Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
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We wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\n
Throughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\n
We wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
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1. Introduction
Wheat is one of the most important cereal staple food crops in the world, both in terms of food production and for providing the total amount of food calories and protein in the human diet [1]. It is believed that bread wheat originated in south western Asia from where it spread to other regions of Asia, Europe, Africa and America [2]. Wheat has adapted itself to diverse climatic conditions and, as such, is grown over a range of altitudes and latitudes under irrigated, severe drought and wet conditions. The global demand for wheat is projected to rise by 60% by 2050 because of the increase in the world’s human population and changing livelihoods. Wheat production has been threatened by unexpected abiotic and biotic stresses due to abrupt environmental changes or movement of pathogens. The monoculture of modern wheat cultivars with low genetic diversity has resulted in pathogen resurgences, which threaten wheat supplies [3].
Biotic stress in plants is caused by several living organisms namely fungi, virus, insects, nematodes, arachnids and weeds. Unlike the stresses caused by environmental factors i.e. abiotic stresses (heat and drought), the biotic stress agents directly affect the host growth and development by depriving them of nutrition resulting into reduced plant vigor and in extreme cases, even death of the host. From the agricultural context, biotic stress has major contribution in pre as well postharvest losses. Of the nearly 200 diseases and pests that have been documented, 50 are considered economically important because of their potential to damage crops and affect farmers’ incomes [4]. Among biotic stresses, pathogenic fungi represent a significant challenge to wheat production globally. The major diseases in wheat involves stripe rust, stem rust, leaf rust, powdery mildew, head blight etc. Historically, yellow rust has caused and is presently causing significant and severe losses in susceptible wheat cultivars worldwide [5]. The major insect-pests attacking wheat are aphid, hessian fly, green bug and borers etc.
In this chapter, the major diseases and pests detrimental to wheat crop along with the molecular basis of stress resistance will be discussed. Moreover, the remarkable global milestones being achieved along with some important tools and prospects for mitigating with these economically important diseases and pests will be focused.
2. Biotic stress resistance in wheat
2.1 Types of disease resistance
There are basically two types of genetic resistances as described by Vander Plank [6] for the different diseases in wheat i.e. Qualitative/Vertical resistance and Quantitative/Horizontal resistance.
2.1.1 Qualitative (vertical) resistance
It is specified to pathogen races controlled by a single or few genes i.e. monogenic or oligogenic. Race-specific is used to describe resistance that interacts differentially with different pathogenic races i.e. it is applied both to complete resistance and components of incomplete resistance that so interact [7]. This kind of resistance is easily detectable with specific pathogenic races or pathotypes which are controlled by genes with major effects. In wheat rust pathosystems, these resistances are recognized by characteristic low infection types. Most of these genes can be detected in seedling evaluations using specific pathotypes. For every resistance gene in the host plant, there is a corresponding virulent gene in the pathogen as stated by gene for gene hypothesis. However the ability of a virulent gene to mutate to avirulent gene, no longer recognizable by the corresponding resistance gene, implies a type of resistance termed race-specific resistance.
2.1.2 Quantitative (horizontal) resistance
This kind of resistance varies in continuous way among the different phenotypes of the host population, ranging from almost imperceptible to quite strong resistance response. The resistance expression depends upon the genotype and environment, where pathogen is the part of that environment. The environment can considerably affect its durability also [7]. Partial resistance is supposed to be under polygenic control and such resistance will be race-nonspecific. Being controlled by minor genes, the quantitative resistance has complex genetic basis which operates against all the pathotypes/races of that specific pathogen. Race-nonspecific resistance is mainly effective at the post-seedling and adult plant stages and adult plant resistance (APR) is often detected as field resistance [8]. The best known APR genes in wheat are Sr2 (stem rust resistance gene) and Lr34, a gene that provides resistance to leaf and stripe rust and powdery mildew. These genes have been used in commercial wheat varieties for almost 100 years. Sr2 and Lr34 have provided partial resistance for decades over large areas and under prolonged disease pressure in the field, proving their durability. Adding to complexity, Ug99 had a very wide spectrum of virulence towards most of the commonly used R genes and rapidly evolved virulence to the important R genes (Sr24 and Sr36) which has impeded the initial emergency breeding response to incorporate resistance to this strain [9].
2.2 Types of insect resistance
Insect resistance on the other hand is typically governed by three main mechanisms.
2.2.1 Single or oligogenic resistance
Single or oligogenic resistance has been observed against some insects such as Hessian fly in wheat. Such resistance is governed by a single or few major genes. This type of resistance has also been reported against Russian wheat aphid and green bug.
2.2.2 Polygenic resistance
Several genes with small additive effects govern the resistant response against some insects. The resistance observed against cereal leaf beetle in wheat is of this type.
2.2.3 Cytoplasmic resistance
Cytoplasmic resistance against insects has not been reported in case of wheat. However, in maize resistance against European corn borer is governed by cytoplasmic genes. Another case of cytoplasmic resistance is observed in lettuce against root aphid.
3. Major diseases of wheat
There are many diseases found in wheat caused by different microorganisms from fungi to bacteria and viruses. But only a few of them caused by pathogenic fungi are economically important with global implications. The major diseases in wheat (Table 1) are stripe rust, leaf rust, stem rust, powdery mildew, loose smut, Fusarium head blight (FHB) and more recently wheat blast (WB) also. Besides Stem rust, which is under control to some extent, Leaf rust and yellow rust have the potential to affect production levels up to 60 and 43 million hectares respectively in Asia if susceptible cultivars were grown [10]. Though fungicidal applications offer control, their use is an added cost to farmers besides being unsafe environmentally. Hence growing resistant cultivars is the most effective and efficient control strategy [11]. The rusts and mildew diseases are caused by biotrophic fungi (survive by obtaining nutrients from living plant tissues). Among these, Puccinia rusts continue to affect and threaten the world’s wheat production [12], although powdery mildew has also emerged as an economically important disease. In case of stem rust, the emergence of Ug99 group of stem rust races placed it among one of the most significant threats to global wheat production [13].
S no
Disease
Causal Pathogen
Behavior
No. of R-genes identified
1.
Stripe rust (yellow)
Puccinia striiformis f. sp. tritici
Biotrophic
95
2.
Leaf rust (brown)
Puccinia triticina
Biotrophic
80
3.
Stem rust (black)
Puccinia graminis f. sp. tritici
Biotrophic
67
4.
Powdery mildew (PM)
Blumeria graminis f. sp. tritici
Biotrophic
70
5.
Karnal Bunt (KB)
Tilletia indica
Biotrophic
6
6.
Fusarium head blight (FHB)
Fusarium graminearum
Necrotrophic
7
7.
Wheat blast (WB)
Magnaporthe oryzae pathotype triticum
Necrotrophic
5
8.
Loose Smut (LS)
Ustilago tritici
Biotrophic
10
Table 1.
Major diseases of wheat with their respective behavior and number of resistance genes identified for each disease (up to 2020).
The other diseases like FHB and WB are caused by necrotrophic fungi (facultative parasites feeding on dead tissue during unavailability of living plants). Wheat blast was first identified in Parana, Brazil in 1985 [14]. It is also of utmost significance as WB outbreaks in Bangladesh [15] and more recently in Africa [16] have attracted immediate global attention from the wheat scientists.
Another economically significant disease, Karnal Bunt (KB) of wheat was first reported in Karnal, India [17], soon extended to Northern and Central India. Later, KB was found to occur in Nepal, Pakistan, Iraq, Afghanistan, South Africa, Mexico and USA [18]. The pathogen is seed, soil and airborne in nature, therefore difficult to control after it is introduced and then established over a region. Although host plant resistance is the most effective and economic method of its management but development of KB resistance varieties is difficult task owing to limited genetic variability in hexaploid wheat [19], quantitative inheritance and considerable impact of environment on KB resistance screening [20].
4. Major insect-pests of wheat
Various insect pests delimit the yields of wheat crop in different agro-climatic zones. Some of these insect pests are foliar aphid complex in irrigated wheat, root aphids in loose soils, pink stem borers in fields having rice stubbles, cut worms in residues, termites in raised beds and brown mites in rainfed conditions [21]. Six different species of aphids are reported to attack cereals. Out of these, Russian wheat aphid and bird cherry-oat aphid are important pests of wheat. The Russian wheat aphid (Diuraphic noxia) is a sucking pest of wheat. Aphid attack is characterized by leaf rolling which is the result of toxic injection by the aphid. The rolled leaves serve as a protection site for the insects. Yield losses up to 40% have been reported in case of aphid infection [22]. The bird cherry oat aphid (Rhopalosiphum padi) has been reported to affect wheats all over the world. Feeding symptoms are almost absent. Yield losses due to R. padi dependent upon the crop stage at which insect attacks. High yield losses upto 24–65% have been reported in case the attack occurs at seedling stage. Losses decrease if attack occurs at later stages [23]. The aphid is also reported to cause significant indirect losses as it is a vector of Barley Yellow Dwarf Virus (BYDV), which is the most important viral disease in cereals. Greenbug (Schizaphis graminum) is another sucking pest of the wheat aphid complex. The green bug feeds on wheat leaves and stems, extracting sap from the phloem. Injection of toxins concomitant with feeding further reduces the chlorophyll content thereby inversely affecting the carbon assimilation and overall plant development [23, 24, 25].
Cephus spp., the wheat stem sawfly has also been reported to cause major losses in wheat. The adult females oviposit into the young stems of wheat. Upon hatching within the stem, the larvae feed voraciously moving up and down in the stem. When the plant attains maturity, larvae migrate to the basal portion of the stem and build a hibernaculum. The stem above the hibernaculum weakens and breaks [26]. The Hessian fly (Mayetiola destructor) is another major pest of wheat crop. Larvae damage stems of plants, thereby preventing internode elongation and disrupting nutrient transport. Significant losses (upto 40%) have been reported upon sawfly attack [27].
5. Molecular basis of disease resistance in wheat
Wheat is an allopolyploid, means a polyploid species that resulted from interspecific or intergeneric hybridization of two or more genomes from different species. Polyploidy, a common form of plant evolution, is associated with promoting the genetic diversity that facilitates adaptation to a range of environments. Because wheat is a global crop, it is under continuous exposure to a large variety of parasite species and strains, many of which have the ability to move around the globe. Long-term co-evolution between plants and their pathogens has equipped plants with a sophisticated multi-layered immune system to guard themselves against pest and pathogens [28]. Specificity between pathogenic variants (races) and plant genotypes (cultivars) follows gene for gene-for-gene interactions, whose outcome is conditioned by alleles of a gene regulating resistance (R gene) in plant and alleles of its corresponding gene regulating avirulence (Avr gene) in pathogen [29]. The plant immune system is typically described in terms of two components: pattern triggered immunity (PTI) which is activated by recognition of microbial or pathogen-associated molecular patterns (MAMPs or PAMPs) and effector-triggered immunity (ETI) involving gene for gene kind of resistance [30, 31]. ETI is often based on the recognition of cytosolic effectors by immune receptors with a conserved nucleotide-binding domain (NBARC) and a leucine-rich repeat domain (LRR) also called NLRs. This type of resistance is usually associated with a hypersensitive response (HR) localized to infection sites. To date, only a handful of these biotic stress resistance genes have been isolated and cloned in wheat (T. aestivum). Donors of the R genes are genetically diverse, including species in the primary gene pool (Triticum spp.), secondary gene pool (e.g. T. timopheevii), and tertiary gene pool (e.g. Aegilops, Secale, and Thinopyrum).
