome and NAFLD or iron deprivation can suppress HCC growth
While tobacco and alcohol are established risk factors for HCC, the most common type of primary liver cancer [92]. Chronic alcohol intake results in the induction of liver cytochrome P450 2E1 leads to generation of ROS with direct or indirect carcinogenic consequences [93]. Many genetic factors regulating alcohol metabolism could predispose in developing alcoholic pancreatitis or cirrhosis. Some studies revealed that alcohol could be metabolized by oxidative and non-oxidative. The main oxidative pathway includes alcohol dehydrogenase, aldehyde dehydrogenase, and cytochrome P450 2E1. In addition, neurocan in neuronal tissue is also expressed in liver and the common polymorphism of its gene rs2228603 is associated with HCC in alcoholic liver disease [94].
Regulating control miRs are highly conserved, small non-coding RNAs (about 18–25 nucleotides in length) regulates transcription or translation of target genes and fatty acid metabolism. Both of miR-197 and miR-99 were associated with liver fibrosis in NASH patients. Altered miRNA expression was associated with activation of major hepatocarcinogenesis-related pathways, including the TGF-β, Wnt/β-catenin, ERK1/2, mTOR, and EGF signaling. The over-expression of the miR-221-3p and miR-222-3p and oncogenic miR-106b~25 cluster was accompanied by the reduced protein levels of their targets, including E2F transcription factor 1, phosphatase and tensin homolog, and cyclin-dependent kinase inhibitor 1. miR-93-5p, miR-221-3p, and miR-222-3p have been confirmed over-expressed in HCC. Aberrant expression of miRNAs may have mechanistic significance in NASH-associated liver carcinogenesis and may serve as an indicator for the development of NASH-derived HCC [94, 95].
Some studies found that miR-122 is a key regulator of glucose and lipid metabolism in livers [96] and significantly higher circulating miR-122, miR-34a, and miR-16 expression were found in NAFLD. During the development of NAFLD patients with simple steatosis to steatohepatitis, the serological levels of miR-122 and miR-34a were positively correlated with disease severity, liver enzyme activities, fibrosis staging, active inflammation, and silencing of microRNA-122 is an early event during hepatocarcinogenesis from NASH [97], suggesting that the alteration of circulating miR-122 could be an early event from NASH to hepatocarcinogenesis..
The development and progression of NAFLD are determined by environmental and genetic factors [10, 98]. The effect of genetic factors has been demonstrated by familial studies, twin studies and several cross-sectional studies. The data from the genome-wide association studies (GWAS) have shown that patatin-like phospholipase domain-containing protein 3 (PNPLA3) involved in metabolism of triglyceride on chromosome 22 is a genetic factor that promotes NASH development, and PNPLA3 gene variant I148M showed a strong relationship with the development and progression of NAFLD, NASH, and NAFLD-related HCC. Single nucleotide polymorphism (SNP, rs738409) is closely related to fatty liver involved in fibrosis progression of NAFLD. The C<G variation in SNP rs738409 also increases HCC risk in NAFLD patients [99, 100].
The whole exome sequencing finds that apolipoprotein B mutations (c.6718A>T, K2240X) represent a paradigm of rare variant influencing liver fat content and HCC risk. Besides, the Patatin-like phospholipase domain-containing 3 [the trans-membrane 6 superfamily member 2 (TM6SF2)] genes variant E167K was associated with NAFLD [101, 102]. Telomerase reverse transcriptase (TERT) mutations have been associated with hepatic steatosis. The deficiency of TERT can reduce the response to liver damage inducing the formation of steatosis and fibrosis. In conclusion, the occurrence of NAFLD-HCC seems to be influenced by common genetic variants as PNPLA3 and by rare genetic variants. Several genes have been proposed as candidate genes to be associated with NAFLD based on case–control studies [103].
NAFLD has become the most common chronic liver disease worldwide and is well-accepted that gut dysbiosis is associated with NAFLD [103]. The gut-liver axis has been proposed as a key player in the pathogenesis of NAFLD, as the passage of bacteria-derived products into the portal circulation could lead to a trigger of innate immunity, which in turn leads to liver inflammation. In intestine, there are trillions of microorganisms including bacteria, archaea, yeasts and viruses collectively called intestinal ecosystem through energy harvesting and fat storage [78, 104]. The relationship between gut microbiota and NAFLD is dependent on levels of choline, bile acid, larger production of endogenous ethanol, higher prevalence of intestinal dysbiosis, higher prevalence of increased intestinal permeability, bacterial translocation, pro-inflammatory molecules, endotoxemia, and cytokines. The hepatic manifestation of the dysregulation of insulin-dependent pathways leads to IR and adipose tissue accumulation in NAFLD patients with liver injury, indicated that the gut liver-axis is the way by which the bacteria and their potential hepatotoxic products (LPS, DNA, RNA, etc.) can easily reach liver [105, 106].
The interaction between the gut epithelia and some commensal bacteria induces the rapid generation of ROS. The main goal of any therapy addressing NASH is to reverse or prevent progression to liver fibrosis/cirrhosis [78]. Recently, a new isoform of human manganese superoxide dismutase (MnSOD) has been shown to be a powerful antioxidant capable of mediating ROS dismutation, penetrating biological barriers via its uncleaved leader peptide, and reducing portal hypertension and fibrosis in rats affected by cirrhosis [107]. Primary bile acids which derived from cholesterol become secondary bile acids under the action of intestinal microbes. If the bile acids bind to G-protein-coupled cell surface receptor (TGR5), it could inhibit inflammation via suppressing NF-κB pathway in macrophages. Many genetic and environmental factors have been suggested to contribute to the development of obesity and NAFLD, but the exact mechanisms might be the issue of further investigations [108, 109].
NAFLD has been implicated in some conditions such as IR, obesity, metabolic syndrome, hyperlipemia, hypertension, cardiovascular disease, and diabetes. Dietary or genetic obesity induces alterations of gut microbiota, thereby increasing the levels of deoxycholic acid, a gut bacterial metabolite known to cause DNA damage [78, 110]. Glyceraldehyde-derived advanced glycation end-products (Glycer-AGEs) are the predominant components of toxic AGEs (TAGE). More data suggested that TAGE with its receptor might change intracellular signaling, pro-inflammatory molecules gene expression, and also elicited the oxidative stress generation in liver cells including hHSCs. Circulating TAGE levels were significantly higher in NASH patients than those with simple steatosis or healthy subjects. Moreover, their TAGE levels inversely correlated with adiponectin. Increased lipid availability in livers might provide ATP and structural support for cancerous cell proliferation [111, 112].
Recent epidemiological studies have identified NASH, a progressive form of NAFLD, as a major risk factor for HCC. Elucidating the underlying mechanisms associated with the development of NASH-derived HCC is critical for identifying early biomarkers for the progression of the disease and for treatment and prevention [97, 113].
Liver derangements in lipid metabolism, importing FFA and manufacturing, storing, and exporting lipids could lead to NAFLD development [114]. The dysregulation of hormonal axes, mitochondrial carnitine palmitoyltransferase-II inactivity, and cytokines in NAFLD promotes a worse cycle between metabolic and inflammatory stimulus lead to malignant transformation of hepatocytes [33, 71]. The majority of NAFLD patients had steatosis about 20% present as NASH that was defined by microscopic finding, and consists of liver injury, steatosis, parenchymal and portal inflammation, and different fibrosis. Alterations of miRNA in hepatocarcinogenesis were associated with TGF-β, Wnt/β-catenin, ERK1/2, mTOR, and EGF signaling pathways. Importantly, miR-93-5p, miR-221-3p, and miR-222-3p were also significantly over-expressed in human HCC. Aberrant expression of miRNAs might have mechanistic significance in NASH-associated liver carcinogenesis and serve as an indicator for the development of NASH-derived HCC [115, 116].
Hepatic lipid accumulation is accompanied by distinct patterns of perilipin expression, suggested that abnormality of hepatic lipid accumulation might promote hepatocyte malignant transformation [33]. The levels of high leptin and low adiponectin are hallmarks of obesity and involved in NAFLD and carcinogenesis [117]. Obesity-promoted HCC occurrence was dependent on increasing IL-6 and TNF levels, which resulted in liver inflammation and oncogenic STAT3 activation. The long-term chronic inflammatory in obesity plus higher IL-6 and TNF might be the risk factor for HCC [118]. The prospective studies (25,337 patients with HCC) demonstrated that both of excess body weight and obesity in males or females are related to an increased risk factor for HCC occurrence [119]. The prospective studies with longer follow-up periods should screen the malignant transformation of hepatocytes with specific biomarkers among NASH or NAFLD populations [3, 120].
In the past decade, the discussion of substantially NAFLD increased by hypernutrition and HCC had become a cocktail party cliché, and its impact on public health cannot be dismissed. With both relationship gradually deepening, more and more evidences have supported that NAFLD might promote the malignant transformation of hepatocytes because of liver lipid accumulation, its toxicity, endoplasmic reticulum dysfunction, IR, and abnormal fat metabolism. Although the exact mechanisms from NAFLD tumor-promoting mechanism triggered by hypernutrition remain to be explored [121], however, the patients with the excessive fat deposition feeds this tumor-promoting inflammatory flame and should be treated in time to avoid the occurrences of hepatocyte malignant transformation [7, 122].
This work was supported by the part grants from the Key Program of Jiangsu Province (BE2016698), the Projects from the National Natural Science Foundations (31872738, 81673241, 81702419), and the International Science & Technology Cooperation Program (2013DFA32150) of China.
CPT | carnitine palmitoyltransferase |
HBV | hepatitis B virus |
HCV | hepatitis C virus |
HSC | hepatic satellite cell |
IL-6 | interleukin-6 |
NAFLD | non-alcoholic fatty liver disease |
NASH | nonalcoholic fatty hepatitis |
NF-κB | nuclear factor kappa B |
MiR | microRNA |
OPN | osteopontin |
HCC | hepatocellular carcinoma |
PNPLA | patatin-like phospholipase domain-containing protein |
ROS | reactive oxygen species |
SREBP | sterol regulatory element-binding protein |
TAGE | toxic advanced glycation end-products |
The poultry industry has witnessed significant improvements over the past several decades achieving higher market weight with improved feed efficiency, thus reducing production cost. During the past 60 years, the amount of time and quantity of feed per pound of meat required to reach broiler market weight had been reduced by 50% [1]; furthermore, according to the National Chicken Council [2], modern broiler chickens can achieve market weight 16 days earlier with 35% higher weight compared to the 1960s broiler chicken. These improvements have resulted from a combination of genetic improvement and progress in nutrition and poultry management.
The U.S. is considered the world’s largest producer of poultry meat; the U.S. provides approximately 17% of the global poultry meat output, followed by Brazil and China, mainly dominated by broiler meat followed by turkey meat and a small fraction for other poultry meat. The production and consumption of poultry meat have increased rapidly worldwide and are expected to continue to grow [3] due to its relatively low price compared to other meats, the absence of cultural or religious obstacles, and its dietary and nutritional properties as it has lower fat, cholesterol, and sodium content [4] with an increased preference of white chicken meat [5, 6].
Additionally, consumers have shifted from the consumption of whole chicken toward portioned (especially breast fillets) and further processed products [7, 8]. These changes were driven by the need for convenience with meal preparation in a fast-paced industrialized era and meeting consumer preference of specific carcass parts. The poultry industry has responded to these changing demands by further enhancing genetic selection for increased breast yield, faster growth rate, and improved feed efficiency. Meanwhile, feed cost has increased, and ethanol production has forced producers to use alternative feed ingredients such as the distiller\'s dried grains with solubles (DDGS) produced as byproducts of ethanol production. However, since the selection of broiler chickens initially focused on increasing growth performance and improving body composition [9], this has led to indirect and often deleterious effects on meat quality traits, such as excessive deposition of abdominal fat, the formation of which represented the inefficient use of feed [10, 11]. Coincidently, several studies have shown an increased incidence of abnormalities, mainly in breast muscles [12, 13]. In the early 1980s, Wight and Siller [14] recognized an abnormal condition in the pectoralis minor, in which the muscle is basically “suffocated” leading to ischemic necrosis; this condition known as deep pectoral muscle myopathy is only the first in a list of fast-growth-related muscle abnormalities that eventually affect meat quality and its functional properties.
