Children’s enrolment country wise in year 2016.
\r\n\tIt is a relatively simple process and a standard tool in any industry. Because of the versatility of the titration techniques, nearly all aspects of society depend on various forms of titration to analyze key chemical compounds.
\r\n\tThe aims of this book is to provide the reader with an up-to-date coverage of experimental and theoretical aspects related to titration techniques used in environmental, pharmaceutical, biomedical and food sciences.
The objective of this chapter is to offer information and evidence on early childhood education and care (ECEC) from an international perspective to those who are, directly or indirectly, involved with young children and their families. Ideological and historical context can explain how a system of ECEC develops within a country, and an understanding of the ECEC system and its characteristics can describe how effects upon children can occur. The chapter draws on the current situation of limited access of young children to early childhood education and care settings in Tanzania. Importantly, it explains how young children access to early childhood education focusing on Tanzanian context.
\nEarly education is the foundation for all formal education worldwide. Early childhood education and care (ECEC) is conceptualised as incorporating both education and care, which has sometimes been called educare [1–3]. However, education and care in many countries, including African countries such as Tanzania, Kenya, Zimbabwe, Lesotho, Zambia, and South Africa has been institutionalised into separate administrative arrangements for care and education [1, 4]. Such separation of administrative arrangements runs counter to a holistic view of learning and development and that education and care should be integrated, with the child and family as the central focus. For example, New Zealand was one of the first countries in the world to integrate all early childhood services under an educational administration, reflecting that education and care cannot be separated and that quality services incorporate both [5]. Also it is important to realise that childcare is diverse, and do not make the mistake, which is too common amongst politicians, of regarding day care for under-ones as basically the same issue as kindergarten for 3–4-year olds. Some forms of ECEC have explicit educational aims and are usually targeted on young children from 3 years upwards, which are nursery schools and kindergartens [2]. There is an overlap between the care and education-oriented divisions with the distinction becoming increasingly blurred, with recognition of the significance of learning in the first 3 years for longer term development.
\nFor many countries worldwide, childcare has traditionally been considered the private problem of families, which often gives rise to resentment to increased childcare provision. However, progressively it is taken for granted that childcare is here to stay given the social changes occurring in developed and developing countries. In industrialised societies, ECEC is now being recognised as part of the infrastructure for economic development [2], since childcare, whether or not accommodates the educational elements, is a necessity for modern societies with women as central to the workforce. The diversity in ECEC provision across countries reflects.
\nHowever, in Tanzanian context, parents and community at large have negative attitude in regard to early investment, they perceive investing in early years like a waste of money [6, 7]. In this regard, their complains include the notion that young children who have access to the ECEC centre just go there to take porridge, sing songs and play and their parents pay for these. Parents argue that at that early age parents and the community should serve as the teachers of young children, until the children grow to the primary school age.
\nViews of children as a distinct social group with rights have developed over time. Pence et al. [8] argue that for much of the twentieth century and throughout most of the world, African countries included, ECEC was largely invisible as a state-policy concern. Young children, in the eyes of most states, were an appendage of their parents, or embedded in the larger family structure [8], and were treated as objects to be shaped and socialised, seen as just properties of their families, and as incomplete human beings [3, 9]. The child as an individual social entity was largely unrecognised [10]. This portrayal contrasts with an understanding that children are persons who, while thriving in conducive, warm, and supportive environments, are “active participants in their social worlds and have a unique part to play in their own development” [5, p. 15].
\nThis section discusses two main arguments as to why ECEC is regarded as valuable and why governments should invest in it. The arguments are concerned with the benefits of early investment for children’s learning and development, society and the economy, and social changes.
\nChildren’s participation in good quality ECEC has benefits for the child’s learning and development at the time of attendance and throughout their life [11, 12]. There is a growing recognition that participation in ECEC from 2 or 3 years before starting school is beneficial for all children and particularly for children from low-income and disadvantaged groups [12, 13].
\nAchievement or breakdown at this early education stage lays the foundation for success or failure in school, which in turn leads to achievements or breakdown in post-school learning [14–16]. A study by [17] reports that the early years (ages 0–6) are the time for brain development; therefore quality ECEC programmes are a key societal as well as personal imperative. Further, [17] emphasise that a child’s environment and experiences start in utero and not only affect brain development, but also physical and mental health, learning and behaviour for a life time. McCain and Mustard [18] also support the view that development of the brain in the early years of life, particularly the 0–3-year olds, establishes the foundation of competence and coping skills for the later stages of life. This view is argued by Smith et al. [13] who state, “there are links between early sensory stimulation and the activation of the arousal system, chaotic environments can produce abnormal reactions to later stress, while nurturing sensitive environments allow children to respond more adaptively” (p. 28). Smith et al. [13] further emphasise, “young children need to be protected from lack of stimulation, over stimulation or aversive stimulation in the early years” (p. 28).
\nRef. [9] asserts that investment in children 0–8 years is important because it gives “a good start in life involving a nurturing, caring, and safe environment” (p. 136) to children who are the future hope of any society and nation. Evidence suggests that providing quality ECEC services can also improve the economic well-being of countries [13, 19]. It is theorised in the literature that children who benefit from early education, especially those from disadvantaged backgrounds, are more likely to succeed in primary schools [12, 20]. Longitudinal studies have also found that children who benefit from a good primary education are more likely to succeed in secondary schools and tertiary education [12].
\nIn support of early investment in young children, [17] report that participation in good quality early interventions leads to increased earnings in later life and stimulates positive social relationships. Many researchers have noted that improving human development in the early years is definitely a way to break out of poverty because early investment has a very high economic rate of benefits [11, 15, 17].
\nECEC is an essential part of the education system worldwide [16, 21]. Many researchers assert that learning starts from birth continues until formal education begins, and continues all the way through life [22]. Early learning is the basis for future learning and early success results in later success, just as early failure can result in later failure [22, 23]. Therefore, investing in good quality ECEC provision from an early age can be seen as an effective means of attaining developmental targets, such as earnings in later life, cost savings, good life for children and families, and breaking cycles of disadvantage [11, 13]. One aim of ECEC has been described as building a bridge from early year’s education to compulsory schooling [24]. ECEC is meant to support parents in the education of their children and also to address any apparent developmental delays.
\nIn summary, current studies of good quality ECEC have shown notable success in promoting children’s learning and development and indicate that the early years are important for early learning [15, 25]. International evidence shows that investing in good quality ECEC can bring cost savings and benefits to governments and economies [25], as well as to children and families.