A few resistance genes have been cloned for race-specific resistance in wheat so far, which belong to a conserved gene family encoding NBS-LRR (Nucleotide binding site-leucine-rich repeat) proteins, also known as R-proteins (NLR) [30]. For example, powdery mildew genes, Pm3 and Pm8 and leaf rust resistance genes Lr10 and Lr21. These R-proteins impart complete but race specific resistance. NBS-LRR proteins are a conserved class of immune receptors that directly or indirectly recognize pathogen-specific effector proteins. These proteins are secreted by pathogens into the host cell to suppress defense response and to establish infection. Recognition of effectors by NBS–LRR proteins triggers a signaling cascade resulting in a strong resistance response called hypersensitive reaction (HR) [31]. HR eventually leads to death of the infected host cell by this means preventing further spread of the pathogen [32]. Since this type of disease resistance depends on the recognition of specific pathogen effectors, even point mutations within effector genes or their loss can disrupt recognition by the corresponding NBS–LRR protein. Such mutations in pathogen effectors result in the emergence of new virulent pathogen races and breakdown of disease resistance. Mutated pathogen spores that avoid recognition by the corresponding R gene will have a huge selective advantage facilitating their rapid multiplication. Dispersal of fungal pathogens by wind over long distances adds to the quick spread of newly evolved virulent pathogen strains. Ug99, for instance, spread out from Kenya to South Africa and the Near East in less than a decade.
So far, only 31 genes have been cloned (Table 2) for biotic stress resistance (30 for disease resistance) from bread wheat and its wild relatives. Among these, most of the genes impart race specific resistance to the plant. These R-genes encode proteins with an NBS-LRR domain with a coiled-coil (CC) domain. This type of gene typically shows a greater degree of variation in LRR-encoding sequences [60, 61]. This is consistent with the idea that the LRR-encoding sequence is important for target specificity [61, 62]. The sequence variation in NBS-encoding region can also play significant role in specificity. For powdery mildew resistance, Pm3 locus encodes seven alleles (Pm3a–Pm3g) providing resistance to different races of Blumeria graminis f. sp. tritici [63]. Sequence analysis indicated that the Pm3 alleles evolved either by gene conversion/recombination or by single point mutations within the NBS and LRR regions [61].
List of major cloned resistance genes in wheat for different biotic stresses.
ABC- ATP binding cassette.
START- Steroidogenic acute regulatory protein-related lipid transfer domain.
PFT- Pore-forming toxin.
5.2 Transporter proteins: basis of durable/adult plant resistance (APR)
Due to rapid pathogen evolution, R gene resistance is often not durable. One strategy to increase the longevity of disease resistance in wheat cultivars is to pyramid several R genes in one cultivar. To overcome such resistance gene stacks, simultaneous mutations in several effector genes would be required in one single pathogen spore. Race-non-specific resistance is supposed to be more durable when deployed in agriculture. Such kind of resistance mechanism sometimes may also be effective against multiple pathogens. These are normally quantitative traits conferring partial resistance that is able to slow down disease development. For example Lr34, Yr36, and Pm21. Lr34 confers non-specific, partial, and slow rusting resistance, and has been deployed worldwide, maintaining its effectiveness in agriculture for decades. Due to its role in conferring resistance to pathogens other than leaf rust, it is also known as Yr18, Pm38, Sr57 and Bdv1 for resistance to stripe rust, powdery mildew, stem rust, and barley yellow dwarf virus, respectively [64]. The successful cloning of Lr34, Yr36, and Lr67 revealed these APRs encode an ABC transporter, a kinase-START protein, and a hexose transporter, respectively (Table 2). They appear to each have their own resistance mechanism, function constitutively and often increase the basal level of resistance of the host, which is different from the recognition based NLRs.
6. Insect resistance in wheat
6.1 Resistance categories
Responses which govern insect resistance in plants can be classified into three categories. Tolerance can be defined as the response of plant which allows the plant to survive insect damage with low or no damage to the yield. Tolerance is generally governed by a complex set of genetic traits. Tolerance does not affect the overall survival of insects thereby poses no selection pressure. Tolerance has been reported in a number of crops [65, 66]. The non-preference of a plant by insect pest or antixenosis is another mechanism used by plants against insects. Generally, antixenosis is manifested by some morphological or chemical factors which hinder feeding of the pest and sometimes rejection as host. Antibiosis, the third category, can be defined as the condition when pest health and reproduction are negatively affected by the resistant plant. Most of the resistance observed in field (up to 90%) is due to antibiosis.
6.2 Resistance mechanisms
Over the due course of evolution traits for direct and indirect defense mechanisms against insect attacks have developed in plants. The classification of these mechanisms has been further done as direct mechanisms and indirect mechanisms. Structural barriers constitute the direct defenses. Tissue toughness, glandular and non-glandular trichomes and plant pubescence are included in these types of defenses. Allelochemicals in plant tissues are also included in direct defenses. These exhibit toxic, anti-feedant, and repellent effects on the attacking arthropods. The digestive enzyme inhibitors, cyanogenic glycosides, glucosinolates, lectins, glucosinolates, terpenoids and alkaloids are involved in this [67, 68]. An extensive review of constitutive & induced morphological & chemical plant defenses has been done [65, 66, 69, 70]. These defenses mediate antixenosis & antibiosis. Volatile organic compounds constitute the indirect defenses. The plants which are damaged by pest arthropod release these compounds. These compounds lead to attraction of arthropod predators & parasitoids or the ones that cause repelling of oviposition of pest arthropods [71]. The specific plant indirect defense responses are represented by herbivore associated molecular patterns (HAMPs). These are the responses to the specific herbivore derived elicitors. This occurs in the in oral or ovipositor secretions. These facilitate indirect defenses against herbivores [72]. The widely researched HAMPs are the insect fatty acid plant amino acid conjugates. These are obtained from the lepidopterous larvae [71, 73].
6.3 Constitutive and induced resistance genes
The arthropod selects host plant tissue substrate based on well-coordinated interactions occurring within evolutionarily conserved protein(s) which are encoded by attacking arthropod & responding host plant. The arthropod successfully manipulates the host plant as a result of suitable arthropod-plant interactions. When there is incompatibility in the arthropod-plant interaction, the arthropod does not succeed resulting in the survival of the plants attacked [74]. The plant and fungal endophytic genes are expressed in both the interactions. These are expressed constitutively or via induced defense responses. These occur following herbivory and find involvement in arthropod resistance [75, 76].
Under field conditions, resistance has been explained more clearly by the effects which are controlled by the constitutive genes. This is concluded based on the limited research done till date. The effects owing to the induced gene expression do not contribute much in this [77, 78]. The generation of reactive oxygen species and the signal cascades which involve salicylic acid (SA), jasmonic acid (JA), abscisic acid, ethylene and gibberellic acid occurs in plants as a response to arthropod herbivory. Direct and indirect defense proteins are resulted by the downstream production [79, 80, 81, 82]. The aphid bacterial endosymbionts could also lead to defense signals [83]. Jasmonic acid based transcriptomes are elicited by the plant tissue damage caused by arthropods with chewing mouthparts. On the contrary, arthropods with piercing-sucking mouthparts induce the jasmonic acid- salicylic acid-based transcriptomes [71]. Recent documentation has been done of the jasmonic acid- salicylic acid signaling induced by both types of herbivory and jasmonic acid- salicylic acid cross talk [68, 74, 84, 85]. The expression of several plant genes which are produced in the initial responses to arthropod herbivory are controlled by the JA, 12- oxo-phytodienoic acid, and jasmonoyl-amino acid conjugates (which are governed by zinc finger protein expressed in inflorescence meristem) repressor proteins [86]. Several defense allelochemicals are produced by the defense response gene upregulation. This occurs via JA and some other pathways [69]. Scanty information is available regarding the arthropod induced expression of the plant metabolism genes. There are very few evidences indicating the down regulation of few of these genes. This is reported to occur in the beginning just after the arthropod herbivory sets in and later on upregulated in the ensuing days [84, 87].
The identification of arthropod pest elicitors of resistance genes is yet to done. An undefined elicitor protein of Diuraphis noxia is recognized by the wheat plant receptors. D. noxia is recognized by plant-signaling gene products feeding in incompatible interactions [88]. Secondary metabolites possessing the Hydroxamic acids (Hx) (1,4-benzoxazin-3-ones) group, find involvement in the resistance of certain cereals against bacteria, fungi and several insects including aphids [89]. In the seed, Hydroxamic acids (Hx) are absent. This increases after germination. The young seedlings exhibit the concentration peak [90]. This is basically located in the mesophyll protoplasts, the vascular bundles [91] and in the sieve elements [92]. In the mature plants, the Hx levels decline after the seedling stage. Even then, the young tissue still exhibits a high concentration of Hx [90]. In the plants, the Hx compounds occur as 2-β-O-D-glucopyranosides [90]. When the tissue is injured, these are enzymatically hydrolyzed by endo-β-glucosides to DIMBOA (2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3- one) [92]. DIMBOA is the main Hx aglucone in the wheat extracts. It leads to antibiosis, decreased performance, feeding deterrence and reduced reproduction in aphids [93].
An enhancement in the overall activity of several enzymes was observed. All the enzymes such as superoxide dismutase, phenylalanine ammonia lyase glutathione reductase, and polyphenol oxidase have a major role in the defense of plants towards the feeding of aphid [94]. An early defense strategy is mounted by the Hessian fly-resistant Ae. tauschii. The production of anti-feedant proteins (lectins), secondary metabolites and ROS radicals is involved in this strategy. These successfully counter the larval extra oral salivary plant cell degrading proteases, lead to fortification of the cell wall and prevention of the Hessian fly larvae from establishing permanent feeding sites [95].
There are different types of carbohydrate binding proteins known as lectins which are present in tissues of plants. Resistance building potential is possessed by these lectins for wheat against insects. To tackle HF, the identification of genes leading to production of this type of lectins seems a potential method. The genes include Hfr-2 called as HF destructor. This is expressed in the leaf sheaths of the resistance genotypes [96] On similar lines, the mannose binding lectins serve as storage protein and accumulate in the phloem sap. This might act against HF. Anti-insect properties are possessed by these lectins. This is attributed to the accumulation of lectin in the midgut of insects, killing them instantly. Another defensive mechanism present in resistant varieties of wheat is the production of Wci-1 mRNAs and Hfr-1. This occurs in response to the attack of HF larvae. The Hfr-1 gene is known as the defender gene against HF. It has the ability to control crop from severe attack [97]. The identification of arthropod pest elicitors of resistance genes is yet to done. An undefined elicitor protein of Diuraphis noxia is recognized by the wheat plant receptors. D. noxia is recognized by plant-signaling gene products feeding in incompatible interactions [88]. An Avirulence (Avr) gene is there on the parasites side. This encodes one of the several effector proteins that the parasite applies to the plant to help in colonization. A Resistance (R) gene is there on the plant’s side. It mediates a surveillance system which detects the Avr protein. The detection is done either directly or indirectly. It triggers effector-triggered plant immunity. The arthropods are responsible for a significant proportion of plant biotic stress but even then they have not been integrated into important models of plant immunity that arise from plant pathology. The absence of molecular evidence for arthropod Avr effectors has been a limiting factor. This evidence was discovered in a plant pathogen around thirty years back. Now, there is evidence for arthropods with the cloning of the Hessian fly’s vH13 Avr gene. Resistance against RWA is supposed to be induced by gene-for-gene model. The resistant gene produces a protein in this mechanism. This protein contains nucleotide binding site-leucine rich repeat (NBSLRR) domain [98, 99]. Firstly, this NBSLRR domain recognizes and then interacts with cognate Avr protein which is produced by the respective insect [100]. It has been reported that another domain (serine/threonine-protein kinases: STKs) is produced by Dn genes. This confers resistance against the RWA [101].