In poultry meat, appearance and texture have been considered the two most important attributes responsible for initial consumer meat evaluation and final product acceptance [15], so consumers are expected to reject meat with observed defects such as bruises and hemorrhages. Several appearance defects have been reported in the poultry industry, such as pinking of raw and cooked meat, bone darkening, red/bloody discoloration, white striping, wooden breast, spaghetti meat, and pale, soft, exudative appearance of breast meat. However, many of the underlying causes of appearance defects have not been fully explained. Understanding the structural organization of the muscle fibers and physiology can help in explaining some of these defects.
The basic structural unit of a muscle has been defined as the muscle fiber, which is constituted of several myofibrils (contractile units). Each muscle fiber is surrounded by a connective tissue called the endomysium; muscle fibers are then grouped into fascicles and surrounded by another layer of connective tissue called the perimysium. Then, the whole muscle is made up of a group of fascicles and surrounded by epimysium that connected the muscle to bones. Collagen is the major constituent of these connective tissues. These connective tissues influenced muscle development and subsequent meat quality.
Skeletal muscles growth was achieved by increasing the size of preexisting muscle fibers (hypertrophy). The number, size, and type of fibers vary with the function and anatomical location of the muscle. Meat quality is also affected by these factors. A muscle that contained high proportion of oxidative fibers tends to have red color due to a greater amount of myoglobin (e.g., thigh muscles) as compared to glycolytic fibers, which tended to appear white in color, which affected the appearance of muscle/meat (e.g., chicken breast muscle). Glycolytic fibers are larger and have lower rate of protein turnover. Therefore, the white muscles are larger and more efficient. In poultry, genetic selection for increased breast yield resulted in pale breast meat color in broilers [16], ducks [17], and turkeys [18], which could result in poor meat quality.
Collagen is the most abundant protein in the body and in connective tissues. The structure of collagen supports its function of providing strength to muscle and other tissues with more than 20 different types of collagen identified in vertebrates [19]. Glycine constitutes about one-third of all the amino acids found in collagen, while proline, which has been classified as an imino acid, and its analog hydroxyproline also constituted about one-third of all amino acids in collagen [20]. Lysine has been considered to be another constituent of collagen where both proline and lysine are covalently modified to hydroxyproline and hydroxylysine, respectively. A collagen molecule (tropocollagen) is composed of three left-handed polypeptide helices coiled around each other to form a right-handed supercoil where glycine is found at every third residue [19].
The strength of the collagen fibrils is due to the covalent bonds formed between and within tropocollagen triple helices, where collagen is cross-linked by lysine side chains that contribute to the strength of the collagen in meat, which has an essential role in the development of meat tenderness [21]. Furthermore, in a recent study, it has been shown that muscle with spaghetti meat abnormality had an altered immunoreactivity to specifically procollagen type III (precursor of collagen type III) suggesting a possible defect in the collagen turnover and synthesis process [22], while Sanden et al. [23] reported that spaghetti meat has poorly packed thin, loose, and immature collagen fiber bundles.
The process of converting muscle to meat in poultry starts immediately upon sacrificing the bird. Exsanguination results in blood/oxygen supply removal, during which the muscle tries to maintain its functions even after oxygen depletion through the anaerobic glycolysis of its glycogen reserves to produce adenosine triphosphate (ATP), but in the absence of blood supply to remove waste, the accumulated heat and lactic acid in the muscle decreases the pH. Owing to ATP depletion, the muscle remains contracted due to actin and myosin binding that leads to muscle stiffness (rigor mortis). This marks the onset of rigor mortis and the conversion of muscle to meat, where muscle proteins start to denature due to high temperature and low pH. Temperature and pH are the main postmortem factors influencing meat quality through affecting the onset and progression of rigor mortis and subsequent resolution [24, 25, 26, 27]. During resolution, the proteolysis of Z-disk proteins takes place, and myofibrillar proteins degrade into myofibrillar fragments by proteolytic enzymes that affect meat tenderness. In chickens, the process of converting muscle to meat has been found to start immediately after slaughter and be resolved within 2–4 h. The extent of meat tenderization postmortem could be altered by the conditions under which the meat is processed. Factors include temperature and chilling duration, deboning time, postchill aging/holding duration, and marination.
Meat quality is a collective term used to describe the indicators of a meat product wholesomeness and freshness, such as color, texture, flavor, pH, and juiciness. The two most important quality attributes for poultry meat are appearance and texture since they influence the initial consumer selection of a product as well as final satisfaction [15]. Appearance quality attributes include skin color, meat color, and appearance defects such as bruises and hemorrhages. Any deviation from a normal appearance would result in meat product rejection, subsequently leading to consumer complaints. Despite the importance of these quality attributes, the poultry grading system used is still based on aesthetic attributes, such as conformation, presence or absence of carcass defects, bruises, missing parts, and skin tears, without taking into consideration the functional properties of meat [28], which have been important for the further processing industry that was mainly interested in the functional properties of meat; the importance of incorporating functional properties and quality indicators is becoming increasingly important as the recent muscle myopathies not only affect consumer acceptance based on appearance but also the quality of further processed meat manufactured using meat with such defects.
Many factors influence poultry meat quality, including sex, strain, age, environmental factors, exercise, diet, and processing practices mainly focused on chilling, deboning time, marination, and electrical stunning [29, 30, 31, 32].
Another important quality attribute that influences customer perception is the tenderness of the meat. This attribute comes second after appearance; consumers usually correlate acceptable appearance with better quality and tenderness. Tenderness development is a function of myofibrillar protein denaturation, connective tissue content, and juiciness. Deboning time, age, and strain are some of the major factors that affect poultry meat tenderness [31, 33]. Lyon and Lyon [34] reported that as the time before deboning increased from 0 to 24 h postmortem, consumer acceptability of the meat texture increased, with fillets deboned at 0 and 2 h postmortem considered tough by a consumer panel, and samples deboned at 6 and 24 h postmortem considered slightly tender to moderately tender. Liu et al. [35] reported a decreased shear force of chicken breast as deboning time increased from 2 to 24 h postmortem. Similar results were also reported by Cavitt et al. [33].
Furthermore, Mehaffey et al. [8] reported that fillets deboned 2 or 4 h postmortem from broilers raised to 7 weeks were significantly tougher than those raised to 6 weeks, indicating that age affected tenderness when deboning was performed shortly after harvest. Northcutt et al. [31] reported that breast fillets harvested at less than 2 h postchill aging were tenderer when taken from broilers slaughtered at 42 or 44 days of age than those harvested from birds 49 or 51 days of age, irrespective of any sex effect. On the other hand, Young et al. [36] reported that females had greater fillet yields than males.
Connective tissue content has been reported to increase with age and is correlated with tenderness; as mentioned earlier, collagen is the most abundant protein in the body, making up the majority of the connective tissue proteins [37, 38]. In young broilers (6–8 weeks), it is expected that connective tissue would not affect tenderness since mature cross-links should have not yet formed between tropocollagen molecules, which are the structural units of the collagen fibril. On the other hand, the contraction of myofibrillar protein, which depends upon time and rate of rigor mortis development after the bird is sacrificed, is related to processing rather than intrinsic factors [15]. Furthermore, tenderness, indirectly associated with connective tissue, is one of the quality attributes that are negatively affected by the emerging muscle myopathies emphasizing the importance of further investigating and attempting to mitigate the negative impacts.
Another important meat quality attribute is meat juiciness, or water-holding capacity, which refers to the ability of raw meat to retain its inherent water during force application and/or processing [39]. Water in muscle has been divided into three general types: bound, immobilized, and free. Bound water is held tightly via myofibrillar protein charges and represents 4–5% of water in muscle [39, 40]; it is resistant to freezing and could only be removed by severe drying processes, not including conventional cooking [41]. Immobilized water is found within the muscle ultrastructure (within the space between actin and myosin), but it is not bound to myofibrillar proteins as in the case of bound water. Immobilized water accounts for the largest portion of muscle-bound water (88–95%). Finally, free water is held within muscle by weak capillary forces [42].
Poultry has been determined to be the only species known to have muscles/parts with apparent differences in color, as meat from poultry has been classified as either white or dark. In chicken, fresh raw breast meat is expected to have a pale pink color, while the raw thigh and leg meat are darker and redder. Meat color plays a significant role in consumer purchase decisions [43, 44, 45]. Consumers tend to associate color with flavor, tenderness, safety, storage time, nutritional value, and satisfaction level [46], and as an indicator of freshness and wholesomeness.
Meat color is what the human eye sees as light is reflected from the meat surface. Poultry meat absorbs most blue and green color spectra and reflects most of the yellow, orange, and red color spectra, which is what the human eye perceives.
The most commonly used colorimetric scale is the CIE Lab [47], even though other color scales have been used, such as the Hunter L, a, b, and YXZ space. However, the accuracy of these instruments has depended upon thickness, background color, and illuminant wavelengths [48, 49].
The CIE Lab system components measures include L* that refers to lightness and has a range from 0 to 100 (black to white), component a* had a range from –60 to +60 (green if negative to red if positive), and b* has the same range as a* (blue if negative to yellow if positive) [50, 51]. Another more recent system used for color measurement is the computer vision system, which has been shown to give reproducible results with the ability to measure the color of the entire sample instead of specific spots, as has been the case with widely used colorimeters [52]; in fact, Tomasevic et al. [53] recommended using computer vision program as a superior approach for poultry color determination.
Meat color is mainly related to the myoglobin pigment present in the muscle fibers. Myoglobin consists of a protein (globin) and a nonprotein heme ring, which has an iron molecule in its center. Iron can bind one of several ligands (e.g., oxygen, carbon monoxide, and nitric oxide) on its sixth coordination site. The forms of myoglobin (deoxymyoglobin, oxymyoglobin, carboxymyoglobin, and metmyoglobin) differ depending upon the ligand bound to iron and on the redox state of the iron. Thus, myoglobin and iron states are the two main ways through which meat color changes.
Myoglobin (or deoxymyoglobin) has a red-purple color in its nature when not bound to any ligands; the state of myoglobin changes to oxymyoglobin when oxygen is present and to carboxymyoglobin when carbon dioxide is present. In both the forms, the color is bright red (bloom), and iron is in the reduced ferrous form (Fe++). The oxidation of myoglobin changes the form to metmyoglobin and the iron to the oxidized ferric form (Fe+++), which has a brown color. These myoglobin color changes are reversible; however, if heat-treated, metmyoglobin becomes denatured and color changes irreversibly to grayish-brown. Curing with nitrites/nitrates causes an irreversible color change to red color that, upon heating, converts to pink. The replacement of iron with zinc results in a stable red color of myoglobin due to the formation of Zn-protoporphyrin IX (ZPP), which has been shown to give Parma ham its stable, bright red color [54, 55]. Within a chicken carcass, chicken breast muscles are mainly composed of white fibers (glycolytic) that have low myoglobin content. Thus, breast meat appears white, while thigh muscles are composed of red fiber (oxidative) and appears darker. Fleming et al. [56] reported a myoglobin concentration of 0.16 and 0.30 mg/g in broiler breast and thigh muscles, respectively. Furthermore, Miller [57] said a lower myoglobin content of 0.01 and 0.40 mg/g in white and dark meat of 8-week-old broilers, respectively.
Froning [58] classified the factors influencing meat color into three main categories (Table 1). Smith et al. [59] investigated the effect of age, diet (carbohydrate source), and feed withdrawal on broiler meat color by slaughtering birds each day from 42 to 45 and 49 to 52 days of age with a carbohydrate source that was either corn, milo, or wheat, with feed withdrawal times of either 0 or 8 h. Color was not affected by age. Still, feed withdrawal increased fillet lightness (L*) from an average of 46.1 to 48.9, decreased redness (a*) from 4.1 to 3.1, and increased yellowness (b*) from 2.8 to 3.7. Fillets from the birds fed the wheat diet were lighter than fillets from the corn or milo fed birds. The milo diet resulted in redder fillets than corn or wheat diets, while the corn diet produced more yellow fillets than milo or wheat diets.