\nThe second main reason for ECEC provision is claimed to be in response to social changes. OECD [26] advocates an increase in women’s labour market involvement, the need to reconcile work and family duties on a more equitable basis, and the need to address issues of child poverty and educational disadvantage. This is because economic prosperity depends on maintaining high employment levels including maternal employment, and this has been a key driver of government interest in expanding ECEC. In other words, ECEC enables mothers of young children to engage in the labour market with consequent positive impacts on the economy and on countries’ policies [2, 12]. However, [3] argue that the availability of early education and child care on the one hand can encourage women to attend to paid jobs, but on the other hand can have some negative effects for the well-being of family members because mothers may have multiple roles, that is, work and child care responsibilities.
\nFurthermore, writers report that developed countries have achieved high levels of quality in ECEC services combined with high rates of maternal employment [26, 27], whereas developing countries, such as Tanzania, despite showing a significant increase in women’s employment, have not shown much advance in ECEC services [1]. Hence ECEC services do not automatically develop when there is a clear need for them. Other factors such as the ideology and politics arising from a country’s history and culture are also important [9, 28].
\nThe situation of ECEC in many African countries is one of the developments due to various reasons. The level of training of staff is poor and many staffs have no training [1, 29]. Access is limited. There are few institutions which care for children aged 0–6 years and most ECEC centres for 3 and 6 years old are found only in urban areas and are of poor quality [28, 30]. Similarly, the ECEC curricula are not helpful for young children, because of their poor consideration of children’s needs and interests. Support from international organisations is mainly used for ECEC of children aged 3 years and above [1], so 0–3 year provision is particularly neglected.
\nA large number of disadvantaged families have found it difficult to get access to ECEC in African countries [1, 9]. Further, it is argued that there are challenges in developing ECEC programmes in under-resourced countries in Africa [9, 17, 31]. Young and Mustard [17, p. 73] assert, “the situation for Africa’s children is alarming” showing examples of limited resources in Tanzania, Kenya, Uganda, Zimbabwe, Lesotho, Zambia, and Senegal. It has been argued that many African countries are looking closely at what services might be developed, at what cost, and for what expected benefits for children immediately prior to their entry into primary school [4].
\nTanzania got its independence from British protectorate in 1961. After independence, Tanzania had to reform its education system in order to match the education provision with the needs of its people. But the government found it too expensive to invest in ECEC due to the country’s low and unstable economic status [32]. So the government opened up doors to private institutions to run ECEC, while it concentrated on investing in primary, secondary, and higher levels of education [33]. Since independence, Tanzania has had a philosophy of Education for Self Reliance (ESR) [34]. This made it essential to enrol children in basic education in order for them to become productive members of society by taking on manual work in the community for self-sufficiency after completion of their primary education. The government’s intention was that after having stabilised basic education it would turn back to ECEC matters [31]. ECEC matters progressed slowly with untrained teachers who had no formalised curriculum. Teachers just taught using their own experiences which were not founded in the ECEC area and they had guidelines which were also not prepared by ECEC experts [35]. This situation continued until the 1990s when the international policy statements about children’s rights were declared [36].
\nAs a response to international and national policies advocating the importance of education for young children as a right, the Tanzanian government also adopted this agenda. The government of Tanzania was one of the first in Africa to ratify the United Nations Convention on the Rights of the Child (UNCROC) 1989 in 1991, as well as the African Charter on the Rights and Welfare of the Child [37]. The government also supports the Jomtien Declaration on Education for All (EFA) and the Dakar Framework for Action [38, 39], both of which consider ECEC as a basic right as well as millennium development goals (MDGS) of the 2000s. The World Conference on Education for All held in 1990 at Jomtien, Thailand, marked a new start in the global quest to universalize basic education and eradicate illiteracy. Through the Jomtien Declaration and the Framework for Action, commitments were made and directions set for a decade of large-scale and sustained efforts [38]. The consensus reached at the 1990 World Summit by the countries present at this conference set a target for all children to be enrolled in primary education by the year 2015 [40]. But this is yet to happen in Tanzania.
\nThe situation of children in Tanzania is still not satisfactory, and children are disadvantaged due to the inadequacy of social services, such as schools, health facilities, and environmental services [41]. In Tanzania 200,000 children under 5 years die each year and more than 2 million children are affected with malnutrition number [33, 41] from a total current population is 47.8 million [42]. Furthermore, a study by [33] reported that the few ECEC settings observed had limited resources. Children have no access to education due to high poverty, poor health services, and likewise, street children, pastoralist families (Maasai family) have no permanent settlement so it becomes difficult for them to get access to education [43]. These are just some of the many issues hindering children from getting opportunities to participate in ECEC.
\nThe government normally gets funds from internal and external sources for various uses. External sources are like international agencies such as the World Bank, UNESCO, and UNICEF. All funds, whether internal or external, are collected in one container and thereafter distributed to various sectors. Therefore, the Ministry of Education in Tanzania also gets funds from the government to run educational matters. Funds from various sources, whether internal or external sources are collected in one container, thereafter the amount is allocated to various sectors according to the requirement and the availability of funds. However, the Ministry of Education did not allocate funds for operating preschools. For example, it is argued that the government through the Ministry of Education should supply Quota Budget Code to preschool education. Quota Budget Code refers to the system of supplying grants to schools, teacher education, and higher institutions in a quarterly basis.
\nIn turn, the implementation is problematic; the allocation of funds for the preschool education through Quota Budget Code is not yet implemented. Preschool education does not have its own budget. Instead the funds are allocated to primary school unit hoping that if any extra could support preschool education, however, in reality even the amount allocated for primary schools is not enough to handle primary education matters [6, 36]. Preschool education is therefore funded through parents and community donations organised by local committees. It is apparent that the situation of ECEC services is not improving due to government’s lack of commitment to this type of education.
\nFor that matter, the situation in early childhood education and care settings in Tanzania is not conducive for children to learn various knowledge and skills. For instance, building facilities are poor and not completed and the local community seemed unable to manage the provision of quality teaching and learning resources, let alone donation in monetary form. Therefore, the government policy-makers need to set clear policies regarding how ECEC could be funded and conducted. These facilities were supposed to be provided by the government through the national policy guidelines on how ECEC could be funded and conducted. However, this is not the case.