7. Sources of biotic stress resistance in wheat
Wheat belongs to the kingdom Plantae and family Poaceae. It is a long day and a self-pollinated crop. The bread wheat (Triticum aestivum) genome is one of the most challenging plant genomes to study. It is highly repetitive (~85%) and approximately 15.4–15.8 Gbp in size, which is five times larger than the human genome [102]. The genus Triticum contains 10 species, out of which six are cultivated and four are wild. Hexaploid wheat (T. aestivum) genome (2n = 6x = 42) encompasses A, B and D sub-genomes which is advantageous for providing useful genetic diversity for crop improvement. There are three ploidy levels in Triticum and Aegilops (encompassing cultivated wheats and their progenitors) genera with 2n chromosomes 14, 28, 42 and the basic chromosome x = 7 in all the species. Other genera of Poaceae such as Secale, Hordeum, Dasopyrum, Agropyron, Elymus, Leymus, Elytrigia, and Thinopyrum are also important for introgression of useful variability into cultivated wheats. On the basis of their genomic constitution, the wild relatives of wheat can be classified into primary, secondary, and tertiary gene pools [103, 104]. These gene pools are affluent source of genes for disease and pest resistance, mitigating abiotic stresses and micronutrient enrichment in wheat. These three gene pools of wheat as sources of resistance can be described as follows:
The primary gene pool consists of species sharing homologous genomes with cultivated wheat. This group includes land races of T. aestivum, T. turgidum and donor species of the A and D genomes of bread wheat-T. monococcum, T. urartu, T. boeoticum and Ae. tauschii. Gene transfer from these species can be achieved by direct hybridization, backcrossing, and selection [104]. Just embryo rescue in certain cases is necessary to produce F1 hybrid. Many genes conferring resistance to diseases and insect pests have been transferred using this method and several of them are still being exploited in cultivar improvement [105, 106]. Among genetic resources, landraces has been reported a crucial germplasm pool contributing to the genes for grain yield [107, 108] high protein content and tolerance to biotic/abiotic stresses [109]. The green revolution semi-dwarfing genes (Rht- B1b and Rht-D1d) [110] and other semi-dwarfing gene, Rht8c, has been a significant contribution of the landraces. The Rht dwarfing gene that was available through the Japanese variety ‘Norin10’ originating from a Japanese landrace Shiro Daruma [111]. Later, these dwarfing genes were utilized by Dr. Norman E. Borlaug to develop the high-yielding semi-dwarf wheat varieties triggering the Green Revolution in late 1960s.At Punjab Agricultural University (PAU), Ludhiana, India, an active collection of 280 Ae. tauschii accessions is being maintained. These accessions have been found to carry resistance genes for various biotic stresses including leaf rust, stripe rust, powdery mildew, and Karnal bunt. Ae. tauschii has a very high level of KB resistance.
The secondary gene pool of bread wheat includes the polyploid Triticum and Aegilops species that have at least one genome in common with wheat. Gene transfer from these species by homologous recombination is possible, if the target gene is located on a homologous chromosome. However, if the genes are present in a non-homologous genome, special cytogenetic manipulations are required. These species have contributed many resistance genes that are being used in cultivar development [103]. At PAU, the genes for disease resistance and HMW glutenin subunits have been successfully transferred from several Triticum and Aegilops species into wheat and durum cultivars with direct hybridization and backcrossing [112, 113].
Species belonging to the tertiary gene pool are more distantly related. Their chromosomes are not homologous to those of wheat. Gene transfer from these species cannot be achieved by homologous recombination, chromosome pairing, and recombination between wheat chromosome and alien chromosomes [103, 104]. Special cytogenetic techniques (in-situ hybridization) are required to ensure compensating transfers with least linkage drag for commercial exploitation of introgressed derivatives. Even though such transfers may include an entire chromosome arm or part of an arm, these have been successfully bred into commercial wheat cultivars because the alien chromosome segment genetically compensates for the missing wheat segment.
8. Major techniques for inducing biotic stress resistance
The route maps followed for a trait improvement particularly stress resistance, both biotic and abiotic remain the same. The Figure 1 graphically depicts various tools and techniques that can be utilized with efficient and effective manner for tackling different biotic stresses in wheat.
Figure 1.
Some major tools and techniques (both in use and under exploration) in wheat breeding for biotic stress resistance.
9. Present scenario
9.1 Fungal diseases
So far, more than 240 rust resistance genes have been characterized and formally designated in wheat or its relatives; most being race-specific resistance genes. At least 67 of these genes are designated as Sr resistance genes [105, 114, 115]. Sr31 was one of the most widely utilized race-specific Sr resistance genes [116]; however, its presence at the International Maize and Wheat Improvement Center (CIMMYT) has been drastically reduced following testing against Ug99 races in Kenya. Evolution of virulence against Sr31 with the emergence of Ug99 led to stem rust susceptibility in most of the wheats grown around the globe. After its new races overcame a number of resistance genes, the genes Sr2, Sr23, Sr25, Sr33, Sr35, Sr45, Sr47, and Sr50 are presently the most efficient for protection against newly evolved races [117]. The QTL-controlling stripe rust resistance in T. monococcum was mapped on chromosome 2A (QYrtm.pau-2A), whereas the QTL from T. boeoticum was mapped on 5A (QYrtm.pau-5A). One stripe rust-resistant gene from T. boeoticum acc. pau5088 was confirmed to be introgressed in cultivated wheat which was indicated by co-introgression of T. boeoticum sequences linked to stripe rust-resistant QTL, QYrtb.pau-5A [118].
For stripe (yellow) rust resistance, 95 genes have been characterized and formally named [105, 114, 115]. However, most of these genes have been rendered ineffective with emergence of virulent races around the globe with exception of a few combinations, such as the combination of Yr5 and Yr15 that remain effective worldwide. At Punjab Agricultural University, Ludhiana, India, about 200 accessions of T. monococcum and T. boeoticum were screened for leaf rust and stripe rust resistance for several years and we found that all the T. monococcum accessions, most of the T. boeoticum and a few T. urartu accessions, were completely resistant to leaf rust. However, a lot of variation was observed for stripe rust resistance. Leaf and stripe rust resistance genes have also been introgressed from diploid species Ae. umbellulata and Ae. caudata using T. durum as bridging species [118, 119].
Similarly, 80 Lr resistance genes have been genetically characterized and documented [115]. Out of these, Lr1, Lr3, Lr10, and Lr20 have been commonly deployed in wheat cultivars [120]. Generally, ASR genes are rendered ineffective with continual emergence of new virulent races of rust pathogens through mutation and recombination [121]. It has been well documented through cloning of 11 race-specific genes in wheat (Sr22, Sr33, Sr35, Sr45, Sr50, Yr5, Yr10, Lr1, Lr10, Lr21, and Lr22) that these genes encode NLR proteins [122, 123, 124, 125, 126].
Till date, only seven race non-specific APR genes have been genetically characterized and formally designated in wheat namely Sr2/Yr30, Lr34/Yr18/Sr57/Pm38, Lr46/Yr29/Sr58/Pm39, Lr67/Yr46/Sr55/Pm46, Lr68, Sr56, and Yr36 [127, 128, 129, 130, 131, 132, 133]. Cloning of the APR genes Yr36, Lr34/Yr18/Sr57/Pm38 and Lr67/Yr46/Sr55/Pm46 has revealed the roles of cytoplasmic protein kinase, adenosine triphosphate (ATP)-binding cassette transporter, and hexose transporter, respectively in mediating resistance [134, 135, 136].
Growing resistant cultivars is the most cost-effective strategy for tackling PM. To date, 70 PM resistance genes have been formally cataloged; most of these provide race-specific resistance in wheat [114, 115]. It is desirable to know the virulence pattern of isolates to generate effective combinations of race-specific resistance genes [137]. More effective method would be deployment of combinations of race non-specific resistance genes is a promising method. As discussed above in the section for rust resistance, only three race non-specific resistance genes have been identified, out of which two pleiotropic genes (Lr34/Yr18/Sr57/Pm38 and Lr67/Yr46/Sr55/Pm46) have been cloned [135, 136].
Genetic resistance to FHB is mainly quantitative and is controlled by multiple moderate to minor genes [138]. Although genetic resistance is the most cost-effective method, it is hard to accomplish in commercial cultivars due to its complex behavior. This complexity is further enhanced by various resistance mechanisms, e.g., invasion (type I), fungal spread (type II), toxin accumulation (type III), kernel infection (type IV) and yield reduction (type V) [139]. FHB resistance also displays significant correlations with heading, plant height, and anther extrusion of the wheat plant [140]. To date, seven genetic loci designated as Fhb1, Fhb2, Fhb4 and Fhb5 from wheat, and Fhb3, Fhb6 and Fhb7 from wild relatives, have been formally named as FHB resistance genes [141]. The cultivars Sumai 3 from China and Frontana from Brazil have been identified as sources of moderate resistance to FHB.
Karnal bunt is among the few quarantine diseases that restrict free trade among countries due to quarantine regulations [142]). Resistance to Karnal bunt has been reported in durum wheat (Triticum turgidum), common wheat, Aegilops, rye and barley under artificial conditions [143, 144]. Susceptibility of T. aestivum to Karnal bunt might be due to presence of an additional D genome [145, 146]. Sharma et al. [147] at PAU developed high yielding Karnal bunt resistant wheat lines by introgression of Karnal bunt resistance from KBRL 22 into the background of high yielding PBW343. Studies on deciphering genetics of resistance have indicated the presence of quantitative rather than qualitative resistance [145, 146, 148]. Fuentes-Davila et al. [145] suggested six genes, designated Kb1, Kb2, Kb3, Kb4, Kb5, and Kb6, while Villareal et al. [149] postulated a minimum of three genes for resistance. Studies on deciphering genetics of resistance have indicated the presence of quantitative rather than qualitative resistance [145, 148].
For loose smut, the majority of genetic studies carried out thus far have demonstrated simple inheritance with one, two or three major genes in hexaploid wheat controlling resistance to several races of U. tritici. The first four loose smut resistance genes Ut1 to Ut4 were named based on segregation of avirulence in U. tritici [150, 151]. Genes Ut1 and Ut3 have no chromosome assignment. Based on pedigree, the gene symbol Ut2 was assigned to the resistance gene on chromosome 6A to race T19 [152]. Ut4 associated with the Thatcher derived differential line TD12A, was located on chromosome 7B [153, 154]. Ut5 was located on chromosome 2BL [155], Ut6 was initially reported on chromosome 5B by Kassa et al. [156] which was later validated by Knox et al. [153]. A gene located to chromosome 7A by Dhitaphichit et al. [157] was subsequently named Ut7 [153]. Knox et al. further identified genes Ut8 on chromosome 3A, Ut9 on chromosome 6B and Ut10 on chromosome 6D. Several studies revealed the additive nature of resistance genes, while in some cases, duplicate complementary action of multiple genes was also implicated [158].
Finally, the genetic resistance to wheat blast at the seedling stage follows a gene-for-gene interaction model [159] and five resistance genes namely Rmg2, Rmg3, Rmg7, Rmg8, and RmgGR119 have been identified in wheat against the Magnaporthe oryzae pathotype triticum [160, 161, 162, 163, 164].
Various molecular markers have been widely used to tag and map resistance genes in wheat; however, SSRs have emerged as the choice of marker in gene-mapping studies. These markers can be strategically used for selection of desirable gene combinations along with phenotypic assays. Wheat has more than 3000 SSR markers mapped so far [165]. Molecular markers can be used for alien gene transfers and understanding the mechanism of gene transfer. Such markers ensure selection of a target gene based on the presence of the linked genotype. The success of selection depends on the close genetic association and robustness of a given marker across different genetic backgrounds. At PAU, a number of genes/QTLs have been mapped for different wheat diseases including stripe rust, cereal cyst nematode, and Karnal bunt. Two QTLs, one each in T. monococcum acc. pau14087, and T. boeoticum acc. pau5088, were detected for resistance in the RIL population. The QTL in T. monococcum mapped on 2A in a 3.6 cM interval between Xwmc407 and Xwmc170, whereas the QTL from T. boeoticum mapped on 5A in 8.3 cM interval between Xbarc151 and Xcfd12 [166, 167, 168].