Heme pigments |
|
Preslaughter factors |
|
Slaughter, chilling, and further processing |
|
Factors influencing poultry meat color [58].
In addition to meat color, skin color has been considered a critical quality attribute, mainly in a whole carcass and skin-on cuts sale. The color of poultry skin has varied from cream-colored to yellow. This variation is primarily the result of genetic variation and natural pigments in feed. Birds had differed in their ability to deposit the black melanin pigment in the epidermis and dermis layers of the skin and varied in their ability to deposit carotenoids from the feed as the combinations of different amounts of melanin and carotenoids produced different skin colors. However, in commercial strains, the ability to deposit melanin has been eliminated through genetic selection. Different skin colors as adopted from [60] are illustrated in Table 2.
Skin color | Dermis | Epidermis |
---|---|---|
White | None | None |
Black | Melanin | Melanin |
Yellow | None | Xanthophyll |
Green | Melanin | Xanthophyll |
Blue (Slate) | Melanin | None |
Combination of possible skin colors due to dietary xanthophyll deposition in epidermis or melanin production in either dermis or epidermis [60].
However, considerable variation in color and discoloration of poultry meat has occurred and remains of great concern for the industry. Discoloration may occur in the entire muscle or only in a portion of a muscle due to bruising or broken blood vessels [58]. Possible poultry color defects are presented in Table 3.
Defect | Description | Possible causes |
---|---|---|
Bruises and hemorrhages | Classic bruises, pin-point blood spots in meat, blood accumulation along bones and in joints | Physical trauma, nutrient deficiencies, mycotoxins, stunning |
Overscalding | Incomplete removal of epidermis, cooked discoloration on surface of meat | Too high scalding temperature, too long in scalder |
Surface drying | Mottled appearance of skin or meat due to surface dehydration | Incomplete removal of epidermis, exposed meat, poor packaging, freezer burn |
Heme reactions | Normal color ranges from raw pink meat, tan to brown raw meat, grey to brown cooked meat, pink cooked meat, cured meat color | Oxidative or redox state of the myoglobin, myoglobin complexing with nitrates/nitrites or other compounds such as carbon monoxide |
Dark meat | Darker than normal appearing meat, possible mottling | High muscle pH due to antemortem depletion of muscle glycogen |
Light meat | Pale breast meat | Low muscle pH (PSE-like condition) |
Dark bones | Dark brown to black bones | Freezing, blood accumulation around bone |
Summary of poultry color defects [60].
The pinking of cooked white meat has been an undesirable color defect found in poultry; its occurrence was noticed sporadically and has negatively influenced consumer purchasing decisions (Maga, I994). According to Maga [61], pink color might have resulted from the presence of high levels of myoglobin that were not completely denatured during heat processing, incidental nitrate/nitrite contamination either in feed or water or during processing. The presence of carbon monoxide and nitric oxide gases in oven gas while roasting has caused pink color on the surface of turkey meat, with carcasses from younger turkeys more susceptible than older ones [62]. The proposed mechanism for pink color development of fully cooked is related to the ligands to which the denatured myoglobin was bound, such as amino acids, denatured proteins, and nitrogen-containing compounds that form denatured hemochromes globin. Therefore, depending on the ligand to which the denatured heme will bind, different pink shades would result.
Binding of nitric oxide to myoglobin from preslaughter contamination (feed and water and gases from the truck exhaust) or during/after processing (processing water, ice, spice mix, and oven gas) has formed the pink nitric oxide myoglobin that, upon cooking, was converted to pink nitrosohemochrome. Furthermore, carbon monoxide binding to myoglobin has led to pink carboxymyoglobin developing upon cooking in oven gases or during irradiation.
Cooking meat harvested from birds before rigor mortis resolution could also cause pink color when meat is cooked when pH was higher than 6.0. At this high pH, myoglobin is not denatured, and cytochrome C (electron transport protein), which is heat stable, increases and contributes to the delayed denaturation of myoglobin since cytochrome C is still able to deliver electrons to myoglobin. Ahn and Maurer [63] showed that a pH above 6.4 leads to binding of myoglobin and hemoglobin with most naturally present ligands, such as histidine, cysteine, methionine, nicotinamide, and solubilized proteins, which leads to pink color of the meat. At high pH, amino acids and protein ligands can donate electrons to Fe, resulting in stable pink ferrohemochrome. High pH also reduces the susceptibility of meat pigments and lipids to oxidation resulting in a cooked pink color [64].
Bone darkening has been described as a dark reddish brown or black discoloration on the surface of bone and muscle adjacent to the bone after cooking. The darkening was due to bone marrow passing from inside the bone onto the bone surface and adjacent tissue, usually after freezing the meat [65, 66] and after cooking of the frozen meat [67]. Lyon and Lyon [30] described the variation in bone discoloration due to different preparation methods (precook, freeze, and reheat). They found that freezing before cooking increased the severity of discoloration more than cooking followed by freezing and reheating. Lyon et al. [65] demonstrated that meat and bone darkening of thigh pieces was related to pigment migration from the femur to muscle tissue. The commercial further processing industry has reported that redness was usually accompanied by blood in bone-in chicken carcasses and parts, which consumers could reject as the product appears undercooked and unsafe for consumption [59].
The migration of pigments from the femur to muscle tissues has created darkening that was more prevalent in younger birds since their bones were less calcified, were more porous, and had more red marrow than older birds. The epiphysis of long bones in older birds is more calcified than young birds, so the pigment is more difficult to escape from bones onto surrounding tissue. However, bone darkening only affects the appearance and not the organoleptic properties of the meat product [67].
Smith and Northcutt [59] studied discoloration prevalence in commercially fully cooked breasts, thighs, and drumsticks from various market sources. They speculated that about 11% of products could face consumer complaints or rejection since they were severely discolored. Furthermore, cooking chicken breast samples with bone marrow collected from femurs increased the darkness and redness of both raw and cooked broiler meat [68].
Red and/or bloody discoloration of poultry meat, raw or cooked, has been a chronic yet sporadic problem for the poultry industry. Raw breast meat with red discoloration is objectionable to many customers, and cooked white or dark meat with red defect is unacceptable to consumers due to the perception that it is undercooked. Red discoloration of white meat is closely related to bone darkening but with higher redness. Little research has been available concerning this red discoloration defect in poultry meat [59]. According to Smith and Northcutt [66], bone marrow is an effective inducer of red, bloody discoloration in breast meat samples. In a previous investigation conducted concerning the color of different parts of chicken, Lyon et al. [65] reported that the initial color of breast was lighter and less red than thighs because breasts had a lower proportion of total bone area to muscle mass, fewer large, calcified bones, a lower proportion of blood vessels per muscle mass (less hemoglobin), or lower myoglobin content than thighs or drums [66].
The bright red color development has been investigated in Parma ham, where this north Italian traditional dry-cured ham “Prosciutto di Parma (Parma ham)” has been made from only the legs of fattened pigs and was salted with sea salt, dried, and matured over 1 year [69]. It was initially postulated that sea salt used was contaminated with nitrate/nitrite. However, that was later investigated, and results showed that this pigment was also formed in a nitrate/nitrite-free environment and that endogenous enzymes as well as microorganisms were involved in this pigment formation [54, 55]. These results suggested that the bright red color in Parma ham is caused by Zn-protoporphyrin IX (ZPP), in which the iron in heme was substituted by zinc heme separated from the native heme protein. Investigations on this lipophylic myoglobin derivative showed that it was a stable red pigment that increased with aging [70]. This process has now been patented for producing red pigments for food use that were heat-stable [71]. The addition of salt accelerated the reaction and increased redness [72]. The process has also occurred in live animals, including humans, as lead poisoning and iron deficiency caused an increase of ZPP in blood as zinc replaced the iron in hemoglobin. The level of ZPP can be evaluated with a simple screening test using a hematofluorometer. The measurement of ZPP has been used with ducks to test for lead poisoning [73]. An increased ZPP/heme ratio indicates that Zn has replaced Fe in the heme, thus changing the color of hemoglobin and myoglobin. Based on findings in Parma ham, ZPP may be responsible for the red discoloration in poultry meat, which could be formed in myoglobin found in muscles or hemoglobin stored in bone marrow. Thus, ZPP leaking out of the bones could cause the increased stable redness observed in white meat.
Green discoloration of live muscles, raw meat, and cooked deli products can be produced by various mechanisms that lead to condemnation by the industry and consumers. In live muscles, green muscle disease (deep muscle myopathy) is caused by the lack of blood supply to the deep pectoral muscle that results in the death of the muscle fibers, thus giving the muscle a green appearance. The bruising of live birds has caused a rupture of blood capillaries and blood accumulation under the skin or in the meat. The color of the bruise subsequently developed over time and turned either yellow or green depending upon heme degradation. Using lactic acid as a decontamination approach resulted in the greening of chicken skin color [74]. The irradiation of fresh beef and pork meat has been thought to affect the stability of iron in the myoglobin and cause the breakdown of the porphyrin molecule and/or the formation of sulfmyoglobin that caused green pigments to appear [75].
In cooked meat, contamination with microorganisms such as Pseudomonas fluorescens has produced a shiny transparent greenish exudate on the meat surface due to microbial degradation of the heme pigment. In sausage-type products, the presence of green rings is an indicator of microbial contamination where the microorganisms oxidized the heme pigment before applying thermal treatment.
Iridescence, which is the appearance of a green-orange color on the surface of meat products such as deli meat, is mainly associated with the meat surface microstructure that could be interpreted as a color diffraction problem related to the ability of certain muscles to split the white light into its component. Thus, the reflection of the meat surface would appear in green-orange. If a sharp knife was used to cut the meat, the smooth surface resulting from the cut causes this color diffraction, but if a dull knife was used instead, this problem would be eliminated.
Deep pectoral muscle myopathy, also known as green muscle disease and Oregon disease, was first identified in turkeys [76] and later in broiler breeders [77] and 7-week-old broiler chickens [78]. This disease affected the wing elevating muscle (
The pectoralis minor muscle is confined in a tight space between the sternum and the pectoralis major muscle (large breast fillet). It is also encased in a rigid fibrous sheath that restricts any increase in muscle volume in response to any physiological changes caused by muscle exercise such as wing-flapping [79] which requires increased blood flow to supply the oxygen and nutrients needed by the muscles. The incidence of green muscle disease has also been reported to be higher in high yielding crosses, especially males.
On the other hand, the incidence of focal pectoral myopathy has increased, and it has been associated with increased growth rate and muscle size [12, 80]. Further investigation is required to determine the causes of this muscular defect since focal myopathy has an even more detrimental effect on the poultry industry. It has affected the pectoralis major muscle leading to consumer complaints and industry economic loss.
The incidence of pale, soft, and exudative (PSE) meat has been well-documented in swine, where meat has a very light gray color, soft texture, and cannot hold water [81, 82]. This condition has been associated with heavy muscling [83]. In poultry, similar PSE characteristics have been reported in turkey meat [84, 85], chickens [86, 87], and ostriches [88]. However, it is more difficult to distinguish and identify these characteristics in poultry meat compared to pork. This condition has been referred to as PSE since characteristics were similar to PSE in pork, which is misleading since both conditions were not exactly the same. Poultry researchers have preferred to refer to the condition in poultry as “PSE-like” or “Pale poultry muscle syndrome” [86, 89]. The PSE and PSE-like conditions are detrimental to the industry profitability since it affects important meat quality attributes involved in the production of value-added products and further processed meat. Affected muscles have been reported to lose their rheological properties and become unable to hold water. For example, mortadella prepared with PSE-like chicken meat has reduced water-holding capacity, altered texture, diminished emulsion stability, and required additives to restore the functional properties of normal meat [90]. In addition, poultry processors have been concerned with the appearance of PSE-like meat in fresh tray packs. The pale color affected color uniformity within the package and, thus, consumer acceptance. The occurrence of PSE-like in poultry meat has been believed to be the result of accelerated postmortem glycolysis (rapid pH decline), while the carcass was still warm [91]. In poultry, normal pH values at 15 min postmortem (pH15) are around 6.2–6.5 [92, 93], whereas normal ultimate pH (pHu) values are approximately 5.8 [60, 88, 94]. If the pH15 value is low (below 6.0) when the muscle is still warm, the proteins are subject to denaturation, which leads to a decreased water-holding capacity and a lighter color of the meat.