\nBriefly, it is imperative that ECEC is recognised within education as the foundation for lifelong learning [2, 12]. Numerous countries worldwide recognise that education in the early years lays down the basis for all levels of education. In developing countries, like Tanzania, the situation of education for young children is not satisfactory. There are large numbers of children who do not have access to ECEC settings for a number of reasons such as lack of support from the government, lack of awareness of parents of the importance of early investment, low socio-economic status of parents, traditional norms and cultural values, and gender discrimination. It is recognised by the World Declaration on Education for All (EFA) and the Framework for Action that education is a child’s right [38, 39], and it needs to be valued from early years. It is therefore of the highest priority that access to early childhood education and care services is enabled for all young children. It is within these early years that young children present the greatest ability to learn and develop. All efforts to develop education from the early years onwards should pay consideration to access, quality provision, and relevance to enable children to reach their full potential.
\nA key factor influencing the enactment of curricula is that of teacher qualifications, teacher education, and professional development. In Tanzania, the Ministry of Education, Science and Technology (MoEST) is responsible for initial teacher education (ITE) and professional development. Tanzania’s Education and Training Policy (ETP) insists that the qualification of teachers and their ability to perform well in the class is a key factor in improving the quality education. However, the ETP is silent about the qualifications of ECEC teachers and as a result the implementation of this policy remains in question [40]. In some areas where children have access to early education settings, unqualified teachers work with young children without having knowledge and skill in relation to ECEC matters. Children are taught by retired teachers and volunteers on contractual bases and in other areas they are taught by primary school teachers who also teach primary school pupils as a result they had a heavy workload which reduce their efficiency. But in both circumstances, no professional development is taking place in order to improve the teaching and learning situation.
\nThe concern of poor human resources is important, because qualified teachers with pedagogical skills to work with young children are reflected in positive learning outcomes. The government is responsible for locating qualified teachers as well as professional development; however, this appears not to be happening. A main argument here is that having primary teachers in the preschool resulted in inappropriate teaching styles; they lack the pedagogical skills for teaching young children, as they are not trained to teach young children, and a theoretical understanding of play-based learning is lacking. Literature shows that ECEC teachers do not get opportunities to attend any professional development for teaching a preschool class [30, 33]. As stated by [44], ECEC is a unique area and requires special preparation for ECEC teachers, and ECEC teacher education has a positive impact on teachers and teaching. Early childhood teacher education is envisaged as addressing both present issues and aspirations.
\nA numerous literature show that qualified teachers rich in pedagogical skills to work with young children can demonstrate social interactions, relationships and activities that promote learning and development [12, 13, 19]. Hence, spontaneous and reciprocal interactions within the context of caring relationships are vital components of ECEC. Enabling environments provide “conditions for the kind of teaching and learning that lead to quality outcomes for children, especially qualified staff, low child: adult ratios, small group size, and staff professional development opportunities” [11, p. 18]. Qualified teachers are expected to draw on their knowledge and experience of working with young children and pedagogy to offer the kinds of cognitive and non-cognitive skills that are linked with gains for children.
\nHowever, the situation indicates that the supply of qualified ECEC teachers is grossly inadequate. The government needs to support more teacher education in ECEC and the school inspectorate to supervise the standards and regulations of preschool education. There is also a need for the government to monitor and control preschool education curriculum enactment and pedagogy, including initial teacher education, qualifications, and certification. The lack of initial teacher education and professional development for preschool teachers in Tanzania, results in children who are not well guided due to the teachers’ lack of pedagogical skills.
\nParent and community involvement in children’s educational experiences plays a significant role in shaping children’s social development, cultural values, and practices [45]. The involvement of parents as partners in ECEC settings provides an ongoing system which can reinforce the effects of the programme while it is in process, and helps to sustain them after the programme ends. The involvement of the parents and community as active participants is critical to the success of an ECEC intervention programme [45, 46]. When parents collaborate with teachers in their children’s learning, they also become experts. Parental involvement is thus both a facilitator and a preserver, and the aim of intervention is neither for the parent nor the child on their own, but the parent-child system. It is argued that when parents participate at school and actively support and encourage learning at home, their children are more successful at all levels of education regardless of the parents’ educational background or social class [45].
\nParental participation should be viewed as a continuous process from home environments up to preschool programmes. Parents’ communications with the early childhood centre have educational significance for the child and also for both parents and teachers [2], who learn more about the child from different perspectives and contexts. A study by [45] reports that collaboration between teachers and parents offers the child security and acceptance, and helps the parents to understand more about the child’s areas of development, psycho-physical abilities [9, 46] and where additional stimulation is needed on the part of the teachers or parents.
\nFurthermore, parents are also involved in school-based activities. For example, they participate in school meetings, school committees, especially at community-managed schools [46]; they do manual labour on the school infrastructure, and help to prepare daily meals or snacks at school [45]. Karwowska-Struczyk [47] in Poland articulates that during parent meetings, it is common for the teacher to inform parents what children learn and do and what kind of curriculum activities the teacher proposes for the children. Then parents are free to ask what they would like their children to learn in the ECEC settings.
\nParent’s engagement in children’s education is progressively viewed as an essential support to children’s early learning, care, and education programmes. Effective parent engagement during the period from preschool through the early grades is a key contributor to children’s positive intellectual, socio-emotional skills outcomes, and healthy development [46, 47]. The involvement of parents in preschools takes various forms that can be broadly classified as, home-based parent involvement, for example, parent-child reading and playing various games with children that offer learning enrichment; or community activities, such as volunteer work in building classrooms or renovations, taking children to the library and/or to study tours. School-based parent involvement could be volunteering in a child care or early grades classroom or serving on school committees as well as parent meetings [45].
\nParents’ commitment in a variety of other home and community activities has also been connected to young children’s learning. Also, in the home environment parents’ engagement can include playing alphabet games, helping children with art activities, and telling stories. A number of studies show that parent warmth and responsiveness to children’s interests and needs are vital dimensions of parent engagement that promote children’s learning [45]. Parents’ responsiveness can be observed through home-based activities such as parent-child book reading and the use of praise and encouragement [2, 46]. Therefore, one way that parent nurturance may promote learning is by helping children acquire self-regulation skills that enable them to manage their socio-emotions and behaviour.
\nThe situation of ECEC in Tanzania is alarming. Children from families with low socio-economic status and low-income backgrounds are less likely to participate in ECEC services. The dire situation of people especially in rural area and their failure to enrol their children in ECEC centres has also been found by various writers in other developing countries. For example, [48, 49] found that in rural India, a large number of the households are involved in agricultural and associated activities, and their children are likely to take up this occupation at an early age with or without schooling.