9.2 Insect-pests
In the last 50 years or so, the HPR concept has been extended to insect-host interactions. As a result, insect resistant cultivars are now in the picture. The variables, both biotic and abiotic which play a major role in deciding the plant reaction to pest, along with mechanisms and categories of resistance are now better understood. Drawing analogy from plant-pathogen interactions, pest-host relationships are now being viewed as (susceptible plant) and incompatible (resistant plant) interactions [74].
Deployment of insect resistance genes in wheat along with other field crops has increased steadily over the years from mid 60s. Marker assisted selection (MAS) and breeding has sped up the process of identification of resistance loci and QTLs and understanding of the mechanisms governing the resistance. Table 3 depicts the genes identified for insect resistance in wheat and their respective categories.
Wheat is an allopolyploid resulted from interspecific or intergeneric hybridization of two or more genomes from different species. Being one of the most consumed and cultivated crop globally, it is under continuous exposure to a large variety of parasite species and strains, many of which have the ability to move around the globe. Long-term co-evolution between plants and their pathogens has equipped plants with a sophisticated multi-layered immune system to guard themselves against pest and pathogens [178]. Despite this, there are a few important challenges which are required to be addressed for effectively mitigating with different biotic stresses in wheat:
New strains of pathogens like the rusts continue to evolve rapidly. It is well documented that the rust pathogens have great pathogenic variability and the frequent emergence of new virulent strains that overcome resistance genes present in cultivated wheat varieties has hindered efforts to achieve durable resistance to these pathogens.
The complex nature of plant–parasite interactions can be overwhelming while breeding for disease resistance in wheat. The standard models of plant pathology i.e. gene for gene model and the expanded model of plant immunity do not elucidate plant immunity and parasite adaptation explicitly in such natural interactions.
The bread wheat (Triticum aestivum) genome is one of the most challenging plant genomes to study. It is highly repetitive (~85%) and approximately 15.4–15.8 Gbp in size [179]. Much of the desirable genetic diversity is present in the wild relatives of wheat, both in progenitors and non-progenitor species. The genomic complexity of bread wheat and various hybridization barriers hinder the potential use of resistance alleles present in that germplasm.
Despite the versatility of transgenic technology with unlimited scope for application in wheat resistance breeding, it has faced increasing public dissent especially against its use in food crops. Other issues include rigorous risk assessments of crop, which are time-consuming and cost-intensive. Such modifications lead to integration of transgenes randomly into plant genomes along with their selection marker genes. Due to which, there is a possibility of pleiotropic effects, potential silencing and varied gene expression in modified plants
Traditional map based/positional cloning is not viable for target genes derived from wild relatives of wheat and which are located in introgressed genome segments that do not recombine with wheat chromatin. Applying this strategy on genes that are located in centromeric regions is also extremely challenging (low recombination rates there).
The foremost challenge in breeding against insect pests is finding sources with reasonable levels of resistance against the pest. Secondly another major hurdle is the difference between resistance at field and protected conditions, since evaluation is carried out in protected conditions, results vary when evaluation is carried out in vivo. Lack of efficient evaluation and selection tools against insects also hinders the insect resistance breeding. Finally, transfer of resistance is often accompanied by linkage drag which sometimes becomes cumbersome to break.
11. Conclusion and future prospects
Genetic control is considered as the most effective and environmentally friendly strategy to control rust disease and involves breeding effective disease resistance genes into wheat cultivars. Many rust resistance genes have been identified genetically, and introgression into wheat lines is increasingly being facilitated by the development of robust molecular markers. However, the massive and complex genome of wheat poses major challenges for the isolation of individual genes. As revealed by the increasing number of newly available whole genome sequences and the more precise bioinformatic pipelines developed for identifying NLR genes, the number of NLR genes varies greatly between species. Based on an analysis of the IWGSC RefSeq v1.0 assembly, a total of 3,400 full-length NLR loci have been documented [180]. The approaches for identifying effective resistance genes therefore, must consider both classical R-genes (immune receptor class genes) as well as other novel classes that may operate via different mechanisms.
Cloning of the genes that controlling resistance to rust pathogens will significantly advance our understanding of the molecular basis underlying expression of disease resistance in wheat. Only a small number of rust resistance genes have been cloned and had their molecular functions studied (Table 2). To overcome the limitations of the map-based cloning strategy in the large genome of wheat, alternative approaches were developed and validated by the rapid cloning of several genes using Target-sequence Enrichment and Sequencing (TEnSeq) pipelines. These include MutRenSeq (Mutagenesis and the Resistance gene Enrichment and Sequencing), AgRenSeq (Association genetics with R gene enrichment Sequencing), MutChromSeq (Mutgenesis Chromosome flow sorting and short-read Sequencing), and TACCA (Targeted Chromosome based Cloning via long-range Assembly). The common component among all these approaches is the intent to reduce the genome complexity prior to the use of next generation sequencing (NGS). Such insight into the molecular mechanisms will be the foremost step towards the functional characterization of the wheat-rust interaction and allow engineering of new resistance by exploiting novel techniques like allele mining and genome editing. Also, approaches like TILLING (Targeting Induced Local Lesions IN Genomes) can be adopted for more precise and efficient characterization of the function of targeted wheat genes for different fungal and bacterial diseases.
The rich genetic diversity available in wheat is a source of numerous novel alleles for both disease resistance and tolerance to abiotic stress. However, there is still a huge gap in characterization of the available genetic resources and their utilization in breeding programs. Over the years, traditional breeding strategies have successfully incorporated novel alleles into elite germplasm, which has significant impacts on production globally. Use of advanced technologies, marker-assisted selection (MAS), genomic selection, transgenics and genome editing will help to increase the efficiency of wheat breeding for biotic stress resilience around the world.
To escape the boom and bust cycle, resistance gene stewardship and deployment strategies such as gene pyramiding, gene stacking (transfer of gene cassettes) could prove to be effective against deadly diseases of wheat (rusts, blight). It is widely reported and agreed upon fact that the most effective and durable means for genetic control of wheat rusts is the use of combinations of multiple broadly effective ASR and APR genes. Using this, the desirable combinations of effective resistance genes can be combined and transformed into wheat as gene cassettes or stacks. This can result in faster improvements in disease resistance of current high-yielding varieties. Also, the advancements in R-gene cloning pipeline like TEnSeq will provide many more tools for MAS in wheat breeding as well as the raw gene sequences to pursue gene stacking (via transgenic gene cassettes). Combining with advances in identifying genetic variation in rust Avr genes, these new tools will lead to more effective deployment strategies to maximize resistance durability.
Genomic selection (GS) is considered one of the best strategies for selection of multiple minor-effect loci in comparison with MAS. Using GS, a training population (after phenotyping and genotyping) is used to standardize a prediction model, which is further used to predict breeding values, thus enabling selection of candidates prior to phenotyping [181]. Recent studies have reported that greater genetic gains can be obtained by using genomic selection than by using MAS [182] and phenotypic selection [183].
More recently, genome editing has emerged as a prominent new plant breeding technique, which involves targeted modification of a native DNA sequence. For instance, it has been observed that a single amino acid substitution (Arg144Gly) in a hexose transporter in wheat results in the gene Lr67 conferring resistance. This substitution evolved recently after common wheat polyploidization. Introduction of the Lr67 transgene into barley conferred seedling and adult plant resistance to the barley leaf rust pathogen [184, 185]. The orthologue sequence of Lr67 exists in the barley genome; hence altering the Arg144Gly by genome editing would be expected to produce resistance to rust in barley. Similarly, a number of homologs/orthologues of the isolated genes exist in related species. Isolating a rust resistance gene from other related species thus can provide deeper insight into rust resistance in the wheat.
Therefore, under a changing global climate, it is of paramount importance to breed for durable and broad-spectrum disease resistance in wheat at a faster pace to reduce losses from attack by rapidly evolving new virulent pathogenic races. Moreover, this would lead to reduction of the use of agrochemicals (fungicides), escaping environmental and human health hazards, an essential component of modern sustainable crop production systems.