The reasons for PSE-like condition have remained unclear, but up to 30% of broiler breast meat and up to 40% of turkey breast meat have shown this defect in commercial processing plants [95, 96, 97]. Furthermore, it has been reported that the occurrence of PSE-like meat in birds may be affected by alteration to the intracellular calcium homeostasis caused by a mutation in the ryanodine receptor gene, which is different from the ryanodine receptor gene in swine, and also depends upon the several aspects of preslaughter and postslaughter management practices [98, 99]. It is thought that the application of “snow chilling” with carbon dioxide intensified meat quality abnormalities [100]. In addition, other factors have been thought to contribute to this problem, such as heat stress during the finisher period or the preslaughter period [86], and stress and struggling before slaughter [101].
Differentiating PSE-like meat from normal meat has been based on the instrumental or visual assessment of color lightness (L*). However, the cutoff value for classifying meat as PSE-like has differed among researchers. Petracci et al. [102] considered an L* value of 56 as the cutoff, while Barbut [28, 103, 104] suggested classifying turkey breast meat as PSE-like when L* values were greater than 52 at 24 h postmortem. Fraqueza et al. [105] classified breast meat as PSE-like when the L* was greater than 50 and pHu was less than 5.8, while Woelfel et al. [106] used L* values greater than 54 in broilers as their standards.
Using L*
White striping, woody breast, and spaghetti meat can be collectively referred to as the myopathies of modern broiler. These nomenclatures were simply based on the appearance of the defective muscles. White striping is a condition described in broiler chickens and characterized by white striations parallel to the direction of muscle fibers on both breast fillets and thighs of broilers. White striping is considered to be an emerging issue by the poultry meat industry that could be associated with enhanced growth rate and heavier body weight in birds [110, 111, 112], especially in the age of 6–8 weeks [110], and higher fat content in broiler breast fillets [111]. The incidence of white striping was evaluated under commercial conditions, and the overall incidence in broiler breast meat was 12.0%, of which 3.1% had severe striping [113]. It is possible that the intense selection for rapid growth rate in birds could have accidentally been accompanied by the selection for inadequate capillary/fascial growth or muscle fiber defects leading to myopathic changes referred to as growth-induced myopathy [13], under which these three different myopathies can be classified.
The precise etiology of white striping has not been defined yet [114]; however, several speculations have been reported. In turkeys, Wilson et al. [80] reported that rapid growth rate may have led to the limited ability of muscle support systems leading to a condition called focal myopathy, which affected the major pectoral muscle.
Ischemia could also result from a rapid growth rate and lead to muscular damage in turkeys [115]. It is also possible that reduced oxygen supply to breast muscle resulted from lower capillary density in fast-growing chickens [116]. A higher growth rate could also lead to defective cation regulation in muscles leading to an increased sodium, potassium, magnesium, and calcium in muscle tissue [117]. An increased level of calcium in muscle tissue could initiate several tissue changes, including the activation of intracellular proteases or lipases resulting in myopathic changes [13, 118, 119, 120]. Kuttappan et al. [114] reported that breast fillets showing severe white striping had reduced protein content and myopathic lesions, while Petracci et al. [113] observed poor cohesion beneath the striation area.
Poultry producers started noticing and complaining about woody breast in the late 1990s [12, 121]. The woody breast muscle is usually characterized by increased firmness in all or parts of the pectoralis major muscle that can start in the live birds and can be detected by palpating the breast muscle. Sihvo et al. [121] reported that woody breast might result from fibrosis, which leads to an accumulation of interstitial connective tissue. This myopathy affects consumer acceptability and meat quality; even when trying to mitigate by diverting to further processed poultry products, woody breast meat is still required to be mixed with normal meat to maintain the quality of the further processed product [122, 123].
Spaghetti meat, or previously known as mushy breast, is the most recent emerging myopathy of breast meat in poultry. As the name implies, the breast muscle loses its structure and firmness. One distinct feature the spaghetti meat has that would differentiate it from white striping and woody breast is the loss of endomysial and perimysial connective tissue that compromises the fiber bundles cohesion, coupled with a loose connective tissue deposition [124] leading to the separation of the fascicles into “spaghetti” strings.
Sanden et al. [23] investigated the collagen of muscles with either woody breast or spaghetti meat abnormalities. They showed that collagen in woody breast muscle was a mix of thin and thick fibers, whereas spaghetti meat had thinner, fewer, and shorter. However, both myopathies generally resulted in a higher content in connective tissue (mainly in perimysium) compared to normal muscle.
Several researchers have investigated these myopathies to understand their etiology and effect on meat products quality [114, 121, 124, 125]. It is believed that cellular stress and hypoxia (ischemia) caused by muscle hypertrophy are the main triggering factors behind white striping and woody breast, in addition to being strapped within a relatively rigid connective tissue that limits the hypertrophy capabilities. However, what is interesting is that spaghetti meat, where the opposite issue is faced concerning connective tissue, started appearing. It is possible that geneticist, while trying to reduce the rigidness of the connective tissue, led to the emergence of the most recent abnormality of spaghetti meat, which is worth investigating in the future with poultry strain companies.
Researchers have investigated multiple factors that may have either contributed or helped in eliminating the emerging myopathies starting at different incubation conditions [126] all the way to management during growing [127, 128] and nutritional manipulations [129, 130, 131, 132, 133].
Several white muscle defects and myopathy have been reported. According to the literature, these problems spiked in the 1970s and 2000s concurrent with increased feed prices. It was suggested that producers were driven to use less expensive feed and use alternative feed ingredients (e.g., DDGS) to control costs. One significant consequence of feeding less expensive feed was that the essential amino acids (e.g., lysine and methionine) became a primary concern when formulating these diets, while the nonessential amino acids (e.g., arginine, glycine, and proline) were neglected despite their essential role in connective tissue formation, which may have contributed to the emerging of muscle defects as genetics for enhanced growth and muscle accretion were improved even further.
The spectacular advancements in genetics witnessed by the broiler industry have resulted in broilers with a higher growth rate, while the role of nutrition has become even more critical in supporting the increased growth demands of what may have become a relatively fragile animal. Profit-driven decisions about formulating feed in a least-cost manner while neglecting the essentiality of nonessential amino acids in nutrition would eventually be evidenced by increased condemnation at the processing plant and increased consumer complaints.
"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges".
\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.
",metaTitle:"About Open Access",metaDescription:"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges.\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.",metaKeywords:null,canonicalURL:"about-open-access",contentRaw:'[{"type":"htmlEditorComponent","content":"The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\\n\\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\\n\\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nOAI-PMH
\\n\\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\\n\\nLicense
\\n\\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\\n\\nPeer Review Policies
\\n\\nAll scientific works are Peer Reviewed prior to publishing. Read more
\\n\\nOA Publishing Fees
\\n\\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\\n\\nDigital Archiving Policy
\\n\\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\\n\\nOpen Science is transparent and accessible knowledge that is shared and developed through collaborative networks.
\\n\\nOpen Science is about increased rigour, accountability, and reproducibility for research. It is based on the principles of inclusion, fairness, equity, and sharing, and ultimately seeks to change the way research is done, who is involved and how it is valued. It aims to make research more open to participation, review/refutation, improvement and (re)use for the world to benefit.
\\n\\nOpen Science refers to doing traditional science with more transparency involved at various stages, for example by openly sharing code and data. It implies a growing set of practices - within different disciplines - aiming at:
\\n\\nWe aim at improving the quality and availability of scholarly communication by promoting and practicing:
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The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\n\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\n\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\n\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\n\nOAI-PMH
\n\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\n\nLicense
\n\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\n\nPeer Review Policies
\n\nAll scientific works are Peer Reviewed prior to publishing. Read more
\n\nOA Publishing Fees
\n\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\n\nDigital Archiving Policy
\n\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\n\nOpen Science is transparent and accessible knowledge that is shared and developed through collaborative networks.
\n\nOpen Science is about increased rigour, accountability, and reproducibility for research. It is based on the principles of inclusion, fairness, equity, and sharing, and ultimately seeks to change the way research is done, who is involved and how it is valued. It aims to make research more open to participation, review/refutation, improvement and (re)use for the world to benefit.