\nA large number of parents/guardians are not enrolling their children in preschools. Amongst other reasons for this is their low socio-economic status and lack of financial support from the government.
\nThis is to say not all parents could afford the continuous demand of school contributions and as a consequence, their children may become involved in child labour, truancy, street children, crimes, and delinquency. Low socio-economic status contributes to poverty, some parents find someone in the community, who seems to be in a good position and requests him to support the family on the promise that he be able to marry their girl child after she has reached a certain age. But that marriage can take place even before her maturity. In the same way, other parents hide their children until they reach school age due to lack of money to pay for ECEC settings. Early marriage is also critiqued by [50] in Kenya, who found that some small girls get married at or before adolescence and begin bearing children as soon as they can. Furthermore, findings from the study conducted by [6] observed that due to poverty, the priority for education was for boys and not a girl child, girls having to remain at home waiting to get married even at a young age. This finding is supported by [51] who found that maternal wage rates and costs of ECEC centres affect children’s enrolment in various settings; an increase in mothers’ wages raises school participation of boys, but lowers that of girls, indicating that girls might substitute for mothers in housework and caring for small children [26].
\nGiven the low socio-economic status of many citizens of Tanzania, it is argued that changes need to be made in order to raise the standard of living of the people. Tanzania is a blessed country with a variety of natural resources including areas of land, mountains, forests, national parks/wildlife, rivers, lakes, coastal zone, fisheries, minerals, coal and natural gas; still the country has failed to utilise the resources in order to support ECEC provision [52]. Many people have low income and no kind of support they get from the government in terms of education for their children. Hence, they fail to enrol their children in the ECEC settings. The Tanzanian government could locate agricultural extension officers in rural areas to give advice on farming inputs and the kind of crops to grow in relation to the weather. This view is supported by [53] who reports that low increases in rural sector productivity are mainly due to inadequate infrastructure investment. The finding is also closely related to that of [54] who reports that in rural areas people live in poverty, they cannot access good social services such as education, clean water, health services, and nutrition.
\nIn Tanzanian context, ECEC is conducted into separate administrative arrangements for care and education as was explained earlier. So, preschool education is a formal school system for children aged 4–5 years. Preschool cycle lasts for 1 year with no examinations for promotion purpose. However, lack of awareness of parents of the importance of preschool education is observed as another reason for parents not sending their children to preschool settings. Based on the lack of awareness and poverty, children do not attend schools as results children look for child labour and for girls end up with early pregnancies. It is also argued that in African context, Tanzanian in particular, a traditional child-rearing system contributes many parents/guardians not enrolling their children in preschool settings [9, 10]. Young brothers and sisters who are also small used to take care of their young children when parents attended individual farms or community activities. African governments need to raise public awareness about the value of preschool education. Low rates of enrolment in preschool education is also explained by [55] in Kenya who found that a lack of public awareness on the value of ECEC for children’s learning and development and a lack of trust of strangers taking care of their children in ECEC settings were amongst the critical issues.
\nExperiences indicate that parents/guardians are not aware of the non-cognitive skills necessary for children’s development. They seem to complain when their children are engaging in play and singing and define it like a waste of time. The view indicates that parents perceive learning as just writing, reading, and arithmetic and not for gaining other skills including motor skills, motivational skills, socio-emotional skills, persistence skills, and self-regulation skills. Indications are that the degree of enrolment of young children in ECEC settings countrywide is low compared to the total number of children. For instance, while the statistics from [56] indicates the total population of children aged 4–5 years old expected to be in enrolled in Tanzania by 2016 was 1,562,770, the actual number of enrolled children was only 710,556 (45.4%). \nTable 1\n below clarifies the situation.
\nEnrolment of 5 -year olds 2016 | \nGross enrolment rate (GER) | \nNet enrolment (NER) | \n(%) of NER | \n||||
---|---|---|---|---|---|---|---|
Country wise | \nM | \nF | \nT | \nM | \nF | \nT | \n\n |
\n | 787,743 | \n775,027 | \n\n1,562,770\n | \n356,127 | \n354,429 | \n\n710,556\n | \n45.4 | \n
The analysis of demands for early childhood education and care prompts a few general conclusions. It can be concluded that not only financial investment in ECEC would change the situation, nevertheless there are a number of other related issues such as governance and financial management, cultural issues, socio-economic status, gender discrimination, awareness of parents/guardians and community of the importance of early education investment, and others that need to receive adequate attention as they tend to strengthen each other in a complementary way. Therefore, to improve the situation, it is recommended that there is need for a forging of partnership between the government, parents, and the community in such endeavour; and that government policy-maker should set clear policies regarding how quality ECEC can be equitably funded and conducted throughout the country. All these issues contribute to the ongoing debate on childhood and family policy in Tanzania. The same matters also deserve consideration in specific research projects and innovative practices.
\nCerebral ischemia is the main disorder of cerebrovascular diseases; currently, according to data from the World Health Organization, it is the second main cause of death worldwide [1] and the third principal cause of disability. In the last 40 years alone, the incidence of this condition has more than doubled in people from low and middle-revenue countries [2].
\nThe increment in the incidence of this condition is due to increased risk factors as diabetes mellitus, hypertension, obesity, hyperlipidemia, and increased longevity of the population [3]. These factors allow the development of atherosclerosis, which is the main cause of ischemia [4]; thereby, it is considered that for the coming years this scenario will be maintained while strategies to reduce these factors are progressing.
\nStroke is distinguished by the brusque reduction of blood flow; therefore, the levels of oxygen and glucose are also reduced significantly, to the point of altering the metabolic activities of the neural tissue [5]. As a consequence of the latter, the low production of ATP and the acidification of the environment induce the depolarization of the membranes causing the intracellular increase of Ca2+ that is added to the one released by the endoplasmic reticulum and mitochondria [6].
\nNeuronal depolarization causes the release of glutamate which, when bound to its ionotropic N-methyl-D-aspartate (NMDA) and -amino-3-hydroxy-5-methyl-4-isoxazolpropionic (AMPA) receptors, achieves greater depolarization and, as a consequence, conditions of excitotoxicity [7]. These conditions are coupled with the production of free radicals [8] and lead to cell death by the activation of molecules that induce necrosis and apoptosis [9].
\nAlong with the lesion caused by the decrease in blood flow, the immune response is added to the events involved in both the detriment of the tissue and its protection.