\n',keywords:"Biotic stress, Durable resistance, Genomics, R-genes, Wheat rusts, Wild relatives",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/76290.pdf",chapterXML:"https://mts.intechopen.com/source/xml/76290.xml",downloadPdfUrl:"/chapter/pdf-download/76290",previewPdfUrl:"/chapter/pdf-preview/76290",totalDownloads:303,totalViews:0,totalCrossrefCites:0,dateSubmitted:"February 25th 2021",dateReviewed:"March 22nd 2021",datePrePublished:"April 15th 2021",datePublished:"May 11th 2022",dateFinished:"April 15th 2021",readingETA:"0",abstract:"Wheat (T. aestivum) is one of the key food grain crops and is a prominent source of calories and proteins globally. In addition to mushrooming population and rising abiotic stresses in this ongoing climate change era, biotic stresses pose a great threat to wheat production over the globe. Fungal diseases such as rusts, mildew, along with pests like aphid, hinder the potential yield performance of the elite wheat cultivars to a huge extent. The complex nature of plant-parasite interactions is shown to be the decisive factor for the ultimate resistance expression in wheat. However, the advancement of molecular genetics and biotechnology enabled the replacement of the tedious, time and resource consuming cytogenetic analyses of locating APR and ASR genes using molecular mapping techniques. Continuous efforts have been made to mine resistance genes from diverse genetic resources such as wild relatives for combating these diseases and pests, which are repositories of R genes. Additionally, they offer a promising source of genetic variation to be introgressed and exploited for imparting biotic stress tolerance in cultivated wheat. Though just a handful of R-genes are cloned and molecularly characterized in wheat so far, more than 350 resistance genes for various diseases have been identified and successfully introgressed into elite varieties around the globe. Modern genomics and phenomic approaches coupled with next-generation sequencing techniques have facilitated the fine-mapping as well as marker aided selection of resistance genes for biotic stress resistance wheat breeding.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/76290",risUrl:"/chapter/ris/76290",signatures:"Harmeet Singh Bakala, Kamalpreet Singh Mandahal, Ankita, Loveleen Kaur Sarao and Puja Srivastava",book:{id:"9670",type:"book",title:"Current Trends in Wheat Research",subtitle:null,fullTitle:"Current Trends in Wheat Research",slug:"current-trends-in-wheat-research",publishedDate:"May 11th 2022",bookSignature:"Mahmood-ur-Rahman Ansari",coverURL:"https://cdn.intechopen.com/books/images_new/9670.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:"978-1-83968-594-1",printIsbn:"978-1-83968-593-4",pdfIsbn:"978-1-83968-595-8",isAvailableForWebshopOrdering:!0,editors:[{id:"185476",title:"Dr.",name:"Mahmood-ur-Rahman",middleName:null,surname:"Ansari",slug:"mahmood-ur-rahman-ansari",fullName:"Mahmood-ur-Rahman Ansari"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"245999",title:"Dr.",name:"Loveleen",middleName:"Kaur",surname:"Kaur Sarao",fullName:"Loveleen Kaur Sarao",slug:"loveleen-kaur-sarao",email:"micro.loveleen@gmail.com",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:null},{id:"285325",title:"Dr.",name:"Puja",middleName:null,surname:"Srivastava",fullName:"Puja Srivastava",slug:"puja-srivastava",email:"pujasrivastava@pau.edu",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:null},{id:"327160",title:"Mr.",name:"Harmeet",middleName:"Singh",surname:"Singh Bakala",fullName:"Harmeet Singh Bakala",slug:"harmeet-singh-bakala",email:"harmeet-pbg@pau.edu",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:{name:"Punjab Agricultural University",institutionURL:null,country:{name:"India"}}},{id:"331896",title:"Dr.",name:"Ankita",middleName:null,surname:null,fullName:"Ankita null",slug:"ankita",email:"suhalia.anki6530@gmail.com",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:{name:"Punjab Agricultural University",institutionURL:null,country:{name:"India"}}},{id:"350483",title:"MSc.",name:"Kamalpreet Singh",middleName:null,surname:"Mandahal",fullName:"Kamalpreet Singh Mandahal",slug:"kamalpreet-singh-mandahal",email:"kamalpreet-pbg@pau.edu",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:{name:"Punjab Agricultural University",institutionURL:null,country:{name:"India"}}}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Biotic stress resistance in wheat",level:"1"},{id:"sec_2_2",title:"2.1 Types of disease resistance",level:"2"},{id:"sec_2_3",title:"2.1.1 Qualitative (vertical) resistance",level:"3"},{id:"sec_3_3",title:"2.1.2 Quantitative (horizontal) resistance",level:"3"},{id:"sec_5_2",title:"2.2 Types of insect resistance",level:"2"},{id:"sec_5_3",title:"2.2.1 Single or oligogenic resistance",level:"3"},{id:"sec_6_3",title:"2.2.2 Polygenic resistance",level:"3"},{id:"sec_7_3",title:"2.2.3 Cytoplasmic resistance",level:"3"},{id:"sec_10",title:"3. Major diseases of wheat",level:"1"},{id:"sec_11",title:"4. Major insect-pests of wheat",level:"1"},{id:"sec_12",title:"5. Molecular basis of disease resistance in wheat",level:"1"},{id:"sec_12_2",title:"5.1 NBS: LRR proteins - basis of race-specific/seedling/all stage resistance (ASR)",level:"2"},{id:"sec_13_2",title:"5.2 Transporter proteins: basis of durable/adult plant resistance (APR)",level:"2"},{id:"sec_15",title:"6. Insect resistance in wheat",level:"1"},{id:"sec_15_2",title:"6.1 Resistance categories",level:"2"},{id:"sec_16_2",title:"6.2 Resistance mechanisms",level:"2"},{id:"sec_17_2",title:"6.3 Constitutive and induced resistance genes",level:"2"},{id:"sec_19",title:"7. Sources of biotic stress resistance in wheat",level:"1"},{id:"sec_20",title:"8. Major techniques for inducing biotic stress resistance",level:"1"},{id:"sec_21",title:"9. Present scenario",level:"1"},{id:"sec_21_2",title:"9.1 Fungal diseases",level:"2"},{id:"sec_22_2",title:"9.2 Insect-pests",level:"2"},{id:"sec_24",title:"10. Key challenges",level:"1"},{id:"sec_25",title:"11. 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Theor Appl Genet 110:550-560'},{id:"B166",body:'Chhuneja P, Kaur S, Garg T, Ghai M, Kaur S, Prashar M, Bains NS, Goel RK, Keller B, Dhaliwal HS, Singh K (2008a) Mapping of adult plant stripe rust resistance genes in diploid a genome wheat species and their transfer to bread wheat. Theor Appl Genet 116:313-324'},{id:"B167",body:'Chhuneja P, Kaur S, Goel RK, Aghaee-Sarbarzeh M, Prashar M, Dhaliwal HS (2008b) Transfer of leaf rust and stripe rust resistance from Aegilops umbellulata Zhuk. to bread wheat (Triticum aestivum L.). Genet Resour Crop Evol 55:849-859'},{id:"B168",body:'Chhuneja P, Kaur S, Singh K, Dhaliwal HS (2008c) Evaluation of Aegilops tauschii (L.) germplasm for Karnal bunt resistance in a screen house with simulated environmental conditions. Plant Genet Resour Charact Util 6:79-84'},{id:"B169",body:'Malik R, Brown-Guedira GL, Smith CM, Harvey TL, Gill BS. Genetic mapping of wheat curl mite resistance genes Cmc3 and Cmc4 in common wheat. Crop Sci. 2003;43:644-650.'},{id:"B170",body:'Lanning SP, Fox P, Elser J, Martin JM, Blake NK, Talbert LE. Microsatellite markers associated with a secondary stem solidness locus in wheat. Crop Sci. 2006;46:1701-1793.'},{id:"B171",body:'Sherman JD, Weaver DK, Hofland ML, Sing SE, Buteler M. Identification of novel QTL for sawfly resistance in wheat. Crop Sci. 2010 50:73-86.'},{id:"B172",body:'Lapitan NLV, Peng J, Sharma V. A high-density map and PCR markers for Russian wheat aphid resistance gene Dn7 on chromosome 1RS/1BL. Crop Sci. 2007;47:811-820.'},{id:"B173",body:'Liu XM, Smith CM, Gill BS, Tolmay V. Microsatellite markers linked to six Russian wheat aphid resistance genes in wheat. Theor. Appl. Genet. 2001;102:504-510.'},{id:"B174",body:'BerzonskyWA, Ding H, Haley SD, Harris MO, Lamb RJ. Breeding wheat for resistance to insects.Plant Breed. Rev. Vol. 22. 2010. DOI: 10.1002/9780470650202.ch5'},{id:"B175",body:'Zhu LC, Smith CM, Fritz A, Boyko EV, Voothuluru P, Gill BS. Inheritance and molecular mapping of new greenbug resistance genes in wheat germplasms derived from Aegilops tauschii. Theor. Appl. Genet.2005;111:831-837.'},{id:"B176",body:'Gharalari AH, Fox SL, Smith MAH, Lamb RJ. Oviposition deterrence in spring wheat, Triticum aestivum, against orange wheat blossom midge, Sitodiplosismosellana: implications for inheritance of deterrence. Entomol. Exp. Appl.2009;133:74-83.'},{id:"B177",body:'Thomas MB. Ecological approaches and the development of “truly integrated” pest management. Proc. Natl. Acad. Sci. USA. 1999; 96:5944-5951.'},{id:"B178",body:'Andersen E J, Ali S, Byamukama E, Yen Y, Nepal M P. Disease resistance mechanisms in plants. Genes. 2018; 9:339.'},{id:"B179",body:'Appels R, Eversole K, Feuillet C, Keller B, Rogers J, Stein N.Shifting the limits in wheat research and breeding using a fully annotatedreference genome. Science. 2018;361:eaar7191.'},{id:"B180",body:'Steuernagel, B.,Witek, K., Krattinger, S. G., Ramirez-Gonzalez, R. H., Schoonbeek, H.-J., Yu, G., et al. (2018). Physical and transcriptional organisation of the bread wheat intracellular immune receptor repertoire. bioRxiv [Preprint].'},{id:"B181",body:'Lorenz AJ, Chao S, Asoro FG, Heffner EL, Hayashi T, Iwata H, Smith KP, Sorrells ME, Jannink JC. Genomic selection in plant breeding: knowledge and prospects. Advance Agronomy. 2011;110:77-123'},{id:"B182",body:'Rutkoski J, Poland JA, Singh RP, Huerta-Espino J, Bhavani S, Barbier H, Rouse MN, Jannik J-L,Sorrells M. Genomic selection for quantitative adult plant stem rust resistance in wheat.Plant Genome. 2014;7(3):1-10'},{id:"B183",body:'Mirdita V, He S, Zhao Y, Korzun V, Bothe R, Ebmeyer E, Reif JC, Jiang Y. Potential and limitsof whole genome prediction of resistance to Fusarium head blight and Septoria triticiblotchin a vast central European elite winter wheat population. Theoretical Applied Genetics. 2015;128:2471 2481'},{id:"B184",body:'Milne RJ, Dibley KE, Schnippenkoetter W, Mascher M, Lui ACW, Wang L, Lo C, Ashton AR, Ryan PR, Lagudah ES (2019) The wheat gene from the sugar transport protein 13 family confers multipathogen resistance in barley. Plant Physiol 179:1285'},{id:"B185",body:'Moore JW, Herrera-Foessel S, Lan C, Schnippenkoetter W, Ayliffe M, Huerta-Espino J, Lillemo M, Viccars L, Milne R, Periyannan S (2015) A recently evolved hexose transporter variant confers resistance to multiple pathogens in wheat. Nat Genet 47:1494-1498'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Harmeet Singh Bakala",address:"harmeet-pbg@pau.edu",affiliation:'