\n\nOpen Science refers to doing traditional science with more transparency involved at various stages, for example by openly sharing code and data. It implies a growing set of practices - within different disciplines - aiming at:
\n\nWe aim at improving the quality and availability of scholarly communication by promoting and practicing:
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His studies in robotics lead him not only to a PhD degree but also inspired him to co-found and build the International Journal of Advanced Robotic Systems - world's first Open Access journal in the field of robotics.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"441",title:"Ph.D.",name:"Jaekyu",middleName:null,surname:"Park",slug:"jaekyu-park",fullName:"Jaekyu Park",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/441/images/1881_n.jpg",biography:null,institutionString:null,institution:{name:"LG Corporation (South Korea)",country:{name:"Korea, South"}}},{id:"465",title:"Dr",name:"Christian",middleName:null,surname:"Martens",slug:"christian-martens",fullName:"Christian Martens",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"479",title:"Dr.",name:"Valentina",middleName:null,surname:"Colla",slug:"valentina-colla",fullName:"Valentina Colla",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/479/images/358_n.jpg",biography:null,institutionString:null,institution:{name:"Sant'Anna School of Advanced Studies",country:{name:"Italy"}}},{id:"494",title:"PhD",name:"Loris",middleName:null,surname:"Nanni",slug:"loris-nanni",fullName:"Loris Nanni",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/494/images/system/494.jpg",biography:"Loris Nanni received his Master Degree cum laude on June-2002 from the University of Bologna, and the April 26th 2006 he received his Ph.D. in Computer Engineering at DEIS, University of Bologna. On September, 29th 2006 he has won a post PhD fellowship from the university of Bologna (from October 2006 to October 2008), at the competitive examination he was ranked first in the industrial engineering area. He extensively served as referee for several international journals. He is author/coauthor of more than 100 research papers. He has been involved in some projects supported by MURST and European Community. His research interests include pattern recognition, bioinformatics, and biometric systems (fingerprint classification and recognition, signature verification, face recognition).",institutionString:null,institution:null},{id:"496",title:"Dr.",name:"Carlos",middleName:null,surname:"Leon",slug:"carlos-leon",fullName:"Carlos Leon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Seville",country:{name:"Spain"}}},{id:"512",title:"Dr.",name:"Dayang",middleName:null,surname:"Jawawi",slug:"dayang-jawawi",fullName:"Dayang Jawawi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Technology Malaysia",country:{name:"Malaysia"}}},{id:"528",title:"Dr.",name:"Kresimir",middleName:null,surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/528/images/system/528.jpg",biography:"K. Delac received his B.Sc.E.E. degree in 2003 and is currentlypursuing a Ph.D. degree at the University of Zagreb, Faculty of Electrical Engineering andComputing. His current research interests are digital image analysis, pattern recognition andbiometrics.",institutionString:null,institution:{name:"University of Zagreb",country:{name:"Croatia"}}},{id:"557",title:"Dr.",name:"Andon",middleName:"Venelinov",surname:"Topalov",slug:"andon-topalov",fullName:"Andon Topalov",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/557/images/1927_n.jpg",biography:"Dr. Andon V. Topalov received the MSc degree in Control Engineering from the Faculty of Information Systems, Technologies, and Automation at Moscow State University of Civil Engineering (MGGU) in 1979. He then received his PhD degree in Control Engineering from the Department of Automation and Remote Control at Moscow State Mining University (MGSU), Moscow, in 1984. From 1985 to 1986, he was a Research Fellow in the Research Institute for Electronic Equipment, ZZU AD, Plovdiv, Bulgaria. In 1986, he joined the Department of Control Systems, Technical University of Sofia at the Plovdiv campus, where he is presently a Full Professor. He has held long-term visiting Professor/Scholar positions at various institutions in South Korea, Turkey, Mexico, Greece, Belgium, UK, and Germany. And he has coauthored one book and authored or coauthored more than 80 research papers in conference proceedings and journals. His current research interests are in the fields of intelligent control and robotics.",institutionString:null,institution:{name:"Technical University of Sofia",country:{name:"Bulgaria"}}},{id:"585",title:"Prof.",name:"Munir",middleName:null,surname:"Merdan",slug:"munir-merdan",fullName:"Munir Merdan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/585/images/system/585.jpg",biography:"Munir Merdan received the M.Sc. degree in mechanical engineering from the Technical University of Sarajevo, Bosnia and Herzegovina, in 2001, and the Ph.D. degree in electrical engineering from the Vienna University of Technology, Vienna, Austria, in 2009.Since 2005, he has been at the Automation and Control Institute, Vienna University of Technology, where he is currently a Senior Researcher. His research interests include the application of agent technology for achieving agile control in the manufacturing environment.",institutionString:null,institution:null},{id:"605",title:"Prof",name:"Dil",middleName:null,surname:"Hussain",slug:"dil-hussain",fullName:"Dil Hussain",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/605/images/system/605.jpg",biography:"Dr. Dil Muhammad Akbar Hussain is a professor of Electronics Engineering & Computer Science at the Department of Energy Technology, Aalborg University Denmark. Professor Akbar has a Master degree in Digital Electronics from Govt. College University, Lahore Pakistan and a P-hD degree in Control Engineering from the School of Engineering and Applied Sciences, University of Sussex United Kingdom. Aalborg University has Two Satellite Campuses, one in Copenhagen (Aalborg University Copenhagen) and the other in Esbjerg (Aalborg University Esbjerg).\n· He is a member of prestigious IEEE (Institute of Electrical and Electronics Engineers), and IAENG (International Association of Engineers) organizations. \n· He is the chief Editor of the Journal of Software Engineering.\n· He is the member of the Editorial Board of International Journal of Computer Science and Software Technology (IJCSST) and International Journal of Computer Engineering and Information Technology. \n· He is also the Editor of Communication in Computer and Information Science CCIS-20 by Springer.\n· Reviewer For Many Conferences\nHe is the lead person in making collaboration agreements between Aalborg University and many universities of Pakistan, for which the MOU’s (Memorandum of Understanding) have been signed.\nProfessor Akbar is working in Academia since 1990, he started his career as a Lab demonstrator/TA at the University of Sussex. After finishing his P. hD degree in 1992, he served in the Industry as a Scientific Officer and continued his academic career as a visiting scholar for a number of educational institutions. In 1996 he joined National University of Science & Technology Pakistan (NUST) as an Associate Professor; NUST is one of the top few universities in Pakistan. In 1999 he joined an International Company Lineo Inc, Canada as Manager Compiler Group, where he headed the group for developing Compiler Tool Chain and Porting of Operating Systems for the BLACKfin processor. The processor development was a joint venture by Intel and Analog Devices. In 2002 Lineo Inc., was taken over by another company, so he joined Aalborg University Denmark as an Assistant Professor.\nProfessor Akbar has truly a multi-disciplined career and he continued his legacy and making progress in many areas of his interests both in teaching and research. 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Insect pests are one of the main causes for losses in agriculture production, and current control technologies based on pesticide application or the use of transgenic crops expressing Bacillus thuringiensis toxin proteins are facing efficacy challenges. Novel approaches to control pests are urgently necessary. RNA interference (RNAi) is a gene silencing mechanism triggered by providing double-stranded RNA (dsRNA), that when ingested into insects can lead to death or affect the viability of the target pest. Transgenic plants expressing dsRNA version of insect specific target genes are the new generation of resistant plants. However, the RNAi mechanism is not conserved among insect orders, and its elucidation is the key to develop commercial RNAi crops. In this chapter, we review the core RNAi pathway in insects and the dsRNA uptake, amplification, and spread of systemic silencing signals in some key insect species. We also highlight some of the experimental steps before developing an insect-pest-resistant “RNAi plant”. Lastly, we review some of the most recent development studies to control agricultural insect pests by RNAi transgenic plants.",book:{id:"5090",slug:"rna-interference",title:"RNA Interference",fullTitle:"RNA Interference"},signatures:"Thais Barros Rodrigues and Antonio Figueira",authors:[{id:"176770",title:"Dr.",name:"Thais B.",middleName:null,surname:"Rodrigues",slug:"thais-b.-rodrigues",fullName:"Thais B. 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Histologically, collagen decreases, and the dermis is replaced by abnormal elastic fibers as a cause of wrinkle formation through the loss of skin elasticity. There have been numerous studies of skin aging performed to elucidate the underlying molecular mechanisms and to develop various antiaging therapeutics and preventive strategies. We summarized the molecular mechanisms and treatments of skin aging. Mainly UV radiation induces ROS formation and DNA damage, leading to increased production of MMPs and decreased production of collagen in keratinocytes and fibroblasts, which reflect the central aspects of skin aging. Besides UV radiation exposure, extrinsic factors including tobacco smoking, exposure to environmental pollutants, infrared radiation, and heat contribute to premature skin aging. Like UV radiation, these factors cause ROS formation and increase expression of MMPs, thus accelerating skin aging by inducing extracellular matrix (ECM) degradation. Accumulated collagen fibrils inhibit the new collagen synthesis and account for the further degradation of the ECM through this positive feedback loop. Accumulating evidence for molecular mechanisms of skin aging should provide clinicians with an expanding spectrum of therapeutic targets in the treatment of skin aging.",book:{id:"5258",slug:"molecular-mechanisms-of-the-aging-process-and-rejuvenation",title:"Molecular Mechanisms of the Aging Process and Rejuvenation",fullTitle:"Molecular Mechanisms of the Aging Process and Rejuvenation"},signatures:"Miri Kim and Hyun Jeong Park",authors:[{id:"47695",title:"Prof.",name:"Hyun Jeong",middleName:null,surname:"Park",slug:"hyun-jeong-park",fullName:"Hyun Jeong Park"},{id:"185767",title:"Prof.",name:"Miri",middleName:null,surname:"Kim",slug:"miri-kim",fullName:"Miri Kim"}]},{id:"49637",title:"RNA Interference Technology — Applications and Limitations",slug:"rna-interference-technology-applications-and-limitations",totalDownloads:4097,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"RNA interference (RNAi), an evolutionarily conserved mechanism triggered by double-stranded RNA (dsRNA), causes gene silencing in a sequence-specific manner. RNAi evolved naturally to mediate protection from both endogenous and exogenous pathogenic nucleic acids and to modulate gene expression. Multiple technological advancements and precision in gene targeting have allowed a plethora of potential applications, ranging from targeting infections in crop plants to improving health in human patients, which have been reviewed in this chapter.",book:{id:"5090",slug:"rna-interference",title:"RNA Interference",fullTitle:"RNA Interference"},signatures:"Devi Singh, Sarika Chaudhary, Rajendra Kumar, Preeti Sirohi,\nKamiya Mehla, Anil Sirohi, Shashi Kumar, Pooran Chand and Pankaj\nKumar Singh",authors:[{id:"176625",title:"Prof.",name:"Devi",middleName:null,surname:"Singh",slug:"devi-singh",fullName:"Devi Singh"},{id:"176744",title:"Ms.",name:"Preeti",middleName:null,surname:"Sirohi",slug:"preeti-sirohi",fullName:"Preeti Sirohi"},{id:"176745",title:"Dr.",name:"Rajendra",middleName:null,surname:"Kumar",slug:"rajendra-kumar",fullName:"Rajendra Kumar"},{id:"176746",title:"Mrs.",name:"Sarika",middleName:null,surname:"Chaudhary",slug:"sarika-chaudhary",fullName:"Sarika Chaudhary"},{id:"176747",title:"Dr.",name:"Kamiya",middleName:null,surname:"Mehla",slug:"kamiya-mehla",fullName:"Kamiya Mehla"},{id:"176748",title:"Dr.",name:"Pankaj Kumar",middleName:null,surname:"Singh",slug:"pankaj-kumar-singh",fullName:"Pankaj Kumar Singh"},{id:"176749",title:"Dr.",name:"Shashi",middleName:null,surname:"Kumar",slug:"shashi-kumar",fullName:"Shashi Kumar"},{id:"176809",title:"Dr.",name:"Pooran",middleName:null,surname:"Chand",slug:"pooran-chand",fullName:"Pooran Chand"}]},{id:"43280",title:"Gene Therapy for Diabetic Retinopathy – Targeting the Renin-Angiotensin System",slug:"gene-therapy-for-diabetic-retinopathy-targeting-the-renin-angiotensin-system",totalDownloads:2458,totalCrossrefCites:2,totalDimensionsCites:2,abstract:null,book:{id:"3509",slug:"gene-therapy-tools-and-potential-applications",title:"Gene Therapy",fullTitle:"Gene Therapy - Tools