\nInflammation is usually present before the development of arterial obstruction that gives rise to the ischemic event. The development of atherosclerosis is accompanied by the production of oxygen free radicals (ROS), expression of cell adhesion molecules, and production of proinflammatory cytokines as IL-1β and tumor necrosis factor-α (TNF-α) by endothelial cells [10].
\nShortly after occlusion, endothelial cells express a greater amount of intercellular adhesion molecules (ICAM), deposition of mannose binding lectin molecules that trigger activation of the complement pathway [11], producing higher amounts of ROS. The overproduction of ROS activates the prostaglandin pathway that stimulates the production of matrix metalloproteinases (MMP) that even though degrading constituents of the extracellular matrix, reshape the vascular endothelium seeking to protect of the blood brain barrier (BBB) [12].
\nThe release of chemokines such as CCL2 allows endothelial permeability [13], leading to the translocation of P-selectin from Weibel-Palade bodies, as well as the expression of ICAM-1 and vascular cell adhesion molecule (VCAM)-1 and E-selectin, on the endothelial surface [14]. Theses phenomena, together with the damage of the extracellular matrix facilitate the extravasation of macromolecules and water, which causes the development of vasogenic edema [15]. Peripheral immune cells then enter the injured cerebral parenchyma [16] facilitating the loss of the integrity of the BBB.
\nNeutrophils are the first leukocytes that migrate to the cerebral parenchyma; they have been detected since the first hour after ischemia and reach their maximum peak in 1–3 days [17]. In the clinic, it has been observed that the higher blood neutrophil count is associated with higher infarction volumes in patients with acute stroke [18].
\nThe second cell type that enters the neural tissue are monocytes, these infiltrate within 24 h of the onset of the ischemic event reaching its peak on day 3 [19]; their differentiation process toward macrophages and their activation will be determined by the molecular environment to which they arrive. This process is similar to that experienced by T lymphocytes, which reach the parenchyma 24–96 h post-ischemia [20].
\nAt the same time, the cells of the injured cerebral parenchyma release damage associated molecular patterns (DAMPs) that activate the microglia. Depending on the activation environment, the microglia can acquire a proinflammatory (M1) or anti-inflammatory (M2) phenotype [21]. In the M1 phenotype, the microglia acquires phagocytic capacity, produces NO, free radicals, and proinflammatory cytokines (e.g. TNF-α, IL-12 and IL-6) [22]. Some regions in the ischemic penumbra present an activation of M2 microglia distinguished by the production of anti-inflammatory and repair molecules, such as insulin growth factor 1 (IGF-1), IL-10, and arginase 1 [23].
\nSome researchers suggest that the M2 phenotype is initially activated during the acute phase in the peripheral zone to the infarction [24], since it has been determined that the levels of IL-10, TGF-β, and CD206 increase from the first day after the lesion and reach the maximum point between 4 and 6 days, possibly trying to keep the viability of tissue. In addition, TGF-β induces the anti-inflammatory phenotype of microglia, related with enhanced proliferation and neuroprotection [25, 26].
\nIn contrast, some authors suggest that the first response is proinflammatory [27], due to the loss of regulatory mechanisms; when a stroke occurs there is an important activation of the M1 microglial phenotype [28].
\nAlthough contradictory, both positions could be correct. The fact is that, M1 and M2 phenotypes actively participate in the response observed after ischemic event; however, in normal conditions, there is an important prevalence of the M1 phenotype leading the response to a proinflammatory reaction that, instead of helping, promotes more damage.
\nOn the other hand, perivascular macrophages and monocytes of peripheral origin that arrive at the injured parenchyma induce the synthesis of chemokines like CXCL1 and CXCL2, which are fundamental for recruiting more neutrophils to the injury site [29, 30]. The dendritic cells (DC) present a greater expression of the major histocompatibility complex II (MHCII) and the co-stimulant molecule CD80. This causes an important enhance in the interaction of T cells around and within the damaged areas inducing then a stronger immune response [31].
\nWhen T lymphocytes are activated by antigen-presenting cells (APCs) toward a Th1 phenotype, the secretion of proinflammatory cytokines like as IFN-γ, TNF, and LT-α [lymphotoxin] increases. This cytokine profile, intensify proinflammatory response and thereby, tissue damage. Contrarily, when T cells are activated toward a Th2 phenotype they produce anti-inflammatory cytokines such as IL-4 and IL-10 [32]. These cytokines have been associated with tissue protection mechanisms and even increased neurogenesis. This immune response that exerts protective effects and limits the damage caused by ischemia [19] can be stimulated by immunomodulatory molecules such as copolymer-1.
\nCopolymer-1 [Cop-1], also known as glatiramer acetate (GA) or copaxone [trade name], is a blend of peptides formed by random sequences of four amino acids: glutamic acid, lysine, alanine, and tyrosine; these have a variable length from 45 to 200 amino acid residues and a molecular weight of 4000–9000 Da [33].
\nCop-1 was originally synthesized from mylelin basic protein (MBP) to identify the precise immunogenic sequence and provoke experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS); however, it did not present encephalitogenic characteristics [34]; on the contrary, it has suppressive and protective effects on EAE [35]. In the clinic, copaxone is able to diminish the relapse rate and improve the disability of patients with relapsing-remitting MS [36]. Copaxone obtained its approvement by the Food and Drugs Administration [FDA] of U.S.A. in 1996 and in Europe in 2001 [33].
\nAt this time, the exact mechanism by which Cop-1 exerts its protective effects is not known at all. Studies carried out in EAE suggest that Cop-1 has greater affinity for the MHCII binding site of APC when competing with peptide complexes derived from the MBP, specifically with the epitope 82–100 [37]. This competition may also be present among the complexes for the TCR binding site of the lymphocytes [38] that, when activated, induces a Th2 response [39].
\nThe Cop-1 response is distinguished by increased synthesis of IL-4, IL-5, IL-10, IL-13, and TGF-β [33, 40, 41, 42, 43]. Cop-1 has also been observed to increase the presence of regulatory T lymphocytes [44] and regulatory CD8+ T lymphocytes in patients with multiple sclerosis [45, 46].
\nAnother important effect of copolymer-1 is the production of growth factors, among which stand out; the brain derived neurotrophic factor [BDNF] [47, 48], IGF-1, [49] and neurotrophins NT-3 and NT-4 [47]. It is known that, in addition to inducing neuroprotection and neurorestoration, these growth factors are related to mechanisms such as memory and learning.
\nThe molecular basis by which Cop-1 exerts its neuroprotective effect has been evaluated in several in-vitro assays. The most explanatory results have been obtained in the analysis of the effect of Cop-1 on APC such as monocytes, microglia, and astrocytes.