'}],corrections:null},book:{id:"9670",type:"book",title:"Current Trends in Wheat Research",subtitle:null,fullTitle:"Current Trends in Wheat Research",slug:"current-trends-in-wheat-research",publishedDate:"May 11th 2022",bookSignature:"Mahmood-ur-Rahman Ansari",coverURL:"https://cdn.intechopen.com/books/images_new/9670.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:"978-1-83968-594-1",printIsbn:"978-1-83968-593-4",pdfIsbn:"978-1-83968-595-8",isAvailableForWebshopOrdering:!0,editors:[{id:"185476",title:"Dr.",name:"Mahmood-ur-Rahman",middleName:null,surname:"Ansari",slug:"mahmood-ur-rahman-ansari",fullName:"Mahmood-ur-Rahman Ansari"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},profile:{item:{id:"221438",title:"Prof.",name:"Ticiana Sidorenko De Oliveira",middleName:null,surname:"Capote",email:"ticapote@gmail.com.br",fullName:"Ticiana Sidorenko De Oliveira Capote",slug:"ticiana-sidorenko-de-oliveira-capote",position:null,biography:null,institutionString:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",totalCites:0,totalChapterViews:"0",outsideEditionCount:0,totalAuthoredChapters:"1",totalEditedBooks:"0",personalWebsiteURL:null,twitterURL:null,linkedinURL:null,institution:null},booksEdited:[],chaptersAuthored:[{id:"57378",title:"Identification of Lower Central Incisors",slug:"identification-of-lower-central-incisors",abstract:"Unlike the other teeth, the permanent lower central incisors have great symmetry between the proximal surfaces, being difficult to distinguish them. It was intended to facilitate the study of the anatomy of the lower central incisor for dentistry students, that this study searched for a better way to differentiate the third quadrant element (31) from the fourth quadrant element (41). The purpose of this chapter was to evaluate 100 permanent lower central incisors of the didactic collection of the Discipline of Anatomy of the Department of Morphology of the School of Dentistry of Araraquara - UNESP and to verify the presence of correlation between the some anatomical features. Besides, it was evaluated if there was difference between 31 and 41. It was verified that the systematic methodology used for the evaluation of the incisors in this study facilitated the identification of the teeth. There was no statistically significant difference between the measurements of 31 and 41. Distinguishing the right from the left central incisor is difficult, even for experienced practitioners. We could observe that the measurements do not facilitate the identification of teeth of different quadrants. Therefore, the anatomical features are relevant for the study of the dental anatomy in the identification of the lower central incisors.",signatures:"Marcela de Almeida Gonçalves, Bruno Luís Graciliano Silva, Marcelo\nBrito Conte, Juliana Álvares Duarte Bonini Campos and Ticiana\nSidorenko de Oliveira Capote",authors:[{id:"199157",title:"Prof.",name:"Marcela",surname:"De Almeida Gonçalves",fullName:"Marcela De Almeida Gonçalves",slug:"marcela-de-almeida-goncalves",email:"marcelagoncalves@foar.unesp.br"},{id:"199243",title:"BSc.",name:"Marcelo",surname:"Brito Conte",fullName:"Marcelo Brito Conte",slug:"marcelo-brito-conte",email:"mbconte@foar.unesp.br"},{id:"199244",title:"Prof.",name:"Juliana",surname:"Álvares Duarte Bonini Campos",fullName:"Juliana Álvares Duarte Bonini Campos",slug:"juliana-alvares-duarte-bonini-campos",email:"jucampos@fcfar.unesp.br"},{id:"221435",title:"Mr.",name:"Bruno Luis Graciliano",surname:"Silva",fullName:"Bruno Luis Graciliano Silva",slug:"bruno-luis-graciliano-silva",email:"bruno.graciliano@hotmail.com"},{id:"221438",title:"Prof.",name:"Ticiana Sidorenko De Oliveira",surname:"Capote",fullName:"Ticiana Sidorenko De Oliveira Capote",slug:"ticiana-sidorenko-de-oliveira-capote",email:"ticapote@gmail.com.br"}],book:{id:"5814",title:"Dental Anatomy",slug:"dental-anatomy",productType:{id:"1",title:"Edited Volume"}}}],collaborators:[{id:"171777",title:"Prof.",name:"Abdolreza",surname:"Jamilian",slug:"abdolreza-jamilian",fullName:"Abdolreza Jamilian",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Islamic Azad University Dental Branch of Tehran",institutionURL:null,country:{name:"Iran"}}},{id:"171873",title:"Dr.",name:"Alireza",surname:"Darnahal",slug:"alireza-darnahal",fullName:"Alireza Darnahal",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"173044",title:"Prof.",name:"Letizia",surname:"Perillo",slug:"letizia-perillo",fullName:"Letizia Perillo",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"179565",title:"Dr.",name:"Nicola",surname:"Mobilio",slug:"nicola-mobilio",fullName:"Nicola Mobilio",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Ferrara",institutionURL:null,country:{name:"Italy"}}},{id:"198961",title:"MSc.",name:"Fabrizia",surname:"D'Apuzzo",slug:"fabrizia-d'apuzzo",fullName:"Fabrizia D'Apuzzo",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"199397",title:"Prof.",name:"Santo",surname:"Catapano",slug:"santo-catapano",fullName:"Santo Catapano",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"199400",title:"Dr.",name:"Alex",surname:"Vargas",slug:"alex-vargas",fullName:"Alex Vargas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/199400/images/5238_n.jpg",biography:"Professor Dr. Alex Vargas Diaz has been an academic at the Pontifical Catholic University of Chile (PUC) since 1995. After graduating from the University of Chile with title of Dentist, he specialized in Oral and Maxillofacial Surgery at the Hospital of the PUC. He later completed internships abroad and a Diploma in Business Administration in Health Organizations and a Diploma in Clinical Teaching. In his hospital training he has dedicated himself mainly to the subspecialties of oncologic pathology, trauma and implantology, in the maxillofacial area.\n\nCurrently is Associate Professor of the Department of Oncological and Maxillofacial Surgery, belonging to the Division of Surgery of the Faculty of Medicine of the PUC. Performs pre and postgraduate teaching for medical and dentistry careers, in addition to teaching-assistance in the UC-Christus Health Network. On the other hand, it conducts research in the area of bioengineering and tissue engineering, in conjunction with researchers from the Faculties of Engineering and Biological Sciences, in the areas of rapid prototyping, scaffolds, bone regeneration and stem cell culture. He has made numerous presentations in national and international congresses and has several publications in national and international magazines.\n\nHe is a member of the Society of Head and Neck Surgery and Maxillofacial Plastic Surgery, the Society of Oral Implantology of Chile, the American Academy of International Dentistry, the International Society of Cell Therapy, the International Dental Research Association and member of The Commission of National Education in Dentistry.\n\nHe is also a member of the Dentistry Education Commission of the Chilean Dentists College; Referee and Project Evaluator of the Research and Development Division of the Universidad Austral de Chile, the National Commission for Scientific and Technological Research (CONICYCT) and the National Council of Science and Technology of Paraguay (CONACYT); and Director in consultation of the Journal of Rapid Prototyping.\n\n\n\nAreas of interest:\nPre and post grade teaching and health-care activities in the areas of:\n-\tMaxillofacial Traumatology\n-\tOral Implantology\n-\tOral and Maxillofacial Pathology and Oncology\n\nResearch activities in the areas of:\n-\tBioengineering: 3D printing (biocompatible scaffolds and simulation models)\n-\tBiomedicine: Hard & Soft Tissue Regeneration and Biocompatibility",institutionString:null,institution:{name:"Pontifical Catholic University of Chile",institutionURL:null,country:{name:"Chile"}}},{id:"202023",title:"Dr.",name:"Paula",surname:"Astorga",slug:"paula-astorga",fullName:"Paula Astorga",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"205059",title:"Dr.",name:"Tomas",surname:"Rioseco",slug:"tomas-rioseco",fullName:"Tomas Rioseco",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"206137",title:"Mrs.",name:"Ludovica",surname:"Nucci",slug:"ludovica-nucci",fullName:"Ludovica Nucci",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null}]},generic:{page:{slug:"OA-publishing-fees",title:"Open Access Publishing Fees",intro:"
The Open Access model is applied to all of our publications and is designed to eliminate subscriptions and pay-per-view fees. This approach ensures free, immediate access to full text versions of your research.
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For Authors who are still unable to obtain funding from their institutions or research funding bodies for individual projects, IntechOpen does offer the possibility of applying for a Waiver to offset some or all processing feed. Details regarding our Waiver Policy can be found here.
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Indexing and listing across major repositories, see details ...
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Long-term archiving
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Visibility on the world's strongest OA platform
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Dissemination and Promotion
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Proven world leader in Open Access book publishing with over 10 years experience
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+184,650 citations in Web of Science databases
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Currently strongest OA platform with over 175 million downloads
As a gold Open Access publisher, an Open Access Publishing Fee is payable on acceptance following peer review of the manuscript. In return, we provide high quality publishing services and exclusive benefits for all contributors. IntechOpen is the trusted publishing partner of over 140,000 international scientists and researchers.
\n\n
The Open Access Publishing Fee (OAPF) is payable only after your book chapter, monograph or journal article is accepted for publication.
\n\n
OAPF Publishing Options
\n\n
\n\t
1,400 GBP Chapter - Edited Volume
\n\t
850 GBP Chapter - Book Series Topic (Annual Volume)
\n\t
10,000 GBP Monograph - Long Form
\n\t
4,000 GBP Compacts Monograph - Short Form
\n\t
850 GBP Journal Article (Across Portfolio)
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\n\n
During the launching phase journals do not charge an APC, rather they will be funded by IntechOpen.
\n\n
*These prices do not include Value-Added Tax (VAT). Residents of European Union countries need to add VAT based on the specific rate in their country of residence. Institutions and companies registered as VAT taxable entities in their own EU member state will not pay VAT as long as provision of the VAT registration number is made during the application process. This is made possible by the EU reverse charge method.
\n\n
Services included are:
\n\n
\n\t
An online manuscript tracking system to facilitate your work
\n\t
Personal contact and support throughout the publishing process from your dedicated Author Service Manager
\n\t
Assurance that your manuscript meets the highest publishing standards
\n\t
English language copyediting and proofreading, including the correction of grammatical, spelling, and other common errors
\n\t
XML Typesetting and pagination - web (PDF, HTML) and print files preparation
\n\t
Discoverability - electronic citation and linking via DOI
\n\t
Permanent and unrestricted online access to your work
\n
\n\n
What isn't covered by the Open Access Publishing Fee?
\n\n
If your manuscript:
\n\n
\n\t
Exceeds the number of pages defined by the publishing guidelines, an additional fee per page may be required
\n\t
If a manuscript requires Heavy Editing or Language Polishing, this will incur additional fees.
\n
\n\n
Your Author Service Manager will inform you of any items not covered by the OAPF and provide exact information regarding those additional costs before proceeding.
\n\n
Open Access Funding
\n\n
To explore funding opportunities and learn more about how you can finance your IntechOpen publication, go to our Open Access Funding page. IntechOpen offers expert assistance to all of its Authors. We can support you in approaching funding bodies and institutions in relation to publishing fees by providing information about compliance with the Open Access policies of your funder or institution. We can also assist with communicating the benefits of Open Access in order to support and strengthen your funding request and provide personal guidance through your application process. You can contact us at funders@intechopen.com for further details or assistance.
\n\n
For Authors who are still unable to obtain funding from their institutions or research funding bodies for individual projects, IntechOpen does offer the possibility of applying for a Waiver to offset some or all processing feed. Details regarding our Waiver Policy can be found here.
\n\n
Added Value of Publishing with IntechOpen
\n\n
Choosing to publish with IntechOpen ensures the following benefits:
\n\n
\n\t
Indexing and listing across major repositories, see details ...