and Potential Applications"},signatures:"Qiuhong Li, Amrisha Verma, Ping Zhu, Bo Lei, Yiguo Qiu, Takahiko Nakagawa, Mohan K Raizada and William W Hauswirth",authors:[{id:"155578",title:"Dr.",name:"Qiuhong",middleName:null,surname:"Li",slug:"qiuhong-li",fullName:"Qiuhong Li"}]},{id:"49416",title:"Microinjection-Based RNA Interference Method in the Water Flea, Daphnia pulex and Daphnia magna",slug:"microinjection-based-rna-interference-method-in-the-water-flea-daphnia-pulex-and-daphnia-magna",totalDownloads:2186,totalCrossrefCites:5,totalDimensionsCites:7,abstract:"It is well known that most daphnid species have several attractive life history characteristics such as cyclical parthenogenesis, environmental sex determination, and predator-induced defense formation. Recent advances in high-throughput omics technologies make it easy to obtain a huge number of potential candidate factors involved in environmental stimuli-triggered phenotypic alterations. Furthermore, our group has developed a microinjection system to introduce foreign materials such as nucleotides and chemicals into the early-stage (one-cell stage) egg of Daphnia pulex and Daphnia magna. Consequently, we established a microinjection-based RNAi system that allows arbitrary gene functions to be investigated. However, this microinjection system does not seem to have pervaded in the daphnid research community due to its low throughput and high level of skills required. In this chapter, we review the microinjection method and its RNAi system in water fleas, D. pulex and D. magna, providing some technical tips and making challenging proposals for the development of novel high-throughput RNAi methods. Finally, we provide an overview of recently developed gene functional analysis methods such as overexpression and genome-editing systems.",book:{id:"5090",slug:"rna-interference",title:"RNA Interference",fullTitle:"RNA Interference"},signatures:"Kenji Toyota, Shinichi Miyagawa, Yukiko Ogino and Taisen Iguchi",authors:[{id:"92826",title:"Dr.",name:"Taisen",middleName:null,surname:"Iguchi",slug:"taisen-iguchi",fullName:"Taisen Iguchi"},{id:"176835",title:"Dr.",name:"Kenji",middleName:null,surname:"Toyota",slug:"kenji-toyota",fullName:"Kenji Toyota"}]},{id:"55603",title:"RNA‐seq: Applications and Best Practices",slug:"rna-seq-applications-and-best-practices",totalDownloads:3743,totalCrossrefCites:7,totalDimensionsCites:8,abstract:"RNA‐sequencing (RNA‐seq) is the state‐of‐the‐art technique for transcriptome analysis that takes advantage of high‐throughput next‐generation sequencing. Although being a powerful approach, RNA‐seq imposes major challenges throughout its steps with numerous caveats. There are currently many experimental options available, and a complete comprehension of each step is critical to make right decisions and avoid getting into inconclusive results. A complete workflow consists of: (1) experimental design; (2) sample and library preparation; (3) sequencing; and (4) data analysis. RNA‐seq enables a wide range of applications such as the discovery of novel genes, gene/transcript quantification, and differential expression and functional analysis. This chapter will encompass the main aspects from sample preparation to downstream data analysis. It will be discussed how to obtain high‐quality samples, replicates amount, library preparation, sequencing platforms and coverage, focusing on best recommended practices based on specialized literature. Basic techniques and well‐known algorithms are presented and discussed, guiding both beginners and experienced users in the implementation of reliable experiments.",book:{id:"5944",slug:"applications-of-rna-seq-and-omics-strategies-from-microorganisms-to-human-health",title:"Applications of RNA-Seq and Omics Strategies",fullTitle:"Applications of RNA-Seq and Omics Strategies - From Microorganisms to Human Health"},signatures:"Michele Araújo Pereira, Eddie Luidy Imada and Rafael Lucas Muniz\nGuedes",authors:[{id:"202103",title:"Ph.D. Student",name:"Michele",middleName:"Araújo",surname:"Pereira",slug:"michele-pereira",fullName:"Michele Pereira"},{id:"202456",title:"MSc.",name:"Eddie Luidy",middleName:null,surname:"Imada",slug:"eddie-luidy-imada",fullName:"Eddie Luidy Imada"},{id:"202460",title:"Dr.",name:"Rafael",middleName:null,surname:"Guedes",slug:"rafael-guedes",fullName:"Rafael Guedes"}]}],onlineFirstChaptersFilter:{topicId:"419",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:31,numberOfPublishedChapters:314,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:11,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:105,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:14,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. The whole process of submitting an article and editing of the submitted article goes extremely smooth and fast, the number of reads and downloads of chapters is high, and the contributions are also frequently cited.",author:{id:"55578",name:"Antonio",surname:"Jurado-Navas",institutionString:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRisIQAS/Profile_Picture_1626166543950",slug:"antonio-jurado-navas",institution:{id:"720",name:"University of Malaga",country:{id:null,name:"Spain"}}}}]},series:{item:{id:"14",title:"Artificial Intelligence",doi:"10.5772/intechopen.79920",issn:"2633-1403",scope:"Artificial Intelligence (AI) is a rapidly developing multidisciplinary research area that aims to solve increasingly complex problems. In today's highly integrated world, AI promises to become a robust and powerful means for obtaining solutions to previously unsolvable problems. This Series is intended for researchers and students alike interested in this fascinating field and its many applications.",coverUrl:"https://cdn.intechopen.com/series/covers/14.jpg",latestPublicationDate:"June 11th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:9,editor:{id:"218714",title:"Prof.",name:"Andries",middleName:null,surname:"Engelbrecht",slug:"andries-engelbrecht",fullName:"Andries Engelbrecht",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRNR8QAO/Profile_Picture_1622640468300",biography:"Andries Engelbrecht received the Masters and PhD degrees in Computer Science from the University of Stellenbosch, South Africa, in 1994 and 1999 respectively. He is currently appointed as the Voigt Chair in Data Science in the Department of Industrial Engineering, with a joint appointment as Professor in the Computer Science Division, Stellenbosch University. Prior to his appointment at Stellenbosch University, he has been at the University of Pretoria, Department of Computer Science (1998-2018), where he was appointed as South Africa Research Chair in Artifical Intelligence (2007-2018), the head of the Department of Computer Science (2008-2017), and Director of the Institute for Big Data and Data Science (2017-2018). In addition to a number of research articles, he has written two books, Computational Intelligence: An Introduction and Fundamentals of Computational Swarm Intelligence.",institutionString:null,institution:{name:"Stellenbosch University",institutionURL:null,country:{name:"South Africa"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:9,paginationItems:[{id:"22",title:"Applied Intelligence",coverUrl:"https://cdn.intechopen.com/series_topics/covers/22.jpg",editor:{id:"27170",title:"Prof.",name:"Carlos",middleName:"M.",surname:"Travieso-Gonzalez",slug:"carlos-travieso-gonzalez",fullName:"Carlos Travieso-Gonzalez",profilePictureURL:"https://mts.intechopen.com/storage/users/27170/images/system/27170.jpeg",biography:"Carlos M. Travieso-González received his MSc degree in Telecommunication Engineering at Polytechnic University of Catalonia (UPC), Spain in 1997, and his Ph.D. degree in 2002 at the University of Las Palmas de Gran Canaria (ULPGC-Spain). He is a full professor of signal processing and pattern recognition and is head of the Signals and Communications Department at ULPGC, teaching from 2001 on subjects on signal processing and learning theory. His research lines are biometrics, biomedical signals and images, data mining, classification system, signal and image processing, machine learning, and environmental intelligence. He has researched in 52 international and Spanish research projects, some of them as head researcher. He is co-author of 4 books, co-editor of 27 proceedings books, guest editor for 8 JCR-ISI international journals, and up to 24 book chapters. He has over 450 papers published in international journals and conferences (81 of them indexed on JCR – ISI - Web of Science). He has published seven patents in the Spanish Patent and Trademark Office. He has been a supervisor on 8 Ph.D. theses (11 more are under supervision), and 130 master theses. He is the founder of The IEEE IWOBI conference series and the president of its Steering Committee, as well as the founder of both the InnoEducaTIC and APPIS conference series. He is an evaluator of project proposals for the European Union (H2020), Medical Research Council (MRC, UK), Spanish Government (ANECA, Spain), Research National Agency (ANR, France), DAAD (Germany), Argentinian Government, and the Colombian Institutions. He has been a reviewer in different indexed international journals (<70) and conferences (<250) since 2001. He has been a member of the IASTED Technical Committee on Image Processing from 2007 and a member of the IASTED Technical Committee on Artificial Intelligence and Expert Systems from 2011. \n\nHe has held the general chair position for the following: ACM-APPIS (2020, 2021), IEEE-IWOBI (2019, 2020 and 2020), A PPIS (2018, 2019), IEEE-IWOBI (2014, 2015, 2017, 2018), InnoEducaTIC (2014, 2017), IEEE-INES (2013), NoLISP (2011), JRBP (2012), and IEEE-ICCST (2005)\n\nHe is an associate editor of the Computational Intelligence and Neuroscience Journal (Hindawi – Q2 JCR-ISI). He was vice dean from 2004 to 2010 in the Higher Technical School of Telecommunication Engineers at ULPGC and the vice dean of Graduate and Postgraduate Studies from March 2013 to November 2017. He won the “Catedra Telefonica” Awards in Modality of Knowledge Transfer, 2017, 2018, and 2019 editions, and awards in Modality of COVID Research in 2020.\n\nPublic References:\nResearcher ID http://www.researcherid.com/rid/N-5967-2014\nORCID https://orcid.org/0000-0002-4621-2768 \nScopus Author ID https://www.scopus.com/authid/detail.uri?authorId=6602376272\nScholar Google https://scholar.google.es/citations?user=G1ks9nIAAAAJ&hl=en \nResearchGate https://www.researchgate.net/profile/Carlos_Travieso",institutionString:null,institution:{name:"University of Las Palmas de Gran Canaria",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"13633",title:"Prof.",name:"Abdelhamid",middleName:null,surname:"Mellouk",slug:"abdelhamid-mellouk",fullName:"Abdelhamid Mellouk",profilePictureURL:"https://mts.intechopen.com/storage/users/13633/images/1567_n.jpg",institutionString:null,institution:{name:"Paris 12 Val de Marne University",institutionURL:null,country:{name:"France"}}},{id:"109268",title:"Dr.",name:"Ali",middleName:null,surname:"Al-Ataby",slug:"ali-al-ataby",fullName:"Ali Al-Ataby",profilePictureURL:"https://mts.intechopen.com/storage/users/109268/images/7410_n.jpg",institutionString:null,institution:{name:"University of Liverpool",institutionURL:null,country:{name:"United Kingdom"}}},{id:"3807",title:"Dr.",name:"Carmelo",middleName:"Jose Albanez",surname:"Bastos-Filho",slug:"carmelo-bastos-filho",fullName:"Carmelo Bastos-Filho",profilePictureURL:"https://mts.intechopen.com/storage/users/3807/images/624_n.jpg",institutionString:null,institution:{name:"Universidade de Pernambuco",institutionURL:null,country:{name:"Brazil"}}},{id:"38850",title:"Dr.",name:"Efren",middleName:null,surname:"Gorrostieta Hurtado",slug:"efren-gorrostieta-hurtado",fullName:"Efren Gorrostieta 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learning consultant from Sweden. \n\nHe is currently at Malmö University in Sweden, but also held positions at Lund University in Sweden and at Moscow Engineering Physics Institute. \nHe holds editorial positions at several international scientific journals and has served as a scientific editor for books and special journal issues. \nHis research interests are wide and include, but are not limited to, autonomous systems, computer modeling, artificial neural networks, artificial intelligence, cognitive neuroscience, cognitive robotics, cognitive architectures, cognitive aids and the philosophy of mind. \n\nDr. Johnsson has experience from working in the industry and he has a keen interest in the application of neural networks and artificial intelligence to fields like industry, finance, and medicine. \n\nWeb page: www.magnusjohnsson.se",institutionString:null,institution:{name:"Malmö University",institutionURL:null,country:{name:"Sweden"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"13818",title:"Dr.",name:"Asim",middleName:null,surname:"Bhatti",slug:"asim-bhatti",fullName:"Asim Bhatti",profilePictureURL:"https://mts.intechopen.com/storage/users/13818/images/system/13818.jpg",institutionString:null,institution:{name:"Deakin University",institutionURL:null,country:{name:"Australia"}}},{id:"151889",title:"Dr.",name:"Joao Luis Garcia",middleName:null,surname:"Rosa",slug:"joao-luis-garcia-rosa",fullName:"Joao Luis Garcia Rosa",profilePictureURL:"https://mts.intechopen.com/storage/users/151889/images/4861_n.jpg",institutionString:null,institution:{name:"University of Sao Paulo",institutionURL:null,country:{name:"Brazil"}}},{id:"103779",title:"Prof.",name:"Yalcin",middleName:null,surname:"Isler",slug:"yalcin-isler",fullName:"Yalcin