\nIt has been showed that through the blockade of the nuclear factor kappa B [NF-kB], Cop-1 reduces the expression of the chemokine CCL5 [RANTES], which is upregulated by the presence of IL-1β [50] and TNF-α in human astroglial cells [51]. A similar effect has also been observed on the monocyte chemotactic protein-1 [MPC-1] and adhesion molecules VCAM-1 and selectin E in endothelial cells as well as COX2 and iNOS [52].
\nIt has also been observed that Cop-1 induces differentiation of type II monocytes independently of the binding of Cop-1 to MHCII. Weber et al. demonstrated that this differentiation is due to the fact that Cop-1 reduces the phosphorylation of the transcription factor STAT-1 by stimulating the expression of IL-10 and TGF-β [53].
\nOn the other hand, it has also been observed that Cop-1 has a direct effect on glial cells [microglia and astrocytes] which are activated in conjunction with T cells reducing STAT-1 and STAT-3 phosphorylation through increased expression of cytokine signaling suppressor (SOCS-1) and independently of IFNϒR, accompanied by a reduction of IL-12 by CD4+ T lymphocytes [54].
\nEven though the molecular pathways by which Cop-1 acts are not yet completely established, the microenvironment induced by this compound is capable of allowing neuroprotection since it reduces the deleterious scenario that leads to neural death. Additionally, the new conditions could facilitate tissue restoration through the synthesis of growth factors.
\nThe beneficial effects showed by copaxone in patients with MS, even though the knowledge of its immunomodulatory mechanisms is partial, encouraged the evaluation of its effect in other experimental models.
\nIn the model of optic nerve lesion—which tries to reproduce the characteristics of secondary degeneration—Cop-1 demonstrated an interesting neuroprotective effect. Kipnis et al. [55] evaluated the effect of adoptive anti-Cop-1 T cell transfer and immunization with Cop-1 immediately after causing optic nerve contusion in Lewis rats; their results were very encouraging as they observed reduction in axonal degeneration, accumulation of T lymphocytes in injured areas and obtained a significant increase in IL-10 and BDNF in-vitro. In contrast, using a model of axon transection of the optic nerve, Blair and coworkers [56] found no beneficial effects of Cop-1. The difference in the results may be due to the different inflammatory response evoked by the type of injury (contusion or transection). Inflammation is more pronounced after contusion as compared to the one observed after a transection. It should be an issue to be studied by future investigations.
\nParkinson’s disease presents gradual reduction of dopaminergic neurons in the region of the substantia nigra and the striatum in the brain, it is not known the reason that causes the death of these neurons, but the pathology is characterized by a significant increase in oxidative stress, mitochondrial dysfunction, neuroinflammation, and cell death [57]. Patients with PD present an increase in TNF-β, IL-1β, and IL-6 and other inflammatory cytokines resulting from the activation of the macrophages and microglia towards a proinflammatory phenotype capable of releasing NO and superoxide radicals that further damage neural tissue facilitating disease progression [58].
\nIn the traditional model to induce Parkinson’s disease in mice [induction by 1-1-methyl-1,2,3,6-tetrahydropyridine], it was observed that Cop-1 reduces the degeneration of dopaminergic cells. This effect is achieved since Cop-1 induces the up-regulation in the protein expression of tyrosine hydroxylase [59, 60]. Additionally, it has been reported an increase in glial cell-derived neurotrophic factor (GDNF), reduction of activated microglia markers, and restoration of BDNF [61]. Based in these findings, several research groups consider COP-1 as a pharmacological alternative for this pathology which should be deeply studied [62].
\nCopolimer-1 has also been tested in models of Alzheimer’s disease (AD). AD is a pathology that produces deposits of the β-amyloid protein, dystrophic neurites, loss of synapses and neurons, and elevated gliosis [63]. From the early stages of the pathology, it has been observed microgial activation toward a M2 neuroprotective phenotype that is modified as the disease progresses [64]. In advanced stages, a proinflammatory microenvironment characterized by the presence of cytokines such as IL-1β, TNF-α, IL-6 has been reported [65].
\nAfter Cop-1 administration, microglia modulation toward a M2 phenotype is observed, in such a way as to promote neuronal survival and neural tissue repair in AD models [66]. Butovsky and coworkers showed that Cop-1 immunizations lead to enhanced infiltration of monocyte-derived macrophages into neural tissue with an anti-inflammatory profile expressing minor levels of TNF-α and high levels of IL-10, TGF-β1, and IGF1. In this scenario, phagocytosis of preformed fibrillar amyloid-β by bone marrow-derived macrophages increased dramatically after the administration of Cop-1. Also, to demonstrate benefits on the preservation of cognitive function, the investigation showed an important synaptic protection, plaque removal, restriction of astrogliosis, and modulation of the immune molecular environment [67, 68].
\nAnother pathology that evidenced the beneficial effects produced by Cop-1 is amyotrophic lateral sclerosis (ALS). This is a neurodegenerative disease known by the progressive depletion of the upper and lower motor neurons [69]. During pathogenesis, glutamate excitotoxicity, structural and functional anomalies of mitochondria, damaged axonal structure, and oxidative stress conducted by free radicals are strongly observed [70].
\nIn this case, Angelov and colleagues showed—in mouse models—that the administration of Cop-1 promotes the survival of motor neurons [71].
\nThe beneficial effects of Cop-1 on ALS have been assessed in a Phase II trial conducted by Mosley. This investigation evaluated the cytokine response of ALS patients treated with copaxone and showed that copaxone is capable of inducing a temporary change in cytokines from Th1 to Th2 phenotype [72].
\nCopaxone is also tested in other pathologies at clinical settings. For instance, a phase III study on optic neuritis is now being conducted to evaluate the thickness of the layer of nerve fiber of the retina after 6 months of treatment. The results of this study have not been published. Finally, copaxone has been tested in Crohn’s disease and various types of carcinomas, studies where copaxone is in evaluation processes [73].
\nThe ability of Cop-1 to modify the proinflammatory milieu and to stimulate the production of growth factors encourages the idea of testing this compound on other pathologies with characteristics of secondary degeneration caused by inflammation. In line with this, the use of Cop-1 after stroke envisions an optimistic result.