\n\t
Long-term archiving
\n\t
Visibility on the world's strongest OA platform
\n\t
Live Performance Metrics to track readership and the impact of your chapter
\n\t
Dissemination and Promotion
\n
\n\n
Benefits of Publishing with IntechOpen
\n\n
\n\t
Proven world leader in Open Access book publishing with over 10 years experience
\n\t
+5,700 OA books published
\n\t
Most competitive prices in the market
\n\t
Fully compliant with OA funding requirements
\n\t
Optimized processes that assure your research is made available to the scientific community without delay
\n\t
Personal support during every step of the publication process
\n\t
+184,650 citations in Web of Science databases
\n\t
Currently strongest OA platform with over 175 million downloads
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Montes-Tapia",authors:[{id:"101498",title:"Dr.",name:"Manuel",middleName:null,surname:"De La O Cavazos",slug:"manuel-de-la-o-cavazos",fullName:"Manuel De La O Cavazos"},{id:"135808",title:"Dr.",name:"Gabriela",middleName:null,surname:"Guajardo Rodríguez",slug:"gabriela-guajardo-rodriguez",fullName:"Gabriela Guajardo Rodríguez"},{id:"135809",title:"Dr.",name:"Consuelo",middleName:null,surname:"Treviño Garza",slug:"consuelo-trevino-garza",fullName:"Consuelo Treviño Garza"}]},{id:"30838",doi:"10.5772/32846",title:"Risk Management in Obstetrics and Neonatal-Perinatal Medicine",slug:"common-allegations-of-professional-liability-against-practitioners-of-neonatal-perinatal-medicine",totalDownloads:5857,totalCrossrefCites:1,totalDimensionsCites:4,abstract:null,book:{id:"2123",slug:"complementary-pediatrics",title:"Complementary Pediatrics",fullTitle:"Complementary Pediatrics"},signatures:"Jonathan Muraskas, Lindsay Ellsworth, Eric Culp, Gretchen Garbe and John Morrison",authors:[{id:"92759",title:"Prof.",name:"Jonathan",middleName:null,surname:"Muraskas",slug:"jonathan-muraskas",fullName:"Jonathan Muraskas"},{id:"96478",title:"Ms.",name:"Lindsay",middleName:null,surname:"Ellsworth",slug:"lindsay-ellsworth",fullName:"Lindsay Ellsworth"},{id:"130957",title:"Dr.",name:"Eric",middleName:null,surname:"Culp",slug:"eric-culp",fullName:"Eric Culp"},{id:"130958",title:"Dr.",name:"Gretchen",middleName:null,surname:"Garbe",slug:"gretchen-garbe",fullName:"Gretchen Garbe"},{id:"130960",title:"Dr.",name:"John",middleName:null,surname:"Morrison",slug:"john-morrison",fullName:"John Morrison"}]}],mostDownloadedChaptersLast30Days:[{id:"66831",title:"Management of Gastroschisis",slug:"management-of-gastroschisis",totalDownloads:1299,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Gastroschisis (GS) is one of the congenital abdominal wall defects, in which the bowel has prolapsed without a covering through a defect adjacent to (and nearly always to the right of) an otherwise normal umbilicus. Proper management of such cases gives them the opportunity to survive and thrive. In this chapter, simplified flowcharts for the initial management of GS, surgical intra-operative decisions and post-operative active follow-up of such cases will be presented and discussed. The first flowchart will discuss how to deal with a GS case from birth till the operative theatre, while the second flowchart will take the lead to guide the surgeon with the available surgical options and how to choose the suitable one for the case. Finally, the post-operative active follow-up fluid management and possible complications are discussed.",book:{id:"8463",slug:"pediatric-surgery-flowcharts-and-clinical-algorithms",title:"Pediatric Surgery, Flowcharts and Clinical Algorithms",fullTitle:"Pediatric Surgery, Flowcharts and Clinical Algorithms"},signatures:"Alaa Obeida and Aly Shalaby",authors:[{id:"273587",title:"Dr.",name:"Alaa",middleName:null,surname:"Obeida",slug:"alaa-obeida",fullName:"Alaa Obeida"},{id:"276899",title:"Mr.",name:"Aly",middleName:null,surname:"Shalaby",slug:"aly-shalaby",fullName:"Aly Shalaby"}]},{id:"67769",title:"Pediatric Choledochal Cysts: Unknowns are Decreasing",slug:"pediatric-choledochal-cysts-unknowns-are-decreasing",totalDownloads:1239,totalCrossrefCites:1,totalDimensionsCites:2,abstract:"Choledochal cysts (CCs) are congenital cystic dilatation of extrahepatic and/or intrahepatic bile ducts. CCs are more common in Asian population, the cause is still unknown. Although the etiology is controversial, the main elements in the natural historical emergence of the type I and type IV, which make up the majority of all types, have become clearer. The majority of CCs are diagnosed in childhood. Clinical presentation varies from jaundice in young patients to nonspecific abdominal pain in older, but morbidity increases with complications such as cholangitis, pancreatitis, perforation, hepatitis, liver failure, and malignancy in delayed diagnosed patients. MRCP is considered the current gold standard diagnostic modality that is able to accurately assess biliary anatomy. Although the treatment approach has been formed over the years, it still has not reached the last state. Eventually, the removal of the entire cyst and the reconstruction of the remaining biliary tract to drainage is the current treatment approach. But the dilemma is the way of reconstruction procedure (hepaticoduodenostomy or hepaticojejunostomy). All patients should be followed up for a long period of time, regardless of the surgery method.",book:{id:"8463",slug:"pediatric-surgery-flowcharts-and-clinical-algorithms",title:"Pediatric Surgery, Flowcharts and Clinical Algorithms",fullTitle:"Pediatric Surgery, Flowcharts and Clinical Algorithms"},signatures:"Hasan Özkan Gezer",authors:[{id:"273381",title:"M.D.",name:"Hasan",middleName:"Özkan",surname:"Gezer",slug:"hasan-gezer",fullName:"Hasan Gezer"}]},{id:"66650",title:"Necrotizing Enterocolitis",slug:"necrotizing-enterocolitis",totalDownloads:2283,totalCrossrefCites:1,totalDimensionsCites:2,abstract:"Necrotizing enterocolitis (NEC) is the commonest inflammatory gastrointestinal disorder of newborn infants, occurring primarily in premature neonates. Presenting as a medical and surgical emergency, it is associated with significant morbidity and mortality. NEC is characterized by acute intestinal inflammation and necrosis with intramural dissection of gas, pathognomically appearing as pneumatosis intestinalis on radiography. The incidence and mortality, with an inverse relationship to maturation, range between 3–11% and 17–20% respectively. Mortality may be up to 50% in extremely premature infants who require surgery for intestinal perforation or gangrene. The exact etiopathogenesis is unknown. Over 90% of infants are premature and more than 98% are enterally fed. NEC presents with feeding intolerance and abdominal distension, which may rapidly progress to cardiorespiratory decompensation and death in severe cases. Intestinal dysbiosis and its functional and immunological immaturity are proposed to play roles in the pathogenesis. While exact triggers are undetermined, the disease is marked by an anomalous immunological response of enterocytes to inflammation, invoking cytokines and chemokines. NEC is treated with bowel rest, antibiotics, cardiorespiratory support, parenteral nutrition, and blood products transfusion. Approximately 30% of cases require surgery and a significant number of survivors suffer from neurological deficits, intestinal dysfunction, and post surgical short bowel syndrome.",book:{id:"8463",slug:"pediatric-surgery-flowcharts-and-clinical-algorithms",title:"Pediatric Surgery, Flowcharts and Clinical Algorithms",fullTitle:"Pediatric Surgery, Flowcharts and Clinical Algorithms"},signatures:"Rita Prasad Verma and Archana Kota",authors:[{id:"278358",title:"Dr.",name:"Rita P.",middleName:null,surname:"Verma",slug:"rita-p.-verma",fullName:"Rita P. Verma"},{id:"296230",title:"Dr.",name:"Archana",middleName:null,surname:"Kota",slug:"archana-kota",fullName:"Archana Kota"}]},{id:"69210",title:"Meconium Ileus",slug:"meconium-ileus",totalDownloads:881,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Meconium ileus is a type of neonatal intestinal obstruction that occurs when abnormally thick meconium impacts in the ileum causing blockage of intestinal flow. Most infants with meconium ileus have cystic fibrosis, a congenital condition characterized by abnormally thick intestinal secretions and pancreatic insufficiency. The pathogenesis of meconium ileus is due to hyperviscous mucus secreted by abnormal intestinal glands, abnormal concentrating processes in the proximal small intestine, and pancreatic enzyme insufficiency. The clinical presentation of meconium ileus is that of abdominal distention, bilious vomiting, and failure to pass meconium. Cases of meconium ileus are usually evaluated with plain abdominal radiograph and contrast enema. Numerous air-filled loops of bowel on the supine view with characteristic absence of air-fluid levels are commonly seen on the radiograph, but the presence of calcification suggests intestinal perforation. Contrast enema examination is useful in cases with microcolon. Uncomplicated meconium ileus obstruction can be relieved by giving one or more dilute diatrizoate sodium enema (with Nacetylcysteine added) under fluoroscopy. Surgery is indicated when there is progressive distention or signs of clinical deterioration despite multiple enemas, as well as in complicated cases like meconium peritonitis, ileal atresia or stenosis, ileal perforation, and volvulus with or without pseudocyst formation.",book:{id:"8463",slug:"pediatric-surgery-flowcharts-and-clinical-algorithms",title:"Pediatric Surgery, Flowcharts and Clinical Algorithms",fullTitle:"Pediatric Surgery, Flowcharts and Clinical Algorithms"},signatures:"Udefiagbon Omogiade",authors:[{id:"273380",title:"Dr.",name:"Omogiade",middleName:null,surname:"Udefiagbon",slug:"omogiade-udefiagbon",fullName:"Omogiade Udefiagbon"},{id:"284652",title:"Dr.",name:"Owolabi",middleName:null,surname:"Oni",slug:"owolabi-oni",fullName:"Owolabi Oni"}]},{id:"30824",title:"Pediatric Ophthalmology / Eye and Disorders",slug:"pediatric-ophthalmology-eye-and-disorders",totalDownloads:9440,totalCrossrefCites:1,totalDimensionsCites:2,abstract:null,book:{id:"2123",slug:"complementary-pediatrics",title:"Complementary Pediatrics",fullTitle:"Complementary Pediatrics"},signatures:"Hikmet Basmak, Nilgun Yildirim, Seyhan Topbas, Ahmet Ozer, Nazmiye Erol, Huseyin Gursoy and Afsun Sahin",authors:[{id:"94622",title:"Dr.",name:"Meselik Saglik Ve",middleName:null,surname:"Egitim Vakfi",slug:"meselik-saglik-ve-egitim-vakfi",fullName:"Meselik Saglik Ve Egitim Vakfi"},{id:"98268",title:"Dr.",name:"Huseyin",middleName:null,surname:"Gursoy",slug:"huseyin-gursoy",fullName:"Huseyin Gursoy"},{id:"98269",title:"Prof.",name:"Nilgun",middleName:null,surname:"Yildirim",slug:"nilgun-yildirim",fullName:"Nilgun Yildirim"},{id:"98271",title:"Prof.",name:"Seyhan",middleName:null,surname:"Topbas",slug:"seyhan-topbas",fullName:"Seyhan Topbas"},{id:"98274",title:"Prof.",name:"Ahmet",middleName:null,surname:"Ozer",slug:"ahmet-ozer",fullName:"Ahmet Ozer"},{id:"98277",title:"Dr.",name:"Nazmiye",middleName:null,surname:"Erol",slug:"nazmiye-erol",fullName:"Nazmiye Erol"},{id:"98278",title:"Dr.",name:"Afsun",middleName:null,surname:"Sahin",slug:"afsun-sahin",fullName:"Afsun Sahin"}]}],onlineFirstChaptersFilter:{topicId:"1112",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 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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:"11",title:"Biochemistry",doi:"10.5772/intechopen.72877",issn:"2632-0983",scope:"Biochemistry, the study of chemical transformations occurring within living organisms, impacts all areas of life sciences, from molecular crystallography and genetics to ecology, medicine, and population biology. Biochemistry examines macromolecules - proteins, nucleic acids, carbohydrates, and lipids – and their building blocks, structures, functions, and interactions. Much of biochemistry is devoted to enzymes, proteins that catalyze chemical reactions, enzyme structures, mechanisms of action and their roles within cells. Biochemistry also studies small signaling molecules, coenzymes, inhibitors, vitamins, and hormones, which play roles in life processes. Biochemical experimentation, besides coopting classical chemistry methods, e.g., chromatography, adopted new techniques, e.g., X-ray diffraction, electron microscopy, NMR, radioisotopes, and developed sophisticated microbial genetic tools, e.g., auxotroph mutants and their revertants, fermentation, etc. More recently, biochemistry embraced the ‘big data’ omics systems. Initial biochemical studies have been exclusively analytic: dissecting, purifying, and examining individual components of a biological system; in the apt words of Efraim Racker (1913 –1991), “Don’t waste clean thinking on dirty enzymes.” Today, however, biochemistry is becoming more agglomerative and comprehensive, setting out to integrate and describe entirely particular biological systems. The ‘big data’ metabolomics can define the complement of small molecules, e.g., in a soil or biofilm sample; proteomics can distinguish all the comprising proteins, e.g., serum; metagenomics can identify all the genes in a complex environment, e.g., the bovine rumen. This Biochemistry Series will address the current research on biomolecules and the emerging trends with great promise.",coverUrl:"https://cdn.intechopen.com/series/covers/11.jpg",latestPublicationDate:"June 29th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:32,editor:{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. Since 1983, he has been a faculty member of the RO Perelman Department of Dermatology, NYU School of Medicine, where he is codirector of a training grant in cutaneous biology. Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. He has published more than 100 peer-reviewed research articles and graduated numerous Ph.D. and postdoctoral students.",institutionString:null,institution:{name:"New York University Langone Medical Center",institutionURL:null,country:{name:"United States of America"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:4,paginationItems:[{id:"14",title:"Cell and Molecular Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/14.jpg",isOpenForSubmission:!0,editor:{id:"165627",title:"Dr.",name:"Rosa María",middleName:null,surname:"Martínez-Espinosa",slug:"rosa-maria-martinez-espinosa",fullName:"Rosa María Martínez-Espinosa",profilePictureURL:"https://mts.intechopen.com/storage/users/165627/images/system/165627.jpeg",biography:"Dr. Rosa María Martínez-Espinosa has been a Spanish Full Professor since 2020 (Biochemistry and Molecular Biology) and is currently Vice-President of International Relations and Cooperation development and leader of the research group 'Applied Biochemistry” (University of Alicante, Spain). Other positions she has held at the university include Vice-Dean of Master Programs, Vice-Dean of the Degree in Biology and Vice-Dean for Mobility and Enterprise and Engagement at the Faculty of Science (University of Alicante). She received her Bachelor in Biology in 1998 (University of Alicante) and her PhD in 2003 (Biochemistry, University of Alicante). She undertook post-doctoral research at the University of East Anglia (Norwich, U.K. 2004-2005; 2007-2008).\nHer multidisciplinary research focuses on investigating archaea and their potential applications in biotechnology. She has an H-index of 21. She has authored one patent and has published more than 70 indexed papers and around 60 book chapters.\nShe has contributed to more than 150 national and international meetings during the last 15 years. Her research interests include archaea metabolism, enzymes purification and characterization, gene regulation, carotenoids and bioplastics production, antioxidant\ncompounds, waste water treatments, and brines bioremediation.\nRosa María’s other roles include editorial board member for several journals related\nto biochemistry, reviewer for more than 60 journals (biochemistry, molecular biology, biotechnology, chemistry and microbiology) and president of several organizing committees in international meetings related to the N-cycle or respiratory processes.",institutionString:null,institution:{name:"University of Alicante",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null},{id:"15",title:"Chemical Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/15.jpg",isOpenForSubmission:!0,editor:{id:"441442",title:"Dr.",name:"Şükrü",middleName:null,surname:"Beydemir",slug:"sukru-beydemir",fullName:"Şükrü Beydemir",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00003GsUoIQAV/Profile_Picture_1634557147521",biography:"Dr. Şükrü Beydemir obtained a BSc in Chemistry in 1995 from Yüzüncü Yıl University, MSc in Biochemistry in 1998, and PhD in Biochemistry in 2002 from Atatürk University, Turkey. He performed post-doctoral studies at Max-Planck Institute, Germany, and University of Florence, Italy in addition to making several scientific visits abroad. He currently works as a Full Professor of Biochemistry in the Faculty of Pharmacy, Anadolu University, Turkey. Dr. Beydemir has published over a hundred scientific papers spanning protein biochemistry, enzymology and medicinal chemistry, reviews, book chapters and presented several conferences to scientists worldwide. He has received numerous publication awards from various international scientific councils. He serves in the Editorial Board of several international journals. Dr. Beydemir is also Rector of Bilecik Şeyh Edebali University, Turkey.",institutionString:null,institution:{name:"Anadolu University",institutionURL:null,country:{name:"Turkey"}}},editorTwo:{id:"13652",title:"Prof.",name:"Deniz",middleName:null,surname:"Ekinci",slug:"deniz-ekinci",fullName:"Deniz Ekinci",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYLT1QAO/Profile_Picture_1634557223079",biography:"Dr. Deniz Ekinci obtained a BSc in Chemistry in 2004, MSc in Biochemistry in 2006, and PhD in Biochemistry in 2009 from Atatürk University, Turkey. He studied at Stetson University, USA, in 2007-2008 and at the Max Planck Institute of Molecular Cell Biology and Genetics, Germany, in 2009-2010. Dr. Ekinci currently works as a Full Professor of Biochemistry in the Faculty of Agriculture and is the Head of the Enzyme and Microbial Biotechnology Division, Ondokuz Mayıs University, Turkey. He is a member of the Turkish Biochemical Society, American Chemical Society, and German Genetics society. Dr. Ekinci published around ninety scientific papers, reviews and book chapters, and presented several conferences to scientists. He has received numerous publication awards from several scientific councils. Dr. Ekinci serves as the Editor in Chief of four international books and is involved in the Editorial Board of several international journals.",institutionString:null,institution:{name:"Ondokuz Mayıs University",institutionURL:null,country:{name:"Turkey"}}},editorThree:null},{id:"17",title:"Metabolism",coverUrl:"https://cdn.intechopen.com/series_topics/covers/17.jpg",isOpenForSubmission:!0,editor:{id:"138626",title:"Dr.",name:"Yannis",middleName:null,surname:"Karamanos",slug:"yannis-karamanos",fullName:"Yannis Karamanos",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002g6Jv2QAE/Profile_Picture_1629356660984",biography:"Yannis Karamanos, born in Greece in 1953, completed his pre-graduate studies at the Université Pierre et Marie Curie, Paris, then his Masters and Doctoral degree at the Université de Lille (1983). He was associate professor at the University of Limoges (1987) before becoming full professor of biochemistry at the Université d’Artois (1996). He worked on the structure-function relationships of glycoconjugates and his main project was the investigations on the biological roles of the de-N-glycosylation enzymes (Endo-N-acetyl-β-D-glucosaminidase and peptide-N4-(N-acetyl-β-glucosaminyl) asparagine amidase). From 2002 he contributes to the understanding of the Blood-brain barrier functioning using proteomics approaches. He has published more than 70 papers. His teaching areas are energy metabolism and regulation, integration and organ specialization and metabolic adaptation.",institutionString:null,institution:{name:"Artois University",institutionURL:null,country:{name:"France"}}},editorTwo:null,editorThree:null},{id:"18",title:"Proteomics",coverUrl:"https://cdn.intechopen.com/series_topics/covers/18.jpg",isOpenForSubmission:!0,editor:{id:"200689",title:"Prof.",name:"Paolo",middleName:null,surname:"Iadarola",slug:"paolo-iadarola",fullName:"Paolo Iadarola",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSCl8QAG/Profile_Picture_1623568118342",biography:"Paolo Iadarola graduated with a degree in Chemistry from the University of Pavia (Italy) in July 1972. He then worked as an Assistant Professor at the Faculty of Science of the same University until 1984. In 1985, Prof. Iadarola became Associate Professor at the Department of Biology and Biotechnologies of the University of Pavia and retired in October 2017. Since then, he has been working as an Adjunct Professor in the same Department at the University of Pavia. His research activity during the first years was primarily focused on the purification and structural characterization of enzymes from animal and plant sources. During this period, Prof. Iadarola familiarized himself with the conventional techniques used in column chromatography, spectrophotometry, manual Edman degradation, and electrophoresis). Since 1995, he has been working on: i) the determination in biological fluids (serum, urine, bronchoalveolar lavage, sputum) of proteolytic activities involved in the degradation processes of connective tissue matrix, and ii) on the identification of biological markers of lung diseases. In this context, he has developed and validated new methodologies (e.g., Capillary Electrophoresis coupled to Laser-Induced Fluorescence, CE-LIF) whose application enabled him to determine both the amounts of biochemical markers (Desmosines) in urine/serum of patients affected by Chronic Obstructive Pulmonary Disease (COPD) and the activity of proteolytic enzymes (Human Neutrophil Elastase, Cathepsin G, Pseudomonas aeruginosa elastase) in sputa of these patients. More recently, Prof. Iadarola was involved in developing techniques such as two-dimensional electrophoresis coupled to liquid chromatography/mass spectrometry (2DE-LC/MS) for the proteomic analysis of biological fluids aimed at the identification of potential biomarkers of different lung diseases. He is the author of about 150 publications (According to Scopus: H-Index: 23; Total citations: 1568- According to WOS: H-Index: 20; Total Citations: 1296) of peer-reviewed international journals. He is a Consultant Reviewer for several journals, including the Journal of Chromatography A, Journal of Chromatography B, Plos ONE, Proteomes, International Journal of Molecular Science, Biotech, Electrophoresis, and others. He is also Associate Editor of Biotech.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorTwo:{id:"201414",title:"Dr.",name:"Simona",middleName:null,surname:"Viglio",slug:"simona-viglio",fullName:"Simona Viglio",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRKDHQA4/Profile_Picture_1630402531487",biography:"Simona Viglio is an Associate Professor of Biochemistry at the Department of Molecular Medicine at the University of Pavia. She has been working since 1995 on the determination of proteolytic enzymes involved in the degradation process of connective tissue matrix and on the identification of biological markers of lung diseases. She gained considerable experience in developing and validating new methodologies whose applications allowed her to determine both the amount of biomarkers (Desmosine and Isodesmosine) in the urine of patients affected by COPD, and the activity of proteolytic enzymes (HNE, Cathepsin G, Pseudomonas aeruginosa elastase) in the sputa of these patients. Simona Viglio was also involved in research dealing with the supplementation of amino acids in patients with brain injury and chronic heart failure. She is presently engaged in the development of 2-DE and LC-MS techniques for the study of proteomics in biological fluids. The aim of this research is the identification of potential biomarkers of lung diseases. She is an author of about 90 publications (According to Scopus: H-Index: 23; According to WOS: H-Index: 20) on peer-reviewed journals, a member of the “Società Italiana di Biochimica e Biologia Molecolare,“ and a Consultant Reviewer for International Journal of Molecular Science, Journal of Chromatography A, COPD, Plos ONE and Nutritional Neuroscience.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorThree:null}]},overviewPageOFChapters:{paginationCount:36,paginationItems:[{id:"82195",title:"Endoplasmic Reticulum: A Hub in Lipid Homeostasis",doi:"10.5772/intechopen.105450",signatures:"Raúl Ventura and María Isabel Hernández-Alvarez",slug:"endoplasmic-reticulum-a-hub-in-lipid-homeostasis",totalDownloads:2,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Updates on Endoplasmic Reticulum",coverURL:"https://cdn.intechopen.com/books/images_new/11674.jpg",subseries:{id:"14",title:"Cell and Molecular Biology"}}},{id:"82409",title:"Purinergic Signaling in Covid-19 Disease",doi:"10.5772/intechopen.105008",signatures:"Hailian Shen",slug:"purinergic-signaling-in-covid-19-disease",totalDownloads:3,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Purinergic System",coverURL:"https://cdn.intechopen.com/books/images_new/10801.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82374",title:"The Potential of the Purinergic System as a Therapeutic Target of Natural Compounds in Cutaneous Melanoma",doi:"10.5772/intechopen.105457",signatures:"Gilnei Bruno da Silva, Daiane Manica, Marcelo Moreno and Margarete Dulce Bagatini",slug:"the-potential-of-the-purinergic-system-as-a-therapeutic-target-of-natural-compounds-in-cutaneous-mel",totalDownloads:9,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Purinergic System",coverURL:"https://cdn.intechopen.com/books/images_new/10801.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82103",title:"The Role of Endoplasmic Reticulum Stress and Its Regulation in the Progression of Neurological and Infectious Diseases",doi:"10.5772/intechopen.105543",signatures:"Mary Dover, Michael Kishek, Miranda Eddins, Naneeta Desar, Ketema Paul and Milan Fiala",slug:"the-role-of-endoplasmic-reticulum-stress-and-its-regulation-in-the-progression-of-neurological-and-i",totalDownloads:6,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Updates on Endoplasmic Reticulum",coverURL:"https://cdn.intechopen.com/books/images_new/11674.jpg",subseries:{id:"14",title:"Cell and Molecular Biology"}}}]},overviewPagePublishedBooks:{paginationCount:32,paginationItems:[{type:"book",id:"7006",title:"Biochemistry and Health Benefits of Fatty Acids",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/7006.jpg",slug:"biochemistry-and-health-benefits-of-fatty-acids",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Viduranga Waisundara",hash:"c93a00abd68b5eba67e5e719f67fd20b",volumeInSeries:1,fullTitle:"Biochemistry and Health Benefits of Fatty Acids",editors:[{id:"194281",title:"Dr.",name:"Viduranga Y.",middleName:null,surname:"Waisundara",slug:"viduranga-y.-waisundara",fullName:"Viduranga Y. 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