Isler",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRyQ8QAK/Profile_Picture_1628834958734",institutionString:null,institution:{name:"Izmir Kâtip Çelebi University",institutionURL:null,country:{name:"Turkey"}}}]},{id:"24",title:"Computer Vision",coverUrl:"https://cdn.intechopen.com/series_topics/covers/24.jpg",editor:{id:"294154",title:"Prof.",name:"George",middleName:null,surname:"Papakostas",slug:"george-papakostas",fullName:"George Papakostas",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002hYaGbQAK/Profile_Picture_1624519712088",biography:"George A. Papakostas has received a diploma in Electrical and Computer Engineering in 1999 and the M.Sc. and Ph.D. degrees in Electrical and Computer Engineering in 2002 and 2007, respectively, from the Democritus University of Thrace (DUTH), Greece. Dr. Papakostas serves as a Tenured Full Professor at the Department of Computer Science, International Hellenic University, Greece. Dr. Papakostas has 10 years of experience in large-scale systems design as a senior software engineer and technical manager, and 20 years of research experience in the field of Artificial Intelligence. Currently, he is the Head of the “Visual Computing” division of HUman-MAchines INteraction Laboratory (HUMAIN-Lab) and the Director of the MPhil program “Advanced Technologies in Informatics and Computers” hosted by the Department of Computer Science, International Hellenic University. He has (co)authored more than 150 publications in indexed journals, international conferences and book chapters, 1 book (in Greek), 3 edited books, and 5 journal special issues. His publications have more than 2100 citations with h-index 27 (GoogleScholar). His research interests include computer/machine vision, machine learning, pattern recognition, computational intelligence. \nDr. Papakostas served as a reviewer in numerous journals, as a program\ncommittee member in international conferences and he is a member of the IAENG, MIR Labs, EUCogIII, INSTICC and the Technical Chamber of Greece (TEE).",institutionString:null,institution:{name:"International Hellenic University",institutionURL:null,country:{name:"Greece"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"1177",title:"Prof.",name:"Antonio",middleName:"J. R.",surname:"Neves",slug:"antonio-neves",fullName:"Antonio Neves",profilePictureURL:"https://mts.intechopen.com/storage/users/1177/images/system/1177.jpg",institutionString:null,institution:{name:"University of Aveiro",institutionURL:null,country:{name:"Portugal"}}},{id:"220565",title:"Dr.",name:"Jucheng",middleName:null,surname:"Yang",slug:"jucheng-yang",fullName:"Jucheng Yang",profilePictureURL:"https://mts.intechopen.com/storage/users/220565/images/5988_n.jpg",institutionString:null,institution:{name:"Tianjin University of Technology",institutionURL:null,country:{name:"China"}}},{id:"29299",title:"Prof.",name:"Serestina",middleName:null,surname:"Viriri",slug:"serestina-viriri",fullName:"Serestina Viriri",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYOalQAG/Profile_Picture_1620817405517",institutionString:null,institution:{name:"University of KwaZulu-Natal",institutionURL:null,country:{name:"South Africa"}}},{id:"315933",title:"Dr.",name:"Yalın",middleName:null,surname:"Baştanlar",slug:"yalin-bastanlar",fullName:"Yalın Baştanlar",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00002qpr7hQAA/Profile_Picture_1621430127547",institutionString:null,institution:{name:"Izmir Institute of Technology",institutionURL:null,country:{name:"Turkey"}}}]},{id:"25",title:"Evolutionary Computation",coverUrl:"https://cdn.intechopen.com/series_topics/covers/25.jpg",editor:{id:"136112",title:"Dr.",name:"Sebastian",middleName:null,surname:"Ventura Soto",slug:"sebastian-ventura-soto",fullName:"Sebastian Ventura Soto",profilePictureURL:"https://mts.intechopen.com/storage/users/136112/images/system/136112.png",biography:"Sebastian Ventura is a Spanish researcher, a full professor with the Department of Computer Science and Numerical Analysis, University of Córdoba. Dr Ventura also holds the positions of Affiliated Professor at Virginia Commonwealth University (Richmond, USA) and Distinguished Adjunct Professor at King Abdulaziz University (Jeddah, Saudi Arabia). Additionally, he is deputy director of the Andalusian Research Institute in Data Science and Computational Intelligence (DaSCI) and heads the Knowledge Discovery and Intelligent Systems Research Laboratory. He has published more than ten books and over 300 articles in journals and scientific conferences. Currently, his work has received over 18,000 citations according to Google Scholar, including more than 2200 citations in 2020. In the last five years, he has published more than 60 papers in international journals indexed in the JCR (around 70% of them belonging to first quartile journals) and he has edited some Springer books “Supervised Descriptive Pattern Mining” (2018), “Multiple Instance Learning - Foundations and Algorithms” (2016), and “Pattern Mining with Evolutionary Algorithms” (2016). He has also been involved in more than 20 research projects supported by the Spanish and Andalusian governments and the European Union. He currently belongs to the editorial board of PeerJ Computer Science, Information Fusion and Engineering Applications of Artificial Intelligence journals, being also associate editor of Applied Computational Intelligence and Soft Computing and IEEE Transactions on Cybernetics. Finally, he is editor-in-chief of Progress in Artificial Intelligence. He is a Senior Member of the IEEE Computer, the IEEE Computational Intelligence, and the IEEE Systems, Man, and Cybernetics Societies, and the Association of Computing Machinery (ACM). Finally, his main research interests include data science, computational intelligence, and their applications.",institutionString:null,institution:{name:"University of Córdoba",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"111683",title:"Prof.",name:"Elmer P.",middleName:"P.",surname:"Dadios",slug:"elmer-p.-dadios",fullName:"Elmer P. 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She is now a lecturer at the University of Witwatersrand, South Africa, and a principal researcher at the Health Economics and Epidemiology Research Office (HE2RO), South Africa. Dr. Moolla holds a Ph.D. in Psychology with her research being focused on mental health and resilience. In her professional work capacity, her research has further expanded into the fields of early childhood development, mental health, the HIV and TB care cascades, as well as COVID. She is also a UNESCO-trained International Bioethics Facilitator.",institutionString:"University of the Witwatersrand",institution:{name:"University of the Witwatersrand",country:{name:"South Africa"}}},{id:"342152",title:"Dr.",name:"Santo",middleName:null,surname:"Grace Umesh",slug:"santo-grace-umesh",fullName:"Santo Grace Umesh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/342152/images/16311_n.jpg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"333647",title:"Dr.",name:"Shreya",middleName:null,surname:"Kishore",slug:"shreya-kishore",fullName:"Shreya Kishore",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333647/images/14701_n.jpg",biography:"Dr. Shreya Kishore completed her Bachelor in Dental Surgery in Chettinad Dental College and Research Institute, Chennai, and her Master of Dental Surgery (Orthodontics) in Saveetha Dental College, Chennai. She is also Invisalign certified. She’s working as a Senior Lecturer in the Department of Orthodontics, SRM Dental College since November 2019. She is actively involved in teaching orthodontics to the undergraduates and the postgraduates. Her clinical research topics include new orthodontic brackets, fixed appliances and TADs. She’s published 4 articles in well renowned indexed journals and has a published patency of her own. Her private practice is currently limited to orthodontics and works as a consultant in various clinics.",institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"323731",title:"Prof.",name:"Deepak M.",middleName:"Macchindra",surname:"Vikhe",slug:"deepak-m.-vikhe",fullName:"Deepak M. Vikhe",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/323731/images/13613_n.jpg",biography:"Dr Deepak M.Vikhe .\n\n\t\n\tDr Deepak M.Vikhe , completed his Masters & PhD in Prosthodontics from Rural Dental College, Loni securing third rank in the Pravara Institute of Medical Sciences Deemed University. He was awarded Dr.G.C.DAS Memorial Award for Research on Implants at 39th IPS conference Dubai (U A E).He has two patents under his name. He has received Dr.Saraswati medal award for best research for implant study in 2017.He has received Fully funded scholarship to Spain ,university of Santiago de Compostela. He has completed fellowship in Implantlogy from Noble Biocare. \nHe has attended various conferences and CDE programmes and has national publications to his credit. His field of interest is in Implant supported prosthesis. Presently he is working as a associate professor in the Dept of Prosthodontics, Rural Dental College, Loni and maintains a successful private practice specialising in Implantology at Rahata.\n\nEmail: drdeepak_mvikhe@yahoo.com..................",institutionString:null,institution:{name:"Pravara Institute of Medical Sciences",country:{name:"India"}}},{id:"204110",title:"Dr.",name:"Ahmed A.",middleName:null,surname:"Madfa",slug:"ahmed-a.-madfa",fullName:"Ahmed A. Madfa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/204110/images/system/204110.jpg",biography:"Dr. Madfa is currently Associate Professor of Endodontics at Thamar University and a visiting lecturer at Sana'a University and University of Sciences and Technology. He has more than 6 years of experience in teaching. His research interests include root canal morphology, functionally graded concept, dental biomaterials, epidemiology and dental education, biomimetic restoration, finite element analysis and endodontic regeneration. Dr. Madfa has numerous international publications, full articles, two patents, a book and a book chapter. Furthermore, he won 14 international scientific awards. Furthermore, he is involved in many academic activities ranging from editorial board member, reviewer for many international journals and postgraduate students' supervisor. Besides, I deliver many courses and training workshops at various scientific events. Dr. Madfa also regularly attends international conferences and holds administrative positions (Deputy Dean of the Faculty for Students’ & Academic Affairs and Deputy Head of Research Unit).",institutionString:"Thamar University",institution:null},{id:"210472",title:"Dr.",name:"Nermin",middleName:"Mohammed Ahmed",surname:"Yussif",slug:"nermin-yussif",fullName:"Nermin Yussif",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/210472/images/system/210472.jpg",biography:"Dr. Nermin Mohammed Ahmed Yussif is working at the Faculty of dentistry, University for October university for modern sciences and arts (MSA). Her areas of expertise include: periodontology, dental laserology, oral implantology, periodontal plastic surgeries, oral mesotherapy, nutrition, dental pharmacology. She is an editor and reviewer in numerous international journals.",institutionString:"MSA University",institution:null},{id:"204606",title:"Dr.",name:"Serdar",middleName:null,surname:"Gözler",slug:"serdar-gozler",fullName:"Serdar Gözler",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/204606/images/system/204606.jpeg",biography:"Dr. Serdar Gözler has completed his undergraduate studies at the Marmara University Faculty of Dentistry in 1978, followed by an assistantship in the Prosthesis Department of Dicle University Faculty of Dentistry. Starting his PhD work on non-resilient overdentures with Assoc. Prof. Hüsnü Yavuzyılmaz, he continued his studies with Prof. Dr. Gürbüz Öztürk of Istanbul University Faculty of Dentistry Department of Prosthodontics, this time on Gnatology. He attended training programs on occlusion, neurology, neurophysiology, EMG, radiology and biostatistics. In 1982, he presented his PhD thesis \\Gerber and Lauritzen Occlusion Analysis Techniques: Diagnosis Values,\\ at Istanbul University School of Dentistry, Department of Prosthodontics. As he was also working with Prof. Senih Çalıkkocaoğlu on The Physiology of Chewing at the same time, Gözler has written a chapter in Çalıkkocaoğlu\\'s book \\Complete Prostheses\\ entitled \\The Place of Neuromuscular Mechanism in Prosthetic Dentistry.