\nAs copolymer-1 has been shown to have beneficial effects in various models where neuroinflammation is a detrimental determinant, our group decided to evaluate its neuroprotective effect on cerebral ischemia. For this purpose, we used the median transient cerebral artery obstruction (tMCAO) model. Sprague-Dawley male rats were used. After being subjected to ischemia for 90 min, the rats were immunized in the interscapular region with a dose of 200 μg of Cop-1.
\nIn the first study, the animals were evaluated for neurological deficit at day 1 and day 7 post-ischemia using the Zea Longa scale [74]. Then, a histological analysis was performed using hematoxylin and eosin staining to determine neuroprotection. The results indicated that Cop-1 is able to avoid up to 85.1% increase in infarct size (4.8 ± 1.5 for Cop-1 vs. 32.2 ± 8 for control group; p = 0.004 mean ± SD; Figure 1A) and is able to reduce neurological deficit on day 7 post-ischemia.
\nNeuroprotective effect of the copolymer-1. (A) Infarction size reduction. (B) Effect of the copolymer-1 on the neurological deficit. n = 8. Each bar represents mean ± SEM. Two-way repeated measure ANOVA. Sidak’s post hoc multiple comparisons test. *p < 0.05; **p < 0.0.
This neuroprotective effect may be due to the reduction of the proinflammatory cytokines TNF-α and IL-1β and the increase of IL-4, as was observed by the Manguin group in a model of ischemia in diabetic mice [75]. Additionally, the production of neurotrophic factors—known to be implicated in the processes of neural survival and proliferation of neuron precursor cells—could also be involved [76].
\nOn the other hand, recovery from neurological deficit can be achieved by diverse mechanisms; for instance, neuroprotection exerted by Cop-1 could be limiting tissue damage caused by inflammation, this could allow the proper functioning of remaining neuronal connections. Functional recovery could also be the result of neurogenesis induced by Cop-1. Neurogenesis is a phenomenon that can replace neurons that died during the ischemic insult by allowing the substitution of neuronal circuits and thus neurorestoration.
\nOur study provided evidences about the neuroprotective effect of Cop-1; however, the fact that Cop-1-induced T cells are able to produce neurotrophic factors, led us to think that, it was imperative to investigate if behind the clinical recovery there was also a possible neurogenesis phenomenon.
\nIn the following study, we evaluated whether Cop-1 induces neurogenesis in the two neurogenic niches of the adult brain: in the subventricular (SVZ) and the subgranular zone of the dentate hippocampus gyrus (SGZ) [77]. To accomplish the evaluation, we performed an immunofluorescence technique using a double marking of 5-bromo-2′-deoxyuridine (BrdU) and doublecortin (Dcx) at 7 and 60 days after ischemia.
\nThe results were very encouraging, the neurological recovery caused by Cop-1 was observed from day 7 post-ischemia as in the first experiment [78] and was improving even in the chronic phase at 60 days (Figure 1B). The number of neuroblasts in the groups treated with Cop-1 was significantly higher in the two neurogenic niches at both 7 and 60 days in the SVZ and SGZ (Figure 2). This neurogenic phenomenon correlated with the clinical recovery of treated rats. Simultaneously, an important increase of NT-3 was observed in the area of the ischemic penumbra [79].
\nEffect of copolymer-1 on neurogenesis at 7, 14, and 60 days. (A) Neurogenesis in SVZ at 7 and 60 days. (B) Neurogenesis in SGZ at 7 and 60 days. (C) Neurogenesis in SVZ and SGZ at 14 days. n = 8 in A and B. n = 5 in C. Each bar represents mean ± SEM. Two-tailed Mann-Whitney U test. Dunn’s post hoc multiple comparison test. *p < 0.05, **p < 0.01, ***p < 0.001. SVZ: Subventricular zone and SGZ: Subgranular zone.
Cop-1-induced neurogenesis has been evaluated in other animal models such as EAE [47], Alzheimer [66], and recently in the model of permanent cerebral ischemia in diabetic male mice C57Bl6 [75]. Regarding the latter, it is important to mention that, in a previous experiment carried out by the same group, they did not observe improvement in the neurological function nor reduction in the volume of the infarction. These findings could be the result of the use of inappropriate evaluation techniques [80] as in their most recent study, they observed a reduction in infarct size of up to 30–40% and an increase in neurogenesis 7 days after permanent ischemia in the SVZ. In addition, they found a reduction of proinflammatory cytokines such as TNF-α, IL-1β, and a significant increase of IL-4 and IL-10 [75].
\nNeurogenesis is a mechanism widely regulated by signals that stimulate the stem cells of neurogenic niches [81]; many of these signals are produced by the choroid plexus (CP), which is a complex structure of cells considered an interface that mediates communication between the immune system and the cerebral parenchyma [82]. Therefore, trying to analyze the mechanism by which Cop-1 induces neurogenesis, we evaluate whether Cop-1 modifies the microenvironment of CP, 14 days after tMCAO.
\nIn the third investigation, we evaluated neurological recovery—which was observed according to our previous experiments [78, 79], neurogenesis and the expression of proinflammatory (IL-1β, TNF-α, INF-ϒ, and IL-17) and anti-inflammatory cytokines (IL-4 and IL-10) as well as the concentration of growth factors (BDNF, NT-3 and IGF-1) at the CP (Figure 3).
\nEffect of the copolymer-1 on the expression of growth factors and IL-10. Gene expression of: (A) BDNF; (B) NT-3; (C) IGF-1; and (D) IL-10. Bars represent mean ± SEM of 5 rats from each group. *p < 0.05, **p < 0.001. Mann-Whitney U test. Dunn’s post hoc multiple comparison test.
In this experiment, we again proved a significant increase of neurogenesis in the groups treated with Cop-1 in both, the SVZ and SGZ [83]. This data was similar to that previously reported [79]. As for the expression of proinflammatory cytokines, we only found significant differences in the expression of IL-17, which was observed reduced in the groups treated with Cop-1. With respect to anti-inflammatory cytokines, only IL-10 was significantly increased. In this investigation, we also found a significant increase of growth factors (BDNF, NT-3, and IGF-1) in the CP [83].
\nBoth growth factors and IL-10 have been reported to be directly involved in the stimulation of SVZ and SGZ stem cells; specifically, IL-10 has been observed to induce stem cell proliferation but not differentiation in primary cultures [84]. Moreover, IL-10 has immunomodulatory capacity as it inhibits the synthesis and release of proinflammatory cytokines such as TNF-α, IL-6, and IL-1β that are known to affect neurogenesis [85]. Moreover, growth factors such as NT-3 maintain viable stem cells from neurogenic niches facilitating plasticity [86]. BDNF promotes the proliferation and survival of neuroblasts [87] and IGF-1 promotes stem cell differentiation and migration of neuroblasts [88]. Therefore, this investigation allowed to demonstrate that Cop-1 is capable of raising the expression of IL-10 and growth factors, which have beneficial effects on neurogenesis.
\nIn order to know if Cop-1 modulates the number of leukocytes in CP and to know if these intervene in the synthesis and release of growth factors and IL-10, we evaluated the cell types present in the cerebrospinal fluid in animals submitted to tMCAO and Cop-1 therapy. The results showed a significant increment in CD8+ T cells, which positively linked with the increase in growth factors and IL-10 [unpublished data].
\nThe increase in CD8+ T lymphocytes has been observed as an effect of copaxone immunization in patients with MS [46]. In addition, experiments performed in the EAE model have considered these cells indispensable for the development of the beneficial effect of Cop-1 [89]. However, it is necessary to identify the nature of these cells and whether the type of CD8 T lymphocytes is of a regulatory phenotype.
\nFinally, the combination of Cop-1 with other strategies like polyunsaturated fatty acids has shown optimistic results as together, they have a greater capacity to significantly reduce the size of the infarction in the tMCAO model [unpublished data].
\nThe existing evidence of the effect of Cop-1 in the tMCAO model has been very encouraging, as it shows a significant neurological recovery. This beneficial effect could be caused by modulatory mechanisms that allow the increase of IL-4 and the reduction of TNF-α and IL-1β at the lesion site, promoting then neuroprotection. Additionally, neurological recovery could also be reinforced by the changes induced by Cop-1 at the CP as the increase of IL-10 and growth factors in this site stimulate neurogenesis after ischemia. We consider that more investigations are needed in order to analyze in greater detail the mechanism by which Cop-1 acts so that in the medium term, it may be considered as a pharmacological alternative for patients suffering from a cerebrovascular event.
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\n\n4.2 Nothing in this Publication Agreement shall have the effect of excluding or limiting any liability for death or personal injury caused by negligence or any other liability that cannot be excluded or limited by applicable law.
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\n\n5.1 IntechOpen has a right to terminate this Publication Agreement for quality, program, technical or other reasons with immediate effect, including without limitation (i) if the Corresponding Author or any Co-Author commits a material breach of this Publication Agreement; (ii) if the Corresponding Author or any Co-Author (being an individual) is the subject of a bankruptcy petition, application or order; or (iii) if the Corresponding Author or any Co-Author (being a company) commences negotiations with all or any class of its creditors with a view to rescheduling any of its debts, or makes a proposal for or enters into any compromise or arrangement with any of its creditors.
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\n\n6. INTECHOPEN’S DUTIES AND RIGHTS
\n\n6.1 Unless prevented from doing so by events outside its reasonable control, IntechOpen, in its discretion, agrees to publish the Chapter attributing it to the Corresponding Author and any Co-Author.
\n\n6.2 IntechOpen has the right to use the Corresponding Author’s and any Co-Author’s names and likeness in connection with scientific dissemination, retrieval, archiving, web hosting and promotion and marketing of the Chapter and has the right to contact the Corresponding Author and any Co-Author until the Chapter is publicly available on any platform owned and/or operated by IntechOpen.
\n\n6.3 IntechOpen is granted the authority to enforce the rights from this Publication Agreement, on behalf of the Corresponding Author and any Co-Author, against third parties (for example in cases of plagiarism or copyright infringements). In respect of any such infringement or suspected infringement of the copyright in the Chapter, IntechOpen shall have absolute discretion in addressing any such infringement which is likely to affect IntechOpen's rights under this Publication Agreement, including issuing and conducting proceedings against the suspected infringer.
\n\n7. MISCELLANEOUS
\n\n7.1 Further Assurance: The Corresponding Author shall and will ensure that any relevant third party (including any Co-Author) shall, execute and deliver whatever further documents or deeds and perform such acts as IntechOpen reasonably requires from time to time for the purpose of giving IntechOpen the full benefit of the provisions of this Publication Agreement.
\n\n7.2 Third Party Rights: A person who is not a party to this Publication Agreement may not enforce any of its provisions under the Contracts (Rights of Third Parties) Act 1999.
\n\n7.3 Entire Agreement: This Publication Agreement constitutes the entire agreement between the parties in relation to its subject matter. It replaces and extinguishes all prior agreements, draft agreements, arrangements, collateral warranties, collateral contracts, statements, assurances, representations and undertakings of any nature made by or on behalf of the parties, whether oral or written, in relation to that subject matter. Each party acknowledges that in entering into this Publication Agreement it has not relied upon any oral or written statements, collateral or other warranties, assurances, representations or undertakings which were made by or on behalf of the other party in relation to the subject matter of this Publication Agreement at any time before its signature (together "Pre-Contractual Statements"), other than those which are set out in this Publication Agreement. Each party hereby waives all rights and remedies which might otherwise be available to it in relation to such Pre-Contractual Statements. Nothing in this clause shall exclude or restrict the liability of either party arising out of its pre-contract fraudulent misrepresentation or fraudulent concealment.
\n\n7.4 Waiver: No failure or delay by a party to exercise any right or remedy provided under this Publication Agreement or by law shall constitute a waiver of that or any other right or remedy, nor shall it preclude or restrict the further exercise of that or any other right or remedy. No single or partial exercise of such right or remedy shall preclude or restrict the further exercise of that or any other right or remedy.
\n\n7.5 Variation: No variation of this Publication Agreement shall be effective unless it is in writing and signed by the parties (or their duly authorized representatives).
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\n\nAny modification to or deletion of a provision or part-provision under this clause shall not affect the validity and enforceability of the rest of this Publication Agreement.
\n\n7.7 No partnership: Nothing in this Publication Agreement is intended to, or shall be deemed to, establish or create any partnership or joint venture or the relationship of principal and agent or employer and employee between IntechOpen and the Corresponding Author or any Co-Author, nor authorize any party to make or enter into any commitments for or on behalf of any other party.
\n\n7.8 Governing law: This Publication Agreement and any dispute or claim (including non-contractual disputes or claims) arising out of or in connection with it or its subject matter or formation shall be governed by and construed in accordance with the law of England and Wales. The parties submit to the exclusive jurisdiction of the English courts to settle any dispute or claim arising out of or in connection with this Publication Agreement (including any non-contractual disputes or claims).
\n\nLast updated: 2020-11-27
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