\\ The book was published five times since by the Istanbul University Publications. Having presented in various conferences about occlusion analysis until 1998, Dr. Gözler has also decided to use the T-Scan II occlusion analysis method. Having been personally trained by Dr. Robert Kerstein on this method, Dr. Gözler has been lecturing on the T-Scan Occlusion Analysis Method in conferences both in Turkey and abroad. Dr. Gözler has various articles and presentations on Digital Occlusion Analysis methods. He is now Head of the TMD Clinic at Prosthodontic Department of Faculty of Dentistry , Istanbul Aydın University , Turkey.",institutionString:"Istanbul Aydin University",institution:{name:"Istanbul Aydın University",country:{name:"Turkey"}}},{id:"240870",title:"Ph.D.",name:"Alaa Eddin Omar",middleName:null,surname:"Al Ostwani",slug:"alaa-eddin-omar-al-ostwani",fullName:"Alaa Eddin Omar Al Ostwani",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/240870/images/system/240870.jpeg",biography:"Dr. Al Ostwani Alaa Eddin Omar received his Master in dentistry from Damascus University in 2010, and his Ph.D. in Pediatric Dentistry from Damascus University in 2014. Dr. Al Ostwani is an assistant professor and faculty member at IUST University since 2014. \nDuring his academic experience, he has received several awards including the scientific research award from the Union of Arab Universities, the Syrian gold medal and the international gold medal for invention and creativity. Dr. Al Ostwani is a Member of the International Association of Dental Traumatology and the Syrian Society for Research and Preventive Dentistry since 2017. He is also a Member of the Reviewer Board of International Journal of Dental Medicine (IJDM), and the Indian Journal of Conservative and Endodontics since 2016.",institutionString:"International University for Science and Technology.",institution:{name:"Islamic University of Science and Technology",country:{name:"India"}}},{id:"42847",title:"Dr.",name:"Belma",middleName:null,surname:"Işik Aslan",slug:"belma-isik-aslan",fullName:"Belma Işik Aslan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/42847/images/system/42847.jpg",biography:"Dr. Belma IşIk Aslan was born in 1976 in Ankara-TURKEY. After graduating from TED Ankara College in 1994, she attended to Gazi University, Faculty of Dentistry in Ankara. She completed her PhD in orthodontic education at Gazi University between 1999-2005. Dr. Işık Aslan stayed at the Providence Hospital Craniofacial Institude and Reconstructive Surgery in Michigan, USA for three months as an observer. She worked as a specialist doctor at Gazi University, Dentistry Faculty, Department of Orthodontics between 2005-2014. She was appointed as associate professor in January, 2014 and as professor in 2021. Dr. Işık Aslan still works as an instructor at the same faculty. She has published a total of 35 articles, 10 book chapters, 39 conference proceedings both internationally and nationally. Also she was the academic editor of the international book 'Current Advances in Orthodontics'. She is a member of the Turkish Orthodontic Society and Turkish Cleft Lip and Palate Society. She is married and has 2 children. Her knowledge of English is at an advanced level.",institutionString:"Gazi University Dentistry Faculty Department of Orthodontics",institution:null},{id:"178412",title:"Associate Prof.",name:"Guhan",middleName:null,surname:"Dergin",slug:"guhan-dergin",fullName:"Guhan Dergin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/178412/images/6954_n.jpg",biography:"Assoc. Prof. Dr. Gühan Dergin was born in 1973 in Izmit. He graduated from Marmara University Faculty of Dentistry in 1999. He completed his specialty of OMFS surgery in Marmara University Faculty of Dentistry and obtained his PhD degree in 2006. In 2005, he was invited as a visiting doctor in the Oral and Maxillofacial Surgery Department of the University of North Carolina, USA, where he went on a scholarship. Dr. Dergin still continues his academic career as an associate professor in Marmara University Faculty of Dentistry. He has many articles in international and national scientific journals and chapters in books.",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"178414",title:"Prof.",name:"Yusuf",middleName:null,surname:"Emes",slug:"yusuf-emes",fullName:"Yusuf Emes",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/178414/images/6953_n.jpg",biography:"Born in Istanbul in 1974, Dr. Emes graduated from Istanbul University Faculty of Dentistry in 1997 and completed his PhD degree in Istanbul University faculty of Dentistry Department of Oral and Maxillofacial Surgery in 2005. He has papers published in international and national scientific journals, including research articles on implantology, oroantral fistulas, odontogenic cysts, and temporomandibular disorders. Dr. Emes is currently working as a full-time academic staff in Istanbul University faculty of Dentistry Department of Oral and Maxillofacial Surgery.",institutionString:null,institution:{name:"Istanbul University",country:{name:"Turkey"}}},{id:"192229",title:"Ph.D.",name:"Ana Luiza",middleName:null,surname:"De Carvalho Felippini",slug:"ana-luiza-de-carvalho-felippini",fullName:"Ana Luiza De Carvalho Felippini",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/192229/images/system/192229.jpg",biography:null,institutionString:"University of São Paulo",institution:{name:"University of Sao Paulo",country:{name:"Brazil"}}},{id:"256851",title:"Prof.",name:"Ayşe",middleName:null,surname:"Gülşen",slug:"ayse-gulsen",fullName:"Ayşe Gülşen",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/256851/images/9696_n.jpg",biography:"Dr. Ayşe Gülşen graduated in 1990 from Faculty of Dentistry, University of Ankara and did a postgraduate program at University of Gazi. \nShe worked as an observer and research assistant in Craniofacial Surgery Departments in New York, Providence Hospital in Michigan and Chang Gung Memorial Hospital in Taiwan. \nShe works as Craniofacial Orthodontist in Department of Aesthetic, Plastic and Reconstructive Surgery, Faculty of Medicine, University of Gazi, Ankara Turkey since 2004.",institutionString:"Univeristy of Gazi",institution:null},{id:"255366",title:"Prof.",name:"Tosun",middleName:null,surname:"Tosun",slug:"tosun-tosun",fullName:"Tosun Tosun",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/255366/images/7347_n.jpg",biography:"Graduated at the Faculty of Dentistry, University of Istanbul, Turkey in 1989;\nVisitor Assistant at the University of Padua, Italy and Branemark Osseointegration Center of Treviso, Italy between 1993-94;\nPhD thesis on oral implantology in University of Istanbul and was awarded the academic title “Dr.med.dent.”, 1997;\nHe was awarded the academic title “Doç.Dr.” (Associated Professor) in 2003;\nProficiency in Botulinum Toxin Applications, Reading-UK in 2009;\nMastership, RWTH Certificate in Laser Therapy in Dentistry, AALZ-Aachen University, Germany 2009-11;\nMaster of Science (MSc) in Laser Dentistry, University of Genoa, Italy 2013-14.\n\nDr.Tosun worked as Research Assistant in the Department of Oral Implantology, Faculty of Dentistry, University of Istanbul between 1990-2002. \nHe worked part-time as Consultant surgeon in Harvard Medical International Hospitals and John Hopkins Medicine, Istanbul between years 2007-09.\u2028He was contract Professor in the Department of Surgical and Diagnostic Sciences (DI.S.C.), Medical School, University of Genova, Italy between years 2011-16. \nSince 2015 he is visiting Professor at Medical School, University of Plovdiv, Bulgaria. \nCurrently he is Associated Prof.Dr. at the Dental School, Oral Surgery Dept., Istanbul Aydin University and since 2003 he works in his own private clinic in Istanbul, Turkey.\u2028\nDr.Tosun is reviewer in journal ‘Laser in Medical Sciences’, reviewer in journal ‘Folia Medica\\', a Fellow of the International Team for Implantology, Clinical Lecturer of DGZI German Association of Oral Implantology, Expert Lecturer of Laser&Health Academy, Country Representative of World Federation for Laser Dentistry, member of European Federation of Periodontology, member of Academy of Laser Dentistry. Dr.Tosun presents papers in international and national congresses and has scientific publications in international and national journals. He speaks english, spanish, italian and french.",institutionString:null,institution:{name:"Istanbul Aydın University",country:{name:"Turkey"}}},{id:"171887",title:"Prof.",name:"Zühre",middleName:null,surname:"Akarslan",slug:"zuhre-akarslan",fullName:"Zühre Akarslan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/171887/images/system/171887.jpg",biography:"Zühre Akarslan was born in 1977 in Cyprus. She graduated from Gazi University Faculty of Dentistry, Ankara, Turkey in 2000. \r\nLater she received her Ph.D. degree from the Oral Diagnosis and Radiology Department; which was recently renamed as Oral and Dentomaxillofacial Radiology, from the same university. \r\nShe is working as a full-time Associate Professor and is a lecturer and an academic researcher. \r\nHer expertise areas are dental caries, cancer, dental fear and anxiety, gag reflex in dentistry, oral medicine, and dentomaxillofacial radiology.",institutionString:"Gazi University",institution:{name:"Gazi University",country:{name:"Turkey"}}},{id:"256417",title:"Associate Prof.",name:"Sanaz",middleName:null,surname:"Sadry",slug:"sanaz-sadry",fullName:"Sanaz Sadry",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/256417/images/8106_n.jpg",biography:null,institutionString:null,institution:null},{id:"272237",title:"Dr.",name:"Pinar",middleName:"Kiymet",surname:"Karataban",slug:"pinar-karataban",fullName:"Pinar Karataban",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/272237/images/8911_n.png",biography:"Assist.Prof.Dr.Pınar Kıymet Karataban, DDS PhD \n\nDr.Pınar Kıymet Karataban was born in Istanbul in 1975. After her graduation from Marmara University Faculty of Dentistry in 1998 she started her PhD in Paediatric Dentistry focused on children with special needs; mainly children with Cerebral Palsy. She finished her pHD thesis entitled \\'Investigation of occlusion via cast analysis and evaluation of dental caries prevalance, periodontal status and muscle dysfunctions in children with cerebral palsy” in 2008. She got her Assist. Proffessor degree in Istanbul Aydın University Paediatric Dentistry Department in 2015-2018. ın 2019 she started her new career in Bahcesehir University, Istanbul as Head of Department of Pediatric Dentistry. In 2020 she was accepted to BAU International University, Batumi as Professor of Pediatric Dentistry. She’s a lecturer in the same university meanwhile working part-time in private practice in Ege Dental Studio (https://www.egedisklinigi.com/) a multidisciplinary dental clinic in Istanbul. Her main interests are paleodontology, ancient and contemporary dentistry, oral microbiology, cerebral palsy and special care dentistry. She has national and international publications, scientific reports and is a member of IAPO (International Association for Paleodontology), IADH (International Association of Disability and Oral Health) and EAPD (European Association of Pediatric Dentistry).",institutionString:null,institution:null},{id:"202198",title:"Dr.",name:"Buket",middleName:null,surname:"Aybar",slug:"buket-aybar",fullName:"Buket Aybar",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/202198/images/6955_n.jpg",biography:"Buket Aybar, DDS, PhD, was born in 1971. She graduated from Istanbul University, Faculty of Dentistry, in 1992 and completed her PhD degree on Oral and Maxillofacial Surgery in Istanbul University in 1997.\nDr. Aybar is currently a full-time professor in Istanbul University, Faculty of Dentistry Department of Oral and Maxillofacial Surgery. She has teaching responsibilities in graduate and postgraduate programs. Her clinical practice includes mainly dentoalveolar surgery.\nHer topics of interest are biomaterials science and cell culture studies. 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After graduating from TED Ankara College in 1986, she attended the Hacettepe University, Faculty of Dentistry in Ankara. \nIn 1993 she attended the Gazi University, Faculty of Dentistry, Department of Orthodontics for her PhD education. After finishing the PhD education, she worked as orthodontist in Ankara Dental Hospital under the Turkish Government, Ministry of Health and in a special Orthodontic Clinic till 2011. Between 2011 and 2016, Dr. Deniz Uzuner worked as a specialist in the Department of Orthodontics, Faculty of Dentistry, Gazi University in Ankara/Turkey. In 2016, she was appointed associate professor. Dr. Deniz Uzuner has authored 23 Journal Papers, 3 Book Chapters and has had 39 oral/poster presentations. She is a member of the Turkish Orthodontic Society. 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Her fields of interest are entomology, toxicology, forensic entomology.",institutionString:"Classes et Events in Sciences (C.E.S.)",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"6",totalChapterViews:"0",totalEditedBooks:"7",institution:null}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null},{type:"book",id:"12223",title:"Sustainable Management of Natural Resources",subtitle:null,isOpenForSubmission:!0,hash:"1881a08bbd8f5dc1102c5cb7c635bc35",slug:null,bookSignature:"Dr. Mohd Nazip Suratman and Dr. Engku Azlin Rahayu Engku Ariff",coverURL:"https://cdn.intechopen.com/books/images_new/12223.jpg",editedByType:null,submissionDeadline:"July 19th 2022",editors:[{id:"144417",title:"Dr.",name:"Mohd Nazip",middleName:null,surname:"Suratman",slug:"mohd-nazip-suratman",fullName:"Mohd Nazip Suratman",profilePictureURL:"https://mts.intechopen.com/storage/users/144417/images/system/144417.jpg",biography:"Mohd Nazip Suratman is a Professor of Forestry at the Faculty of Applied Sciences, and a Principal Fellow at the Institute for Biodiversity and Sustainable Development, Universiti Teknologi MARA (UiTM), Malaysia, He earned a B. Sc in Forestry from Universiti Putra Malaysia (UPM) and an M. S from the University of Nebraska-Lincoln (UNL), USA. He was then honored with a prestigious fellowship from the Canadian Commonwealth to pursue a Ph.D. degree at the University of British Columbia (UBC), Canada, where he worked on the application of remote sensing for forest resources management. He has been involved in numerous collaborative international research projects that led to publications in reputable journals. Altogether, he has published a total of 14 books and more than 200 research publications. His research interests cover several aspects of forestry, mainly forest modeling, forest ecology, and biodiversity. He received the UiTM’s Best Researcher and Top Talent Awards in 2015 and 2021, respectively. 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